JOURNYS Issue 4.2

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Journys Journal of Youths in Science


The Science Behind Sleep 4 Phantom Limbs: Plasticity of the Brain 9 Time Travel: Is it Possible? 11 What are the Ten Dimensions? 14 Eat Less, Live Longer? 24


The Journal of Youths in Science (JOURNYS) 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 Westview High School, San Diego CA Del Norte High School, San Diego CA Beverly Hills High School, Beverly Hills CA Alhambra High School, Martinez CA Walnut High School, Walnut CA Blue Valley Northwest, Overland Park KS


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: 7501500 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: 1000-2000 Op-Ed: An op-ed is a persuasive article or a statement of opinion. All oped 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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Journal of Youths in Science Spring 2012 Volume 4, Issue 2 Hope Chen

The Science Behind Sleep

Varun Bhave

The End of ... Everything?

Fabian Boemer

Queueing Theory Apoorva Myavarapu

Phantom Limbs Amy Chen

Time Travel

4 5 7 9 11

William Hang


Kenneth Xu


The Computer Science

Imagining ten Dimensions Madeline Pesec

Assessment of Ethnobotanical Treatments

Front cover photography: Kevin Tong Fack cover photography: Ben Pu


Sarah Bhattacharjee


Frances Hung


Why Yes, I Actually Can Smell Your Fear

Synesthesia A Mind Mystery Negin Behzadian

Uncontrollable Prejudice Emily Sun

Eat Less, Live Longer? Cindy Yang

Cancer and Oncogenes Sarah Lee

22 24 26

Soy Food Intake and Breast Cancer


Rachael Lee


Precocious Puberty M. Solovykh, G. Bradley

A Novel Inhibitor of Metalloprotease


Harshita Nadimpalli


Born This Way

Graphic by Mandy Wang

The Science behind Sleep By: Hope Chen Edited by: Emily Sun The shrill cry of the alarm clock pierces through your wonderful dream. Groggily, you reach out to slam the alarm silent. Then you fall back into a waking sleep, at least until you realize you have school today. With all the tasks for the day in mind, you grudgingly clamber out of bed. Little do you think of the last eight hours or so that you just spent in bed, sleeping. Now, let’s backtrack to last night, when you first started feeling drowsy. This natural sensation is induced by a neurotransmitter associated with the bodily processes that occur during wakefulness. This tiny molecule, adenosine, is built up in the bloodstream when the body is awake and is broken down when the body is asleep. It binds to adenosine receptors, which measure the concentration of adenosine in the body and send signals telling the brain to sleep [1]. The body uses adenosine to keep track of and trigger sleep when necessary, which is why people cannot simply adapt to sleeping less. After a few nights of sleeping less than necessary, people must catch up for the lost sleep and have the excessive adenosine broken down [1]. After climbing under the covers, the average person falls into a light sleep after ten to fifteen minutes. A typical sleep-deprived person falls asleep within five minutes of getting into bed and has a big sleep debt, and therefore should sleep more. If it takes more than twenty minutes to fall asleep, your body is not tired enough, or the adenosine receptors are blocked, usually by caffeine or some other anti-drowsiness substance [2]. Caffeine tends to speed up nerve cell activity and prevent adenosine from delivering fatigue signals so the brain is fooled into thinking the body is not tired when it actually is. These substances act like adenosine and interfere by binding 4

to adenosine receptors [2]. When you finally do fall asleep, you first fall into the first stage of non-rapid eye movement (NREM) sleep. Though it is unknown why, there are two types of sleep, NREM, and rapid eye movement (REM) sleep. NREM is divided into four stages; the first and second stages are considered light sleep while the third and fourth stages are considered deep sleep. During NREM sleep, the muscle activity is minimal but still able to function. In REM sleep, vivid dreams occur, eyes dart back and forth, and muscles are paralyzed. When people sleep, they experience cycles of NREM and REM sleep that last approximately 90-110 minutes each. A typical night would follow the pattern: NREM 1, NREM 2, NREM 3, NREM 4, NREM 3, NREM 2, NREM 1, REM, NREM1, NREM2, and so forth. People generally spend about 50% of their sleeping time in NREM2, 20% in REM, and 30% in the other stages [1]. So how does sleep work? The biological clock, also known as the circadian rhythm, is an internal timekeeper that controls temperature fluctuation and enzyme release and cooperates with adenosine. This rhythm is controlled by the suprachiasmatic nucleus (SCN), a pair of pinheadsized brain structures located above the hypothalamus of the brain, which is just above the point where optic nerves cross. The SCN also regulates the sleep-wake cycle, body temperature, hormone secretion, urine production, and changes in blood pressure [3]. Then REM sleep begins with signals from an area at the base of the brain called pons. These signals travel to a brain region called the thalamus, which relays them to the cerebral cortex, the outer layer of the brain that is responsible for learning, thinking, and organizing information. The pons also emits signals that shut off neurons in the spinal cord, causing temporary paralysis of the limb muscle. When people wake up, light that reaches photoreceptors in the retina creates signals that go from the optic nerve to the SCN. This signal goes to several brain regions, including the pineal glands, which responds to light induced signals by switching off the production of melatonin, a substance that also makes people lethargic. Hence, it is easier to wake up in a room full of sunshine than in a dark room.

Journal of Youths in Science

Although people spend about a third of their lives sleeping, scientists are still unclear of the function of sleep, though many have come up with hypotheses. One such hypothesis is that the restoration and recovery of body systems occurs when sleep takes place. It especially helps the nervous system by allowing the neurons to shut down and repair. If it does not, the neurons become so depleted in energy or so polluted with byproducts of normal activities that they begin to malfunction [1]. A study also found that wound-healing is affected by sleep and that deprivation of sleep hinders the healing process. Another hypothesis states that sleep aids in memory consolidation and brain development, which is why newborns and younger children need more sleep than adults. A study with rats showed that certain nerve-signaling patterns during the day were repeated during deep sleep. This helps encode memories and improve learning, which accentuates the importance of sleep for young children and students. Another test also showed that people deprived of sleep for a few days suffered from concentration difficulties, memory lapses, loss of energy, fatigue, lethargy, and emotional instability [1]. Though the function of sleep is unknown, it is vital. Knowing how sleep works can help people obtain better sleep. The circadian rhythm is actually 25 hours long, which is why the body needs to reset itself every day, and why it is easier to sleep in than wake up early [3]. Thus, it is good to go to bed and wake up at the same times every day. Disrupting the circadian rhythm by having irregular sleep patterns or changing between time zones resets your sleep cycle even more. A study conducted by the University of California, San Diego (UCSD) found that out of more than one million adults, those who lived the longest slept for generally more time than those who didn’t—about six to seven hours a day [1]. Sleeping much more or much less than this optimal amount increases mortality. Another study with rats found that rats kept awake indefinitely developed skin lesions, hyperphagia, loss of body mass, and hypothermia. Young people need much more sleep than elderly people because their brains are still developing, hence why an infant requires about eighteen hours of sleep a day, whereas an average seventy year-old only requires six hours a day [2]. So, although students in high school and college often suffer from sleep deprivation in order to finish homework and study for tests, they should still try as much as possible to sleep a healthy amount every night. Works Cited: 1. National Institute of Health, “Information about Sleep”, http:// (2003). 2. Sleep Disorders Guide, “Sleep Science Basics”, http://www. (2012). 3. American Academy of Sleep Medicine, (2012).

Volume 4, Issue 2. 2012

The End of…Everything? By: Varun Bhave Edited by: Nathan Manohar Reviewed by: Andrew Corman

The term “universe” encompasses, according to the Webster’s New World College Dictionary, “the totality of everything that exists.” [1] It may seem extremely hard to comprehend such a broad term, but the universe – the entire cosmological world, including stars, planets, and galaxies – has been a subject of scientific discourse for centuries. Despite its seemingly endless and timeless nature, the universe clearly had a beginning and will (possibly) have an end. The question of the universe’s ultimate fate has spawned many scientific theories, but the answer is still unclear. Nevertheless, the concept is intriguing – what is the timeframe of the universe? How did it begin? And, eventually, how will it end? Today, the most accepted hypothesis on the origin of the universe is the “Big Bang” Theory, which postulates that around 12-14 billion years ago, the universe began expanding from a highly hot and dense state to the much cooler and spread out version that we view today [2]. The Big Bang Theory has been supported by many independent observations, particularly Edwin Hubble’s 1929 observation that the universe is expanding, with galaxies moving away from each other and drifting apart into previously nonexistent territory. In addition, the theory is supported not only by the observation of galaxies, but also by the universe’s composition. The universe’s abundance of the elements helium, hydrogen, and lithium uphold the idea, since the fusing of protons and neutrons in the early stages of the universe would have created massive quantities of these elements. Finally, the detection of cosmic microwave background (CMB) radiation in 1965 added even greater scientific credibility to the concept, as CMB radiation is the remnant heat radiation from the Big Bang itself [3]. The concept of an expanding universe (corroborated by Hubble and others’ observations), ultimately determines the scientific theories about its fate. At the core of the issue is the shape of the expanding universe itself. The universe’s shape is either a) open, or b) closed. If the universe is closed, then it must be of a spherical nature, with all curved lines over its surface eventually meeting at its poles. An open universe refers to a universe that is negatively curved, and forms a hyperbolic plane, shaped similarly to the saddle on a horse. [4] In that case, how is the universe actually shaped? 5

Recent scientific evidence seems to suggest that the universe is open. In 1998, the observations of distant supernovae by Saul Perlmutter, Brian P. Schmidt, and Adam G. Riess led them to conclude that the universe’s expansion is actually accelerating. The scientists shared the 2011 Nobel Prize in Physics for their discovery [5], which would appear to confirm the open universe concept, since a negatively curved, hyperbolic universe will expand forever [6]. The concept of an open universe has interesting implications. If the universe continues to expand forever, then its most probable fate is heat death, otherwise known as the “Big Freeze.” The theory is as follows: since the universe is continually expanding and cooling, then eventually the universe’s density of matter will be so low that the universe will be essentially frozen, chilled and lifeless at near absolute zero (the lowest temperature possible) [7]. A variation of this theory is the idea of the universe reaching maximum entropy – “waste” heat given off by the usage of energy. Since the matter and energy in the universe is limited, the amount of energy available will continue to decrease as the universe expands, thus eventually leading to heat death, with almost infinitely low energy density and a state of thermal equilibrium [8]. However, the universe may not necessarily expand forever, since eventually the force of gravity, which causes all objects to be attracted to each other, may pull the universe together into a state of singularity. The entire concept (in a closed universe) depends on the density of the universe to start with. If the density of the universe is greater, then the attraction between its particles will be stronger – based on Newton’s Law of Gravity. Therefore, if the density of the universe reaches a critical amount, then the attraction between the particles of the universe will slowly pull it together in an event known as the “Big Crunch.” Although the universe is currently expanding, it is extremely difficult for scientists to predict the density of the universe as a whole, and thus the Big Crunch theory cannot be ruled out – we may be seeing the accelerating expansion of the universe simply because the force of gravity has not yet overcome the energy release of the Big Bang [9]. A variation of this theory is that the universe will contract in a Big Crunch, then re-expand in another Big Bang. In fact, this may repeat itself an infinite amount of times. This cyclic repetition of the universe’s expansion and contraction is known as the “Big Bounce.” [10][11] Despite all these scientific theories, humanity may never know the true fate of the universe. However, we can continue to speculate, hypothesize, and observe in the hope of 6

one day understanding the nature of our biggest home, and its future. In the end, the deciphering of the mysteries surrounding the origin and end of our universe may be humanity’s ultimate goal, for then, as legendary cosmologist Stephen Hawking said, “It would be ultimate triumph of human reason…then we would know the mind of God.” [12]

Graphic by Crystal Li

Works Cited: 1. Webster’s New World College Dictionary. Wiley Publishing, Inc.. 2010. 2. Wollack, Edward J. (10 December 2010). “Cosmology: The Study of the Universe”. Universe 101: Big Bang Theory. NASA. Retrieved 11/20/11. pg. 2 3. Wollack 7 4. Wollack 5-6 5. “Nobel physics prize honours accelerating Universe find”. BBC News. science-environment-15165371. Retrieved 11/20/11 6. Wollack 39 7. Wollack 39-40 8. Hawking, Stephen. “A Brief History of Time.” 10th Anniversary Edition. New York: Bantam, 1996. pgs. 45-47 9. Hawking 48-54 10. ScienceDaily, 15 May 2006. Web. Retrieved 21 Nov. 2011. ( 11. Vaas, R., 2006, “Dark Energy and Life’s Ultimate Future,” in Burdyuzha, V. (ed.) The Future of Life and the Future of our Civilization. Springer: 231–247. pg. 4 12. Hawking, 191

Journal of Youths in Science

Queueing Theory By: Fabian Boemer Edited by: William Hang Reviewed by: Samantha Greenstein Photograghy by Ginelle Wolfe


he average person spends three to five years of his lifetime waiting in lines and queues and spends six months of his lifetime waiting for traffic lights. Considering an average lifespan of roughly 70 years, the average person spends at least 4% of his life waiting [1]. That is over an hour a day spent simply waiting. While people generally adapt to long waits by occupying themselves, the short waits are much more prevalent. Queueing takes the form of waiting in line to purchase groceries, waiting at stop signs and traffic lights, waiting to see a film play in the cinema, waiting for commercials, waiting for movies to stream and web pages to load. The list goes on. People wait to be served at restaurants, wait for someone to answer the phone, and wait for food to be heated in the microwave. As we waste away our lives waiting on an event, some are bound to consider: why am I waiting? Why doesn’t the line go faster? Why do I have to wait longer than others? Volume 4, Issue 2. 2012

The answers to these questions form the basis of queueing theory, the mathematical study of waiting in lines, or queues. Queueing theory, apart from being a hassle to spell, analyzes the processes of a queue, including arriving at the back of the queue, waiting in the queue, and being served when at the front of the queue. The effectiveness of a queueing system is determined by several performance measures, such as average waiting time, length of the line, and availability of a server. Maximizing the efficiency of the system is critical to the applications of queueing theory. Such systems include telecommunications, traffic engineering, computing, and the designs of factories, shops, offices, and hospitals [2]. Before a system can be evaluated, one must first understand the basic principles of queueing theory. The server is defined as an object or person providing a service. Servers include traffic lights, cashiers, or computers. The customers are defined as the individuals seeking a service. These individuals include people, but also computer jobs, and 7

cars. The basic queueing model is characterized by six elements. First is the arrival process of customers. Customers may arrive one at a time or in groups. The distribution of customers is usually a common distribution, often the Poisson distribution, characterized by exponential arrival times. Second is the customer’s behavior. Impatient customers may leave the line, shortening the queue. A third element is the server’s behavior. Service times are usually assumed to be independent of arrival times for mathematical ease. In reality, however, this is not always true; for instance, cashiers in a grocery store, fearful of a growing line, may quicken service.

