A T U R E S
Carbon Nanotubes: Bearing Stress Like Never Before Aditya Limaye 6
Earthquakes Induced By Stress Harjit Singh B S J
t r e s s Fall 2013
Cancer Due to Prolonged Inflammation Nithya Lingampalli
Effects of Cortisol On Physical and Psychological Aspects of the Body and Effective Ways By Which One Can Reduce Stress Preethi Kandhalu 14
The Experimental Effects of Stress On Fertility & Possible Solutions to the Problem Jenna Koopman 17
Fracking: An Industry Under Pressure Jo Melville 22
The Language of Science: What Ideas Do We Stress? Jahlela Hasle 29
The Potential for Abuse: Addiction Ramandeep Dhillon 38
Poverty and Stress Neel Jani 42
Spider Silk: Stronger Than Steel? Alexander Scott Powers 46 i • Berkeley Scientific Journal • Stress • Fall 2013 • Volume 18 • Issue 1
Optimizing Stress Abigail Chaver
R E S E Arē’sûrch’ R C H & I N T E /̓intər,vyōō/ R V I E W
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Building a Bridge for the Future with Professor Abolhassan Astaneh-Asl Ali Palla, Kuntal Chowdhary, Jingyan Wang, Joshua Hernandez, Kaitlyn Kraybill-Voth, Mariko Nakamura, Jessica Evaristo 50 An Afternoon with Professor George Bentley Kuntal Chowdhary, Harshika Chowdhary, Manraj Gill, Atiriya Hari, Rhea Misra, Jess Evaristo, Ali Palla 55 A Discussion on an Integrative Society with Professor Amani Nuru-Jeter Kuntal Chowdhary, Joshua Hernandez, Jessica Evaristo, Jingyan Wang, Ali Palla, Harshika Chowdhary, Mariko Nakamura, Kaitlyn Kraybill-Voth, Rhea Misra 61 An Interview with Professor Michael Shapira Kuntal Chowdhary, Manraj Gill, Mariko Nakamura, Kaitlyn Kraybill-Voth, Atiriya Hari, Ali Palla 65
Research: Managing the Weed-Shaped Hole: Improving Nitrogen Uptake and Preventing Re-invasion in Urban Riparian Restoration Nathan Bickart 71 Evolution of the phosphatase gene family across nematode worms and flies Paulina Tsai and Melissa A. Wilson Sayres 87 ii • Berkeley Scientific Journal • Stress • Fall 2013 • Volume 18 • Issue 1
C O N T A C T
/stāf S T/ A
Mailing Address Berkeley Scientific Journal 5 Durant Hall #2940 Berkeley, CA 94720-2940 Phone Number (510) 643-5374
B /S J
bē ěs jā/
Alvin Huang Jessica Robbins Nithya Lingampalli
Email firstname.lastname@example.org Online bsj.berkeley.edu
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Dear Reader, I am pleased to introduce the first issue in Berkeley Scientific’s 18th volume. Twice each year, Berkeley Scientific publishes undergraduate research, interviews with distinguished Cal faculty, and feature articles spanning diverse scientific disciplines. This semester, we chose to explore stress in different realms of scientific thought. How does one clearly define stress? In the human body, stress takes on the form of various chemicals and stress-inducing hormones, thereby altering the body’s physiology. Preethi Kandhalu explores the biological mechanisms of stress on page  and Jenna Koopman provides a cautionary description on the dangers stress can have on fertility on page . On pages  and , Integrative Biology Professors George Bentley and Michael Shapira talk about their research and how it pertains to biological mechanisms of stress. However, stress is not limited to the biological systems. Engineers depend heavily on creating safe structures in which extreme levels of physical stress are applied. Structural failures result in perilous consequences, as witnessed by the devastating building collapse in Savar, Bangladesh earlier this year. On page , Aditya Limaye sheds light on the current technology surrounding carbon nanotubes and its properties that make it a suitable candidate for 21st century infrastructure. Tensile strength is not limited to large physical objects, however—on page , read Alex Power’s entertaining article on how spider silk is perhaps strong enough to withstand an oncoming train. With new scientific information filling new textbooks annually, how do we decide what particular ideas to stress? On a more philosophical level, Jahlela Hasle writes about the “language of science” and its inevitable evolution over the years on page . We invite you to join us in exploring the many ways in which stress factors in our lives, from the social to the biological, to the mechanical, to the linguistic. Go Bears! Sincerely, Prashant Bhat Editor-in-Chief
Interview Editors Associate Interview Editor and Team
Abigail Chaver Aditya limaye alexander Scott Powers Harjit Singh Jahlela Hasle Jenna Koopman Jo Melville Neel Jani Nithya Lingampalli Preethi Kandhalu Ramandeep Dhillon Kuntal Chowdhary Ali Palla Atiriya Hari Harshika Chowdhary Jessica Evaristo Jingyan Wang Joshua Hernandez Kaitlyn Kraybill-Voth Manraj Gill Mariko Nakamura Phyllis Wang Rhea Misra
David Ding Eric Huang
Alexander Yang Kevin Antony Renee Salz
( ) 18 1 Design & Layout Editors
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Lucy Zhang Spring Chau
Hadrien Picq Isabeth Mendoza Jingting Wu Kim Li Liza Polyudova
Cancer Due to Prolonged Inflammation Nithya Lingampalli
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Inflammation has long been accepted as the most standard, and perhaps the most effective, response that the body has in place to fight both external and internal pathogens.
What mechanisms are activated when your body is invaded by pathogens? How do these mechanisms interact with other pathways in the body? Scientists have considered these questions for years in order to determine exactly how we fight diseases and how we can amplify our body’s defense system. Inflammation has long been accepted as the most standard, and perhaps the most effective, response that the body has in place to fight both external and internal pathogens. This mechanism is considered useful because it activates whenever a threat is present,
“Trouble can arise when these immune cells have been genetically damaged or attacked by mutagenic cells (initiated cells). When this DNA mutation occurs, the immune cells continue to proliferate at the site of an injury even though they are no longer needed (Coussens and Werb). “
http:// web.mit. edu/
Figure 1: Endoscopic biopsy showing granulomatous inflammation of the colon in a case of Crohn’s disease.
and becomes inactive upon restoring health. However, in some instances this inflammation continues to propagate, now harming cells and threatening to expand throughout the body. This prolonged inflammation gives rise to multiples forms of cancer. In this article we will consider the mechanism of inflammation and how it is activated in the body. To understand how this mechanism can become
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uncontrollable, we will look at the possible Trouble can arise when these immune cells routes of mutation, factors that can trigger such have been genetically damaged or attacked by mutations, and the negative effects they cause. mutagenic cells (initiated cells). When this DNA Finally, we will consider everyday actions that mutation occurs, the immune cells continue to cause this prolonged inflammation that can proliferate at the site of an injury even though eventually develop into cancer. Inflammation is a mechanism triggered “This uncontrolled proliferation when pathogens invade our sensitive, highly is a trademark of all forms advanced immune system. When you are injured, either externally or internally, immune of cancer, and hence we can cells around the affected area release a variety see that there is a reflexive of proteins and other factors that promote cell proliferation and regeneration. However, relationship between cancer and release of factors occurs only for a limited inflammation (Rakoff-Nahoum, period of time, and positive feedback of the 2006). “ repaired area prevents the immune cells from releasing more factors. As the damaged cells are repaired or regenerated, they cease to excrete the chemicals that attracted the immune cells. they are no longer needed (Coussens & Werb, This decrease in signaling factors conveys a stop 2002). This uncontrolled proliferation is a message to the immune cells, which then cease trademark of all forms of cancer, and hence their reparative mechanism and recede. This we can see that there is a reflexive relationship process of inflammation is vital in the body as between cancer and inflammation (Rakoffit is responsible for reparative processes such Nahoum, 2006). as, “tissue remodeling, angiogenesis, and other wound-healing features” (Demaria, Pikarsky, Although the link between prolonged Karin, Coussens, Chen, El-Omar, Trinchieri, inflammation and cancer has become a major Dubinett, Mao, Szabo, Krieg, Weiner, Fox, topic of study recently, the link between the two Coukos, Wang, Abraham, Carbone, Lotze, was noticed as early as 150 years ago. In 1863, 2010). Virchow observed that there was an unusually strong correlation between sites where chronic inflammation was present and sites where cancer later manifests (Lu, Ouyang, Huang, 2006).
Figure 2. Inflammed cancer cells
Numerous studies have found that there are more factors involved than simply the uncontrollable production of cells that cause cancer. Rather, this proliferation requires the support of an environment that is, “rich in inflammatory cells, growth factors, activated stroma, and DNA-damagepromoting agents…” (Coussens & Werb, 2002). Thereby, it is now understood that not only is cell proliferation necessary, but it must also be supported by a cell environment that both supports the cell growth and its rate of regeneration. Both of these features combined promote neoplastic risk, which is
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the probability of the appearance of abnormal tissue growth (tumors) (Coussens & Werb, 2002).
responses through changes in cell proliferation, cell death, cellular senescence, DNA mutation rates, DNA methylation, and angiogenesis (Schetter et al, 2010).
A supportive cell environment not only supports the expansion of cancer, but may also Nuclear factor kappa B, a particularly important factor, plays a role in perpetuating make it more deadly. After the initial infection, cancer when it is activated from its dormant the mutated cells and the surrounding cell factors develop a type of communication system that can aid them in their proliferation. Cancerous cells themselves hijack some of “Hence, since the cells are no longer the communication mechanisms present in the inflammatory system and use them to able to die, they continue to grow and further their own growth and development develop, promoting chemoresistance throughout the host (Coussens & Werb, 2002). and tumorigenesis. While this factor After hijacking these signaling systems, the seems to be clearly implicated in tumor cells have a much more elaborate and propagating cancer, it has also been powerful system at their disposal that they can found to be a potential therapeutic then use to mutate beyond their initial purpose target.” of reparation through the use of processes such
“A supportive cell environment not only supports the expansion of cancer, but may also make it more deadly.” as “transformation, survival proliferation, invasion, angiogenesis, metastasis, Figure 3. Prostate cancer cells chemoresistance, and radioresistance…” (Aggarwal & Gehlot, 2009). This hijacking process progresses to the extent that the survival and proliferation of most types of cancer stem state in the cytoplasm. The activation of this genetic factor causes a suppression of cells seem to be dependent on the activation apoptosis, or cell death. Hence, since the cells of these inflammatory pathways (Aggarwal & are no longer able to die, they continue to grow Gehlot, 2009). Hence, through deep integration and develop, promoting chemoresistance and with the inflammation pathway, the cancer tumorigenesis. While this factor seems to be cells are able to further their own infection of clearly implicated in propagating cancer, it has the host. also been found to be a potential therapeutic target. Most chemopreventative agents are The specific factors through which the thought to primarily suppress Nuclear factor inflammatory system can be commandeered kappa B production, indicating that it is a into helping cancer cell proliferation are, major factor in facilitating the spread of cancer. “nuclear factor kappa B, reactive oxygen Further optimization of this method may lead and nitrogen species, anti-inflammatory to further developments in more efficient and cytokines…” (Schetter, Heegaard, Harris, successful cancer treatment and prevention 2010). The collective activity of these factors programs (Bharti & Aggarwal, 2002). can induce pro-tumorigenic inflammatory 3 • Berkeley Scientific Journal • Stress • Fall 2013 • Volume 18 • Issue 1
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When considering cytokines, there are two types that are of interest: anti-inflammatory and inflammatory. Generally, anti-inflammatory cytokines play a vital role by acting as inhibitors regulating the inflammatory system after the necessary repairs have occurred. However, sometimes they may fail to properly control the inflammatory activity within the cell or overcompensate by decreasing the immune response from the necessary levels needed for protection. In the first case, when the antiinflammatory cytokines are unable to properly control the inflammatory response, there is an increase in cell proliferation and growth, which then promotes cancerous growth (Opal & DePalo, 2000). Cellular senescence refers to the aging of the cells. “Senescence, perceived as a cancer barrier, is paradoxically associated with inflammation, which promotes tumorigenesis” (Pribluda et al, 2013). This is because although cells that undergo senescence prevent cancer in that they lose their ability to produce viable offspring, they also increase their production of inflammatory cytokines. As discussed previously, these inflammatory cytokines prevent cytokine inhibitors from controlling the inflammatory response and allow it to
perpetuate over a prolonged period of time, thus promoting tumorigenecity. (Ren, Pan, Lu, Sun, Han, 2009). The factors discussed above play a major role in mutating a DNA sequence from its original strand to a more powerful viral strand. Mutation rate refers to the rate at which base pairs within a given sequence are mutated. A faster mutation rate is characteristic of developing cancer cells as their high rate of proliferation makes them more prone to mutation accumulation. A factor that is linked to increasing the mutation rate is known as miR-155, and further research may indicate that this is a viable therapeutic target for controlling these pro-tumorigenic factors (Ohio State University Medical Center, 2011). Non-genetic factors that can increase the inflammation-cancer risk include free radicals, which are considered the hallmarks of tumor progression. Free radicals, molecules that are unstable due to extra outer shell electrons, have been shown to play a role in tumor initiation and development by increasing metastatic potential (the potential for cancer to spread from one organ to another), especially in tumors (Arrabal, Cordon , Leon, Román-Marinetto, Del Mar Salinas-Asensio, Calvente, Núñez, 2013).
Figure 4. (1) Acute inflammation (2) chronic inflammation with hyperplasia and dysplasia (3) and carcinoma (4) Hematoxylin and eosin
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Everyday factors that have long-reaching effects in abnormally activating these inflammatory pathways, and increasing the risk of inflammation-induced cancer include tobacco, mental stress, diet, and alcohol. These factors are responsible for up to 95% of all cancers as a result of many mechanisms, including the inflammation-induced pathway (Aggarwal & Gehlot, 2009). In conclusion, although the inflammatory pathway is vital for our survival as it repairs and restores the body’s cells, it can also be turned against the body due to the negative influence of many everyday factors. Once the inflammatory pathway begins to produce regenerative cells, despite having fixed the necessary problem, this becomes a trademark site of tumor production. The further prolonging of this regeneration increases the metastatic potential of these tumors, and makes it more likely that the cancer will spread to organs throughout the body. Many factors such as nuclear factor kappa B, reactive oxygen and nitrogen species, and anti-inflammatory cytokines have been shown to play having key roles in this mechanism. The direction of future cancer research is to better understand the activation pathways of these factors so that they can be manipulated to prevent or slow tumor growth. Although the stress that prolonged inflammation places on one’s cells is deadly, there is still hope for a cure in the near future.
References: Arrabal SR, Cordon FA, Leon J, et al. Involvement of free radicals in breast cancer. Springerplus. 2013; 2:404. doi: 10.1186/21931801-2-404. Aggarwal BB, Gehlot P. Inflammation and Cancer: How friendly is the relationship for cancer patients. Curr Opin Pharmacol. 2009; 9(4): 351-369. doi: 10.1016/j.coph.2009.06.020. Bharti AC, Aggarwal BB. Nuclear factor-kappa B and cancer: its role in prevention and therapy. Biochemical Pharmacology.
Coussens LM, Werb J. Inflammation and cancer. Nature. 2002 December 19; 420(6917): 860-867. doi: 10.1038/nature01322. Demaria S., Pikarsky E., Karin M., Coussens L.M., Chen Y.C., El-Omar E.M., Trinchieri G., Dubinett S.M., Mao J.T., Szabo E., et al. Cancer and inflammation: Promise for biologic therapy. J. Immunotherapy. 2010;33:335–351. doi: 10.1097/ CJI.0b013e3181d32e74. Lu, Haitian, Weiming Ouyang, and Chuanshu Huang. Inflammation, a Key Event in Cancer Development. Molecular Cancer Research 4.221 (2006): 5-261. Web. 7 Oct. 2013. <http:// mcr.aacrjournals.org/content/4/4/221.full#cited-by>. Ohio State University Medical Center (2011, April 19). How inflammation can lead to cancer. ScienceDaily. Retrieved October 7, 2013, from http://www.sciencedaily.com¬ / releases/2011/04/110419091159.htm Opal SM, DePalo VA. Anti-Inflammatory Cytokines. Chest Journal. 2000; 117(4): 1162 – 1172. Doi: 10.1378/ chest.117.4.1162 Pribluda A, Elyada E, Wiener Z, et al. A senescenceinflammatory switch from cancer-inhibitory to cancerpromoting mechanism. Cancer Cell. 2013; 24(2): 242-256. doi: 10.1016/j.ccr.2013.06.005 Rakoff-Nahoum S. Why cancer and inflammation? Yale Journal of Biology and Medicine. 2006;79(3-4):123–130. Ren JL, Pan JS, Lu YP, et al. Inflammatory Signaling and Cellular Senescence. Cell Signal. 2009; 21(3): 378-383. doi: 10.1016/j. cellsig.2008.10.011 Schetter AJ, Heegaard NH, Harris CC. Inflammation and cancer: interweaving microRNA, free radical, cytokine and p53 pathways. Carcinogenesis. 2010; 31(1): 37–49. doi: 10.1093/ carcin/bgp272.
Image References: http://web.mit.edu/newsoffice/2012/ cancer-inflammation-h-pylori-0611.html http://ajpgi.physiology.org/content/286/3/G361 http://www.33rdsquare.com/2012/06/ prostate-cancer-drug-trial-stopped-so.html
2002; 64(5-6): 883-888.
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Evolution of the
phosphatase gene family across nematode worms and flies Paulina Tsai and Melissa A. Wilson Sayres
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Department of Integrative Biology, College of Letters and Science, University of California at Berkeley Keywords: evolution, phosphatase, nematodes, Drosophila, phylogeny
Abstract Phosphatase genes have been shown to be involved in male meiosis in the nematode worm, Caenorhabditis elegans, and are expressed in the testis in the fruit fly, Drosophila melanogaster. However, the evolution of this multi-gene family among nematodes and flies had not previously been investigated. We conducted a phylogenetic analysis of all genes in the phosphatase gene family across nematodes and flies using sequences from a 6-way alignment of nematode worms and a 15way alignment of insects, including 12 Drosophila species. We found that: 1) multiple alignments contain spurious alignments that should be filtered for quality control; 2) several gene sequences with incomplete open reading frames are highly conserved, so may actually be functional genes; and, 3) the phosphatase gene family appears to have expanded independently in the common ancestor of nematodes, and again in the common ancestor of flies (but not all insects). Introduction Protein Phosphatase Type 1 (PP1) is a major eukaryotic protein serine/threonine phosphatase that regulates a large variety of cellular functions and processes, such as glycogen metabolism, muscle contraction, cell division, and many more, through the dephosphorylation of many substrates (1, 2). Phosphorylation of specific serine, threonine, and/or tyrosine residues controls the expression of about onethird of all eukaryotic proteins (3). Over 400 protein serine/threonine kinases and ~25 protein serine/ threonine phosphatase have been identified across eukaryotes (4). Global analyses of proteins and protein domains performed on Caenorhabditis elegans reveal that protein kinases comprise the second largest family of protein domains in nematodes (5). It seems that while the number of protein kinases has steadily increased during eukaryotic evolution, the serine/
threonine phosphatases have not increased to the same extent, but the diversity of their interacting polypeptides has increased enormously (3). PP1 has been shown to be necessary for mitotic progression in Drosophila, and that the other loci cannot supply sufficient activity to complement loss of expression of this gene (6). Further research has shown that PP1 genes are essential for male meiosis in C. elegans (7). Curiously, phosphatase genes are also expressed in the testis in many species, including Drosophila melanogaster (8). Both C. elegans, and D. melanogaster have large phosphatase gene families, but it is not clear whether these genes families expanded in the common ancestor of invertebrates, in the common ancestor of nematodes independent of the common ancestor of flies, or only in the C. elegans and D.melanogaster lineages. We used bioinformatics methods and comparative genomics
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Reference species C. elegans C. elegans C. elegans C. elegans C. elegans C. elegans C. elegans C. elegans C. elegans C. elegans C. elegans C. elegans C. elegans C. elegans C. elegans D. melanogaster D. melanogaster D. melanogaster D. melanogaster D. melanogaster D. melanogaster D. melanogaster D. melanogaster D. melanogaster D. melanogaster
name C25A6.1 C34D4.2 C47A4.3 F23B12.1 F25B3.4 F52H3.6 gsp-1 gsp-2 gsp-3 gsp-4 phophatase pph-1 T16G12.7 Y71G12B.30 ZK938.1 flw Pp1-13C Pp1-87B Pp1alpha96A PP1Y1 PP1Y2 PpD5 PpD6 PpN58A PpY-55A
tree code C25 C34 C47 F23 F25 F52 gp1 gp2 gp3 gp4 phos PpH1 T16 Y71 ZK9 flw P13C P87B P96A
accession NM_072031 NM_068724 NM_070249 NM_074173 NM_073069 NM_063766 NM_073332 NM_001027445 NM_059028 NM_058836 NM_072685 NM_073333 NM_066828 NM_001026652 NM_063716 NM_167229 NM_080182 NM_080198 NM_079760
chr chrV chrIV chrIV chrV chrV chrII chrV chrIII chrI chrI chrV chrV chrIII chrI chrII chrX chrX chr3R chr3R
cdsStart 5408511 7154706 13741009 14429030 9565600 10026571 10682502 7336549 4709356 3838390 8084099 10702539 10038436 1818989 9829413 10280544 15253461 8250501 20344380
cdsEnd 5410055 7155913 13742233 14430478 9568680 10027785 10685823 7338116 4710422 3839433 8085221 10704457 10039983 1822932 9830618 10301512 15254370 8251410 20346216
homologs 4 1 1 1 3 2 5 4 2 1 4 6 4 4 4 15 12 12 12
Pp1Y1 PP1Y2 PpD5 PpD6 P58A P55A
AF427493 AF427494 NM_079968 NM_080208 NM_058036 NM_057341
chrU chrYHet chr2R chr2L chr2R chr2R
8549613 279994 17929317 3109719 17768978 13843048
8550146 291785 17930358 3110730 17769953 13843993
1 1 14 9 7 10
Table 1. Phosphatase gene information. analyses to take advantage of recent large-scale sequencing efforts, to better understand the evolution of the phosphatase gene family. Specifically we asked when, evolutionarily, the phosphatase gene family expanded. In doing so, we also addressed issues relating to sequencing quality and alignment.
Materials and Methods Sequences PP1 DNA sequences (Table 1) were downloaded from UCSC for the 6-way nematode alignment and the 15-way Drosophila alignment (7). We analyzed the currently sequenced nematode genomes in the 6-way nematode alignment (Caenorhabditis elegans: WS190/ce6, C. brenneri: WUGSC 6.0.1/caePb2, C. briggsae: WUGSC 1.0/cb3, C. remanei: WUGSC 15.0.1/caeRem3, C. japonica: WUGSC 3.0.2/caeJap, and Pristionchus pacificus: WUGSC 5.0/priPac1), and the insects available in the 15-way insect alignment including 12 Drosophila species, mosquito, honeybee
and red flour beetle (Drosophila melanogaster: BDGP R5/dm3; D. simulans: droSim1; D. sechellia: droSec1; D. yakuba: droYak2; D. erecta: droEre2; D. ananassae: droAna3; D. pseudoobscura: dp4; D. persimilis: droPer1; D. willistoni: droWil1; D. virilis: droVir3; D. mojavensis: droMoj3; D. grimshawi: droGri2; Anopheles gambiae: anoGam1; Apis mellifera: apiMel3; Tribolium castaneum: triCas2). We also downloaded the yeast phosphatase gene sequence (Table 1). Quality control All phosphatase sequences from the multiple alignments were analyzed within a species. Spurious alignments, where the same genomic location was mapped to more than one gene, were removed, retaining only the sequence with the highest quality alignment. Sequences were analyzed for potential functionality by assessing open reading frames for frameshift and nonsense mutations. Sequences with premature stop codons, frameshift insertions, or
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frameshift deletions were tagged as being potential pseudogenes for downstream analysis. Alignments Homologous sequences were aligned using ClustalW2 (9), PRANK (10) and MAFFT (11).
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Phylogenetic and evolutionary analysis Consensus neighbor-joining and parsimony trees with 1000 bootstrap replicates each were constructed using phylip (12). We built maximum likelihood trees and computed branch-specific substitution rates using PhyML (13). Selection analysis The alignments were screened for putative pseudogenes and internal stop codons, which were removed before computing the sequences into DataMonkey (www. datamonkey.org) to detect site-specific selection (14).
Results Sequence quality We assembled homologous sequences of phosphatase genes from 6 nematodes and 15 insects, and conducted sequence similarity searches across them. We used perl programs to compare the genomic mapping of all sequences within a species, and removed sequences where the genomic location overlapped (suggesting an in silico duplication), retaining the sequence with the most sequence coverage relative to the reference. 46 of the 49 nematode sequences were retained, while 81 of 150 insect sequences were retained.
We used Datamonkey (14) to determine the mean dN/ dS ratio and positive and negative selection on our alignments. Our results yielded a mean dN/dS ratio of 0.18357 across the tree, which is indicative of purifying selection. There were no positively selected sites detected across the alignment of phosphatase genes, but 337 negatively selected sites (with 0.1 significance) were identified. After applying a Bonferroni correction for multiple testing (one test for each of the 561 codons: 0.05*561 codons = corrected p-value of 8.91266 x 10-5 or less) Datamonkey reported 223 negatively selected sites, suggesting that this gene family evolves under strong purifying selection across lineages.
Discussion This study showed that the phosphatase gene family appears to have expanded independently in the common ancestor of nematodes, and again in the common ancestor of flies. There was an additional lineage-specific expansion of phosphatase genes in C. elegans. In addition, we determined that great care must be taken when using publicly available multiple alignments to avoid in silico errors that may mislead results.
Phylogenetic analysis We tested three different tree-building programs: Neighbor Joining (NJ), Maximum Parsimony (MP), and Maximum Likelihood (ML). All three treebuilding methods yielded qualitatively similar results; we present the findings from the ML trees.
Sequence quality During preliminary analyses with the multiple alignments for nematodes and insects, we noticed peculiar clusterings. Upon further investigation, we identified that, in a many species, the same genomic location was mapped to several phosphatase homologs. This led to artificially identifying homologs. To remove these in silico alignment errors, we analyzed all paralogous genes in each species individually, and conducted sequence similarity searches. We compared the genomic mapping of all sequences within a species. We retained the sequences with unique mappings, and, in the case of overlapping segments, we retained only the sequence with the highest coverage relative to the reference. 46 of the 49 nematode sequences were retained, while only 81 of 150 insect sequences were retained. It is noteworthy that nearly all sequences identified as orthologs in the mosquito, honeybee and red flour beetle, are excluded using this quality filter. Although it is possible that all of these orthologs were lost independently in mosquito, honeybee, and red flour beetle, these results suggest that these phosphatase genes likely do not have homologs in the common ancestor of all insects, but that any expansions must have happened after Drosophila diverged from other insects.
Alignments We tested three alignment algorithms, ClustalW2, PRANK and MAFFT, aligning both the nucleotides and amino acids with all methods. Similar to previous analyses (14), we observed that PRANKC (PRANK, aligning the codons) and MAFFT outperformed ClustalW2, but observed similar alignments between PRANKC and MAFFT, except that PRANKC failed multiple times to run for the full dataset of 128 sequences. As such, we proceeded with the analysis using the MAFFT alignments.
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pseudogenes, might bias the results, so we attempted to computationally define sequences that were likely to be nonfunctional. For the sequences that were uniquely mapped, we defined a set of putative pseudogenes as those sequences that had disrupted open reading frames, including missing start or stop codons, or if the nucleotides were not in multiples of three (frameshift insertions or frameshift deletions). We labeled these sequences with a “q” at the beginning of the file names, for “questionable”. Phylogenetic analysis Maximum likelihood is a parametric statistical method that uses an explicit model of character evolution, which gives a large number of parameters that can account for differences in the probabilities of particular states, changes, and differences in probabilities of change among the characters. This makes ML more powerful than both NJ and MP, non-parametric statistical methods (15). We used PhyML to compute the Maximum Likelihood tree
for each set of alignments. PhyML uses Maximum Likelihood algorithm to estimate phylogenies from alignments of nucleotide or amino acid sequences, which we created in MAFFT. PhyML is good for large data sets, has a large number of substitution models coupled to various options to search for phylogenetic tree topologies, and also incorporates branch-length estimation (13). Assessing putative pseudogenes We first analyzed the phylogenetic relationship and branch lengths of all sequences (Figure 1). We expected that the putative pseudogenes might have long branch lengths, relative to orthologs in other species with functional open reading frames. This assumes that the pseudogenization event was old, and so the pseudogenized orthologs have been evolving under relaxed constraints (and so might accumulate more mutations, particularly nonsynonymous mutations) than functional coding orthologs. Curiously, however, the branch length analysis shows that many putative
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pseudogenes have quite short branch lengths. This would result if the pseudogenization event was very recent, and so there hasn’t been enough time for the nonfunctional sequence to accumulate many mutations. Alternatively, because many of these sequences are low coverage, it is possible that many putatitive pseudogenes only have a nonfunctional open reading frame because of a sequencing or assembly error. We do note, however, that some putative pseudogenes do have extremely long branch lengths relative to orthologs with functional open reading frames. These are likely to be nonfunctional sequences. Figure 1. Maximum likelihood phylogenetic tree comparing all aligned phosphatase homologs across insects, nematodes, and yeast. The aligned MAFFT sequences were run through PhyML. All aligned sequences, including putative pseudogenes, were retained for this analysis for protein alignments. Putative pseudogene sequences, those with an incomplete open reading frame, are highlighted in green (also start with
q). For both figures, the species names are abbreviated using the species and genome build (Caenorhabditis elegans: ce6; C. brenneri: caePb2; C. briggsae: cb3; C. remanei: caeRem3; C. japonica: caeJap; Pristionchus pacificus: priPac1; Drosophila melanogaster: dm3; D. simulans: droSim1; D. sechellia: droSec1; D. yakuba: droYak2; D. erecta: droEre2; D. ananassae: droAna3; D. pseudoobscura: dp4; D. persimilis: droPer1; D. willistoni: droWil1; D. virilis: droVir3; D. mojavensis: droMoj3; D. grimshawi: droGri2; Anopheles gambiae: anoGam1; Apis mellifera: apiMel3; and, Tribolium castaneum: triCas2). Including all sequences, we still observe that most sequences group by orthologous family (Figure 2), and not by paralogs within a species, suggesting that these phosphatase genes expanded prior to the diversification of flies independent of nematodes. However, not all genes are monophyletic by species, so we investigated this further by removing the potentially confounding putatitve pseudogenes.
