volume x ix issue í î ì í ñ - bronx high school of ... 2015...receptors (1). the synapse is...
TRANSCRIPT
VOLUME XCIX | ISSUE 1 | 2015
AL
SO
IN
TH
E
J
OU
RN
AL
SPECIAL FEATURE The Year in Biology FEATURED STUDENT RESEARCH
Spinal Pulse Inducing Neuro-Electric Stimulator S.P.I.N.E.S. (Bionic Spine Connector)
Neuroscience
2
"The brain is the organ of destiny. It holds within its
humming mechanism secrets that will determine the future of the human
race."
Quote by Wilder Penfield , Penfield, W. (1963). The Second Career.
Boston: Little, Brown.
3
Volume XCIX
2015
SENIOR STAFF Betty Chen ‘15 Jessica Ho ‘15 Yiwen Huang ‘15 Tangirul Islam ‘15 Jiayi Lily Ma ‘15 Keti Vaso ‘15 Aaron Zhang ‘15
JUNIOR STAFF
Crystal Wu ‘16 Yan Zhang ‘16 FACULTY CONSULTANT
Erin O’Leary, PhD
THE BRONX HIGH SCHOOL of SCIENCE
75 West 205th Street
Bronx, New York 10468 Telephone: (718) 817 -7700
Fax: (718) 733 -7951 www.bxscience.edu
JEAN M. DONAHUE, PhD
Principal
ALLISON WHEELER, PhD Assistant Principal
The Journal of Biology is published annually by
the students of the Bronx High School of Science
4
It can be said that neuroscience is the central science, with the central nervous
system and the vast, interconnected network of the peripheral nervous system (PNS)
containing billion of neurons. Billions of neurons are firing away right now. They con-
duct messages between sensory neurons, inter-neurons, and motor neurons to elicit
what we might perceive as simple responses that range from lifting an arm, to moving
your leg, to creating feelings of joy and anger, and to controlling the beating of your
heart. Neuroscience, therefore, is in no way a simple science. It is an intricate science
that today, still remains enigmatic to the best scientists around the world. How does the
brain enable individuals to form dreams, hopes, and nightmares? How does the circuit-
ry of the brain contribute to the development of diseases and mental conditions? How
is the brain influenced by our environment? How does neuroscience influence who we
are as a person and our lifestyle? As important discoveries are made in neuroscience,
we are learning more about our brain, our mind, and ourselves.
What is Neuroscience ?
by Jessica Ho „15
Co
mm
enta
ry
5
The Table of Contents
I. Overview of the Brain Tangirul Islam- Page 6
II. Interview: Dr. Gensert
Keti Vaso and Yiwen Huang - Page 8
III. Neuroplasticity Jiayi Lily Ma - Page 12
IV. “Bak Yeh”
Betty Chen - Page 15
V. Effect of Sleep Deprivation on Adolescent Brain and Behavior Keti Vaso- Page 17
VI. Effect of Drugs on Brain
Tangirul Islam - Page 19
VII. What is schizophrenia, what underlies its etiology, and what are its current cases and research?
Jessica Ho-Page 21
VIII. Amnesia: Memory Loss Crystal Wu-Page 23
IX. Brain Tumors: The Facts and the Problems
Aaron Zhang- Page 25
X. Featured Student Research: Spinal Pulse Inducing Neuro-Electric Stimulator (S.P.I.N.E.S.) (Bionic Spine Connector)
Page 28
XI. Student Research Abstracts - Page 36
XII. Award Winners in Biology - Page 51
6
The brain is the focal point of all neu-
rological activity, averaging 3 pounds and con-
trolling all conscious and unconscious deci-
sions. The brain is what makes us human be-
cause it enables us to read, write, speak, think
rationally and so much more. Every time we
walk, raise our hands, or turn our heads, it is
our brain that is both simultaneously compre-
hending information from the environment and
sending messages throughout the body to react
to the environment.
You may wonder what enables the
brain to perform all of its intricate tasks. The
brain contains a hundred billion nerve cells
called neurons, which are electrically excitable
cells that process and transmit information
through electrochemical signals. Three major
types of neurons are motor, sensory and inter-
neurons. Motor neurons control muscle move-
ment and sensory neurons carry messages from
the outside of your body such as your skin and
send it to your central nervous system. For ex-
ample, your motor neurons are responsible for
your reflex when your hand moves to touch a
hot object and your sensory neurons are used
to tell you that the object is hot, which then
causes your hand to jerk away. This reaction is
called a reflex. The neuron is made up of an
axon that is covered in a myelin sheath. This
myelin sheath consists of fat and protein that
speeds up the movement of the message be-
tween neurons, through a small gap known as
the synapse. Dendrites finally connect the neu-
ron to another neuron and the process contin-
ues as such (1).
In the most general terms, the brain is
made up of the cerebrum, brain stem, thalamus
and hypothalamus. The cerebrum is the largest
part of the brain responsible for controlling
intelligence judgement and voluntary activities
such as moving your shoulders up when you
don‘t know something. In the back of the skull
lies the cerebellum, the second largest region
of the brain that is responsible for balance in
the body (3). The brain stem serves as the inter
connecting region of the brain that connects
the brain and the rest of the spine and central
nervous system for the purpose of regulating
the flow of information between the brain and
the rest of the body (2). It also regulates blood
pressure, heart rate, breathing and swallow-
ing.The thalamus internally receives messages
from the sense organs such as the cerebrum.
These messages are subsequently sent to the
cerebrum in order to be interpreted. The cere-
brum controls voluntary actions which is the
reason humans can do hard math problems or
kick a soccer ball (4). The hypothalamus is the
control center for recognition and analysis of
hunger, thirst, fatigue anger and body tempera-
ture.
Figure 1. A message goes to the axon terminal through
the synapse onto another neuron picked up by dendrites.
The messages goes from the terminal bud and then through the axon and in the synapse where they attach to
receptors (1). The synapse is located between the den-
drites and the previous axon terminal (2).
In order to perform everyday functions
such as running, the brain must have some type
of protection, and it does! The skull covered by
layers of membranes called meninges (1). Me-
ninges protect the brain from rubbing against
Overview of the Brain By Tangirul Islam ‗15
AR
TIC
LE
Neuroscience: Overview of the Brain
7
the bones of the skull and spine. Furthermore
the brain and spinal cord have cerebrospinal
fluid which aids in protecting the brain from
damage during accidents such as getting hit on
the head by a basketball (4).
Development of the Brain
The first part of the brain that develops is the
brainstem and midbrain which is the top and
middle portion of the brain. These regions are
significantly responsible for autonomic func-
tions such as digesting food in your stomach or
regulating hormones (4). When a baby is born,
the lower portions of the nervous system must
be well developed before the higher regions.
For humans, newborn babies develop the high-
er portions of their brain after birth (2). The
higher portion of the brain controls emotions
language and abstract thought. Each region
manages its assigned function through process-
es with chemical messenger. (neurotransmitters
and hormones) to transmit info throughout the
body and the rest of the brain.
Conclusion
The inner mechanisms of the brain are very
complex. Neurologists have spent many years
to figure out how it works. The brain is respon-
sible for a persons personality, memory, move-
ment and senses. Thanks to neuroscience re-
search, we are able to find out specifically
which part of the brain does what and how it
affects our lives. Our brain is like a computer
that controls every part of our body!
References:
1. David Borsook ( 2012, February. Neurologi-
cal Diseases and Pain Brain. National Geo-
graphic ; 135(2): 320–3
2. Clikeman Margaret. Research in Brain Func-
tion and Learning Retrieved from <http://
www.apa.org/education/k12/brain-
function.aspx>.
3. University of Michigan. "The Human Brain."
The Human Brain. N.p., n.d. Web. 01 Jan.
2014.
4.Helen Philips. (2006) The Human Brain.
NewScientist.
Neuroscience: General Overview of Brain
Figure 2: As shown in the diagram above, the forebrain,
midbrain and the hindbrain are developed first for babies.
8
Interview Conducted by Keti Vaso ‘15 and Yiwen Huang ‘15
SP
EC
IAL
FE
AT
UR
E
9
Dr. JoAnn Gensert:
Q. Please introduce yourself and talk about your position here at Bronx Science
A. My name is JoAnn Gensert, and I‘m at Bronx Science as a biology teacher. I teach research
projects, AP Biology, and Research Literacy.
Q. What did you do before coming to Bronx Science?
A. I was a research scientist. I got my doctorate at Columbia University Medical Center. I did a
post doc and fellowship at NYU School of Medicine. I was also on the faculty at Cornell and I
worked at a research institute as well.
Q. What were you studying during college?
A. Biochemistry. I did research as an undergrad as well. My research as an undergrad involved
examining the function of the 5‘ planking region of the estrogen gene. It had to do with manipu-
lating a particular region of the DNA for a gene that encodes for a hormone.
Q. We heard from Dr. O’Leary that you were involved with neurobiology. Could you tell
us a little bit more about that?
A. Certainly. I did my doctorate in the lab of the director of neuropathology at Columbia. My
research is specifically in rodents, but it applies to mammals. I was the first one to identify that
proliferating cells that persist in adult mammals are able to be stimulated to differentiate into a
cell type called an oligodendrocyte. Oligodendrocytes actually myelinate the neurons. So, these
immature dividing cells that are in the adult brain, even in your brain, are able to be induced to
become oligodendrocytes and to repair lesions. The type of lesions that they can repair are those
seen in diseases like multiple sclerosis. Multiple sclerosis is a disease of the brain. For example,
when you touch something hot, your brain will tell you that ―Its hot! Its hot!‖ And the brain will
say ―Pull your hand away,‖ and a healthy person will pull his/her hand away hard. In multiple
sclerosis, then this breaks down so the message doesn‘t go through completely, and the person
can‘t pull their hand away as a reflex. These cells are actually in the brain so you don‘t have to
put any cells into the person and there‘s no rejection issues; they‘re already there. So we labeled
these oligodendrocytes so we created a lesion and we showed that these oligodendrocytes were-
able to repair the induced lesion. Oligodendrocytes make myelin, and myelin covers the neuron
so that the message can travel long distances.
Interview with Dr. JoAnn Gensert
10
In conclusion, we showed that these cells in the brain could differentiate and mature into
oligodendrocytes. They could repair lesions in a therapeutic approach. Naturally in cross-
sections of post-mortem brain tissues there might be myelin on the axon like a swirled lollipop.
However in MS brain, there is some myelination, but it is not as thick with not as many swirls.
Q. What kind of implications do you think your research could have in medicine or the
future?
A. My research employs a more therapeutic approach to MS but it is not a cure. It is a method
used to enhance lesion repair so that a person would be able to regain some functions, or not
lose function as quickly. However, the actual signals that cause the progenitors to mature into
oliogodentrocytes are unknown. And so, these signals must be identified.
Q. What made you interested in this topic?
A. I love glia. There are many different types of glia, mainly micro and macro glia. Macro glia
consists of astrocytes and oligodendrocytes, and hold the brain together. It these weren‘t in your
body, your brain would just mush and drip out of your nose. When I first started, I did a project
in a lab involving glia, and I am passionate about glia. Everybody thinks that the brain is just
composed of neurons, but glia are also present in neurons and allow signals to travel long dis-
tances. Astrocytes put their endfeet around a synapse to protect the communication between one
neurons.
Q. More generally, how did you become interested in the field of neurobiology?
A. I have always been interested in science. I‘ve always been interested in asking questions and
trying to understand how things work. As an undergrad I didn‘t do neuro initially as I did re-
search that was more molecular in nature. I love cells and love working with whole animals be-
cause you can see the effect. I don‘t know for sure why it‘s neuro, but I know it is my passion.
Q. What was your favorite part about being involved in neurobiology?
A. Discovering something in neuroscience could make a difference in peoples lives. My thesis
advisor and I had the opportunity to do things such as brain sectioning. Columbia has a brain
bank where the brains are cut in half. One half is frozen and the other half is fixed in+ para-
formaldehyde. Some diseases are identified post mortem only, although the symptoms may
point to a disease before a person passes away, you have to cut the brain and look to verify the
disease. The other thing I liked is that if there was a certain incident where the physicians were
removing a tumor, for example, my mentor would have to go while the person was still being
operated on, my mentor would have to go and section the pieces of the tumor removed to get
the edges. That is exciting to me, and I think it‘s a lot of fun. The other thing I liked that I
worked on in terms of neuro was we showed that someone did a comparison of a type of brain
tumor which is glioma and normal astrocytes. And when they did that comparison, they pulled
out a couple of molecules that are expressed in one part but not expressed in another.