Notice as traffic intensity approaches zero, the number of customers approaches zero. Conversely, when ρ approaches 1 (this occurs when average arrival rate approaches average service rate), the number of customers approaches infinity. Note, this is bad. Any system with infinite customers, the majority of them waiting, will fail. Finally, the total waiting time (T) is given by the formula:

The fourth factor is service time, or the processing rate of the server. The service discipline varies between systems. Customers may be processed one by one, or in batches. Additionally, there are many possibilities for service order: first come, first serve (common in human service, such as in grocery stores); last come, first serve (as in computer stacks), priorities (as with rush orders), or processor sharing (as in a computer that evenly divides processing power between all jobs). A fifth element is service capacity, the presence of one or multiple servers in a system helping the customers. Finally, the size of the waiting room, where jobs wait before being processed, determines the maximum number of customers in a given system [3]. The understanding of complex queueing models begins with the basic understanding of the simplest model. The simplest queueing system is notated as M/M/1, in which both the arrival and service processes have exponential probability densities, and one server is present. Imagine a store with a single cashier serving customers. Three basic formulas guide the understanding of this system. If we let rho (ρ) equal traffic intensity, or occupancy, lambda (λ) equal average customer arrival rate, and mu (µ) equal average service rate, occupancy can be defined as:

A functioning system will always have a higher average service rate than average customer arrival. Otherwise, queues would rapidly approach infinity. Therefore, occupancy should always be less than one. Next, the mean number of customers (N) in the system can found with the following equation: 8

Again, as average arrival rate (λ) approaches average service rate (µ), total waiting time (T) approaches infinity [2]. Together, these three formulas allow for the basic understanding of the simplest queueing model. Application of these formulas comes in the familiar experience of waiting in lines at amusement park rides. California Screamin’, the prominent roller coaster in Disney’s California Adventure, provides a prime example. The coaster has 7 cars, of which 6 can run simultaneously. Thus, the number of servers is 6, while the population is the number of impatient customers in line. Each coaster can seat up to 24 people. With 5 cars operating (in 96 observed departures, the coaster never operated 6 cars), average departure time was 40.75 seconds. The ride time was 156 seconds, yielding a total service time of 196.75 seconds [4]. Using this information, we calculate an average service rate, µ, of (24 customers per car*5 cars)/(196.75 seconds) = 0.61 customers per second, or 2195 customers per hour, roughly equal to the posted ride capacity of 2200 customers per hour. An average wait time, T, on a reasonably busy day hovJournal of Youths in Science

ers around 25 minutes [5]. Inserting the numbers into the third formula, we solve for average arrival rate, λ. Solving the equation, 25 minutes = 1/(36.67 customers per minute- λ) yields λ = 36.54 customers per minute. Notice the minimal difference between service rate and arrival rate. Using λ and µ, we further calculate traffic intensity, ρ. Solving ρ = 36.54/36.67 = .997, indicating the coaster is operating at nearly full capacity. Finally, we are able to solve for the mean number of customers in line, N. N = .997/(1-.997), so N=296 customers in line. This information is critical to engineers and park management. Expecting up to 300 customers to wait in line, queues must be constructed to allow enough waiting room. Utilizing these hard numbers, Disney’s “Imagineers” are able to plan and adapt queues to accommodate expected customers. Indeed, Disney’s Hollywood studios conducted an experiment testing a new “queue-less” wait system. Rather than waiting in line, guests are split into groups and assigned a group number. Entertaining themselves in an air-conditioned tent, guests are free to enjoy their waits. Once their group number is called, guests are free to board the ride, having escaped the drudgery of waiting in a never-ending line [6]. The application of queueing theory extends beyond planning a roller coaster. The designing of restaurants, traffic lights, grocery stores, and computer jobs all employ queueing theory. Indeed, anytime individuals queue for a service, queueing theory is applicable. While the expanse of entire queueing theory cannot be covered in a short article, resources are available and easily accessible. Deeper understanding of queueing theory will take many hours of research and dedication. Yet, if you use the time you spend waiting to learn, the server of your mind will process the job of understanding with minimal waiting time. Works Cited [1] Ward, J. "How Much Time People Spend Doing Stuff In Their Lifetime.” how-much-time-people-spend-doing-stuff.html (2010). [2] Adan, I. & Resing, J. Queueing Theory. (Eindhoven Univ., Eindhoven, 2001). [3]"Queueing Theory Basics." http://www.eventhelix. com/realtimemantra/congestioncontrol/queueing_theory.htm (2011). [4] Tibben-Lembke, R. S. Maximum Happiness: Amusement Park Rides as Closed Queueing Networks. Management Science 1, summer07/MS-happiness16.pdf (2007). [5] Testa, L. “Disney California Adventure Crowd Levels.” (2002). [6] Caldwell, L. "No lines at Walt Disney World?." http:// iines-at-walt-disneyworld-theme-park-tests-new-queue-less/ (2010). Volume 4, Issue 2. 2012


The doctor tells you to move your left hand, and you do. He tells you to reach for the pen in his hand, and you do. His grip on the pen doesn’t loosen, and you feel a sharp pang of pain shoot up your arm. Suddenly, you realize that your arm was amputated three years ago after a car accident. Then why is it that your arm extends and retracts unexpectedly? Why do you feel jolts of pain in your arm when you touch your cheek? Why do you still feel voluntary movements in your arm, years after its amputation? Approximately 98% of amputees experience a phantom limb, a sensation that an amputated limb is still present and occasionally painful. First observed in 1872, this ghostly sensation has always been a mysterious phenomenon.1 Amputations result in severed nerve endings, called traumatic neuromas, which cause tumors in the nerve tissue. These neuromas continue to send pain signals to the brain even after the limb has been removed, causing the brain to believe that the limb is still there. A study conducted by V. S. Ramachandran and William Hirstein reveals that this mysterious sensation is caused by a cross-wiring of neurons in the somatosensory cortex, the main receptive region for touch in the brain.1 Signals that are received from touch receptors in the skin pass via sensory nerves to the spinal cord. Here, connecting neurons pass the information to the thalamus and the sensory cortex in the brain. This information is highly topographic, meaning that the body is represented at different levels in the nervous system.2 Larger areas of the sensory cortex are devoted to sensations from the most sensitive areas of the body, including the hands and the lips. Less sensitive parts of the body are represented by smaller cortical regions. The somatosensory cortex, located in the parietal lobe, consists of a sensory homunculus: a map of sensory space, often connecting the legs to the arms, the arms to the face, the face to the mouth, and so on. This homunculus is dependent on how much sensory input it receives, so if a 9

movement in their nonexistent limb. The roofless box consisted of two holes in the front and a mirror placed vertically between the holes.3 Patients would place their working hand into one hole, and their phantom limb into the other. As they looked into the mirror, they would move their working hand and see that their nonexistent hand was also moving, relieving them of the pain caused by phantom limbs fixed in painful positions. A recent study by Jonathan Cole and Simon Crowle in the United Kingdom brings another virtual reality (VR) technique to the treatment of phantom limb sensations. Rather than reflecting input from the patient’s opposite, existing limb, this new technique uses motion from the patient’s stump itself and translates it into desired movement of a virtual limb enacted by an avatar in the VR environart by apoorva mylavarapu ment. This portable and inexpensive method was shown to have equally high rates of relieving pain as Ramachandran’s VR mirror box.4 limb is amputated, the brain reorganizes this homunculus to adapt The existence of phantom limbs proves that, conto the missing sensory input. Referring to the side figure1, any sen- trary to previous belief, the brain has the ability to sory input to the face is characterized as input to that missing limb. reorganize neural connections even through adultTherefore, neural connections previously attached to the ampu- hood, and allows neurons to grow into new dentated limb adjust to other parts of the body, and the brain receives dritic connections. This plasticity of the brain is sensory input to this part of the body as input from the phantom what allows us to accomplish the complex feats of applying information from experience, of recoverlimb. As patients begin to recover from experiencing their phantom limb, ing from learning disorders, of even treating brain they normally lose all consciousness of it. However, in 50% of damage. The brain, a three pound mass of neurons cases, the phantom limb grows progressively shorter, until just the that distinguishes humans from all other forms of stump and the hand or foot remains. The explanation behind this life, has yet again proven to be far more complex phenomenon, known as telescoping, is again based on the sensory than anything we could imagine. homunculus. Since the limb is still represented in the homunculus yet does not provide any input, the brain gradually telescopes the phantom limb as it reduces its sensory representation. In some studies, the length of the telescoped phantom limb extended and Works Cited Ramachandran, Vilayanur S., and William Hirstretracted variably. For example, one patient’s phantom limb was 1. ein. “The Perception of Phantom Limbs. The D. O. pushed into his stump at the elbow. When he attempted to grab Hebb Lecture.” Brain 121.9 (1998): 1603-1630. Web. a mug, which was suddenly pulled away from him, his phantom 2. Brain Facts: A Primer on the Brain and Nervouslimb extended unexpectedly, causing him jolts of pain. In their study, Dr. Ramachandran and Dr. Hirstein observed that the phantom limbs of several patients were fixed in awkward, often painful postures (partially flexed at the elbow, twisted behind the head, etc.) Further study of this phenomenon revealed that these positions were often the positions the limbs were in prior to amputation. In several patients, the phantom limb was permanently lodged in painful positions. In another experiment conducted by Dr. Ramachandran, patients used a “virtual-reality box” to regain sensations of voluntary 10

System. Washington, D.C.: Society for Neuroscience, 2008. Print. 3. Ramachandran, Vilayanur S., and Diane RogersRamachandran. “Phantom Limbs and Neural Plasticity.” Archives of Neurology 57 (2000): 317-320. Web.

4. Cole, Jonathan, Simon Crowle, Greg Austwick, and David Henderson Slater. “Exploratory Findings with Virtual Reality for Phantom Limb Pain; from tump Motion to Agency and Analgesia.” Disability & Rehabilitation 31.10 (2009): 846-854. Web. Journal of Youths in Science

a much smaller radius, generating an extremely strong gravitational field that even light cannot escape [5].

Time Travel By: Amy Chen

Edited By: Rekha Narasimhan Reviewed By: Brooks Park Graphic By: Eun jin Kim


ime travel, the concept of moving to and from different periods in time without the individual experiencing the lapse of time [1] has always been widely referenced in pop culture and literature. Movies such as A Time Traveler’s Wife and Butterfly Effect show the main characters’ ability to sporadically travel back or forward in time as well as the consequences that often ensue. Though time travel had previously been a fictitious notion deemed impossible by spectators as well as theologians alike, scientists’ close analysis of Einstein’s relativity theories and the black hole phenomenon has shown that, theoretically, time travel could exist. The first general evidence given regarding the possibility of time travel involves Einstein’s special relativity theory. There are two main principles proposed in the theory. First is the consistency of the speed of light, proven in Maxwell’s equations of electromagnetism, in which constant c represents the speed of light [2]. Second is the principle of relativity, which basically states that in essence, the laws of physics remain constant regardless of the observer [1]. Time travel in a Newtonian universe would be impossible because time and space are presented as absolute matters. However, Einstein’s special relativity proposes that since the value of the speed of light and laws of physics always remain the same, something else must change in order to keep those values constant [3]. This theory leads to the idea that the length and distance of time and motion are not fixed quantities. In contrast to the cosmos previously assumed true in the Newtonian universe, special relativity suggests a lack of simultaneity for observers of different frames of references, or inertial frames, because external time is defined within one’s own frame of reference [1]. In other words, there is no set reference frame for an inertial observer, and the value of space and time are different for every individual, depending on their own personal velocity.

Black holes are created during the end evolutionary cycle of massive stars. There are two general types of black holes: Schwarzschild, or the static and not revolving black holes with impenetrable centers; and Kerr black holes, the ones that rotate in a spiraling motion [6]. The singularities of stationary black holes are so dense and impenetrable that anything sucked in would be crushed and annihilated instantly. However, if an observer were to place himself in the singularity of a Kerr black hole, the unusual disturbance in spacetime would create a region that acts in such non-correspondence with the external time frame that the observer would possibly witness the elapse of long periods of time with little time passing by on his part. This provides another form of theoretical time travel, but restricts participants to traveling into the future [1]. Theoretically, if a fourth dimension tunnel, or “wormhole”, were to link the singularity of two rotating black holes, and remains stable enough for traversing, it would be possible for an observer to travel back in time. If one black hole could be made to move at a velocity that approaches the speed of light whereas the other remains stationary, the spiraling end of the worm hole would be progressing on a relatively slower time frame than the still end. If a traveler were to go through the stationary end and emerge from the rotating end, the individual would arrive at a time a few years prior to when he had entered. Hypothetically speaking, wormholes would serve as a connection between two points in space and time, and exist as a natural time machine. However, even if wormholes could be created naturally, which still remains disputable and highly improbable, they would be extremely unstable and collapse so quickly that no object could be sent through it. Any naturally existing wormhole would require expansion using exotic matter such as negative energy to achieve the minimum stability [1]. The forms of time travel depicted in books and movies where an individual simply steps through a portal or falls into a deep pit is indisputably simple fantasy. Einstein’s theories and the physics of black holes present the idea that time travel would not defy the laws of nature, though the scenarios in which it exists are impossible as of now. Until scientists uncover more secrets of the universe, time travel zealots will have to fulfill their curiosity with reading scientific fiction novels.