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Figure 2. Maximum likelihood phylogenetic tree comparing phosphatase homologs with intact open reading frames across insects, nematodes, and yeast. The aligned MAFFT sequences were run through PhyML. Putative pseudogenes were excluded for this analysis for protein alignments. All gene families are colored in a unique color, and all nematode sequences are highlighted in blue, while insects are highlighted in green. Evolutionary relationship between genes and species In the maximum likelihood tree with only sequences with functional open reading frames, we observe a complicated history of the phosphatase gene family. It seems that some phosphatase genes (namely gp1 and gp2) are quite ancestral, whereby the nematode orthologs group closely with a set of homologs in flies. In nematodes, gp1 groups closely with the Drosophila flw genes. Alternatively, the gp2 gene from nematodes groups with an expanded set (P87B, P96A, and P13C) in flies. All of these genes have relatively short branch lengths, suggesting they may be highly conserved. In contrast, the rest of the phylogenetic tree is composed of genes with much longer branch lengths. Notably, there was an expansion of phosphatase genes in C. elegans that has no homologs in any of the flies or in other nematodes, suggesting that, although there was some expansion of these gene families in the common ancestor of nematodes and flies, there has also been a lineage-specific expansion within C. elegans (Figure 2). The C. elegans specific expansion can also be viewed in the tree with putative pseudogene sequences (Figure 1), but is much clearer in the tree without putative pseudogenes (Figure 2). Selection analysis 223 out of 561 codons (40% of the entire alignment) show evidence of being negatively selected, suggesting that a high proportion of the positions across this gene family are evolutionarily constrained.
Future directions This study was designed to determine whether or not the phosphatase gene family expanded independently in C. elegans and also in Drosophila flies or if it was more ancestral. To expand upon the results of this project, we can resequence these genes in the non-model organisms, to see if the ORFdisrupting mutations were due to sequencing errors, or are actually ORF-disrupting mutations. We can further investigate lineage-specific selection, and look at the protein domains to detect evidence of neofunctionalizatino or subfunctionalization across
this gene family. We can also assess the expression of these genes across the different fly and nematode species, to see if they are sex-specific, or involved in meiosis, as they appear to be in C.elegans. Lastly, we can look at diversity information, and see if there are any signals of selection acting on these genes across or within species.
Conclusion This study found that 1) multiple alignments may contain spurious alignments, where the same genomic location is mapped multiple times, which is especially a problem for multi-gene families; 2) low quality sequences may result in several ORF-disrupting mutations that may appear to be pseudogenes, but may in fact just be sequencing errors; and 3) the phosphatase gene family appears to have expanded in the common ancestor of nematodes, and again in the common ancestor of flies, with an additional lineagespecific expansion in the nematode C. elegans.
1. Cohen, P.T.W., Protein phosphatase 1 – targeted in many directions, Journal of Cell Science, 115, 241-256, 2002. 2. Fong, N.M., Jensen, T.C., Shah, A.S., Parekh, N.N., Saltiel, A.R., and Brady, M.J., Identification of Binding Sites on Protein Targeting to Glycogen for Enzymes of Glycogen Metabolism, Journal of Biological Chemistry, 275, 35034-35039, 2000. 3. Ceulemans, H., and Bollen, M., Functional Diversity of Protein Phosphatase – 1, a Cellular Economizer and Reset Button, Physiological Reviews, 84:1, 1-39, 2004. 4. Plowman, G.D., Sudarsanam, S., Bingham, J., Whyte, D., and Hunter, T., The protein kinases of Caenorhabditis elegans: a model for signal transduction in multicellular organisms, PNAS, 96:24, 13603–13610, 1999. 5. Ceulemans, H., Stalmans, W., and Bollen, M., Regulator-driven functional diversification of protein phosphatase-1 in eukaryotic evolution, Bioessays, 24:4, 371–381, 2002. 6. Axton, J.M., Dombradi, V., Cohen, P.W., and Glover, D.M., One of the protein phosphatase 1 isoenzymes in Drosophilia is essential for mitosis, Cell Press, 63:1, 33-46, 1990. 7. Wu, J., Go, A.C., Samson, M., Cintra, T., Mirsoian, S., Wu, T.F., Jow, M.M., Routman, E.J., and Chu, D.S., Sperm Development and Motility are Regulated by PP1 Phosphatases in Caenorhabditis elegans, Genetics, 190:1, 143-157, 2012. 8. Wu, T.F., and Chu, D.S., Sperm Chromatin: Fertile Grounds for Proteomic Discovery of Clinical Tools, Molecular & Cellular Proteomics, 7, 1876-1886, 2008. 9. Larkin M.A., Blackshields, G., Brown, N.P., Chenna, R., McGettigan, P.A., McWilliam, H., Valentin, F., Wallace, I.M., Wilm, A., Lopez, R., Thompson, J.D., Gibson, T.J., and Higgins D.G., ClustalW and ClustalX version 2, Bioinformatics, 23:21, 2947-2948, 2007. 10. Loytynoja A., Goldman N., An algorithm for progressive multiple alignment of sequences with insertions, PNAS, 102:30, 10557-10562, 2005. 11. Katoh, K., Misawa, K., Kuma, K., Miyata, T., MAFFT: a novel method for rapid multiple sequence alignment based on fast Fourier transform, Nucleic Acids Research, 30:14, 3059-3066, 2002. 12. Edgar, R.C., MUSCLE: multiple sequence alignment with high accuracy and high throughput, Nucleic Acids Research, 32:5, 1792-
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1797. 13. Guindon S., Dufayard, J.F., Lefort, V., Anisimova, M., Hordijk, W., Gascuel, O., New Algorithms and Methods to Estimate MaximumLikelihood Phylogenies: Assessing the Performance of PhyML 3.0., Systematic Biology, 59:3, 307-321, 2010. 14. Delport, W., Poon, A.F., Frost, S.D.W., Pond, S.L.K., Datamonkey 2010: a suite of phylogenetic analysis tools for evolutionary biology, Bioinformatics, 26:19, 2455–2457, 2010. 15. Jordan, G., Goldman N., The effects of alignment error and alignment filtering on the sitewise detection of positive selection, Molecular Biology Evolution, 29:4, 1125-1139, 2012. 16. Graur, D., and Li, Wen-Hsiung, Fundamentals of Molecular Evolution: Second Edition, pp. 181-216, 2000.
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We would like to thank Dr. Diana Chu for preliminary discussions of this topic. Funding for this project was provided by the Miller Institute for Basic Research fellowship to MAWS.
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Conservation and Resource Studies, Alumni, Class of 2013 Research Sponsor: Dr. Katharine Suding Nathan Bickart
Managing the Weed-Shaped Hole: Improving Nitrogen Uptake and Preventing Re-invasion in Urban Riparian
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Keywords: restoration ecology, invasive species control, trait-based filtering, limiting similarity, stable isotope tracer analysis, native plants, riparian restoration, Strawberry Creek, nitrogen pollution, volunteer-based restoration.
As the field of ecological restoration grows, novel methods to improve the effectiveness of restoration projects are being advanced and tested. Here, measured plant functional traits are used to select a native planting palette for the restoration of riparian habitat at Strawberry Creek, a heavily invaded urban ecosystem in Berkeley, CA. I partnered with an active restoration program and together we focused on methods to prevent re-invasion by a dominant non-native understory species and reduce nitrogen pollution of the riparian ecosystem. uptake study revealed a marginally significant (0.05<p<0.10) result suggesting that shrubs may be more proficient at taking up nitrogen, though further research is needed to clarify this finding. This work points to the potential benefits that ecosystem science research and on-the-ground restoration efforts can offer one another.
The field of ecological restoration is growing rapidly in response to increasing humaninduced degradation of the Earth’s ecosystems (1, 2). Despite this growth, there is still much to learn regarding how best to carry out ecosystem restoration (2, 3, 4). Realistic and tangible goal setting (5, 6), scientifically supported restoration techniques (3), and novel theoretical frameworks (7) have all been suggested as mechanisms to improve the success of restoration projects in achieving desirable outcomes.
Rivers, creeks, and streams are often at the epicenter of restoration work (8, 9). Along the West Coast of the United States, efforts to improve fish habitat, particularly for salmon, have directed significant restoration efforts towards these waterways (10). While dense human settlement near creeks may lead to their degradation, human proximity also facilitates connection with these natural spaces and interest in restoring the ecosystem. The restoration of urban creek ecosystems is tremendously challenging: human community needs (e.g. public safety), heavy pollutant inputs (e.g. nitrogen deposition due to combustion processes; see (11)), hydrologic alterations, and frequent disturbance (e.g. trampling) complicate management and make many noble restoration goals infeasible (12).
One significant challenge that many restoration projects face is that of invasive non-native plant species (13), an issue that can be particularly pronounced in urban areas due to the connectivity of urban centers in an increasingly globalized world (14). Restoration of native flora is frequently cited Figure 1. Evidence for the weed-shaped hole near Strawberry Creek on the UC as a goal in restoration projects (15), but can be Berkeley campus: Ivy (Hedera helix, right) previously covered this site. After exceedingly difficult. the ivy was removed from this area, another invasive species, panic veldtgrass (Ehrharta erecta, left), quickly colonized the niche vacated by the ivy.
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Removing invasive species without effectively establishing other desired (typically native) species leaves a “weed-shaped hole” (a niche well-suited for non-native invasive species) that non-natives can quickly re-colonize (16), (Figure 1). Though the hope behind earnest non-native removal efforts is that native species will re-colonize the area once niche space becomes available, the evidence that this occurs without further intervention is limited (12, 17), particularly if the native species have been extirpated from the area and thus propagule material does not exist.
Funk et al. propose the concept of “limiting similarity” to reduce the possibility of re-invasion by non-natives (4). The idea is that non-invasive native species that have similar functional traits to non-natives (i.e. utilize a similar set of resources) are expected to be better competitors and prevent the reinvasion of non-native species (4). ‘Functional traits’ are species’ attributes relating to how the species takes up resources and its effect on the resource pool in the ecosystem (4). The limiting similarity concept encourages practitioners to fill the ‘weedshaped hole’ with native species that will prevent non-native invaders from accessing resources in the ecosystem. Nitrogen is a critically important resource in ecosystem management. Nitrogen deposition has been implicated in facilitating invasion of nutrientpoor California ecosystems by non-native plant species, particularly near urban areas with abundant fertilizer use and combustion-powered machinery (11, 18). Furthermore, nitrogen has the potential to cause eutrophication of downstream waterways if it is provided in excess by urban runoff (19). This work builds off of Cadenasso et al. (20) in that I suggest urban riparian restoration plantings as a method to preventnnitrogen pollution of the watershed. In this article I operationalize limiting similarity in the context of a working, volunteer-based restoration project on the University of California – Berkeley (UC Berkeley) campus. Plant functional traits were measured to filter the regional species pool (‘trait-based filtering, as suggested in (21)) to a set of native plant species best suited to achieve desired project goals, namely to prevent re-invasion by non-native ivy species (Hedera canariensis, canary ivy; and Hedera helix, English ivy), and to prevent nitrogen pollution of the creek and riparian habitat. Within the broader trait-filtering framework, I hone in on the selection of native species with
high rates of nitrogen uptake, as determined by a stable isotope tracer analysis. Enhancing riparian nitrogen uptake has the potential to both slow the rate of nitrogen delivery to the stream (alleviate downstream nutrient pollution) and help prevent reinvasion of riparian habitat by nonnatives (i.e. achieve limiting similarity). Finally, this research serves as an example of the sort of collaboration encouraged by Palmer (3), in which campus scientists inform the work of an ‘onthe- ground’ restoration program, which can then provide feedback with regard to the success of different approaches.
Methods Project Site
Strawberry Creek (37°52’N; 122°15’W) is an urbanized watercourse that runs east to west through Berkeley (Alameda County), California, from the Berkeley Hills (immediately east of the UC Berkeley main campus) to the San Francisco Bay (Figure 2a). The creek has two forks North and South) that converge near the west entrance to the UC Berkeley campus (Figure 2b). The 4.7 km2 watershed drained by the creek is relatively undisturbed in the hills east of the campus, but is for the most part heavily urbanized, with impervious surfaces becoming the norm as the creek flows west through the flatlands of Berkeley (22, 23). The creek flows in underground culverts for the majority of its path, including immediately east and west of the UCB campus. This study focuses on the reaches of the creek within the confines of the UCB main campus, to match the spatial scope of the work done by the partner restoration program. The establishment of the university along the banks of Strawberry Creek led to substantial degradation of its aquatic and riparian habitat. Trash dumping, sewage discharges, and campus lab waste made the creek a toxic site for most of the 20th century (24, 12). The creek’s course and riparian habitat were substantially modified to prevent flooding of campus buildings, which has led to significant incision and channelization (12). In the late 1980s, the Strawberry Creek Restoration Program (SCRP) was born, which led to substantial water quality improvement and native fish reintroduction to the creek (22). Understory habitat at Strawberry Creek is dominated by English (Hedera helix) and canary ivy (Hedera canariensis), both non-native, invasive species. In recent years, the SCRP has shifted its focus to student-led, volunteer-driven understory
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B S J Figure 2. (a) Berkeley, CA, with the University of California’s property and Strawberry Creek highlighted. The UC Berkeley main campus, referred to as the ‘campus’ in the document, is the small rectangle at the western-most point of the UC Berkeley property, west of Memorial Stadium (the Stadium can be seen near the middle of the picture, where the culverted line of the creek splits into two lines). The creek flows in a culvert for nearly the entirety of its trip from the west side of the campus (left edge of this image) to San Francisco Bay (approximately 2.5 miles). (b) The UC Berkeley main campus, with aboveground stretches of Strawberry Creek highlighted and labeled. Green areas represent the campus’ ‘natural areas,’ in which the Strawberry Creek Restoration Program has permission to work. Sites where planting plans were implemented are also highlighted, in neon.
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vegetation management; perhaps the program’s biggest impact has been the removal of vast swaths of ivy from the shores of the creek. Other invasive species like periwinkle (Vinca minor) and panic veldtgrass (Ehrharta erecta) have also been removed, which has resulted in largely unoccupied understory habitat for substantial stretches of Strawberry Creek. To date, re-colonization of this habitat by native plant species has not occurred, and re-invasion of these habitats by weedy species (either that which was removed or a new species) occurs frequently (for example, see Figure 1). Ivy frequently returns to sites from which it was removed, usually as a result of incomplete removal of root biomass. The SCRP has recently increased its native plant output in an attempt to reintroduce native species to the banks of Strawberry Creek; the Program’s interest in discovering which native plant species will do best in this urbanized ecosystem guides this research. Volunteers with the SCRP (both UCB students and members of the Berkeley community) helped clear nonnatives and plant native species at all of the sites mentioned below.
Nine functional traits were measured on 38 plant species native to Alameda County, following from the methods in Cornelissen et al. (25). The regional species pool was narrowed to 38 species through a variety of considerations, most notably through the elimination of native species for which I did not have access to propagule material or species that did not grow well in the SCRP’s on-campus nursery (for species list, see Appendix 1). The 38 species were
almost entirely understory species, a function of the SCRP’s focus on understory management. Species were selected from a variety of different habitat types (e.g. redwood forest, riparian, wetland, grassland) to minimize the possibility of ‘pre-selecting’ species assumed to do well at Strawberry Creek. In addition to the native species, functional traits were measured on two non-native species: canary and English ivy. These species were included to discern the relative differences in traits between the native and nonnative species, an important prediction of limiting similarity. Ages and propagation methods were standardized across functional groups, to the extent practicable (Appendix 2); the SCRP’s long-standing nursery program had some gaps in records, making it difficult to determine the exact age or geographic origin of some individuals.
The selected traits relate to diverse aspects of species morphology (Table 1). When possible, ratios were used instead of raw values (e.g. proportion of fine roots rather than mass of fine roots) to minimize the effect of any age differences. All trait measurements were taken on plants grown in nursery settings (e.g. in potting containers and a standardized potting soil). Trait measurements were taken on five replicate individuals for each plant species, then averaged across the replicates. The five replicates were spaced across five blocks in the nursery and species position within each block was randomized to minimize neighbor effects or the effects of divergent growing conditions.
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N tracer analysis
Plant nitrogen uptake is a focal point of this research, but was treated differently from the traits listed above. I aimed to discover how nitrogen uptake rates vary across species of different growth forms (functional groups) and geographic origins (native/ non-native). A nitrogen-15 stable isotope tracer analysis was conducted to address these questions. For this analysis, five species representing four 15 functional groups were given N-labeled ammonium chloride injections (Table 2). These species were also included in the broader trait-based filtering study. Individuals used for the nitrogen uptake analysis were all of the same age (approximately 6 months since propagation) and were all sourced from the Strawberry Creek watershed. Our interest in controlling these factors, in addition to cost constraints, motivated the choice to evaluate nitrogen uptake only on representative species from
each functional group, rather than test all species. As above, propagation methods were standardized within functional groups. Inaddition to four native species, the nitrogen uptake rate of canary ivy (the more prevalent of the two ivy species at Strawberry Creek) was also analyzed, to allow for the comparison of native and non-native uptake rates. Five replicate 15 individuals of each species were given N injections.
This work follows from James & Richards (28) in terms of quantity of nitrogen delivered to the system. I assumed that in an urban setting, nitrogen will most likely be delivered to the riparian corridor in ‘pulse’ events carrying large amounts of nitrogen, e.g. rainstorms. However, Imodified the methods in James & Richards (28) to adjust for the size of the SCRP’s planting containers (i.e. surface area and amount of soil) and different percent enrichment of 15 N (98% atom enrichment compared to 10% atom 15 enrichment in (28)). In total, I added 2 mg of N (as
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7.64 mg of NH4Cl, molar mass 53.491 mg) in a 176.7 mL solution with de-ionized water (simulating a 10 mm rain event over the surface area of exposed soil, as in (28)) to each plant. 15
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The labeled nitrogen solution was added to the soil via syringe injection. The solution was delivered via 18 injections in a circle around the base of the plant, to a depth of 10 cm. I attempted to label all parts of the soil column uniformly, injecting the solution into the soil at a slow and steady pace as I moved the syringe up through the soil column (29). The plants were harvested 13 days after injection. I chose to wait for a relatively long period of time between injection and harvest because this analysis was carried out in the non-growing season (injections on December 21st, harvest on January 3rd). The decision to perform the injections in the winter was pragmatic, based on this project’s timeline. Plants were kept dry (not watered) for the week prior to injection and were not watered for the 13 days following injection. After the 13 days had passed, the plants were harvested and all plant biomass was dried and weighed. Leaf samples (youngest fully formed leaves, as above) and root samples (a representative sample incorporating different root sizes) were collected for each plant; each sample was then ground and homogenized. Roots and leaves remained separate throughout this process. Approximately 5.5 mg of each sample was then weighed into tin capsules, yielding 50 samples: 5 species x 5 replicates x 2 samples/individual (1 leaf sample and 1 root sample). These samples were combusted in an elemental analyzer, and isotopic ratios were analyzed by a mass 15 spectrometer, yielding leaf and root N content for each individual plant.
To visualize the interspecific differences in species’ traits, a principal component analysis (PCA) was conducted for the nine traits (listed above) across forty species. Specifically, I looked to see how the native plant species would group, in terms of species traits, relative to the nonnative species and one another.
To evaluate how much labeled nitrogen each species had taken up in the 13-day study period, I 15 examined the δ N (per mil) values for the roots and leaves of the five focal species, calculated relative to an ACM Peach standard sample according to Formula (1) below: (1) δ N(per min, compared to standard)= [(Rsample-Rstandard)/(Rstandard)]*1000 15 14 Where R = (Atom% N)/(Atom% N) 15
In addition to evaluating the δ N data by species, I also conducted of set of t-tests, for which 15 I grouped the N species into binary categories: shrub or non-shrub, and native or non-native. This allowed me to maximize the number of replicates in a group while still addressing the question at hand: how does nitrogen uptake vary across species of different growth forms (specifically, woodier versus less woody species) and geographic origins (native/ 15 non-native)? The δ N data was analyzed through a series of two-way t-tests assuming unequal variance: native shrubs (n=10, 2 species) v. all non-shrubs (including ivy, n=15, 3 species); native shrubs v. native non-shrubs (excluding ivy, n=10, 2 species); native species (n=20, 4 species) v. the non-native ivy (n=5); and native shrubs v. ivy. To compare total 15 plant nitrogen uptake of each group, the δ Nleaf and 15 the δ Nroot values for each individual plant were summed and then averaged across the species or group in question. This method emphasizes total plant uptake of nitrogen, rather than the relative proportion of nitrogen taken up into roots or shoots. Upon noticing that most of the interspecific variation 15 in δ N rates was a result of differences in leaf uptake rates, the same t-tests were conducted using only the 15 δ Nleaf data, yielding 8 t-tests in total. 15
Results Trait-based filtering
The first two axes of the PCA explained almost half of the trait variation in the dataset, with axis 1 explaining 25% of the variation, and axis 2 explaining 19.6% of the variation (Figure 3). Importantly, the two ivy species grouped together at very high root-to-shoot and chlorophyll values, and very low proportion of fine root values. These non-native species are also notably separate from the rest of the species within the trait space. Of the native species, Oxalis oregana (oxor, redwood sorrel) and Polystichum munitum (pomu, sword fern) appear to be the most similar, in terms of functional traits, to the non-native ivy species (heca and hehe, Figure 3).
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were only marginally significant at best. Two of the t-tests to discern differences in leaf uptake rates by group showed marginally significant differences (0.05<p<0.10), while the others were not significant (p>0.10) (Figure 4b). The comparisons of δ15Nleaf between native shrubs and all non-shrubs (p=0.084, t=2.18, df=12) and between native shrubs and ivy (p=0.084, t=2.2, df=11) suggested that shrubs had marginally higher uptake rates. There were no differences in leaf uptake rates between native shrubs and native non-shrubs (p=0.136, t=2.18, df=12) and natives and the ivy (p=0.157, t=2.36, df=7).
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Figure 3. PCA for the 40 species and 9 traits studied. Species are in black, traits in red. Species codes correspond to the code names given in Appendix 1. Note that the ivy species (hehe and heca) group together at very high root-toshoot (rts) and chlorophyll values, and very low proportion of fine root (propF) values. Trait codes correspond to those given in Table 1.
By measuring plant functional traits on the regional species pool, we now have a database of information to help ‘filter’ the pool to an appropriate list of species and guide restorative plantings. Below, I suggest a few ways to utilize this data and create planting plans to achieve the desired project goals: preventing re-invasion of riparian habitat by the nonnative ivy species and reducing nitrogen pollution of the riparian corridor.
The combined root and shoot δ N values were not significantly different for any of the intergroupcomparisons conducted: native shrubs v. all non-shrubs (two-tail p=0.249, t=2.12, df=16),native shrubs v. native non-shrubs (p=0.272, t=2.2, df=11), native species v. the non-native ivy(p=0.57, t=2.57, df=5), or native shrubs v. ivy (p=0.425, t=2.36, df=7) (Figure 4a). 15
Figure 4. a) Combined root and leaf N uptake rates (δ N, summed by individual plant, then averaged by species. Species codes correspond to those given in Table 2. No significant results were found for the pairwise t-tests between native shrubs and all non-shrubs, native shrubs compared to native non-shrubs, native species compared to the non-native ivy, or native shrubs compared to the 15 15 non-native ivy. b) Leaf N uptake rates (δ N), averaged by species. Marginally significant results (0.05<p<0.10) were found for the t-tests between native shrubs and all nonshrubs, and between native shrubs and the non-native ivy. The comparisons between native shrubs and native nonshrubs and between natives and the ivy showed no statistically significant differences.
Most of the interspecific variation in uptake rates appeared to come from differences in leaf uptake rates, but these differences in leaf uptake
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Trait-based planting plans
The PCA was analyzed in two ways to design planting plans in accordance with project goals. First, in an effort to achieve limiting similarity, species that grouped with the ivy species (and thus have traits similar to the ivy) were identified in the PCA and a planting plan was designed around these species. Oxalis oregana (oxor, redwood sorrel) and Polystichum munitum (pomu, sword fern) were both included in this planting plan. Full planting plans are shown in Table 3.
The second planting plan maximizes functional diversity in traits, in an attempt to fill all available niche spaces and thus prevent reinvasion by any non-native species. Species for this planting plan were selected from all around the PCA trait space; for example, Claytonia perfoliata (clpe, miner’s lettuce), Eriophyllum staechadifolium (erst, lizard tail), and Juncus phaeocephalus (juph, brown-headed rush) were all included in this planting plan.
Statistically marginal evidence indicated higher nitrogen uptake rates in native shrub species, particularly for leaf uptake, when compared against non-shrubs and the non-native ivy. A third planting plan was developed based off this information, in which woodier species like Cornus sericea (creek dogwood) and Mimulus aurantiacus (sticky monkey flower) were prioritized in an attempt to maximize nitrogen uptake at these sites (Table 3). Each of the three planting plans was implemented four times, once at each of four similar sites along the South Fork of Strawberry Creek (Figure 2b). Over 100 SCRP-led volunteers, many of whom had earlier cleared ivy from the sites, planted the plans over two days in early February 2013. Total plant biomass must be considered when 15 evaluating the nitrogen uptake data. δ N values are effectively per gram values, such that if two individual plants have the same δ15N as reported here, the plant with more biomass will have taken up more nitrogen, in total. With this in mind, a better 15 way to evaluate δ N data in the future would be to 15 scale the δ N by plant biomass (or by the biomass
Table 3. Planting plans established at 4 sites along the South Fork of Strawberry Creek. Each subplot was planted with 29 individuals according to the planting plans below, such that each planting plan (subplot design) was planted once at each planting site (four times total). The orientation of the planting plans with respect to one another within a site was randomized across the four sites to reduce neighbor effects. The location of each plant within each subplot was also randomized. Species not included in the trait-filtering analysis but included in the planting plans are asterisked.
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of the specific plant part being analyzed, e.g. total leaf weight). The data collected for this study was 15 insufficient to properly scale up the δ N value to account for total plant biomass. Particularly because 15 the (albeit marginally significant) differences in δ N values observed here occurred across functional groups, future research that explores shrub versus non-shrub species uptake, while scaling for biomass, could resolve some of the questions left unanswered by this research.
Also of note is that most of the interspecific or inter-group variation in uptake rates was observed in the leaf data, rather than the root data. While a representative sample of all root sizes was taken 15 for the root δ N-analysis, only the youngest fullyformed leaves were taken for the leaf analysis. This suggests that interspecific differences in uptake of nitrogen may be more pronounced in new growth: 15 perhaps the trend of increased δ N in shrub species would become clear given more time to grow in the presence of the added nitrogen. However, the experimental framework used here related to a ‘pulse’ of nitrogen to the system, and thus was unable to address questions of nitrogen uptake operating over longer time scales.
More detailed analyses should be completed in the future to uncover inter-functional group differences in nitrogen uptake. Here, coverage of several functional groups was prioritized over replication of individual species or functional groups; study with more than five replicates for each species, or with more than two or three species for each functional group, might be better equipped to evaluate inter-group differences.
work. In this case, both parties benefitted from the collaboration: the restoration program received invaluable expertise and a quantifiable database on which to base the season’s plantings, and the academic lab gained access to a nearby ‘outdoor laboratory’ that could serve as a testing ground for developing ecological theory. Though this approach had some limitations (e.g. limits to what species could be outplanted at Strawberry Creek), it also had extraordinary benefits, particularly in terms of outreach, as volunteers working on the creek were able to participate in and learn about the research being conducted. A transparent goal-setting and decision-making process for species selection engages volunteers and stakeholders in a way that is lacking in many restoration efforts (e.g. projects that plant natives just because they are natives, without further explanation).
In addition to serving as an example of researchinformed restoration practice, this work also uncovered a marginally significant trend indicating higher nitrogen uptake in native shrub species when compared against a dominant non-native species or members of other understory functional groups. Though this trend needs to be confirmed in future research, it suggests a path forward for restoration work on Strawberry Creek in which native plantings both prevent reinvasion of a non-native species and enhance nitrogen uptake in the riparian corridor.
Post-project monitoring will be the true test of the effectiveness of the trait-based framework in achieving project goals. In addition to collecting data on percent ivy reinvasion and nitrogen content in the soil surrounding Strawberry Creek, survivorship data on the native species outplanted will help us to determine which species do well in the unique urban ecosystems at Strawberry Creek, and which traits might predict this success.