11
I looked at a couple of these molecules and based on DNA structure, we proposed that it may
respond to certain really cheap drugs to cause the gene to be re-expressed. And when we re-
express the molecule that was in one part but was missing in the tumor, the tumor stopped di-
viding and stopped moving around. So that can also be a possible therapeutic treatment. And
that‘s exciting, because to me, you take the logic, look at system, you apply simple biological
concepts, ask the right questions and do the right experiments to come up with answers that can
change the lives of people.
Q. How did you end up from researching neurobiology to teaching at Bronx Science?
A. I‘ve always been a teacher. I‘ve taught Sunday school, I‘ve coached volleyball on a high
school and college level, I‘ve taught swimming and tennis from when I was in high school all
the way up, and so I‘ve always been a teacher. I love teaching, and believe it or not, I love kids,
including high school kids. I wanted to apply what I know to a different type of atmosphere and
environment.
Q. Do you have any advice for students who may be interested in pursuing neuroscience in
college?
A. Start learning basics as early as you can. There are many students who come up to me and
say they‘re interested in neuroscience and biology, but they don‘t understand how a neuron
functions, and that is just part of the basics. There are so many things online that you can ac-
cess, or get a good neuroscience book and just go through it. So my advice would be to start
learning and to read as early as you can, because who knows, somebody who‘s interested in
neuroscience and research can be one of you guys to discover the cure for MS, for example.
The cure is coming from you, young people.
12
Neuroplasticity
For decades, neuroscientists believed
that the functions carried out by specific re-
gions of the brain are fixed; any incidents of
brain change or recovery were considered ex-
ceptions.(1) However, during the 1970‘s and
80‘s, scientists changed their conventional
view of the brain and accepted neuroplasticity
as an important characteristic of this vital or-
gan.
Neuroplasticity is the ability of neurons
and neural networks in the brain to change
their connections and behavior in order to ad-
just to new information, sensory stimulation,
development, damage or dysfunction.(1) Neu-
ral networks exhibit modularity and carry out
specific functions. Nevertheless, they can di-
verge from their regular functions and reorgan-
ize themselves when necessary.(1)
Rapid alterations or reorganization of
the brain‘s neural networks can happen in
many forms and under many circumstances.
During developmental plasticity, neurons in
the young brain branch out quickly and form
synapses. Some of these synapses are strength-
ened while others are weakened as the brain
begins to process information. In a process
called synaptic pruning, unused synapses are
eliminated, leaving behind efficient networks
of neural connections.(1) Other forms of neu-
roplasticity that are induced by various circum-
stances have a similar mechanism as the one
described above. These circumstances include
physical changes of the body; for example, the
loss of a limb or sense organ.(1) In addition,
the brain employs neuroplasticity during the
reinforcement of sensory information gathered
through activities such as learning.(1)
Adult Neurogenesis
The ability of the adult mammalian
brain to generate new neurons from neural
stem cells and progenitor cells in a process
called neurogenesis is one of the most fascinat-
ing examples of neuroplasticity.(2) Neurogene-
sis has sparked new interest in stem cell re-
search because of the possibility to discover
ways to enhance the regeneration of neurons in
adults who suffer from neurological disease
and impairment, stroke, and depression.
For years, scientists believed that cer-
tain cells in the body, such as brain cells, were
nonrenewable. However, many later studies
indicated that these cells can be regenerated
from stem cells that exist throughout life. In
the 1960s, Joseph Altman reported the first
evidence of adult neurogenesis in rats. (3) Yet,
the idea of adult neurogenesis wasn‘t widely
accepted until the 1990s, when researchers
found self-renewing neural stem cells that
could give rise to new neural cells in the sub-
ventricular zone of the lateral ventricles and
the subgranular zone of the hippocampal den-
tate gyrus.(3)
Similar to the neurogenesis process
during development, adult neurogenesis in-
volves a multistep process that includes cell
proliferation, cell cycle exit, a choice between
survival and death, cell migration, cell differ-
entiation, and cell-fate decisions.(4) Despite
this similarity, there are several significant dif-
ferences between the two. The most important
difference is that adult neurogenesis creates
fewer proliferating cells and produces limited
Neuroplasticity By Jiayi Lily Ma ‘15
A
RTI
CLE
Neuroscience: Neuroplasticity
13
neuronal cell classes.(4) The cause of the adult
neural stem cells (NSC) to have a more re-
stricted neurogenic potential could be the mi-
croenvironment or the ―niche‖ of these cells.
During development, embryonic NSCs origi-
nate from radial glia and neuroepithelial cells
lining the neural tubes. Adult NSCs, however,
come from the embryonic neuroepithelial radi-
al glia, with a subset of cells found in highly
specialized regions of the brain such as the
subgranular zone and subventricular zone. (3)
Implications of Adult Neurogenesis in Various
Diseases and Disorders
Adult neurogenesis is affected by brain
injuries and neurological diseases and disor-
ders such as traumatic brain injury and ischem-
ic stroke. Neurodegenerative diseases like Alz-
heimer‘s and Parkinson‘s diseases; demye-
linating diseases like multiple sclerosis; epilep-
sy and seizure; and psychiatric disorders such
as depression also have an impact on adult
neurogenesis.(3) The following explores sever-
al of these diseases and disorders and how they
are connected with adult neurogenesis.
Brain Injury Traumatic brain injury (TBI) occurs
when sudden trauma causes brain injury. Gen-
erally, TBI leads to neuronal loss and neuro-
logical deficits, especially in hippocampus-
dependent cognitive functions.(3) Many ani-
mal studies of both focal and diffuse TBI indi-
cate that neurogenesis is increased in the sub-
granular zone (SGZ) of the dentate gyrus and
the subventricular zone (SVZ) of the lateral
ventricles after TBI.(3) However, whether neu-
rogenesis contributes to the recovery process
after TBI is another question. Stroke, a leading
cause of death in humans, occurs because of
ischemia blockage or hemorrhage to the brain.
Studies have shown that focal or global ische-
mia could induce neurogenesis in adult rats
and monkeys. Researchers have also demon-
strated functional neurogenesis in the hippo-
campus and discovered that ―newborn‖ neu-
rons in the SVZ migrate to the damaged cor-
tex. (3) Despite these findings, the specific role
that ischemia-induced neurogenesis plays in
the recovery process remains unknown.
Alzheimer's disease (AD)
AD is a progressive neurodegenerative disease
of the central nervous system; the main feature
of AD includes the accumulation of plaques
and tangles in the brain, especially in the hip-
pocampus. Another characteristic of AD is the
loss of connections between neurons.(5) The
role that neurogenesis plays in AD is ambigu-
ous and complicated. In some animal model of
AD, increase in hippocampal neurogenesis is
reported.(3) Other evidence has indicated the
opposite, however. An important characteristic
of AD is the reduction of overall cholinergic
signaling. The loss of cholinergic signaling has
been shown to decrease adult neurogenesis in
the hippocampus and olfactory bulb.(3) On the
other hand, treatment with cholinergic drugs
that increase cholinergic signaling has been
found to induce neurogenesis.(3)
Amyotrophic Lateral Sclerosis (ALS) ALS is a fatal, progressive neurodegen-
erative disease that affects neurons and the spi-
nal cord. It causes rapid muscle weakness, dis-
ability, and ultimately, death.(6) There is an
increase in progenitor cell proliferation, migra-
tion, and neurogenesis in mice with a mutation
of superoxide dismutase 1, a mutation found in
rare familial patients with ALS.(3)
The neurodegenerative diseases de-
scribed above influence both adult neurogene-
sis and neural plasticity. The genes that are of-
ten involved in these diseases (Parkinson‘s dis-
ease and Alzheimer‘s disease) seem to play a
key regulating role in adult neurogenesis, too.
(3)
Major Depression Disorder (MDD)
MDD is a psychiatric disorder that
causes low mood, low self-esteem, and a loss
of interest in activities that are usually enter-
taining.(3) In 2000, researchers suggested that
depression is linked to impaired adult neuro-
genesis. Many experiments have both support-
ed and opposed this hypothesis. Patients with
chronic MDD usually have smaller hippocam-
Neuroscience: Neuroplasticity
14
pi. The high stress and cortisol levels usually
experienced by people with MDD have been
shown to decrease adult hippocampal neuro-
genesis.(3) Conversely, antidepressants in-
crease cell proliferation in the adult hippocam-
pus. Recent findings suggest that impaired
adult neurogenesis affect MDD patients; nev-
ertheless, MDD is not completely caused by
weakened neurogenesis. (3)
Treatments Involving Adult Neural Stem Cells
Adult neural stem cells (NSCs) are
multipotent cells that have the ability to self-
renew. It has been found that adult mammalian
NSCs can give rise to functional neurons and
glia.(3) Although it is known that adult neuro-
genesis plays a key role in maintaining homeo-
stasis and contribute to the plasticity of the
central nervous system (CNS), scientists are
still investigating the specific role that adult
neurogenesis plays.
Adult neurogenesis seems to help to
repair the CNS after a brain injury or disease.
Acute brain damage usually causes an accrue-
ment of cell proliferation temporarily; chronic
brain damage, however, leads to a decrease in
adult neurogenesis overtime.(3) Studies have
indicated that in rats, NSCs are responsible for
replacing dying neurons caused by direct inju-
ry or ischemic stroke.(3) In addition, in many
seizure models and neurodegenerative diseases
such as Alzheimer‘s Disease (AD) and Hun-
tington‘s Disease (HD), cell proliferation and
neurogenesis seems to escalate initially at the
sites of damage.(3) In patients with neuro-
degenerative disorders, an increase in neuro-
plasticity is also found.(3) Thus, treatments
involving NSCs may be the cure for many neu-
rological disorders.
Currently, there are two such NSC-
based treatments: Transplantation of exoge-
nous neural stem or progenitor cells and stimu-
lation of endogenous neural stem or progenitor
cells.(3)
Scientists have found some degree of
success transplanting fetal neuronal precursor
cells to animals with spinal cord injury, TBI,
Parkinson‘s Disease (PD), and spinal muscular
atrophy. But when similar transplanting is ap-
plied to humans with PD or HD, mixed results
were found.(3) The transplanting of adult neu-
ronal precursor cells has also been tested.
When adult spinal cord stem cells were trans-
planted locally into the adult dentate gyrus in
rats, the generation of new neurons was ob-
served.(3) Despite these discoveries, neuro-
transplantation of adult or embryonic stem/
progenitor cells in humans still present chal-
lenges to neuroscientists due to issues such as
improper delivery and migration, mass effect
and cell death, cell manufacturing problems,
tumor formation, and adverse immune system
interactions.(3)
Another promising way of treating neu-
rological disorders or diseases is the stimula-
tion of endogenous neural stem or progenitor
cells. Active adult neurogenesis is mostly con-
fined in the SGZ and SVZ regions of the brain;
however, incidence this process is also found
throughout the CNS.(3) Consequently, recruit-
ing and activating these endogenous cells
could induce regeneration and healing in in-
jured or diseased CNS.(3)
Conclusion
Many cells in the body have the ability
to repair and self-renew because of stem cells
and of various regulating mechanisms.(3)
Since the brain can regenerate, it may be possi-
ble in the future to use NSC-based therapy to
cure neurological diseases like AD and brain
injuries.
References: 1. Rugnetta, M. (2012). Neuroplasticity. In Britannica.
Retrieved September 5, 2013
2. Gage, F. H., Kempermann, G., & Song, H.
(2008). Adult Neurogenesis. (p. blurb). Cold Spring Har-
bor, NY: Cold Spring Harbor Laboratory Press. Re-
trieved September 6, 2013
3. Doze, V. A., & Perez, D. M. (2012, July). G-Protein-
Coupled Receptors in Adult Neurogenesis [Electronic
version].Pharmacological Reviews, 64(3), 645-675.
doi:10.1124/pr.111.004762
4. Gage, F. H., Kempermann, G., & Song, H.
(2008). Adult Neurogenesis (p. 7). Cold Spring Harbor,
NY: Cold Spring Harbor Laboratory Press. Retrieved
September 6, 2013 In National Institute on Aging. Re-
trieved September 5, 2013
Neuroscience: Neuroplasticity
15
Bak Yeh (Uncle)
I've always wondered deep inside
how you've managed to stay so kind.