One famous example is the twin paradox; the principle suggests that if one twin were to be placed on a spaceship that’s traveling at a velocity approaching the speed of light whereas the other remains relatively stationary on earth, the effects of time dilation would show that the twin traveling at a higher velocity ages slower than the one that remains stationary, since her personal clock (or time) ticks slower as she nears the speed of light [3]. The concept of time dilation, achieved only when an object is traveling at high velocities, creates a miniscule but natural form of time travel in the Works Cited 1: Felder, G. “General Relativity” [4]. beria/NumRel/GenRelativity.html (2003) Another view on time travel concerns Einstein’s general relativity theory. Space is described as a four-dimensional plane, with time being its last dimension; and the measure of space and time is combined to make spacetime [5]. Central to the general relativity theory is the idea of a curved space. Matter in the universe generates such enormous gravitational pull that time slows when it comes within the vicinity of those gravitational fields, creating the said curvature. Time travel, therefore, could occur at regions in the universe where an enormous disturbance in spacetime is present. A black hole forms an area in space that has an even greater density than the sun but Volume 4, Issue 2. 2012

2: Hunter, J. “Time Travel [Internet Encyclopedia of Philosophy].” (2004) 3: Watson, C. “Did You Know…Special Relativity” (2007) 4: Nova Online. “NOVA Online | Time Travel | Think Like Einstein (2).” (2000) 5: University of Illinois. “General Relativity: Einstein: Physics.” http:// html (1995) 6: Anonymous. “Black Holes.” stars_blackhole.


The Computer Science Million-Dollar Problem By: William Hang Edited by: Fabian Boemer

P = NP? Any person that provides a proof to the question above will have elucidated one of the most important problems in computer science that has far-reaching applications and broad impacts across many disciplines of science. As a byproduct of his success, the solver will re-

ceive not only $1,000,000 in cash from the Clay Mathematics Institute, but will also garner the admiration and jealousy of millions of mathematicians, computer scientists, and computer engineers worldwide. The question of whether P = NP is an abbreviation of a more descriptive problem statement: “If the solutions to a problem can be verified in polynomial time, can they themselves be computed in polynomial time?” First proposed by Stephen Cook in his 1971 paper [1], this problem is one of seven highly important and challenging mathematical problems known as Millennium Prize Problems. Only one of them, the Poincare conjecture, has been solved. Let’s start with some of the basics. Most computer problems are classified as “NP.” NP means that solutions to the problem can be verified in an amount of time closely related to the size of the problem. This amount of time needed is represented by O(nk), where n is the problem size and k is some constant, usually determined by external factors, such as choice of algorithm. This time needed is often called “complexity”, and is approximated by an nth order polynomial, hence the name “polynomial time.” For example, let’s recall a very frustrating and indomitable puzzle toy from our childhood: the 15-puzzle [2]. This is a sliding square puzzle with one slot missing, where the 12

objective is to rearrange the squares so that they are correctly numbered. The time needed to find the solution increases exponentially with the amount of squares, which makes this problem intractable with a large amount of squares. However, given a solution consisting of the steps to solve the puzzle, we can verify it by duplicating the steps. This will only take an amount of time linearly related to the number of steps, and can be performed in very little time. This is a prominent example of the N-puzzle problem, or any sliding square problem with N squares. It belongs to a subset of problems within NP called NP-complete, abbreviated as NPC [2]. NPC-problems are defined as “some of the most difficult NP-problems,” and are known for not having any fast algorithm for their solution [3]. Although they are difficult to solve, NPC-problems have important applications in real life. One of these applications includes microprocessor scheduling, where the computer must efficiently route tasks to a number of microprocessors to perform parallel processing. Another of these applications includes finance and capital investments, where the knapsack problem can be applied. The goal of the knapsack problem is to achieve the greatest value while adhering to a weight limit when choosing out of a collection of items [4]. On the other hand, P problems are generally solvable in polynomial time. This makes their complexity predictable and

Journal of Youths in Science

consistent. P-problems can also be solved relatively quickly, depending on the problem and what algorithms are used to solve it. One example of a P-problem is finding the greatest common divisor of two numbers. Now, we go back to the million-dollar problem. The P = NP? problem amounts to whether or not any NP-problem is solvable in polynomial time on a deterministic Turing machine, or a normal computer. These NP-problems also include NP-complete problems such as the N-puzzle problem or the knapsack problem. A solution to P = NP? can spark enormous change and advance in many scientific disciplines from mathematics biology, and may potentially allow all NP-problems to be solved in polynomial time.

Although no solution has been achieved, people are already taking sides. Many computer scientists agree that P ≠ NP due to the fact that over the course of computer science history, there has not been a single known discovery of a polynomial time algorithm for any one of over 3000 known NPcomplete problems [5]. Despite the skepticism, its solution and proof will have drastic positive impacts on computer science, information technology, mathematics, and other disciplines. If it were shown that P = NP, many important problems classified as NPcomplete could have realizable polynomial algorithms for their solutions [6]. This would spur considerable advances in many disciplines. For example, protein folding and protein structure prediction are NP-complete problems, and their efficient solutions would have an enormous positive impact on biology and pharmacology [7]. Mathematics would also be revolutionized, as computers may finally be able to efficiently find proofs for existing unsolved mathematical problems. On the other hand, if it were shown that P ≠ NP, this would definitively show that not all NP-problems can be solved in polynomial time. This would resolve countless quesVolume 4, Issue 2. 2012

tions about the problem, and would cause many researchers to abandon the problem and focus their efforts on other areas, such as finding partial solutions to the most important NP-complete problems. The question of whether or not P = NP continues to confound countless researchers and mathematicians. It has been the subject of many research efforts and proof attempts, none of which have succeeded. However, its solution will generate an immense impact on many disciplines, and will reveal the solutions to thousands of important problems in computer science with many real-life applications.

Graphic by Amber Seong

Citations: 1. Fortnow, M. The Status of the P versus NP Problem. Comms. of the ACM 52, 78-86 (2009). 2. Ratner, D. & Warmuth, M. Finding a Shortest Solution for the N×N Extension of the 15-Puzzle is Intractible. AAAI-86, 168-172 (1986). 3. Dasgupta, S., Papadimitriou, C. & Vazirani, U. Algorithms Ch. 8 (UC Berkeley, Berkeley, 2006). 4. Black, P. E. “Knapsack problem.” HTML/knapsackProblem.html (2010). 5. Gasarch, W. I. The P=?NP Poll. SIGACT News 33, 34-47 (2002). 6. Pavlus, J. “What Does ‘P vs. NP’ Mean for the Rest of Us?” http:// (2010) 7. Berger, B. & Leighton, T. Protein folding in the hydrophobichydrophilic (HP) model is NP-complete. J. Comput. Biol. 5, 27-40 (1998). 13

Brain Twister: Imagining the Ten Dimensions BY: KENNETH XU


magine going to the movies. As soon as you walk in, the smell of popcorn assaults your nose, while the colorful, flashing movie advertisements clamor for your attention. After deliberating for a while, you choose the latest action film. The next decision: will you watch it in 2D or 3D? The former is traditional and relatively boring. The latter confuses and tires your eyes. Without realizing it, you have just distinguished between two dimensions. Everyone knows the first three dimensions: the line, the plane, and our world. However, few know anything beyond this. There are actually ten dimensions, ten ways to visualize time and space. We, three-dimensional beings, can see the lower dimensions, but can only imagine the higher ones. Once you understand all the dimensions, you will never look at the universe, the world, or your life the same way again. First, we must define a dimension. A dimension is the structure of space in a certain position of time. The number of the dimension is the minimum amount of numbers needed to specify a specific point [1]. For example, a point in the 1st dimension, which is a line, can be defined by the number 1. The first three dimensions are critical for understanding the higher ones, since higher dimensions are built on the principles of lower ones. 0th dimension: The point. It has no particular size or direction, so no numbers are needed. It’s just a point.

1st dimension: The line. When you take two 0th dimension points and connect them, a line segment is formed. Only one number is needed to specify a point on this line, so this is the first dimension.

Graphics by: Aisiri Murulidhar

was not folded, the ant would not be able to get to the other side of the paper instantly. Thus, by folding through the 2nd dimension, we have created the 3rd dimension. By definition, the 3rd dimension is what you fold through to jump from one point to another in the 2nd dimension [2].

The two points are in different places in the 2nd dimension


2 Two dimensional plane (horizontal view)

If the plane is folded in the arrow direction, then the two points connect (3rd dimension). An ant at point 1 would be instantly transported to point 2.

As we progress to the higher, more complex dimensions, remember these two processes: connecting and folding. These processes are the basis of imagining the higher dimensions.

2nd dimension: The plane. There is a length and a width, but there is no depth. The two dimensional world is infinitely thin. In order words, it is composed of many 1st dimension lines connected to each other on the same plane. Two numbers are needed to define a point.

4th dimension: A line. This is often known as the space-time dimension. Pretend you are a dot. Imagine yourself ten minutes ago, then look at yourself now. Now draw a hypothetical line from the past self to your present. You have just imagined the 4th dimension. If you were to look at yourself in the 4th dimension, you would look like a snake, with birth at one end and death at the other. As we progress through time, all we can see are the cross sections of this snake. We can only see ourselves at a particular moment. We cannot actually see ourselves in the 4th dimension.

The points are connected by many 1st dimension lines to form a 2nd dimension plane

To us, three-dimensional humans, we travel through time in a seemingly straight line. However, this “line” is actually twisting and turning through space. Our lives, our timelines, are defined by our choices, other’s choices, and pure chance [2].

3rd dimension: A fold. This is the dimension we live in, with length, width, and depth. However, another way to imagine the third dimension is folding. Imagine a two-dimensional piece of paper. Then, imagine we fold one end of the paper to the opposite end, forming a circular cylinder. If an ant were on one end of the paper, he would find himself instantly transported to the other end. However, if the point

One more way to think of this: treat the entirety of three-dimensional space, at a certain state, as a point (remember, a point has no definite size), and draw a line from it to another point, representing three-dimensional space at a different state [2]. If we expand this idea further, the line between the beginning of the universe and the end of the universe is also in the 4th dimension.


Journal of Youths in Science

Brain Twister: Imagining the Ten Dimensions by K. Xu

(Line in 4th dimension)

Beginning of time

Beginning of our Universe

End of time

A possible ending Imagine it as a single point (Actual undulating “Line” in 4th dimension)

All possible timelines of our universe (Starting with some initial condition, ending with the possible

5th dimension: A plane. How you ever wondered about fate? For many, their lives seem like a straight timeline, moving directly from birth to death. But what if you had made different choices in life? What if, by chance, your luck, was different? Suppose you accidentally discovered the world’s biggest diamond in your backyard, and had become rich. Your life would be different. If this new timeline of your life branches out from your old one, the 5th dimension is formed. Imagine all the possible timelines of your life. The plane they form would be in the 5th dimension. The timeline you follow Birth


Also imagine it as a single point All possible timelines of a different universe (Starting with a different initial condition) Connect the two points to form a line in the 7th dimension

Our universe

Another universe

8th dimension: A plane. Imagine all possible universes stemming from different initial conditions as points, and connect them with lines. The plane formed from these 7th dimensional lines would be in the 8th dimension. Possible universes

Lines in the 7th dimension

All the possible timelines your life could have followed (ending in death) These branches form the plane of the 5th dimension:

Any 4th dimensional lines branching off from or crossing another would be in the 5th dimension. This applies to everything, including the beginning and end of the universe. 6th dimension: A fold. Remember when we converted the 2nd dimension into the 3rd dimension by folding? Well, we can do the same here. Just as folding the 2nd dimension allowed two discrete points to connect, so folding the plane of all possible timelines (5th dimension) allows you to jump from one possible timeline/world, to the next. In this 6th dimension, you could walk from a world in which you are a debt-laden college student into a one where you are a outrageously rich businessman. The 6th dimension therefore allows us to jump around in the 5th dimension, between possible (4th dimensional) timelines, just as the 3rd dimension allowed us to jump around the 2nd dimension.

Possible worlds


(Horizontal View)

The two worlds come together in the 6th dimension

The plane of the 5th dimension is folded into the 6th dimension

7th dimension: A line. The timelines we were thinking of before all had one thing in common: initial conditions. No matter what, your timeline(s) always started at the same origin. The 7th dimension has different initial conditions. Imagine all of the possible timelines, all the possible endings, stemming from the same origin of the universe. Now, take all that, and make it a point, just like you did with the 3rd dimension when creating the 4th dimension. This point is commonly referred to as “infinity” [2]. Now, if we imagine a different beginning of our universe, that universe would have different laws and different timelines. All the possible timelines stemming from the origin of that universe would form its own separate point, its own “infinity.” If we connect the two points we have just imagined into a line, voila! We have reached the seventh dimension. Volume 4, Issue 2. 2012

9th dimension: A fold. Now fold the plane containing all the possible universes (which, in turn, contain all possible timelines and endings of that universe). We can now compare all possible universes. That is, in the 9th dimension, you could jump around from one universe to the next instantly. Plane with all possible universes (horizontal view)

Two different universes are compared

10th dimension: A point. We are stuck. There is nothing more imaginable. We have covered all possible beginnings, all possible endings, and all possible timelines leading to those endings. The 10th dimension is simply a point containing everything [2]. There is no other point to connect to. This is where we stop. All these dimensions are helpful in understanding such outlandish concepts as wormholes and string theory. In fact, it is believed that superstrings vibrating in the 10th dimension create the subatomic particles of our universe (atoms), as well as all other universes [2]. Hopefully, this was a thought-provoking exercise that helped you gain insight into the many ways the universe can be perceived. If not, well, at least you should feel smarter.

Works Cited:

[1] “What is a Dimension Anyway?” (2008). [2] Bryanton, Rob. Imagining the Tenth Dimension: A New Way of Thinking About Time, Space, and String theory (Talking Dog Studios, Victoria, Canada, 2006).



