JOURNYS Issue 7.1

Page 1

Journal of Youths in Science

Booming Cities is algae the new


sounds of a


gillyweed? star trek

in the present

Art by Chelsea Xu


The Journal of Youths in Science (JOURNYS), formerly known as Falconium, is a student-run publication. It is a burgeoning community of students worldwide, connected through the writing, editing, design, and distribution of a journal that demonstrates the passion and innovation within each one of us.


Torrey Pines High School, San Diego CA Mt. Carmel High School, San Diego CA Scripps Ranch High School, San Diego CA Del Norte High School, San Diego CA Cathedral Catholic High School, San Diego CA Beverly Hills High School, Beverly Hills CA Alhambra High School, Alhambra CA Walnut High School, Walnut CA Lynbrook High School, San Jose CA Palo Alto High School, Palo Alto CA Mills High School, Millbrae CA Lakeside High School, Evans GA Blue Valley Northwest, Overland Park KS Olathe East High School, Olathe KS Delhi Public School, New Delhi, India Korean Youth Math Association

All submissions are accepted at Articles should satisfy one of the following categories: Review: A review is a balanced, informative analysis of a current issue in science that also incorporates the author’s insights. It discusses research, concepts, media, policy, or events of a scientific nature. Word count: 750-2000 Original research: This is a documentation of an experiment or survey that you did yourself. You are encouraged to bring in relevant outside knowledge as long as you clearly state your sources. Word count: 1000-2500 Op-Ed: An op-ed is a persuasive article or a statement of opinion. All op-ed articles make one or more claims and support them with evidence. Word count: 750-1500 DIY: A DIY piece introduces a scientific project or procedure that readers can conduct themselves. It should contain clear, thorough instructions accompanied by diagrams and pictures if necessary. Word count: 500-1000 For more information about our submission guidelines, please see




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SPRING 2016 Volume 7 Issue 1

CHEMISTRY 4 Air Purification from Photocatalytic Oxydization | EMILY STUART 6 The Dilemma: Booming Cities and PM 2.5 | JACK HU 8 The History of Superconductors | AN NGUYEN



BIOLOGY Is Algae the New Gillyweed? | NATHAN LIAN 9 A Heart Transplant: A Life’s Miracle | MIHIKA NADIG 10 Effectiveness of Contact Lens Solutions | JANIE KIM 12 Microbiota in the Body | STEPHANIE HU 14 Prion Treatment: Steps Towards a Cure | JANIE KIM 16 RNAi: A New Approach to Medicine | HANA VOGEL 18

PHYSICS & APPLIED MATHEMATICS 20 Star Trek in the Present | SUNG BIN ROH 22 The Uncertainty Principle and Monochromatic Light |




PSYCHOLOGY Alice in Wonderland Syndrome | CLAIRE WARRENFELT 25 More Than Meets the Eye | MELBA NUZEN 26 Sounds of a Rainbow: Synesthesia | ALEXANDER DIEBOLD 28 The Science of Sensory Deprivation | JESSICA GANG 30 Walking Corpses | CLAIRE WARRENFELT 32 3 | JOURNYS | SPRING 2016

AIR PURIFICATION FROM PHOTOCATALYTIC OXYDIZATION Brown smog hangs heavy on the horizon as you drive down from the hills into Orange County, California. While gazing at the dirty smudge across the sky, you find it difficult to comprehend the number of people who live and work in a sea of polluted air. The harrowing effects of airborne toxins seem inescapable. Fortunately, methods to clean the air we breathe exist. Air purification is a necessary process in the modern world, as it removes toxins from the air we breathe. For example, the 2013 average amount of lead present in United States air was .24 ug/mg3, almost twice the national standard [1]. To avoid the inhalation of toxins, the air must be cleaned. However, the majority of the air purifiers on the market today, which pump air through a filter to remove particles of pollutant, cannot effectively combat toxins such as lead or carbon monoxide [2]. This is because these filter-based air purifiers allow gaseous pollutants and smaller particle pollutants to pass through the filter and back into the atmosphere. In addition to their inefficiency, filter-based air purifiers are costly, use electrical energy to pump air, and must have their filters periodically replaced. Luckily, there is another type of air purification system that uses photocatalysis to reduce gaseous and smaller particle toxins. Photocatalysis works through sunlight, where UV light excites electrons in

a sheet of semiconductor material, usually titanium dioxide, causing them to be released. These electrons interact with water molecules in the air, binding to one hydrogen atom in the molecule. The hydrogen disconnects with the rest of the molecule, leaving an uncharged hydroxyl radical (the unstable neutral form of a hydroxide ion: oxygen bonded with a hydrogen atom) [3]. The hydroxyl radicals can then oxidize, or take electrons away from, the pollutant molecules, causing them to break apart and rebind into harmless molecules, such as water and carbon dioxide. All that is needed to make a photocatalytic oxidizing air purifier is a sheet of titanium, a much cheaper alternative to the fans and filters present in most purifiers. Despite the simple, cost-effective build of photocatalytic oxidation air purifiers, research of the technology only began a few years ago. Like with all new technologies, many people remain skeptical of the usefulness of these air purifiers, and scientists are currently debating whether their effect on the environment is truly beneficial. Their arguments are founded on the fact that these generators release a small amount of ozone, a toxic pollutant. However, ozone is already present in Earth’s high atmosphere, where the gas blocks harmful UV rays from entering the lower atmosphere. The levels of ozone produced

Written by Emily Stuart Art by Kristina Rhim 4 | JOURNYS | SPRING 2016

The Manuel Gea González hospital Image Courtesy of Sensing Cities

by photocatalysis remain significantly lower than the international guideline standard of .05 parts per million [3]. Thus, though photocatalytic oxidizing air purifiers produce small amounts of ozone, they do not generate enough of this pollutant to do any harm. By ridding the air of pollutants, photocatalytic oxidization’s positive effects greatly outweigh any negative ones. Because photocatalysis removes chemical and fine-particle toxins from the air, it has been shown to reduce the occurrences of acid rain, when normal raindrops form around acidic pollutant particles instead of grains of dust. The precipitation then carries the pollutants into soil, lowering the pH. Acid rain is described by the United States Environmental Protection Agency as “wet or dry deposited material from the atmosphere containing higher than normal amounts of nitric and sulfuric acids” [4]. The harmful increase in the acidity of soil and water effectively kills the wildlife living in the damaged habitats. By breaking up airborne nitric and sulfuric acids, photocatalytic oxidization reduces the toxicity and occurrence of acid rain. Although photocatalysis is extremely effective against acid rain and air toxicity, scientists have been attempting to make use of this technology on a larger scale. The Manuel Gea González hospital in Mexico

A close up of the photocatalytic “lace” Image Courtesy of Medical Daily

City has discovered several solutions. The side of the hospital is layered with a lace-like webbing to increase surface area of titanium dioxide-covered materials, which has already begun to affect the city’s pollution. Two thousand square feet (185.8 square meters) of titanium dioxide, like those on the side of the Manuel Gea González Hospital, can potentially erase pollution produced from 10,800 miles of driving ­— a distance more than three times longer than the length of the United States [5]. Because only a microscopically thin layer of titanium dioxide is needed to purify air, the system can be put on buildings for little to no cost or structural damage. With the use of titanium dioxide on buildings, photocatalytic air purifiers can be implemented on a large scale. Dirty air is becoming an increasingly significant problem each year. In 2012, the World Health Organization reported that air pollution caused at least 7 million deaths worldwide [6]. In order to stop deaths such as these, preventative measures must be taken. Photocatalytic air purifiers, unlike filter-based air purifiers, are capable of removing gaseous toxins from the air. Because of their low cost, photocatalysis can be used on a large scale to rid the atmosphere of pollutants. Photocatalytic oxidizing air purifiers are an effective, efficient way to clean the air we breathe.

REFERENCES 1. United States Environmental Protection Agency. “Lead”. (2014) 2. United States Environmental Protection Agency. “Indoor Air Publications: Guide to Air Cleaners In The Home”. airclean.html (2014) 3. Woodford, Chris. “Photo Catalytic Air Purifiers”. (2014) 4. Environmental Protection Agency. “Acid Rain”. (2014) 5. Mathews, Daniel. “A Titanium Skin Destroys Air Pollution”. (2013) 6. World Health Organization. “Burden of Disease in Ambient and Household Air Pollution”. databases/en/ (2014)


The Dilemma: Booming Cities and PM 2.5 by Jack Hu When you walk through the busy streets in a metropolis on a smoggy day, you probably sense the pungent air in your surroundings. This smell is caused by the fine particulate matter of 2.5 μm or less in aerodynamic diameter (PM2.5) in the air, and it is common in various booming cities of developing countries around the world. Over the last decade, researchers have extensively studied the respiratory failures and cardiovascular diseases brought about by PM2.5 [1]. Governments and the general public have also given considerable attention to the health risks of this matter. Since the Industrial Revolution, it seems that economic growth and environmental issues cannot be accommodated for at the same time. Nonetheless, many cities have been motivated to increase government expenditures to develop advanced public transportation systems and to change from conventional energy sources to alternative ones. The dilemma of booming cities and PM2.5 is also being brought to the global scientific stage. Today, researchers from different countries are cooperating to combat this dilemma, and Beijing is their chosen experimental field. In the first half of 2013, the concentration of PM2.5 in Beijing had a daily average of 194 micrograms per cubic meter. The intraday peak of 886 micrograms per cubic meter occurred on Jan. 12, 2013, which well exceeded t h e


hazardous level of 301 μg /m³ -500 μg /m³ [2]. This extremely high concentration of PM2.5 has multiple causes. The major components of the PM2.5 are generally either natural or related to human activity. Additionally, dust is one of the most abundant aerosols, as sandstorms whip small pieces of mineral dust from deserts into the atmosphere. The geographical location of Beijing makes this metropolis seemingly fit into this category of aerosols. To the north of Beijing is the Inner Mongolian desert, and the northwest-wind carries the sand to the capital, creating sandstorm-related weather. However this factor isn’t quite convincing enough to explain the presence of PM2.5. Phoenix, Arizona, located in the Sonoran Desert, is sometimes affected by the dust storms as well; however Phoenix’s PM2.5 concentration has a five-month-average (from June 2,2008, to October 31, 2008) of 9.7 μg /m³ with very few outlier data of around 20 μg / m³ [3]. Besides the natural causes, other contributors of PM2.5 are considered anthropogenic, or human-made, and they come from a variety of sources. Though less abundant than natural forms, anthropogenic aerosols can dominate the air downwind of urban and industrial areas. Fossil fuel combustion produces large amounts of sulfur dioxide, which reacts with water vapor and other gases in the atmosphere to create sulfate aerosols. Biomass burning, a common method of clearing land and consuming farm waste, yields smoke that is comprised mainly of organic carbon and black carbon. Automobiles, incinerators, smelters, and power plants are prolific producers of sulfates, nitrates, black carbon, and other particles. Deforestation, overgrazing, drought, and excessive irrigation can alter the land surface, increasing the rate at which dust aerosols enter the atmosphere [4]. Beijing, the capital of China, has experienced rapid growth in the past two decades. The expanding city attracted a population in the millions; from 2005 to 2012, 5.31 million people moved to become permanent residents of Beijing [5]. Corresponding to the growth in population was the increased need of private cars and coal—one being the major transportation­, the other, the vital energy source. As the economy grew, the demand for cars skyrocketed. By 2012, the private automobiles possessed in Beijing reached 4 million, and this number is still increasing. Every day, the cars on the road produce car exhaust that adds up to 900,000 tons a year. Additionally, the burning of coal is still the dominant source of energy and heat supply. Though there are no fossil fuel plants within the Beijing city limits, Beijing still owes 25% of its daily energy to the numerous fossil fuel power plants within the 50-mile-radius circle of Beijing. The total amount of 23 million tons of coal burnt in these plants in 2012 speaks on its own, releasing toxic gases that contribute sulfur dioxide, hydrogen sulfide, and nitrogen monoxide to the city’s atmosphere [5]. Most importantly, city expansion required the destruction of farmland and forests for the construction of estates and skyscrapers. The deforestation around Beijing and the transportation of sand from construction sites significantly increase the amount