This project serves as an example of a pragmatic collaboration between university scientists and on-the-ground, volunteer-driven restoration
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References 1. Young, T.P., Restoration ecology and conservation biology, Biological Conservation, 92, 73-83, 2000. 2. Suding, K.N., Toward an Era of Restoration in Ecology: Successes, Failures, and Opportunities Ahead, Annu. Rev. Ecol. Evol. Syst., 42, 465-487, 2011. 3. Palmer, M.A., Reforming Watershed Restoration: Science in Need of Application and Applications in Need of Science, Estuaries and Coasts, 32, 1-17, 2009. 4. Funk, J.L., Cleland, E.E., Suding, K.N., and Zavaleta, E.S., Restoration through reassembly: plant traits and invasion resistance, Trends in Ecology and Evolution, 30.10, 2008. 5. Hobbs, R.J., Setting Effective and Realistic Restoration Goals: Key Directions for Research, Restoration Ecology, 15.2, 354-357, 2007. 6. Hobbs, R. J., and Norton, D.A., Towards a conceptual framework for restoration ecology, Restoration Ecology, 4.2, 93–110, 1996. 7. Hobbs, R.J., Higgs, E., and Harris, J.A., Novel ecosystems: implications for conservation and Restoration, Trends in Ecology and Evolution, 24.11, 599-605, 2009. 8. Bernhardt, E.S., Palmer, M.A., Allan, J.D., Alexander, G., Barnas, K., Brooks. S., et al., Synthesizing U.S. River Restoration Efforts, Science, 308, 636-637, 2005. 9. Kondolf, G.M., Anderson, S.D., Storesund, R., Tompkins, M., and Atwood, P., Post-Project Appraisals of River Restoration in Advanced University Instruction, Restoration Ecology 19.6, 696-700, 2011. 10. Kondolf, G.M., Personal communication, September 2011, Department of Landscape Architecture and Environmental Planning, College of Environmental Design, University of California-Berkeley, 2011. 11. Weiss, S.B., Cars, Cows, and Checkerspot Butterflies: Nitrogen Deposition and Management of NutrientPoor Grasslands for a Threatened species, Conservation Biology, 13.6, 1476-1486, 1999. 12. Pine, T., Personal communication, January 2012, Office of Environmental Health and Safety, University of California-Berkeley, 2012. 13. D’Antonio, C., and Meyerson, L.A., Exotic plant species as problems and solutions in ecological restoration: a synthesis, Restoration Ecology, 10.4, 703–713, 2002. 14. Cohen, A.N., and Carlton, J.T., Accelerating Invasion Rate in a Highly Invaded Estuary, Science, 279, 555558, 1998. 15. Hallett, L.M., Diver, S., Eitzel, M.V., Olson, J.J., Ramage, B.S., Sardinas, H., Statman-Weil, Z., and Suding, K.N., Do we practice what we preach? Goal setting for ecological Restoration, Restoration Ecology, 21.3, 312-319, 2013. 16. Buckley, Y.M., Bolker, B.M., and Rees, M., Disturbance, invasion, and re-invasion: managing the weed-
shaped hole in disturbed ecosystems, Ecology Letters, 10, 809-817, 2007. 17. Adams, C.R., and Galatowitsch, S.M., The transition from invasive species control to native species promotion and its dependence on seed density thresholds, Applied Vegetation Science, 11, 131-138, 2008. 18. Bidwell, S., Attiwill, P.M., and Adams, M.A., Nitrogen availability and weed invasion in a remnant native woodland in urban Melbourne, Austral Ecology, 31, 262-270, 2006. 19. Conley, D.J., Paerl, H.W., Howarth, R.W., Boesch, D.F., Seitzinger, S.P., Havens, K.E., Lancelot, C., and Likens, G.E., Controlling Eutrophication: Nitrogen and Phosphorus, Science, 323, 1014-1015, 2009. 20. Cadenasso, M.L., Pickett, S.T.A., Groffman, P.M., Band, L.E., Brush, G.S., Galvin, M.F., Grove, J.M., Hagar, G., Marshall, V., McGrath, B.P., O’Neil-Dunne, J.P.M., Stack, W.P., and Troy, A.R., Exchanges across Land-waterscape boundaries in Urban Systems: Strategies for Reducing Nitrate Pollution, Ann N Y Acad Sci, 1134, 213-232, 2008. 21. Brudvig L.A., and Mabry, C.M., Trait-based filtering of the regional species pool to guide understory plant reintroductions in Midwestern oak savannas, U.S.A., Restoration Ecology, 16.2, 290-304, 2008. 22. Charbonneau, R., and Resh, V.H., Strawberry Creek on the University of California, Berkeley Campus: A case history of urban stream restoration, Aquatic Conservation: Marine and Freshwater Ecosystems, 2, 293-307, 1992. 23. Purcell, A.H., Corbin, J.D., and Hans, K.E., Urban Riparian Restoration: An outdoor classroom for college and high school students collaborating in conservation, Madrono, 54.3, 258-267, 2007 24. Charbonneau, R., Strawberry Creek I: The making of an urban stream, 1860–1960, Chronicle of the University of California, 3, 1–19, 2000. 25. Cornelissen, J.H.C., Lavorel, S., Garnier, E., Diaz, S., Buchmann, N., Gurvich, D.E., Reich, R.B., ter Steege, H., Morgan, H.D., van der Heijden, M.G.A., Pausas, J.G., and Poorter, H., A handbook of protocols for standardised and easy measurement of plant functional traits worldwide, Australian Journal of Botany, 51, 335-380, 2003. 26. Spasojevic, M.J., and Suding, K.N., Inferring community assembly mechanisms from functional diversity patterns: the importance of multiple assembly processes, Journal of Ecology, 100, 652661, 2012. 27. Roumet, C., Urcelay, C., and Diaz, S., Suites of Root Traits Differ between Annual and Perennial Species Growing in the Field, New Phytologist, 170.2, 357367, 2006.
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28. James, J.J., and Richards, J.H., Plant nitrogen capture in pulse-driven systems: interactions between root responses and soil processes, Journal of Ecology, 94, 765-777, 2006. 29. Ashton, I.W., Miller, A.E., Bowman, W.D., and Suding, K.N., Nitrogen Preferences and Plant-Soil Feedbacks as Influenced by Neighbors in the Alpine Tundra, Oecologia, 156.3, 625-636, 2008. Acknowledgements We would like to thank Lauren Hallett, Lawrence Fernandez, Katie Suding, Tim Pine, Martin Alexander, Jesse Fried, and all the SCRP volunteers. I also thank The Green Initiative Fund, The Chancellors Advisory Committee on Sustainability, and the Sponsored Projects for Undergraduate Research Program for their support of this project.
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Notes: ‘Geographic origin’ codes give the location from which the genetic stock of the plant was collected originally: RFS: Richmond Field Station, a UC Berkeley property, or surrounding areas within the same watershed. SC: Strawberry Creek Watershed. Larner: purchased from Larner Seeds, with the precise origin of the genetic material unknown.
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‘How acquired’ indicates whether the plant was propagated in the Strawberry Creek Native Plant Nursery (labeled ‘Nursery’), or originally purchased from another nursery before being housed at the SCNPN. Nursery codes: SBM: San Bruno Mountain’s Mission Blue Butterfly Native Plant Nursery in Brisbane, CA. OTN: Oaktown Native Plant Nursery, Berkeley, CA. NHN: California Native Plant Society’s Native Here Nursery, East Bay, Berkeley, CA. The ‘field division’ propagation method implies that both aboveground and belowground plant parts were taken from a field site and then re-located to a container within the nursery. ‘Cutting’ implies that only aboveground shoot material was removed from an individual in the field. Cuttings were grown in a 3:1 perlite:vermiculite growing medium in the nursery, then transplanted to individual containers once new root growth emerged.
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An Interview with Professor Michael Shapira
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Kuntal Chowdhary, Manraj Gill, Mariko Nakamura, Kaitlyn Kraybill-Voth, Atiriya Hari, Ali Palla The BSJ Interviews Crew had the opportunity to interview Professor Michael Shapira. Professor Shapira received his B.Sc. and his Ph.D. in biochemistry and molecular biology from the Hebrew University in Jerusalem. Following receipt of his doctorate, Professor Shapira moved to the Genetics department at Stanford University School of Medicine, where he trained with David Botstein and Man-Wah Tan as a Life Sciences Research Foundation postdoctoral fellow. Currently, Professor Shapira’s research is focused on understanding the fundamentals of host-pathogen interactions in the context of the whole organism. Through the use of his unique model organism, the soil nematode Caenorhabditis elegans, Professor Shapira’s current point of interest at the lab is pathogen recognition.
BSJ: To start things off, how did you get interested in your research? Prof. Shapira: Well, things have happened as they sometimes do in science. I wasn’t always focusing on C. elegans; I used what seemed to be the most appropriate system at the time to answer a biological question. As my interests in stress and environmental stress conditions evolved to consider genome-wide responses, I moved to work with a eukaryotic unicellular model organism, in which analysis could be more complete, but actually, I was more interested in studying similar stress responses in multicellular organisms. By chance, a nearby lab was working with C. elegans, studying how it dealt with infection. I figured that that was a type of stress, and the system seemed overall very attractive: typically you study a one-sided response to stress, but when studying host-pathogen interactions, you have two sides that are responding to each other. I became increasingly fascinated with this host-pathogen interaction story. Again, nothing really stays the same, I started with stress and moved to the host-pathogen interactions, and before you know it, I’m back to stress.
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BSJ: Why did you choose to work with C. elegans? Much of your research is based on this nematode. Many labs in Berkeley use the mouse or rat as their model organisms. Prof. Shapira: First, the question is “how appropriate is the particular system to answer the biological question” and “what new insights can you get by using this system unlike other organisms that people have been using for a long time”. In that respect, studying host pathogen interactions in C. elegans was new, and we thought we could get new insights by using this system. There were two other factors. Firstly, I did work with mice and human tissues, while I was completing my Ph.D.; I didn’t like working with these models; I preferred to work with invertebrates -- to me it was cleaner. But the main reason was that I wanted to simplify the system I used. For my first postdoc I chose yeast to be able to study genome-wide stress responses. Microarray technology was new then, and with yeast, I felt that I could get the most. I could get into the nitty gritty of the mechanisms, be able to do serious bioinformatics and get new insights. It’s a great system. Working with yeast made me grow affectionate with simple model organisms and the kind of things that you could do with them, both nasty things, but more importantly, the depth of information you can get from that. From yeast, moving to C. elegans was a step up to the ‘real world’ of multicellular organisms, and back to multitissue physiology. In a sense, it’s the middle of the road between the well-defined and genetically tractable model and a complex organism. BSJ: Could you elaborate a little more on your current research now and how it’s related to stress? Prof. Shapira: As I mentioned earlier, we started with infections and stumbled back into stress. We were initially aiming to examine a mechanism of the worm innate immune
Professor Shapira in the lab showing C. elegans, the nematode he works with.
system. The adaptive immune system with all the antibodies and lymphocytes is something that is unique to vertebrates. It’s a relatively recent invention. Innate immunity is something we vertebrates use alongside the adaptive immune system, but invertebrates are completely dependent on it. The innate immune system is quite similar in its function in all animals. We were interested in a mechanism that is activated during exposure to a pathogen. We have a mutant strain, in which a disruption in a gene encoding a MAP kinase is unable to activate the protective response. MAP kinases are enzymes, which play roles in organismal and cellular signaling. They work as part of a ‘pathway’ in which one protein modifies the structure of another protein, which modifies the structure of another protein, leading to changes in the expression of a bunch of genes, many of them serving protective roles. We wanted to generate a situation where we have control over activation of that enzyme that was
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regulating this protective response, a MAP kinase of the p38 family. By ‘knocking-down’ the expression of a negative regulator of the p38 MAP kinase, we were able to activate it. That’s what nice about having C. elegans as a model organism. You can easily decrease the expression of any gene of interest to examine its function. When we knocked down the expression of the negative regulator, we increased the activation of the p38 MAP kinase and the worms were better protected from infection. However, to our surprise, this was true only in developing worms, and when the same knock-down was performed in young adults we saw the opposite effect: worms became more sensitive to infection! It turned out that the negative regulator we targeted regulated not only the p38 kinase, but also a second MAP kinase of the JNK family (pronounced “Junk”), called KGB-1, which when activated in adults showed a new and dominant detrimental contribution to infection resistance. The detrimental contribution of KGB-1 to stress resistance appearing in adults was not unique to infection resistance, but more general, affecting resistance to various environmental stress conditions and further shortening lifespan. Importantly, this experiment exposed an age-dependent reversal in the contribution of a stress-protective mechanism. It turns out that JNK signaling seems to be doing similar things in mammals. It is generally protective, a stress activated protective mechanism, but it’s also associated with a large array of diseases, most of them associated with old age; e.g. tissue damage after stroke, insulin resistance, and neurodegenerative diseases. We thought we might have a handle on conserved mechanisms that are affecting first, how we respond to stress; and second, aging and aging-associated pathologies. Therefore, this experiment has led us into a very basic mechanism of aging.
BSJ: So, is this a transregression mechanism wherein you suppress some of the immune systems first defense? Prof. Shapira: No, not quite. It does suppress the ability to resist infection, but its effects are more general. Let me elaborate on that. Animals have two stress-activated MAP kinase pathways, the P38 and the JNK. In developing animals, both have protective effects. The p38 protects mostly against infection and oxidative stress, and JNK signaling, in C. elegans at least, is mostly for heavy metals and stress due to misfolded proteins, a fundamental problem in aging by the way. However, in young adults (which in worms means two days later), while the activation of the p38 pathway is still protective, activation of the KGB-1 JNK kinase becomes detrimental. It decreases heavy metal resistance, makes the worm more sensitive to infection and shortens life span. A reversal in the contribution of this important mechanism. The characteristics of the KGB-1 switch, responsible for agedependent antagonistic contributions, were apparently described before, or rather predicted. More than 50 years ago, an evolutionary biologist called George Williams suggested a general theory for the evolution of aging, built on a conceptual mechanism he called Antagonistic Pleiotropy. We know that many proteins have pleiotropic effects, which means they can contribute to more than one biological process. Antagonistic Pleiotropy in turn suggests that some proteins are sometimes good and sometimes bad, specifically, good early in life, but bad late in life. It is possible that such mechanisms will be positively selected during evolution because the strength of natural selection decreases as we age. As the extreme, contributions of biological processes appearing past reproductive age have no effect on fitness. So, species can select for mechanisms that are good at the beginning of life although they may be really bad later. These mechanisms together would be the cause of aging.
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BSJ: So along that line, do organisms that undergo stress tend to age more quickly? Or tend to have other side effects that you haven’t talked about.
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Prof. Shapira: Considering that our stressactivated KGB-1 has long-term detrimental effects (including lifespan reduction) when artificially activated in adult animals, it would seem so. This is of course in addition to the damage caused by the environmental stress itself, which is a part of the natural scenario. BSJ: Could you elaborate on how JNK pathways and insulin signaling interactions affect stress resistance and lifespan? Prof. Shapira: Yeah, that’s the one million dollar question that we are interested in. The C. elegans insulin signaling is an important regulator of lifespan and aging, and its relevant human counterpart is the one responding to insulin-like growth factors. It is known that a C. elegans JNK homolog, expressed specifically in neurons (not our KGB-1), positively regulates a transcription factor called DAF-16, which is the main receiver of inputs from the insulin signaling pathway, driving it into the nucleus. This transcription factor can increase stress resistance and extend lifespan. In vertebrates, the homolog that serves similar functions is called FOXO3A. FOXO-3A, as well as DAF-16, are the hallmarks of longevity regulation. They integrate many signals and accordingly induce many stress-protective genes: antioxidants, detoxifying enzymes, etc. The Insulin Signaling pathway keeps DAF-16 phosphorylated which prevents it from going into the nucleus. The C. elegans neuronal JNK homolog also phosphorylates DAF-16, but in a way that drives it into the nucleus, allowing it to increase protective capacities against oxidative stresses. What we found with the other JNK homolog, our KGB-1,
Picture of the nematode is that it also promotes nuclear localization of DAF-16, but only in developing animals Going into adulthood, KGB-1 activation does the opposite, removing DAF-16 from the nucleus. We still don’t understand how this age-dependent antagonistic regulation of DAF-16 occurs. But we have hypotheses, based on the interesting bit that the switch occurs when the animal enters into reproductive age. Initiation of reproduction is a junction point where decisions are made between reproduction and maintenance. In C. elegans, you can easily disrupt germline proliferation and generation of gametes. You have the somatic gonad, but you no longer have any eggs in it. What others have shown was that germline disruption leads to a huge increase in the secretion of steroid hormones from the somatic gonad. Results from the Kenyon, Ruvkun and Antebi labs showed that when these hormones are secreted, they extend lifespan tremendously, which makes some sense because if there is no reproduction there is more investment in maintenance i.e. stress resistance. So, the clue we were given was that KGB-1 activation can reverse some of the effects of these steroid hormones, which suggests that KGB-1 may interact with components of this hormonal signaling
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BSJ: In an ideal organism, there is a mechanism whereby reproduction supersedes maintenance of the organism itself? Prof. Shapira: It’s always a trade-off and the trade-off has been well known for many years. There are exceptions, but typically, mutations that cause increased reproduction would come at the expense of lifespan or stress resistance. Long-lived mutants, in many cases, have smaller brood size. With limited resources, you have to balance how you use your resources. When germline proliferation is inhibited and animals live longer, there are at least two signaling mechanisms that are activated. There is a lot of redundancy in biology. One of the mechanisms is involves the increase in the hormone secretion from the somatic gonad. These hormones act both directly and indirectly, though mostly indirectly, to drive nuclear localization of DAF-16, thereby increasing lifespan. However, when we activated KGB-1, we were able to reverse that. DAF-16 was removed from the nucleus. So, we think that KGB-1may interact with the same signaling mechanism that first sent DAF-16 into the nucleus, downstream to gonadal signaling. This guides our current experiments. BSJ: When a worm becomes reproductive, or it has the capability to reproduce, it’s not in a stressed environment. It’s in an environment where there is an appropriate amount of food, resources that it will be able to use to create the next generation. Thus, you have a greater number of the reproductive hormones in the worm. Would these reproductive hormones have a sort of negative feedback mechanism through which it would affect “the switch”? Prof. Shapira: Well you are asking an interesting question, a little bit complicated because it assumes that we know everything, which we don’t. I think that much of the
mechanisms enabling such choices operate before reproduction, as adverse conditions rarely appear all of a sudden. In C. elegans, one of the first choices is made during early development, in the second of four larval stages. If conditions are not favorable, worms will leave the normal developmental course leading to adulthood and reproduction. They will go to an alternative larval stage called “Dauer ”, which is stress resistant and longer lived. Consider that the entire lifespan of the worm is about 2 weeks, Dauers can live more than a month. If the conditions become favorable again, it can return to the normal developmental course and continue to reproduction. The good decisions are typically made before reproduction. To a certain extent, once reproduction begins it is already a commitment. BSJ: Pertaining to your work specific to C. elegans, do you have any aspirations for any clinical applications that could evolve to prevent aging? Prof. Shapira: To connect our results to aging in humans, we need to know how relevant are mechanisms we’re observing in C. elegans to those playing roles in human aging, or in aging-associated disease. We have a collaboration where we use mammalian cell cultures and human tissues to examine if there’s a relationship between the age of individuals and the outcome of JNK activation, and whether some of the mechanisms that we exposed in C. elegans play a role in age-dependent outcomes in mammalian systems as well. Specifically we’re looking at people with Alzheimer’s Disease, where JNK activation was shown to be an exacerbating factor. But this is just the beginning, so I have nothing to report about it yet. More generally, C. elegans is one of the best models to study aging, because it is a tractable genetic system and because it is short lived, but also because it turns out that many of the mechanisms that were characterized in C. elegans to affect aging
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were also found to be very important for mammals. One of these is insulin signaling; certain variations in the insulin receptor affect the longevity of C. elegans. Genetic studies in centenarians, people around 100 years old, identified linkage between old age and mutations in genes that affect insulin signaling. So, studying the genetic programs of aging in C. elegans could unravel conserved mechanisms that play similar roles in human aging, and thus may have clinical applications. However, this is usually not an immediate translation. Nevertheless, all considered, I’m pretty sure that our work in this invertebrate model organism could provide valuable insights into our understanding of the process of aging. BSJ: Where do you see your research going? What other facets are you looking into? Prof. Shapira: We are still interested in hostpathogen interactions. A third project in the lab that I have not mentioned yet, focuses on the characterization of the C. elegans gut microbiota, how the host shapes it and what is the significance of microbiota members for their host. I would love to see the three projects come together: for us to understand the contribution of the microbiota to its host physiology – to infection resistance, to environmental stress resistance, and to aging; and also understand how priorities change with age. I believe that the host and its microbiota are one system, with its compound behavior determining the success of all system members. I also believe that aging disrupts relationships in this system leading to misrepresentation and malfunction. I hope that we could prevent, or slow down these changes and help improving the quality of life, now and later in life.
BSJ: Thank you again so much for your time. 70 • Berkeley Scientific Journal • Stress • Fall 2013 • Volume 18 • Issue 1
A Discussion on an Integrative Society with
Professor Amani Nuru-Jeter
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Kuntal Chowdhary, Joshua Hernandez, Jessica Evaristo, Jingyan Wang, Ali Palla, Harshika Chowdhary, Mariko Nakamura, Kaitlyn Kraybill-Voth, Rhea Misra
Though the phrase “stress can kill you” is often used in jest, the broader implications of chronic stress are often overlooked. Chronic stress is the slow poison that kills from within. BSJ Interviews had the pleasure of interviewing Professor Amani Nuru-Jeter to understand the broader implications of the “wear and tear” of stress and explore the root causes of the issue. Professor Nuru-Jeter’s broad research interest is to integrate social, demographic, and epidemiologic methods to examine racial inequalities in health, as they exist across populations, across place, and over the life-course. Professor Nuru-Jeter is also Principal Investigator of the African American Women’s Heart and Health Study, which examines the association between racism stress, cardiovascular biomarkers, and biological stress among Black women in the Bay area with particular focus on coping mechanisms; and Co-Principal Investigator of the Bay Area Heart Health Study which examines similar associations among Black men with particular emphasis on coping mechanisms and internalized racism. BSJ: How did you get involved in your research? Prof. Nuru-Jeter: I have several lines of research
and my work on stress is one of those lines of research. I was working at the department of Health in Washington D.C. where I was getting my M.P.H. at George Washington University. I was doing a lot of work there, around trying to help communities of color and low-income communities navigate the public healthcare system, the Medicaid system, and other social service systems in order to meet their needs. I became very interested in the topic of social equity and inequity. I worked at the department of health and I did that for a year or so. After that, I worked at a non-profit organization and I am still doing similar work. It is interesting to do similar work from different perspectives. There is the government perspective, where we are creating and delivering programs to meet the needs of the community, and the nonprofit
perspective, where you are advocating on the behalf of the community. In both of those positions, I had the opportunity to work with various community groups and that was really my introduction to the disconnect between our service organizations with what we say are communities needs and what communities are saying their real needs are along with their barriers to access these services. I became really interested in the disconnect between service organizations in meeting community needs to better understanding the issues around equity and inequality and why, generally, colored and lower-income communities end up not being served as well as other communities. This sparked my interest in the idea of social inequality and I went back to school for my Baccalaureate and started doing more work in that area. The work that I do is in a field called “social epidemiology”, trying to better understand better how
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social factors, what we call “social determinants of health”, impact population health and health disparity. With my dissertation work in graduate school, one the issues I was working on the community, was one of the issues related to accessing care in relation to high degrees of racial residential segregation and economic residential segregation that isolates these communities from many of the services that they needed. When I went to graduate school, I did my doctoral work on racial residential segregation, concentrated poverty, and differences in mortality between racial groups. That was all pre-Berkeley, when I came to Berkeley as a post-doc with the Johnson Health Society College Program and then joined the faculty two years later. As a post-doc, I began to talk to several psychologists just because of where our offices were situated. There was another post-doc program in the same office space. When I came to Berkeley, I used to think, “People don’t matter, places matter”. These “places” are what we call “macro-level social determinants of health”, structural ways that neighborhoods are set up disadvantaging certain groups and advantaging other groups. As I started talking to more psychologists, I grew to have a greater appreciation for the fact that environmental structures, like racial segregation, impact health in many different ways. Some examples include: having access to care, not having fresh fruits and vegetables in certain neighborhoods, having a greater police presence, or poor housing. One of the things I asked myself in doing this segregation work is, “How does one come to internalize their social position relative to others?” For example, are you aware that your neighborhood is different from other neighborhoods? This issue brought me to this idea of stress, living in these neighborhoods and then perhaps knowing that your neighborhood is systematically different from other neighborhoods. Is there a process of internalizing stress that could impact health? This is how I got to my current work on the embodiment of social stress. Now, I’m greatly focusing on racial discrimination, which, again, has its roots in racial residential segregation. I would consider that to be a marker of institutional discrimination, but there are other forms of racial discrimination. What most people think about are one-on-one interpersonal experiences with racial discrimination. That is what I am studying right now, interpersonal discrimination and how that impacts health disparities among African Americans.
BSJ: What would you define as stress that is caused by this racial discrimination?
Prof. Nuru-Jeter: I define stress as a process. When
I teach about this, I usually start out by saying, “How do you define stress?” Usually I get answers like “The test that I have to take next week”. The type of stress that I am talking about is the kind of stress that actually impacts the body. The “macro-level social determinants of health” that I previously mentioned can be perceived as stressors, so I would say that from social epidemiologist perspective, I would consider these macro-level social environmental factors as the root causes that set everything into process, from the physiological to psychological stresses. Racial residential segregation, including institutional and other forms of racial discrimination, along with environmental stressors impact health by being filtered through individual-level processes. A certain environmental factor can’t be considered a stressor without an individual perceiving it as a threat that begins the biological processes, typically associated with stress. If I had to intervene, reducing people’s biological stresses would be a short-term strategy and would be focused on threat appraisal and coping, which are parts of how we deal with these types stressors. However, those aren’t the root causes, so we can mitigate the short-term problem, but on the other side, this “fix” teeters on the edge of putting the responsibility on the victim to learn to how to cope better. What we really want to do is to create a more equitable society to certain groups of people, who are not disproportionately exposed to social stressors that are going to force them to have to cope with these stressors in the first place. This was the empirical finding in the analysis of our research. I wouldn’t make that as a blanket statement across the board, but for that particular analysis, that is what we found. This initially seemed counterintuitive, so we starting digging into the literature. One of the hypotheses stated: When there are racial minority groups in marginalized social positions, occupying social positions that are stigmatized, the higher a member of these stigmatized social groups climbs the social ladder, the higher the likelihood of them interacting with people that are not like them. Therefore, those with higher educations or higher incomes are more likely to spend most of their time or most of their day in a work environment with people that are not like them. There is greater opportunity to experience racial discrimination. For example, those with lower incomes or lower levels of education tend to be clustered in certain neighborhoods, working certain kinds of jobs. We hypothesized that when someone breaks free and climbs the ladder, they have a greater chance of experiencing racial discrimination
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because they are near more out-group members, as opposed to in-group members, such as middle class from where they originated. There is also a racial discrimination in African American communities. An interesting finding is that higher income Blacks, more so than lower income Blacks, might live in neighborhoods that are more integrated. When you are in a more integrated neighborhood or a more integrated workplace, you feel your minority status, you are aware of it more. So, there is terminology that we use for minorities in this kind of workplace, coined “solo status”. You are used to being “solo” because you are the only person that looks like you. I, personally, was often the only person that looked like me in my biology classes in college. When I was with other African Americans, I wouldn’t feel like a minority. Social marginalization is enough to cause stress. That is the theory behind why higher income minority groups experience more stress. It is basically biology; there is a term called “allosteric load” commonly known as chronic stress. When one physiologically perceives threats, there is a natural way that our bodies adapt to those environmental demands through regulation of a variety of stress hormones like epinephrine, cortisol, and cortical inflammatory cytokines, which cause heightened inflammation in the body. All of these can be regulated in the body, and they are helpful in warding off immediate stressors, but in the long term, overproduction of these stress hormones can become toxic in the body and create susceptibility or a biological vulnerability to adverse health outcomes. With increased stress, we often see heightened inflammation in the body, which can be a concerning issue in pregnant women. An inflammatory pathway can makes some women more susceptible to having with babies low birth weight or premature rupture of membranes. Another issue with this comprisable biological state is that one can be more prone or more susceptible to infections. Infection is a big issue with respect to birth outcome. We know Black women, for example, have a higher incidence of bacterial vaginosis, which is an infection that can cause premature delivery and or other adverse birth outcomes. We also know that bacterial vaginosis is associated with the experience of chronic stress, so there has been research that has linked different parts of the puzzle and we are trying to put it all together to try to make sense of it. I am very interested in inflammatory pathways and I am interested in doing work that examines whether that inflammatory pathway, as an outcome of chronic stress, might be a pathway linking chronic stress to a variety of health outcomes like low
birth weight, preterm birth rate, and cardiovascular disease. The public health intervention doesn’t just intervene on this particular outcome or that outcome, but we intervene on the stress process or the biological mechanisms.
BSJ: Are you currently working on or involved in trying to find a solution to racial segregation and the connection to the inflammatory response?
Prof. Nuru-Jeter: I’ve moved a bit away from my
research in racial segregation. Now, I’ve become very interested in individual-level processes related to stress. Currently, I am doing much work on the individual-level and my hope is to, at some point, bring it all to a full circle. I’ve done work on the macrolevel – racial segregation concentrated poverty, income and equality. Now, I’m hoping to bring together, both macro-level and, what I call, micro-level factors or individual factors and to look at the intersection between the two. I just finished a project called the “African American Women Heart and Health Studies”. This project examined the association between chronic social stresses and, in particular, racial discrimination, but we also look at other forms of social stress – both in mental and physical health outcomes in African American women. We’re just starting to look at the data now. Some of the preliminary findings show that it supports stress theories. One of the things that motivated this work for me is that much of the public health research starts by looking at discrimination in health outcomes. They look at discrimination as the stressor and some distant health outcome, like hypertension, without capturing a few key aspects of the stress response process like coping style. The goal of this study was to accurately depict all the stages of the stress process, so we developed some measures. We call them “culture-specific measures” of stress appraisal and coping style-specific to a African American women and what we’re finding is the prevalence of “anticipatory racism”, the idea that regardless of whether one experiences the threat or not, just anticipating the threat is enough to initiate the biological stress response. We found that people who experience high level of “anticipatory racism” threat end up having heightened inflammation in the body. This finding motivated our continued interest in inflammation; it looks like coping styles are moderating or influencing the relationship between discrimination and inflammation. It’s not just the stressor, but it’s the intersection between experiencing the stimulation in conjunction with how one appraises
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that stressor and how they cope with that stressor. So, that’s where the cusp of my work is right now and we’re getting very interesting findings in this project. We’re submitting grants for larger projects to continue doing work in this area.
One area that much of my work has been focused on is Black women. We know that because of issues they are very exposed to, like gender role norms (men have higher measures of masculinity compared to women). Women rank higher in “network stress”. “Network stress” extends beyond individual stress, which means that women tend to be stressed out more so than men, not only from their only stress experience, but also the experiences of others in their social network, like their children, their spouse, and others. One of the things I’m interested in looking into is the degree to which Black men and women differently appraise their stresses and cope with their stresses. Those differences might impact inflammatory response.
two different schools of thought. Some scholars will call one is “colorblind racism”, where we say that race doesn’t matter at all. After all, we have our first Black president. Well, if we say that race doesn’t matter, we don’t look at it, we don’t try to improve racial relation. That creates a challenge.