Your passion to learn,
to laugh and
to stay firm,
is definitely a mentality that many can learn from.
Although we're many miles away,
and our visits have been timed,
each visit has surely been infinitely sublime.
The things that you have shown me though are beyond the depths of this rhyme.
You've taught me to stand strong,
to know no limits
and to be wrong.
You've truly defined the quote,
"It's not about the cards you're dealt,
but how you play the hand."
You chased after your education
and worked hard conducting your job.
After many years of toil, you've finally made it to the top.
You've gone above and beyond your possible limits,
all the while,
staying vivid.
Over the years, your health has greatly deteriorated.
But you're still very much extraordinarily bold.
As this poem is drawing to a close,
one thing is for sure,
ALS may be within you,
but it will surely
never define you.
Written by Betty Chen ‘15
16
Figure 1. Normal nerve cell vs ALS nerve cells.
Amyotrophic lateral sclerosis (ALS), often also known as "Lou Gehrig's Disease‖, is a progres-
sive neurodegenerative disease that targets nerve cells in the brain and the spinal cord. Motor
neurons spread from the brain to the spinal cord and then to the muscles in the body. When these
motor neurons begin to degenerate, they are then unable to send impulses to the muscle fibers
which would normally cause muscle movement. As a result, the brain is unable to initiate and
control muscle movement. Patients in the later stages of this disease are often paralyzed. Howev-
er, the current cause of this disease is unknown.
Symptoms of ALS include increasing muscle weakness, especially in the arms and legs,
and inhibited speech and breathing. This may lead to difficulty in projecting one's voice, as well
as twitching and cramping of muscles in hands and feet. Limbs also begin to look "thinner" as a
result of muscle tissue atrophies, which is when the muscle tissues decrease in size since they are
unable to receive messages from the motor neurons.
In order to diagnose someone with ALS, a list of cumulative tests must be done, includ-
ing a spinal tap, x-rays, muscle/nerve biopsy, etc. There is not one specific test or procedure to
diagnose one with ALS. Many who do develop ALS are between the ages of 40 and 70, but there
are also cases in those who are in their twenties and thirties. Once diagnosed with ALS, half of
all people affected live at least three years or more. Twenty percent live at least five years and
ten percent live more than ten years.
Although there is currently no cure for this disease, there is an FDA approved drug
known as Riluzole which shows clinically that it slows the progression of ALS.
Neuroscience: ALS Disease
Neuroscience: ALS By Betty Chen ‘15
17
Bronx Science is arguably one of the
most widely known high schools in New York
City. Nearly everyone who‘s heard of it is
aware of how hard working and motivated all
of the students in our school are. But the public
is not entirely familiar with a fact more widely
known among the students in our school: many
Bronx Science students suffer from lack of
sleep. But are those two hours of sleep lost to
cram for an upcoming test really beneficial in
the long run? Sleep deprivation is thought to be
undermining teenagers‘ health as it has nega-
tive effects on the developing brain which, con-
sequently, affects how teenagers behave. Not
only is it becoming a rising issue for students in
Bronx Science, but also for high school stu-
dents all around the nation. According to the
National Sleep Foundation, teenagers in Ameri-
ca are advised to sleep 9 hours every night. But
a follow up study published in the Journal of
Adolescent Health reveals that only 8% of
teenagers in America are receiving the required
amount of sleep. (1) Even more shocking is the
fact that as many as two thirds of American
teenagers get, on average, 7 hours of sleep or
less. (2) But how can we stop this rising issue?
In order to answer that question, the effects of
sleep deprivation must first be considered.
Sleep is crucial, especially for developing
teenagers, to provide rest for the brain and en-
sure it works optimally. The effects of sleep
can be considered in relation to the cerebral
cortex. For example, the temporal lobe of the
cerebral cortex is associated with the process of
language. MRI scans on subjects who are fully
rested reveal very active brain activity in this
region. (3) However, in sleep deprived sub-
jects, MRI scans have shown very little to no
activity occurring in the temporal lobe. These
effects on the cerebral cortex are seen to greatly
impact behavior as well. The inactivity in the
temporal lobe is thought to be associated with
the fact that, after verbal learning tests, sleep
deprived subjects were seen to exhibit slurred
speech patterns, as opposed to the normal
speech patterns seen in the subjects who did
receive sufficient sleep.
Limited amounts of sleep not only af-
fect speech patterns, but also performance in
school. In an 1998 study conducted by psy-
chologists from the College of the Holy Cross
and Brown University Medical School, stu-
dents who reported lower grades (D‘s and F‘s)
were reported to receive 25 less minutes of
sleep when compared to students who reported
higher grades (A‘s and B‘s). (2) Furthermore, a
connection between sleep deprivation in teens
and decreased levels of human growth hormone
has been seen. This hormone is an essential
component to the physical growth, brain devel-
opment, and maturation of the immune system
in a teenager. (3) A study conducted in 2010 by
the journal, Sleep, revealed that teenagers who
stay up past midnight are 24% more likely to
Neuroscience: Sleep Deprivation
Effect of Sleep Deprivation on Adolescent Brain and Behavior
By Keti Vaso ‘15
A
RTI
CLE
18
suffer from depression and other psychological
disorders. (1) Lack of sleep can affect the deci-
sions that teenagers make. In order to cram for
tests or try to stay more alert, they may rely on
caffeine, energy drinks, as well as ampheta-
mines such as Adderall, which may have severe
neurologic and cardiovascular effects on a de-
veloping teen‘s body.
What steps can be taken to help increase
the amount of sleep for teens and decrease their
reliance on unhealthy habits to stay awake? It is
important that teens develop a schedule to
properly balance their school work and extra-
curricular activities, while fulfilling the neces-
sary nine hours of sleep every night. Routines
such as listening to soft music or reading, or
being in an optimal environment that is cool
and dark can help one fall asleep easily. Fur-
thermore, caffeine intake should be limited after
lunchtime. There is no set cut off time one
should stop taking caffeine, but it is recom-
mended that caffeine intake should be stopped
four to six hours before bedtime.
If more teenagers and parents become
aware of the serious health risks sleep depriva-
tion poses, then perhaps more steps can be tak-
en to ensure teenagers receive the amount of
sleep their body really needs.
References
(1) Strauss, V. (2012, March 10). Sleep deprivation and
teens: ‗Walking zombies‘. Washington Post. Retrieved
April 1, 2014, from http://www.washingtonpost.com/
blogs/answer-sheet/post/sleep-deprivation-and-teens-
walking-zombies/2012/03/10/gIQAr0QP3R_blog.html
(2) Carpenter, S. (2001, October 1). Sleep deprivation
may be undermining teen health. http://www.apa.org.
Retrieved March 31, 2014, from http://www.apa.org/
monitor/oct01/sleepteen.aspx
(3) The Effects of Sleep Deprivation on Brain and Behav-
ior. (n.d.). Serendip Studio. Retrieved March 30, 2014,
from http://serendip.brynmawr.edu/exchange/node/1690
Neuroscience: Sleep Deprivation
19
Have you ever wondered why drinking
an energy drink makes you wide awake? Have
you ever thought of the reasons that some drugs
put you sleep? Most drugs work by enhancing
or restricting the effects of natural chemicals in
your body. In fact, this is the way that energy
drinks, which can contain up to eighty milli-
grams of caffeine, work. Caffeine is a stimulant
contained in these drinks. Caffeine is chemical-
ly similar to a neurochemical called adenosine,
which functions by binding to receptors to
cause drowsiness. Caffeine, which neurons mis-
takenly identify as adenosine, enables caffeine
to bind to adenosine receptors. Since caffeine
has binded to all the available adenosine recep-
tors, adenosine is unable to bind to the surface
of neuron cells. The result is the feeling of alert-
ness that you get from energy drinks (4).
Some drugs can become addictive be-
cause they activate the brain‘s ―reward system‖.
The reward system in your brain releases a
chemical called dopamine from neurons called
the dopaminergic neurons found in the substan-
tia nigra. Dopamine is naturally released when
we do something that is pleasurable, such as
eating food or accomplishing something. Some
drugs increase dopamine release which leads to
addictions. For example, people can be addicted
to candy because of dopamine (1).
When you inhale the smoke of marijua-
na, chemicals such as tetrahydrocannabinol
(THC) travel to the brain through the blood-
stream and affect something called cannabinoid
receptors. Cannabinoid receptors affect your
physical and mental activities such as problem
solving, short term memory loss, coordinating
and learning. THC can affect the ability to carry
out these essential processes. Cannabinoid re-
ceptors are activated by a neurotransmitter
called anandamide, and THC, a cannabinoid
chemical, interferes with this interaction. THC
as a result of its similar chemical nature to
anandamide mocks the neurotransmitter. In-
stead of having anandamide bind to the canna-
binoid receptors, THC molecules bind to these
chemicals and cause the hazy and drowsy feel-
ing that marijuana users feel when they are
―high‖(2).
Neurotransmitters allows the neurons to
communicate. They fill in the gaps between
neurons and bind to protein receptors which al-
lows functions to be carried out and it allows
the body to be turned on and off (3). THC
blocks the neurotransmitters actions, thus creat-
ing difficulties in the functions that need to be
carried out by the body. Marijuana overac-
tivates the endo-cannabinoid system, which
heightens a person's appetite, pain sensation,
mood and memory.
Neuroscience: Effect of Drugs on the Brain
Effect of Drugs on the Brain By Tangirul Islam ‘15
A
RTI
CLE
20
Some drugs, such as medicines, are ben-
eficial for your health until over consumed.
Drugs usually enhance or block chemicals al-
ready inside your system, or can increase or de-
crease the levels of certain chemicals (4). This
can undeniably lead to catastrophic results to
your mind and body. So please, talk to your
doctor about drugs before taking them as they
may have potentially harmful side effects.
References (1) Vince, Gaia. (2005, December). Dopamine Blockers
Lead Faithful Voles Astray. NewScientist Retrieved from
http://www.newscientist.com/article/dn8412-dopamine-
blockers-lead-faithful-voles-astray.html.
(2) Frood, Arran. (2011, October).Drug Hallucinations
Look Real in the Brain. NewScientist,.
(3) Nutt, D. (2008). Drugs on the brain. Live Well. Re-
trieved June 12, 2014, from http://www.nhs.uk/Livewell/
drugs/Pages/Dodrugsdamagebrain.aspx
(4) Pubchem. Adenosine.. Retrieved June 12, 2014, from
http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?
cid=60961#x281
Neuroscience: Effect of Drugs on the Brain
21
Schizophrenia, literally meaning ‗split
mind‘, is a serious, chronic mental disorder that
affects approximately 1.1% of the population in
the United States. Schizophrenia most com-
monly develops in individuals who have
reached adulthood. Individuals diagnosed with
schizophrenia may find difficulties in maintain-
ing normal lifestyles and find it harder to inter-
act with others. In fact, those diagnosed with
schizophrenia might experience what research-
ers and medical doctors called positive and
negative symptoms. Positive symptoms include
delusions, withdrawal, disorganized behavior,
hallucinations, and abnormal perception of true
reality. The distinction between positive and
negative symptoms is that the former is primar-
ily associated with behaviors not seen in men-
tally healthy individuals while the latter is more
associated with disruptions of normal behavior.
As such, negative symptoms of schizophrenia
describe behaviors such as lack of drive or
pleasure in life, and withdrawal from associat-
ing with others; in fact, when approached by
others, schizophrenics tend to talk very little
and even if they do, they may do so with mo-
notony and with little emotion (called a ‗flat
effect‘). (1)
Paranoid, catatonic, disorganized and
residual schizophrenia are the four most promi-
nent subtypes of schizophrenia. As denoted by
its name, paranoid schizophrenia is identified
by a mistaken perception of reality, meaning
that a paranoid schizophrenic loses touch with
reality and begins to imagine things that are not
really there. Moreover, the term catatonia, de-
scribing a prolonged state of stupor, or motion-
lessness and observed in conditions like depres-
sion, is additionally characteristic of catatonic
schizophrenia. Catatonic schizophrenia is a less
common subtype of schizophrenia. Individuals
diagnosed with this type of schizophrenia expe-
rience vastly different episodes of emotions.