of PM2.5 in the urban atmosphere. There is no wonder that human-influenced air pollution, the byproduct of this aggressive development, has become one of the main sources of the growing problem of PM2.5 in Beijing. Despite its picayune size, PM2.5 has a profound effect on every person in its vicinity. The Air Quality Guidelines Global Update 2005 from World Health Organization assesses that more than two million premature deaths each year can be attributed to the effects of urban outdoor air pollution and indoor air pollution (caused by the burning of solid fuels). More than half of this disease burden is borne by the populations of developing countries. People living in an urban environment where PM2.5 concentration reaches 35 μg/ m³ on a yearly average have a 15% higher risk of premature death than those living in an environment with a concentration of 10 μg /m³ [6]. With an estimation of 800,000 PM2.5-related premature deaths, the WHO has ranked high concentration of PM2.5 as the 13th leading cause of worldwide mortality [7]. Among the various clinically diagnosed cases on premature deaths caused by PM2.5, lung cancer stands out as a typical case. Dr. Chen from McGill University in Canada points out that “The … long-term exposure to PM2.5 increases the risk of non-accidental mortality by 6% per a 10 μg /m³ increase, independent of age, gender, and geographic region. Exposure to PM2.5 was associated with an increased risk of mortality from lung cancer (range: 15% to 21% per a 10 μg / m³ increase) and total cardiovascular mortality (range: 12% to 14% per a 10 μg /m³ increase)” [8]. Exposure to elevated levels of PM2.5 over a few hours to weeks can also trigger cardiovascular disease related mortality and nonfatal events [1]. The evidence is the strongest for ischemic heart disease (IHD), a common PM2.5 related clinical case, including myocardial infarction and heart failure hospitalizations [7]. Unlike PM10 or larger particulates, PM2.5 has such a small diameter that it is much easier to be transited through the respiratory system into the lungs or the blood vessels, causing lung and cardiovascular diseases. Knowing the snake in the grass, developing countries’ citizens who live in major cities such as Beijing are faced with the same dilemma. Should they choose to stay in the booming cities where they can enjoy the growing economy and suffer from the deteriorating air quality, or should they move to the suburbs or countryside where the air is fresh but the opportunities are less? Instead of passively accepting the situation, many of the developing city officials and dwellers are choosing to fight the problem. The Beijingers are taking the initiative to lead the world’s developing countries in combating PM2.5. In 2008, when Beijing was criticized for not having a decent air quality to hold the 29th Olympics and many national Marathon teams and race-walking teams were questioning the safety of competing in long-distance racing sports in the mist of smog, Beijing citizens undertook the policy of odd-even number plate restriction, which prohibits people from using cars every other day. In fact, according to Professor Rich from University of Rochester in his research monitoring the change in air pollution before, during, and after the Olympics, Beijing had significant reduction in the mean concentration of sulfur oxide (-60%), carbon monoxide (-48%), nitrogen dioxide (-43%), fine particles (particulate matter less or equal to 2.5 μm in aerodynamic diameter [PM2.5]; -27%), and sulfate (-13%) [9]. If Beijing could accomplish this feat once, why wouldn’t it succeed in this second round of actions? On September 12, 2013, China unveiled its first comprehensive

plan to fight air pollution, promising significant improvements in air quality in key regions by 2017. On a global scale, China is also seeking international cooperation to battle the PM2.5 in the long run. California Governor Jerry Brown and China's top climate negotiator have signed the first agreement between a US state and China that seeks greater cooperation on clean energy technologies and research meant to reduce greenhouse gas emissions. The two-year agreement establishes collaboration to enhance pollution control strategies for industrial sectors and the transportation sector. It encourages joint efforts to protect public health, promotes clean and efficient energy, protects the environment and natural resources, and supports sustained economic growth. “Reducing pollution takes great political struggle,” said Governor Brown in a meeting with China’s Minister of Environmental Protection Zhou Shengxian. “We know in America it’s not easy, so it won’t be easy in Beijing. But to the extent that we can help, we would like to help” [10]. China and the US, two of the world’s top-ranked greenhouse gas emitters, are putting the means of global implications in to combat PM2.5. Some cities in developed countries such as Los Angeles and London have already undergone the process of changing to alternative energy resources and developing convenient public transportation systems. However, there are more cities in developing countries that are in the same situation as Beijing, such as New Delhi, São Paulo, and Mexico City. Clean air is a shared global resource, and it is a common interest for people around the world to protect air quality in order to promote global health. The struggle against PM2.5 is an on-going battle; it will not be finished until we see the whole world under the same clear blue sky. REFERENCES 1. Roger D. Peng, PhD, et al. “Coarse Particulate Matter Air Pollution and Hospital Admissions for Cardiovascular and Respiratory Diseases Among Medicare Patients.” JAMA. 299(18): 2172-2179. doi: 10.1001 / jama.299.18.2172 (2008). 2. Embassy of the United States Beijing, China. “Beijing Air Quality Current Reading.” (2013). aqirecent3.html 3. Environmental Protection Agency. Download detailed AQS (air quality system) data. (June 2,2008, to October 31, 2008). http://www.epa. gov/ttn/airs/airsaqs/dataildata/downloadaqsdata.htm 4. M. Hardin and R. Kahn. “Aerosols: Tiny Particles, Big Impact.” NASA earth observatory (2010 Nov. 2). 5. Beijing Municipal Bureau of Statistics. “Beijing city data” (2013). http:// 6. World Health Organization. “WHO air quality guidelines for particulate matter, ozone, nitrogen dioxide and sulfur dioxide. Global update 2005. Geneva, Switzerland: World Health Organization.” 2006. http:// index.htm 7. Diane R. Gold, MD, MPH, DTM&H et al. “New Insights into pollution and the cardiovascular system 2010 to 2012” Circulation. 127(18): 1903-13. doi: 10.1161/CIRCULATIONAHA.111.064337. (2013 May 7). 8. H. Chen et al, “A systematic review of the relation between long-term exposure to ambient air pollution and chronic diseases.” Rev Environ Health. 23(4):243-97. (2008 Oct-Dec). 9. Rich DQ, et al. “Association between changes in air pollution levels during the Beijing Olympics and biomarkers of inflammation and thrombosis in healthy young adults.” JAMA. 307(19): 2068-2078. (2012). 10. C. Tian. “California, China Officials Sign Clean Air Cooperation Pact.” Environmental News Service (2013 April 10).



Superconductors are materials Magnetic levitation (maglev) for transport that possess no resistance to the vehicles like trains is an example of the flow of electricity, and are recent application of superconductors in public milestone discoveries in the field of transportation. Because the trains “float” on chemistry. However, much remains the rail tracks due to the strong repulsion, to be discovered about the numerous friction is virtually eliminated and heat energy theories and limits of the application of is not lost [3]. The Ministry of Transport superconductors. of Japan authorized the construction Physicist Heike Kamerlingh of Yamanashi Maglev Test Line, Onnes of Leiden University which was opened on April 3, discovered superconductivity 1997, and the maglev vehicle in 1911 when he cooled the can now reach a speed temperature of mercury of 361 mph. In addition, to 4° Kelvin (-452° F or electrical generators made -269 °C) [1]. Onnes found with superconducting that mercury’s electrical wire have proven to be far resistance seemed to more efficient than those disappear entirely at this made with copper wire, as temperature; this major discovery their calculated potential efficiency won him the Nobel Prize in 1913, and is above 99 percent. Not only that, but Art by Nick Hand the size of the generator would be half of that of opened the door for new experiments seeking to exploit superconductors’ lack of electrical resistance. conventional generators [4]. Another possible, though slightly A significant breakthrough in understanding the properties idealized, application of superconductors is to use them in of superconductors came in 1933 when Walther Meissner and transmitting electrical power to cities, as the wires would have Robert Ochsenfeld discovered the extreme extent to which a no resistance to the flow of electricity [4]. Finally, the so-called superconducting material will repel a magnetic field and the SQUID (Superconducting Quantum Interference Device) is amount of time it is maintained. When a magnet moves by a currently in use by the U.S. Navy to detect mines and submarines. conductor, a current is induced. However, in a superconductor, This is the most sensitive type of detector known to science the induced current mirrors the field, causing a strong repulsion. and consists of a superconducting loop used to measure any This effect, also known as the “Meissner effect,” exhibits strong strong magnetic field [4]. Unfortunately, the cost and difficulty diamagnetism [1]. In addition, although an induced current of cooling miles and miles of wire to very low temperatures has in an ordinary metal substance would decay rapidly from the made the realization of this technology challenging in real life. dissipation of resistance, a superconducting ring has been shown The endless applications for superconductors are to exhibit a decay constant of over billions of years; that is, a extraordinary. But unfortunately, their nature and workings have superconductor would never develop resistance to the flow of not yet been fully uncovered by scientists and researchers nearly electrons and therefore has huge practical applications to many 100 years after their discovery. It is difficult to say when we will future inventions. attain a full understanding of superconductivity, but along the The first widely accepted theory about the nature of way, it is certain that new innovations practical to society will superconductivity was put forth in 1957 by John Bardeen, be invented in the process of utilizing the unique properties of Leon Cooper, and John Schrieffer. Their BCS theory explains superconductors. why superconductivity happens at temperatures close to References absolute zero for elements and simple alloys [2]. At higher 1. Eck, J. “Superconductors Information for the Beginner.” http:// temperatures and different superconducting systems, though, BCS theory is not applicable and cannot fully explain the nature 2. Bellis, M. “History of Superconductors.” od/sstartinventions/a/superconductors.htm. of superconductivity. To this day, a theory to explain high3. Halder, P. and Abetti, P. “Superconductivity’s First Century.” http:// temperature superconductivity has not been found, limiting our of superconductivity [2]. century (2011). Still, superconductors have many possible uses and 4. “Superconductivity Concepts.” applications, with many more possibilities being researched. hbase/solids/supcon.html. 8 | JOURNYS | SPRING 2016

Is Algae the New Gillyweed? In Harry Potter and the Goblet of Fire, Harry Potter ingests gillyweed, a magical plant that allows a witch or wizard to process oxygen from water, in order to complete the second task of the 1994 Triwizard Tournament. Although such a plant exists only in the wizarding world, Dr. Ryan Kerney and his colleagues at Dalhousie University in Nova Scotia, Canada may have come close to unlocking the key to breathing underwater in the Muggle World in their study, “Intracellular invasion of green algae in a salamander host,” published in the Proceedings of the National Academy of Sciences.” In the study, Kerr and his team attempt to attribute a tangible cause to the symbiotic relationship between the green algae Oophila amblystomatis and the spotted salamander Amblystoma maculatum, a relationship that has puzzled scientists since the late 19th century. Through a series of time-lapse videos, Kerr arrived at the hypothesis that the appearance of algae within the embryos of salamanders could only be explained by uptake of O. amblystomatis through an opening in the developing embryo known as the blastopore. This would also explain why previous scientists studying algal-salamander symbiosis have failed to identify any visible signs of algal invasion of embryonic salamander tissues and cells during development. In fact, identifying such interactions between a photosynthetic organism and a vertebrate at all goes against the fundamental mechanisms of biological processes. In vertebrae, there exists a biological system known as an adaptive immune system, an immune system that destroys biological materials not characterized as “self”. Algae would fall into such a category. How then is a symbiont like O. amblystomatis able to stably reside in a vertebrate like A. maculatum? While the origin of this unique relationship between two such organisms is unknown, two hypotheses have been proposed: a) O. amblystomatis fully integrates within A. maculatum before the complete development of its immune system and b) A. maculatum has an inherently “weak” immune response in terms of specificity, speed of onset, and memory, which contributes to its ability to easily regenerate lost limbs. Regardless of how O. amblystomatis becomes integrated into A. maculatum, Kerney and his team’s identification of this unique symbiotic relationship between two seemingly incompatible organisms has immense implications in many fields of biological study. However, in order to add depth and credibility to their findings, they must first address a number of questions revolving around the way in which the system operates. According to the study, O. amblystomatis provides an oxygen ART BY ALEXANDER HONG

By Nathan Lian

rich environment for A. maculatum, and A. maculatum provides nitrogen rich waste and carbon dioxide for O. amblystomatis. Should the amount of oxygen generated by O. amblystomatis suffice in sustaining A. maculatum, it would be the sole oxygen source for A. maculatum to carry out cellular respiration underwater. However, in order for oxygen to be generated by O. amblystomatis, it must undergo photosynthesis, a process by which autotrophic organisms are able to sustain themselves by producing glucose; oxygen is a byproduct of this process and sunlight is necessary to initiate it. While this symbiotic relationship is plausible in the early stages of A. maculatum development when the embryonic sac is light-permeable, once the salamander is fully grown, O. amblystomatis is effectively shielded from the light by a thick layer of skin, an adaptation which allows the salamander to spend most of its adult life underground. Therefore, even if sunlight is able to penetrate its skin and supply the energy required to initiate photosynthesis in O. amblystomatis, the layers of earth covering A. maculatum would stop the sunlight from even reaching the surface of its skin in the first place. Some may argue that many eukaryotic algae are capable of growing heterotrophically in the absence of light; and while this is undoubtedly true, the interaction between such algae and a eukaryotic host would merely reflect a one-sided symbiotic relationship. Not only would the host’s stores of sugar be depleted more readily as sugar becomes the initiator of heterotrophic growth in both the host and the algae, but the algae would also provide nothing more to the host than fixed carbon dioxide as a result of intermediate steps in the Calvin Cycle. As far as A. maculatum is concerned, and all animals for that matter, carbon fixation does not impact cellular respiration in any way and therefore provides no support for Kerney’s study. In fact, even if O. amblystomatis is able to sustain itself through the nitrogen waste produced within a. maculatum, it provides A. maculatum with absolutely no oxygen required for it to survive underwater, meaning that the supposed mutualism embodied by this interaction is nothing more than commensalistic. The only way for the interaction to be mutualistic, therefore, is if O. amblystomatis grows autotrophically, a notion confirmed by Kerney in a 2010 conference. Because it has now been established that O. amblystomatis does in fact grow autotrophically, that then begs the question, how does O. amblystomatis even sustain itself now, let alone another organism in the absence of an adequate light source such as the sun? Should these questions be effectively and comprehensively answered in future years, the entire dogma of vertebrate cells disposing of foreign materials would be sufficiently challenged, paving the way for enormous bounds in all fields of biological study. Perhaps, breathing underwater via natural means is not so magical after all. References 1. Kerney Ryan, et al. “Intracellular invasion of green algae in a salamander host.” (2011). 2. Petherik, A. “A solar salamander: Photosynthetic algae have been found inside the cells of a vertebrate for the first time.” http://www.nature. com/news/2010/100730/full/news.2010.384.html (2010).