AN ASSESSEMENT OF ETHNOBOTANICAL TREATMENTS AS MEASURED BY A BRINE SHRIMP LETHALITY ASSAY By: Madeline Pesec Edited by: Sarah Bhattacharjee Abstrat This study was performed to determine if plants chosen through ethnobotanical consultation had more potential to be used in anti-cancer treatment, than plants chosen at random. Ethnobotanical consultation is the process of speaking with a medicine man, or shaman, to find medicinal plants. Two groups of plants from the Costa Rican rainforest were tested: one group of 22 plants chosen through ethnobotanical consultation and one with 20 plants chosen at random. Potential for anti-cancer treatment was measured by a Brine Shrimp Lethality Assay (BSLA). The lethal concentration needed to kill 50% of the brine shrimp (LC50) was established for each plant and the groups were then compared. It was shown that the plants chosen through ethnobotanical consultation had a statistically significant higher median and mean lethality than those chosen at random. These results demonstrate a correlation between the traditional practitioner’s advice and possible applicability of the plant for anti-cancer therapeutics. Despite having a lower LC50, none of the plants tested were especially potent. Additional tests are needed to better delineate the anti-cancer potential of these rainforest plants. INTRODUCTION Throughout natural history, mammals and plants have evolved together. Plants that were able to adapt their seed dispersal methods to take advantage of animals’ movements had a much greater chance of survival. On the other hand, mammals that were able to eat plants and gain a competitive advantage that the plant provided were more successful. As a result, the effects of plants on mammals are numerous, and many plants have unique characteristics that affect the body in different ways [1]. Botanical research has identified over one thousand plants used for the treatments of diseases in Central America alone and over 10,000 plants used medicinally worldwide [2][3]. In developed nations, between 33-40% of medicines originate from plants, fungi, and animals [1][4]. Researchers trying to identify plants with potential pharmaceutical benefits need to narrow their search, and consultation with traditional practitioners often proves to be valuable. Unfortunately, loss of biodiversity through habitat destruction, as well as disappearance of ethnobotanical knowledge through urbanization, has made it urgent to determine the value of preserving this knowledge and the plants, fungi, and animals of the rainforest [5]. The main objective of this research was to determine if plants chosen through ethnobotanical consultation had a higher probability of potential use in an anti-cancer treatment than plants chosen at random. A secondary objective was also to discover especially potent, and thus useful, plants that were previously untested. METHOD The Brine Shrimp Lethality Assay (BSLA) was shown by Dr. Meyer in 1982 to be a good indicator of a plant’s probable results in an anticancer assay [6]. The BSLA subjects the crustacean Artemia salina (brine shrimp) to different concentrations of plant extract to determine the lethal concentration of plant extract needed to kill 50% of the brine shrimp (LC50). To test this hypothesis, plants identified as having anticancer properties by traditional practitioners local to Sarapiqui, Costa Rica were compared with plants chosen at random. To choose the me16

dicinal plants, the ethnobotanical database from the biological reserve, La Selva, in Sarapiqui, Costa Rica was used. This database contains over 500 plants identified to have medicinal properties by over dozens of traditional practitioners. This breadth and depth avoids any bias that could result from relying on a single person. Plants that were noted to have anti-cancer or anti-tumor effects were selected. To randomly select plants from the rainforest, a number generator was used to select different genera from an electronic database of all of the plants at La Selva. Then, depending on availability, a species within that genus was selected. Within six hours of collection, plant extracts were prepared by mixing 500 mg of chopped plant leaf with 10 mL of 50%(v/v) ethanol in water. After 24-78 hours of extraction, leaf-free samples of the extracts were evaporated to dryness to remove ethanol, which is toxic to brine shrimp, and rehydrated to the original volume with water. Each plant test, done in triplicate using a single 24-well plate, comprised, per well, 20 or more shrimp hatchlings, various amounts of rehydrated extract (50, 100, 200, 350, or 500 uL), and sufficient artificial salt water to bring the final volume to 2700 uL. Negative controls omitted any extract and usually had no dead shrimp. Positive controls included potassium dichromate, a known shrimp toxin, and always showed 100% killing. Occasional tests in which the negative controls had any dead shrimp were excluded from the analysis. After 24 hours, the percent kill of each concentration was calculated. This was done by counting the number of dead shrimp at 24 hours. Then potassium dichromate was added to the wells, killing all of the remaining shrimp, and the total number of shrimp in the cell was recorded. The percent kill was established by dividing the number of shrimp dead after 24 hours by the total number of shrimp in the well. These results were then analyzed in three different ways. The first was a prediction of the LC50 with the raw data. Then Probit Analysis and the Reed-Muench methods were also used. Once numbers from each of these methods had been calculated, the three were averaged to give an approximate LC50. Journal of Youths in Science

DATA Randomly Selected Plants: Plant

LC50 (ppm)


Clussia Flava



Sloanea Laevigata



Vittaria Lineata



Anaxagorea crassipetala



Neea Laetevirens



Justicia comata



Rhodospatha wendlandii



Chamaedorea tepetilote



Ficus costaricana



Polypodium dulce



Gliricidia Sepium



Souroubea Gilgii



Licaria sp.



Asplundia Utilis



Miconia Nervosa



Cyperus Thryrsiflourus



Stachytarpheta jamaicansis



Codonanthe crassifolia



Cissus microcarpa



Citrus limon



Plants Selected through Ethnobotanical Consulatation: Plant

LC50 (ppm)


Annona Muricata



Catharanthus roseus



Cocos Nucifera



Eclipta Prostrata



Vernonia cinerea



Crescentia Cujete



Momordica charantia



Jatropha gossypiifolia



Manihot esculenta



Sida hirsutissima



Mimosa pudica



Virola Koschnyi



Mirabilis Jalapa



Petiveria alliacea



Hamelia patens



Morinda citrifolia



Uncaria tomentosa



Citrus aurantium



Impatiens balsamina



Ocimum Campechianum



Artocarpus altilis



Gliricidia sepium



RESULTS The mean of LC50 of the plants selected through ethnobotanical consultation was 6800ppm, while that of the random plants was 2.5x more (17000ppm) after statistical outliers were discarded from the group. Since the LC50 is a concentration, the lower the LC50, the more toxic the plant was. Both the mean and median were lower

Volume 4, Issue 2. 2012

for medicinal plants when compared to the plants chosen at random. The LC50 of the two groups were compared in a one-sided t-test to determine if one of the groups was more toxic. The test also showed that the difference between the means was statistically significant with a p-value of .0295.

A box graph showing the distribution of the LC50 of the different plants tested. Plants with a LC50 greater than 80,000ppm were excluded. Four plants from each group were excluded

DISCUSSION These results show that the medicinal plants are indeed more likely to have a lower LC50. Consequently, there is a correlation between the traditional practitioner’s advice and the applicability of the plant in cancer treatment. While the LC50 was lower with the medicinal plants, none of the plants tested were excessively potent (with an LC50 less than 1,000 ppm). As the test had a p-value less than .05, the test was statistically significant, which is especially impressive with the small sample size. More studies examining the validity of ethnobotany in regard to other diseases could corroborate this study’s conclusion about the validity of ethnobotanical consultation. The results of this study are promising, as they show the importance of a branch of medicine that has long been considered unscientific. Traditional practitioners, rather than believing in “magic,” have an understanding of the forest built on thousands of years of trial and error. The importance of learning from the traditional practitioners and cataloguing their knowledge before it is lost is paramount. Capturing this information, along with a systematic analysis of plants recommended during that process could lead to thousands of new medications. Preserving the fragile habitat of these plants is crucial to sustainable medicine as well as a healthy planet. Ethnobotany may be a way to help more effectively develop solutions for drug therapy and devoting resources to this field could be invaluable. ACKNOWLEDGEMENTS I am deeply appreciative to Dr. Bryan Hanson of DePauw University for all of his help throughout every stage of this project. Many thanks to Dr. Ron Coleman who provided invaluable brine shrimp survival tips and kind words of encouragement during the wee hours of the morning. I am also very grateful to Nikolai Sopko, Tatiana Ioudovina, and Jose Gonzalez for their support in everything from statistical p-values to plant-hunting in the jungle. REFRENCES: 1. Old Yet New – Pharmaceuticals from Plants. Journal of Chem. Edu.78, 175-184 (2001). 2. Cáceres, A., et al. Multidisciplinary Development of Phytotherapeutic Products from Native Central American Plants. In Review. 3. Kinghorn, A. D., et al. The Relevance of Higher Plants in Lead Compound Discovery Programs. Journal of Nat. Products.74, 1539–1555 (2011). 4. Newman, D. J. Natural Products as Leads to Potential Drugs: An Old Process or the New Hope for Drug Discovery?. Journal of Medicinal Chemistry. 51, 2589-2599 (2008). 5. Kingston, D. G. I. Modern Natural Products Drug Discovery and Its Relevance to Biodiversity Conservation. Journal of Nat. Prod. 74, 496-511 (2001). 6. Meyer, et al. Brine Shrimp: A Convenient General Bioassay for Active Plant Constituents. Planta Medica. 45, 31-34 (1982).



edited by Ruochen Huang

We’ve all seen those horror movies or read those books in which the villain will say in an utterly chilling voice, “I can smell your fear…” to the hero or heroine. Smell composes one of the five senses of the human, and it is an extremely important one. Without it, we would be unable to taste food and appreciate many other things in our lives. In comparison to other animals, however, a human’s nose is one of the weakest at sifting through smells and recognizing them. Though the idea of smelling a person’s fear might sound absurd, it might actually be feasible. Fear: a four-letter word that represents one of the broadest sections of the human scale of emotions. Brought on by impending doom, pain, or an AP Chem test, fear is a very distressing emotion. Fear is actually one of the most powerful emotions that a human possesses. We have classified it far more than any other, and we have created names for the numerous types of fears a person can have. Arachnophobia: fear of spiders, acrophobia: fear of heights, coulrophobia: fear of clowns and many, many others are all fears that affect people, and in some cases, can rule over their lives. Pale faces, clammy palms, goosebumps, and many other responses are all very familiar results of this well-known emotion.



reviewed by Amiya Sinha-Hikim

Interestingly, eau de fear is actually quite distinct from a scientific viewpoint. When a person becomes anxious, the sweat they release has an odor different from that of normal I-was-just-outfor-a-run sweat. In a study conducted by psychologist Bettina Pause of the University of Dusseldorf in Germany, the brain activity of sniffers would react in a different pattern when given a sample of anxious sweat as opposed to regular sweat. What exactly does this anxious sweat do? Testers, or rather sniffers, reported a sense of discomfort at the smell of anxiety. This sense is the nearest thing to a sixth sense in humans. How does the sweat work? When a person smells the socalled anxious sweat, a certain section of the brain is activated. This cluster of areas in the brain is related to empathy and is what triggers the sense of discomfort testers had felt. “That suggests,” Pause says, “that anxiety—and maybe also other emotions— can be chemically transferred between people.” Chemical transfers of emotions and feelings have long been a topic of debate among scientists. The study of pheromones, chemical substances reart by joy li leased by an animal that influence the behavior of other members of its species, can directly correlate to the concept of smelling fear. Though numerous animals such as seals, bears, and rodents have exhibited the use Journal of Youths in Science

of pheromones, scientists are at a standstill in the debate of whether or not humans possess pheromones. However, the development of the idea of being able to sense fear and stress in humans through smell adds solid ground to the argument of humans possessing pheromones. How are pheromones used? Animals utilize their pheromones for two reasons: attraction and defense. Most people are familiar with the concept of animals utilizing pheromones to defend their territory, and may have seen their own dog marking its territory every so often. Animals also use pheromones to attract potential mates and announce that they are open for mating. However, the idea of being able to smell the emotion of fear is a completely new concept. The discovery of the possibility of actually being able to smell fear, and possibly other emotions, has a profound effect on the psychology of empathy. Imagine being unable to hide your feelings from someone else, and the manner in which people would be able to understand you. For animals in the wild, the potential of smelling fear would be a great tool in hunting and battles for dominance. The ability to smell fear would help an animal, or even a human, gain an edge over their competitor, and this could even boost the animal’s chance of survival. Research is still being conducted over the existence of pheromones in humans as scientists debate the possibility of them and the manners in which they could help us. Evolution has granted us with numerous adaptations, and this new development that could possibly act as a so-called sixth sense could influence our abilities immensely. Though it is still a very strange thing to think about as it seems to invoke those cliché horror movies and stories (“I can smell your fear”), this new discovery has brought about new knowledge of the potential of the human senses and brain. For now at least, I would advise you to invest in a good perfume or deodorant.

Works Cited “The Smell of Love,” Psychology Today,, (1996) “You Really Can Smell Fear, Says Scientists,” The Guardian,, (2008) “Yes, You Really Can Smell Fear,” Discover Magazine,, (2009)

art by haiwa wu

Volume 4, Issue 2. 2012


Synesthesia a mind mystery

by Frances Hung

edited by Sarah Watanaskul

For centuries, the musical world has been both plagued and blessed by a mysterious phenomenon which has affected composers like Liszt, Rimsky-Korsakov, and Sibelius, giving them the ability to instinctively associate musical notes with color. Due to this condition, they were either mocked, like Liszt, or forced to keep quiet throughout their musical careers to avoid suspicion of paranoia. On the other hand, it also allowed them to literally compose with sight as well as hearing, so that each piece they wrote turned into an auditory painting—the composer deciding the most relevant color scheme to complement the composition’s mood. However, as the 19th century drew to a close, more cases of this condition were recorded. Symptoms ranged from matching colors with the days of the week to experiencing sounds with certain sights or movements. Despite the public’s obvious fascination, research went nowhere, and the topic—now known as synesthesia—was abandoned for the next 50 years. With the rise of the Internet in the 1990s, though, people with synesthesia began to reach out to their fellow synesthetes via online organizations, which have evolved today into major groups like the American Synesthesia Association.1 According to the University of Washington, the probability of anyone having synesthesia ranges anywhere from 1 in 100,000 to 1 in 200.2 While possible types of synesthesia can theoretically consist of any combination of the five senses, five major combinations recognized by the American Synesthesia Association appear the most: grapheme-color, sound-color, number form, personification, and lexical-gustatory.3 In the most widespread form, grapheme-color, individuals see individual letters and numbers as shaded or tinted a certain color. While no whole set of characters looks alike to each person with grapheme-color synesthesia, there are some which are nearly universally the same (for example, the letter “a” is often red). People with this condition often report using it to help them spell and memo-


reviewed by Ricardo Borges

rize words and number strings. Sound-color, the form of synesthesia first noticed in composers, causes individuals to see a corresponding shade of color upon hearing a certain note, key, or sound. Like grapheme-color synesthesia, each person’s set of symptoms is highly individualized, yet there are certain guidelines as well. Loud and high-pitched tones are always matched to bright, bold colors, and soft and low-pitched tones correspond with a more muted tint. Number form synesthesia is perhaps the most distracting to those affected: every time that person thinks of numerals, a fixed arrangement of numbers appears. It was first detailed and named by Francis Galton in 1881 in his book The Visions of Sane Persons. Another synesthesia type discovered in the 1800s was personification. An individual with personification synesthesia assigns human characteristics, such as personality and appearance, to sequences like days, letters, and numbers. These characteristics can also be extended by synesthetes to everyday objects to the extent that items like teapots and telephones can be endowed with distinct personalities. The rarest of the five, lexical-gustatory, is a condition wherein spoken, heard, or written language causes someone to experience specific tastes. Scientists suspect that each association between a word and a food is influenced by one’s upbringing and simple phonics (for example, the taste of mince is triggered by the sounds /s/ and /n/). The cause of synesthesia remains a mystery, but scientists have developed two solid theories. One, developed by V.S. Ramachandran and E.M. Hubbard in 2005, states that synesthetes experience their condition when two regions of the brain are more connected than normal, perhaps due to excessive brain synapses. Normally, these excessive brain synapses would be pruned during early childhood, but in synesthetes, these connections fail to vanish due to a single sexlinked mutation in the X chromosome.4 Based on prior knowledge, Ramachandran and Hubbard also hypothesized that the two cross-linked brain sections were usually located within one of two regions: the angular gyrus and the fusiform gyrus. Respectively, the angular and fusiform gyri are responsible for out-of-body experiences and interpreting sensory information. Therefore, any cross-wiring within these sections can lead to imagined connections between senses where none should exist. The alternate theory suggests that Journal of Youths in Science