For instance, a catatonic schizophrenia may be
extremely silent, emotionless and catatonic one
moment and in the next, become extremely er-
ratic and disarrayed the next. These unpredicta-
ble episodes of behaviors, therefore, represent
the quintessential nature of catatonic schizo-
phrenia. The third subtype of the mental disor-
der is disorganized schizophrenia. Signs of this
subtype include disorganized thinking and
speech as well as the lack of facial expressions
during speech (called the ‗flat‘ or ‗blunted af-
fect‘) (1). Those with this chronic disorder may
find it readily difficult to organize their
thoughts and speech well enough and may ca-
priciously jump from subject to subject. When
speaking, they might do so in a monotonous
voice and a stolid expression without a hint of
emotion whatsoever.
Those with a history of schizophrenia,
but do not have current positive symptoms of
schizophrenia are said to have residual schizo-
phrenia.
What are the current views on the etiology of
schizophrenia?
There is a much higher prevalence of
schizophrenia in individuals with familial his-
tory of the disorder. Scientists currently believe
that molecular and biochemical imbalances in
the brain underlie the development of schizo-
phrenia. Research has dawned light on two par-
ticular types of neurotransmitters called dopa-
mine and serotonin, molecules that researchers
have learned to be essential to the normal func-
tioning of the brain. Dopamine is a neurotrans-
mitter secreted by the dopaminergic neurons in
the substantia nigra and has a crucial role in the
brain, regulating the reward and pleasure cen-
ters part of the limbic system, which include
the striatum. Dopamine transmits messages
from dopaminergic neurons to its target cells
by binding on their specific dopamine recep-
tors. The binding of dopamine regulates a
plethora of things such as physical movement,
emotions, alertness, pleasure, and memory (2).
Neuroscience: Schizophrenia
What is schizophrenia, what underlies its etiology, and what are its
current causes and research? By Jessica Ho‘15 A
RTI
CLE
22
In many individuals who have schizo-
phrenia, additionally, seem to be hyperactive.
Research has also shown that lowered levels of
dopamine can cause hyperactivity, a diagnostic
symptom of ADHD. Drugs such as cocaine can
accelerate dopamine buildup in the brain, lead-
ing to maladaptive effects. Evidence of a posi-
tive correlation between the introduction of a
dopamine antagonist (D2 antagonists) to a
schizophrenic subject and the presence of dopa-
mine‘s breakdown product, called homovallinic
acid, in urine, cerebrospinal fluid, and plasma
support the hypothesis that abnormalities in do-
pamine levels contribute to the mental disorder.
MRI studies have also demonstrated increased
levels of dopamine co-transporters in the cau-
date nucleus and the putamen, two regions re-
sponsible for memory and motor functions re-
spectively. These research findings have
strengthened the assertion that dopamine level
abnormalities contribute the etiology of schizo-
phrenia (2).
In addition to the dopamine hypothesis,
mounting evidence over the years has led re-
searchers to formulate the serotonin hypothesis
which uses the abnormalities of serotonin levels
as a possible basis for the development of schiz-
ophrenia. Serotonin comes from tryptophan,
and was first hypothesized to play a role in the
disorder in the 1950s when researchers ob-
served similarities between serotonin and lyser-
gic acid. Lysergic acid, which is in higher levels
at serotonin‘s receptor sites, induces symptoms
somewhat similar to a psychosis effect, allow-
ing researchers to raise a possibility of whether
serotonin may hold a degree of responsibility in
eliciting the symptoms observed in schizo-
phrenics. Despite having collected contradictory
evidence as to serotonin‘s role in schizophrenia,
researchers have discovered that serotonin lev-
els are abnormally elevated in the putamen,
caudate, and the prefrontal cortex, which might
be due to reduced serotonin reuptake sites). (2)
Lastly, gamma-amino butyric acid (GABA) has
become of interest to researchers; the produc-
tion of dopamine by dopaminergic neurons are
regulated by the GABAergic neurons, which are
in turn regulated by an enzyme called glutamate
decarboxylase (GAD). Studies have shown that
decreased production of GABA promotes dopa-
mine production, therefore possibly creating the
symptoms of schizophrenia (2).
Interesting Case Involving Schizophrenia
A seven year old girl named Jan
Schofield was different from other children the
day that she was born. While other babies sleep
about 16-17 hours a day, Jani never slept for
more than twenty minutes at a time and no more
than four hours per day. At age 2, she began to
‗see‘ and interact with her imaginary friends
(hallucinations). Although it is normal for kids
this age to have imaginary friends, what was
different about Jani‘s situation was that her in-
teractions with her imaginary friends became
violent. She felt as if her friends were ‗out to
get her,‘ and wanted to attack her. Episodes of
violent behavior soon followed afterwards-she
began to scratch and attack her parents-later
on, became a danger to herself. In many situa-
tions, she would try to choke herself. In another
situation, when Jani was locked in her room as
punishment for trying to hurt herself, her par-
ents found Jani attempting to jump out of the
window. These instances exemplify that the
symptoms of schizophrenia are in some cases,
dangerous and can be developed at a very
young age. (3) References
1 Goldberg, J. (2013, May 1). Types of Schizophre-
nia: Paranoid, Residual, and More. Retrieved No-
vember 17, 2014, from http://www.webmd.com/
schizophrenia/guide/schizophrenia-types
2. Milind, P. (2013). Biomarkers/causative factors
of Schizophrenia. International Research Journal of
Pharmacy, 4(4), 78-85.
3. The 7-Year-Old Schizophrenic. (2009, October
6). Retrieved November 17, 2014, from http://
www.oprah.com/health/The-7-Year-Old-
Schizophrenic/3
Neuroscience: Schizophrenia
23
What is Amnesia? Amnesia is the loss of memory and is also
sometimes characterized by the difficulty to
remember due to a traumatic event, injury, dis-
ease, drug abuse, or tumor. Loss of memory
can be permanent, but not always. In some cas-
es, memories can be recovered with the help of
psychotherapy. These memories are usually
memories of traumatic events or accidents.
However, amnesia can also result in a perma-
nent loss of memories. This can result in a
lapse between two time periods. Depending on
the length of the time, the person with amnesia
can return to their normal lives with minimal
help and treatment. (1)
Causes of Amnesia Amnesia can be caused in multiple ways. Two
major causes are organic causes and functional
causes. Organic causes include the use of seda-
tive drugs, which damage parts of the brain that
hold memories. The areas that are damaged are
usually the temporal or diencephalic parts of
the brain. The temporal part of the brain in-
cludes the hippocampus as well as the cortical
areas that surround it. The diencephalic area
consists of a group of subcortical structures that
are located in the middle of the
brain. Damage to these areas can also be
caused functionally, or by the mind‘s reaction.
The brain has defense systems that can result in
the loss of memories if hey are traumatic. The
memories will then trigger the mind to defend
itself by blocking out or forgetting the memo-
ries. (2)
Memories can also be lost due to dis-
eases or tumors. If the disease or tumor damag-
es the temporal or diencephalic areas of the
brain, then amnesia is a possible effect. One
rare case was that of Clive Wearing, an English
musician. His brain was damaged due to the
encephalitis virus, resulting in an inability to
make memories that last more than 7 to 30 se-
conds. However, he was still able play the pi-
ano and conduct a choir since these actions
were procedural actions and that part of the
mind responsible for this function was not
damaged (3).
Symptoms of Amnesia
The symptoms of amnesia include the loss of
memories. People affected with amnesia might
not know that they are missing memories.
When they suffer memory loss, they forget the
event and occurrences. If the memory is not
brought to their attention, they might not even
know that they are missing memories. For ex-
ample, if a person encounters a traumatic inci-
dent, then forgets about it, the person would
not know that anything is out of the ordinary
unless someone tells them. If people with am-
nesia do know about the missing memory, they
would not be able to remember anything that
happened. Sometimes, however, people re-
place their forgotten memories with false ones.
(4)
Treatment for Amnesia
Amnesia can sometimes be treated and lost
memories can be restored. To make this possi-
ble, psychotherapy is often required. A psycho-
therapist can help people recover their memo-
ries by focusing on what happened before and
anything that can link them to their memory.
Neuroscience: Amnesia
Amnesia: Memory Loss By Crystal Wu ’16
AR
TIC
LE
24
This sometimes triggers them to retrieve their
memory. However, when it is not possible to
get the memory back, a psychotherapist can
help a person cope with the memory loss. As of
today, there are no drugs or any form of medi-
cation that can cure amnesia. (5)
Amnesia vs. Dementia The terms amnesia and dementia are often as-
sumed by many to mean the same, but in actu-
ality, they are different mental conditions that
have different symptoms. However, there are
symptoms that differentiate the two. Although
both impair memory, amnesia is the loss of
memories. This is different from dementia be-
cause amnesia is only the loss of memories and
sometimes difficulty remembering future
events while dementia can impair the ability to
perform basic functions. Also, dementia can
often worsen over time while amnesia usually
stabilizes and does not get worse unless another
problem causes it to. People with dementia
have difficulties living in society without help.
People with amnesia can often live normally
since it is memories that are forgotten.
References (1) Web MD (2013). Retrieved from
http://www.webmd.com/brain/tc/confusion-memory-loss
-and-altered-alertness-topic-overview
(2) Kwon JT, Jhang J, Kim HS, Lee S, Han JH. Brain
region-specific activity patterns after recent or remote
memory retrieval of auditory conditioned fear. Learning
& Memory 2012;19(10):487-494.
(3) Mastin, L. (2010). Retrieved from http://www.human
-memory.net/disorders_amnesia.html
(4) Mayo Clinic Staff. (n.d.). Mayo Clinic. Retrieved
from http://www.mayoclinic.com/health/amnesia/
DS01041/DSECTION=symptoms
(5) Nordqvist, C. (2014). Medical News Today. Re-
trieved from http://www.medicalnewstoday.com/
articles/9673.php
Neuroscience: Amnesia
25
Brain tumors are the abnormal growth
of cells in the brain or central nervous system.
In a healthy individual, when cells age, the
cells are eventually replaced with new healthy
cells. Cancer prevents this natural cycle of re-
cycling cells from happening, leading to the
build up of unhealthy cells that eventually end
up becoming tumors. A synonym for tumor is
neoplasm, which is defined as an abnormal ag-
gregation of tissue that results from abnormal
growth patterns of cells. These abnormal
growth patterns include metaplasia or dyspla-
sia, which can lead to neoplasia. A micrograph
of pancreatic acinar metaplasia is shown above.
The former term means the abnormal growth of
mature cells in order to adapt to environmental
stress and if this stress is removed, the cells re-
turn to their original state. The latter term de-
scribes the abnormal growth of immature cells
or developmental delay including maturation
and differentiation of cells. Neoplasia is the
progressed form of metaplasia or dysplasia and
usually develops in malignant cancers (1).
There are two types of tumors; they are
malignant tumors and benign tumors. Benign
tumors are non-cancerous and not as rooted or
attached onto the brain or as compared to ma-
lignant tumors, but are still dangerous since
they can cause inflammation and place pressure
on the surroundings. Thus, most benign tumors
are surgically removed since they have clearly
defined boundaries that separate the tumors
from the surrounding tissues. The benign tu-
mors also have a lower chance of relapse. Ma-
lignant tumors are the dangerous and cancerous
tumors that grow faster and spread quicker as
compared to benign tumors. The malignant
brain tumors invade surrounding tissue in the
brain and central nervous system but rarely
spread to other organs. The exact cause of for-
mation of brain cancer is unknown, which
makes the disease so dangerous and hard to di-
agnose (2).
However, there have been speculations
of the cause through research. These causes
include mutations in the DNA of brain cells
and history of cancer, which means that cancers
that occur elsewhere spread to the brain. These
mutations usually occur in membranes cover-
ing the brain, cranial nerves, or glands found in
the brain. This type of tumor is known as a pri-
mary brain tumor because they originate in the
brain. The other cause of a brain tumor is con-
sidered a metastatic brain tumor or secondary
brain tumor. This type of tumor is more com-
mon as compared to the primary brain tumor.