A Heart Transplant:

A Life’s Miracle written By Mihika Nadig Art by Nick Hand At every tick of the clock, an infinite series of critical processes takes place in the human body for one sole purpose: to live. One instrument that contributes to this purpose, often considered the most vital organ, is the heart. With its constant rhythm, it indicates a sign of life. From the moment of birth to the moment of death, the heart has the utmost priority of maintaining a uniform rhythm, a constant reminder that life exists within a human being. With every beat, the heart pumps blood into each crevice of the human body, but when it deteriorates to the point where it can no longer perform its task, it causes a life-threatening situation. The heart may become diseased with serious ailments such as severe coronary heart disease, angina, or end stage heart failure. In such cases, the diseased heart of a patient can be replaced with a healthy heart — a heart transplant. In order to find an appropriate donor heart, a transplantation team must evaluate a patient’s eligibility for a heart transplant through procedures like blood tests, X-rays, pulmonary function tests, and psychological assessments. To reduce the chances of a patient’s body rejecting the transplant, it is critical that the donor heart closely matches the patient’s disease severity, blood type, and tissue type. After the transplant team determines that a patient is eligible for a heart transplant, the patient is placed on the National Organ Donors List. When a match is found, a group of surgeons carefully review the heart to ensure eligibility and begin preparations for the surgical procedure. The cardiac allograft, or heart tissue, is then 10 | JOURNYS | SPRING 2016

injected with potassium chloride (KCI) to stop the heart from beating before the heart is removed from the donor’s body. The allograft must be used within four to six hours of preservation. Prior to the procedure, IV fluids may be administered to the patient [1]. Catheters are also inserted into the patient’s neck and wrist, bladder, and possibly the subclavian area and groin. In order to ensure normal breathing, a tube is inserted through the mouth and into the lungs and attached to a ventilator. Additional tubes are inserted into the patient’s chest in order to drain postoperative fluids and blood that often accumulate around the heart. During this entire process, an anesthesiologist monitors the patient’s heart rate, blood pressure, and other involuntary processes. The cardiac allograft can be sutured in either an orthotopic or a heterotopic position. In an orthotropic procedure, the patient’s diseased heart is removed, while in a heterotopic procedure, the patient’s heart is left in place and the donor heart is implanted; in a sense, the two hearts support each other. In rare cases, a patient will undergo the latter method because of certain inherent complications, which include pulmonary compression of the recipient, difficulty obtaining endomyocardial biopsy, and the need for anticoagulation [4]. In cases of pulmonary hypertension, a heterotopic transplant is the optimal solution. An orthotropic procedure can be performed with the Shumway-Lower technique or as a bicaval anastomosis [4]. The Shumway- Lower technique shortens

the ischemic time by about ten minutes [4]. However, surgeons find the bicaval method to be significantly more advantageous because they can avoid the right atrium, allowing for a better atrial transport in the heart. In an orthotropic procedure, a median sternotomy is performed in which the mediastinum, or the partition between the two body cavities, is exposed [3]. Here, the pericardium, or the membrane that encompasses the heart, is opened, followed by the dissection of the great vessels, which include the superior and inferior vena cava, pulmonary arteries and veins, and the aorta [3]. Afterwards the patient is attached to a cardiopulmonary bypass or a heartlung machine, and his or her diseased heart is removed by transecting the great vessels and a portion of the left atrium, leaving the pulmonary arteries in place. The cardiac allograft is then trimmed to be properly positioned and sutured on top of the patient’s remaining portion of the left atrium. This new heart can be restarted through electrical shock. After proper heart rate is detected, the patient is removed from the cardiopulmonary bypass, tubes are attached to a suction device that drains the fluids away from the heart, and both the sternum and the skin over it are sewn together. In order to cover the initial incision, surgical staples or sutures are put into place, marking the end of the surgical procedure. During the initial period of recovery, temporary wires may be inserted to the pacemaker in order to monitor the rate of beating. One of the biggest challenges that a patient faces is his or her body’s response to such a drastic change. A human’s

immune system is naturally trained to fight against the presence of any foreign substance, which includes both infectious pathogens and transplanted tissue. As a result, when the new organ is placed in the recipient’s body, the immune system falsely identifies the organ as an invader of the body. In order to reverse this instinct, the patient is given immunosuppression medications such as cyclosporine, azathioprine, Prednisone, or Methotrexate in order to help the body accept the donor and treat it as a beneficial unit [2]. These medications are given to the patient before and after the procedure [2]. After the heart transplant, the patient is moved to the ICU, or intensive care unit, where his or her body’s progress and response are carefully monitored. Human beings have a right to live their lives without the constant fear of a failing heart. However, a time may come when the body’s deterioration is unendurable. At these times, only the miracle of a heart transplant is capable of restoring healthy life back to the body. References 1. “Heart Transplantation Procedure.” http://www.hopkinsmedicine. org/healthlibrar y/test_procedures/cardiovascular/hear t_ transplantation_procedure_92,P07974/. 2. “Patient's Guide to Heart Transplant Surgery.” ht-pg-hearttransplantprocedure.html. 3. McRae, Donald. Every Second Counts: The Race to Transplant the First Human Heart. New York: G.P. Putnam's Sons, 2006. Pri nt. 4. Botta, D. M., Jr. “Heart Transplantation Technique.” http://emedicine. (2014).

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Analysis of Antimicrobial Effectiveness of RGP Contact Lens Solutions Abstract

against MRSA and P. aeruginosa

The objective of the experiment was to determine which out of five rigid gas permeable (RGP) contact lens solutions—Boston Advance Conditioning Solution, Lobob Soaking Solution, Boston Simplus Multi-Action Solution, Menicare Multipurpose Solution, and Opti-Free GP Multi-Purpose Solution—prohibits the growth of MRSA TCH 1516 and Pseudomonas Aeruginosa PA01 the most effectively. Both bacterial species were tested against the five lens solutions and a saline control using a minimum inhibitory concentration method (the percentage of solution is tested at different decreasing percentages). Boston Simplus was the most effective against MRSA, while MeniCare was the most potent against Pseudomonas. With these results, RGP lens wearers can avoid potential infections by understanding which solutions work best against either of these two bacteria. Introduction/Background Contact lenses are directly placed onto the cornea of the eye, which means sterility is critical to avoid infection. Because of this, the solution the lenses are stored in and its effectiveness in eradicating bacterial growth plays a major role in contact lens users’ eye health. A common bacteria species found naturally in the eye’s fauna is Staphylococcus aureus, a bacterium capable of bringing about serious infections that has a deadlier strain called Methicillin-Resistant Staphylococcus aureus. Another bacterium notorious for causing eye infections is Pseudomonas aeruginosa: the most frequent bacterial cause of microbial keratitis [1]. Because bacteria and other pathogens can infect the eye, choosing the right lens solution is essential. Just why is Methicillin-Resistant Staphylococcus aureus so notorious? Often referred to as MRSA, it is a pathogen gaining increasing attention in the medical research community due to its high, steadily growing number of long-lasting infections. As stated in its name, MRSA possesses the ability to flourish despite applications of methicillin, a form of the blue-moldderived group of antibiotics, penicillin. The number of infections is increasing due to more frequent surgeries and lifesupport treatments, ineffective hand washing, and the failure to completely sterilize medical equipment [2]. This leads to the development of diseases such as conjunctivitis, keratitis, corneal ulcers, fungal infections, and even blindness as the bacteria begins to grow in the eyes and contact lenses. Like MRSA, Pseudomonas aeruginosa is noted for its versatility and tendency to become resistant to antibiotics [3]. It is a Gram-Negative bacteria found ubiquitously in water and soil, and is motile by means of a single flagellum [4]. Because of its ability to flourish in a wide range of environments, Pseudomonas is a prominent pathogen in hospitals. It is also difficult to eliminate due to its outer membrane, which is characteristic to Gram-Negative bacteria and acts as an extra barrier for drugs and antibiotics.

Written by Janie Kim Art by Haiwa Wu 12 | JOURNYS | SPRING 2016

Methods For the MRSA trials, MRSA TCH 1516 was taken from the stock and grown onto a Todd Hewitt Agar plate at room temperature for twelve hours. A single colony was then put into 5 mL of Todd Hewitt Broth, grown for about 7 hours, spun in a centrifuge for six minutes, and diluted to an optical density of 0.40 using a spectrophotometer. This suspension was diluted to a 1:20 ratio in phosphate buffered saline. For this experiment, there were two types of contact lens solutions used: one-step and two-step. One-step solutions (Boston Simplus Multi-Action Solution, Menicare GP Cleaning, Disinfecting, Storing Solution, Opti-Free GP Multi-Purpose Solution) are contact lens solutions that require only one solution for both cleaning and storage of lenses, and twostep solutions (Boston Advance Conditioning Solution, Lobob Soaking Solution) are contact lens solutions that require separate solutions for cleaning and storing. The two-step solutions were tested only by their storing solutions for the purposes of this experiment. Two hundred µl of each solution were then pipetted into Row A of an assay plate, with two columns per solution. After 100 µl of CA-MHB broth was added to all other wells beneath, 100 µl of solution from Row A was moved to Row B, then from Row B to Row C, etc. until the last row. 90 µl of every well was moved to a fresh assay plate and a positive and negative control were added. The negative control was a column of only CA-MHB, and the positive control consisted of 10 µl of the bacterial solution and 90 µl of CA-MHB. Ten µl of the prepared bacterial solution was added to every well except the negative control. Finally the plates were parafilmed and placed in a shaker incubator for 15 hours. After incubation, 10 µl of resazurin was added, and the plates were incubated for 24 hours. Resazurin is a blue indicator dye that turns a pinkish hue in the presence of live bacterial organisms. It changes into a purple color in the presence of low levels of bacterial growth and a bright pink in the case of high levels of growth. The experiment was repeated three more times for a total of four trials. For the Pseudomonas trials, the P. aeruginosa PA01 bacteria was tested using the same procedures as in the MRSA trials. The only variances were using Lysogeny agar in the place of Todd Hewitt agar, using Lysogeny broth in the place of Todd Hewitt broth, and having three trials instead of four.

Results/Conclusions Boston Simplus was more effective in discouraging growth of MRSA than any of the other tested solutions, and the average percentage of the solution in which bacteria began to grow was approximately 0.53%. Boston Advance was the second most effective overall and the most effective out of the twostep solutions, averaging 1.58%. The three other solutions— Menicare, Lobob, and Opti-Free—did not perform as well as Simplus or Advance. The sterile saline control averaged 45%, which proved that the preservatives did make a difference in antimicrobial strength. The two preservatives that seemed to be most effective in combination were Chlorhexidine Gluconate at 0.003% and Polyaminopropyl Biguanide at 0.0005%, both contained in the top two solutions. Polyaminopropyl Biguanide is a preservative used for its antimicrobial properties, while Chlorhexidine is a more commonly used antiseptic, often applied topically to patients before surgery [6]. For P. aeruginosa, Menicare was the solution that was able to kill all bacterial colonies at the lowest concentration of 9.375%. Simplus and Advance both averaged 11.25%, Lobob and OptiFree averaged 18.75%, and bacteria grew at 45% saline for all trials. Menicare contained the preservatives Benzyl Alcohol at 0.3% and Disodium Edetate at 0.5%. All solutions eliminated all bacteria at much higher concentrations than against MRSA.

Discussion It was predicted that Benzyl Alcohol’s bacteriostatic characteristic [7] would stop bacterial growth, during which the Disodium Edetate would kill all the bacteria while it was unable to multiply. Disodium Edetate and Benzyl Alcohol were not potent enough against MRSA, but were comparatively much more effective against P. aeruginosa. This may have been due to the extra cell wall that Gram-Negative organisms possess, and the effectiveness of a bacteriostatic agent and an antimicrobial agent working in combination against hardier bacteria. The extra cell wall may also have been the reason Simplus and Advance’s Chlorhexidine and Polyaminopropyl Biguanide were ineffective against Pseudomonas. The addition of a bacteriostatic preservative along with an antimicrobial preservative (as in Menicare) may have been more effective against a pathogen like Pseudomonas with a hardier cell wall, as opposed to two antimicrobial preservatives (as in Simplus and Advance). In conclusion, contact lens wearers who use the information from this research can decrease the chance of contracting an infection from MRSA or Pseudomonas. Possible future additions to this project include testing the popular “soft” contact lens solutions, or testing the five solutions against Acanthamoeba—another concern in the contact lens user community, as it is an amoeboid pathogen that causes infections difficult to diagnose and treat—and multiple other species of bacteria such as Streptococci for an even more thorough analysis of the solutions and their preservatives. Expansions on the information gained from this project could include testing numerous preservatives and combinations of preservatives in order to find which are the most effective against a wider range of pathogens, opening the gateway for specialized contact lens solutions designed for use in areas with a high chance of infection by certain bacteria.