in some cases, normal synaptic passageways are overly stimulated, causing feedback from some senses to interfere with others.5 When sensory information is sent back to its corresponding brain area, it normally doesn’t interfere with other regions reserved for other senses. In synesthetes, however, certain types of sensory information interact with other sections of the brain and, as a result, cause synesthesic experiences. Though genes play a role in synesthesia, the surrounding environment and its influence on gene expression determine the majority of the chances of getting any one type of synesthesia. The gene coding for this characteristic has been linked to chromosome 2, near the genes associated with autism and epilepsy, which explains why a higher percentage of synesthetes than the general population suffers from these two ailments. At the very least, most synesthetes don’t mind their current condition. Synesthesia helps them enhance their memories to extraordinary lengths, as David Tammet demonstrated in 2004 when he recited 22,514 digits of pi by memory.6 Since the 1980’s, however, some scientists have linked synesthesia to difficulty in arithmetic, right-left coordination, and sense of direction. This may be because of the interference of synesthesia with

the angular gyrus, a region linked not only to out-ofbody experiences but also to mathematical calculation and spatiovisual coordination. Lisa Emerson, a synesthete herself, attests that the syndrome sometimes has a negative pychological effect on those affected.7 When a color, sound, or object is not portrayed ideally, synesthetes are often shocked or annoyed, sometimes to comic effect; Liszt and Rimsky-Korsakov famously quarreled over the colors of various musical keys. Synesthetes are struck with both a blessing and a curse, for while their mnemonic capabilities are boosted greatly, they are forced to confront a world where nothing is always the perfect color, texture, or character they can instinctively imagine. Though the media often portrays synesthetes as unhappy and troubled, most have learned to see the bright side of their condition. They consider synesthesia a gift which sets them apart from the rest of the world population and gives them a private landscape only they can take in. Those who study synesthetes at times liken their subjects’ symptoms to those of epileptics, monks, and certain drug users; voluntarily or involuntarily, they live in a world they can make surreal and intensely personal in an instant. art by cassie sun

Works Cited 1 Jensen, Amber. Synesthesia. Lethbridge Undergraduate Research Journal. Vol. 2, vol2n1/synesthesia.xml#documentHeading-HistoryofSynesthesia (2007). 2 Phillips, Melissa L. “Synesthesia.” (1996). 3 “Do Your Numbers Have a Color? The Concept of Color Synesthesia.” (2011). 4 Ramachandran, Vilayanur S. and Edward M. Haubbard. Neurocognitive Mechanisms of Synesthesia.Neuron. 48, 509520 (2005). 5 Grossenbacher and Lovelace. “Mechanisms of Synesthesia: Cognitive and psychological constraints.” http://www. (2001). 6 Konto, Neues. “Does synaesthesia lead to better memory capacities?” lernen/lernen (2009). 7 Emerson, Lisa J. “Mixed Signals—synesthesia online”. (2002).

Volume 4, Issue 2. 2012


Uncontrollable Prejudice:

Fear and the Fault of the Amygdala

by negin b e


It’s human nature. Or is it? Can we consciously avoid it, or is the prevalence too strong? Without its impacts where would we be today? Would we all be blatantly frank or rude with each other? All of these are questions we may struggle to answer. Discrimination has certainly been an enduring issue, contributing to countless disagreements and wars from the Civil Rights Movement to World War II. Fear, an uncontrollable response to stressful stimuli, is known to be a crucial factor in causing it. However, humans have assumed that it is one’s “automatic” tendency to discriminate.1 What is it really that is causing prejudice? Is there a specific part of the brain that controls fear and in turn, discrimination? Learning about the mechanisms behind prejudice may lead to a society in which people understand discriminatory tendencies and try to eliminate them. Recently, several research projects were undertaken to discover the neurological reasons behind prejudice. Rhesus macaques, a group of monkeys which diverged evolutionarily from humans about 25 to 30 million years ago1 with 93% genome similarity to humans,2 have been useful in research on discriminatory behavior. Like humans, these macaques live in packs and form social groups, leading them to be the first non-human species to discriminate against members of their own species.2 In a 2011 experiment, 37 adult rhesus macaques were shown a screen containing two full-color headshots of macaques: one of an ingroup monkey, and one of an outgroup monkey that had never lived with the subject. Since macaques tend to be more vigilant towards the monkeys they are afraid of, the subjects looked at the outgroup macaque images an average of 6.58 seconds longer, as shown in Figure 1. Thus, the results demonstrated an increased distrust towards outgroup members, revealing that monkeys, like humans, discriminate due to fear of the unknown.1 In another experiment in 2011, the same macaques were shown pictures of ingroup or outgroup monkeys next to ones of spiders or fruits.1 The macaques tended to associate images of ingroup monkeys with objects that carried a positive connotation, such as fruits, and correlated outgroup monkeys with unpleasant images, like those of spiders. On the other hand, juxtaposing the ingroup monkey with the spider, or the outgroup monkey with the fruit, would startle the monkeys. The outgroup/fruit and ingroup/spider Figure 1: Comparing the Amount of Time Spent Looking at Ingroup vs. Outgroup Macaques



edited by

margaret g uo

combinations were looked at for an average of 6.05 seconds longer than the other two, indicating that they were inconsistent with the monkey’s expectations, while the ingroup/fruit and the outgroup/spider combinations were consistent with the monkey’s expectations.1 The fact that the outgroup/fruit sequence was looked at the longest emphasizes the existence of fear and prejudice towards outgroup members.

art by katherine luo

These experiments confirmed the presence of a primitive form of discrimination, and raised questions about the existence of a physiological mechanism that has endured for approximately 25 million years. To understand the reason behind this, the researchers first had to understand the parts of the brain associated with fear. The portion of the human brain most closely related to the fear response is the amygdala, located in the anterior inferior temporal lobe of the human brain. The fear response through the amygdala consists of four steps: starting with the stimulus, the thalamo-amygdala pathway first activates the amygdala, generating a basic reaction. Second, the thalamo-cortico-amygdala pathway is followed to the cortex, by which the amygdala is told the specifics of the stimulus. Third, the signal travels via the stria terminalis pathway to the hippocampus. Lastly, the physiological responses of fear are initiated by the amgydala, through symptoms such as pupil dilation and sweating.3 By establishing the amygdala as the cause of the fear response, scientists believe it is also the root of prejudice. In order for a true relationship to exist between amygdala activity and prejudiced behavior, however, the inverse of this statement must also be proven true: that the lack of amygdala activity leads to a lack of fear,

Journal of Youths in Science

and in turn, a decrease in discriminatory behavior. In order to test the accuracy of this statement, patients with a condition known as Williams Syndrome (WS), a genetic mutation on chromosome 7, were studied. WS patients exhibit symptoms such as mental retardation, physical deformities, and extreme sociability, especially with strangers. The lack of biases and social fears in the affected individuals seems to be due to a faulty linkage between the amygdala and the decision-making orbitofrontal cortex (see Figure 2).4 Figure 2: The MRI brain scan of a Williams Syndrome patient

on the right compared to that of a normal subject shows a significantly lower activity in the amygdala region (yellow spot)

In other words, a defective amygdala leads to lack of fear in an individual. An experiment in 2010 in the UK attempted to confirm this by scanning the brains of Williams Syndrome patients using MRI, while showing the subjects a sequence of various facial expressions shown in Figure 3:4 Figure 3: The sequence of pictures of human faces with various facial expressions shown to Williams Syndrome patients to monitor the subjects’ reactions to each expression.

role of the amygdala in fear response and discriminatory behavior.

A second experiment in 2010 endeavored to further confirm that lack of a fear response leads to lack of discriminatory behavior. In this experiment, groups of healthy children and children affected by Williams Syndrome were read a story and told to point to the picture of the person who they thought the story was about. The healthy Caucasian children showed proCaucasian bias, while the Williams Syndrome children were considerably more impartial, giving an average of 20% fewer stereotype-consistent answers than normal children.5 By demonstrating that the lack of amygdala activity ultimately leads to a lack of prejudiced behavior, researchers established the amygdala as a crucial physiological factor in discrimination. Although it is great that the physiological mechanisms behind prejudice are now realized, perhaps more important is devising a method for controlling this behavior. Many have wondered if selfcontrol is a solution. In a recent experiment, a group of white subjects were shown a sequence of pictures of weapons and tools and told to identify them as gun or tool as quickly as possible with minimal error. Before each of the pictures appeared, however, a picture of the face of an African American or white individual quickly flashed on the screen. After seeing the flash of an African American face, most subjects reported the following picture to be a gun even if it were a tool, based on common stereotypes. Electroencephalography (EEG) was used to monitor the subjects’ brains during the experiment. Participants with fewer reported errors in identifying objects had greater brain activity in the left prefrontal cortex of the brain—particularly in the anterior cingulate, the area which monitors behavioral intentions and ongoing motor responses—enabling them to overcome their stereotyping tendencies the easiest. It was thus concluded that exercising more self-control leads to the development of the anterior cingulate, which in turn allows the individual to overcome his or her automatic biases.6 In the future, researchers hope to study the difference in fear mechanisms between men and women, and also find the phylogenetically oldest animal exhibiting prejudiced behavior and study the role of fear in causing it. Also, with countless differences among humans, why has race become the most salient characteristic to influence our prejudices? Although discrimination is a natural tendency based on fear, there perhaps is a way to curb it. The ability to control this supposed “uncontrollable” response may eliminate the detrimental social effects of prejudice and pave the way for a unified, fully integrated world in the future. Hopefully, that day is coming soon.

Would the amygdalae in WS subjects be activated by looking at the fearful face, a typical response in normal individuals? Brain scans indeed revealed minimal activity in the amygdala region. Additionally, the individuals expressed a high degree of sociability, even towards the fearful face. The results of the brain scans and the subjects’ reactions confirm the cause of sociable approach towards strangers and minimal fear in WS patients as lack of amygdala activity, as shown in Figure 4.4 Figure 4: It is shown that as the degree of sociability increases, the activity of the amygdala decreases, which emphasizes the

art by eric tang Works Cited 1 Mahajan, N. et al. The Evolution of Intergroup Bias: Perceptions and Attitudes in Rhesus Macaques. J. Pers. Soc. Psychol. 100 (3), 387-405 (2011). 2 Youngsteadt, E. “Monkey Business.” php?id=40 (2007). 3 Dubuc, B. “The Amygdala and its Allies.” a_04/a_04_cr/a_04_cr_peu/a_04_cr_peu.html (2004). 4 Haas, B., W. et al. Individual differences in social behavior predict amygdala response to fearful facial expressions in Williams syndrome. Neuropsychologia. 48(5), 1283-1288 (2010). 5 Santos, A., Meyer-Lindenberg, A. & Deruelle, C. Absence of racial, but not gender, stereotyping in Williams syndrome children. Curr. Biol. 20(7), 307-308 (2010). 6 Amodio, D. M., Kubota, J. T., Jones, E.H. & Devine, P.G. Alternative Mechanisms for Regulating Racial Responses According to Internal vs External Cues. Soc. Cogn. Affect Neurosci. 1(1), 26–36 (2006).

Volume 4, Issue 2. 2012



caloric restrIction and longevity Emily Sun edited by Jenny Li by

Since the earliest of days, mankind has led an unwavering quest for immortality, but so far to no avail. Juan Ponce de Léon pursued the legendary Fountain of Youth, but it turned out to be only a myth. Countless times, alchemists claimed to have produced the Elixir of Life, but these concoctions were ineffective, oftentimes even toxic. Even with today’s technological advancements, we still haven’t found a cure to our mortality. However, scientists have discovered various means of delaying aging, one being caloric restriction, or CR. Proven to prolong life expectancy by controlling the total number of calories consumed daily, CR has also been shown to postpone numerous age-related diseases [1]. CR is a dietary regimen that restricts food intake while still providing adequate nutrition, as opposed to ad libitum consumption, or unlimited caloric intake [1]. Various studies have been conducted to gauge CR’s ability to improve health and to lengthen the life spans of several different organisms. More than seventy years ago, it was found that restricting food intake could increase the life span of laboratory rodents in an experiment conducted by C.M. McCay at the Animal Nutrition Laboratory at Cornell University. Both the magnitude and the duration of caloric restriction were found to vary directly with the length of the life span. When calorie intake was lowered to 30-40% of the control group’s, which operated at ad libitum level, the average and maximum life spans of the rodents were increased by 30-40% [2]. Similar observations have been made in primates. In a study conducted by the Wisconsin National Primate Research Center, a population of rhesus monkeys was subjected to CR in which food intake was limited to 70% of the control group’s. The average life span of the animals in the control group was 27 years, and at 30 years of age, 50% of the control group had died. In contrast, more than 80% of the 30 year-old CR animals were still alive. The appearances of the CR monkeys were also much younger than those of the same age in the control group. Moreover, CR diminished the incidences of age-associated pathologies in the monkeys, the most prevalent being diabetes, cancer, cardiovascular disease, and brain atrophy [3]. Additional studies have investigated the mechanisms underlying this extension of life span, indicating that CR lessens the damage that ordinarily accumulates in cells as the body grows older and becomes more susceptible to diseases. Several additional animal trials have also found that CR improves cardiovascular health by mitigating levels of triglycerides, phospholipids, inflammatory markers, and atherogenic low-density lipoproteins (bad cholesterol), while increasing levels of atheroprotective high-density lipoproteins (good cholesterol) [4]. Blood pressure and heart rate declined 24

significantly as well, and cardio-protective alterations in gene expression have been noted. CR also improves glucoregulatory function and insulin sensitivity by balancing fasting blood glucose and insulin levels, which may result in serious health problems including hyperglycemia if left unchecked by CR or another method. Furthermore, CR is most likely responsible for the inhibition of tumor growth, decrease in body weight, and deceleration of sarcopenia, or the loss of skeletal muscle mass associated with aging. In addition, CR reduces oxidative stress biomarkers called reactive oxygen species, which are substances such as protein carbonyls, nitrotyrosine, and hydrogen peroxide [1]. The accumulation of these agents can damage DNA, which encodes proteins crucial for cell functions. It is widely believed that DNA damage is the main contributor to aging of cells. Besides rodents and primates, multiple studies have also indicated that CR could delay the aging process in dogs, fruit flies, worms, and bacteria. The universality of the effects of CR in lower organisms raises the possibility that it may impact aging in humans as well [5]. Indeed, analysis of CR in humans has already begun. These experiments include programs such as CALERIE (Comprehensive Assessment of Long Term Effects of Reducing Caloric Intake), which investigates the responses to CR in freeliving humans [6], and Biosphere 2, which places subjects in an “ecological mini-world” with limited food resources [1]. Most of these studies have been conducted on healthy, non-obese, middle-aged humans, both male and female, oftentimes under conditions in which caloric intake is reduced by 20-25% of the average number of calories consumed daily. Most humans would consume 1200-2000 of their 2000-3000 calories when undergoing CR [1]. Some CR investigations have also included diabetic, obese, elderly, and young individuals as well. Ideally, though, CR should be started after the body has completely matured and developed, as low calorie diets could stunt growth even when the diet contains all essential nutrients. CR during pregnancy or illness should also be avoided; at these times the body requires sufficient nutrition as well [7]. These studies have so far yielded positive results, especially those related to biomarkers associated with glucoregulatory and cardiovascular functions, oxidative stress, and mental health. These analyses reveal that CR reduces blood pressure, triglycerides, total cholesterol, and the thickness of artery walls in humans, and further enhances insulin sensitivity while retarding circulating insulin and glucose levels. Simultaneously, CR attenuates levels of oxidative agents and stimulates verbal memory performance in the elderly [1]. Journal of Youths in Science