The name metastatic brain tumor is derived
from how tumors from other parts of the body
―metastasizes‖ or spreads to the brain. The dia-
gram to the top illustrates a tumor shown with
an arrow. This tumor is a metastatic tumor in
the right cerebral hemisphere originating from
the lungs. The image is created using magnetic
resonance imaging (MRI) technique, which is a
very common method used to locate cancers
and tumors around the body (3).
There are five stages in cancer and
many types of brain cancer fall under stage four
– the final and most malignant phase. Malig-
nant cells begin to metastasize. Stage four
Neuroscience: Tumors
Brain Tumors: The Facts and the Problems
By Aaron Zhang ‘15
A
RTI
CLE
26
cancers are a very serious problem and are ex-
tremely hard to treat even with the extensive
medical knowledge available today (4). Certain
stage four brain cancers include Ependy-
moblastoma, Glioblastoma, Medulloblastomas,
and Pineoblastomas. Ependymoblastoma oc-
curs mainly in young children and infants that
usually occurs in the area of the brain that con-
tains the cerebrospinal fluid. The cerebrospinal
fluid is the bodily fluid found between the brain
and the spine.
Glioblastoma is a common brain cancer
that includes 12% of all brain cancer cases and
is located in the cerebral hemisphere of the
brain. This type of brain cancer targets astro-
cytes, which are the most abundant type of
brain cell. The reason why this is a very dan-
gerous cancer is because astrocytes serve a va-
riety of functions for the brain and nervous sys-
tem and making their growth abnormal is fatal
for the patient. Medulloblastoma is another
type of childhood brain cancer and originates in
the cerebellum. This cancer metastasizes to
many other parts of the body.
Pineoblastoma is a type of brain cancer
that occurs in the pineal gland of the brain. The
pineal gland secretes the hormone melatonin,
which monitors the sleep and wake cycles (or
circadian cycles) and seasonal functions. The
prefix of the word Pineoblastoma is ―pine,‖
which is due to the shape of the pineal gland,
which is the shape of a pinecone (5). The
symptoms of these stage four brain cancers in-
clude hearing problems, loss of memory and
coordination, vision problems, seizures and
hallucinations, and weakness of the arms and
legs.
A recent case involving a stage four
brain cancer is Riley Brilliant, a five year old
child who was diagnosed with a stage four
brain cancer since he was eight weeks old. His
doctors said that Riley‘s survival rate was only
a mere five percent and that if he survived, he
would be impaired in this ability to walk and
talk. However, thanks to the doctors at St. Jude
Children‘s Research Hospital, Riley‘s tumor in
the left side of his brain was successfully re-
moved at the expense of most of the left side of
his brain. However, Riley is now able to talk
and walk with limitations such as walking us-
ing crutches and talking with a habit of repeti-
tion. Although Riley‘s story is one of happiness
and success, there are still many cases of brain
tumors that remain unresolved. Riley‘s story
raises awareness of the disastrous effects can-
cer has on people and their family and loved
ones. This story also shows how the under-
standing of neurology can help more people
like Riley survive (6).
Riley‘s treatment to his stage four brain
cancer was through surgery. Today, there are
many other brain cancer treatments which in-
clude radiation therapy, chemotherapy, proton
therapy, and targeted therapies. Surgery is used
to reduce tumor size or completely remove the
tumor before it gets too large and malignant.
Brain surgery is usually the first attempted
treatment for brain cancer and little to no dam-
age to the brain is dealt undergoing surgery.
However this is not the case for many and a
majority of the time, many important parts of
the brain are removed or destroyed. Radiation
therapy is used to target brain tumors that can-
not be removed using surgery. This treatment
uses radioactive rays to target and kill tumor
cells. However, the therapy may also harm
healthy cells. This is why radiation therapy is
sometimes paired with chemotherapy to lessen
the stress of healthy cells. Targeted therapies
are also used to remove remaining cancer cells.
Chemotherapy is sometimes also used to treat
brain cancer. Chemotherapy consists of the in-
jection or oral intake of drugs that target the
tumor cells. This method is not always the best
for brain cancers because the blood-brain barri-
er and small blood vessels in the brain prevent
many chemotherapeutic drugs from entering
the brain. Proton therapy is similar to radiation
therapy with a few differences. In proton thera-
py, there are high doses of radiation targeting
specific areas and deals less harmful effects to
nearby healthy cells. This leads to fewer side
effects. Proton therapy is also used to target
sensitive areas of the brain that would normally
be damaged using radiation therapy and sur-
gery. Thus, this treatment is most suggested for
Neuroscience: Tumors
27
children to reduce radiation to healthy parts of
the brain and avoid long-term radiation prob-
lems. Targeted therapies are relatively new in
that the drugs target the genes that cause the
abnormal growth of cancer cells. There have
been many clinical trials regarding this new
type of therapy (7).
As one can see, brain cancer is a very
serious issue. Even with the advanced medical
treatments available, there is still much that sci-
entists and doctors do not know about this ma-
lignant disease. However, the understanding of
neurology and medical science is increasing
each day, and hopefully one day everybody
with a brain disorder or brain cancer can be as
successful as Riley Brilliant‘s story.
References:
(1) Abrams, G. D. (2008, August 25). DIS-
TURBANCES OF GROWTH NEOPLASIA I.
University of Michigan. Retrieved December
12, 2013, from http://open.umich.edu/sites/
default/files/082508.gabrams.neoplasiai.pdf
(2) Brain Tumors (Benign and Malignant):
Symptoms, Causes, Treatment. (n.d.). WebMD.
Retrieved December 15, 2013, from http://
www.webmd.com/cancer/brain-cancer/brain-
tumors-in-adults
(3) Brain Tumor Treatment. (n.d.). Cancer
Treatment and Cancer Research. Retrieved De-
cember 15, 2013, from http://
www.mdanderson.org/patient-and-cancer-
information/cancer-information/cancer-types/
brain-tumor/treatment/index.html
(4) New Health Guide. (n.d.). Stage 4 Brain
Cancer. Retrieved December 15, 2013, from
http://www.newhealthguide.org/Stage-4-Brain-
Cancer.html
(5) Pineal gland (anatomy). (n.d.). Encyclope-
dia Britannica Online. Retrieved December 12,
2013, from http://www.britannica.com/
EBchecked/topic/460967/pineal-gland
(6) Shinn, S. (2013, December 15). Diagnosed
with brain cancer as infant, Riley Brilliant
about to turn 5. Salisbury Post. Retrieved De-
cember 15, 2013, from http://
www.salisburypost.com/article/20131215/
SP01/131219787/1184/diagnosed-with-brain-
cancer-as-infant-riley-brilliant-about-to-turn-5
(7) Staff, M. (2012, June 14). Definition. Mayo
Clinic. Retrieved December 15, 2013, from
http://www.mayoclinic.com/health/brain-
tumor/DS00281/DSECTION=causes
Neuroscience: Tumors
28
Spinal Pulse Inducing Neuro Electric Stimula-tor S.P.I.N.E.S. (Bionic Spine Connector) Lakshmi Singh ‘13, Maliha Sultana ‘13, Phoebe Wong ‘13, and Zejia Yu ‘13 REGIONAL 1 Winners,2012
Abstract
Paraplegia, also known as paralysis, is the complete or partial loss of muscular con-trol, leading to the lack of feeling and mobility in the affected area. This growing problem distresses millions across the world. Although there are several types of therapy available for paraplegics, no definitive cure exists. Currently, scientists are regenerating functioning neurons using stem cells. However, due to ethical and technical concerns, these regenera-tions often lead to numerous detrimental side effects like scar tissues. Therefore, our pro-posal suggests a novel technique that uses electrical pulses to stimulate damaged neurons and muscles, enabling movement and alleviating pain in damaged areas. In a similar experi-ment, the paraplegic was eventually able to exhibit ambulation, showing potential in the success of electrical stimulation in spinal cord injury. Our vision is to create a wireless bion-ic spine that functions as a neuro-stimulator, to cure paraplegic cases concerning the body from waist-down.
FE
ATU
RED
STU
DEN
T R
ESEA
RC
H
29
PRESENT TECHNOLOGY
Currently, there are no known defini-
tive treatment strategies that can bring a sig-
nificant change to the condition of patients
suffering from this injury. Although complete
recovery of function in an injured spinal cord
is still not possible, research is being conduct-
ed to promote regeneration and repair the in-
terruption of impulses. Current technology has
allowed for the repair of damages in the spinal
cord so that patients could regain some move-
ment. However, the repair of damaged neu-
rons responsible for spinal cord injury remains
limited to the area of stem cell research. Exo-
skeleton suits, bionic spinal discs and spinal
cord stimulators bring new insight and possi-
bilities. Scientists are currently in the process
of researching the further use of spinal cord
stimulation devices. Spinal cord stimulation
devices are mostly used to relieve pains in
limbs and ineffective areas affected by nerve
damage. Pope et al (1) theorized that this neu-
ro-stimulation produced from the device re-
flects the ―gate control theory‖. This states
that a neuro-stimulus would cause the ―gate‖,
which releases noxious stimuli at nerve ends
to ―close‖ and reduce the intensity of pain to a
lower sensation.
However, in a recent study (2) , a spinal
cord stimulation device composed of 16 elec-
trodes was surgically implanted into a para-
plegic (from neck down) on key parts of his
spine. After three days of therapy, the patient
was capable of standing for at least four
minutes and exhibits some ambulatory move-
ments. During this process, he also regained
some control of his autonomic functions of his
bladder and bowel. Consequently, the electri-
cal stimulation device may be used for more
advanced techniques and devices in the future.
Another present technology is a motor-
ized exoskeleton REWALK bionic suit. (3)
This technology provides an alternative to
wheelchairs and enables patients to stand,
walk and climb stairs. The device features a
computer-based control system as well as DC
motors at joints, rechargeable batteries and
sensors. It is designed for durability of a wide
array of moments so that it accommodates
most of the patient's needs.
Another rehabilitation method is the
Functional Electrical Stimulation technique.
(4) Functional Electrical Stimulation (FES)
applies small electrical pulses to paralyzed
muscles to restore or improve their function.
FES can help some to improve bladder, bowel
function, and reduce the frequency of pressure
sores. An example of the FES is the Parastep
method. It is a computerized
―neuroprosthesis‖ system in which users hold
on to a front-wheeled walker fitted with a key-
pad wired to a microprocessor on the belt.
Electrodes are placed on the quadriceps, the
muscles and the nerve. The user initiates am-
bulation by positioning muscles in the proper
sequence. Stimulation of the quadriceps caus-
es a contraction leading to a knee extension,
which enables the user to stand. Some re-
search today demonstrates that such a pattern
may not even be necessary, in Summer‘s case,
muscle memory and spinal signals were initi-
ated by the pressure of weight exerted on his
legs which allowed him to stand on his own
with just non-patterned electrical stimulus. (2)
Though FES devices are known to use elec-
trodes to stimulate certain points of the spine,
the connector would be programmed to emit a
pulse necessary to reach the point or enough
to initiate a reaction that could relay the mes-
sage through the stimulated neurons.
The goal is to find a type of surgical
battery that would provide the spine connector
with enough energy so that it could last for a
sufficient amount of time. Research indicates
that the different types of implantable batter-
ies: the implantable battery and various re-
chargeable batteries function in different ways
to sustain a relatively long battery life. The
implantable battery, usually found in pace-
makers, is implanted under the skin and would
30
have to be eventually replaced surgically. As
for rechargeable batteries, two methods exist.
One requires the battery to be charged through
an electrical wire that protrudes from the pa-
tient connected the battery inside the body to
recharge it. A more popular approach is the use
of radio waves. Radio waves would be emitted
from an external source to recharge the im-
planted battery. Instead of using the current
models we plan on adopting a battery re-
charged by different means. Present studies
plan to develop a battery in the future that is
self rechargeable or recharges by exploiting its
surrounding environment , which we hope to
use for our device. A possibility for such an
occurrence in our device would be the depend-
ency of the battery on the pulse generator, uti-
lize part of the electricity to charge itself.
Another change that can be incorporated
into this future technology is the capability of
the device to function wirelessly. Current con-
cepts of spinal chord stimulation devices re-
quire a machine or small portable device to be
connected to the patient to program and moni-
tor the electrical pulsing pattern. We hope to
create a connector device that would not dis-
rupt the human body like the implantable pace-
maker, as an abnormal device attached above
the heart. Overall we are looking forward to
discover the success of independent ambula-
tion by paraplegics through our device.