REFERENCES 1. “Why We’re Stuck on Pseudomonas”. http://www.revoptom. com/content/d/research_review/i/2191/c/37831/ (2012). 2. “MRSA and the Workplace”. mrsa/ (2013). 3. Todar, K. “Pseudomonas”. pseudomonas.html (2012). 4. Windsor, GL. “Pseudomonas aeruginosa”. http://www. (2011). 5. Hill, M. “UNSW Cell Biology: Methods—Enzyme-linked immunosorbent assay (ELISA).” 6. Bennett, E.S., Veissman, B.A. Clinical Contact Lens Practice, (Lippincott Williams & Wilkins, 2005). 7. Doughty, M., Field, A. “EDTA.” pharmacy/edta.htm.

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Microbiota in the Body By Stephanie Hu It is difficult to imagine that the average human body is made up of a trillion or so cells, and yet the number of microbes in the body still outnumbers that by at least a factor of ten [1]. These minute organisms exist largely in areas that are open to the environment, such as the skin surface, oral cavity, and upper respiratory tract, where they generally live commensally in the human body [2]. More recently, there has also been a rising interest in the gastrointestinal (GI) tract microbiome and their influence on different aspects of the human physiology, including metabolism, immunity, and nervous system function. For many years it has been well known that intestinal microbes contribute significantly to metabolic processes in the human body. Many bacteria in the gut help synthesize vitamins like vitamin K and various vitamin B compounds, such as folate and biotin [5]. In the colon, the major metabolic function of microbes is the fermentation of nondigestible carbohydrates, such as pectins, cellulose, and some undigested oligosaccharides. This results in the production of short-chain fatty acids, namely acetate, proprionate, and butyrate, which have been shown to influence the stimulation of colonic epithelial cell proliferation and differentiation [5]. Another important role of gut microflora is in the maturation of the immune system in the GI tract. Their colonization affects the composition of the gutassociated lymphoid tissue, whose development is heavily dependent on exposure to microorganisms [3, 5]. Bacteria in the intestinal mucosa are able to “teach� immune cells to recognize antigens present on bacterial cell surfaces that do not exist in higher-level human cells, which in turn helps the immune system to generate a faster response to pathogen invasion of the body [5]. In the absence of microflora in the intestines, there is reduced expression of Toll-like receptors, which are present on the cells of the innate immune system and recognize certain pathogenic molecules [6]. Furthermore, it has been suggested that resident bacteria in the gut help prevent the colonization of external microbes by competing for available nutrients 14 | JOURNYS | SPRING 2016

and preventing the attachment of pathogens to epithelial cells along the tract; this is known as the barrier effect, or colonization resistance [5]. This helps reduce the number of pathogenic microorganisms that are allowed to settle inside the human digestive tract. However, what may be the most interesting effect of the gut microbiome is its relationship to the human nervous system. While it might not seem obvious at first, recent research has elucidated evidence that point to intestinal microbiota regulation of both brain and nerve function [3]. Interestingly, stress has been linked to a change in the composition of the gut microbiome of an individual by promoting the growth of diseasecausing microorganisms like Escherichia coli O157:H7 [3]. This is caused by increases in both the release of epinephrine and norepinephrine in the host and in the permeability of the gut, which allows bacteria to cross into the mucosa [3, 6]. These bacteria can then induce an immune response that leads to the activation of the hypothalamic-pituitary-adrenal (HPA) axis. On the other hand, one study showed that a hyper-response of the HPA axis in germ-free mice subjected to restraint stress could be reversed by mono-association with Bifidobacterium infantis, a major bacterial species in the infant GI tract [7]. This demonstrates that the human microflora play an influential role in monitoring the development of the HPA. Although the exact mechanisms in which intestinal bacteria are able to communicate with the brain have yet to be elucidated, there has been research that implicates neurotransmitters and short-chain fatty acids as two possible pathways [3]. Many microorganisms produce neuroactive molecules like gamma-aminobutyric acid, serotonin, and acetylcholine. Although these chemicals are formally involved in intermicrobe signaling, they have now also become involved in communication between bacteria and host [3]. Previously it was mentioned that short-chain fatty acids can influence the development of the lining of the large intestine; those same fatty acids can regulate mood and other activities in the brain. For example, injection of butyrate into the brain resulted in antidepressant-like effects by increasing the levels of

brain-derived neurotrophic factors in the frontal cortex [3]. While it is unclear whether or not butyrate produced in the intestines can exert effects on the brain at the same magnitude as direct injection, it is nevertheless an intriguing speculation. Due to the extensive influence that the gut microbiota has over various bodily functions, researchers in the past couple of years have been trying to find patterns in the microbiomes of healthy individuals versus those who are afflicted with various types of diseases [4]. But each person has his or her own unique gut microbiome profile, and various analyses in more recent years has indicated that there is a significant level of variation in the composition of gut microflora between human beings [4]. This is due to differences in the environments in which each individual is raised. Infants are generally born with sterile guts, but immediately after delivery microbes rapidly begin colonizing the GI tract [4]. After about a year, they begin showing characteristics of their adulthood microbiome profile, which is rarely altered permanently as the individual grows; in other words, while external factors like stress, diet, and disease may momentarily change the intestinal microbe composition, it will eventually revert back to what was established during infancy [3]. Even so, scientists remain curious about the possibility of altering the gut microbiome to treat afflictions like depression and obesity. In order to answer these questions, and much more, further research will have to be conducted to elucidate the mysteries of the human’s “hidden metabolic organ” and its relationship to the rest of the body.

References 1. Costello, E. K. et al. Bacterial Community Variation in Human Body Habitats Across Space and Time. Science 326, 1694–1697 (2013). 2. Tannock, G. W. Normal Microflora: An Introduction to Microbes Inhabiting the Human Body (Chapman & Hall, London, 1995). 3. Forsythe, Paul et al. Mood and gut feelings. Brain Behav. Immun. 24, 9-16 (2010). 4. Guinane, Caitriona M. & Cotter, Paul D. Role of the gut microbiota in health and chronic gastrointestinal disease: understanding a hidden metabolic organ. Therap Adv Gastroenterol. 6, 295–308 (2013). 5. Canny, G. O. & McCormick, B. A. Bacteria in the Intestine, Helpful Residents or Enemies from Within? Infect. Immun. 76, 33603373 (2008). 6. Dinan, Timothy G. & Cryan, John F. Regulation of the stress response by the gut microbiota: Implications for psychoneuroendocrinology. Psychoneuroendocrinology 37, 1369-1378 (2012). 7. Sudo, Nobuyuki. Stress and gut microbiota: Does postnatal microbial colonization programs the hypothalamicpituitary-adrenal system for stress response? Psychosom. Med. 1287, 350–354 (2006).


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Prion Treatment: Steps Towards A Cure Written by Janie Kim

Art by Nick Hand 16 | JOURNYS | SPRING 2016

are deadly infectious agents that were first correctly identified in the 1960s. This headache of the medical world has left rampant death in its wake, yet it is invisible to both the naked eye and the microscope. For many years, there was no cure to the wraithlike prion; however, recently, a team of scientists at the U.S. Geological Survey, the University of Wisconsin, Montana State University and the Universidad de Antioquia has proposed a novel potential cure. This new find, a gold mine for the medical community, involves the unassuming lichen. The prion, or a proteinaceous infectious particle, is an incorrectly folded version of a protein called PrP (a protein also found in uninfected people, whose normal functions are unclear and are still being researched). Unlike diseasecausing bacteria, prions contain no nucleic acid and are therefore unaffected by common bacterial treatments that target the nucleic acid. Prions also have a special way of replicating themselves: their attachment to normal prion proteins causes them to refold themselves into the infectious versions [1]. Although normal prion proteins are naturally broken down by proteases, the pathogenic proteins are resistant due to inaccessible “attachment sites” for the proteases. The expression of the gene responsible for the PrP protein in a healthy human normally results in an accumulation of PrP proteins around nerve cells’ myelin sheaths. However, when infected by prions, the infectious versions of the protein will surround and kill those cells (the mechanics of which are still unclear) [2]. This causes human diseases such as Creutzfeldt-Jakob Disease and Fatal Familial Insomnia, both of which cause symptoms such as dementia, hallucinations, and psychosis. Neuron death by infectious prions causes scrapie in goats and sheep, Bovine Spongiform Encephalopathy in cattle—the cause of several epidemics throughout history—and Chronic Wasting Disease in deer [3]. Prions have been under medical scrutiny for years now because of their resistance to destruction; since prions are only proteins, they are not alive, and are resistant to heat, acidity, alcohol, radiation, and autoclaving methods that normally denature proteins and kill living pathogens [4]. The dense aggregates that prion proteins often form allow them to avoid denaturation in conditions that would destroy regular proteins. Prions also do not “go away” or “die”; they can wait for years upon years, perhaps lying on a rock or a fence, and still be able to infect organisms. They have proved themselves difficult opponents in the medical field, but intense research has been underway to discover a method to combat these hardy pathogens. Such attempts have yielded a potential candidate for a cure: lichen. Lichens are composed of two organisms: a fungus, called the “mycobiont,” and a photosynthetic organism, called the “photobiont.” The 13,500 different species of lichen currently known contain different combinations of mycobionts and photobionts [5]. Researchers from the


aforementioned institutions, Cynthia Rodriguez, James Bennett, and Christopher Johnson, decided to investigate if these unique organisms could interfere with prions. Lichens seemed promising because they create special chemicals called secondary metabolites that serve many purposes in their growth and survival; it defends against microbes and UV light, and provides herbicidal and antibiotic action—the key in this case. Rodriguez, Bennett, and Johnson performed experiments to test lichens and lichen extracts containing these substances for anti-prion activity. The researchers conducted their experiment by preparing extracts containing special molecules from numerous lichen species. Using infected brain samples, they also created a PrP preparation that was then exposed to the lichen extracts. After incubating these mixtures, the researchers found that three of the tested lichen species—Parmelia sulcata, Cladonia rangiferina and Lobaria pulmonaria—were able to cut the PrP levels down twofold. After conducting their first set of experiments, the researchers tried to find the specific lichen substance that was responsible for destroying prions. They discovered that the ability of the lichens and their extracts to cut down PrP levels was due to lichen serine protease (an enzyme that, unlike other types of proteases, can break down proteins at body temperature and at a neutral pH.) [6]. Furthermore, they found that the lichen extracts were able to degrade PrP in infected hamster brain tissue. Interestingly enough, simply incubating a mixture of water, prions, and intact lichen could destroy the prions as well [7]. The research on lichens has also revealed that lichen serine protease functions well at body temperature and neutral pH, unlike the established prion-destroying procedures such as exposure to high temperatures and extreme pH conditions. This evidence suggests that lichen proteases may become a viable method to treat prion diseases in the future. From these discoveries in the unique ability of lichens and progress in uncovering an effective degrader of prion proteins, researchers may be able to develop a reliable cure to prion diseases: hope for the previously hopeless.

References: 1. “BSEinfo.” (2014). 2. Prusiner, Stanley B. Prions. PNAS 95, content/95/23/13363.full (1998). 3. Prusiner, Stanley B. “Prion Diseases and the BSE Crisis.” http://www. 4. “Prions: On the Trail of Killer Proteins.” content/molecules/prions/ (2014). 5. Rodriguez, C., Bennett, J., Johnson, C. Lichens – Unexpected AntiPrion Agents? Prion 6, PMC3338958/ (2012). 6. Frazer, J.“Lichens vs. the Almighty Prion.”http://blogs.scientificamerican. com/artful-amoeba/2011/07/25/lichens-vs-the-almighty-prion/ (2011). 7. Johnson, C., et al. Degradation of the Disease-Associated Prion Protein by a Serine Protease from Lichens. PLOS One. http://www.plosone. org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0019836 (2011).