BSJ: In your opinion is it hard to get people to talk about racial problems
Prof. Nuru-Jeter: It is. I think it’s because there are
with these stressors? Is there anything we can do to reduce this inflammatory response?
Another school of thought states that race does matter, but the experience of racism might look different than it did 50 years ago. We’re now still dealing with some acute insult, but also what we call “micro-aggression”. Small subtle daily experiences or mistreatment, whether it’s in the classroom or walking around campus, builds up and creates this swell of feelings of mistreatment that can wear down on a person. This is the “wear and tear” stated in my research papers that the body experiences from the accumulation of chronic stresses related to race over time.
Prof. Nuru-Jeter: We’re still working on trying to
BSJ: To conclude, in 20 words or less, can you
BSJ: How can we, as UC Berkeley students, hope aid
learn more about that. We’re still trying to see what works and what doesn’t. So, I don’t feel comfortable saying we should do this or that. Researchers are trained to always say we need more research, but one of the things we know about the UC Berkeley campus is that, again a lot of the work I do is about race, there are issues around race and other forms of social stigma whether it’s sexual orientation, gender issues, or disability issues. Our most recent climate survey has shown us that there are groups that feel disrespected and its creating low levels of trust on campus from certain groups of people. If we really believe that we want to cut the chord, we have to cut the fact that people are experiencing those stressors to begin with. Thus, concerning racial discrimination or other types of discrimination, what I am trying to create a more inclusive type of community, where we celebrate differences, so that no group feels left out, so that no group feels like they are part of the marginalized or stigmatized group. If we just appreciate that we are one big community, it could make a lot of difference. If we do that, then maybe we could actually eliminate the stressor in the first place and teach people how to cope or act a certain way to protect our health. It has to be taken to a personal level and that is not something that can just be created by people. Like they say in the business world, the leaders of an institution have to set the tone of an environment that creates a more
please define what you want to see in a nonracial, unsegregated society?
Prof. Nuru-Jeter: That is a good question. I just want
to see people, all working together towards a common goal. Towards creating a society that uplifts everybody, that doesn’t just uplift one group of people or another, but creates the kind of system and infrastructures in society that gives everyone an equal chance from the start.
BSJ: BSJ Interviews would like to thank you for your time!
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An Afternoon with Professor George Bentley
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By: Kuntal Chowdhary, Harshika Chowdhary, Manraj Gill, Atiriya Hari, Rhea Misra, Jess Evaristo, Ali Palla
This year, BSJ had the pleasure of interviewing Professor George Bentley. Professor Bentley’s research interests include avian reproductive biology, neuroendocrinology and behavior. As an ornithologist, Professor Bentley has completed extensive studies on song control systems. Endocrine and behavioral responses to stimuli such as vocalizations have been documented for decades, yet the “black box” approach has been applied to any explanation of the brain’s involvement. Any external stimulus has to be first monitored by and then responded to by the brain for the stimulus to have a physiological effect. To affect the reproductive axis, these stimuli must influence the gonadotropin-releasing hormone (GnRH) system. Much of Professor Bentley’s recent work has been on the recently identified neuropeptide, gonadotropin-inhibitory hormone (GnIH). BSJ had the opportunity to learn more about the role of stress in the GnRH system.
How did you get involved in your research in stress regarding birds?
I started my research career looking at what is called “photoperiodism” -- how birds and other mammals respond to changes in day length and how their reproductive system changes. I was interested in how this phenomenon occurs on a basic level -- how birds change from breeding to a nonbreeding status. I ended up working in a lab in Seattle that focused on the role of stress influencing different behaviors within discrete stages of the annual breeding cycle. I am not a stress biologist, historically. When I moved here, because of my interest in regulation of photoperiodism in seasonal breeding, I started working on a neuropeptide called Gonadotropin-Inhibitory Hormone (GnIH), which was discovered in Japan by a friend of mine, Kazu Tsutsui (Kazuyoshi Tsutsui). We started working on GnIH and we knew nothing about how peptides are regulated and their associated regulators. We initially thought this discovery was very exciting because this inhibitory peptide could explain or could be part of the mechanism with which birds and mammals terminate (switch-off) reproduction at the end of the breeding system when their gonads regress. Turns out that was not the case. We started to
look at different hormones that might modulate the expression of GnIH. The obvious thing to look at was the HPA (Hypothalamic-pituitary-adrenal) axis. We wanted to see if stress hormones could modulate the GnIH. A graduate student of mine, Becca Calisi (Dr. Rebecca M. Calisi-Rodriguez), started by doing some work on stress at different times of the breeding season in house sparrows. We saw that GnIH was regulated differently at the start of the breeding season as compared to the end of the breeding season. We caught these birds from the wild and simulated a predation event -- we catch them, put them in a cloth bag, and hang up them for an hour. While the birds are sitting there in the bag, we assumed that they perceive that they would be eaten by predators and this elicits a strong stress response and allows us to see how GnIH was regulated. We found that it was regulated more at the start of the breeding season than later in the breeding season. This makes sense, as at the start of the breeding season, breeding can be delayed or advanced depending on what kinds of supplementary cues these birds are receiving. The drive of changing day length can switch on the reproduction system, so the birds do not enter full reproduction until everything is just perfect. Now in birds, we have been historically limited in terms of the tools we have to manipulate at the level of the gene. We first have to clone the gene. Daniela Kaufer and I, we were talking about collaborating and see how GnIH can respond to stress. One of her graduate students, Liz Kirby (Elizabeth Kirby), did a lot of this early work and culminated in a
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PNAS paper about stress influencing the mammalian form of GnIH in male rats, inhibiting reproduction.
Stress has several effects on the brain. BSJ: As mentioned earlier, there would be different effects for different types of stress, how do you classify types of stress?
What parts of the brain does stress affect the most?
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Prof. Bentley: There is
It depends on what type of stress you are talking about, because stress is an overarching term for many different kinds of stress, such as food stress, emotional stress, psychological stress, and predation stress. Yes, stress feeds back to the hypothalamus and then influences the endocrine status of the animal by binding to peptide neurons. It can also influence the hippocampus. It influences the fate of neuronal precursor cells. If you were talking to me thirty years ago, no one would have believed that, because neurogenesis in the adult vertebrate brain was not thought to occur until it was discovered in a songbird study. Songbirds have this network of interconnected brain nuclei called the “song control system” and this allows them to learn vocalizations. The song control
also nutritional stress that is thought to influence the size of the song control system. So, if young were fed an impoverished diet, then their song control system will be smaller and they will be less able to learn songs as well. That may be partially mediated by glucocorticoids and nutritional status.
BSJ: In terms of measuring the reproductive ability, what type of stress do you use? How would you classify that? Prof. Bentley:
I would say that is simulated predation stress. To understand this concept, we’ll have to delve a bit into acute vs. chronic stress. You can have a single predation event. Imaging a zebra being chased across the plain of Africa by a lion or cheetah, it leads to an elevation in the glucocorticoid to get the energy reserves mobilized. So, acute stress is actually quite adaptive and in some ways can help you survive. Chronic stress can be very detrimental because we haven’t really adapted to deal with chronic stress.
...acute stress is actually quite adaptive and in some ways can help you survive. Chronic stress can be very detrimental because we haven’t really adapted to deal with chronic stress. system grows and shrinks seasonally in response to changing gonadal steroids and melatonin. In the early 1980s, Fernando Nottebohm from Rockefeller University discovered this shrinkage and growth of particularly HVC, Area X, and RA. It is not just cells changing size. It is new neurons being born and migrating to different brain areas. Since then, there is a debate whether mammals can exhibit neurogenesis in adulthood. Some people pooh-poohed the idea and other people stuck with it. Now, we know that humans and primates can exhibit neurogenesis in adulthood. So, returning to the topic of stress, neurons are born from neuronal precursor cells. With stress, the fate of the neuronal cells will be changed. They will become astrocytes, for example, versus neurons. This process can occur in the hippocampus, which is involved in memory.
BSJ: What initial indicators do you look for when stress is first induced in birds?
Prof. Bentley: Well, one thing we typically do is we take blood samples and we have to get a baseline measure of the bird’s stress response. We have aviaries at the field station where we can catch birds and take a blood sample in under three minutes -- that is how long glucocorticoids remain in the blood. First, we take that initial blood sample and then take several subsequent blood samples. However, typically, we can’t see the bird in the bag, so I don’t know if you’re talking about the internal indicators or external indicators?
BSJ: I guess both. I was just curious as to how you measure that
We measure glucocorticoid in the blood. But, if they aren’t hunched up, it’s very hard to tell if they’re exhibiting a stress response. But, if they are, we
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really don’t want to use those measurements.
animal models like sheep come in very handy because you can cannulate this portal system, using live X-ray, taking quite large blood samples of the portal system over a long period of time. Then, you can see the pulsatile release of the neuropeptides once you do the assay. We’ve collaborated with some people on that; we don’t have sheep here. I’ve thought about it, it would be a bit useful for that. But, we know people who have a long history of studying sheep and can help us measure these neuropeptides.
...early in the breeding season, the birds that had successfully competed under these natural stresses had lower GnIH content in the brain than the birds, which had not been successful in nesting on the same day. BSJ: You mentioned the HPG axis, Could you elaborate on that? Specifically the tropic effects of GnIH on GnRH (Gonadotropin-releasing hormone)?
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Prof. Bentley: On the HPG axis, you have GnRH at the
top. The hypothalamus ejects GnRH to the pituitary gland and GnIH is released to the pituitary portal system, which is separated from the rest of the blood supply. So, that neuropeptide can be released in small amounts and not have large effects. If they were released in the peripheral blood supply, then it’ll just be diluted. The pituitary releases gonadotropins, LH (Luteinizing hormone) and FSH (Follicle-stimulating hormone). GnIH neurons project to GnRH neurons, as the GnRH is receptive to the GnIH. Moreover, we know, not from our work, but work done in some other labs, Yale in particular, that GnIH can inhibit the firing of GnRH neurons and inhibit their activity. In most species, GnIH projects to the anterior pituitary gland and can be released in the portal system that is receptive to the GnIH expressed in the pituitary gland, thereby directly inhibit the synthesis and release of LH and FSH. GnIH is also made in the gonads, so that the gonads can make it even though it’s called a “neuropeptide”. The receptor of GnIH is also found in the gonads. We have data to support that GnIH can inhibit gonadal steroid release. And not just in birds!
BSJ: How would you measure the levels of GnIH and GnRH since they are very localized, especially in the median eminence?
It’s very hard to do in birds. We can measure the transcription of the genes with qPCR or PCR. Through in-situ hybridization, we can check for the expression in birds. We can do immunohistochemistry and label the neurons in the brain with antibodies specific to those neuropeptides. We can also cut out the hypothalamus, extract the neuropeptides, and then perform an ELISA assay to measure the quantities of the neuropeptide in question. That doesn’t tell us about the release to the pituitary gland, though! This is where
BSJ: So, in terms of what you mentioned initially about what your research focus has been: the differences in the GnIH levels in the spring and the fall/non-breeding seasons. Would there be a relationship of stress in there whereby they would not produce as much GnIH if exposed to stress and impact reproductive activity?
Yes, we’ve done some studies looking at that, what we call a type of “social stress”. A graduate student of mine looked at a type of social stress. In this experimental pyridine, we limited the number of nest sites available for the pairs of starlings. She found that early in the breeding season, the birds that had successfully competed under these natural stresses had lower GnIH content in the brain than the birds, which had not been successful in nesting on the same day.
BSJ: So this would be during the spring? Prof. Bentley: Yes, during early spring! BSJ: So, you would say that since they’ve been exposed to
those stressful conditions… Everyone would be equally exposed to the stress, right?
Prof. Bentley: Yes! But, some are dealing with it a different way. Some are successfully competing. There might be different factors coming into play here to modulate the GnIH. It might not be a stress effect, it might be a perception of “Oh, I’ve successfully competed for the nest spot, and now I can go into the next stage of my breeding cycle!” and therefore, to put it simply, GnIH decreases. So, maybe not a stress response per say, but you can see social competition as having been “stress-induced”.
How does GnIH affect LH and FSH? Are these hormones involved in a negative feedback pathway?
Prof. Bentley: This gets quite complicated the more that
people work on it! There are many factors to consider, such as the species or the length of daytime. In general, GnIH inhibits the synthesis of LH and FSH. LH and FSH are glycoprotein hormones and these glycoproteins have an alpha-subunit that is identical in LH, FSH, and TSH
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(thyroid-stimulating hormone). All have the same common alpha-subunit, but they have a different beta-subunit, which confers their differential biological activity. We know that in vitro and in vivo can inhibit synthesis of both, the common alpha-subunit and the beta-subunits of the gonadotropins. So, presumably, that’s acting via binding to its receptor, a G-protein covered receptor. In terms of the simple steroid negative feedback pathway, I know of no evidence that testosterone is involved in negative feedback to the GnIH system. Lance Kriegsfeld has done some work looking at the role of estrogen in terms of its action on GnIH and negative feedback. He’s interested in ovulation and he studies female mammals, specifically hamsters, prior to ovulation. Estrogen, of course, is involved in negative feedback. But just before ovulation, there is a switch to positive feedback and Lance has some data indicating that GnIH is responsive to estrogen and it may be involved in this switch between negative to positive feedback but he’s still working on that.
BSJ: So would you refer to GnIH as a “stress hormone”? Prof. Bentley: I would not call it “the stress hormone”, only because I think it’s doing many other things, as well responding to many different kinds of input. They can influence sexual behavior, regulate feeding behavior, and of course, stress response. They respond to melatonin, which is secreted at night. They probably do much more, but keep in mind GnIH was just discovered 13 years ago, so there is a lot more to be discovered. I think it’s a mediator of stress, well a mediator of a perception of a stressor, whether it is psychological or physiological, and then integrating that stress signal into the appropriate endocrine response.
that encodes three mature peptides -- there’s a precursor polypeptide that’s encoded and then cleaved into three mature peptides. We’ve only been working on GnIH. We don’t know much about the other peptides that are called GnIH-related peptide 1 and related peptide 2. We know from in vitro binding studies that they can bind in a similar way to the GnIH receptor, so it may just be that the precursor is cleaved differently under different circumstances, but it ends in the same result. Alternatively, it may be that there is another receptor that we haven’t discovered yet and this differential cleavage is a precursor in different brain areas to perform different processes. Now, in mammals, typically, there is a precursor polypeptide, but only two mature peptides: RFRP-1 and RFRP-3. In humans, it seems that there may be three mature peptides, but we’ve only managed to isolate two; however, based on the genome, it seems that there ought to be another one in there. And functional differences? Well, there are some functional similarities. One interesting difference is that, in hamsters - I don’t remember which species, RFRP-3 is administered to these hamsters on long days, so when they should be breeding you can inhibit the HPG-axis, you can inhibit LH release. But, if it is administered to the same species on short days, when the reproductive system is regressed, you can increase LH release. We have not looked at that in birds yet to see whether there is a differential response to the administration of GnIH under different day lengths, but there are many similarities in RFRP-3 and GnIH. Both influence sexual behavior, feeding behavior and the response to stress.
BSJ: What does it mean for humans to have more than two to have three?
Prof. Bentley: Evolutionarily or functionally?
BSJ: So if
Prof. Bentley: Depending on how low, yes I believe so.
Prof. Bentley: Possibly, if
you have low levels of LH and FSH would that directly correspond to an ability to successfully reproduce.
From our understanding GnIH and RFRP3 are orthologs. What are the structural and functional differences between mammalians and birds?
Prof. Bentley: It’s interesting, in birds, there is one gene
Both maybe? Would you say there is greater variety between how those would function? there is a third mature peptide it looks like it’s probably an RSamide, instead of an RFamide. I don’t know if I want to speculate too much on that because we haven’t isolated it.
BSJ: Is it an ability to react to different types?
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Maybe. Several of these neuropeptides haven’t been looked at in great detail across all vertebrates; the most studied organisms are rats and mice. So, there are neuropeptides that we know of that were probably present early on in the evolution of vertebrates like GnRH2 more basal vertebrates have more forms of GnRH than rats and mice. Typically rats have one form, fish have three or four forms. Humans have expressed GnRH2, as well as GnRH1, whereas rats don’t. You have to think about how we evolved and what type of accidents that occurred along the way for us to lose one or keep one.
BSJ: Do high levels of stress affect the production of RFRP3 in mammals like stress triggers the production of GnIH in avians?
Prof. Bentley: Yes. In male rats, that’s certainly the case.
This was the experiment I was talking about that Daniela Kaufer’s graduate student Liz Kirby performed. Daniela now is actually doing some cool work. We’re collaborating on this with another graduate student, Anna Geraghty. She’s looking at stress and RFRP3 in female rats. People typically don’t study female model organisms. In birds, its because it is hard to get them to breed in captivity if they’re a wild bird. You get this nice testicular response in the lab; in the wild, you don’t get that with the ovary unless they are in the correct conditions, which we have at the field station. With rats, people are worried about the data being muddled by the stage of the estrous cycle that the female is in at the time. Therefore, they just find it much easier to work on males. And that’s a little shortsighted, I think, because you’re missing half of the population of your studied organism. So, Anna very bravely wanted to look at the effects of stress on GnIH in female rats and how that might influence pregnancy success and eventual total reproductive success. And, doing some very cool manipulations, she’s found that yes, stress increases RFRP3, yes it influences reproductive success. Using a very cool viral vector technique, she can knock out RFRP3 and then block those stress effects. Those virustreated animals with RFRP3 knocked out showed the same reproductive success as the controls. BSJ: Are GnIH and RFRP3 conserved evolutionarily across
species or observed only in birds or mammals?
Prof. Bentley: They are pretty well conserved across species. When I first started working on GnIH, I was submitting around proposals and getting comments back along the lines of, “Yeah this is very interesting, but it may only be in birds. We don’t know if this substance even exists in mammals, let alone humans.” When I came here, I made it one of my missions to see if GnIH was conserved across vertebrates. Obviously, you can’t study every vertebrate. But I wanted to look in rodents, fish, nonhuman primates and humans. We ended up isolating GnIH or RFRP3 from the monkey brain and the human brain. We’ve also been looking at GnIH and RFRP3 in carnivores because nobody had been doing any work on carnivores. We were approached a while ago by a private foundation interested in creating a novel technique for sterilizing cats and dogs. They looked at how GnIH worked and thought, “Well, maybe you could apply that to create this single injection sterilization technique for cats and dogs”. Its established by a billionaire, who basically is very upset that there are millions of cats and dogs euthanized every year in this country and around the world. We are in the process of isolating GnIH from cats. We’ve cloned it from cats, and we think we can manipulate GnIH in cats, hopefully to sterilize these animals. So yes, quite a long answer, it does appear to be conserved from fish to humans.
BSJ: So just to bring it a little bit back home, do you see your research being applied to the effects of stress on humans and as Berkeley students, we have many different types of stresses upon us. How would it affect humans?
Prof. Bentley: Well, we need to do the studies, but one
would predict that you probably have elevated GnIH because of chronic stress and it may well influence the libido or fertility. But, we simply don’t know really in humans, yet, what the effects of chronic stress are on reproduction via GnIH. What we do know is that chronic stress in humans can affect fertility and libido, as well. But, bear in mind that there are other factors that affect GnIH. Melatonin can increase GnIH release, staying up late at night messes with your melatonin rhythm. Similarly, you might be influencing GnIH in that way, too.
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BSJ: With birds, would you be able to test acute stress versus chronic stress? What are the ways you would do that?
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Prof. Bentley: We’re starting to look at chronic stress in
birds now. With acute stress, we typically use this very well defined paradigm - you go and catch the birds, put them in a bag for 30 minutes to an hour. Many labs have used this technique to measure different aspects of the stress response in birds. Chronic stress, again, it can come in different forms. The stress could be a worry about being eaten; it could be being forced to live in a poor habitat as compared to a good habitat. Now, we’re able to house birds in a nice outdoor environment, which we call a “semi-natural environment”. At the same time, we have birds indoors in an environment, where we know they won’t breed. We know from data from many different animals that have been housed in a non-natural environment that such conditions can elevate the baseline glucocorticoid level. I think the chronic elevation of that baseline glucocorticoid level could be classed as a chronic stressor, but the effects might be subtler than a potent chronic stressor. Some labs go up to the birds’ aviaries every day and spray them with water, or blow wind at them, or make startling noises. Those would be really strong chronic stressors.
That’s something I’m very excited about working on. In terms of other aspects of GnIH biology, I’m interested in going the other way. So, rather than sterilizing animals, I’m interested in finding out how GnIH is modulated by captivity, and I think I mentioned to you that it is really hard to get wild species to breed in wild captivity, especially birds. We think GnIH might be something we can manipulate to enable captive breeding of endangered species. I’m starting a collaboration with some people from the Smithsonian, on the East coast, to look at that as well. So two very different endpoints—sterilization and reproduction—but using the same mediator.
BSJ: We would like to thank you for your time.
Since “stress” can be used in many contexts, do you have a term that you prefer to use in lieu?
Prof. Bentley: I would have to think about that. I don’t
have one. Even if I coined one, I think other stress biologists would disagree with me. They would have their own word that they want to use. I think stress is a whole spectrum of physiological responses to a whole spectrum of different cues. If I picked a word, I might be thinking about a specific part of the spectrum, but someone else might be thinking about the next.
BSJ: Where do you see your current research heading in the future?
Prof. Bentley: I am currently collaborating with Daniela
Kaufer on this study, where we are trying to develop a non-sterilization technique on cats and dogs. I think that would be fantastic; this would be one very applied aspect of our research. It really could change the world, really, if we did it. It’s just the mission of the foundation that’s funding us is to develop this single injection sterilization technique that could be used without any surgical expertise and could be used in developing countries, for example. If you travel around the world, in some countries, there are dogs running everywhere. In this country, you tend not to see it so much, but there are millions of animals euthanized every year and we wouldn’t need to do that.
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Building a Bridge for the Future with Professor Abolhassan Astaneh-Asl
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By: Ali Palla, Kuntal Chowdhary, Jingyan Wang, Joshua Hernandez, Kaitlyn Kraybill-Voth, Mariko Nakamura, Jessica Evaristo Although stress is primarily interpreted from the psychological or biological perspective, the term stress is widely used in the realm of civil and structural engineering as well. Buildings and bridges must be able to withstand a wide variety of stressors, ranging from natural phenomena such as earthquakes to blasts and terrorist attacks. Individuals like Professor Abolhassan Astaneh-Asl, professor of civil and environmental engineering at the University of California, Berkeley, are leading the charge in making our buildings and bridges safe from whatever stressors they may face. Professor Astaneh-Asl also had the privilege of being one of the few researchers who had access to the engineering blueprints for the World Trade Centers following their tragic collapse in the 9/11 terrorist attacks. This past semester Professor Astaneh-Asl was in Turkey conducting research as a Senior Fulbright Scholar; he graciously took time out of his busy schedule to speak with us over Skype. Currently, Profession Astaneh-Asl added an additional focus on blast protection. In conjunction, he works with a large team of UC Berkeley undergraduates to create an archive of the information gathered from the collapse of the World Trade Centers. BSJ: How did you first get interested in your line of research? Prof. Astaneh-Asl: It goes back to how I got interested in structural engineering, specifically bridge engineering. The research you get interested in is specific to your background and your education. My background and my education are in structural engineering. My interest was sparked in the first undergraduate course I took, which was a statics course, where we looked at stresses and equilibrium and forces. When I went to this class, this was the first time that I saw buildings and bridges. I thought, “Wow, this is amazing!” Imagine, you come into a classroom and sit there with the Bay Bridge and all these wonderful structures. Everyone is fascinated with buildings and bridges. Taking that course was a defining moment where I decided, “This is
it. I’m going to be a structural engineer.” I got my undergraduate degree and started working. I had 10 years of practice in design of structures. Then I came to the United States in 1978, I’m originally from Iran. I completed my Masters and Ph.D. at the University of Michigan in Structural Engineering, and of course, that was my life by then. I did design work on buildings and bridges. Then, I went to University of Oklahoma for 4 years, where I was a professor. I came to Berkeley in 1986. I was still working on buildings, but not so much on bridges. I started working on building bridges specifically in the Bay Area. My friends were in structural engineering, so I got involved. Just three years after I joined this “super group”, there was a big earthquake. This earthquake collapsed a small part of the Bay Bridge. The Bay Bridge was closed for a month. As a faculty member who specialized in steel bridges, I was the only one in Berkeley working on steel, long standing bridges. Other faculty in our group were working on concrete bridges. Therefore, I was in a unique position as the only professor in California, not just Berkeley, who knew something about steel bridges. Berkeley
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became the center of the universe, in term of long span steel bridges, surpassing even Japan, which is known for earthquake engineering. We ended up being the leaders for many years for research into seismic studies of long span bridges.
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In 1995, there was the terrorist attack on a federal building in Oklahoma. In fact, it was a little personal because that building that the terrorists, Timothy McVeigh and others, attacked was the federal building where I had my interview for US citizenship. I went to Oklahoma as a faculty and the university helped processed citizenship for me. I went to this building with my family, wife and two kids. There were federal agents there who fingerprinted us and talked to us. They were, of course, very kind. Moreover, that was a historic day in the life of any immigrant. It was like Ellis Island. That federal building collapse was like our Ellis Island collapsing. We passed through that building to become US citizens. This is our home. We are very, very proud. As any proud immigrant, we remember that day, even the faces of the federal agents. That was 5 or 6 years later, when I had seen the building collapse. At that time, I had no interest in blast protection and terrorist protection. I was only interested in seismic activity, earthquakes. Having that sort of personal attachment to the Alfred P. Murrah building, and having this feeling that the attack was not just like any other bombing, but a personal attack, was a very defining moment. They attacked and killed people that I knew personally. During that time, I had decided to look into protection of buildings and bridges against terrorist attacks, including car bombs. I, then, got involved with the Lawrence Berkeley National Lab. I spent 3 years learning the basics -- studying, reading papers and researching results. It was a very new area for me. It wasn’t earthquake engineering; it was different dynamic effect. So, I educated myself for about 3 or 4 years. Then, we started to do research on blasts and started thinking about how you can make bridges and buildings that can withstand blasts, especially car bombs. Then in 2001 came the attacks on the World Trade Center. When Al-Qaeda attacked the World Trade Center, I was very focused on how you protect tall buildings and bridges against terrorists attacks. I ended up being the only researcher to receive a National Science Foundation (NSF) grant to go to Ground Zero in New York to investigate and
document the collapse, and do a reconnaissance. I went there one week after 9/11, on September 18, when the airplanes started flying again. It was a very fast operation, from the time I submitted the proposal, received the grant, and landed in New York at Ground Zero. I stayed there for 3 weeks and went through hundreds, probably even thousands, of tons of steel to document it, to photograph it, to inspect it, to videotape it and make comments on what I discovered, so later, other researchers can use this information when they study what happened. This was the most important structural building collapse and the toughest project of my lifetime.
Later, I testified before the Committee on Science of House of Representatives. The Committee of Science is the committee that oversees disasters, like natural disasters or any major disasters. I ended up testifying and answering questions about what I thought. The committee gave me the drawings, engineering drawings, of the World Trade Center. The engineering drawings of the World Trade Center, even today, are sealed and you cannot look at them. No one had the drawings to look at, but I was very lucky when I testified. The Chair of Committee asked me, “Astaneh, what do you want to continue to research?” I immediately jumped on the chance, “I need the drawings, I have to study the drawings and give them up”. So to keep it short, the Chair ordered FEMA, the Federal Emergency Management Agency, which was in charge of drawings and everything else. They gave me the drawings in 2002 and then I did 5 years of very extensive research on the World Trade Center.