History:
One of the most common disabilities
today is paralysis: the loss of control over the
movement of a part of the body due to an inju-
ry to the nerves. In fact, according to the Na-
tional Injury Database, 250,000 Americans
have spinal cord injuries every year, with 52%
being paraplegic. (6) Paralysis can be classi-
fied as local or generalized and may even fol-
low a particular pattern, depending on the af-
fected area. In addition, a person can experi-
ence one of the various levels of paralysis such
as spasticity and flaccidity. Spasticity is a form
of paralysis which results in an increased tight-
ness in the muscles when they are immobile
and often cause a person to display abnormal
limb positions. Flaccidity, on the other hand, is
a form of paralysis in which skeletal muscles
become unresponsive due to a problem with
communication to a somatic nerve.
SCI can be described as a disconnec-
tion syndrome that disrupts the motor fibers
from the motor cortex to the spinal neurons,
and the ascending somatosensory fibers from
the spinal cord to the brain. This disruption of
electrical impulse conduction is what causes
loss in lower body function in SCI. In the
event of a nervous system injury, regrowth of
axons is not possible because the central nerv-
ous system has multiple additional factors that
act as barriers towards regeneration and ren-
ders the environment hostile to inherent regen-
erative ability.
Paralysis had been thought to be incur-
able due to the aforementioned reasons. How-
ever, over the recent years, there have been
developments in the treatments for paralysis.
In fact, it was not until the recent few decades
that spinal cord injury survivors have reached
life expectancy that is in close proximity to the
normal population. Yet, many still struggle
with immobility and its complications such as
respiratory infections, urinary tract infections,
decubitus ulcers, cardiovascular diseases, etc.
Depending on the level and the cause of paral-
ysis the patient is diagnosed with, treatments
vary. For example, a patient may work with an
occupational therapist who focuses on training
the patient in doing normal activities in order
to allow him to develop basic skills for self-
care. Another form of treatment that patients
have been exposed to in the past is physical
therapy. A physical therapist concentrates on
the patient‘s mobility skills by working on the
muscles that can still function. Although these
techniques have often shown progress in pa-
tients‘ conditions, they have not occurred at
the desired rate and cases in which therapy has
been able to completely cure paraplegics have
been rare. Thus, research in this area is still
required.
31
Future Technology:
Our vision is to create an implantable
device that can replace damaged or missing
sectors of the spine to restore control of the
lower body called a ―Bionic Spine Connector.‖
Spinal cord injury often leads to paralysis due
to the damaged central nervous tissue, which
does not have the capacity in self-healing, such
as the tissue in the peripheral nervous system.
Current studies are focused on the repairs of
central nervous system; however our idea is
focused on reestablishing connection of the
neurons in the central nervous system to pro-
vide the ability for functional limbs again.
Recently, a new technique utilizing
electrical stimulus has shown to succeed in in-
ducing nerve reactions. It gradually allowed
the paraplegic to not only stand but also take a
few steps following three days of use. If this
concept were to be incorporated onto the spine,
it would allow the nerves to connect to the
nervous system with greater proximity and
promote further movement. In addition, vari-
ous electrical patterns created by an enhance
program may be induced to regulate the type
of movement, required by the user. For in-
stance, if consecutive electrical impulses could
move the leg four inches or if alternating elec-
trical impulses would move the leg two inches.
Therefore, by coordinating electrical impulse
patterns with leg movement, we can know
what impulse pattern should be used to induce
a specific leg movement. Some research today
demonstrates that such a pattern may not even
be necessary, in Summer‘s case (2) muscle
memory and spinal signals were initiated by
the pressure of weight exerted on his legs
which allowed him to stand on his own with
just non-patterned electrical stimulus. Though
FES devices are known to use electrodes to
stimulate certain points of the spine, the con-
nector would be programmed to emit a pulse
necessary to reach the point or enough to initi-
ate a reaction that could relay the message
through the stimulated neurons.
One goal is to find a type of surgical bat-
tery that would provide the spine connector
with enough energy so that it could last for a
sufficient amount of time. Research indicates
that the implantable battery and various re-
chargeable batteries function in different ways
to sustain a relatively long battery life. As for
rechargeable batteries, two methods exist. One
requires the battery to be charged through an
electrical wire that protrudes from the patient
connected the battery inside the body to re-
charge it. A more popular approach is the use
of radio waves. Radio waves would be emitted
from an external source to recharge the im-
planted battery. Instead of using the current
models we plan on adopting a battery re-
charged by different means. Present studies
plan to develop a battery in the future that is
self rechargeable or recharges by exploiting its
surrounding environment , which we hope to
use for our device. A possibility for such an
occurrence in our device would be the depend-
ency of the battery on the pulse generator, uti-
lize part of the electricity to charge itself.
Another change that can be incorporated
into this future technology is the capability of
the device to function wirelessly. Current con-
cepts of spinal chord stimulation devices re-
quire a machine or small portable device to be
connected to the patient to program and moni-
tor the electrical pulsing pattern. We hope to
create a connector device that would not dis-
rupt the human body like the implantable pace-
maker, as an abnormal device attached above
the heart. Overall we are looking forward to
discover the success of independent ambula-
tion by paraplegics through our device.
Breakthrough:
32
The design for a bionic spine connector
is far more advanced than the current technolo-
gy. In order to successfully create such a
mechanism, several technical and theoretical
advances are needed to accommodate our envi-
sioned project. Further developments include
an everlasting or easily replaceable battery,
wireless FES control, and a small portable de-
vice to monitor and program the bionic con-
nector by processing patterns for electrical
stimulus. In terms of organics, the knowledge
of reestablishing nerve connection is essential
to our project and is currently one of the most
difficult topics to study since researchers of the
past decade are still dealing with stem cells
and electrical stimulus to attempt and repair
nerves.
Batteries used for current FES devices
all either need to be recharged or replaced sur-
gically, otherwise to have a battery wire exten-
sion from the patient‘s back to the device. Our
goal is to eliminate the need for surgical re-
placement of the battery or possibly to have an
everlasting battery that is self-rechargeable. If
the patient were to continuously replace the
battery once worn through surgery, as is the
current method, it would be troublesome for
many who use the bionic connector. To relieve
their problem, a small minute whole could be
created small enough to connect to the device
and change the battery when needed by using a
small tool. The minute hole would be made of
titanium with a closing to prevent any objects
from entering the body.
We proposed that the wireless controller
device, usually implanted into the body, be re-
moved to eliminate any unnecessary room or
damage it may cause. It would also be much
easier to control the device from outside than
have to surgically operate on a patient to fix
the device. If such a hand-held technological
device could be made to program and com-
municate simultaneously to the bionic spine
connector, then the efficiency for the patient
would increase and be much faster than the
current ―steps‖ that are now taken by the RE-
WALK exoskeleton and Parastep device. The
hand-held transmitter would also prove as a
safety device in manual shutdown in case the
product malfunctions. Obstacles faced by this
procedure would be the signal transmission
from the spine connector to the device that
would be intercepted by the human torso.
Types of frequency waves, such as radio
waves, used to communicate with the device
may also cause side effects that may damage
the body so a safer method must be found in
the communication process.
Lastly, nerve reconnection is the key
step for the device to function properly. Nerv-
ous tissue is known for its low capacity to self
regenerate and repair. Damaged nerves hardly
heal, leaving people paralyzed in certain areas.
A possible function that could be achieved in
the future is to create nanomachines or other
substances to mimic the neurotransmitters re-
leased by nerves to relay messages allowing
the entire body to move. Another approach
could be to interpret the ―messages‖ sent by
the brain and either reroute the message or al-
low the bionic connector to interpret the move-
ments and carry them out with electrical stimu-
lation of the spine.
Design Process:
After we decided to focus on the spine
we decided to find a solution to paralysis. This
would be done by creating a bionic spine that
would be located inside the body. This spine
would be charged by a battery that would be
connected to the spine. The battery, lithium
iodide, would be the same as those used in
pacemakers since they are currently the best
known batteries of today to use in implanted
devices. We realized that some people only
have some ineffective spine segments and re-
moving the entire spine of a human would be
dangerous. Therefore, to adapt to all individu-
als, the spine connector would reconnect the
separate or damaged spine segments to restore
its ability to function properly. Contemporary
studies have begun the experiment of using
Schwann and stem cells in an attempt to
reestablish nerve connection through differen-
tiation. (8) We avoided the use of such devel-
opmental factors because little is known about
33
nerve reconnection and stem cells are prone to
become scarred tissue instead of a functioning
nerve. This idea requires more experimenting
and a risk that could not be incorporated into
our design.
In current studies for repair of degener-
ating spinal discs, Dr. Kennedy and Dr. Boyan
are working to develop a bionic spine disc re-
placement made of hydrogel that would have
the same strength and flexibility of a natural
disc (9). For the design of our connector, the
hydrogel discs would be placed at both ends of
the bionic connector to imitate a more natural
environment of the spine and protect the sur-
rounding segments. Many therapies in the past
only used titanium grafting which would be
uncomfortable and not flexible considering we
needed to implant it into the spine so the more
advanced discs are to be used.
Like pacemakers, the bionic connector
would be composed of a pulse generator, lead
systems, and battery. The rechargeable lithium
iodide battery would be placed towards the
back of the connector like a small capsule so it
can be removed through a minute hole instead
of having to replace it surgically. The pro-
grammed pulse generator would be monitored
by an external device that would control the
frequency, memory, and programming of the
pulse generator. Most of the electrical pulse
would be transferred to the leads that are
placed on key points of the spine, depending
on the type of paralysis, to stimulate the move-
ment. A small portion of the electrical pulse
would be transferred to the lithium iodide bat-
tery to recharge itself.
We have also decided on having a palm
monitor that controls and shows the pulses,
patterns, and status of the bionic spine con-
nector. In case of a malfunction in the connect-
or this palm device possesses the ability to shut
it off manually. Present treatment requires the
monitoring device to be connected to the stim-
ulation device resulting in a protruding wire
from the person‘s back which may result in
several limitations for the person to live a nor-
mal, industrious life. This palm sized external
aide seems fitting for current technology of
iPads, iPhone, and other small electronic hand
held devices. Furthermore, we hope to use oth-
er methods of telemetry other than radio-waves
to establish a communication link between the
palm monitor and bionic spine connector to
avoid any overheating or radiation issues that
are known to occur.
The implantation of this device requires
a surgical procedure to fix the bionic spine
connector in a stable position and connect the
leads from the device to key areas of the spine.
A small hollow titanium tube, no more than 2
cm, would also be placed directly above the
battery (if it is not everlasting/ self-
rechargeable) and sealed securely to alleviate
the irritating process of having to surgically
remove the battery. A skin patch (like a fiber
enforced water resistant medical tape) would
be placed over it. This minute hole would be a
backup for manual shut down, where each pa-
tient will be given a small screw-like tool the
size of a key to manually shut down the battery
by removing the skin patch and adjusting the
battery off.
Consequences:
Once this technology is designed and
fully perfected, the Bionic Spine Connector
will be able to bring benefits to paraplegics.
The 12,000 paraplegics who could benefit
from this device each year significantly
demonstrate the practicality of this technology.
This device will be capable of facilitating and
improving functions of the respiratory, sexual,
bladder, bowel, and lower limb mobility that
are associated with paraplegia through the ap-
plication of electrically controlled stimulus to
incite the paralyzed muscles to contract and to
function. By restoring the damaged segment of
the spine and simultaneously stimulating the
spine, the device will ―connect‖ the neurons
that transmit signals up and down the spine. In
doing so, the electrical stimulus will enable
messages to be sent to other parts of the body
and coordinate movement. It would be conven-
ient for the patients because it is easy to con-
trol. Once inserted, the device will function
34
and operate on a pulse-charged battery. Using
a rechargeable battery shows it is cheaper than
maintaining a non-rechargeable system. In
addition, because the device would be capable
of functioning wirelessly, it would maximize
the ease and convenience of usage to benefit
the patients.
A negative effect of this experiment
would be that the battery would need to be re-
placed about every ten years. In addition, hav-
ing the water proof skin patch would make the
replacement more accessible and less painful
to the patient. Future research could develop
this device so that it could help more than just
paraplegic patients. A difficulty with the con-
cept of the battery will be the obstruction of
the minute hole in the back and the possibility
that batteries may overheat during its use.