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RNAi: A New Approach to Medicine by Hana Vogel Art By nick hand For years, scientists have been searching for new and better approaches to treating life-threatening and often terminal diseases such as cancer or AIDS. Traditionally, drugs have been small molecules that interact with cellular receptors or enzymes, but more recently, large biological molecules like monoclonal antibodies have become the best treatment for diseases like arthritis and some cancers. Based on the rapidly growing knowledge of the genetic machinery of disease, a new and promising solution is coming close to clinical application—RNA interference (RNAi) drugs. This method has the potential to facilitate research on the roles of genes in various cellular pathways and to develop new treatments for diseases. What is RNAi and why is its potential so great? RNAi drugs work by inhibiting gene expression, usually by causing the breakdown of specific messenger RNA (mRNA) molecules making specific proteins important in the pathology of a specific disease. The exquisite selectivity of RNAi drugs ensures potent therapeutic action with little risk of the “off target” side effects almost always seen with traditional drugs. However, the big challenge in turning RNAi drugs into practical medicines is “delivering” them into the cells where they can have a therapeutic effect. This is because they are fragile snippets of RNA, which would be digested if they were simply swallowed in pills. Several biotech companies are addressing this challenge, and it is expected that the FDA will approve several breakthrough RNAi drugs within the next five years or so. This simple yet revolutionary process is able to not only aid medicine but also serve as a tool for the investigation of genes. Small interfering RNAs (siRNAs) can be designed to bind to multiple specific sites on particular gene(s), and therefore, if allowed to spread throughout the body, let scientists examine the role of that particular gene(s) in several pathways. For example, this function can prove useful in the treatment of infectious diseases, both bacterial and viral, which are prone to mutation and need quick and lasting treatment. 18 | JOURNYS | SPRING 2016

How was RNAi discovered and how does it work? It started with plant biologists, Dr. Richard A. Jorgensen and Dr. Carolyn Napoli, in their attempt to alter the coloring of petunias with proteins that produce purple pigment. To their surprise, the petals became white. In the process, they had accidentally discovered the phenomenon that is now known as “gene silencing.” Dr. Jorgensen called this phenomenon “co-suppression” because he observed the loss of the RNA for the protein’s genes. Later, Dr. Andrew Fire and Dr. Craig Mello of the Carnegie Institute of Washington received the Nobel Prize for their work on gene silencing in worms. In their experiments, they investigated the effects of the par-1 gene, where they injected a synthesized complementary RNA sequence for the gene, preventing the production of the corresponding protein [1]. Their results caused a storm in the biomedical community because it was evident that gene silencing with RNAi drugs had vast potential as therapeutic agents.

How does gene silencing work? Gene silencing is an intrinsic ability of the cell, although RNAi drugs can artificially induce the effect. Three subtypes of RNA—dsRNA, siRNAs and microRNA—can cause inhibition of genes by preventing the expression of specific mRNA sequences. These subtypes of RNA attach to complementary sequences of RNA and induce its cleavage. Therefore, the expression of that region will be suppressed. Depending on the sequence, the expression of a specific gene will not occur and could potentially change the organism beneficially. Unlike other RNA, dsRNA is double-stranded and can induce the beginning of gene silencing. The introduction of a virus causes the cell to create dsRNA and form the RNA-induced silencing complex (RISC). Once dsRNA is formed, the enzyme Dicer proceeds to cut dsRNA into several fragments which are called siRNAs. Shorter than the original dsRNA, siRNAs possess sequences complementary to specific mRNA sites and contain two overhanging, unpaired segments on the leading strand, which makes it the most efficient agent for RNAi. This unique structure allows siRNAs to potentially silence all genes in the body. “In theory, siren genes silence all complementary genes” [2]. Its efficiency is derived from its compatibility with the RISC. The siRNAs then proceed to bind to proteins specific to RNAi and form a RISC. Scientists have theorized that the presence of ATP incites the activation of the RISC by allowing a strand of the siRNA to be exposed. Once the RISC has finished forming, it binds to the mRNA and the siRNAs suppress the expression of its corresponding sequences. As a result, the mRNA is cleaved and degraded by proteins. As a catalytic event, the degradations continue for several rounds, eventually resulting in a decreased number of target mRNAs and by extension, the protein product. The cleaved mRNA is later degraded by exoribonucleases [2, 3]. While it is possible for microRNA, which composes part of the RISC, to silence genes, they usually do not have matching sequences with the target sites due to their multi-step creation process. In addition, they also usually cause translational inhibition instead of cutting the target site.

What are current challenges and recent progress in drug development? The initial surge in interest in RNAi drugs declined when a major pharmaceutical company, Roche, chose to discontinue its research in 2010 [4]. They had difficulty finding a way to actually incorporate the engineered siRNAs into target cells and were reluctant to further invest in developing a drug with dubious prospects for commercialization. As RNA is a large and fragile molecule, it cannot cross the cell membrane without assistance from some sort of delivery vessel to keep it intact while traveling in the blood. Furthermore, even if the vessels take the siRNAs into the cell, there is no guarantee that the siRNAs will work within in the cell. The cell is sensitive to foreign agents, so if the RNA poses any similarity to pathogens, the cell might reject it [3]. Hopefully this obstacle can be surmounted and a way will be found to deliver RNAi agents to their targets. Recently preliminary clinical research indicates that successful implementation of RNAi drugs in treating humans may become a reality. For example, in July, the biotech company Alnylam reported preliminary “proof of concept” results in patients with TTR-mediated Amyloidosis, a rare genetic disease that is progressively debilitating and fatal. The disease is triggered by the overproduction of an abnormal TTR protein which causes a change in the shape and function of the affected organs. In a small ongoing study, a formulation of an RNAi specific to blocking TTR production was subcutaneously injected—and the TTR levels in the patients dropped dramatically [5]. Hopefully over the coming years, this and other RNAi applications will prove to be extraordinarily effective and safe treatments for serious diseases and make their way into pharmacies around the world.

REFERENCES 1. “RNAi Fact Sheet.” factsheet-rnai.aspx (2012) 2. Alnylam “About RNA” about-rnai/ 3. Agrawal, Neema, Asif Mohmmed, Pawan Malhotra, Raj K. Bhatnagar, Sunik K. Muhkerjee, and Dasaradhi “RNA Interference: Biology, Mechanism, and Applications” articles/PMC309050/. (2003) 4. Landford, Heidi. “Drug Giants Turn Their Backs on RNAi.” http:// (2010) 5. Clayton, Cynthia. “News Release.” (2013)

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“Beam me up Scotty!”

is an iconic phrase associated with the television series “Star Trek.” The “Star Trek” transporter, along with many other gadgets, has been an essential component to science fiction; now, however, some of this technology exists in the real world. Although some of these gadgets like warp engines or transporters are currently out of reach, communicators and handheld computers are prevalent in 2015. Other technologies, such as food replicators and the famous tricorder, are also being developed. There are many reasons why warp drive and teleportation are not yet possible. Warp engines, as described in “Star Trek,” require antimatter, a substance that possesses high volatility when in contact with matter [10]. Currently, the creation of antimatter is extremely inefficient and consumes more energy than it produces. Furthermore, warp engines must also be able to contain the explosions when antimatter and matter are combined. This is achieved with dilithium crystals, whose 20 | JOURNYS | SPRING 2016

magnetic properties can be used to channel matter and antimatter. Although dilithium is a completely fictional element, named after an allotrope of lithium [3], it could actually be replaced by a high-frequency electromagnetic field in real life. In “Star Trek,” the Romulans were also able to use small artificial singularities as an alternate source of energy, though the show does not specify how the energy was harnessed. The energy expended by antimatter and matter reactions must then be used to create a subspace bubble around the ship that can envelop the starship and distort the surrounding spacetime continuum. Channeling the energy occurs in the warp nacelles, which are constructed from verterium cortenide, another fictional material that can create a subspace displacement field around the ship. Teleportation like warp engines will not be possible in the near future because of technological restrictions. Teleportation in “Star Trek” is the dematerializing and rematerializing of an object or life form [8]. Even in the

TV series, it was not possible to transport objects until the early 2270s and 2280s; in fact, teleportation was not perfected until the 24th century. Right before transport, a molecular imaging scanner scans the target to the quantum level and the Heisenberg compensators create a map of the object being disassembled. The object or life form is then broken down into a stream of subatomic particles called a matter stream. The matter stream is stored in a pattern buffer to compensate for Doppler shifts and is transmitted to the destination across a subspace domain. A confinement beam is used to maintain the integrity of the information carried in the matter stream, and when the matter stream reaches its destination, it is reassembled as the object of lifeform. Unfortunately, the science behind this has not yet been researched; indeed, many people have even called teleportation impossible. Although this may be true, unlike the warp engine or transporters, other technology from “Star Trek” has become a reality in our world. Technology from “Star Trek” that exists in our current time period includes communicators and handheld computers. Although they may seem commonplace to us, they still serve an important role in our everyday lives. Communicators like the ones in “Star Trek” range from computer-like displays to small, wearable walkietalkies. The earliest communicators included flip phones, but as time progressed, they evolved into pager-like devices used to communicate and transmit information of the wearer’s location [1]. Phones have also become an integral part of our lives, especially since, over time, they have advanced in function from just communicators to devices that can also transmit information about the user

and provide a source of entertainment and knowledge. Handheld computers in “Star Trek” look like modern tablets and seem even simpler than the ones we have now — the touchscreens we have today are much more advanced and sensitive than the ones from the TV series. Computers from the original series have an interactive voice much like Apple’s Siri and use memory cards similar to floppy discs; in comparison, modern computers are more advanced and can access many types of memory storage from cloud data to microSD cards. Some of the technology from “Star Trek” currently undergoing development includes replicators and tricorders. Replicators from “Star Trek: The Next Generation” simply materialize whatever the user desires as long as the molecular structure is programmed into the computer [6]. In the real world, 3D printers now have the capability to print basic foods like candy and are often used in mechanical industries to produce exact replicas of certain objects. This relatively new technology is still evolving and someday, after many improvement, it may become a true “Star Trek” replicator. The tricorder, an icon of “Star Trek,” has appeared several times since the original series and although its design has changed, it has not altered in function. The basic functions of a tricorder are to sense, analyze, and record data [9]. A medical tricorder is a specialized tricorder because it can assess a patient’s condition without any intrusion into the body. The technology for the tricorder is promising and is certain to be a success when it is released to the public. No longer will the technology of the future remain so as we “boldly go where no man has gone before.”

ART BY ALEXANDER HONG REFERENCES 1. ”Communicator.” Memory Alpha. Web. 24 Nov. 2014. <>. 2. ”Computer.” Memory Alpha. Web. 24 Nov. 2014. <>. 3. ”Dilithium.” Memory Alpha. Web. 24 Nov. 2014. <> 4. ”Guidelines.” Qualcomm Tricorder XPRIZE. <> (2014) 5. Kakaes, Konstantin. “Faster-Than-Light Drive.” <>. (2014) 6. ”Replicator.” Memory Alpha. Web. 24 Nov. 2014. <>. 7. Star Trek. Roddenberry, Eugene. NBC. 1966. Television 8. ”Transporter.” Memory Alpha. Web. 24 Nov. 2014. <>. 9. ”Tricorder.” Memory Alpha. Web. 24 Nov. 2014. <>. 10. ”Warp Drive.” Memory Alpha. Web. 24 Nov. 2014. <>.

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Uncertainty Principle’s Effect Monochromatic Light


by Abdelrhman Saleh

ABSTRACT The experiment was carried out to show how the properties of waves are altered in order to avoid violating the uncertainty principle. A laser beam was passed through a narrow slit of known width and projected on a screen. The image on the screen was then analyzed to determine how the momentum of light had changed. From the results it was concluded that there is a negative correlation between the uncertainty in momentum and the uncertainty in position if their product is comparable to ħ. INTRODUCTION


The laws of classical physics do not apply to measurements on the miniscule scale of atoms. On such a small scale, energy does not vary smoothly, but rather in small discrete quantities. Planck’s constant, h = 6.63 x 10-34 J sec [1], indicates how close together these quantities are [2]. The Heisenberg uncertainty principle is crucial to understanding quantum physics. The principle shows that the more precisely the position of a particle is determined, the less precisely its momentum can be known at that instant, and vice versa [3]. The uncertainty principle arises due to a fundamental property of all quantum systems, not because of an inadequacy in the measuring device. The uncertainty relation is shown as an inequality [4]

An ordinary green laser beam was pointed through a narrow slit in a box. I conducted three experiments, varying the slit width in each one. The slit’s width was 5 x 10-5 m, 5 x 10-5 m and 5 x 10-6 m in experiments one, two, and three, respectively. The length of the box was 0.65 meters. I measured the slit’s width using a micrometer. I attached a ruler to the screen so that when the light hit the screen, the length of the image could be measured. In all the experiments, the same laser source was used with the same wavelength and frequency. I used a clamp to ensure that the light hit the slit from the same position in each experiment. The whole setup was placed inside a closed box to maintain complete darkness for the effect to be observed clearly. The experimental setup is shown in figure 1.

ΔxΔp ≥ ħ


where Δx is the uncertainty of the position of the particle, Δp is the uncertainty in momentum of the particle and ħ is h/2π where ħ is 1.05 x 10-34 J•s. I carried out an experiment to investigate the effect of the uncertainty principle. To do this, I passed a laser beam through a small slit of known width. On the other side of the slit there was a screen and the emergent light beam hit that screen. The uncertainty in momentum was seen on the image shown on the screen.

PURPOSE I conducted the experiment to show how the uncertainty principle affects all experiments and how the properties of waves or particles change in order to agree with the uncertainty relationship. Furthermore, I show why the Uncertainty Principle should be taken into account when doing highly precise experiments and how it can be used to give a lower bound of the electron’s speed in a hydrogen atom. 22 | JOURNYS | SPRING 2016

FIGURE 1. Experimental setup.