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I ended up being the only researcher who was able to do the research and publish the results, as I was the only researcher to receive drawings from Congress and because of that, I did not accept any restrictions on my research at Berkeley. With this privilege, we published our results based on actual data from the field. No other researcher was allowed this unique opportunity, other than the few of us at Berkeley. The analysis that we did demonstrated a structural collapse. Last year, we had an opportunity to revisit this project. I have a few undergraduate students who organized the entire archives on the World Trade Centers. About a month ago, in October, we established World Trade Center archives at UC Berkeley. I am very proud of this work. There are many prestigious universities and UC Berkeley ended up being the only university that actually worked on this project, the archives especially, and we are adding more. BSJ: In recent years you have co-authored a number of papers focused on blast protection of bridges. Can you explain conceptually how an explosion of blast places stress upon a bridge, and how these effects may compare to another event such as an earthquake?
member then the effect is just local. Earthquakes affect all the members of the structure, all the connections. BSJ: In your paper on blast protection of suspension bridges, mild steel is found to be more blast resistant than high strength steel. Can you please elaborate on how the properties of these materials may contribute to these observations, and the significance of such an observation? Prof Astaneh-Asl: The issue comes down to what can be called “ductility”. Ductility is the capacity of the material to absorb energy, the character of material that allows it to bend but not break. If you take a paper clip and bend it back and forth, it takes maybe ten or twenty bends before you break the paper clip. The reason it takes so many cycles to break it is because steel is highly ductile. Therefore, low strength steel is more ductile than high strength steel. High strength steel is very strong but is very brittle, which means it can take a lot of force, but cannot bend too much. So the difference between high strength steel and low strength is that low strength steel can yield and deform quite a lot before it breaks which is important in a blast of earthquake. Every time I’ve
So the difference between high strength steel and low strength is that low strength steel can yield and deform quite a lot before it breaks which is important in a blast of earthquake. Prof. Astaneh-Asl: That’s a very good question. Some think that if you design a bridge for earthquakes, it will be just fine for blasts as well. However, earthquakes are dynamic forces that shake a whole structure. The dynamic forces come from the foundations all the way up; every cubic foot of bridge is affected. Earthquakes are also relatively slow: the waves come in cycles, one cycle per second so you can think of it like average. That is slow actually in terms of groundbreaking. When you look at a blast, it’s just a local effect. The blast force is very large compared to an earthquake, but just at the mass that is affected. It’s like taking a hammer and hitting a small piece of bridge. You are just going to damage the local area and it is one thousand times faster than an earthquake. If a blast hits a very critical member, it can be devastating, but if it doesn’t hit the critical member or you have a mechanism to prevent collapse of that critical
presented, I’ve see engineers who think you can resist a blast by making the structure stronger. That is an absolutely incorrect solution. You make your structure stronger and it becomes very brittle, like glass. Because it’s very strong, it generates large dynamic forces. But it doesn’t have ductility to absorb it, which causes the structure to break and fly all over the place. Low strength steel bends, but it does not break. BSJ: Many of the papers you have co-authored contain performance criteria for structures subject to specific conditions and stressors. What role do these performance criteria play in the design and construction of buildings and structures on a greater scale? Prof Astaneh-Asl: Whenever you design something, you have to put on paper what you want this
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structure to do. Nevertheless, you cannot design structures to avoid all damage. Now, we have the technology to design a structure that will not take any damage during a magnitude 9.0 earthquake. But we cannot afford that. So, the performance criteria come into play. For example, if you are designing a building for earthquakes, the performance criterion focuses on life safety. During a major earthquake, there will be glass broken, doors jammed, walls cracked, this and that, but the floors should not collapse and people should not be killed. We have been very successful in the US as compared to other countries. Now when we started looking at blast protection for bridges, I realized that not much had been done. Then, the question was “What should be the performance criteria for blast protection of bridges?” We cannot just design every bridge, such that if a car bomb goes off, the bridge will not have any damage, otherwise every bridge would be like a tank. It’s very important to come up with performance criteria that are economical because society can afford only certain amount of money to spend on certain risks. It’s a balancing act between how much risk we should accept and how much money, accepting that risk, we will need to spend. We started to formulate this, considering one very important criterion, life safety. When there is a car bomb on a bridge, there will always be casualties. You can’t do anything as engineers to stop the tragedy of cars next to the explosion. And the bridge will be damaged. What we don’t want is the collapse of the whole span. If the whole span collapses, then many cars will go down; that would be catastrophe. So establishing that level is important. BSJ: In addition to your own research, you are in charge of the undergraduate research program within the Civil and Environmental Engineering Department. What drew you to become so involved in undergraduate research? Prof Astaneh-Asl: From the beginning, I always had undergraduates involved in my research, probably because our students are just amazing. In the undergraduate classes I teach, I have heard
This phenomenon of resonance is very important because if resonance occurs, we see really large forces.
questions that I’ve never heard in my 8 years of teaching. Also, I work with all of my undergrads directly and make sure that each undergrad has a special well-defined project. They’re not just helping graduate students plot curves. Last year was very exciting because I had 10 undergraduates to work on the World Trade Center archives. We had a request for information, for me to submit all my World Trade Center data during that first year I was in New York. I anticipated that my undergraduates and I are going to go through a lot of storing, a lot of indexing, and a lot of paperwork, which makes it hard for an undergrad to do a self standing unit of research that can be published in a paper. So, I decided that I would hire 10 undergraduates, and they would spend half their time on the World Trade Center archives and the other half on their own projects. Each student had one building or bridge that they worked on for the semester with me, with no graduate student involvement. The goal was to establish how these structures would respond to long distance earthquakes. In 2011, the Washington Monument in Washington D.C. was damaged by an earthquake. However, Washington D.C. is not a seismic hotspot. The earthquake was about 120 miles to the south of Washington D.C., 5.5 magnitude, and only the Washington monument was damaged. Why? It wasn’t close to the epicenter; it wasn’t even a big earthquake. Other things in Washington had no damage. This is a phenomenon called the “Long Distance Earthquake”. Tall buildings are very flexible, like the Washington Moment, and they are very safe if the earthquake is nearby. But if an earthquake is that far away, the seismic waves traveling through the ground become longer and longer. These long waves are very weak. So usually, when they get to a city far away they don’t do any damage. But, because they have a long period, they can create resonance with very flexible buildings or bridges. This phenomenon of resonance is very important because if resonance occurs, we see really large forces. So, now if the structure is very tall and very flexible - like the Washington Monument - or if it is a long span bridge that is also very flexible, - like the Golden Gate Bridge or the Bay Bridge - due to their flexibility, these structures have very long periods of vibration. The earthquake that is coming in, if it comes from very far away it creates long waves, long period waves. Those waves coming into the structure can create
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resonance. Those long period waves hit the tall and flexible Washington Monument and it took serious damage; it’ll be under repair for three years.
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We started looking into this phenomenon in 2005. That year there was an earthquake in southern Iran, which was about 100-150 kilometers from Dubai. That earthquake was magnitude 6 and for Iran, that’s not that big a deal. But, the shockwaves of that earthquake traveled about 150 km through the Persian Gulf and reached Dubai, and became long period waves. Dubai is full of tall buildings and resonance occurred. In the morning at about 11 o’clock, all these tall buildings in Dubai started shaking. There was big chaos and Sheikh Zayed, the Amir of the United Arab Emirates, was panicked that all these tall buildings were going to collapse. That was when Lawrence Livermore National Lab (LLNL) and I got involved. We realized that the United Arab Emirates and Dubai are in “bad neighborhoods” as far as seismic activity, due to the seismic activity in Iran to the north.
Long distance earthquakes are phenomena that most structural engineers, almost all of them, don’t look at. We don’t design for it, we just design for earthquakes next door, If the San Andreas fault ruptures in San Luis Obispo, it would be worse for Los Angeles, as compared to an LA earthquake – for tall buildings at least. These ten undergrad students each had a structure, and only one parameter, long distance earthquakes. For example, one student had the Campanile, and she was comparing what would happen if the Hayward fault ruptures on campus, just next to Campanile versus if it ruptures in Santa Cruz. What she found was an earthquake in Santa Cruz could cause more damage to Campanile than an earthquake right on our campus. This research has been very successful. Our Department of Civil Engineering has started a research program that we offer certain people who are admitted called Undergraduate Research Opportunity Program, UROP. Usually we get top applicants applying, but we don’t get those very top students coming to Berkeley, mostly because Stanford and MIT offer more money. So, we offered the 20-30 top applicants some money. They are also guaranteed an opportunity to do research when they get to their third or fourth year. Suddenly, the whole picture changed – we now have the brightest students coming in and registering. I ended up being in charge of this program now.
We have 14 freshmen now. Next semester, when I come back from sabbatical, I will be teaching an undergraduate research seminar. Once a week, faculty from our Department of Civil Engineering will come in, lecture these students, and hold discussions with them. Next semester, this group moves into another course, which teaches them how research is done – how you work with a team, how you discuss questions, etc. Research requires very close relationships; everyone is responsible for other people to succeed. The most important thing in research is to dispute advice, of course in a nice way. Undergrads, in my experience, sometimes are a little bit scared. But that’s just natural. You’re going to break that, make sure they’re confident, and they feel there is no consequence asking questions. If there is some risk, and the results are not quite as expected, so what?
Then they write a proposal, and they reach out to faculty whose work they are interested in. The faculty select a few students, and that student and faculty spend a semester together. Having an undergrad as a team member is very exciting! Even though they are not as knowledgeable as graduates are, they bring in all kinds of new ideas.
I’ve seen for so many years that undergrad research is getting so much attention, and many faculty members are very excited. As an engineer, when I design, there is a client. Nowadays, I always tell my students that you’re my client. My salary comes from tuition that he or she has paid as a student. Undergrads are very important and we need to take care of them.
BSJ: I think that’s a great place to end. Thank you for everything. It was a great interview.
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train full of passengers is about to plummet into a river. The brakes are stuck. Who will save the day? Who else but Spider-man! He slings thick strands of spider silk onto adjacent buildings, bracing himself on the front of the train until it comes to a grinding halt at the last moment of safety. Spider-Man might be a fictional superhero, but the incredible properties of his spider webs are not so far-fetched. In a recent study published in The Journal of Physics Special Topics, graduate students at the University of Leicester decided to myth-bust the above scene from SpiderMan 2. To their surprise, theoretical calculations showed that spider silk is, in fact, strong enough to stop a runaway train (Bryan, 2012). They began by estimating the force needed to stop the train: about 300,000 newtons. After analyzing the web, the geometry, and the anchor points, they calculated the tensile strength required of the silk fibers (the maximum stress they can withstand while being stretched before breaking). This type of strength is reflected in a value called Young’s Modulus which in this case worked out to be 3.12 gigapascals. As it turns out, spiders produce silk with Young’s Moduli ranging from 1.5 to 12 gigapascals — meaning that Spider-Man could indeed have stopped a fast moving train with spider silk (Bryan, 2012). In fact, biologist William K. Purves (2003) writes that, “The movie Spider-Man drastically underestimates the strength of silk - real dragline silk would not need to be nearly as thick as the strands deployed by our web-swinging hero in the movie”.
ver the past few decades, spider silks have attracted the attention of the scientific community for their amazing mechanical properties and endurance under stress. Of course, silk and its relationship to
humanity is nothing new. According to Confucius, it was in 2600 B.C.E. that a silkworm cocoon fell into the tea cup of Chinese princess Leizu. Attempting to remove it from her beverage, she began to unroll the silken thread of the cocoon. By the 3rd Century B.C.E., Chinese silk fabrics were traded throughout Asia and the West by way of the famous Silk Road. However, silk production remained a closely guarded secret. Most Romans, who highly prized the cloth, were convinced that the fabric came from trees. The Chinese monopoly was defended by an imperial decree, condemning to death anyone attempting to export silkworms or their eggs. In 552 C.E., the Roman Emperor Justinian sent two monks on a mission to Asia, and they returned with silkworm eggs hidden inside their bamboo walking sticks. Soon, sericulture (silk farming) spread across the world (Silk Association, 2012). During the 19th and 20th centuries, modernization and industrialization of sericulture in Japan made it the world’s foremost silk producer. During World War II, western countries were forced to find substitutes as supplies were cut off. Recently invented synthetic fibers such as nylon became widely used. Now silk has largely been replaced by these artificial polymers which are far more cost effective. However, silk polymers (of which scientists have only recently understood the full potential) are poised for a possible comeback if they can be mass produced cheaply and efficiently (Silk Association, 2012). pider silk may seem weak and flimsy, useful for nothing better than haunted house decor. Yet for its miniscule weight and size it can absorb a surprising amount of energy. It’s also stretchy - it can stretch 30% farther than the most pliable nylon. If spider silk were as thick as a steel beam, it would be very difficult to
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break, a lot more difficult than the comparatively sized and much heavier steel. In fact, it would take about 100 times more energy (Gosline, 1986). Actually, spider silk has a tensile strength comparable to that of steel, about 1.5 gigapascals, but silk’s much lower density means that for equal weights of the materials, silk wins. “One strand of pencil thick spider silk can stop a Boeing 747 in flight,” say Xiang Wu and colleagues at the National University of Singapore. Spider silk of the species Caerostris Darwini is among the strongest silk yet measured. These spiders spin some of the largest webs in nature, often spanning streams and canyons. In one study, spider were captured from the wild and allowed to build webs inside a greenhouse. The silk was then analyzed with a tensile tester - basically by
became a subject of interest. The first basic model of silk was introduced in only 1994 and described “amorphous flexible chains reinforced by strong and stiff crystals”(Termonia, 1994). A more thorough analysis was published in Science in 1996. Silk consists of very repetitive blocks of mainly glycine and alanine (glycine and alanine are types of amino acids - the molecules that make up the long protein chains) (Simmons, 1996). These are the simplest and smallest amino acids allowing strands to be packed together. Strands are “glued” together by hydrogen bonds to form tightly packed, highly ordered crystalline regions. The hard crystals make up only 10-15% of the total volume (Keten, 2010). Other regions contain bulky amino acids like tyrosine or arginine that
“One strand of pencil thick spider silk can stop a Boeing 747 in flight,” tugging on the ends of the fiber. It was found that C. Darwini silk is far higher performing, absorbing about ten times more energy before fracturing, than the manmade fiber Kevlar (Agnasson, 2010). Silk’s unusual combination of high strength and stretch leads to toughness values never attained in synthetic highperformance fibers. Even compared to silkworm silk, spider silk has a tensile strength 3 to 20 times greater, can strech almost 3 times further, and absorb 3 times as much energy (Shao, 2002). But what is responsible for spider silk’s ability to endure so much stress?
Fig 1. Tensile Strengh of Spider Silk
ll silks are proteins; they reflect millions of years of evolution toward a material perfectly suited for its biological purpose. Although silk has been a well-known material for decades the intricacies of its chemical and molecular properties only recently
prevent close packing. These regions form amorphous, disordered areas that allow the silk to stretch. The interplay between the hard crystalline segments and the elastic regions gives spider silk its extraordinary properties.
pider silks hold great promise as a material with an impressive array of potential applications ranging from artificial body parts to microelectronics. Randy Lewis, a professor at Utah State University, writes that “The major efforts for the commercial use of spider silk are for artificial ligaments, tendons and bone repair materials.” Silks are scleroproteins, the same protein type used to provide support in collagen, tendons, and muscle fibers. Yet, silks are 100 times stronger than natural ligaments. During ACL reconstruction (the anterior cruciate ligament), surgeons often replace the torn knee ligament with a ligament transplanted from a cadaver or the patient’s own hamstring muscle. However, the new ligament is weak and at high risk for reinjury. Spider silks could be used to construct tear-resistant artificial ligaments. In addition, spiders silks are biocompatible, triggering little, if any, immune response. “We can make something that mimics the size, shape, and elasticity [of a ligament] without any trouble at all,” says Lewis (USTAR, 2012). Spider silk proteins may one day mimic not only connective tissues but actual muscles. Researchers at the University of Akron are designing biomimetic muscles utilizing another little explored property of spider silk; contraction. When morning dew or rain drops weigh down a spider web, rather than collapse or stretch, the fibers actually contract
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and tighten to maintain tension. At high humidity spider silk ‘supercontracts’ - shrinking up to 50% of its length due to disruptions and changes in protein bonding. This change is enough for a single 40 mm long, 5 micrometer diameter fiber (more than 3 times smaller than human hair) to lift at least 100 mg (1/10 weight of paperclip). This may seem insignificant but the work density is actually 50 times higher than biological muscles. Scaled up, a 1 mm diameter fiber could lift as much as 5 kg and a 2 cm diameter fiber could lift 2 metric tons. Driven by humidity alone, silk offers potential for lightweight and compact actuators for robots and micro-machines (Agnarsson, 2009). Ever notice spiderwebs glinting in the sunlight? Light can propagate along strands of spider silk just as it does through a fiber optic cable. Physicist Nolwenn Huby of the Institut de Physique de Rennes in France recently demonstrated silk fibers in a small photonic chip (which uses light instead of electricity to relay
other, and aren’t necessarily easy to handle. For example, it took over 4 years and a million golden orb spiders to produce only an 11ft by 4ft tapestry now hanging in the American Natural History Museum (Legget, 2009). One current approach uses genetic engineering in which the spider genes responsible for producing silk are placed in other more easily controlled organisms with more efficient protein production. So called recombinant spider silk proteins have been produced in bacteria, yeast, and plant systems with limited success. The complexity and size of the genes have made expression in bacterial systems nearly impossible (Romer, 2008). Research continued with eukaryotic cells such as yeast which manufactured the desired proteins but posed problems for purification and extraction in a useful form. Similar problems were encountered with plants (such as potato or tobacco) which are particularly attractive for larger scale production. Production in mammalian cells is the subject of current research. A study employed bovine mammary cells and baby hamster kidney cells as expression systems with some success (Lazarus, 2002). The researchers successfully spun these proteins into fibers. However, the highest tenacity value (tenacity is the strength of a fiber) obtained was 2.26. This is much lower than the reported values for dragline silk (7 to 11).
Fig. 2. Physicist Nolwenn Huby of the Institut de Physique de Rennes in France recently demonstrated silk fibers in a small photonic chip. Light propagates along strands of spider silk just like fiber optic cables.
information). Although the silk fibers had brightness losses much higher than glass or plastic, they are much thinner than conventional fibers while maintaining strength and flexibility. Plus, tiny glass cables and metals wires are expensive and not very compatible with human tissue. Silk’s biocompatibility opens the gate for a range of medical applications including minimally invasive internal imaging or even implanted electronics (Huby, 2013).
he current problem with using s p i d e r silk-based material lies mainly in production. Farming spiders would be incredibly difficult for obvious reasons: they do not produce a lot of silk, like to eat each
company Nexia Biotechnologies continued the use of mammalian cells for silk protein expression. Scientists removed the genes that encodes dragline silk from an orb-weaver spider and placed them into the DNA responsible for milk production in the udders of goats. The altered genes were then inserted into an egg and implanted into a mother goat (the process used in mammalian cloning). It was thought that the manner in which mammary glands create long amino acid chains found in milk would enable the formation of spider silk proteins. Nexia then precipitated the proteins from the milk, creating a web-like material trademarked as BioSteel (Mansoorian, 2006). Although this technique initially produced promising results, the concentration of soluble protein in the milk was found to be low and the proteins could not be efficiently purified for thorough analysis. Although the company went bankrupt, Professor Randy Lewis at Utah State University, has continued research with the so-called “spider goats” at a university-run farm (Romer, 2008). pider silk technology is still in the very early stages and it may be decades before it enters into the lives of the average consumer. However, the future is bright considering dozens of universities and labs are focusing their efforts on unraveling the secrets of nature’s toughest fiber.
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References Agnarsson, I., Dhinojwala, A., Sahni, V., Blackledge, TA. (2009). Spider silk as a novel high performance biomimetic muscle driven by humidity. Journal of Experimental Biology, 21. 1990-1994. doi: 10.1242/ jeb.028282. Agnarsson, I., Kuntner, M., Blackledge, T. (2010) Bioprospecting Finds the Toughest Biological Material: Extraordinary Silk from a Giant Riverine Orb Spider. PLoS ONE, 5. Retrieved from http://www.plosone.org/ article/info%3Adoi%2F10.1371%2Fjournal.pone.0011234.
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Bryan, M., Forster J. (2012). A2 4 Doing Whatever a Spider Can. Journal of Physics Special Topics, 10. 1-2. Retrieved from https://physics.le.ac. uk/journals/index.php/pst/article/view/548/354. Gosline, J., DeMont, E., Denny, M. (1986). The Structure and Properties of Spider Silk. Endeavour, 10. 37-43. doi: http://dx.doi. org/10.1016/0160-9327(86)90049-9. Huby, N., Vie, V., Renault, A. (2013). Native spider silk as a biological optical fiber. Appl. Phys. Lett. 102. http://dx.doi.org/10.1063/1.4798552. Keten, S., Buehler, M. J. (2010). Nanostructure and molecular mechanics of spider dragline silk protein assemblies. Journal of The Royal Society Interface. Retrieved from http://hdl.handle.net/1721.1/61713. Lazaris, A., Arcidiacono, S., Huang, Y., Zhou, JF., Duguay, F., Chretien, N. (2002). Spider silk fibers spun from soluble recombinant silk produced in mammalian cells. Science, 295. 472-476. doi: 10.1126/ science.1065780. Legget, H. (2009) 1 Million Spiders Make Golden Silk for Rare Cloth. Wired. Retrieved from http://www.wired.com/wiredscience/2009/09/spider-silk/. Mansoorian, A. (2006). Comparing Problem Solving in Nature and TRIZ. The TRIZ Journal. Retrieved from http://www.triz-journal.com/ archives/2007/04/04/. Purves, W. (2003). Why is Spider Silk So Strong?. Scientific American. Retrieved from http://www.scientificamerican.com/article. cfm?id=why-is-spider-silk-so-str. Römer, L., Scheibel, T. (2008). The elaborate structure of spider silk. Prion, 2. 154-161. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/ articles/PMC2658765/. Shao, Z., Vollrath, F. (2002). Surprising strength of silkworm silk. Nature, 418. 741. doi:10.1038/418741a.
Image Source http://www.flickr.com/photos/aviansky/10907613954/ http://www.sandstormreptiles.com/#!invertabrates/c1bbt http://d3gtl9l2a4fn1j.cloudfront.net/t/p/original/ waZqriYTuBE3WqXI3SDGi3kfDQE.jpg http://pbmo.files.wordpress.com/2011/03/spider-silk-protein.png
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Poverty & Stress By Neel Jani The poorest children are 10 times more likely to die Physically, those in poverty experience greater environmental toxins, air pollution, and hazardous waste. Cognitively underprivileged children face significantly higher levels of turmoil, violence, and strife at home. Overall, children in impoverished households experience much more chaos than do middle and upperincome children growing up, and such instability impairs their cognitive development in the future. Evans found that children who live in prolonged stressful environments endure higher blood pressure (approximately 2 mm/Hg) when exposed to math problems relative to their counterparts who live in in non-stressful environments. Moreover, these children took a longer time for their blood pressure to reach the baseline levels after the problem was handed out.
Hence, research concluded that this was one of the reasons as to why the underprivileged in general perform worse on cognitive tests than those who do not face the adverse conditions of poverty. Interestingly enough, Evans and colleagues found that those who are poor but somehow evade the stress of poverty perform just as well as their non-poor counterparts (Evans, Brooks-Gunn, & Klebanov, 2007). This finding is vital in understanding the relationship between poverty and stress. Poverty in of itself does not lead to poor cognitive ability but rather causes the stressful reaction that accompanies it.
Poverty in of itself does not lead to poor cognitive ability but rather causes the stressful reaction that accompanies it.
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The poorest children are 10 times more likely to die Physically, those in poverty experience greater environmental toxins, air pollution, and hazardous waste. Cognitively underprivileged children face significantly higher levels of turmoil, violence, and strife at home. Overall, children in impoverished households experience much more chaos than do middle and upperincome children growing up, and such instability impairs their cognitive development in the future. Evans found that children who live in prolonged stressful environments endure higher blood pressure (approximately 2 mm/Hg) when exposed to math problems relative to their counterparts who live in in non-stressful environments. Moreover, these children took a longer time for their blood pressure to reach the baseline levels after the problem was handed out. Hence, research concluded that this was one of the reasons as to why the underprivileged in general perform worse on cognitive tests than those who do not face the adverse conditions of poverty. Interestingly enough, Evans and colleagues found that those who are poor but somehow evade the stress of poverty perform just as well as their non-poor counterparts (Evans, Brooks-Gunn, & Klebanov, 2007). This finding is vital in understanding the relationship between poverty and stress. Poverty in of itself does not lead to poor cognitive ability but rather causes the stressful reaction that accompanies it.
Overall, children in impoverished households experience much more chaos than do middle and upperincome children growing up, and such instability impairs their cognitive development in the future. Research indicates that more detrimental psychological problems were experienced by those exposed to poverty related stress (Bauer and Boyce, 2004). Specifically, they found that stressful environment conditions alter neuroendocrine response systems, primarily the sympatheticadrenomedullary and hypothalamic-pituitary-adrenal systems. Significantly increasing activity within these response systems leads “to a host of biomedical
diseases and psychiatric disorders responsible for significant population morbidity” (Bauer and Boyce, 2004). Hence, the increased activity of these systems is inevitable for the poor, whose daily life is inherently connected to stressful environments. Unfortunately such high levels of activity within these systems are associated with the degradation of later health. Such health consequences are in fact more devastating toward children. This finding reveals that the poverty cycle is in a sense a feedback loop, since the more poor one gets the less healthy he and his children are; the less healthy his children are the greater the chance that they will also grow up in poverty. The researchers attribute this finding to two reasons. First, children feel helpless in their adverse conditions and bear more stress than the parents; they perceive themselves as lacking control over the negative outcomes surrounding them. Secondly, parents tend to neglect kids during stressful moments in poverty as they prioritize other immediate obligations such as money for food over interacting with their children. In fact, Shepherd a researcher at Oregon State University finds this to be true holistically. She finds that poverty causes caregiver stress, which in turn causes physical neglect for the child (Shepherd, 2012). In fact, child abuse and neglect are found to be statistically higher among underprivileged families. The child is neglected the parent prioritizes economic obligations over maintaining the condition of their child’s health and education. In fact, 22% of children in the lowest income group lived with a depressed parent and 12.5% with a chronically stressed parent compared with 6% and 3.5% respectively among children in the highest income group (Spencer 2008). Clearly, underprivileged parents are generally more overwhelmed and have more reason to neglect their kids. Shepherd also finds, similar to Evans, that poverty in of itself does not cause physical neglect. Instead, it is the caregiver’s stressful reaction to the poverty that causes the physical neglect. Several other hypothesis and alternative explanations exist regarding relationship between poverty, stress, and cognitive function. Mani finds that poverty in of itself reduces cognitive capability; however this is not due to stress (Mani et al., 2013). Rather “poverty-related concerns consume mental resources, leaving less for other tasks” (Mani et al.,
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the limited cognitive resources we possess, and limits the cognitive resources available for other activities. These findings appear to be similar to what was discussed earlier; for instance, it can be argued that stress is holding our attention and reducing our mental capacity. However, the typical biological responses that are associated with increased stress, such as an increase in cortisol levels, are absent even with diminished cognitive capacity. Thus, this research reveals that even if poverty causes stress, it’s not a factor in diminished cognitive capacity.
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Poverty in of itself does not cause physical neglect. Instead, it is the caregiver’s stressful reaction to the poverty that causes the physical neglect.
Solving for poverty at its root is evidently very difficult. As shown earlier, the majority of research, excluding that of Mani, concludes that stress caused by poverty, not poverty itself, leads to impaired cognitive development for children and child neglect. Thus, a majority of the research concludes that a method of reducing poverty can be the amelioration of health that is impaired through stress. This would increase cognitive functions and help educate the underprivileged, which would then allow them to develop critical thinking skills. This development of critical thinking is important as it allows for underprivileged people to solve problems facing them, without burdening themselves with stress as they had done previously. This in turn would decrease all the negative effects associated with stress on health and cognitive function (Bauer and Boyce, 2004). Interestingly, it has been empirically proven that health improvement is maximized through indirect effects from increases in education rather than direct efforts to enhance health. Therefore, education not only directly helps one to remove himself from the poverty cycle but promotes healthier behaviors and increases health literacy to alleviate stress and subsequent diminished cognitive function (UNICEF 2002).
the association between poverty and stress opens up a field of solutions that have not been extensively explored. Specifically, the research indicates that poverty causes stress, which in turn causes adverse health and cognitive outcomes as well as child neglect. These consequences are huge barriers for any child to escape the clutches of poverty. By solving for stress and the health outcomes associated with it, we limit stress’s negative impacts on underprivileged individuals. The optimal solution seems to be advances in education. In fact, research suggests that childhood programs such as Head Start Program by the US Department of Health and Human Services can result in improvements in cognitive development in the future (Bauer and Boyce, 2004). If one does not accept stress as the internal link from poverty to negative cognitive outcomes, then the above assertions might not hold true. However, if one accepts that poverty causes stress, which then causes decreased health outcomes, education seems to be the answer in thwarting poverty.
Overall, poverty represents a problem that has been unsolved for millennia. Recent research into 44 rkeley Scientific Journal Stress18• F• all 2013 • Berkeley Scientific Journal • Stress • Fall•2013 • Volume Issue 1 •
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References Bauer, A. M., & Boyce, W. T. (2004). Prophecies of Childhood: How Children’s Social Environments and Biological Propensities Affect the Health of Populations. International Journal of Behavioral Medicine, 11(3), 164-175. Evans, G. W., Brooks-Gunn, J., & Klebanov, P. K. (2011). Stressing Out the Poor. Retrieved from http://www.stanford.edu/group/scspi/_media/ pdf/pathways/winter_2011/PathwaysWinter11_ Evans.pdf Haushofer, J., de Laatu, J., & Cheminu, M. (2012, October). Poverty Raises Levels of the Stress Hormone Cortisol: Evidence from Weather Shocks in Kenya. Mani, A., Mullainathan, S., Shafir, E., & Zhao, J. (2013). Poverty Impedes Cognitive Function. Science, 341(976), 976-980. Retrieved from http://www2. warwick.ac.uk/fac/soc/economics/staff/academic/ mani/mani_science_976.full.pdf Shepherd, J. R. (2012, March). Poverty and Child Neglect: Subtypes of Neglect and Stress as a Mediator. Spencer, N. (2009). Health Consequences of Poverty for Children. 2002 UNICEF ANNUAL REPORT (UNICEF, Comp.). (2002). Retrieved from http://www.unicef. org/publications/files/pub_ar02_en.pdf Image Sources “CoR - European Platform against Poverty and Social Exclusion.” CoR - European Platform against Poverty and Social Exclusion. Europe 2020 Monitoring Platform, n.d. November 31, 2013. Straub, Gerry. “Poverty and Prayer.”March 10, 2008. Gerry Straub’s Blog. Wordpress.
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The potential for Abuse: Addiction Stress of prolonged substance abuse/addiction on Brain
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Figure 1. MRI scans of rat brains for a brain abnormalities study.
The U.S. Food and Drug Administration (FDA) defines abuse potential as a drug used for recreational use repeatedly and sporadically for the positive psychoactive effects that are produced on the central nervous system (FDA, 2010). These drugs include, but are not limited to, opioids, nicotine, amphetamine, ethanol, and cocaine (FDA, 2010). Drugs of potential abuse may in certain circumstances lead to addiction, more commonly referred to as substance dependence (FDA, 2010). Addiction is a chronic disorder characterized by a compulsive use of substances despite the adverse consequences involved (FDA, 2010). Recent studies indicate that addiction may be a chronic brain disease caused by abnormalities in the mesolimbic system.
studied by Olds and Milner (1954) who first identified the regions of the brain in which direct electrical stimulation produced a positive reinforcing effect. Olds and Milner conducted laboratory experiments in which they implanted electrodes in various
Dopamine, a neurotransmitter in the central nervous system associated with motor function, motivation, and pleasure is involved in the action of many drugs of potential abuse (Arias-Carrión, Stamelou, Murillo-Rodríguez, Menéndez-González, & Pöppel, 2010). Of the various dopaminergic pathways found in the body, the mesolimbic dopamine system in particular plays a crucial role as the “pleasure center” of the brain by reinforcing rewarding behavior (Hyman, 2005). This pathway contains dopaminergic neurons along which signals are carried from one region of the brain to another.
regions in the rat’s brains and allowed the rats to self-administer their own electrical stimulation with a lever (Olds & Milner, 1954). They found that in the areas of the brain in which electrical stimulation was most rewarding, the rats stimulated themselves in these areas most frequently and regularly and for a longer duration of time if they were allowed to do so (Olds & Milner, 1954). These studies indicated that the most sensitive areas of the brain that were able to produce the highest rewarding effects were also all connected through the neural pathway of the medial forebrain bundle (Olds & Milner, 1954).