Although the data indicates that CR can improve human health, these studies are still in their early phases and have yet to provide direct evidence demonstrating that CR indeed extends human life spans, as humans are already relatively long-living organisms. The analyses of human life spans would therefore need to rely on the observations of several generations before a solid conclusion can be drawn, something bound to be costly and difficult to maintain [6]. This is one reason why most human CR studies have been carried out for periods of only 6-12 months, or at most several years, at a time. In many cases, scientists have had no choice but to measure surrogate markers for longevity, which include fasting insulin levels, body temperature, and markers of oxidative stress [1]. Some are also concerned that due to differences in dietary habits, the increases in life spans via CR in other organisms may not be applicable to humans. We might have already reached our optimal level of energy intake, as unlike other animals, we do not eat ad libitum, and further limiting our diets may not yield such drastic changes. However, correlative evidence does exist supporting that people subjected to CR may live longer. For example, a study of the monks of Mount Athos in Greece between 1994 and 2007 found that their restricted diet—they only eat two small and ascetic, albeit nutritious, meals a day—contributes to their long lives and lower rates of cancer, heart disease, Parkinson’s disease, Alzheimer’s disease, and prostate cancer [8].

But cutting down on calories, despite its observed positive results, might not be a wholly enjoyable experience. Selecting foods that provide all the nutritional requirements but which are low in calories may sound easy, but refraining from consuming anything more than the bare minimum may prove to be more difficult: no sweet treats, no second helpings, and no dessert. Few people in today’s society would be able or willing to step up to this challenge. Nevertheless, the discovery of CR as a potential promoter of human longevity represents one significant step t o w a r d s achieving man’s desire f o r immortality. O t h e r p a r t i a l solutions to our age-old predicament e x i s t — a myriad of drugs, operations, or complicated diet regimens—but currently CR seems to be the most natural and promising method to extend lifespan and enhance health. Although we may never unlock the secret to living forever, modern science combined with something as simple as a well-controlled diet may allow us to enjoy longer, healthier lives.

Graphic by Amy Ng Works Cited 1. Trepanowski, J. F., Canale, R. E., Marshall, K. E., Kabir, M. M. & Bloomer, R. J. Impact of caloric and dietary restriction regimens on markers of health and longevity in humans and animals: a summary of available findings. Nutr. J. 10, <> (2011). 2. Mattson, M. P. Energy intake, meal frequency, and health: a neurobiological perspective. Annu. Rev. Nutr. 25, < annurev.nutr.25.050304.092526> (2005). 3. Coleman, R. J., et al. Caloric restriction delays disease onset and mortality in rhesus monkeys.” Science. 325, < full.pdf?sid=c3e8babf-cf10-4444-aa76-dbe925ba3d6f> (2009). 4. Berrougui, H. & Khalil, A. Age-associated decrease of high-density lipoprotein-mediated reverse cholesterol transport activity. Rejuvenation Res. 12, <http://> (2009). 5. Lane, M. A., Ingram, D. K. & Roth, G. S. The Serious Search for an Anti-Aging Pill. <> (2002). 6. Gertner, J. “The Calorie-Restriction Experiment”. <> (2009). 7. Zamora, A. “Calorie Restriction with Optimum Nutrition (CRON) - The Longevity Diet”. <> (2010). 8. Katz, N. “How Do Mount Athos Monks Stay so Healthy?”. <> (2011).

Volume 4, Issue 2. 2012


Graphic by

th Julia Yang was e life of t A a ke pp know n as n by a m le co-fou Rece one ys nd nt c a o thro ut of m ncer. H terious a er Stev ly, e ugh owev illion n Taki er, J d fatal d Jobs ng i the me s of vic o isea bs ts ti n the s Unit place a acing s ms who was onl e y ed S s th t s as m a u g ffere es en tat a furti lignant es, canc umber-t of canc d wo k ve a e neop er (m bilit iller r. lasm warn edic y i ) a n to se in lly k is n iz o now then g and n to s e victim torious resu for i po s’ rf of al ts l me ace onc ntaneou lives w i e n s thou ly v and agai Stat t onea n es d third . Overa nish an is ca evelop l d l o , f abou can all w nce t ha om of ye r? How cer in th eir li en in the lf ars, is it fetim scie Unit cre unso ed es [ lved ntists h ated? F or th 1]. Wha ave ques t puz tio yet ou dead ns of thi zled ov sands e s l r y rem In the a dise rkable, brief, ase. cancer is a term for a large group of

diseases involving uncontrolled cell growth. In regulated cell growth, a parent cell provides one complete set of genes to each of the two daughter cells. The cells then undergo a period of normal cell growth and activity. Cancer cells do not necessarily grow faster than normal cells, but they continue to grow under conditions where normal cells would stop. Normally, when the cell membranes of two cells touch each other, they exchange signals, called contact inhibition, which turn off the portion of the DNA that controls cell growth and division; as a result, the cells stop growing [2]. However, in cancerous cells, the affected portion of the DNA does not seem to respond to this signal, and the cells continue to grow and divide uncontrollably. Eventually, as the cancerous cells divide and pass on their affected DNA, a tumor begins to form. Cancer can be stimulated by faults in proto-oncogenes, which are genes potentially capable of causing cancer. Mutated protooncogenes are converted into oncogenes, which lead to cancer development. According to the oncogene theory, all vertebrates contain the genetic information for producing a type-C RNA tumor virus that remains in an unexpressed form throughout hundreds of cell generations. The endogenous virogenes (genes that code for the production of type-C viruses) and oncogenes (the portion of the virogene accountable for the transformation of a normal cell into a cancerous cell) are usually maintained in an unexpressed form by the tumor suppressor genes [3]. However, when agents such as carcinogens and viruses invade the cell, they “switch on” the oncogenes, which then direct the production of proteins that affect cell growth and contact inhibition. Carcinogens, one of the agents that turn on the oncogenes, are substances or exposures that potentially cause cancer.

CANCER and oncogenes by Cindy Yang edited by Achi Mishra Environmental factors such as inhaling poisonous particles of asbestos, certain dioxins, tobacco smoke, and intense exposure to radioactive substances including gamma rays and alpha particles can easily damage cell genome and metabolic processes. Retroviruses play an important role in activating, or even creating oncogenes. While some viruses contain DNA encased in a protein shell, retroviruses are composed of RNA. These viruses cannot directly inject their genetic information into the host’s nucleus because of the host’s DNA composition, so reverse transcription takes place. The particles involved in this process are known as enzyme reverse transcriptase (RTase), which aid in synthesizing a complementary DNA by using the virus’ RNA as a template [4]. Furthermore, most retroviruses contain one or more additional genes. When invading eukaryotic host cells, some retroviruses may pick up copies of the host’s proto-oncogenes and then convert it into an oncogene [5]. Several of the cancers in animals are caused when the virus injects its RNA containing the oncogene into another eukaryotic cell. Once the oncogenes are activated, the production of proteins that affect cell growth and contact inhibition commences. The cells divide uncontrollably and clump together to form a tumor. As the cancerous tumor grows, blood vessels may start flowing through it, providing the swelling clump with nourishment. The tumor cells grow wild and undergo dedifferentiation, in which the cell loses its normal distinguishing characteristics and functions. Cancer cells can lose molecules on their surface that keep them intact with other cells. This causes the cells to detach, which partly contributes to tumor metastasis, or the spreading of cancer to other parts of the body. When malignant tumors undergo metastasis, the cancer cells migrate through the body by means of blood and lymph circulation [6]. Once transported to a new tissue, the cells again take root and develop into a tumor. This is one of the reasons why cancer is one of the most feared killers—because of its stealthy ability to drift to other parts of the body and regain new life. Fortunately, as scientists developed new advancements in technology to help treat and prevent cancer, the percentage of cancer deaths has slowly abated over the years. In centuries to come, scientists from all around the world will continue to unite and endeavor to end the battle against the relentless cancer. But for now, even with the numerous advancements in technology, scientists have only grazed the surface of understanding and answering the endless questions of this mysterious disease.

Works Cited 1. American Cancer Society. “What is Cancer.” (2011). 2. Silverstein, A. & Silverstein, V. Cancer: Can it be Stopped? (Lippincott, New York, 1987). 3. Todaro, G.J. & Huebner R. J. “The Viral Oncogene Hypothesis: New Evidence.” (2011). 4. “Diagram of a Retrovirus.” 5. “Retroviruses.” (2011). 6. “The Cancer Cell.” (2011).


Journal of Youths in Science


Soy Food Intake


Graphic by Kerry Luo

In a shining era of better healthcare, research, and innovative medicine, life spans have increased drastically from those in previous centuries. This has been accompanied by equally great advances in the quality and convenience of lifestyles. Yet while these improvements may seem like jewels in our ever-growing society, they have also revealed one of the darker sides of life: an increase in cancer patients. As more people are diagnosed with cancer each day, the fear and struggles with this disease only grow larger and darker. Breast cancer, one of the most common forms in women, is perhaps among the most infamous. It has been strongly correlated with estrogen, a hormone that stimulates cell division [1]. As a result, many treatments for breast cancer have been centered on blocking or inhibiting the effect of estrogen by reducing its production in t h e body [2]. Tamoxifen is one type of drug widely used to prevent estrogeninduced effects [3]. This treatment works best for estrogen receptor (ER) positive patients. E R -

Volume 4, Issue 2. 2012

by Sarah Lee edited by Anita Chen reviewed by Saswati Hazra

positive patients have receptors that bind to estrogen to yield chain reactions. The resulting chain reactions cause dysregulation of signal transduction pathways, potentially causing complications in cell division and triggering the production of cancerous cells [3]. Tamoxifen effectively competes with estrogen to bind with these estrogen receptors, but unlike estrogen, it does not produce chain reactions. Ultimately, the treatment severely cuts down the amount of estrogen-induced reactions and in turn lowers the harmful effects of abnormal results from this hormone. ERnegative patients do not have cells with these receptors, so it is much more difficult to treat these patients with methods that utilize competitive inhibitors like tamoxifen [4]. The connection between estrogen and breast cancer has also led many to believe that avoiding foods containing high levels of estrogen, like soy foods, will help prevent breast cancer. Indeed, soy foods are packed with plant estrogen (phytoestrogen), particularly a group of compounds called isoflavones, which possess both estrogen-like and anti-estrogenic properties. There has been debate over whether these isoflavones will produce estrogenic effects and promote cancer recurrence, or exert their anti-estrogenic properties. There has also been concern about the effect of soy isoflavones on other treatments, like tamoxifen. A team of scientists conducted an experiment in 2009 to shed light on these controversies, and their research has shown that the consumption of soy foods may actually be beneficial in treating breast cancer [5]. Under the Shanghai Breast Cancer Survival Study, permanent female residents of Shanghai, China who were diagnosed with primary breast cancer were recruited in the study. Their ages ranged from 20 to 70 years, and the sample size started with roughly 5000. Qualitative data was first collected through interviews and questionnaires on demographics, disease history, medication use, reproductive history, diet, and other lifestyle factors. Clinical information, including cancer history, progression, and previous treatments, was also obtained. The sample size was then split into four quartiles, with each consuming varying amounts of soy foods. Using food frequency questionnaires, the soy food intake, including tofu, soy milk, soy beans, meat, fish, and other soy products, was measured accurately and designed to control various variables. Dietary intake was then assessed at specific time windows: 6 months after cancer diagnosis for baseline survey, then the 18, 36, and 60 month mark. At these times, interviews were conducted again to reassess disease progression [5].


The results indicated that overall, soy food intake was inversely associated with mortality and breast cancer recurrence. This was evident in both ER-positive and ER-negative patients. The group with the lowest amount of soy intake had a 13.1% mortality rate and 13.0% recurrence rate, while the group with the greatest soy intake had a 9.2% mortality rate and 8.9% recurrence rate. Looking at both figure 4 and 5 shown below, this trend of decreasing percentages is apparent as the quartile number (and soy food intake) increases. The association follows this rough linear pattern until around the 11 grams of soy protein per day mark indicating that soy consumption over 11 grams per day will not lower morality and recurrence rate any more significantly [5]. Figure 4. Total Mortality by Soy Protein Intake Figure 5. Breast Cancer Recurrence by Soy Protein Intake. The results also indicate that soy food intake does not decrease the effectiveness of tamoxifen. In fact, when soy was consumed in high quantities, the use of tamoxifen had no effect on mortality and recurrence rates. At moderate and lower levels of soy intake, however, administering tamoxifen continued to improve patient prognoses [5]. In conclusion, the anti-estrogenic effects in isoflavones of soy foods override the estrogen-like characteristics, thus accounting for lower mortality and recurrence rates of breast cancer. Concern regarding the interaction between estrogen-inhibiting medicines like tamoxifen and foods with high levels of estrogen was also cleared, as results clearly showed no detrimental effects. Though these results may bring uplifting news for the masses, there are still some issues that must be addressed before definite conclusions can be made. First, the follow-up period of the study is still relatively short compared to the life spans of the patients. The long-term follow up study will give a more accurate evaluation of the long-term effects of soy intake [5]. Second, this study was done entirely in Shanghai, China. Soy foods are more abundant there than in the U.S. and many other regions due to cultural and dietary differences. As a result, it is possible that soy food intake may have less pronounced or even harmful consequences if the experiment were repeated with a new sample size in a different location. However, it can be expected that as soy food becomes increasingly widespread and popular in other places in the world, the effects can only be beneficial for the breast cancer patients and survivors. So for now, pass me the tofu, please!