RESULTS AND CONCLUSION Since the slit used had a fixed width d, the photons could not travel anywhere except through the width of the slit. Thus it is safe to conclude that Δx=Δd. By using slits of different widths and derivations from equations, the effect of the Uncertainty Principle can be predicted. Due to the fact that light consist of photons it would seem that the uncertainty relation cannot be fulfilled because the image would be expected to appear as one small spot of light where it hit screen. However, since light has wave-like properties [5], we can consider light as a wave and thus the momentum is given by, (2) where, p is the momentum of the photon and λ is the wavelength. Note the difference between p and Δp. The former is a definite momentum, while the latter is the uncertainty in momentum. The size of the slit in experiment 1 was 5 x 10-5 m. Thus, Δx = d = 5 x 10-5 m. (3) Substituting everything in the equation yields Δp ≥ 2.1x10-30


By making the slit narrower, we are reducing the uncertainty in the position Δx, as all photons must pass through this very small slit. As the uncertainty of the position of the photons decreases, it follows from the uncertainty principle that the uncertainty in momentum increases. As a result, the laser beam is scattered on the screen.

It is now obvious from equation 3 that there is an inverse relationship between the uncertainty in momentum and the width of the opening [6]. We can calculate the momentum of the individual photons using (2) since the wavelength of green laser is known to be 600 nm [7]. This yields p = 1.1x10-27 kgm/s


The angle at which the laser beam scatters is called angle θ (fig 2). Due to the small angle approximation, we have sinθ≈ θ (6)

Therefore, θ is

If the image is projected on a screen at distance L, where L is 0.65 m, the width of the spot on the screen can be calculated by, sinθ x L (7) Thus, the width on the screen is θL


2.1 x 10-3 x 0.6 = 1.365 x 10-3m Having mathematically derived the above value, we predicted that the light appearing on the adjacent screen at 0.65 m away will veer at least 1.365 mm to the right and 1.365 mm to the left rather than a single round spot.

... I used three slits with different lengths. The slit in experiment 1 had a width of 5 x 10-5 m, the slit in experiment 2 had a width of 5 x 10-5 m, and the slit in experiment 3 had a width of 5 x 10-6 m. It follows that the uncertainty in momentum in experiment 2 will be increased by a factor of five due to the increase the certainty in position of particles by a factor of five caused by making the slit five times narrower. Thus, a divergence of at least 6.825 mm in each direction was predicted. Moreover, the uncertainty in momentum in experiment 3 will be increased by a factor of ten, due to increasing the certainty in position of particles by a factor of ten. Thus, we predict a divergence of at least 13.65 mm in each direction.

FIGURE 2. Diagram of conducted experiment showing measurements taken.


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FIGURE 3. The laser spot before passing through a slit.

The results of the experiments confirm the equations within the limits of experimental uncertainty. The Uncertainty Principle states a minimum uncertainty, so by calculating uncertainty in momentum we can deduce the least possible divergence of the light rays. The hydrogen atom has a diameter of 10-10 m [6] and a mass of 9.10x10-31 kg [8]. This indicates that the electron must be present somewhere within this diameter. (3) (3a)

A bright single spot appeared on the screen when no slit was used, seen in figure 3. In experiment 1 (fig 4), the length of the brightest spot in the center was 3 mm, and the prediction was that the emerging length of the spot would be at least 2.73 mm. In experiment 2 (fig 5), the length of the spot was 14.5 mm, which is slightly more than the predicted 13.65 mm. In experiment 3 (fig 6), the length of the spot in the center was 28 mm seen. The results are shown in table 1 below. Slit












Table 1

FIGURE 4. Experiment 1 result.

FIGURE 5. Experiment 2 result.

FIGURE 6. Experiment 3 result. 24 | JOURNYS | SPRING 2016

Since, the uncertainty in momentum of a particle is Δp= ΔmΔv, (9) (9a) We may speculate that the oscillation of electrons in atoms is due to their confinement to a small diameter and that the speed of the electron in a hydrogen atom must be at least 1153846 m/s. Theoretically, this principle does not apply only to waves but also to particles treated as waves [9]. Thus, it is predicted that particles, when projected through narrow slit, should show the same divergence as waves.


REFERENCES 1. Boyer, T. H. “Is Planck’s Constant h a “Quantum” Constant?” (2012). 2. Bettin, H. et al. Precision Measurements of the Planck and Avogadro Constants. Annalen Der Physiks. abs/1303.0825 (2013). 3. Heisenberg, W. The Physical Principles of the Quantum Theory. (Dover Publications, Mineola, New York, 1950). 4. Heisenberg, W. The Actual Content of Quantum Theoretical Kinematics and Mechanics. Zeitschrift f¨ur Physik. 43, 172-198 (1927). 5. Rashkovskiy, S. A. Is a Rational Explanation of Wave-particle Duality Possible? Proc SPIE. (2013). 6. Lewin, W. “The Wonderful Quantum World.” https://www. (1999). 7. Wikipedia contributors. “Laser.” Laser (2014). 8. The NIST Reference on Constants, Units, and Uncertainty. 9. Serway, R. A., and Vuille, C. College Physics (Brooks/Cole, Cengage Learning, Pacific Grove, CA, 2012). 10. Caves, C. M. Quantum-mechanical Noise in an Interferometer. Physical Review D. abstract/10.1103/PhysRevD.23.1693 (1981).

Alice in Wonderland Syndrome by Claire Warrenfelt

The sizes of the people and objects around you fluctuate There is no effective treatment for AIWS when it is not wildly; one arm seems to lengthen and dangle through the caused by migraines, and little is being done to research possible floor while the other feels alarmingly short and small. This is a cures. This results from the fact that it is such a rare condition, description of life with Alice in Wonderland Syndrome (AIWS). so it receives minimal attention from both the public eye and AIWS is a neurological condition involving delusions of size the scientific community. But when the cause of the AIWS is distortion, along with other symptoms. It has been closely migraines, preventing the migraines will also inhibit the AIWS associated with migraines and epilepsy, but may often be symptoms. This can include traditional methods of treating confused with psychosis or drug use [1]. Though rare in adults, migraines, such as avoiding dark chocolate and strong cheese it is quite common in childhood and in the first stages of sleep; and keeping a regular sleep pattern [7]. however, most people “grow out of it” during their teens [2]. It has often been said that truth is stranger than fiction. In AIWS is sometimes called Todd’s Syndrome, after the English the case of Alice in Wonderland Syndrome, truth may have psychiatrist Dr. John Todd, who first described the syndrome in influenced the creation of one of the most well-known fictional 1995 [3]. Todd characterized the disorder in great detail, but he universes: Wonderland. But instead of eating something to was especially interested in the fact that his patients had no grow or drinking something to shrink, people who are problem distinguishing hallucinations from reality. He afflicted with AIWS in the real world and his colleagues even speculated that Lewis Carroll, often have no way of controlling the the author of Alice’s Adventures in Wonderland, had perceived size and shape distortions AIWS, which he used as inspiration for his novel. caused by the disorder. Many Indeed, it is well known that Lewis Carroll sufferers are unaware that their suffered from migraines, which are condition even has a name, let alone closely associated with AIWS [4]. that it could be a form of migraine In AIWS, the optical system that they could banish simply itself is entirely normal; it is the by making some lifestyle perception that is altered. AIWS changes. Unfortunately, the affects the senses of vision, touch, same is true of many rare hearing, and body image (including conditions; they should not the size and shape the body parts). be ignored just because Two of the most prominent they are uncommon. symptoms are micropsia (seeing Greater public awareness objects or people as smaller can help people with rare than they actually are) and conditions like AIWS obtain macropsia (seeing them as proper diagnoses, which will larger than they are) [5]. ultimately help them find treatment. One patient, a 20-yearold man with a family REFERENCES history of migraines, 1. Ospedaliera, A., Addolorata, described it this way: G. “The Alice in Wonderland Syndrome.” http://www.ncbi. “Quite suddenly, objects appear small and distant or large and close. (1999). I feel as if I am getting shorter and 2. Eisenhower, L. J. “Alice in smaller and also the size of persons Wonderland Syndrome.” http://sites. ART BY ALEXANDER HONG are not longer than my index finger. I hear the voices of people quite loud wonderland-syndrome/ (2014). 3. “Alice in Wonderland Syndrome.” and close or faint and far. Occasionally, I experience attacks of raredisease/alice-in-wonderland-syndrome (2014). migrainous headache” [6]. Much rarer symptoms include loss of 4. Persch, J. A. “When the World Looks Like a Real-Life Wonderland.” limb control and loss of memory [2]. is actually considered to be a rare form of migraine. real-life-wonderland-f1C9926899 (2010). However, other possible triggers for AIWS include stress, 5. Brumm, K., Walenski, M., Haist, F., Robbins, S. L., Granet, D. B., Love, encephalitis (inflammation of the brain), brain tumors, epilepsy, T. “Functional MRI of a Child with Alice in Wonderland Syndrome During an Episode of Micropsia.” and Epstein-Barr virus infection (which also causes infectious pmc/articles/PMC2928409/ (2010). mononucleosis, or “mono”) [3, 4, 7]. One study found that a 6. Hamed, S. A. “A Migraine Varient with Abdominal Colic and Alice in child with AIWS showed decreased activity in the visual cortices Wonderland Syndrome: A Case Report and Review.” http://www. (brain areas responsible for processing visual information), (2010). but increased activity in parietal lobe cortical regions (which 7. Hemsley, R. “Alice in Wonderland Syndrome.” (2012). integrate information from the various senses) [5]. 25 | JOURNYS | SPRING 2016

more than meets the eye

Sleep is a mysterious and bizarre concept that has puzzled people for centuries. We need sleep to function, but what are our bodies really doing while we sleep? Does our body just replenish energy during the precious time we spend asleep? Within a single night, our bodies transition through four stages and two types of sleep. The four stages occur in cycles and the two types of sleep are NREM (non-rapid eye movement) sleep and REM (rapid eye movement) sleep. As we fall into unconsciousness, our bodies begin the sleep cycle with Stage 1. Stage 1 normally lasts five to ten minutes and is the transition between consciousness and sleep. It is also the stage where some people begin to experience hallucinations, the feeling of falling, or weightlessness. The brain will begin to produce sleep spindles, or rapid, rhythmic brain waves, during Stage 2 [1]. Stage 2 lasts for about 20 minutes, during which body temperature decreases and heart rate begins to slow, followed by delta sleep, or Stage 3. Here, the brain starts to produce deep, slow brain waves called delta waves. As Stage 1 is the transitional period between consciousness and sleep, Stage 3 is the transitional period between light sleep and deep sleep. Up until the end of Stage 3, our bodies are in NREM sleep, but As Stage 3 concludes, the body begins to enter REM sleep [2]. REM sleep, also known as Stage 4, is characterized by the fluttering of eyes under the eyelids, irregular and shallow breathing, and loss of muscle control, and occurs about an hour after a person first falls asleep. The body is still and relaxed except a few occasional twitches, and blood pressure rises. This is also the stage in which dreaming occurs [3]. The structure of sleep follows a pattern alternating between NREM sleep and REM sleep. The body usually goes through Stage 1 once during the night before passing through Stages 2 and 3 and finally entering REM sleep. After about 10 minutes of REM sleep, the body will return to Stage 2 and repeat this cycle throughout the night. The first time your body enters REM sleep, the stage only lasts about ten minutes, but by the end of the night, the last cycle of REM sleep may be up to 60 minutes long. For every cycle of sleep the body experiences, the length of REM sleep increases and length of delta sleep decreases. By morning, there is almost no delta sleep left in the cycle, which takes approximately 90 minutes and occurs four to five times a night. When you awaken naturally, you will have just finished a period of REM sleep [1]. Sleep is vital to human health. When our bodies fall into unconsciousness, they do a lot more than just lie motionless. Although it does not seem like it, the amount of energy consumed by the brain does not decrease when the body enters sleep, primarily because several systems in the brain are active during sleep. The first is a system that flushes waste from the brain. During consciousness, byproducts of neural activity build up, but are cleared away during nightly sleep. Since the brain is enclosed by a set of molecular gateways — the bloodbrain barrier — the system that clears waste in the body does not extend to the brain. During sleep, cerebrospinal fluid (CSF) is pumped through the brain’s tissue and the waste is then flushed back into the circulatory system where it eventually works its way to the liver. As this system, known as the glymphatic system, cleans the brain, brain cells shrink to allow CSF to flow more smoothly through the tissue. The glymphatic system is ten times more active during sleep than during consciousness [4]. The brain also stays active in producing brain waves during each stage of sleep. These different waves are characterized by frequencies corresponding to the nature of the stage they are released in and show the amount of activity in the brain and our level of consciousness.