“A comparison of brain imaging pictures demonstrated that there is a significant difference between the brains of an addict as compared to a non-addict”
The brain reward system was comprehensively
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associated with conditioned learning involving the beneficial biological value of stimuli (Hyman, 2005). This structure conditions an individual to be able to associate an external stimulus as either rewarding or aversive (Hyman, 2005). The VTA also interacts with a nearby structure known as the hippocampus, located in the temporal lobe’s medial portion. The hippocampus plays a crucial role in memory, adaptive behavior, and the maintenance of homeostasis (Nestler, n.d.). Lastly, the medial prefrontal cortex of the brain functions in decision making related to a reward or aversive stimuli (Hyman, 2005).
Figure 2. PET scans of human brain showing addictive substances and their consequences
The mesolimbic pathway begins in a region of of the midbrain referred to as the ventral tegmental area (VTA) that connects to the limbic system through projections to the nucleus accumbens, amygdala, hippocampus, and medial prefrontal cortex (Hyman, 2005). The VTA is composed of various types of neurons that include a specific cluster of dopaminergic neurons that communicate foremost with the nucleus accumbens via the medial forebrain bundle (Hyman, 2005). Although the number of dopaminergic neurons housed in the VTA is miniscule compared to other regions of the brain, these individual neurons run extensively throughout the brain, with axonal lengths approximating 74 cm and synaptic connections containing roughly 500,000 terminals (Arias-Carrión, et. al., 2010). As a result, dopaminergic neurons are able to play a specialized role in influencing complex regions of the brain such as the reward system. The dopaminergic neurons of the VTA communicate with the medium spiny neurons of the nucleus accumbens (NAc) through synaptic connections that release dopamine neurotransmitters into the NAc (Hyman, 2005). The VTA- NAc circuit is involved in mediating the rewarding effects of both natural rewards and drugs of potential abuse (Hyman, 2005). The amygdala is another structure within the limbic system that interacts with the VTANAc pathway through neural circuitry. Located in the temporal lobe anterior to the hippocampus, the amygdala functions in regulating emotions and is
Under normal conditions, the mesolimbic system of the brain reinforces positive behavior provides a positive reinforcement of behavior that is serves to be beneficial to an individual and species. The mesolimbic system creates a sense of pleasure and reward when an individual engages in behavior that pertains to water, food, exercise, or reproduction (Nestler, n.d.). These naturally rewarding stimuli activate the mesolimbic system, resulting in a release of dopamine neurotransmitters in the shell of the nucleus accumbens (Hyman, 2005). This positive reinforcement of pleasure results in this particular behavior to be repeated again. Similarly, all drugs of potential abuse also act directly on the mesolimbic pathway by releasing dopamine and producing the same sense of pleasure (Arias-Carrión, et al., 2010). However, drugs of potential abuse differ from natural stimuli due to their ability to release a more substantial concentration of dopamine into the extracellular space of the nucleus accumbens, resulting in an increase in rewarding effects (Volkow, Fowler, Wang, Swanson, 2004). In essence, the brain adapts to the over stimulating effects of these drugs through homeostatic mechanisms that result in the production of tolerance in which an individual is forced to increase dosage of a drug in order to receive the same effects (Volkow, et al., 2004).
“Located in the temporal lobe anterior
to the hippocampus, the amygdala functions in regulating emotions and is associated with conditioned learning involving the beneficial biological value of stimuli”
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Further studies have illustrated that in vivo administration of different drugs of abuse results in a common an increase in synaptic strength of dopamine neurons in the VTA-NAc circuit (Saal, Dong, Bonci, Malenka, 2003). A study compared five different drugs of abuse that differed in their molecular mechanisms within the brain: cocaine, amphetamine, morphine, nicotine, and ethanol (Saal, et al., 2003). First, cocaine and amphetamine were compared together due to similarities they share as both being a psychoactive stimulant that increases dopamine concentrations within the brain (Saal, et al., 2003). These two drugs of potential abuse were found to both increase excitatory transmission onto dopamine neurons (Saal, et al., 2003). Similar results were found in morphine’s effect on opioid receptors, (which acts on opioid receptors), nicotine’s on nicotinic receptors, and ethanol’s on various neurotransmitters (which acts on nicotinic receptors), and ethanol (that acts on various neurotransmitters) (Saal, et al., 2003). However, there were no apparent increases in the changes in synaptic adaptations on dopamine neurons with non-abusive drugs (Saal, et al., 2003). “Similarly, all drugs of potential
abuse also act directly on the mesolimbic pathway by releasing dopamine and producing the same sense of pleasure”
Although drug reward does play a role in drug addiction, it does not necessarily constitute the main underlying factor causing addiction. As a psychological disorder, addiction can also be attributed to various factors that can be influenced by environmental and genetic factors. However, the sense of euphoria and pleasure that is felt by selfadministration of a drug can promote addiction by causing an individual to engage in repeated drug use (Chiara, 1999). Increased levels of dopamine release in response to salient stimuli such as drugs of abuse play a role in learning and motivation. Both addictive drugs and natural stimuli result in dopamine release that promotes an individual to engage in a certain behavior through positive reinforcement that is able to associate salient stimuli with a distinctive memory. However, the substantial release of dopamine from
drugs of abuse can overtime result in neurobiological changes in the brain that alter the thresholds in which natural stimuli and drug stimuli are able to activate dopamine release (Volkow, et al., 2004). Brain imaging studies have indicated a decrease in the release of dopamine and the number of dopamine receptors in the mesolimbic pathway associated with an addicted individual (Volkow, et al., 2004). As a result of these decreased dopaminergic effects on the brain, an individual must increase dosage of a certain drug of abuse due to the tolerance that the brain has developed. As the levels of dopamine decrease, an individual becomes desensitized to natural stimuli that once were salient and the sense of pleasure subsides (Volkow, et al., 2004). With the memories stored in the amygdala and hippocampus, an individual may attempt to recreate these euphoric feelings through compulsive use of drugs despite the negative consequences involved (Volkow, et al., 2004). Drugs of abuse can be potentially hazardous in their abilities to alter the brain in which natural stimuli become desensitized and behavior that once promoted survival is no longer reinforced. Although the linkage between drug reward and drug addiction is not entirely developed, there is evidence that supports that certain factors of drug reward have the potential to lead to addiction (Pierce, 2005).
Figure 3. A rat with a fiber-optic cable, which applies a laser signal to the brain to stimulate specific brain cells.
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References: 1. Saal, Daniel, & Dong, Yan, & Bonci, Antonello, & Malenka, C. Robert (2003). Drugs of Abuse and Stress Trigger a Common Synaptic Adaptation in Dopamine Neurons. Neuron, 37 (4), 577-582. http:// dx.doi.org/10.1016/S0896-6273(03)00021-7
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2. Old, James, & Milner, Peter (1954). Positive Reinforcement Produced by Electrical Stimulation of Septal Area and Other Regions of Rat Brain. Journal of Comparative and Physiological Psychology, Vol 47 (6), 419-427. doi: 10.1037/h0058775 3. Ikemoto, Satoshi, & Bonci, Antonello (2014). Neurocircuitry of Drug Reward. Neuropharmacology, 76 (B), 329-341. http://dx.doi.org/10.1016/j. neuropharm.2013.04.031 4. Pierce, R. Christopher, & Kumaresan, Vidhya (2005). The Mesolimbic Dopamine System: The Final Pathway for the Reinforcing Effect of Drugs of Abuse? Neuroscience & Biobehavioral Reviews, 30 (2), 215-238. http://dx.doi.org/10.1016/j. neubiorev.2005.04.016
Psychiatry, 162 (8). http://dx.doi: 10.1176/appi. ajp.162.8.1414 10. Nestler Laboratory, Laboratory of Molecular Psychiatry, Icahn School of Medicine at Mount Sinai. Brain Reward Pathways. http://neuroscience.mssm.edu/nestler/ brainRewardpathways.html 11. Arias-Carrión, Oscar, & Stamelou, Maria, & MurilloRodríguez, Eric, & Menéndez-González, Manuel, & Pöppel, Ernst (2010). Dopaminergic reward system: a short integrative review. International Archives of Medicine, 3. doi:10.1186/1755-7682-3-24
Image references: http://www.deviantart.com/customization/wallpaper/ fractals/?view_mode=2&order=5&q=vista http://news.emory.edu/stories/2013/09/ lab_land_biomedical_blog/campus.html http://www.nyu.edu/about/news-publications/ news/2012/08/22/ researchers-find-benefits-to-early-interventionin-addressing-brain-abnormalities-.html
5. Volkow, D. N, & Fowler, S. J, & Wang, J. G, & Baler, R., & Telang, F. (2008). Imaging Dopamine’s Role in Drug Abuse and Addiction. Neuropharmacology, 56 (supplement 1), 3-8. http://dx.doi.org/10.1016/j.neuropharm.2008.05.022 6. Chiara, Di Gaetano (1999). Drug Addiction as dopamine-dependent associative learning disorder. European Journal of Pharmacology, 375(1-3), 13-30. http://dx.doi.org/10.1016/S0014-2999(99)00372-6 7. US. Department of Health and Human Services, Food and Drug Administration (2010). Draft Guidance/ Guidance for Industry. Assessment of Abuse Potential of Drugs. [http:/ / www.fda.gov/ downloads/ Drugs/ GuidanceComplianceRegulatoryInforma tion/ Guidances/ UCM292362.pdf] 8. Volkow, D. N, & Fowler, S. J, & Wang, J. G, & Swanson, M. J (2004). Dopamine in drug abuse and addiction: results from imaging studies and treatment implications. Molecular Psychiatry, 9, 557-559. doi:10.1038/sj.mp.4001507 9. Hyman, E. Steven (2005). Addiction: A disease of learning and memory. The American Journal of 41 • Berkeley Scientific Journal • Stress • Fall 2013 • Volume 18 • Issue 1
Optimizing Stress Abigail Chaver
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You glance at the clock for the third time this minute. You’ve got twelve minutes and 13 — no, 23, no, 13, 12 seconds left. Your limbs are rigid and vibrating, your heart is pounding, and your cheeks are hot. You’re trying to remember how to take the integral of a square root and all you can hear is the scratching of others’ pencils. You did this just two days ago, but right now you can barely remember the times tables. When stress reaches extremely high levels, it becomes debilitating. But when it’s not overwhelming, and instead moderate, stress is a crucial factor in success. Without it, our minds are disengaged, slow, and unproductive. This idea is captured well in a classic Buddhist teaching: A person has to be tuned like the string of an instrument: If it is too taut, it will snap. If it is too slack, it will not play. We can benefit from “tuning” to this ideal tension. The question is, how? The theory of stress tuning is well displayed by the Inverted-U graph, which plots stress against productivity (Figure 1). Finding actual data to fit this graph is difficult. The science of stress can be approached from several angles including biology, psychology and economics. However, data from these three fields looks quite distinct. Understanding the method of data collection and its precision will help determine its usefulness in stress management at both the individual and organizational levels.
a 4 indicating high stress), and then the numbers are summed, giving the score from 0 to 40, where 40 is the maximum stress level. This survey, and others like it, attempts to measure feelings of frustration, emotional instability, and failure. This makes it a very poor metric for identifying a good stress level – it implies that the ideal amount of stress is 0. In fact, most stress research presents a negative relationship between stress and productivity. A review analyzing this correlation concluded that these findings were constrained by methodology. Because of stress’s negative connotations, most research focuses on its negative effects— surveys rarely ask questions about feeling under-stressed. (Muse, 2003) The PSS is a good example of a survey that fails to measure the under-stressed condition. The review suggests adding questions to stress surveys regarding feelings of boredom and levels of engagement.
Psychology Metrics Surveys are commonly used in psychology and are fairly easy to administer. However, stress-related surveys often fail to differentiate constructive stress from destructive stress. For example, the Perceived Stress Scale uses a survey to rate an individual’s stress Figure 1: Inverted U Model level. The PSS asks subjects to report the frequency of thoughts, on a scale of 0-4 (never - extremely frequently), relating to both positive and negative Part of the problem may be the ambiguous items. For example, a negative item might be, “In the definition of “stress,” which is inconsistently defined last month, how often have you been upset because in research (Muse, 2003). Language varies: sometimes of something that happened constructive stress is unexpectedly?” A positive called “Eustress,” while item might be “In the last the destructive stress “However, stress-related month, how often have you is called “Distress.” surveys often fail to differentiate felt that you were on top Others describe a of things?” (Cohen, 2013) positive stress condition constructive stress from The results for the positive as being “arousal,” a destructive stress.” items are reverse scored (a 0 condition separate from on a positive item becomes stress. A more uniform 34 • Berkeley Scientific Journal • Stress • Fall 2013 • Volume 18 • Issue 1
understanding of stress as a continuous gradient with both positive and negative aspects may improve psychological metrics and research.
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Biological Metrics A chemical indicator of stress, such as adrenalin or cortisol levels, is a less subjective measure (Figure 2). There are blood, urine and saliva tests. These tests must be processed by a lab and therefore require some resources beyond the scope of personal home testing (ADAM, 2013). Cortisol levels reliably fluctuate throughout the day (ADAM, 2013). They also fluctuate in response to specific events, so chemical levels taken once are not necessarily indicative of long-term stress levels. For these reasons, chemical indicators may not be ideal for managing stress. However, they do have the advantage of measuring stress at excessively low and high levels. This could be useful in identifying an optimal range.
Economic Metrics An economic approach would consist of looking at productivity figures rather than stress directly. This approach is somewhat risky as it might encourage increasing stress until productivity begins to fall. There is likely to be a lag before stress begins to seriously affect performance. Productivity metrics depend on the situation. Sales revenue, grade point average, time frame to complete a project, or number of bugs in a product are all possible metrics. None of these external indicators offer much information about stress levels. However, if they were paired with a direct measure of stress levels, like the previously mentioned psychological or biological metrics, they could be insightful. Economics can also illuminate why stress has become a severe problem. Economies that increasingly rely on automation shift humans into jobs that require more responsibility and critical thinking (Figure 3). While these jobs are more mentally stimulating, they are associated with higher stress levels (Maxon, 1999).
Figure 2: The molecular structure of the hormone cortisol. A less direct measure of stress that is subject to fewer short-term fluctuations is health data. Most companies pay for their employees’ health insurance and lose money when employees are ill. They would have an interest in following figures like health care costs and frequency of stress-related illnesses, and would have an incentive to reduce stress if it was correlated with tangible costs such as sick days (APA, 2010). Being under-stressed has less discernible health effects and thus measuring health care costs is not ideal for finding the optimal range of stress as it cannot provide insightful or actionable data about being understressed.
A practical approach might be to find proxy indicator of stress rather than a direct measure. For example, low reaction time is a plausible indicator of optimal cognitive function and is highly influenced by stress levels. Using a test of mental reaction time could be low-cost, and could yield an excellent metric. The activity itself would be a small stressor that could raise stress levels moderately, which should be accounted for when considering the data. An activity that tracks both speed and correctness, like a timed sorting game, would be helpful for determining peak mental faculties and when anxiety has become destructive. An activity done over a computer interface would allow mouse tracking, another source of anxiety-related data. Frequent and unnecessary mouse movements might be a good indicator of stress above optimal levels. This data would not be trackable on a touchscreen device, somewhat limiting the utility of this test.
“An activity that tracks both speed and correctness, like a timed sorting game, would be helpful for determining peak mental faculties and when anxiety has become destructive.”
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1991) Evaluations of psychological hardiness are typically subjective and qualitative, but many of them avoid the self-reporting trap by soliciting information from supervisors and peers.
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What insights does this theory provide? Commitment is fairly easy to understand: A person’s belief in the importance of what they’re doing will increase their tolerance for setbacks and their desire to persevere. Challenge is almost circular reasoning: Figure 3: Macroeconomic trends are partly responsible for increased stress levels in the workforce. A person’s belief that they can handle Finding a proxy with an already established data a challenge is probably based on past experiences stream would be ideal, but this would differ across successfully handling challenge. This would correlate organizations. The amount of time it takes to respond to being good at handling challenge. Control is the to an email could be a good corollary, or it could most insightful— a feeling of power over one’s own indicate high distractibility. Other interesting indicators life is strongly correlated to high stress tolerance. The could be speed of movement or speech, but these are application of this idea would be increasing individuals’ difficult to measure. autonomy. This requires trust in the judgment of people as well as their ability to function without close This data could be tracked by individuals or oversight. aggregated. If optimal stress levels varied widely between people, aggregation of data would make it There is question as to whether psychological difficult to track specific trends. There could be some hardiness is a personality trait or a skill that can be effort to normalize the data or plot inverted-U curves learned. For example, some theorize that psychological for individuals. It might also be extremely valuable to hardiness is simply low neuroticism, as measured on an organization, especially while hiring, to have data Big 5 personality scales. There does seem to be some about a person’s stress curve. Many professions are correlation, but whether the two are equivalent remains self-selecting for stress levels, but adding more data as to be seen. (Bartone, 2009) Building psychological a reference for this process can help many make better hardiness seems more plausible if it is not a personality decisions regarding the external stressors in their lives. trait.
Stress Coping Ability A study of a high-stress occupation, military combat, identified a trait that showed a high positive correlation to excellent leadership performance: psychological hardiness. (McDonald, 2013) While this study was specifically about military leadership, psychological hardiness has been studied in employees, social workers, and other groups. Psychological hardiness has been broken down into three components: Commitment, Challenge, and Control. Respectively, these can be understood as a person’s commitment to their pursuits, belief in their ability to handle a challenge, and their belief that they have a measure of control over the rewards and punishments they receive. (Bartone,
Solutions While none of the metrics discussed are perfect, they can be useful, especially when combined. Using a self-reported or chemical indicator of stress and a measure of productivity can help individuals and organizations set reasonable productivity goals and stress boundaries. Awareness of stress levels and stress tolerance should guide decisions regarding beginning a new activity or cutting down on responsibilities. Sources of stress that don’t contribute to productivity, such as unclear communication of expectations, should be eliminated first when stress is too high. Stressors like workload and novel problems are appropriate to increase when stress is too low. Lastly, a conscientious
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effort to increase psychological hardiness can help stress tolerance rise, improving productivity.
Works Cited ADAM. (December 11, 2011) Cortisol Level. Retrieved October 28, 2013 from: http://www.nlm.nih. gov/medlineplus/ency/article/003693.htm
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American Psychological Association Practice Organization. (2010). PsychologicallyHealthyWorkplaceProgramFactSheet: BytheNumbers. Retrieved from http://www.phwa.org/ dl/2010phwp_fact_sheet.pdf Bartone, Paul T., “Development and Validation of a Short Hardiness Measure,” Third Annual Convention of the American Psychological Society (June 1991) Retrieved October 28, 2013 from: http://www. hardiness-resilience.com/docs/aps91b.pdf Bartone, Paul T., Eid, Jarle, and Snook, Scott, “Big five personality factors, hardiness, and social judgment as predictors of leader performance,” Leadership and Organization Development Journal 30 (6) (March 2009): 498-521. Cohen, S., Kamarck, T., Mermelstein, R. (1983) A global measure of perceived stress. Journal of Health and Social Behavior, 24, 385-396. http://www.psy.cmu. edu/~scohen/scales.html Cortisol [Graphic]. (2013). Retreived October 28, 2013 from: http://www.huck.psu.edu/about/newsarchive/susman-adolescent-violence Maxon, Rebecca. (1999). Stress in the Workplace: A Costly Epidemic. Fairleigh Dickinson University Magazine, http://www.fdu.edu/newspubs/ magazine/99su/stress.html McDonald, S. P., (2013). Empirically Based Leadership: Integrating the Science of Psychology in Building a Better Leadership Model. Military Review, 93(1), 2. Muse, Lori A., Harris, Stanley G., Feild, Hubert S. (2003) Has the Inverted-U Theory of Stress and Job Performance Had a Fair Test?, Human Performance, 16:4, 349-364, DOI: 10.1207/S15327043HUP1604_2 US Manufacturing Jobs as a Percentage of All Jobs [Graph]. (2012). Retrieved October 28, 2013 from : http://research.stlouisfed.org
Image Sources stuff4educators.com http://research.stlouisfed.org 37 • Berkeley Scientific Journal • Stress • Fall 2013 • Volume 18 • Issue 1
The Language of Science
What ideas do we stress?
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On April 24, 1990
Edwin Hubble, the astronomer who realized in 1929 that the universe is expanding uniformly in ,a all directions. It was a ground-breaking discovery, piece of equipment roughly the size of a schoolbus fundamentally reshaping how we view our was launched into space (Hubblesite, nd). At the universe. As a memorial, NASA elected to honor time the unit cost $1.5 Hubble’s discovery billion ($4.3 billion naming their own today), weighed as “When a scientist identifies a new by ground-breaking much as two large protein, invents a better test for optical space telescope elephants and was due to become the world’s cervical cancer, or finds a new spe- after the astronomer. It’s a great story. Or first space-based optical cies of pufferfish, how do you pick would be a great story, telescope (BLS Inflation Calculator; Wolfram the most important feature? What had Edwin Hubble made the discovery Alpha). The contraption do you name it?” first. Two years earlier, was the Hubble Space a little-known Belgian Telescope, and chances priest and astronomer are that you have seen named George Lemaître published a finding that the striking images the HST has collected in the the universal rate of expansion is accelerating, decades since. The telescope was named after
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and included a mathematical constant, much like Hubble had, which could account for that expansion (HubbleSite News Center, nd). However, Lemaître’s name is not recognized beyond the smallest circles, and we maintain Edwin Hubble as the pioneer. What happened? Lemaître originally published his work in French in 1927, and when it was translated to English in 1931, he elected to omit the crucial passages about his version of Hubble’s constant. He believed they were “of no actual interest”, certain that others would publish more appropriate figures. Lemaître was humbly uninterested in receiving credit for his discovery, and as he slipped into obscurity, time granted his wish. So what is in a name? Does it matter that history remembers Hubble, and not Lemaître? When a scientist identifies a new protein, invents a better test for cervical cancer, or finds a new species of pufferfish, what is the most important feature? How do you name it? What idea about that discovery is so fundamental or important that this is the one feature you stress? This is a big decision to make because at the end of the day, the goal of scientific communication is to share ideas about the world. When human curiosity moves us to look out into the world, then back into our own minds, we wonder: How? Why? What if? Once we answer the questions, we turn to recording those answers. This is the moment that we face the name decision. Each word carries within it some idea that its inventor believed had future value, and was therefore worth remembering by name. Which name to choose? Hopefully one that in some way relates to the form or function of the thing described. T a k e , for example the task of naming a flower. About a year ago, I toured the historical district of Monterey, CA. Passing through a garden, I spotted a bush whose flowers had enormous, floppy, white petals, with a great golden dollop in the center. I chuckled and remarked to a companion, “And here we have the fried egg plant!” Moving closer, I spotted a small plaque sitting at the bush’s base. Imagine my surprise
Figure 1. George Lemaître (left) with Albert Einstein (right), California, 1933.
when I read: ‘Fried Egg Flower, Romenya Coulteri, S. California and Mexico’. Imagine my delight. The name made sense, of course, but there are almost infinitely many other possibilities. For instance, the fried egg flower has great, sweeping white petals and a splash of yellow. The plant just as easily could have been named after Marilyn Monroe: Romenya Marylini. The name is relatable; it would probably go undisputed in western countries. However, a trip east might reveal a botanist in Cambodia who does not recognize the significance of Romenya Marylini, having no prior knowledge of the great actress. With so many options, naming a discovery or invention can be a stressful. Sometimes there is guidance ( t a p p i n g into extant etymological traditions), but other times the decision exists in isolation. Lewis and Clark had no name for the pronghorn antelope they first encountered on their journey across North America in 1704. They chose to call it a “buck goat”, in the absence of any other available name (Ambrose, 2002). Looking at an antelope, one can clearly understand the description, but the question remains: Why didn’t buck goat stick? It does look like a hybridized goat deer. The answer
“(...) at the end of the day, the goal of scientific communication is to share ideas about the world (...) Which name to choose? Hopefully one that in some way relates to the form or function of the thing described.”
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Figure 2. Romneya, the fried egg flower (left). Can you see why the flower may also invoke Marylin Monroe (right)?
is that we now recognize pronghorns to be more closely related to other antelope species than goats. Even Clark noted “he is more like the Antilope or Gazella of Africa than any other Species of Goat” (Smithsonian Museum of Natural History, nd). The name ‘pronghorn antelope’ would not show up until 1826 (Oxford English Dictionary, 2013). The switch to stress a more phylogenetically accurate name would seem almost inevitable, but science is not always so self-correcting. Systemically, science is full of misnomers that stem from situations similar to the Hubble and buck goat stories. Misnomers can stem from publishing in an obscure language, in a country distant from intellectual centers, even naming a discovery with terminology that is simply not obvious enough -all of these factors contribute to the at-times chaotic field of scientific taxonomy. Sometimes the confusion happens by accident. One can’t help but be charmed by the 17 distinct ways Clark spells ‘mosquito’ in his journals chronicling the transcontinental journey. Misspellings aside, the synonym can be just as tricky. In practice, there is considerable overlap between the field of applied psychology and that of user experience, but if a user experience researcher doesn’t know to use the search term ‘applied psychology’, he or she might entirely miss a key reference or potential collaboration. A more serious incident occurred in 1999. The new Mars satellite disappeared from NASA’s communication lines after dipping too close to the planet. It later surfaced that a misunderstanding between the collaborating American and European teams had led to the accident. One team was using imperial units, while the other was using metric. At $94 million dollars ($1.48 billion today), losing the satellite was a costly mistake. Accidents happen in scientific communication,
but what happens when the scientist intends to confuse or obscure? What if the author chooses to stress non-intuitive features, or to emphasize complexity at the expense of readability? Sir Isaac Newton chose to publish Principia Mathematica in Latin, to ward off any who might pester him about its content. Indeed, William Cropper called it “one of the most inaccessible books ever written” (Cropper, 2001). Newton aimed to exclude amateur readers with the Principia’s impossibly dense prose, but he was also serving a personal vendetta against Robert Hooke -- Hooke had published statements crediting himself with Newton’s equation for the inverse square law. Newton vengefully struck Hooke out of the acknowledgments, and went on
“When we step back to consider the amount of confusion that can arise from nomenclature fraught with error and inconsistency, why bother to name something at all?” to write the key section in propositional logic and Latin thicker than molasses (Inverse Square Blog, nd). When we step back to consider the amount of confusion that can arise from nomenclature fraught with error and inconsistency, why bother to name something at all? The physicist Richard Feynman’s father once taught him, “You can know the name of that bird in all the languages of the world, but when you’re finished, you’ll know absolutely nothing whatever about the bird. You’ll only know about humans in different places, and what they call the bird (Feynman 1988). Was Feynman’s father right? Is naming something far less important than knowing its nature? In part, the wisdom holds. Naming all of the periodic elements is impressive, but doing so without regard for how they interact in the world, or with each other, seems to defeat the purpose of chemical knowledge. Can’t we just stress their properties? Well, sure, but at the end of a day, we come back to our naming traditions. Naming systems are ingrained within our ability -- and human tendency – to categorize and catalogue information (Tran, 2012). At the end of the day, it is simply inefficient to refer to ‘neon’ as
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‘that gas naturally occurring in our atmosphere that rarely reacts with anything, and is frequently found in Las Vegas signs.’ What’s more, there are features of the physical world we can never observe directly. For example, we could hardly hope to understand the activity of subatomic neutrino particles passing through the space between our atoms without someone telling us about them -- and that telling requires some standard of scientific language. As natural categorizers, it is unsurprising that humans spend quite a bit of time classifying everything we encounter. We have been classifying things since the dawn of language, but perhaps the most significant shift in science taxonomy came in 1753 when Carolus Linneaus began published the tenth edition of his Systema Naturae (Systems of Nature). It became the first text to consistently use what we now call the ‘Binomial Nomenclature,’ a system for naming and cataloguing organisms based on their most prescient features (Bellows & Fisher, 1999). We have since adopted the system, and nearly every discovered organism now has its own dedicated name that follows Linneaus’s original patterns. This is not to say that the naming is easy. “Taxonomy is described sometimes as a science and sometimes as an art, but really it’s a battleground” (Bryson, 2003). There are constant skirmishes in the physical and life sciences regarding names. We can look to the recent discovery of several skulls in Dmanisi, Georgia to hear a modern debate about our ancient ancestry (Sample 2013). Anthropologists are now disputing whether several specimens previously thought to be separate species are actually one and the same. Where does that leave us then, in the 21st century? Are we improving our science communication? Should we focus more on how to teach individuals varying levels of scientific specificity? For the child, the language of science begins with a first question like, “Why are the cows walking away?” The parent might answer simply and truthfully, “They are looking for something to eat.” In these first years, gathering scientific information happens purely through direct sensation. In time, the child will discover reading. The textbook, the science fiction novel, newspaper, magazine, internet article -- these have all become standard media for communicating ideas in science through written language. By the time the child has grown to young adulthood, and entered college, the scope of scientific education will begin to shrink with specialization. The language becomes more specific, tailored, and precise. Now “the
bovine strategically positions itself to maximize alimentation through the harsher winter months.” With each additional degree -- Masters, PhD., etc. -- the scope of discourse will narrow to the point of novelty – with hope leading to new discoveries that will each require tailored names – names which stress the vital features of the discovery. These names will then enter books and classrooms, and so the cycle continues. As we learn more about the world, our experience becomes more rich. “This small cluster of white flowers, fanning out atop a spindly green stem? We call this plant ‘Queen Anne’s Lace’ -- doesn’t it look like lace?” You may know this plant in another context entirely. Pull it up by the roots and under the dirt you will find a wild carrot. Furthermore, in the academic community of botany, the flower is known as Daucus carota. Can we afford this kind of layered lexicon for so many of our plants, proteins, planets? Sure. We can afford them, and we need them, if we want to continue conducting science at so many distinct levels of detail. It can be confusing, or even stressful, when one level leaks into another. However, new knowledge is where curiosity and learning intersect to add meaning to our world, and for that we can thank the language of science.
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24,500 pounds - Wolfram|Alpha. (n.d.). Retrieved from http://www. wolframalpha.com/input/?i=24%2C500+pounds
Ambrose, S. E., & Abell, S. (1998). Lewis & Clark: Voyage of discovery (p. 62). Washington, D.C.: National Geographic Society.