References
(1) Spinal Cord Stimulation Devices Peripheral
Neuropathy FBSS CRPS (2010, December). In
MISS Spine Brain Surgeon Neurosurgeon
Sydney Australia . Retrieved December 15,
2011, from http://www.spinesurgeon.com.au/
modalities/
Spinal_Cord_Stimulation_Devices.html
(2) Haugh, Thomas M. "Former Beaver
regains ability to walk." Gazette Times 19
Mar. 2011. Web. 30 Jan. 2012. <http://
www.gazettetimes.com/news/local/
article_b8000682-8278-11e0-91e6-
001cc4c002e0.ht
(3) Brand, Howard. ReWalk-Bionic Research.
N.p., 18 Dec. 2010. Web. 30 Jan. 2012.
<http://rewalk.us/>.
(4) RégineBrissot, R., Gallien,, P., Le Bot,, M.,
Beaubras, A., Laisné, D., & Jocelyne, . (2000,
February 15). Clinical Experience With
Functional Electrical Stimulation-Assisted Gait
With Parastep in Spinal Cord–Injured Patients.
Spine, 25(4), 501-508. Retrieved December
20, 2011, from http://journals.lww.com/
spinejournal/Abstract/2000/02150/
Clinical_Experience_With_Functional_Electri
cal.18.aspx
(5) Spinal Cord Stimulation Devices (2002). In
Virture Medical Centre . Retrieved December
15, 2011, from http://
www.virtualmedicalcentre.com/Devices.asp?
sid=2
(6) Gilbert, Ronald R.Spinal Cord Injury Facts.
Foundation for Spinal Cord Injury Prevention,
C, 2001. Web. 30 Jan. 2012. <http://
www.calvin.edu/library/knightcite/index.php>.
(7) Hobson, K. (2011, May 20). An Electrical
Jolt for Paralysis Research . In Wall Street
Journal . Retrieved December 15, 2011, from
http://online.wsj.com/article/
SB10001424052748704083904576333672813
390298.html
(8) Samar, H., & Hayek, R. (2008, August 2).
Role of electrical stimulation for rehabilitation
and regeneration after spinal cord injury: an
overview. Europe Spine Journal, 17(9), 1256-
1259. Retrieved December 21, 2011, from
http://www.ncbi.nlm.nih.gov/pmc/articles/
PMC2527422/
(9) Mallela, Venkateswara, V Ilankumaran,
and N Rao. "Trends in Cardiac Pacemaker
Batteries."Indian Pacing Electrophysiol
Journal‖4.41 Oct. (2004): 201-12. Web. 30
Jan. 2012. <http://www.ncbi.nlm.nih.gov/pmc/
articles/PMC1502062/>.
(10) Maugh, T. (2011, May 19). Former
Beaver regains ability to walk. Gazette Times.
Retrieved December 21, 2011, from http://
www.gazettetimes.com/news/local/
article_b8000682-8278-11e0-91e6-
001cc4c002e0.html
(11) Kennedy, S., & Boyan, B. (2005, July 4).
Bionic Spine-New Discovery to Aid Treatment
[Electronic version]. Retrieved January 17,
2011 from http://www.wowt.com/news/
features/2/1658247.html
(12) Ludbrook, K. (2011, October 3). Bionic
Spine Enables Girl to Walk Again [Electronic
version]. IOL Scitech.
35
(13) Biomaterial of the Month. (2007, June 1).
Society for Biomaterials. Retrieved December
21, 2011
(14) Hamilton, M. (n.d.). In What is an EMS
Muscle Stimulator Unit and How Does It
Work?. Retrieved January 3, 2012, from http://
www.lgmedsupply.com/whisemsmusta.html
(15) Hornberger, J, K Kumar, E Verhulst, MA
Clark, and J Hernandez. "Rechargeable spinal
cord stimulation versus non-rechargeable
system for patients with failed back surgery
syndrome: a cost-consequences
analysis."Clinical Journal of Pain‖ 24.3 Apr.
(2008): 244-52. Web. 30 Jan. 2012. <http://
www.ncbi.nlm.nih.gov/pubmed/18287831>.
Webpage References:
(1) Henry F. Duston D.D.S, M.S. Web. 30 Jan.
2012. < http://4.bp.blogspot.com/
_g_KhGa4HxMw/TQFr0oTOLNI/
AAAAAAAAANM/eaqvGdIq5os/s1600/
man_fifties.casual.jpg
(2) Bambi SCI Revoery Project. Web. 30 Jan.
2012. <http://www.bambi.net/bob/
thesis_paraplegic.jpg >.
(3) Spinal Cord Stimulator. Web. 30 Jan. 2012.
<18. http://www.njsrlaserspine.com/
Portals/16887/images/C--Users-dgoldberg-
Desktop-eon-mini-spinal-cord-stimulator-3.jpg
>.
(4) Spine. Web. 31 Jan. 2012. <http://
wordsandpicturesareras-
cals.files.wordpress.com/2011/04/
spine_jpg.jpg>.
(5) Medical Pace Maker. St. Jude. Web. 31
Jan. 2012. <http://upload.wikimedia.org/
wikipedia/commons/8/82/
St_Jude_Medical_pacemaker_in_hand.jpg>.
(6) Color Pal Multi Parameter Patient Monitor.
Web. 31 Jan. 2012. <http://image.made-in-
china.com/2f0j00BeKaWEnRgTob/Color-
Palm-Multi-Parameter-Patient-Monitor-
JERRY-I-.jpg>.
(7) Bionic Suit. Web. 31 Jan. 2012. <http://
cdn.medgadget.com/img/robodudes.jpg>.
(8) Nanomachines. Web. 31 Jan. 2012. <http://
www.def-logic.com/articles/nano1.jpg>.
Spinal Cord Stimulator. Web. 31 Jan. 2012.
<http://www.njsrlaserspine.com/Portals/16887/
images/C--Users-dgoldberg-Desktop-eon-mini
-spinal-cord-stimulator-3.jpg>.
36
Art
icle
Ref
eren
ces
R
esea
rch
Knockdown of c-Myc in Rhabdoid Tumor Cells In-
hibits Cell Growth
By Anna Bao
Rhabdoid tumor (RT) is a rare and lethal pediatric can-
cer. INI1/hSNF5, a component of the chromatin remod-
eling SWI/SNF complex, is a tumor suppressor deleted
in RT. Our lab had demonstrated that Cyclin D1 and
Aurora A are the direct downstream targets of INI1 and
that INI1 interacts with cMYC, an oncogene in many
types of cancer, including lymphoma and breast cancer
and regulates cMYC-mediated transcription. Interesting-
ly, previous experiments shown that there is an overex-
pression of cMYC, Cyclin D1 and Aurora A in RT cells
and that Aurora A is upregulated by cMYC in B-cell
lymphoma and cMYC transcriptionally activates Cyclin
D1. The association of cMYC with INI1 suggests its
possible involvement in affecting Cyclin D1 and Aurora
A transcription in RT and thereby affecting cell prolifer-
ation. To determine the role of cMYC in RT, knock-
down of cMYC were performed in RT cells and its ef-
fect on tumor cell growth was determined. Western blot
was used to confirm that cMYC was knocked-down.
The proliferation assay indicated that complete cMYC
knockdown inhibits RT cell growth and western blot
confirmed that knockdown of cMYC was successful.
These results suggested that knockdown of cMYC in-
hibits Rhabdoid tumor cell growth. Therefore, cMYC is
an oncogene necessary for RT cell survival and may be
a potential drug target.
No Double Strand Breaks induced after 1900 MHz
(cell phone) Irradiation in Saccharomyces cerevisiae
By: Tyler Bell
As human exposure to cell phones has increased, the
public has expressed concerns with the possible effects,
the most detrimental being the development of cancer.
The effect of cell phone radiation on DNA integrity in
Saccharomyces cerevisiae was measured in live cells in
this study using two assays: Rad52 protein localization
and Sml1 protein degradation. Results from both assays
suggest that the low frequency radiation emitted by cell
phones does not damage DNA. The effect of cisplatin
on DNA integrity in S. cerevisiae was also measured
using a Rad52 protein localization assay. Cisplatin is a
cross-linking agent commonly used for chemotherapy.
This study confirmed that the repair pathway of the
DNA interstrand crosslinks and intrastrand crosslinks
formed by cisplatin utilize homologous recombination
proteins as the assay showed an increase in Rad52 foci.
Furthermore, damage is seen within just a few hours of
cisplatin treatment. This work is important to under-
standing the potential dangers of cell phone usage and
towards understanding how the cisplatin chemotherapy
drug works.
Abstracts of Student Research (‘12-’13)
37
A Structural Analysis of a Novel Dendrite Arborization
Regulator Menorin in the Nematode C. elegans
By: Shyam Bhatt
The novel protein Menorin was identified through chemical
mutagenesis and an SNP mapping strategy as an important
factor in dendrite development and structuring in the nema-
tode Caenorhabditis elegans. The protein is encoded for by
the gene mnr-1, an ortholog of the human genes FAM151A
and FAM151B. The protein Menorin contains two do-
mains, a DUF domain that is conserved throughout all
orthologs of the gene in different species. The question
asked was if the DUF domain alone could do the job of
guiding dendrite arbors of the worm neuron PVD into the
hypodermis where they belong, and maintain their
"menorah" structure as in wild type. A truncated form of
mnr-1 was inserted into mutant worms deficient for Men-
orin. This produced a truncated form of the protein Menorin
that was expressed in the hypodermis (where Menorin is
normally expressed) due to the help of a dumpy-7 promoter.
A GFP promoter was added to the worms to enable visibil-
ity of dendritic branching patterns in PVD and it was ob-
served that the truncated form of Menorin does not rescue
the phenotype of normal arborization in PVD. The same
phenotype of abnormal branching was observed as in the
Menorin deficient mutants.
Assessing Anxiety and Depression in ?9-
Tetrahydrocannabinol Treated Adolescent Rats Using
an Elevated Plus Maze and Forced Swim Test
By: Rita Black
The rate of teenaged adolescents abusing illicit substances,
most notably of marijuana, has been rising steadily over the
past decade. Previous studies on marijuana (?9-
Tetrahydrocannabinol) abuse have remained primarily fo-
cused on the repercussions to the cognitive abilities of adults
but have overlooked adolescents as a significant marijuana-
user group. As a result, it is imperative that the effects of
the abuse of this substance on adolescents be assessed.
However, current behavioral studies are limited in their abil-
ity to adequately collect data from consenting human sub-
jects through ―check-in‖ reports and unreliable, personal
information. Additionally, behavioral studies involving
adolescents are often not feasible due to the age of the par-
ticipants not allowing for consent. Therefore, a behavioral
study that can (1) perform as a rigidly controlled experiment
to yield consistent results and (2) measure the effects of
marijuana use on mental health during adolescence specifi-
cally would be of considerable value to the scientific com-
munity. The techniques of behavioral testing that evaluate
comprehensive mental disorders involve exposing the ani-
mal test subjects to engineered stresses in the form an ele-
vated plus maze (EPM) and a forced swim test (FST). The
elevated plus maze acts as an assessor of anxiety whereas
the forced swim test analyzes depressive symptoms.
This study evaluates the application of these behavioral
tasks in determining the consequences of marijuana abuse
on the mental stability, relating to anxiety disorders and
depression, of adolescent aged Sprague Dawley rats. Re-
sults affirm that ?9-Tetrahydrocannabinol presents both anx-
iety-related and depressive symptoms specifically in female
rats more so than male rats. Thus, behavioral testing in rat
test subjects to assess anxiety and depressive symptoms
following drug abuse has significant implications in rein-
forcing current marijuana research pertaining to adolescents.