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art by mai saito by melba nuzen

In Stage 1 and REM sleep, the brain produces theta waves, which are usually measured at 4 to 7.5 cycles per second, or 4 to 7.5 hertz. These waves can also be experienced during deep meditation. Theta state heightens receptivity and can be produced fleetingly as the body wakes or falls asleep. In addition, during REM sleep, the brainstem blocks information from leaving the brain’s motor cortex, causing muscles to be relaxed and unmoving [5]. Throughout Stage 2, sleep spindles occur periodically as rhythmic waves unvarying in form. The sleep spindles are measured between 10 and 14 hertz [6]. In Stage 3, delta waves are produced. Their frequency ranges from 0 hertz to 4 hertz, and they are the lowest set of frequencies a human brain can experience. Certain frequencies of delta waves trigger the release of growth hormone and are essential to the restorative process of sleep [5]. These active portions of the brain during sleep contribute to its remedial nature, meaning that our time sleeping is absolutely critical to our performance; the human body is actively working and cleansing itself while we are unconscious. Dreams are perhaps the least understood stage of unconsciousness. What is their purpose? What do they mean? Although there are no solid facts on the purpose of dreams, there are many theories as to why dreaming occurs. Dr. John Allan Hobson, a psychiatrist and sleep researcher, believes that since we always wake up after a period of REM sleep, dreaming is a way for the brain to “warm up.” In dreams, we anticipate the emotions, sights and sounds we’ll experience upon waking up. In this sense, dreams prepare our bodies to return to consciousness [7]. Another theory comes from Carl Jung, who proposed that dreams are meant to recompense for the parts of our personality that are less developed when we are awake. However, Calvin Hall, who studied 2-week journals from test subjects, has a contradicting theory. Hall states that dreams are continuous with the ideas and behaviors when we are awake [8]. Even still, there are more opinions and arguments over the function of dreaming. Nobel laureate Francis Crick believed dreams were a way for the brain to discard bits and pieces of memories that were deemed irrelevant. Crick theorized that dreams were the accumulation of excess thoughts and ideas that did not make it into the brain’s memory [9], explaining why we hardly ever remember our dreams. At a glance, the mechanics of sleep seem simple: four stages of sleep and dreaming in between. However, looking closer, it is evident that sleep is intricately complex and entails much more than meets the eye. The time that we spend asleep is not just our body lying around doing nothing — our bodies use the same amount of energy during sleep as during consciousness, and the process of sleeping is just as complicated as being awake. Even today, experts are discovering more and more about previously unknown aspects of sleep and dreams.

REFERENCES 1. Russo, M. "Sleep: Understanding the Basics Causes, Symptoms, Treatment - Stages of Sleep." the_basics/page3_em.htm. 2. "What Happens When You Sleep?" 3. Dement, W., and Kleitman, N. "Cyclic Variations In EEG During Sleep And Their Relation To Eye Movements, Body Motility, And Dreaming." http:// (2003). 4. Iliff, J. et al. "A Paravascular Pathway Facilitates CSF Flow Through the Brain Parenchyma and the Clearance of Interstitial Solutes, Including Amyloid β." (2012). 5. "The Four Brain States." 6. Lüthi, A. "Sleep Spindles: Where They Come From, What They Do." (2013). 7. Hobson, J. A. "REM Sleep And Dreaming: Towards A Theory Of Protoconsciousness." (2009). 8. Domhoff, G. W. "The Purpose of Dreams." 9. Breecher, M. "The Biology of Dreaming: A Controversy That Won't Go to Sleep."

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THE SOUNDS OF A RAINBOW Written by Alexander Diebold Art by Carolyn Chu Everyone has a distinct view on life, but there are some who see things differently. Due to superfluous cross-talking between areas of the brain, people with the condition known as “synesthesia” experience the world in a unique manner, with combinations of senses providing a “tasteful look” on life. From color-auditory correlations to determining the source of pain through color-flooded vision, synesthetes can experience life in ways unimaginable to most. Synesthesia comes from the Greek roots “syn-” meaning together and “-esthesia” meaning sensation. Thus, the word synesthesia literally translates to “sensations coming together.” People with synesthesia, also known as synesthetes, feel activated senses that are completely unrelated to what they are currently experiencing [1]. Synesthetes will typically link together perceptions and physical objects. Any combination of senses is possible with synesthesia; usually two senses are interconnected, with three or more possible, albeit rare [2]. Within synesthesia, there are many subdivisions dependent on specific combinations of senses. Currently there are more than 35 different known subtypes, the most common of which are color-grapheme (associating letters with colors) and color-auditory (associating sounds with colors). The range of variance can differ from seeing colors that look flat to seeing complex patterns in three dimensions. Other synesthetes may taste food and nonfood items in extremely particular ways. Although it is being researched, a definite cause for synesthesia has yet to be discovered. In 2007, psychologist Edward Hubbard conducted research concerning synesthetes and discovered a relationship between functional magnetic resonance imaging (fMRI) signals and a synesthete’s performance on certain perceptual tasks. (Functional MRI signals show blood flow to the areas of the brain that are being used.) Synesthetes who were able to segregate tactile textures at an above-average performance had a correspondingly larger fMRI signal in some visual areas of the brain [3]. This correlation may eventually lead to the discovery of the neural cause of synesthesia. In 2002, Julia Nunn conducted research to determine whether synesthetes had a normal amount of crosstalking between areas of the brain or simply lacked the ability to separate the senses. Nunn found that spoken 28 | JOURNYS | SPRING 2016

words would lead to activation of the color-vision region in the brain, thus establishing that synesthetes actually have an abnormally large amount of cross-talking. Nunn’s additional research saw that non-synesthetes trying to imagine colors or simple word association would not produce the same results [3]. The case rate of synesthesia is thought to be somewhere between 1 in 5,000 people to 1 in 100,000. Case reports have been increasing recently, although it is uncertain whether this is because of an actual increase in the number of synesthetes versus an increase in self-reports generated by greater public awareness and scientific interest. People who are true synesthetes have had synesthesia from a very young age. Because synesthesia is not easily recognized, it is hard for physicians to describe the average synesthete. They can only make estimates about traits of those with synesthesia from the data they have [1]. Synesthesia is more common in women than men. In the United States, the ratio of female to male synesthetes is 3:1, while in the UK the ratio is 8:1. Synesthetes are also more inclined to be left-handed, neurologically normal, and have a family history of synesthesia. This could be explained if synesthesia is found to be a dominant X-linked genetic trait; that would also explain the greater number of female-to-male synesthetes [2]. The two characteristics that define synesthesia are: (1) the perceived sensation that is an involuntary response to an outer stimulus and (2) an irrepressible and very constant reaction to stimuli. The effect of synesthesia is not simply a recollection of a memory in response to something, as it is with normal people. If a normal person was to smell pie, he would imagine a picture of a pie because that is the object that he has associated with the smell. A synesthete’s mental picture, however, would not look like a pie but instead would look like an unrelated texture and color. This is not simply a memory response though—synesthetes will perceive colors and textures for new experiences as well [1]. Physicians look for the following symptoms when diagnosing someone with synesthesia: “irregular sensory experiences, consistent reactionary triggers, involuntary and automatic perception, [and] simple and objective sensations” [4]. Synesthesia is not a result of hallucinogenic drugs such as LSD or MDMA, although

these drugs can induce synesthetic experiences for a brief period of time [1]. Synesthesia is not characterized as a disease, but rather, a disorder. There are no treatments to “cure” synesthesia. Synesthesia typically confers some benefits such as performing better on certain tests of memory and intelligence. Synesthetes as a group are not mentally ill; they test negative on scales that check for schizophrenia, psychosis, delusions, and other disorders [1]. Many famous artists are synesthetes and express their synesthesia in their artwork. Vasily Kandinsky is a famous synesthetic painter, Olivier Messiaen and Frank Liszt are synesthetic composers of the nineteenth and twentieth centuries, and Charles Baudelaire and Arthur Rimbaud are famous poets with synesthesia who lived in the nineteenth century [2]. Carol Steen is a modern-day example of a synesthete. Carol first learned she had synesthesia from a psychology colleague at the University of Michigan where she was an art teacher [3]. Her symptoms of synesthesia included discerning colors in letters, numbers, and sounds, interpreting colors and numbers through acupressure and acupuncture, and color flooding vision when feeling pain. Carol is able to incorporate many of these perceptions into her art [5]. Carol has a rarer form of synesthesia that allows her to see colors with acupressure and acupuncture. When she is sick, she can only perceive black; when she is feeling well, she will see colors when she is poked in certain areas. Carol describes her condition, thusly, “I also see the color in layers. Like if the needle goes in to a particular depth, it’s not the same color all the way down” [5]. When she experiences pain, Carol uses the color flooding in her vision to diagnose the source of the pain. As an example, when she had tooth pain, Carol was able to discern which tooth needed a root canal by using the color flooding method. Her dentist then verified that she was right [5]. There have been research attempts made to determine whether a person could be taught through training to perceive things the way a synesthete does. Olympia Colizoli at the University of Amsterdam gave seven volunteers a novel with certain letters consistently colored a specific way throughout the novel. After having the volunteers read the novel, she then proceeded to administer a synesthesia test. The test subjects scored higher on the synesthesia test than “normal” people, showing that there is some possibility of training a person to combine senses like a synesthete [7]. Other research concerning synesthesia includes a test done by Daniel McCarthy at the University of Nevada. Professor McCarthy gave three synethetes a math test in which some of the numbers were replaced with just a color. “Each volunteer was shown equations such as 4 + white = 5 and asked whether it was true or false. All

three answered just as quickly and accurately to equations where colors replaced numbers as when numbers were used” [8]. This demonstrates that numbers do not only correlate to colors, but vice versa as well. There is also scientific proof that synesthetes actually perceive the world in abnormal ways and are not simply “making things up”. Functional MRI scanning of their brains shows an activation of V2/V4 visual cortexes when color-sound synesthetes are presented with auditory stimuli. Color-grapheme synesthetes are able to replace letters in words with color and read it as normal, and there is also the “test of genuineness itself”—believing that people are telling the truth when speaking of experiencing synesthetic moments [1]. Synesthesia does not get in the way of living everyday life. Just as normal people grow up with their five senses and are accustomed to experiencing the world through them, synesthetes grow up perceiving the world with the combination of senses they have. The way their senses are combined to perceive things is “normal” for them. Having synesthesia, though, can be irritating, such as, when: “…a stimulus produces an adversive synesthetic experience. Some words may taste like cigarette smoke or sour milk … synesthete[s] may dislike some letters because they have ugly colors … it is disturbing to find people whose names produce colors incongruent with their personalities; for example, a boring person whose name has a vibrant, exciting hue” [1]. Synesthesia is a unique disorder that gives a person an extraordinary look on life. While it may be easy to recognize synesthesia because of its specific symptoms, many people do not realize what they have because of a lack of knowledge about the disorder. Synthesia comes in many different combinations and it affects synesthetes’ lives every day, and yet they are still able to live perfectly normal and functional lives. And while some people with synthesia are not able to comprehend this phenomenon, it is very real and allows them to experience life in truly distinctive, remarkable ways. References 1. Gross, Veronica. “The Synesthesia Project | Frequently Asked Questions about Synesthesia.” (2013). 2. Phillips, M. L. “Neuroscience for Kids: SYNESTHESIA.” http://faculty. (2013). 3. Cytowic, R. E. & Eagleman, D. M. Wednesday Is Indigo Blue: Discovering The Brain of Synesthesia (MIT Press, Cambridge, MA, 2009). 4. Synesthesia Test. “Symptoms of Synesthesia.” http://www. (2013). 5. Synesthesia and the Synesthetic Experience. “Synesthete Perspectives – Carol.” (2013). 6. Synesthesia and the Synesthetic Experience. “Synesthete Perspectives –Karen.” (2013). 7. Geddes, L. “Self-taught synaesthesia.” New Scientist 207:2769, 1 (2010). 8. Reardon, S. “5 + yellow = 7. True or false?” New Scientist 218:2914, 19 (2013).w

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Art by Haiwa Wu

Science of Sensory Deprivation by Jessica Gang

At any given moment, the brain processes information at a rate of 13 milliseconds. The average number of thoughts that humans are believed to experience each day is approximately 70,000 [1]. The brain is the most important organ that we as humans possess and is essentially the “crown jewel” of the human body. As the center of the nervous system, the brain’s job is to process information it receives from every other organ it connects to. After absorbing that information, the brain creates visual and audio recognition signals able to recognize objects seen before and catalogue new 30 | JOURNYS | SPRING 2016

and unfamiliar ones. The brain is a complex machine, one capable of translating an astronomical amount of sensory information it receives from nerve endings in the body into a singularly vivid world. The process of completely isolating the body from all forms of sensory communication is known as “sensory deprivation.” Sensory deprivation is touted as a way to block as much sensation from the brain as possible, allowing the brain to relax, recharge, and perhaps even function on a higher level than previously thought capable.