Bellows, T. S., & Fisher, T. W. (1999). Handbook of biological control: Principles and applications of biological control (p. 45–55). San Diego: Academic Press.
Bryson, B. (2003). A short history of nearly everything (p. 360). Toronto: Doubleday Canada.
Cropper, W. H. (2001). Great physicists: The life and times of leading physicists from Galileo to Hawking (p. 31). Oxford: Oxford University Press.
Feynman, R. P., & Leighton, R. (1988). What do YOU care what other people think?: Further adventures of a curious character. New York: Norton.
Friday (Isaac) Newton blogging: “On the Shoulders of Giants” or, Revenge
is a Dish Best Eaten Cold Edition. | The Inverse Square Blog. (n.d.).
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Retrieved from http://inversesquare.wordpress.com/2008/03/07/ friday-isaac-newton-blogging-on-the-shoulders-of-giants-or-revengeis-a-dish-best-eaten-cold-edition/
Home: Oxford English Dictionary. (2013). Retrieved from http://www. oed.com/view/Entry/152534?redirectedFrom=pronghorn+#eid
HubbleSite - The Telescope - Hubble Essentials - Quick Facts. (n.d.). Retrieved
HubbleSite - NewsCenter - Was the Real Discovery of the Expanding
Universe Lost in Translation? (11/09/2011) - The Full Story. (n.d.). Retrieved
Inflation Calculator: Bureau of Labor Statistics. (n.d.). Retrieved from http://www.bls.gov/data/inflation_calculator.htm
Smithsonian Museum of Natural History. Lewis and Clark as Naturalists. (n.d.).
Sample, I. (2013, October 17). Skull of Homo erectus throws story of human evolution into disarray. The Guardian. Retrieved October 2013, from http://www.theguardian.com/science/2013/oct/17/skull-homoerectus-human-evolution
Tran, D. N. & Yoshida, H. (2012). Honoring different ontological boundaries:
The role of language in category formation. In N. Miyake, D. Peebles,
& R. P. Cooper (Eds.), Proceedings of the 34th Annual Conference of the Cognitive Science Society (pp. 2457-2462). Austin, TX: Cognitive Science Society.
1) George Lemaître with Albert Einstein
http://www.catholiceducation.org/articles/science/sc0022.html 2) Romneya and Marilyn Monroe
Cover image and background: created by Hadrien Picq
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Fracking: An Industry Under Pressure
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Three miles beneath the surface of the earth and at pressures exceeding one thousand atmospheres, a complex concoction of chemicals spurts, rupturing stone and cracking sheet rock through sheer force. As fractures creep out from the shattered bedrock, the fluid continues its destructive course, splitting millennia-old stone as if it were soft timber. As the pressure ebbs away further from the epicenter of the event and the initial pressure surge subsides, the wash of gushing liquid gives way to a tide of granular particles almost like a wave of quicksand. The particulate matter penetrates deep within the myriad ruptures, wedging them open so that the rocks themselves can release their precious bounty -- energyrich shale gas trapped between layers of stratified rock. The process that has just taken place is known as hydraulic fracturing, but is far more ubiquitous under a different name -- fracking. Fracking has had its fair share of the media spotlight recently, with innumerable reports and studies showing that it taints everything from our atmosphere to our water tables while similar amounts of reports and studies declare it not only perfectly safe, but vital for the stability of the energy economy. Both sides have convincing evidence and plenty of scientific clout; it is very likely that neither side is completely right. Whatever the case, it is vitally important that we acknowledge the benefits and consequences of hydraulic fracturing. Because of its vital importance to the extraction of natural gas and oil, both central tenets of the energy industry, banning fracking could hugely destabilize energy prices. However, if fracking is polluting our air and water, allowing it to continue could be even worse. To fully understand the controversy behind fracking, it is necessary to understand what it is and how it works. Hydraulic fracturing is a method of treating wellbores to increase the production rate and efficiency of collection of resources. It is most commonly used to increase the yields of natural gas or oil mining operations, though adapted versions of the process see insignificant amounts of usage harvesting more exotic resources (Brown, 2007). True to its name, it works by pumping highly pressurized fluid into a borehole, causing ruptures in the side of the well through which gas or oil can seep in, which are often wedged open using a granular “proppant” to facilitate flow through the fissures. While fracking has existed commercially since the 1960s, prototypi-
cal forms of the process date back to over a hundred years before that (Montgomery & Smith, 2010). In its long lifespan, fracking has been fine-tuned dozens of times by hundreds of innovative new processes, chemicals, and instruments that allow it to drastically increase the yields of wells. While many regulatory agencies have and continue to consider fracking a safe process, some recent studies (and indeed, reported contamination incidents) make it seem ever more likely that fracking is far from the golden boy of the energy industry that it was once thought to be. Even now, several governments around the world have passed legislation restricting or banning the use of fracking, and it is increasingly possible that we may see it phased out altogether. It is almost laughable to compare fracking in its historic sense to the modern usage of the term -- indeed, the sheer scale of the growth of the process boggles the mind. While early fracking treatments in the 1950s used on the order of 750 gallons of fluid to rupture the rock and 400 pounds of sand to prop open the fractures, some of the largest modern fracking treatments can exceed 1,000,000 gallons of fluid and 5,000,000 pounds of proppant (Montgomery & Smith, 2010). While much of this vast increase in scale is due to increased demand for fuel and larger wells, a large extent of it is due to a clearer understanding of the mechanics of fracking, a gradual and unending perfection of the process, and a better sense for the maximum amount of fracking that is cost-efficient. It is easy to think of modern fracking as a science, and like all sciences, fracking evolved from highly disorganized roots through careful observation and improvement. In 1865, Lieutenant-Colonel Edward Roberts, inspired by memories of artillery from the Civil War, christened his “Explosive Torpedo”, a gunpowder-filled iron shell with an explosive tip that would detonate upon a firm impact. By filling an oil well with water, then deploying and detonating a torpedo in the well, Roberts was able to utilize the power of the explosion to carve fissures into the rock well in a process he called “superincumbent fluid tamping” (Montgomery & Smith, 2010). In the years that followed, roughneck oil workers in New York, Pennsylvania, and West Virginia often employed nitroglycerine, a potent explosive, to increase the yields of shallow, hard oil wells. By disintegrating substantial portions of the oil-containing structures, the workers hoped to increase the flow of oil to the well and the total amount of
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oil that could be effectively recovered. This process, known as “shooting” an oil well, was incredibly dangerous, highly illegal, and above all, spectacularly successful in liberating black gold from its rocky prison. This process was artfully painted by John J. McLauren in his 1896 book Sketches in Crude Oil —
Some Accidents and Incidents of the Petroleum Development in all parts of the Globe:
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“A flame or a spark would not explode Nitro-Glycerin readily, but the chap who struck it a hard rap might as well avoid trouble among his heirs by having had his will written and a cigarbox ordered to hold such fragments as his weeping relatives could pick from the surrounding district.” Despite the notorious and well-document risks, this prototypical form of fracking quickly became a standard in the incipient petroleum industry, due in no small part to increases in
yield as high as 1200%. The practice also spread to similar industries, who found that “shooting” was equally effective in releasing gas and water from otherwise impermeable reservoirs. In the 1930s, experimentation with less explosive methods of well stimulation led to the development of acidization, a process in which strong acids capable of etching rock formations (but incapable of damaging the hydrocarbon reservoirs) are injected into wellbores, creating fractures that are less susceptible to collapse and “cleaning up” existing fractures such as to increase the flow of reservoir fluids. Acidization is still used today, as a way of purging the formation of rubble and unwanted chemical side products that are formed by previous treatments (Fjaer, 2008). Acidization, however, was only the first foray into nonexplosive fluid stimulation. In 1947, Floyd Farris of Stanolind Oil, noticing a correlation between treatment pressures of acidization and well productivity, first conceived of hydraulic fracturing as we know it today. In Kansas City later that year, the first experimental “Hydrafrac” treatment was performed, with 1000 gallons of napalm-thickened gasoline injected into a well in an attempt to rupture a natural gas formation through pure pressure as opposed more chemical means (Montgomery & Smith, 2010). Though the process
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suitable fluid is formed. Nowadays, acids, alcohols, did not significantly alter the output of the well, Hydrafrac brines, foams, gelling agents, and crosslinkcontinued to perambulate around Stanolind Oil ing agents all see usage to optimize the until it papers about it were released to properties of the fracking fluid to the oil industry in 1948, culminatto perfectly fit the situation ing in Halliburton Oil acquiring (Fjaer, 2008; Montgomery an exclusive patent to the treat& Smith, 2010). Modern ment. Halliburton performed fracking fluid consists on the first commercial frackaverage of 99.5% freshing treatments later that year, water and sand and a mere using crude oil and gasoline as 0.5% additives. These a fluid and adding sand to the additives include, but are mixture in an attempt to wedge not limited to, guar gum (to the hydraulic fractures open. thicken the fluid to allow it to After early treatments produced insuspend the proppant), isoprocreases in production averaging 75%, panol (to increase the viscosity of the fracking took the oil industry by storm, fluid), various borate salts (to topping out at over 3000 treatModern fracking operations utilize powerful maintain viscosity indepenments per month in the midpumps and vast amounts of water and dence with temperature), and 1950s and drastically increasing the US oil supply (United chemicals to liberate trapped gases and oils. hydrochloric acid (to dissolve rubble and facilitate the creStates Department of Energy ation of fissures), along with a myriad assortment of sup[US DoE], 2011). At this point, the concept behind plements that serve to minimize the amount fracking was fundamentally complete; of unwanted chemical side reactions however, since that time, improvethat take place. It is this fluid that ments in the materials, equipment, is of supreme concern to oppoand processes of fracking have nents of fracking, as the princontinued to improve the efcipal environmental danger ficacy of the treatment. of fracking is that of these Possibly the most imunwanted chemicals leaching portant component of any into the surrounding ecosysfracking treatment is the tem via water tables during fluid used to rupture the the fracking process. rock. It is impossible to use The propping basic fluids like water for this agents, by contrast, are of far less task, which lack the necessary interest to both environmentalists and viscosity to convey proppant to the petroleum engineers alike. The first frackformation that it might hold open the ing treatments used screened ruptures formed. The visAfter a fracking operation, little river sand or construction cosity of the proppant also remains except for vastly increased wellflow sand to wedge open crevices affects the properties of the and -- according to some -- widespread in sheet rock, and though breached well; high-viscosity environmental harm. many exotic, even unusual fluids tend to form large, proppants have seen use prominent fissures of large over the years (ranging from metal shot or plastic pellets to penetration, whereas lower-viscosity (also known as “slickwaglass beads or even rounded nutshells), ordinary sand has ter”) treatments tend to create numerous spread-out microalways been the most common propping agent. The usage fractures (Fjaer, 2008). For this reason, early treatments utiof proppant has varied over the years, mainly due to changes lized crude oil, gasoline, or kerosene, which were inexpensive in the propping fluid; the viscous oils and water-based gels of at the time and facilitated large volumes at low cost. Water the 50s to mid-1960s tend toward lower concentrations of was first used as a fracking fluid in 1953; through the use of larger-grained particulate, whereas less viscous modern fluids various gelling agents, it can serve as a ‘base’ with which a
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necessitate much higher concentrations of sand. While early fracking treatments averaged approximately half a pound of sand per gallon of fluid, modern treatments range between 2 to 5 pounds of proppant per gallon, and can actually reach as high as 20 lbs/gal during some stages of the fracking process (Fjaer, 2008). Nevertheless, due to the relative ubiquity of sand as a propping agent, even the high volumes used do not make the propping agents of serious concern to those concerned about the environmental ramifications of fracking. Simultaneously, sand’s low price and efficiency as a proppant mean that propping optimization is by and large not as important as fluid optimization when it comes to maximizing the efficacy of the fracking process. However, there is a tertiary concern beyond the consumable resources applied during the process of fracking. In order to create the incredible pressures used to crumble brittle rock like dry toast, heavy machinery is needed. While early fracking treatments made do with existing acid- or cementpumping equipment, specialized instruments were rapidly created to produce the necessary pressures and flow rates that fracking requires. Modern fracking equipment uses around 1500 horsepower to pump 800 gallons of fluid per minute at pressures of around 500 psi. Some of the largest equipment for the deepest wells can utilize in excess of 10,000 horsepower to pump more than 4200 gallons of fluid per minute at pressures that can exceed 20,000 psi (Fjaer, 2008). The amount of pollution and runoff that these instruments can produce makes them unexpected factors to fracking’s environmental damage. When it comes to the health risks of fracking, it is undisputable that several of the chemicals used in fracking fluids are known toxins and can be poisonous not just to local ecosystems but also nearby residents. Health and Safety Agencies in Colorado and New York found detectable and not insignificantly harmful concentrations of carcinogens such as benzene, toluene, and xylene (which are used as thickening agents), as well as and toxins like ethylene glycol (which is used to prevent the formation of limestone “scales” on the boreholes) in groundwater near fracking operations (Brown, 2007). In July 2011, the EPA released new emissions guidelines, stating that “previous standards...could lead to unacceptably high cancer risks for those living near drilling operations” (United States Environmental Protection Agency [US EPA], 2011). Fracking is also known to produce high emissions of greenhouse gases, both via uncaptured methane from fractured rock and emissions from fracking equipment (Brown, 2007). Fracking also consumes large volumes of water, only 30-70% of which is recovered after it is pumped into the well, and in an environmentally unusable state (US Energy Information Administration [US EIA], 2011). While much of this
water is recycled, the simple fact that less is recovered than is needed means that fracking treatments will continually draw water while they are in progress. As if this laundry list of malignancies was not enough, fracking has also been shown to liberate or otherwise lose significant quantities of radioactive nuclides. While some of these radiation sources are naturally-occurring minerals like uranium or thorium that are freed during the fracking process, a significant quantity of the radioactive output is due to the loss of radioactive “tracers” that are used to map fractures in the rock and are subsequently leached into the surrounding area (Brown, 2007). Despite reported contamination incidents of many of these scenarios in Colorado, Pennsylvania, Texas, and many other states, the drilling industry maintains its position that properly maintained and secured fracking operations pose a negligible risk to the environment, a position that is largely supported by the official EPA stance that fracking contributions to pollution, both atmospheric and groundwater, were negligible comparative to more significant emission sources. After a 16-month investigation, EPA regulators concluded that high methane levels in Franklin Forks, Pennsylvania, were unrelated to local natural gas drilling, and were instead the product of local geothermal anomalies. The head of the EPA, Lisa Jackson, stated during Senate testimony that “[She was] not aware of any proven case where the fracking process itself has affected water” (US EPA, 2011). An EPA report
“Advocates state that fracturing has been performed safety without significant incident for over 60 years, although modern shale gas fracturing of two mile long laterals has only been done for something less than a decade. Opponents point to failures and accidents and other environmental impacts, but these incidents are typically unrelated to hydraulic fracturing per se and sometimes lack supporting data about the relationship of shale gas development to incidence and consequences.”
published in 2011 reiterated this stance, stating: Despite this stance, however, environmental health and Background picture: The Kern River Oil Field in California is one of the most densely-developed oilfields in the continental United States.
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safety commissions in Colorado, Ohio, and California have proposed or imposed moratoriums on hydraulic fracturing, and the EPA is compiling a definitive study on fracking’s effects on groundwater, to be released in 2014.
ing will go away, but when. While there are innumerable reports of fracking contamination, many studies on individual contamination incidents are skewed by confounding variables, and as a result few cases can clearly show a documented cor-
Because, on a very fundamental level, fracking breaks down barriers between the resource-rich environment and mining operations, it is inevitable that it will conversely break down barriers between pollutant-ridden mining operations and the environment in the process.
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Ultimately, the most important decision that regulatory agencies must make about fracking is not whether or not it is eminently harmful, but whether it has the potential to do more harm than good. Due to the comparatively gigantic increases in yield that fracking is able to squeeze out of oil and gas wells, it is a huge contributor to the energy economy, and thereby the stability of the the entire energy market. A Yale University Energy Study Group performed a cost-benefit analysis on natural gas fracking, and calculated that the direct economic benefit of hydraulic fracturing in the US totaled over $100 billion per year (Ames, 2012). In North Dakota and South Texas, where fracking contributes hugely to the local oil and gas industries, household income rose during the 2008 recession, leaving the states comparatively unscathed by the economic crisis (US EIA, 2011). Fracking has greatly reduced US dependence on foreign oil imports -- which fell 19% in the first half of 2013 -- which functionally lowered the country’s trade deficit by $31.6 billion. More importantly, the oil and gas industry -- mostly through fracking -- has produced 2.1 million new jobs since the recession (US DoE, 2011). Increasing regulations on fracking would inevitably lead to a decrease in national oil production, and -- depending on whom you talk to -- could put the energy industry into a slump as demand for oil and gas far outstrips their supply. In this sense, the time is simply not right for fracking restrictions and moratoriums, with an unstable economy that is probably unable to cope with the added stress of losing half of its oil and gas production and is certainly not ready to make the transition to more viable alternative energy sources so quickly. From this standpoint, it is not just a matter of environmental safety but also of economic viability whether fracking should be allowed to exist. While increased containment and pollution regulations are possible, widespread moratoriums (or even outright bans) on fracking as a practice are unlikely simply because they upset the status quo too much. Fracking is far too vital to the energy industry for it to disappear without long-lasting and far-reaching consequences. The most important question we must ask is not if frack-
relation. Despite this, the fact that there is no clear scientific consensus on the issue makes a strong case for increased regulations -- after all, it only takes one major spill to make fracking a serious environmental concern. Unfortunately, while increased regulations can certainly decrease the risk of contamination and seepage, the simple fact remains that fracking is difficult to contain by its very nature. Because, on a very fundamental level, fracking breaks down barriers between the resource-rich environment and mining operations (and, more importantly, does so in a crude, uncontrollable manner), it is inevitable that it will conversely break down barriers between pollutant-ridden mining operations and the environment in the process. However, fracking is simply too important to the integrity of the current energy ecosystem for us to expect it to become obsolete in the near future. Because of the multiplicative returns it induces upon fuel sources that are now higher in demand than they have ever been, banning fracking is a poor economic decision. While environmental regulations and restrictions are clearly necessary to limit the consequences of reckless fracking, until there is a fundamental restructuring of the energy economy -- a true green revolution -- fracking is here to stay. REFERENCES • Ames, R. M., Corridore, A., Ephross, J. N., Hirs, E., Macavoy, P. W., & Tavelli, R. (2012). The Arithmetic of Shale Gas. Retrieved from http://papers.ssrn.com/sol3/ papers.cfm?abstract_id=2085027 • Brown, V. J. (2007). Industry Issues: Putting the Heat on Gas. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/ articles/PMC1817691/ • Fjaer, E. (2008). Mechanics of hydraulic fracturing. In Petroleum related rock mechanics(2nd ed., pp. 369-389). Amsterdam, Netherlands: Elsevier. Retrieved from http://books.google.com/books?id=l6CfasFxhzYC&pg =PA369#v=onepage&q&f=false • Montgomery, C. T., & Smith, M. B. (2010). Hydraulic Fracturing: History of an Enduring Technology and The
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Fuss, the Facts, the Future. Journal of Petroleum Technology, 26-41. Retrieved from http://www.spe.org/jpt/ print/archives/2010/12/10Hydraulic.pdf • US Department of Energy (n.d.). Hydraulic Fracturing Technology. Retrieved from http://www.doe.gov/fe/ hydraulic-fracturing-technology • US Energy Advisory Board, Shale Gas Subcommittee. The SEAB Shale Gas Production Subcommittee NinetyDay Report (2011). Retrieved from http://www.shalegas. energy.gov/resources/081111_90_day_report.pdf • US Energy Information Administration (n.d.). Review of Emerging Resources: US Shale Gas and Shale Oil Plays(2011). Retrieved from US Energy Information Administration website: ftp://ftp.eia.doe.gov/natgas/usshaleplays.pdf PICTURE SOURCES • http://www.popfi.com/2010/12/03/new-yorkto-ban-natural-gas-drilling-technique/ • http://www.theepochtimes.com/n2/images/ stories/large/2012/08/20/figure_2_horizontal-fracking-process_propublica.jpg • http://www.rockymountainenergyforum.com/ uploads/files/45/Understanding-Fracturing-Fl.gif • http://www.oerb.com/Default.aspx?tabid=357 • http://en.wikipedia.org/wiki/ File:Frac_job_in_process.JPG • http://upload.wikimedia.org/wikipedia/commons/e/ e2/Well_head_after_all_the_Fracking_equipment_has_been_taken_off_location.JPG • http://cdn.zmescience.com/wp-content/ uploads/2013/02/shale-gas-drilling-diagram.jpg • http://en.wikipedia.org/wiki/ File:ViewintoHell-KernRiver.jpg
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The Experimental Effects of Stress on Fertility & possible solutions to the problem
By Jenna Koopman 17 • Berkeley Scientific Journal • Stress • Fall 2013 • Volume 18 • Issue 1
Imagine entering a pharmacy and going into the fertility and prenatal aisle. You might see a few pregnancy tests, an ovulation predictor kit, and perhaps even some contraceptives. These all make sense: you might already be pregnant, you could be trying to get pregnant, or you may want to avoid pregnancy altogether. Now imagine that right next to the ovulation kit sits a little box that tells you how stressed you are. Is this relevant when it comes to pregnancy?
menstrual cycle ends, LH levels increase, surging in anticipation of ovulation, at which point LH decreases. When luteinizing hormone is inhibited, the ovary does not release an egg, and conception becomes impossible (WebMD, 2013). Beyond conception, cortisol still plays a role in fertility: high levels of cortisol are strongly associated with miscarriage (“Stress and Fertility,” 2013). Example of normal menstrual cycle and Lutenizing hormone levels.
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The scientific answer is yes. Studies from the past several decades demonstrate that high stress levels strongly correlate to infertility in both humans and non-human mammals. However, the solution to stressinduced infertility remains under debate, with both Western and Eastern methods of medicine weighing in on the argument. Defining Fertility and Stress Fertility is an organism’s ability to bring viable offspring into being. Infertility can be due to any number of problems affecting reproductive health, such as low sperm count or immature ova (eggs). Scientifically, stress can have any number of definitions. In the context of mammals, two main forms of stress exist in biology: physical stress (such as carrying a heavy load) and emotional stress (such as grieving the death of a loved one). However, both forms of stress elicit a similar hormonal response. The body responds to different types of stress largely by activating the endocrine organ system, releasing stress-related hormones such as cortisol and adrenalin. Hormonal Control of Stress When stressed, the concentration of cortisol, a glucocorticoid produced in the adrenal glands, increases in the body. As a result of the increase in cortisol concentration, the concentration of luteinizing hormone (LH) decreases in the ovaries of females, disrupting or even halting ovulation. Luteinizing hormone controls whether or not an ovary releases a mature egg, a process known as ovulation. As the
Adrenalin (also known as epinephrine) is another stress-related hormone in the body. Adrenalin is the hormonal factor which triggers the fight-or-flight response in humans usually associated with a physical stressor. When the body undergoes physical stress, the adrenal glands produce adrenalin to promote increased blood flow to muscles, allowing the body to respond more quickly to external stimuli (“Adrenaline”, 2013).
Studies from the past several decades demonstrate that high stress levels strongly correlate to infertility in both humans and non-human mammals.
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Adrenalin correlates to fertility levels as well. In patients undergoing IVF, or in-vitro fertilization, hormones are injected into the body to encourage eggs to mature. These eggs are then removed from the body and fertilized with sperm in a petri dish in order to create embryos. These embryos are then placed back into the uterus, at which point it is hoped that some will implant and begin to grow into a baby. In IVF patients, studies show that when daily adrenalin levels are lower, the rates of implantation increase. Other studies have shown a similar correlation when measuring cortisol levels. These results indicate that when patients lead less stressful lives, they are more successful at reproduction (Csemiczky, Landgren, and Collins, 2001; Facchinetti, Matteo, Artini, Volpe, and Genazzani,1997).
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Example of in-vitro fertilization:
the theory that schizophrenic (i.e. highly stressed) females are much more likely to deliver female offspring (Lane & Hyde, 1973). This suggests that the male gamete does not survive well in a female’s uterus under stressful conditions, although the exact mechanism through which this occurs remains unclear. With regard to human reproduction, stress in the form of mental illnesses and mood disorders can increase infertility as well. In one study, (Ramezanzadeh et al., 2004) both depression and anxiety levels in women trying to get pregnant positively correlated with length of infertility. However, this study does not prove that depression or anxiety cause infertility because the women were already infertile at its outset. Instead, infertility and the emotional connotations thereof could lead to anxiety and depression. Medication
Studies Link Stress and Infertility In the laboratory, studies consistently show stress to be a highly significant factor in infertility. Correlations between high stress levels and infertility have been found in non-human species as well. For example, 30% of stressed male mice placed with receptive females for four days were unable to impregnate the females as compared to only 4% of unstressed male mice (Crump & Chevins, 1989). In another study with female rats, (Lane & Hyde,1973) stressed females gave birth to significantly smaller litters than their unstressed counterparts even when mated with the same males. Additionally, the litters were more likely to be mostly females rather than an equal distribution of gender, helping to confirm
Although anti-anxiety medications may reduce stress, they also have disadvantages which hinder fertility as well. This is due to the occurrence of certain side effects such as a decrease in sexual drive and inability to orgasm that result from taking anti-anxiety medications and antidepressants. For example, certain SSRIs (selective serotonin re-uptake inhibitors) can reduce anxiety and help patients with Major Depressive Disorder and Obsessive-Compulsive Disorder. These same SSRIs cause reduced sexual drive and can cause erectile dysfunction in males, making conception unlikely if not impossible. (Zoloft Oral: Side Effects, 2013.) Thus, faced with these potential complications, patients sometimes seek out alternative treatments for infertility.
Stress in the form of mental illnesses and mood disorders can increase infertility as well.
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Essentially, there are no foolproof methods of increasing one’s fertility in spite of stress, but there may be some ways of reducing stress through traditional Eastern medicine which can lead to a decrease in infertility and better health overall. On the other hand, for those hoping to prevent pregnancy for now or forever, overcommitting to too many different classes, jobs, and other engagements may serve as a slightly effective birth control.
Example of SSRI blocking reabsorption of serotonin.
Acupuncture may be one of the best treatments for stress-induced infertility. Acupuncture is a traditional Chinese form of medicine which requires a patient to lay down while an acupuncturist places needles into the patient’s body at certain locations, called meridians. In one study, female patients undergoing IVF had much lower self-assessed levels of anxiety if they received acupuncture in the four weeks prior to the procedure (Isoyama & Cordts, 2012). These women were then more likely to have successful implantation occur postprocedure. Another method of stress reduction and a way to boost fertility is yoga. A study conducted on women over a three-month time period demonstrated that practicing yoga regularly can actually lower salivary cortisol levels (Michalsen et al, 2005). As cortisol levels are in part to blame for infertility, it could be highly beneficial to practice yoga for its stress-reduction benefits in order to increase one’s fertility. Benefits from yoga are not limited to the fertility of women. Studies show that many fertility benefits for males come from regular yoga practice. Both sperm count and motility show improvement in men who practice yoga. Prostate size can decrease as well. All of these factors can help improve fertility in males. (Sengupta, Chaudhuri, & Bhattacharya, 2013). 20 • Berkeley Scientific Journal • Stress • Fall 2013 • Volume 18 • Issue 1
Sources “Adrenaline.” You & Your Hormones. Society n.d. Web. 27 Oct. 2013.
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Crump, C. J., and P. F. D. Chevins. “Prenatal Stress Reduces Fertility of Male Offspring in Mice, without Affecting Their Adult Testosterone Levels.” Hormones and Behavior 23.3 (1989): 333-43. Science Direct. Web. 30 Sept. 2013. Csemiczy, G., Landgren, B.-M. and Collins, A. The influence of stress and state anxiety on the outcome of IVF-treatment: Psychological and endocrinological assessment of Swedish women entering IVFtreatment. Acta Obstetricia et Gynecologica Scandinavica, 79 (2000): 113–118. Facchinetti, F., Matteo, M.L., Artini, G.P., Volpe, A., and Genazzani, A.R. An increased vulnerability to stress is associated with a poor outcome of in vitro fertilization-embryo transfer treatment. Fertil Steril, Vol 67(2), Feb 1997: 309-14. Isoyama, D Cordts, de Souza van Niewegen, A.M., de Almeida Pereira de Carvalho, W., Matsumura, S.T., Barbosa, C.P. Effects of acupuncture on symptoms of anxiety in women undergoing in vitro fertilisation: a prospective randomised controlled study. Acupunct Med, 2012 Jun 30(2): 85-8. Lane, E. A. and Hyde, T.S. “Effect of maternal stress on fertility and sex ratio: A pilot study with rats.” Journal of Abnormal Psychology, Vol 82(1), Aug 1973, 78-80.
Ramezanzadeh, F., Aghssa, M.M, Abedinia, N. Zayeri, F., Khanafshar, N., Shariat, M., Jafarabadi, M. “A Survey of Relationship between Anxiety, Depression and Duration of Infertility.” National Center for Biotechnology Information. U.S. National Library of Medicine, n.d. Web. 30 Sept. 2013. Sengupta, P., Chaudhuri, P., Bhattacharya, K.. Male reproductive health and yoga. Int J Yoga 2013;6:87-95. “Stress and Fertility.” White Lotus Naturopathic Clinic and Integrative Health. N.p., n.d. Web. 30 Sept. 2013. “Zoloft Oral: Side Effects.” Drugs and Medications. WebMD, n.d. Web. 5 Oct. 2013.
Image Sources Steiling, Evie. “Still Here”. February 2011. The Steilings. Blogspot. November 13th 2013. Lutening Hormone levles < http://www.gpnotebook.co.uk/ menst.gif> In-vitro fertilization method < http://lakecharlesobgyn.com/ Images/PCOS-9-ivf.gif> SSRI effects < http://www.alanpriest.f2s.com/images/ Synapse.jpg>
“Luteinizing Hormone.” Women’s Health. Web MD, n.d. Web. 5 Oct. 2013. Michalsen, A., Grossman, P., Acil, A., Langhorst, J., Ludtke, R., Esch, T., Stefano, G.B., Dobos, G.J. Rapid stress reduction and anxiolysis among distressed women as a consequence of a three month intensive yoga program. Medical Science Monitor (2005);11:55561.