Figure 4

Figure 5

Works Cited 1. Clark, R. A., Snedeker, S. & Devine, C. “Estrogen & Breast Cancer Risk: The Relationship”. BCERF Cornell University. http://envirocancer. (2001). 2. Szabo, L. “Soy Foods could help breast cancer survivors.” USA Today. (2009). 3. National Cancer Institute. “Estrogen Receptors.” National Cancer Institute. estrogenreceptors/page3 (2010). 4. Bankhead, C. “ENDO: ER Negative Breast CA Cells Turn Positive with Trastuzumab.” therapies/new_research/20090618c.jsp (2009). 5. Xiao O. S. Soy Food Intake and Breast Cancer Survival. The Journal of the American Medical Association 302.22 (2009): 2399 - 2502.


Journal of Youths in Science

PRECOCIOUS PUBERTY: Becoming a Lady Far Too Fast

by Rachael Lee edited by Sarah Bhattacharjee

Adolescence is a transitional period between childhood as agonists, antagonists, or manipulators that change the way and adulthood. But what exactly happens when the biological hormones are metabolized and excreted [4]. processes behind it occur in extremely young ages? Alarmingly, an Perhaps it may be irregularities in the most basic foundation increasing amount of girls hit puberty at abnormally young ages, of humans: genetics. Mutations in the KISS1 gene may have a going as far as 6. role in disorders of puberty. The KISS1 gene produces kisspeptin, Puberty begins when the hypothalamus, the master gland which stimulates GnRH secretion. In the study “Mutations of the that directs a multitude of important functions in the human KISS1 Gene in Disorders of Puberty” done by Silveira LG et al, body, begins to produce abnormally large amounts of GnRH, the two KISS1 mutations were identified in unrelated patients with hormone that stimulates the activity of the sex organs. These idiopathic CPP. The mutation also was associated with higher high-amplitude pulses of GnRH signal the pituitary gland to kisspeptin resistance to degradation when compared to normal increase its production of gonadotropin-luteinizing hormone KISS1, meaning that the kisspeptin of the mutated gene would be (LH) and follicle-stimulating hormone (FSH). These hormones more likely to remain in the body and stimulate GnRH secretion travel through the bloodstream to the gonads and stimulate the even more [6]. production of sexual hormones. Increased LH causes the physical Currently, the most prominent treatment for affected children developments of puberty, while increased FSH levels enlarge is monthly medication to neutralize the effect of GnRH. One of the ovaries and promote follicular maturation in girls [1]. These these medicines, Lupron, stops puberty by acting as an agonist processes, which evolve over time to fit the conditions of each at pituitary GnRH receptors [3]. It fills the gaps between the era, are triggered naturally around ages ten to fourteen for girls pulsatile release of GnRH by the hypothalamus, and this steady[2]. But multiple factors, both environmental and hereditary, are GnRH state is perceived by the body as no GnRH at all [7]. Thus, beginning to accelerate the process a lot faster than what evolution it indirectly decreases the secretion of LH and FSH and ceases the would expect it to. mechanisms of puberty. There are two types of early puberty. Central precocious Precocious puberty may not seem that significant. However, puberty (CPP) is caused by the early maturation of the chain link there are several serious risks that ensue from it. There are higher between the hypothalamus, the pituitary gland, and the gonads incidences of breast cancer among women who develop early that trigger the early release of gonadotropins, LH and FSH [1]. due to the additional years that the sensitive breast tissues are Precocious pseudopuberty is due to early release of estrogen and exposed to hormones [4]. It also plays a significant role in growth testosterone in their respective gonads [3]. They differ in the and skeletal problems. Since LH controls pubertal growth spurt, location of prematurity, yet both types are the products of an early production of this hormone leads to sudden growth spurts irregular endocrine system. that cause kids to become taller at a younger age [4]. However, the There are multiple factors that doctors look to as the growth is only temporary and actually concludes much earlier possible source of early puberty. One of the biggest than normal. As bone development advances, growth suspects is obesity due to the fact that fat is crucial plates can closer prematurely and children can end up in the onset of puberty. An adequate amount of a lot shorter than they could be [4]. Even before all adipose tissue, a more sophisticated term for this, the emotional damage inflicted upon girls due fat, is required for child bearing. Thus, fat acts to unwanted attention by boys and even men can as a natural cue to prepare the reproductive lead to psychological issues [4]. system for pregnancy. To do this, adipose Girls often want to grow up fast; tissue produces a hormone called leptin. hence, they love dress up and secretly Besides the regulation of normal bodily try on their mother’s lipstick. But when processes, leptin regulates the release their bodies develop a lot faster than their psyche of GnRH by the hypothalamus[4]. Thus, does, they do not enter adolescence or adulthood increased fat stores, which is perceived by faster. All they will lose is their childhood. the body as a good time for reproduction, induces Works Cited the activity of sexual hormone production. Kaplowitz, P.B. “Precocious Puberty.” http://emedicine.medscape. But dieting a child won’t simply remove com/article/924002-overview (2010). all chances of precocious puberty. In "Puberty." 1973, a fire retardant chemical called (2011). Polybrominated biphenyls (PBBs) "Precocious Puberty (Early Puberty)." http://www.cincinnatichildcontaminated over 500 Michigan (2010). farms and their domesticated animals Kluger, J. "Little Women." [5]. The Michigan population was article/0,9171,2097388,00.html (2011). exposed to the chemical through meat "PBBs (Polybrominated Biphenyls) in Michigan." http://www.michiand dairy products. This caused the (2011). daughters of pregnant women to Silveira, L. G. et. al. "Mutations of the KISS1 gene in disorders of have their menarche at the average puberty." J. Clin. Endocrinol. Metab. 95, 2276-2280 (2010). age of 11.6 years [4]. In this manner, "Leuprolide Injection.” chemical contaminants of the health/PMH0000852/. (2011). environment trigger the early Graphic by Rebecca Wang onset of puberty. They act either

Volume 4, Issue 2. 2012



The Antibiotic, Brefeldin, is a Novel Inhibitor of the Metalloprotease, Meprin A By: Mikhail Solovykh1 and Gaylen Bradley2 Edited by: Florine Pascal3 Abstract

The research is focused on the zinc metalloprotease, Meprin A, an enzyme found in intestines, kidneys, and white blood cells. Meprin A degrades cartilage and gelatin and has been found to have a role in diseases such as inflammatory bowel disease, urinary tract infections and acute renal failure [1]. An effective inhibitor of human Meprin A may have therapeutic potential, and is the focus of this research. Meprin A is known to be inhibited by ethylene diamine tetraacetate (EDTA) and actinonine [1], confirming that substances binding to the active site or to zinc are possible inhibitor candidates. Meprin A also has numerous sugar molecules along its protein backbone [2], leading to the proposition that chemicals binding to sugars may inhibit Meprin A. Here it is shown that sugar-binding lectins, or proteins with highly specific functional groups, from Sambucus bark and red kidney beans do not inhibit Meprin A, but Concanavalin A, another lectin, reduces Meprin A activity by half. To test compounds that display better safety profiles in animal toxicity tests than Conconavalin A, we chose three additional compounds to test: E-64 (L-transepoxysuccinyl-leucylamido-[4-guanidino] butane), dichloro-iso-coumarin and Brefeldin. Of the three compounds tested, only Brefeldin achieved 50% or above inhibition of Meprin under the test conditions, deserving further testing in animal disease models where meprin overexpression is suspected as a contributing factor.


The metalloprotease Meprin A is a large protein that is formed by dimeric subunits binding together to form large complexes (see figure at right). Homomeric Meprin A is only composed of Meprin alpha subunits in contrast to other forms of Meprin, such as heteromeric Meprin A, which is composed of both Meprin alpha and Meprin beta subunits, and Meprin B, which is composed only of Meprin beta subunits. Unlike heteromeric Meprin A, homomeric Meprin A is released from cells and is found in body fluids such as urine and the fluids in the intestines. Meprin A is produced in the kidneys, intestinal lining, and white blood cells. Because it has been found to play a role in diseases such as inflammatory bowel disease, urinary tract infections and acute renal failure [1], an effective inhibitor for Meprin A might have therapeutic potential. Of the eight compounds tested, five showed at least 50% inhibition. The rationale for testing these compounds was as follows: two of the compounds, EDTA and actinonine, 1. Hershey High School, Hershey, PA and 2. Penn State Hershey Medical Center, Hershey, PA 3. Torrey Pine High School, San Diego, CA


The dimer structure of Meprin A. This study focuses on the protease subunits (the catalytic sites of the enzyme) as well as the lectin-binding MAM subunits. (Graphic by Angela Wu)

Journal of Youths in Science

ORIGINAL RESEARCH are known inhibitors of Meprin and served as positive controls. As it was thought that sugar-binding lectins might restrict Meprin A activity by binding to mannose residues, three were tested in the experiment: Concanavalin A, Red Kidney bean lectin and Sambucus bark lectin. Dichloro-iso-coumarin and L-transepoxysuccinylleucylamido-[4-guanidino] butane (E 64) were tested due to previous studies demonstrating their ability to inhibit serine and cysteine proteases, respectively [3,4]. Brefeldin A, an antibiotic which is isolated from yeast and is known to cause a disruption of intracellular microfilaments (thereby impairing enzyme secretion [5]) was tested to see if it could also inhibit Meprin enzymatic activity.

responses interpreted.


A panel of chemicals was tested for their ability to inhibit Meprin A’s digestion by the protein azocasein. To confirm the reliability of the experimental design, two known inhibitors of Meprin A, actinonine and EDTA, were tested for inhibitory activity. Indeed, 5 µM actinonine and 25 µM EDTA reduced release of the azocasein dye by 50%, as shown in Figures 1 and 2 below.

Enzyme Assay Method

Homomeric Meprin A was provided by Timothy Keiffer (Penn State Hershey Medical Center), who purified the enzyme from mouse kidneys. The enzyme was produced, harvested, and purified from human embryonic kidney (HEK 293) cells. The stock latent enzyme was stored at -20°C before use. At the start of each enzyme assay, Meprin was activated by trypsin, which cleaves off a peptide at the amino-terminal end of the enzyme molecule, leading to full activation [1]. The procedure for assaying Meprin A relied on the release of azo dye bound to casein [7]. First, a small amount (25 µL) of pH 8.5 ethanolamine buffer was dispensed into Eppendorf tubes to facilitate the mixing of later additions. A constant amount of activated Meprin A was then added to the Eppendorf tubes. More buffer or test material was then added to bring the volume to 125 µL. Then 125 µl of azocasein substrate was added. The reaction mixtures were incubated for 1 hour at 37°C. Next, 1000 µL of 5% trichloroacetic acid was added to precipitate the protein. The reaction mixtures were then centrifuged for 5 min at 5000 rpm to sediment the protein. The clear fluid was transferred to cuvettes, and the absorbency of the clear fluid at 340nm was measured using a spectrophotometer. The procedure for detecting inhibition of Meprin A activity includes a series that consists of a blank with no enzyme or test material, a positive control with enzyme but no test material, and varying amounts of potential inhibitor with enzyme. The chemicals tested included: actinonine, EDTA, concanavalin A, dichloroiso-coumarin, L-transepoxysuccinyl - leucylamido- (4 – guanidine) butane (E64), dicyclohexylcarbodiimide, Sambucus bark lectin, red kidney bean lectin, and brefeldin A. The data was then graphed and the inhibitory Volume 4, Issue 2. 2012

Figure 1. Actinonine inhibits Meprin A activity

Figure 2: EDTA inhibits Meprin A activity

It has been reported that a protein that binds to the sugar residue, mannose (mannan binding protein) inhibits Meprin activity [2]. In the present study we tested three different proteins that also bind sugars, including Concanvalin A, Sambucus Bark Lectin, and Red Kidney Bean phaseola lectin. Of these, only Concanavalin A at 20 µM resulted in a 50% reduction of digestion of azocasein by Meprin A, as shown in Figures 3, 4, and 5 below. 31

ORIGINAL RESEARCH as a therapeutic agent [6]. In an attempt to identify other novel inhibitors of Meprin activity that may have therapeutic potential, other protease inhibitors that had better safety profiles in animal toxicity studies [6] were tested, including dichloro-iso-coumarin, E64 and brefeldin. The first two compounds tested, dichloro-iso-coumarin and E64, showed limited inhibition of Meprin A activity even at very high concentrations (465 ÂľM and above) as shown in Figures 6 and 7.

Figure 3: The lectin, Concanavalin A, is an effective inhibitor of Meprin A

Figure 6: Dichloro-iso-coumarin is not an effective inhibitor of Meprin A Figure 4: The lectin from Sambucus bark is not an effective inhibitor of Meprin A

Figure 5: The lectin from red kidney beans is not an effective inhibitor of Meprin A

From the above enzyme assays, we were able to conclude that Concanavlin A was a novel inhibitor of Meprin. However, this molecule has shown toxic effects in animal experiments that would limit its usefulness 32

Figure 7: E-64 is not an effective inhibitor of Meprin A

Brefeldin A, however, a known inhibitor of Meprin secretion [5], was also found to inhibit Meprin A proteolytic activity at 80 ÂľM as seen in Figure 8 below. Journal of Youths in Science

ORIGINAL RESEARCH tivity against Meprin A. In addition, tests on mice would have to be conducted to study the therapeutic potential and hazards of the chemicals, especially brefeldin A.


1. Bylander, John, Greg Bertenshaw, Gail Matters, Simon Hubbard, and Judith Bond. Human and mouse homo-oligomeric meprin A metalloendopeptidase: substrate and inhibitor specificities. J. Biol. Chem. 388. (2007): 1163-1172.