The idea of ridding the body of as much external stimuli as possible was first pioneered by neuroscientist John C. Lilly in 1954 [2]. Lilly was a leader in the field of electrical brain stimulation, and was known for his personal eccentrics. The first person to map out pain and pleasure pathways in the brain, Lilly also conducted extensive experimentation with mind-altering drugs such as LSD and spent a considerable amount of time in the isolation tank that he in large part invented. It does bear mentioning, however, that Lilly’s experiences with illusion-causing hallucinogens often overlapped with his episodes in the isolation tank [3], contaminating the results significantly. The most easily accessible approach to achieve sensory deprivation is through the isolation tank. Isolation tanks have become increasingly popular throughout the years as a method to relieve stress and achieve a state of relaxation. In the original isolation tank, the subject was suspended in up to 160 gallons of water with everything submerged except for the top of his head, and a “blackout mask” similar to the equipment used at insane asylums was required to block out light and supply the subject with air. As technology advanced, the black-out masks were done away with and the isolation tank began to evolve into a more modern model. The present-day isolation tank contains water saturated with 800 pounds of Epsom salt, rendering the water dense enough for participants to float near its surface or at a shallow depth [4]. Inside the isolation tank there is no light, no sound, no gravity—nothing but the type of quiet that allows you to count your heartbeats and hear your muscles contract. The experience of the isolation tank has been compared to the sensation of a drug-induced high. The buoyancy of the water and the inability to distinguish temperature while inside the tank combine to give the illusion of a zero gravity environment, one where it is nearly impossible to discern where your body ends and the water begins. On the popular television show Fringe, the isolation tank served as a bridge between two alternate realities, and Lilly believed he had experienced the same effect. Lilly’s experiences, however, are in the vast minority, and many report having experienced the sensations of heightened levels of introspection and hallucinations. Controversy has arisen over the decision of several national governments to adopt and enforce violent sensory deprivation techniques a part of their advanced interrogation program, especially after the European Court of Human Rights ruled that the use of the five sensory deprivation techniques of wall standing, hooding, subject to noise, deprivation of sleep, and deprivation of food and drink used by British security forces in Northern Ireland amounted to inhumane and degrading treatment [5]. One of the most notorious

cases of sensory deprivation being used as an instrument of interrogation is the case of José Padilla, who was convicted of aiding terrorists in 2007 and sentenced to 17 years and 4 months in prison [6]. After reports that Padilla was being tortured for information using several of those five sensory deprivation techniques, his consul argued that Padilla had been rendered mentally unstable by the interrogation period. Contradicting these examples of negativity, however, are more optimistic reports from the general public, who report that they experience heightened feelings of relaxation while floating in isolation tanks as part of the growing push to make isolation more accessible in everyday situations. The contrast between Padilla’s situation and the one experienced by average citizens worldwide highlights the thin line between therapeutic sensory deprivation conducted in a relaxed, controlled environment, and sensory deprivation used as cruel and unusual punishment. The practice of sensory deprivation in itself is for the most part a new and largely undiscovered field of science, but has the capacity to greatly advance neuroscience as whole. By advancing their knowledge of sensory deprivation and how it affects the mind, researchers can contribute and apply their knowledge of the brain to a wide variety of current neurological and psychological issues.

REFERENCES 1. Nursing Assistant Central. “100 Fascinating Facts You Never Knew About the Human Brain.” http://w w blog/2008/100-fascinating-facts-you-never-knewabout-the-human-brain/ (2008) 2. Gonzalez, R.T “Everything You Ever Wanted To Know About Sensory Deprivation Chambers” http:// (2012) 3. Ireland v. the United Kingdom. Paragraph 167. European Court of Human Rights. 1978. 4. Rosenthal, A. “Tortured Logic” http://takingnote. r=0 (2012)

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Walking Corpses by Claire Warrenfelt ART BY ALICE JIN In today’s world, there is an entire class of people who believe themselves to be dead, despite their beating hearts and breathing lungs. These are people whose organs function perfectly, yet they are dead in their own minds. Cotard’s Syndrome, also known as Cotard’s Delusion or Walking Corpse Syndrome, triggers this phenomenon. The syndrome is a rare mental disorder in which sufferers believe themselves to be dead and decaying, or to have lost blood and internal organs. In extreme cases, the patient may believe that they are immortal [1]. The name “Cotard’s Syndrome” is coined after Jules Cotard, a French neurologist who first diagnosed this condition. At a Paris lecture in 1880, he called it “Negation Delirium.” Cotard noted that the disorder was characterized by perceptions of missing or dead body parts, or “delusions of negation” [1]. Cotard explained that a mild state of the disorder was characterized by despair and self-hatred, while a severe state involved intense delusions of negation and chronic depression. In one of his lectures on the neurological disease, Cotard exemplified a patient known only as Mademoiselle 32 | JOURNYS | SPRING 2016

X. Mademoiselle X believed that several parts of her body were missing and that she no longer needed to eat. As the disorder progressed, she gradually became convinced that she was “eternally damned,” and that she could no longer die. She eventually starved herself to death [2]. Cotard’s Syndrome still exists today. In a 1990 case of the disorder, the patient suffered a brain injury after a severe motorcycle accident. When the patient left the hospital, his mother took him to South Africa, where he became convinced that he had died from AIDS or from a yellow fever injection, and that he had “borrowed [his] mother’s spirit to show [him] round hell” [2]. Another modern case was delineated in a 2005 study of a 14-year old child with epilepsy, a disorder in which people suffer from continuous seizures triggered by sudden increases of electrical activity in the brain [6]. This child in particular was characterized by extreme cynicism, an unhealthy obsession with death, and social withdrawal. He often experienced episodes of negation delusions, each of which lasted anywhere between three weeks to three months. During these episodes the child would describe himself as a dead body and obsess over a nihilistic belief that the world was soon coming to its end. He showed no interest in social activities and demonstrated no reaction to “pleasurable stimuli” such as play or food [2]. Three distinct stages of Cotard’s Delusion are seen in all diagnosed patients. In the first stage, germination, patients exhibit psychotic depression and become hypochondriacal. Psychotic depression is an episode of severe depression accompanied by delusions or hallucinations [4]. Hypochondriasis, more commonly referred to as “health anxiety”, is excessive concern with contracting a certain illness, even without any evidence to suggest a medical condition [3]. In the second stage, blooming, sufferers fully develop delusions of negation. In the third stage, chronic, patients experience severe

delusions and chronic depression. People with Cotard’s Syndrome often become withdrawn from their family and friends and tend to neglect their hygiene. The disorder makes it impossible for them to make sense of the world. Thus, it makes sense that Cotard’s Syndrome is most commonly found in patients also suffering from schizophrenia, a disorder in which people perceive voices in their head or believe others are trying to harm or control them [5]. Cotard’s Syndrome causes delusions similar to those found in schizophrenics [2]. From a neurological standpoint, Cotard’s Syndrome is thought to be related to Capgras Delusion, a disorder in which the patient believes that a friend, spouse, parent, or any person close to them has been replaced by an impostor who is identical to the real person in every way. Capgras Delusion is believed to be caused by a disconnect between the fusiform areas (areas located near the brainstem that recognize faces) of the brain and the amygdala (an area, located closer to the center of the brain, that controls emotion). The connection between these two areas of the brain can be severed by events like brain injuries and seizures. According to this theory, a recognized person evokes no emotional response in the viewer’s brain, and is therefore interpreted as an impostor [7]. It is widely believed that Cotard’s Syndrome is caused by the same disconnect, but a person afflicted with Cotard’s can’t recognize their own face. If the patient sees his own face and feels no association between that face and his sense of self, they may interpret this as an indication that they no longer exist or have died [10]. In more recent studies, Cotard’s Syndrome has also been shown to be the result of abnormal reactions to the drug Valacyclovir. Valacyclovir is most often used to treat herpes simplex virus infections, varicella zoster (chickenpox), and herpes zoster (shingles). Less than 1% of the people who take Valacyclovir experience abnormal reactions. The adverse reactions are associated with high concentrations of a main ingredient of Valacyclovir, experience abnormal reactions. The adverse reactions are

“During these episodes the child would describe himself as a dead body and obsess over a nihilistic belief that the world was soon coming to its end.”

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associated with high concentrations of a main ingredient of Valacyclovir, 9-Carboxymethoxymethylguanine (CMMG). Thankfully, in most cases of Cotard’s Syndrome that stem from abnormal drug reactions, the effects are temporary; dose reduction and haemodialysis cure the delusions of negation within a few hours [11]. Fortunately, there are several possible forms of successful treatment for Cotard’s Syndrome. Antidepressants, antipsychotics, and mood stabilizers have proven effective. Many sufferers and their families have reported positive results from a combination of p h a r m a c o t h e r a p y, the treatment of a disease with drugs, with Electroconvulsive Therapy (ECT). Electroconvulsive Therapy, formerly called electroshock therapy, is a treatment that uses electrically

induced seizures to provide a patient relief from a psychiatric illnesses. This may seem inhumane, but in western countries is always administered when the patient is under anesthetic and with a muscle relaxant [8]. Cotard’s Syndrome is a formidable neurological disorder that leaves its victims confused and depressed. Though there are many theories and promising studies regarding its cause, it is still a largely misunderstood disease. The lack of public knowledge about Cotard’s Syndrome and other rare neurological diseases, like Capgras Delusion, can cause sufferers to feel confused and alone in their fight against the disorder. Fortunately, there has been success in treating Cotard’s. These treatments might spell the end of the nightmare that is the Walking Corpse Syndrome [9].

REFERENCES 1. “What is Cotard’s Syndrome?” what-is-cotards-syndrome.htm (2013) 2. Soniak M. “Plight of the Living Dead: 10 Case Reports of Cotard’s Syndrome.” http://mentalfloss. com/article/50197/plight-living-dead-10-case-reports-cotard’s-syndrome (2013) 3. “Hypochondriasis.” (2013) 4. Vorvick L. J. “Major Depression with Psychotic Features.” ency/article/000933.htm (2012) 5. “What is Schizophrenia?” (2012) 6. Nordqvist C. “What is Epilepsy?” (2013) 7. Abumrad J., Krulwich R. “Seeing Imposters: When Loved Ones Suddenly Aren’t” http://www.npr. org/templates/story/story.php?storyId=124745692 (2010) 8. “Electroconvulsive Therapy (ECT).” MY00129 (2012) 9. Thomson H. “Back From the Dead: Reversing Walking Corpse Syndrome.” http://www.newscientist. com/article/mg22029392.600-back-from-the-dead-reversing-walking-corpse-syndrome.html#. UotevGR4bVS (2013) 10. “Capgras and Cotard’s Syndromes.” Capgras%2527+and+Cotard%2527s+Syndrome (2001) 11. Hellden A., et al. “Death Delusion.”

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STAFF POSITIONS EDITORS IN CHIEF Alice Qu, Carolyn Chu ASSISTANT EDITORS IN CHIEF Stephanie Hu, Jessica Gang SECTION EDITORS MinJean Cho, Stephanie Hu, Jessica Gang, Mihika Nadig MEDIA MANAGER Maggie Fang GRAPHICS MANAGER Kristina Rhim GRAPHIC ARTISTS Nick Hand, Connie Chen, Alice Jin, Jenny Li, Alexander Hong, Teresa Chen, Mai Saito, Carolyn Chu, Haiwa Wu DESIGN EDITOR Alice Qu DESIGNERS Dimei Wu, Alexander Hong COPY EDITOR Tasia Mochernak CONTRIBUTING AUTHORS Emily Stuart, Jack Hu, An Nguyen, Nathan Lian, Mihika Nadig, Janie Kim, Stephanie Hu, Hana Vogel, Soo Jung Lee, Sung Bin Roh, Abdelrhman Saleh, Claire Warrenfelt, Melba Nuzen, Alexander Diebold, Jessica Gang STAFF ADVISOR Mr. Brinn Belyea

PRESIDENT Chris Lu VICE PRESIDENTS Abishek Chozhan, Frank Lee, Kalyani Ramadurgam, Caroline Zhang COORDINATORS Erica Hwang, Abishek Chakraborty, Mihika Nadig SCIENTIST REVIEW BOARD COORDINATOR Abhishek Chakraborty SCIENTIST REVIEW BOARD Dr. Aaron Beeler, Dr. Akiva Cohen, Dr. Amiya Sinha-Hikim, Mr. Andrew Corman, Dr. Aneesh Manohar, Dr. Arye Nehorai, Dr. Benjamin Grinstein, Mr. Brooks Park, Dr. Bruno Tota, Mr. Craig Williams, Mr. Dave Ash, Mr. Dave Main, Mr. David Emmerson, Dr. Dhananjay Pal, Dr. Erika Holzbaur, Dr. Gang Chen, Dr. Gautam Narayan Sarkar, Dr. Greg J. Bashaw, Dr. Haim Weizman, Dr. Hari Khatuya, Dr. Indrani Sinha-Hikim, Ms. Janet Davis, Dr. Jelle Atema, Dr. Jim Kadonaga, Dr. Jim Saunders, Dr. Jody Jensen, Dr. John Allen, Dr. John Lindstrom, Professor. Joseph O’Connor, Ms. Julia Van Cleave, Dr. Kathleen Boesze-Battaglia, Dr. Kathleen Matthews, Ms. Kathryn Freeman, Ms. Katie Stapko, Dr. Kelly Jordan-Sciutto, Dr. Kendra Bence, Dr. Larry Sneddon, Ms. Lisa Ann Byrnes, Dr. Maple Fung, Mr. Mark Brubaker, Dr. Michael Plewe, Dr. Michael Sailor, Mr. Michael Santos, Dr. Reiner Fischer-Colbrie, Dr. Ricardo Borges, Dr. Rudolph Kirchmair, Dr. Sagartirtha Sarkar, Ms. Sally Nguyen, Ms. Samantha Greenstein, Dr. Saswati Hazra, Dr. Simpson Joseph, Dr. Sunder Mudaliar, Dr. Sushil Mahata, Ms. Tania Kim, Dr. Tanya Das, Dr. Tapas Chakravarty, Dr. Tapas Nag, Dr. Thomas Tullius, Ms. Tita Martin, Dr. Todd Lamitina, Dr. Toshinori Hoshi, Ms. Tracy McCabe, Dr. Trilochan Sahoo, Ms. Trish Hovey, Professor. Xin Chen, Dr. Yifeng Xiong

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Journal of Youths in Science


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