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EFFECTS OF CORTISOL ON PHYSICAL AND PSYCHOLOGICAL ASPECTS OF THE BODY AND EFFECTIVE WAYS BY WHICH ONE CAN REDUCE STRESS Preethi Kandhalu
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ver the past years, reports of increased stress levels in millennials have been on the rise; Stress in America, a study, from the American Psychological Association found “half of all millennials are so stressed out that they can’t sleep at night, and 39 percent of millennials have stress levels that have increased in the past year” (Yandoli, 2013) and “On a 10-point scale, Americans ages 18-33 reported an average stress level of 5.4 compared to the national average of 4.9” (Kingkade, 2013). Consequently, there are a plethora of suggestions regarding ways to reduce stress – common tips include keeping a positive attitude, exercising and eating healthy (WebMD). A popular website also indicates that eating berries help combat stress since “Blueberries are naturally rich in vitamin C, which helps fight increased levels of cortisol, a stress hormone”1 (Oz, 2010). Unfortunately, for most people, it is difficult to evaluate whether such tips are effective stress reducers. The aim of this article is to explain why stress exists. The cortisol hormone, i.e. “stress hormone” that’s secreted by the Hypothalamic-Pituitary-Adrenal (HPA) affects our body in both physical and mental ways that can be detrimental to our overall health. Some of the effects of stress can be due to our genes, while some effects can be due to external environmental factors. However, there do exist effective ways by which one can reduce cortisol levels.
n order to understand why we feel stressed, it is important to understand the mechanism of the Hypothalamic-Pituitary-Adrenal (HPA) axis, an axis
(“Hypothalamic–pituitary–adrenal axis”). In the first step of the process, the hypothalamus contains neuroendocrine neurons that synthesize proteins, which act as hormones when released. While some hormones target distant tissues, some hormones – including vasopressin and corticotropin releasing hormone (CRH) – are released in the blood circulation of the axis for delivery to the pituitary gland. The CRH is received by the anterior pituitary gland, which in turn secretes Adrenocorticotropic Hormone (ACTH) within the blood circulation of the axis. ACTH further
Fig 1. HPA Mechanism
acts on the two of the three zones of the adrenal gland – zona fasciculate and the zona reticularis – this action leads to the secretion of glucocorticoids (which mainly consists of cortisol in humans) among other hormones (Mitrovic). Also, 90% of the cortisol is eventually
“Some ailments caused by increased levels in cortisol include a suppressed immune system, insomnia, severe mood swings, depression and severe hypotension” along our brain that secretes cortisol. The hormones produced by the hypothalamus results in a cascade of events down the HPA axis which ultimately leads to the secretion of cortisol from the adrenal gland
bound by proteins, whereas 10% of the free cortisol is unbound, and therefore biologically active – this free cortisol creates a negative feedback loop whereby it binds to hypothalamus and the pituitary gland to inhibit secretion of CRH and ACTH (Mitrovic).
Scientific experiments done to determine correlation between Vitamin E and C levels, and cortisol levels actually suggest that cortisol production did not change with different concentrations of Vitamin E and C. In other words, blueberries do not fight increased levels of cortisol. (Montalvo, Diaz, Galdames, Andres & Larrain, 2011)
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There exists a scientifically proven way by Cortisol affects various parts of our body, both which one can reduce cortisol levels – Yoga. Results
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psychologically and physically. Some ailments caused by increased cortisol levels include a suppressed immune system, insomnia, severe mood swings, depression and severe hypotension. Glucocorticoids inhibit inflammatory response; specifically, cortisol suppresses the synthesis and secretion of arachnidonic acid, a key precursor for a number of mediators of inflammation. However, heightened levels of glucocorticoid hormones can lead to suppression of the body’s immune response due to stabilization of lysosomes, decrease in number of circulating T4 lymphocytes and a decrease in production of key mediators in immune response (Mitrovic). A decrease in immune response reduces the body’s ability to recognize and defend itself from foreign entities such as bacteria and viruses (David C. Dugdale).
ortisol also acts on the central nervous system by directly changing the electrical activity in the limbic system and the hippocampus; this modulation can decrease REM sleep and increase slow-wave sleep and time spent awake. Increased levels of cortisol can cause insomnia and also severe mood swings (Mitrovic).
hough one may experience ailments caused by increased levels of cortisol, females are more prone to stress as a result of a specific variation in their genomes. 5-HTTLPR is a repeat polymorphic region that occurs in the promoter, a sequence upstream of the gene that’s required for transcription, of the SLC6A4 gene, the gene that encodes serotonin transporter. There are two alleles (variants) that are normally reported; the short (s) allele and the long (l) allele. Evidence from a study of 67 girls reported that girls who were homozygous for the s-allele produced higher and prolonged levels of cortisol in response to the stressful stimuli in comparison to that of girls who were heterozygous, or homozygous for the l allele. Results suggest that females who are homozygous for the s allele may have an increased susceptibility to depression in response to stressful events during her life due to a specific variation in her genome (Gotlib, Joormann, Minor & Hallmayer, 2008).
from a study suggested that the levels of cortisol in people with Major Depressive Disorder dropped significantly after three months of practicing yoga, suggesting that yoga has antidepressant effects (Thirthalli, Naveen, Rao, Varambally, Christopher &
“when you change your mind about stress, you can change your body’s response to stress” Gangadhar, 2013).
here also exist environmental factors that can alter one’s cortisol levels. Following the recent major financial crisis in Greece, a comparison in cortisol levels and a questionnaire with different health indicators was administered to 124 Greek youth and 112 Swedish youth, who were much less affected by the economic turmoil. The Greek youth reported significantly higher perceived stress, experience of serious life events, low hope for the future and, significant and widespread symptoms of anxiety and depression compared to their Swedish counterparts. However, it was found that the Greek youth had low cortisol levels (Faresjo, Theodorsson, Chatziarzeni, Sapouna, Claesson, Koppner & Faresjo, 2013). This suggests that a prolonged exposure to highly stressful situations lead to lowered free cortisol levels as a result of the negative feedback loop of the HPA axis. The level of inhibition is directly proportional t o the concentration o f glucocorticoids initially secreted (Mitrovic).
o w e r levels of cortisol c a n further affect
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the body in detrimental ways. For example, cortisol aids in maintaining the responsiveness of vascular smooth muscles to proteins, and therefore participates in blood pressure regulation. However, when exposed to low levels of cortisol, the smooth muscle becomes unresponsive to proteins. This decreased responsiveness can lead to severe low blood pressure, otherwise known as hypotension (Mitrovic).
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While some of the popular tips on reducing
stress may or may not be true, there exist scientifically proven ways to reduce stress. In addition to yoga, another effective way to reduce stress concerns itself with how you think about stress! On her TED talk titled “How to make stress your friend”, Stanford University psychologist, Kelly McGonigal, says that “when you change your mind about stress, you can change your body’s response to stress” (McGonigal, 2013). When one feels stressed, the person may interpret it as anxiety or signs that you’re not handling the situation very well, however, it’s healthier to view stress as something that energizes your body and is preparing you to meet the challenge. Because in a typical stress response, you might be breathing faster, your heart rate might go up – as a result, your blood vessels constrict. However, when you view stress as a positive phenomenon, your blood vessels stay relaxed, making for a healthier cardiovascular profile. The next time you feel stressed, think to yourself, “This is my body helping me rise to this challenge” (McGonigal, 2013).
References 1. David C. Dugdale. (n.d.). Retrieved from http://www.nlm.nih.gov/ medlineplus/ency/article/000821.htm 2.
Faresjo, A., Theodorsson, E., Chatziarzeni, M., Sapouna, V., Claesson, H., Koppner, J., & Faresjo, T. (2013, September 16). Higher perceived stress but lower cortisol levels found among young greek adults living in a stressful social environment in comparison with swedish young adults. Retrieved from http://www.plosone.org/article/ info:doi/10.1371/journal.pone.0073828
Gotlib, I., Joormann, J., Minor, K., & Hallmayer, J. (2008). Hpa-axis reactivity: A mechanism underlying the associations among 5-HTTLPR, stress, and depression.NIH Public Access, 847-851. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2373542/pdf/ nihms46269.pdf
4. Hypothalamic–pituitary–adrenal axis. (n.d.). Retrieved from http:// en.wikipedia.org/wiki/Hypothalamic–pituitary–adrenal_axis 5. Kingkade, T. (2013, 2 8). Millennials are more stressed out than older generations: Stress in america survey. Retrieved from http://www. huffingtonpost.com/2013/02/08/millennials-stress_n_2646947.html 6.
McGonigal, K. (Performer) (2013). Ted: How to make stress your friend [Theater]. Available from http://www.ted.com/talks/kelly_ mcgonigal_how_to_make_stress_your_friend.html
Mitrovic, I. (n.d.). Introduction to the hypothalamopituitary-adrenal (hpa) axis. Retrieved from http://biochemistry.ucsf.edu/programs/ ptf/mn links/HPA Axis Physio.pdf
Montalvo, C., Diaz, N., Galdames, L., Andres, M., & Larrain, R. (2011). Short communication: Effect of vitamins e and c on cortisol production by bovine adrenocortical cells in vitro. Journal of Diary Science , 94(7), 3495-3497. doi: 10.3168/jds.2010-3760
9. Oz, M. (2010, February). Seven ways to reduce stress. Retrieved from http://www.oprah.com/health/Dr-Oz-on-Stress-Reduction 10. Stress Management. Retrieved from http://www.webmd.com/ balance/stress-management/reducing-stress-tips 11. Thirthalli, J., Naveen, G. H., Rao, M. G., Varambally, S., Christopher, R., & Gangadhar, B. N. (2013). Cortisol and antidepressant effects of yoga. Indian Journal of Psychiatry , doi: 10.4103/0019-5545.116315 12. Yandoli, K. (2013, 2 12). Teens and stress: Millennials, experts talk ‘most stressed generation’. Retrieved from http://www.huffingtonpost. com/2013/02/12/experts-talk-what-stress-_n_2670234.html
Image Sources: 1.
2 http://www.balancewinnipeg.com/wp-content/uploads/2013/09/ yoga-meditation.jpg 3. h t t p : / / w w w. b e n g r e e n f i e l d f i t n e s s . c o m / w p - c o n t e n t / uploads/2013/08/Basic_HPA_Axis.jpeg
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Stress is one of the most destructive forces in nature. We all know the negative impacts that stress can have on humans. But what happens when rocks on continents and oceans become stressed? The result is an earthquake.
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EARTHQUAKES Induced by STRESS
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Stress is one of the most destructive forces in nature. We all know the negative impacts that stress can have on humans. But what happens when rocks on continents and oceans become stressed? The result is an earthquake. Large magnitude earthquakes with great destructive potential are unleashed due to the release of stress and strain in rocks near tectonic plate boundaries. The theory of plate tectonics explains the world’s earthquakes, volcanoes, and mountains. The rigid surface of the earth (its lithosphere) is broken into many pieces called tectonic plates, shown in Figure 1. These tectonic plates move around the surface of the Earth and are driven by the underlying mantle convection. This is analogous to dropping a handful of pasta shells into boiling water and seeing them move around, where the shells are tectonic plates and the boiling water represents mantle convection. The surfaces of these plates interact in three different ways at their boundaries. The three plate boundaries are convergent, divergent, and transform. At convergent boundar-
ies, plates move towards one another. This type of boundary is typically associated with mountain and volcano-building. Most earthquakes occur at convergent boundaries. At divergent boundaries, plates move away from one another. Magma from Earth’s interior rises up and solidifies into new crust at these boundaries, as is seen in the mid-ocean ridges of the Atlantic Ocean. Few earthquakes occur at divergent boundaries. Lastly, tectonic plates slide past one another at transform boundaries. The San Andreas Fault is a prime example of a transform plate boundary. Strike-slip earthquakes occur at these boundaries. Stress is the cause of all earthquakes but it is easiest to imagine at transform boundaries. Stress is the same as pressure; it occurs when a force is applied over an area (Ormand & Baer, 2012). Strain is the deformation of rocks that results from stress. Imagine taking your hands and pressing them together tightly. You are exerting a force over the area of your hands and this leads to a buildup of stress. Now if you try to slide your hands past one another they will not
Figure 1. Diagram of Earth’s tetonic plates
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move. But slowly they become strained and start slipping until there is a large slip and all the built up stress has been released. This is precisely what happens “Large magnitude earthquakes with great during a strike-slip earthquake. The destructive potential are unleashed due vious comparison is that to the release of stress and strain in rocks your hands are two “large” distinct plates and near tectonic plate boundaries” earthas those plates try q u a k e to slide past one defined as another stress is built up in the fault until an even- (where large is relatively tual release. Note that the limits of this simple greater than magnitude 5.5) struck the Hayward model do not explain that two plates actually fault in 1889; it was a magnitude 5.6 earthquake create an array of faults rather than just one large (CA Department of Conservation, 2008). That was 124 years ago. This hiatus is troubling fault. As Berkeley students, we do not need to look because there is a common scientific notion about far to see an example of a transform boundary. earthquakes: the longer an active tectonic boundThe sliding motions of the North American and ary goes without an earthquake, the greater the Pacific plates create a network of faults through- chance for there to be an upcoming large earthout California. In the Bay Area, the principle fault quake. This makes sense in terms of stress. The as a result of the transform boundary is the San longer a boundary goes without an earthquake, Andreas Fault. The Hayward Fault lies parallel more stress builds up and the built up stress holds to the San Andreas Fault, shown if Figure 2. The more destructive power. Since earthquakes are a Hayward Fault is 74 miles long, running from relevant natural disaster, it is important to think Richmond to San Jose, and it runs just under the about how to predict earthquakes. famous California Memorial Stadium (CA De- There are arguments both for and against the partment of Conservation, 2008). Due to previous feasibility of earthquake predictions. Critics of earthquakes and decades of creep (the slow shift- earthquake prediction say that tectonic boundaring of tectonic plates) Memorial Stadium has essen- ies are a complicated system. Thus, it is difficult to tially split into two parts. If an earthquake were to say with good certainty when an earthquake may happen, Memorial Stadium would collapse due to occur. For example, in Parkfield, CA, between surface rupture that occurs from ground motion. 1857 and 1966, earthquakes of magnitude 5.5 or The engineering task of seismically retrofitting larger would occur nearly every 22 years. Based Memorial Stadium was completed by breaking on this trend, a prediction was made that there the stadium into fault rupture blocks where the is a 95% chance that an earthquake greater than fault crossed, so that these portions of the build- magnitude 5.5 will occur between 1985 and 1993 ing could move in response to possible surface (Kanamori, 2003). However, an earthquake of that rupture without affecting the rest of the structure magnitude did not occur in Parkfield until 2004. (Forell / Elsesser Engineers). Now that we have a This is an example of how short-term predictions retrofitted stadium, how soon will its engineering are not possible. The National Research Council be tested, or in other words “when will we expe- has deduced that “based on the relative timescales, rience a large earthquake in Berkeley?” The pre- predicting the size, location, and time of an earth11 • Berkeley Scientific Journal • Stress • Fall 2013 • Volume 18 • Issue 1
ments in seismology, reliable estimates on the location and size of earthquakes can be collected within minutes of the initiation of rupture if the earthquake is far away. For nearby earthquakes, the ground will have begun shaking before these estimates can be made. If seismographs can quickly pick up an earthquake under way, then an earthquake early warning system can be enforced. Regions that will be subject to dangerous shaking can be warned through telecommunications before the shaking arrives because the speed of electromagnetic waves in telecommunications exceeds that of seismic waves. Within the seconds
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“In a good scenario, a 10Figure 2: Hayward Fault and the adjacent San Andreas Fault
quake to within a week corresponds to predicting the size, location, and time of a lightning bolt to within a millisecond.” The closest we can come to “predicting” an earthquake in the short term is saying that “large shallow earthquakes are immediately followed by aftershocks that are triggered by the main shock. Large earthquakes sometimes trigger other large earthquakes” (DePaolo, 2008). An example of the latter is when a series of large earthquakes ruptured most of the North Anatolian fault during the 20th century. In addition, by monitoring the stress and strain in small areas, for example, the San Andreas Fault, in great detail we can hope to predict when renewed activity in that area is likely to take place (U.S. Geological Survey, 2012). This methodology may not seem very satisfying, but it is all we have right now as there is active but unfinished research in improving short-term forecasting for earthquakes. The next best option is early warning forecasting. The earliest that people can be undeniably warned of a coming earthquake are a mere seconds before it hits. With the use of high-quality instru-
15 second warning can be provided before an earthquake hits a city.” of warning from an incoming earthquake, public transportation systems can be halted, people can take cover under desks, sensitive and dangerous manufacturing equipment can be paused, and dangerous chemicals in labs can be isolated. In a good scenario, a 10-15 second warning can be provided before an earthquake hits a city (DePaolo, 2008). This might not seem like much time but it is enough to save lives and money. Professor Richard Allen, director of the Berkeley Seismological Laboratory, is a leading advocate for early warning systems. Early warning technology was tested when a magnitude 9 earthquake hit Japan in 2011. The closest large city received a 15 second warning which saved many lives and even more money from reduced damage costs. Professor Allen is calling for a US early warning system. He first proposes a West Coast system that will cost $120 million for the first five years to build and operate early warning technologies. This would include California, Oregon,
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and Washington because these are the states most likely to be affected by an earthquake. A partnership between the public and private sectors would manage the early warning system. The private sector would pay for “the installation and long-term operation of geophysical networks” including sensors and GPS technology that detects the earthquakes (Allen, 2013, p.30). The private sector would deliver the alerts through mobile apps. Besides the obvious benefit for human lives, with increased data from sensors and GPS, scientists can better study plate motion and have more information to further nuance our model of Earth’s interior. In September 2013, Governor Jerry Brown signed into law a bill to build an earthquake early warning system in the state. Thus, the momentum for early warning technology is increasing. Stress can come in many different forms. It is deadly at an individual scale and on a large geologic scale. Rocks being stressed from the coming together or sliding of tectonic plates are the cause of earthquakes. When the built up stress is released, the energy that is released travels through Earth’s crust and creates ground motions. The intensity of these ground motions depends on the type of rock that is present in that area. Some areas are more prone to higher intensity shaking than others. Those who live in seismically unsafe buildings can be crushed in a building collapse, representing a significant risk when an earthquake strikes. Trains may be derailed from earthquakes. Also, as seen from the great 1906 earthquake in San Francisco, gas lines can burst and there may be widespread fires. However, a lot of damage can be prevented through early warning technologies. Even with just a few seconds notice, the proper adjustments can be made to save many lives. Now the only question is can we allocate the money that is required to build a nationwide early warning system. It worked for Japan. Let’s make it work for us.
References 1. Ormand, C & Baer, E. (2012).”Stress and Strain.” Teaching Quantitative Skills in the Geosciences. National Science Foundation. Retrieved from http://serc.carleton.edu/quantskills/methods/quantlit/stressandstrain.html 2. Hayward Fault Fact Sheet. (2008) Retrieved from California Department of Conservation Web site: http:// www.conservation.ca.gov/index/Pages/HaywardFaultFactSheet.aspx 3. UC Berkeley California Memorial Stadium. (n.d.) Retrieved from Forell / Elsesser Engineers Web site: http://www.forell.com/case-studies/uc-berkeley-california-memorial-stadium/ 4. DePaolo, D. J., et al. (2008). Origin and Evolution of Earth: Research Questions for a Changing Planet. The National Academies Press, Washington D.C. 5. Earthquakes and Plate Tectonics. (2012). Retrieved from U.S. Geological Survey Web site: http://earthquake. usgs.gov/learn/topics/plate_tectonics/rift_man.php 6. Allen, R. (2013). Seconds Count. Nature, 502, 29-31. Retrieved from http://seismo.berkeley.edu/~rallen/ pub/2013allen/Allen-EEW-Nature-2013.pdf 7. Kanamori, H. (2003). Earthquake Prediction: An Overview. International Handbook of Earthquake and Engineering Seismology, 81B. Retrieved from http://www. gps.caltech.edu/uploads/File/People/kanamori/ HKees03.pdf Image Sources 1. http://www.learner.org/interactives/dynamicearth/ images/new_map.jpg 2. http://geomaps.wr.usgs.gov/3D4Dmapping/html/ images/hayward_fault_map.jpg
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Carbon Nanotubes: Bearing Stress Like Never Before Aditya Limaye
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arbon, element number six, is often considered the backbone of life on Earth. With four valence electrons and many different bonding geometries, carbon is present in all biological macromolecules and plays an integral role in fundamental biological processes, making it truly deserving of its own field, organic chemistry. While carbon is usually anecdotally known for its abundance in biological systems, carbon’s many bonding geometries and versatile electronic configurations make it an exceptional material for synthetic molecules for physical applications, such as building materials or semiconductors. Serious investigation into carbon for physical applications began in 1985, when a group of researchers at Rice university designed a “buckyball,” a molecule known as buckminsterfullerene with the chemical formula C60 arranged in a structure akin to a soccer ball, with six and fivemembered rings positioned adjacent to each other. In fact, buckminsterfullerene, named after the American architect R. Buckminster Fuller, who built geodesic domes resembling the molecule’s shape, was only one molecule in a class of many fullerenes, molecules made entirely out of carbon, arranged in the shape of a hollow sphere or tube. After the 1996 Nobel Prize in Chemistry was awarded to a team for the discovery of fullerenes, research into the fullerenes was taken up in earnest by much of the scientific community. During this time of high interest in the fullerene molecules, a Japanese team of scientists led by Dr. Sumio Ijima designed a tubular fullerene designed entirely out of six-membered carbon rings; forming a large cylindrical structure they termed the “carbon nanotube” (Popov, 2004). Since this fortuitous discovery in 1991, research into carbon nanotubes increased rapidly, spanning from the original field of chemistry into related disciplines such as physics, materials science, and biology. Research into the properties of carbon nanotubes continues in full force even today, and new applications for carbon nanotubes are currently being studied at the forefront of scientific research. One of the most important properties of the carbon nanotube is its incredible ability to withstand applied
Buckminsterfullerene Ball tensile forces. When choosing the appropriate material for structural applications, materials engineers often need to consider the way in which a material responds to outside stresses, such as the tensile forces applied in cabling for bridges or the compressive forces applied against reinforcement beams in buildings. In these cases, it is important to select a material that can withstand an appreciable amount of stress without fracturing, and the carbon nanotube presents quite an enticing choice. The stress response of materials is often quantified using the Young’s modulus or elastic modulus, which is the ratio of the stress applied to a material to the subsequent strain, either compressive or expansive, that the applied stress causes. Materials with high elastic moduli, such as a steel beam, are stiff, while materials with low elastic moduli, such as rubber bands, are flexible. For most building applications, a delicate balance must be struck between stiffness and flexibility, since very stiff materials such as ceramics can break very easily, while very flexible materials support little weight. Based on these constraints, the carbon nanotube presents a very good choice for a structural material, with an elastic modulus five to ten times greater than high-strength steel, but an ability to flex under certain stress conditions. Based on these properties, carbon nanotubes have been studied in many different stress-bearing applications, with the goal of exploiting the molecular structure and mechanical properties of the carbon
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Carbon Nanotube Synthesis nanotube to design strong materials for myriad applications. While carbon nanotubes present extraordinary properties useful for a wide range of physical applications, the properties of any material are inherently limited by its ability to be synthesized properly, and carbon nanotubes are no exception. Since carbon nanotubes derive their unique mechanical properties from their carefully arranged hexagonal bonding structure, even small deviations, such as a void or a similar defect at one point along the nanotube can cause a severe degradation in the mechanical properties of the nanotube (Popov, 2004), making it important to use a highly precise synthesis process. Carbon nanotubes were originally discovered through arcdischarge synthesis, which runs a current through two carbon electrodes spaced 1 millimeter apart, stripping the carbon atoms from the electrode and forming a nanotube structure on the opposite electrode (Popov, 2004). Unfortunately, this synthesis also leads to the creation of other fullerenes and amorphous carbon by-products, such as soot and ash, which lower both the purity and quality of the final product, making it unsuitable for industrial-scale generation (Popov, 2004). In order to improve the nanotube product yield, new methods such as chemical vapor deposition (CVD) were developed in order to create long nanotubes with very few imperfections. This process involves using small organic molecules such as acetylene or ethylene in the vapor phase, stripping away the carbon from them and “growing” the nanotube by depositing the carbon atoms stripped from the vapor phase onto a metal catalyst, creating a large, tubular assembly of carbon atoms. The CVD process shows much promise for industrial production of carbon nanotubes, and can be used to produce very high-purity products with very few defects or voids. While carbon nanotubes can now be synthesized
nearly perfectly, nanotubes by themselves, due to their small size, are not well suited for structural and stressbearing applications. Instead, these nanotubes must be embedded into a different material to enhance its mechanical properties. Currently, this is accomplished by using carbon fiber, a carbon-based material drawn or woven into fibers 5-10 micrometers in diameter and embedded into a host matrix, or surrounding material. At the moment, carbon fiber represents a $13 billion market worldwide, with an annual growth rate of over 7% and expanding applications in areas such as aerospace, wind energy, and automobiles. Most of these applications use carbon fiber oriented in one direction embedded into a host matrix such as a metal airframe in the aerospace industry or a structural polymer in the automotive industry. While current carbon fiber composites show promise for building materials, carbon nanotube nanocomposites offer an opportunity for much greater property enhancement due to their small size. Industrial focus on these polymer-nanoscale filler nanocomposites began when industrial researchers at Toyota demonstrated they could create a five-fold increase in the strength of nylon composites by embedding nanoscale mica sheets into the material instead (Balazs et al., 2006). While these mechanical property improvements are certainly enticing, the advent of carbon nanotubes as composite fillers presents even greater opportunity for structural polymer nanocomposites to replace the current carbon-fiber market. Not only does the carbon nanotube independently have superior elastic properties as compared to woven carbon fiber, but the nano-scale size of the carbon nanotube unlocks a much larger range of interactions with the polymer that strengthen the structural properties of the overall composite. When materials are embedded into a composite, the total surface area of interaction between the polymer and the filler often determines the property changes it effects. Since the carbon nanotube is so small, it can span a much larger surface area of interaction while maintaining the same weight fraction in the material as a regular carbon fiber composite. Due to their size, many more nanotubes can be inserted into the material at the same weight fraction, leading to a stronger composite overall. Due to this surface area effect, carbon nanotubepolymer composites have been created that confer a 23% increase in the stiffness of an epoxy resin at a paltry 1 wt% loading (de Volder et al., 2013), meaning that even at such sparse dispersion, the nanotubes can change the stiffness of a composite by an appreciable amount. Another team of researchers was able to combine Kevlar, an incredibly stiff polymer, with carbon nanotubes to form a nanocomposite with an elastic modulus of 1
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TPa (Endo et al., 2008). For comparison, the elastic modulus of steel is only 200 GPa, five times lower than the modulus of this composite. Given these dramatic mechanical property improvements, the carbon nanotube appears to be poised to take over the carbon fiber composite market share as a structural material, as they perform nearly all of the same functions that polymer-carbon fiber composite materials do, but to a greater extent. While most applications for carbon nanotubes show significant amounts of promise, some barriers, both economic and scientific, exist that currently block the widespread use of carbon nanotubes. One major obstacle for carbon nanotubes in the polymer nanocomposite market is the tendency of carbon nanotubes to aggregate when placed into a larger polymer matrix. Since carbon nanotubes are usually grown to large lengths that span a significant fraction of the composite’s length, they can entangle very easily, especially
Balazs, A.C., Emrick, T., Russell, T.P. (2006). Nanoparticle Polymer Composites: Where Two Small Worlds Meet. Science, 314. 1107 – 1110.
Coleman, J.N., Khan, U., Blau, W.J., & Gun’ko, Y.K. (2006). Small but strong: A review of the mechanical properties of carbon nanotube– polymer composites. Carbon, 44. 1624 – 1652
De Volder, M.F.L., Tawfick, S.H., Baughman, R.H., & Hart, A.J. (2013). Carbon Nanotubes:
Present and Future Commercial Applications. Science, 339. 535 – 539
Endo, M., Strano, M.S., & Ajayan, P.M. (2008). Carbon Nanotubes. A. Jorio, G. Dresselhaus, & M.S. Dresselhaus (ed.). Berlin: Springer-
at <http://www.owlnet.rice. edu/~Robert.Vajtai/Ajayan/Springer%20book%20 chapter%20ajayan.pdf> Popov, V.N. (2004). Carbon Nanotubes: properties and application. Materials Science and Engineering, 43. 61 – 102. doi: 10.1016/j.mser.2003.10.001 Verlag.
Picture Sources Aligned Composite Image due to the favorable interactions between adjacent carbon nanotubes. Not only does this aggregation effect lower the overall mechanical properties of the composite, but it also confounds any process to predictably align the carbon nanotubes within the composite, one of the main reasons why carbon fiber composites achieve such a high elastic modulus to begin with (Coleman et al., 2006). While this does present a pressing problem for industrial adoption of polymer-carbon nanotube composites, current research is making leaps and bounds in finding a solution, from computationally modeling the energy effects that cause aggregation in the first place to attaching molecules to the outside of carbon nanotubes in order to discourage, at a molecular level, the observed aggregation behavior. Based on the current trajectory of carbon nanotube research and the extraordinary properties this unique molecular arrangement brings to the table, it is clear that carbon nanotubes will undoubtedly play a large role in the future of structural materials, especially polymer-nanotube composites in the aerospace, automotive, and renewable energy sectors. If the past is any indicator of the future trajectory of carbon nanotubes, it appears that new applications and interesting properties will be discovered in the future, paving the way for new and exciting structural, stress-bearing applications of carbon nanotubes.
http://nanochop.lgcgroup.com/wpcontent/uploads/2012/06/Carbonnanotube_000015223149Medium.jpg http://mathspig.files.wordpress.com/2013/04/99-9bucky-balls.gif h t t p : / / o n l i n e l i b r a r y. w i l e y. c o m / d o i / 1 0 . 1 0 0 2 / adma.200500467/abstract http://me1065.wdfiles.com/local--files/hydrogenstorage-in-carbon-nanotubes/CNTs
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