Figure 8 Brefeldin Inhibits the Enzyme Activity of Meprin A


Three lectins with different sugar-binding preferences were tested for their abilty to inhibit the enzyme, Meprin A. Concanavalin A selectively binds to mannan residues, Sambucus Bark lectin to N-acetyl-D-glucosamine, and Red Kidney Bean Phaseola lectin to glycosyl side chains [8][9]. Only Concanavalin A inhibited Meprin A, consistent with previous reports [10]. Indeed, mannose residues are more abundant on the Meprin backbone than Nacetyl-D-glucosamine and galactose residues. It would appear that attachment of lectins to the mannose residues on Meprin molecules impedes proteolysis by altering access of the azocasein substrate to the active site. It is noteworthy that inhibition of meprin’s proteolytic activity tapered off as concanvalin A concentration increased, consistent with the proposition that the large molecule is covering up the active site of the enzyme rather than directly binding to the active site. Dichloro-iso-coumarin and E64 are serine and cysteine proteases, respectively [3][4] confirming the general specificity of these inhibitors. Brefeldin causes a disruption of intracellular microfilaments [5] and thereby impairs secretion of the proenzyme. It is not clear how this relates to the inhibition of proteolysis that we demonstrated in the study above. Experimental errors include the tendency of Meprin to deteriorate during storage at 5° C, thus varying its control activity. Further experiments would be directed at testing these same inhibitors against different zinc metalloproteases to determine the specificity of the inhibitors. The therapeutic potential of a selected inhibitor would be enhanced if it could be established that it only had acVolume 4, Issue 2. 2012

2. Hirano, Makato, Bruce Ma, Nana Kawasaki, Kazumichi Okimura, and Makato Baba. Mannan-Binding Protein Blocks the Activation of Metalloproteases Meprin (alpha) and (beta). Journal of Immunology. 175. (2005): 3177-3185. 3. Harper, Wade, Keiji Hemmi, and James Powers. Reaction of serine proteases with substituted isocoumarins: discovery of 3,4-dichloroisocoumarin, a new general mechanism based serine protease inhibitor. Biochemistry. 24. (1985): 18311854. 4. Matsumoto, k, K Mizoue, K Kitamura , Tse WC, and Huber TP. Structural basis of inhibition of cysteine proteases by E-64 and its derivatives. Biopolymers. 51.1 (1999): 99-107. 5. Fujiwara, T, K Oda, S Yakota, A Taktsuki, and Y Ikehara. Brefeldin A causes disassembly of the Golgi complex and accumulation of secretory proteins in the endoplasmic reticulum. J Biol Chem. 263.34 (1988): 18545-52. 6. Porter, Robert S and Justin Kaplan, editors, The Merck Manual, 19th edition, 2010. 7. Iversen, Stig, and Mogens Jorgensen. Azocasein Assay for Alkaline Protease in Complex Fermentation Broth. Biotechnology Techniques. 9. (1995): 573-576. 8. Shibuya, Naoto, Irwin Goldstein, Willem Brokaert, Makuta Lubaki, and Ben Peeters. The Elderberry (Sambucus nigra L.) Bark Lectin Recognizes the GlcNAc or β1–6-Linked Branch Structures. Journal of Biological Chemistry. 262. (1987): 1596-1601. 9. Kaneda, Yuko, Robert Whittier, Hidenori Yamanaka, Enrique Carredano, and Masonori Gotoh. The High Specificities of Phaseolus vulgaris Erythro- and Leukoagglutinating Lectins for Bisecting GlcNAc or β1–6-Linked Branch Structures, Respectively, Are Attributable to Loop B. Journal of Biological Chemistry. 277. (2002): 16928-16935. 10. Solovykh, Mikhail and Bradley, Gaylen. Identifying New Inhibitors of the Human Metalloprotease Meprin A. National High School Journal of Science, July 26, 2011(online issue). 33

Born This Way by harshita nadimpalli

Murders. Kidnappings. Thefts. Massacres.

In the world we live in, there is a constant and seemingly endless stream of crime. What prompts a person to commit these moral transgressions? The answer is not one most would expect. Surprisingly, over the last century, a theory has emerged suggesting that the actions of some criminals may be programmed into the way their brains or bodies were built, rather than the result of their conscious choice to become a criminal. This theory may have implications for our justice system and for society as a whole. Many scientists have been examining the structures in the brain to better understand how abnormalities in certain brain structures may affect behavior. The majority of these studies analyzed two specific structures of the brain: the amygdala and the vmPFC. The amygdala is the structure that controls emotions, including remorse, memory, and fear. The ventromedial prefrontal cortex, or vmPFC, is crucial to understanding brain functions as well, due to its association with decision making. In a study conducted by the University of Wisconsin, it was found that psychopaths have weaker connections between the amygdala and the vmPFC than non-psychopaths do [1]. In another study, Adam Raine, a professor of criminology, psychiatry, and psychology at the University of Pennsylvania discovered that adult psychopaths have an amygdala that is 18% smaller than that of a regular adult [2]. A brain study comparing 27 psychopaths to 32 non-psychopaths was published in the September 2009 Archives of General Psychiatry, and directly supported this finding. A second study of 21 people with antisocial personality disorder, typically found among criminals, spotted an 18% decrease in the volume of the brain’s middle frontal gyrus, associated with decision making, and a 9% decrease in the volume of the orbital frontal gyrus, associated with both decision making and sensitivity to punishments and rewards [3]. These studies demonstrated that a smaller volume of the brain in the amygdala or the frontal gyrus occurs more frequently in humans with psychological disorders. Thus many have concluded that criminals tend to have a higher likelihood of showing these characteristics. graphic by megan chang

edited by selena chen

There has also been speculation regarding the future of the justice system [4]: would, and should, criminals whose brain scan images show abnormalities be given an alternate to serving their sentence? One example is the case of a man named Herbert Weinstein who was found guilty of killing his wife in 1991. Brain scans showed a large cyst in his frontal cortex which ruined his cognitive abilities, and as a result, his sentence was reduced [3]. It has been adequately shown that many criminals are indeed born with a brain which differs from that of a “normal” individual. A few people have already proposed and evaluated solutions to the “condition” of being born with an abnormal brain. One scientific team has found that the cerebral circuits responsible for empathy and violence are very similar and even overlap at some points, so increasing stimulation and activity in one area may reduce activity in the other area. As a result, encouraging empathy may reduce violence [5]. Nathalie Fontaine, a criminologist from Indiana University, has suggested implementing intervention and support systems in children who have been identified with risk factors early on [3]. While such measures may be seen as a means of preventing children from eventually becoming criminals, they have also raised concerns about the ethics of intervening so soon, before more accurate conclusions can be drawn. Moreover, despite all of the findings claiming that characteristics of the brains of criminals are different from those of non-criminals, Stanford University’s Hank Greely argues, “… that’s fine that you found this person has an abnormal brain – but how many other people have similar abnormalities and don’t commit crimes? The answer will be: quite a few”[6]. A growing number of studies have shown that criminals may have differences in their brains that other humans do not. As a result, it is quite possible that criminals with atypical brains may be shown sympathy by some rather than being punished for their actions. These discoveries have the potential to make a great impact on future lifestyles and attitudes toward crime. Meanwhile, skeptics have laid out some tough queries which hold back the implementation of this newfound knowledge and technology in the justice system, as well as solutions to helping change the paths of individuals who are categorized as “risks.” Only time and more proof will conclusively determine whether criminals make conscious decisions that define their identities, or if their fate is set in stone the moment they enter the world, and they are really “born this way.” Works Cited

1. Parry, W. “Inside the Brains of Psychopaths.” Live Science. (2011). 2. Lerner, E. “Neurocriminology: How Early Can We See a Brain Basis for Crime?” (2011). 3. Moskowitz, C. Criminal Minds Are Different From Yours, Brain Scans Reveal. Live Science. (2011). 4. Juan, S. The Odd Brain: Mysteries of Our Weird and Wonderful Brains Explained (Andrews McMeel Pub., Kansas City, 2006). 5. “Empathy and Violence Have Similar Circuits in the Brain.” (2011). 6. “Stanford’s Hank Greely Puts Neuroscience on Trial.” http://esciencenews. com/articles/2010/02/20/stanfords.hank.greely.puts.neuroscience.trial (2010).


Journal of Youths in Science

STAFF LIST President: Rebecca Su (Torrey Pines) Chapter President: Angela Wang (Westview), Elizabeth Brajevich (Beverly Hills), Kenneth Xu (Scripps Ranch) Vice President: David Koh (Scripps Ranch), George Bushnell (Scripps Ranch), Kevin Li (Westview), Melodyanne Cheng (Torrey Pines), Myung-hee (Rachael) Lee (Torrey Pines), Parul Pubbi (Torrey Pines), Sarah (Hye-In) Lee (Torrey Pines), Sharon Peng (Torrey Pines), Yuri Bae (Torrey Pines) Staff Advisor: Mr. Brinn Belyea Treasurer: Avinash Chaudhary (Torrey Pines), Eden Romm (Torrey Pines), Jim Liu (Scripps Ranch), Keming Kao (Westview) Secretary: Alwin Hui (Scripps Ranch), Claire Chen (Torrey Pines), Karina Lin (Westview), Maarya Abbasi (Torrey Pines), Selena Chen (Torrey Pines) Scientist Review Board: Amiya Sinha-Hikim, Andrew Corman, Brooks Park, Bruno Tota, Craig Williams, Dave Ash, Dave Main, David Emmerson, Dhananjay Pal, Gautam Narayan Sarkar, Hari Khatuya, Indrani Sinha-Hikim, Janet Davis, Julia Van Cleave, Karen B. Helle, Kathryn Freeman, Katie Stapko, Lisa Ann Byrnes, Maple Fang, Mark Brubaker, Michael Santos, Reiner Fischer-Colbrie, Ricardo Borges, Rudolph Kirchmair, Sagartirtha Sarkar, Sally Nguyen, Samantha Greenstein, Saswati Hazra, Sunder Mudaliar, Sushil K. Mahata, Tania Kim, Tanya Das, Tapas Nag, Tita Martin, Tracy McCabe, Trish Hovey SRB Student Coordinator: Sumana Mahata Contributing Authors Alex Jen, Amy Chen, Apoorva Mylavarapu, Cindy Yang, Daniella Park, Emily Sun, Fabian Boemer, Frances Hung, Gaylen Bradley, Gha Young Lee, Harshita Nadimpalli, Hope Chen, Jeffrey Coleman, Kenny Xu, Madeline Pesec, Matthew Paddock, Mikhail Solovykh, Negin Behzadian, Rachael Lee, Sarah Bhattacharjee, Sarah Lee, Varun Bhave, William Hang. Web Design Alice Fang (Stanford), Tiffany Sin (Torrey Pines), Tushar Pankaj (Westview) Blog Editor Marina Youngblood Assistant Blog Editor Shannon Lee Comics Editor Choohyun (Kristine) Paik Assistant Comics Editor Lucy An Photography: Kevin Tong, Benjamin Pu For full list of staff and chapter members, please see

Volume 4, Issue 2. 2012

Editor in Chief: Angela Zou (Torrey Pines) Managing Editor: Carolyn Lee (Westview), Fabian Boemer (Scripps Ranch), Michelle Banayan (Beverly Hills) Assistant Editor in Chief: Apoorva Mylavarapu (Torrey Pines), Sarah Bhattacharjee (Torrey Pines) Design: Eric Tang (Torrey Pines), Grace Chen (Torrey Pines), Heather Chang (Torrey Pines), Sophie You (Torrey Pines), Yang Li (Torrey Pines) Graphics Manager: Wenyi (Wendy) Zhang (Torrey Pines) Senior Editor: Bethel Hagos (Torrey Pines), Christine Li (Westview), Florine Pascal (Torrey Pines), Jimmy Huang (Westview), Margaret Guo (Torrey Pines), Michelle Oberman (Torrey Pines), Nathan Manohar (Torrey Pines), Ruochen Huang (Torrey Pines), Sarah Hsu (Torrey Pines), Sarah Watanaskul (Torrey Pines), Snow Zhu (Westview) Physics Editor: Ethan Song (Torrey Pines), Harrison Qi (Westview), Rekha Narasimhan (Torrey Pines) Chemistry Editor: Daniel Guan (Westview), Hyeimin (Lucy) Ahn (Torrey Pines), Nandita Nayyar (Torrey Pines), Rebecca Kuan (Torrey Pines) Biology Editor: Amber Seong (Torrey Pines), Anita Dev (Westview), Brandon Huang (Westview), Eva Lilienfeld (Torrey Pines), Serin You (Torrey Pines) Editor: Achi Mishra, Achinthya Soordelu , Alex Jen, Alwin Hui (Scripps Ranch), Anvesh Macheria (Scripps Ranch), Austin Su (Scripps Ranch), Caleb Huang (Scripps Ranch), Daniella Park, David Boemer (Scripps Ranch), David Koh (Scripps Ranch), Eric Tang, Frances Hung, Frank Pan, George Bushnell (Scripps Ranch), Hannah Tang (Westview), Jenny Li, Jim Liu (Scripps Ranch), Joy Li, Leonard Chen, Keming Kao (Westview), Kenneth Xu (Scripps Ranch), Michael Do (Scripps Ranch), Michael Zhang (Westview), Nick Wu (Westview), Selena Chen, Sharon Liou (Westview), Taylor Shaw (Beverly Hills), Wenhao Liao (Scripps Ranch), William Huang (Scripps Ranch), Zachary Fouladian (Beverly Hills) Assistant Editor: Ahmad Abbasi, Anita Chen, Emily Sun, Eric Chen, Hope Chen, Maggie Zhang, Pranav Perimbeti, Sarah Lee, Shayun Pedram Graphics Editor: Crystal Li (Torrey Pines) Contributing Graphic Designers Aisiri Murulidhar, Amber Seong, Amy Ng, Angela Wu, Apoorva Mylavarapu, Cassie Sun, Cindy Yang, Crystal Li, Danielle Watson, Eric Tang, Eun jin Kim, Ginelle Wolfe, Haiwa Wu, Jennifer Fineman, Joy Li, Julia Yang, Katherine Luo, Kerry Luo, Mahama Avanti, Mandy Wang, Megan Chang, Melinda Wang, Michelle Oberman, Rebecca Wang, Sarah Bhattacharjee. Stephanie Yuan, Tenaya Kothari. 35


2012 36

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