Hermaphroditism and Social Evolution in Synalpheus
Snapping Shrimp
By: Gillian Carling
Social behavior in the sponge-dwelling snapping shrimp
Synalpheus includes asociality, communal living, and euso-
ciality. Through examining the distribution of hermaphro-
ditism among communal, eusocial, and asocial species of
shrimp, it may be possible to find out if hermaphroditism
and social structure have a connection. The two alternative
hypotheses addressed in this investigation were (1) her-
maphroditism will be more prevalent in asocial species than
social species due to the nature of asocial living, or, (2) her-
maphroditism will be more prevalent in social species than
asocial species due to competition between shrimp in a colo-
ny. Samples from 28 species of Synalpheus were dissected
and sexed through the position of gonopores, or sexual
ducts, on the pereopods of the shrimp. We found that her-
maphroditism was most common among social species of
Synalpheus, with a 50% rate of hermaphroditism among
communal species and a 43% rate of hermaphroditism
among eusocial species. Asocial species only had an 11%
rate of hermaphroditism. This indicated that hermaphrodit-
ism is correlated with social behavior in general rather than
a particular social structure. This supported the second hy-
pothesis, that hermaphroditism will be more prevalent in
social species than asocial species due to competition be-
tween shrimp in a colony. The combination of very diverse
social systems and ecological uniformity found among Syn-
alpheus makes these shrimp an ideal model for studying
how hermaphroditism evolved with social structure
Investigating the Role of Microtubules in Vertebrate
Cardiac Development
By: Jessica (Mei Wai) Chan
Cardiogenesis, the development of the embryonic heart, is a
process investigated in a variety of organisms but particular-
ly suited for this developmental study is the specimen zebra
fish. In the zebra fish, key steps in heart development have
been largely understood through studies over the years but
despite knowledge of these basic steps, understanding of the
mechanisms controlling the process remains vague. The
goal of experimentation is to assess the role of microtubules
in cardiac development. Microtubules, the largest compo-
nent of the cytoskeleton is known to aid during mitosis
38
as well as support cell form and cell migration. Drug treat-
ments with the drug Colchicine, a drug known to disrupt
microtubule formation by binding to tubulin, allowed its
role to be assessed. From preliminary data from the lab, it
was expected that the groups affected by the tubulin- bind-
ing drug would result in trumpet shaped hearts. Results
from the experiments indicated a mild version of what was
anticipated, demonstrating a slightly flared cardiac tube. It
was also observed that the drug-treated embryonic hearts
experienced a lack of cellular migration leftward, and for-
wards in the heart, relative to the control embryos at 24
hours post fertilization (hpf). These findings suggest the
lack of microtubules result in a defective heart lacking prop-
er cellular migration and cell formation at the 24 hpf. These
results are beneficial in filling the gaps of knowledge in the
cardiac process and may lead to future diagnosis of congeni-
tal heart disease.
Compounds Extracted from Dianthus Superbus (Qu
Mai) Inhibit B-cell Lymphocyte Production of Immuno-
globulin-E
By: Vincent Chan
An increase in the frequency of food allergies in recent
times, sometimes life threatening, behooves us to find better
treatments for those who suffer. The immunoglobulin E
(IgE) antibody is one of the main proteins involved in aller-
gic reactions to food. In a previous study, whole extracts of
the Chinese medicinal herb Dianthus superbus (Qu Mai)
were shown to inhibit IgE production in human B-
lymphocytes in culture and to inhibit peanut specific IgE in
whole mice, causing reduced allergic reaction. The purpose
of this study was to more specifically identify the com-
pounds in D. superbus responsible for inhibition of IgE pro-
duction toward finding a treatment for food allergies. Com-
pounds found in D. superbus were separated from each oth-
er through extraction with dichloromethane followed by
silica gel chromatography. The resulting fractions were
then analyzed by high-pressure liquid chromatography and
then tested for their ability to inhibit IgE production in hu-
man lymphocytic cells. One fraction isolated here was able
to inhibit IgE production, and it will serve as the basis for
further characterization of the specific active compounds.
Identification of these compounds would help develop a
general treatment for patients suffering from many types of
food allergy.
Testing the Geographic Mode of Speciation in Indo-
Pacific Chondrichthyes
By: Andrew Chen
The Indo?Pacific region, especially the Coral Triangle, con-
tains the largest amount of marine biodiversity. In this
study, we are trying to determine the mode of speciation that
sharks and rays in the Indo?Pacific region have undertaken
in the last few million years. We used the C01 genes of 25
sister species of sharks and rays from the Indo?Pacific Re-
gion. The C01 sequences of these species were obtained
from the database Genbank and were aligned on a program
called Geneious. MTML?msBayes, a program that analyzes
data from multiple species and examines it under a hierar-
chal model, was used. Two pulses (times when many diver-
gences occurred simultaneously) were confirmed for the 18
sister species pairs that had detectable pair?wise differences.
The first pulse contained 12 sister species, and occurred
near present daytime. The second pulse occurred 2?4 mya
(million years ago), and contained six sister species pairs.
The results support allopatric speciation. The divergences
correspond to the closing of the Indonesian seaway 3?4
mya. The data supports the Center of Origin hypothesis for
the IMPA (Indo?Malay Archipelago) because more of the
species pairs that diverged a few million years ago con-
verged at the IMPA than the species pairs that have recently
diverged near present daytime.
APOBEC1-mediated Editing of Amyloidogenic RNA
Transcripts in Microglia
By: Yashaswini Chittampalli
Microglia, the immune cells of the brain, plays a crucial,
though controversial role in the central nervous system.
Microglia trim synapses, a process important for learning.
However, defective microglia can cause neurological disor-
ders, such as Alzheimer‘s disease (AD). This study focuses
on three genes of microglia: beta 2-microglobulin (B2M),
amyloid precursor protein (APP), and a disintegrin and met-
alloproteinase domain-containing protein 10 (ADAM10).
These genes are involved in the creation of amyloid
plaques—the hallmark AD. It was hypothesized that
Apolipoprotein B-editing enzyme, catalytic polypeptide-1
(APOBEC1)—a cytidine deaminase—edits the 3' UTRs of
these transcripts of microglia. By means of RNA and DNA
isolation, cDNA synthesis, PCR amplification, bacterial
transformation, DNA purification, gel electrophoresis and
sequence analysis using the MacVector program, we have
concluded that APOBEC1 is responsible for editing of APP
in murine microglia from brain tissue, and that cytidine-to-
uridine (C to U) RNA editing occurs in the 3‘ UTRs of
B2M, APP and ADAM10 in an immortalized, murine, mi-
croglial cell line (BV2). It is likely that APOBEC1 is re-
sponsible for the editing present in the BV2 cell line, be-
cause the sites edited correspond with the editing prefer-
ences of APOBEC1.
Dynamics of Emulsion Separation: A Microscopic Inves-
tigation at the Interface
By: Daniel Donenfeld
This study examined the dynamics of phospholipid-
stabilized emulsions, and how the emulsion dynamics affect
self-assembly of the phospholipid. An emulsion droplet of
water and 3-hexanol was imaged using fluorescence
39
microscopy to observe activity on the air/water interface. An
experimental system was designed with a hydrophobic sub-
strate and control over the humidity, early stage coales-
cence, and ambient light using a vacuum grease sealant and
a cover. We obtained data on the spreading of the oil phase
and assembly of the phospholipid from the interfacial activi-
ty. Our data suggests that the emulsion separates in two
ways, coalescence, and creaming, which correspond to dif-
ferent rates of 3-hexanol spreading on the interface. Cream-
ing is also coupled with free lipid going to the interface and
slowing down of the spreading of the oil phase. Previous
studies have examined the stability of phospholipid-
stabilized emulsions, and this research looks at the micro-
scopic dynamics involved. This could allow for a more
tailored design of industrial emulsions through knowledge
of emulsion separation. The results of this research could be
used in designing future food products and pharmaceuticals
with phospholipid surfactants as stabilizers.
Application of Carcinoma Precursors and Cell Polarity
in Intestinal Epithelium
By: Timothy Gao
In recent years, the study of cell polarity has increased, due
to discoveries linking the change in polarity of certain pro-
teins to tumorigenesis. Epithelial cell polarity, defined as
the formation of distinct apical and basolateral domains,
causes proteins to localize in specific areas of the cell; this
often leads to a change in the role that a protein may play
within its cellular surroundings. Proteins, TGF-? receptor,
TNF-? receptor, and ErbB2, have all exhibited signs of tu-
mor initiation in previous studies. While they are promi-
nently known in their research as tumor suppressors, evi-
dence has proven that they can sometimes become tumor
promoters in later stages of development; we believe that
the reason for this change in function is caused by cell po-
larity. The implementation of AP1B, a major basolateral
protein sorter that is found only in epithelial cells, is a possi-
ble player in sorting these three proteins mentioned to ab-
normal areas of the cell when it is abnormally expressed.
As a result, we hypothesize that TGF-? receptor, TNF-?
receptor, and ErbB2 are basolaterally expressed in entero-
cytes because they are AP1B cargo. Based on this hypothe-
sis, immunohistochemistry was performed on intestinal and
kidney sections obtained from mus musculus to be analyzed
via confocal microscopy and morphological identification.
Staining cells of the MDCK cell line and the MDCK µ1B-
KD cell line of AP1B presence was also attempted. Results
demonstrate that TGF-? receptor, TNF-? receptor, and
ErbB2 polarize distinctively in the intestinal epithelium, as a
possible result of AP1B‘s sorting ability.
Preferential Splicing of Full Length CTLA-4 in Activat-
ed, Cultured T Cells
By: John Gilheany
When T cells are activated, they proliferate and undergo a
massive expansion that increases the potency of the immune
response. Cytotoxic T Lymphocyte-Associated Antigen 4
(CTLA-4) is a protein that has regulatory effects on the im-
mune system and it can be spliced to give rise to three dif-
ferent unique isoforms: full length (fl), soluble (s), and a
CTLA-4 isoform with only exons 1 and 4 (1/4). The pur-
pose of the experiment was to see if there is any difference
in the relative levels of each isoform in a T cell prior to and
after activation. Primers were designed to detect each vari-
ant accurately, T cells were cultured with anti-CD3, RNA
was isolated and reverse transcriptase done. A semi-
quantitative PCR was then run, to compare splice variant
expression levels between the activated and non-activated
cells. In the end, after activation of the T cell, it was con-
cluded that flCTLA-4 expression increased, while sCTLA-4
and 1/4 CTLA-4 expression decreased; there was a clear
preferential splicing of full length CTLA-4 over the others
when the cell was activated. This could be because flCTLA
-4 is a strong immune regulator, and as the only splice vari-
ant with a trans membrane domain, it can regulate the im-
mune system the quickest and most effectively. My results
will be applied and compared to the case of ipilimumab pa-
tients, where their T cells are activated. In ipilimumab, a
recent melanoma therapy drug, an antibody blocks CTLA-4
on the surface of the cell to indirectly activate the immune
system. The purpose of the project was to see if there was
any correlation between expression of CTLA-4 splice vari-
ants, and patients who respond to treatment. In total, it can
also help us understand more about T cell activity after acti-
vation, regulation of T cells by CTLA-4, and selective splic-
ing.
Testing the Interactions of Drugs and Modulators in a
Neuromuscular System of Aplysia
By: Joshua glynn
Neuromodulators are a primary component of the nervous
system in biological organisms. They are responsible for
not only the neural development of the organism, but also
for mediating specific muscle activities by forming specific
motor neuron outputs that regulate muscle activity. Neuro-
modulators are very difficult to study, as their effects can be
unpredictable when combining different neuromodulators in
various concentrations are to form different cocktails. This
project addresses the validity of a mathematical combinato-
rial algorithm that is proposed to be able to define the func-
tion of each neuromodulator. The combinations tested in
this experiment were successful in indicating what factors of
modulatory systems we need to pay attention to. Data from
physiological experiments suggests that there are two main
factors that should be taken into account: (1) the order in
which individual modulators are applied and (2) the number
of modulators interacting in any given scenario. Focusing
on these particular aspects in depth in future experiments
will undoubtedly allow for better insight into the dynamics
of these modulatory systems.
40
Location of HIVAN Susceptibility Gene in HIVAN Lo-
cus
By: Ekramul Gofur
HIV-Associated Nephropathy (HIVAN) is a relatively re-
cently discovered which leads to end stage renal disease.
The disease results from HIV-1 infection of renal epithetical
cells and podocytes. The prevalent form of treatment cur-
rently for HIVAN is highly active antiretroviral therapy.
HIVAN primarily occurs in people of African descent; ap-
proximately 90% of known HIVAN cases are from people
of African descent. Previous studies in mice using genetic
linkage have shown four loci, which could potentially have
a susceptibility gene leading to the infection of HIVAN.
This project focuses on determining the location of a sus-
ceptibility gene in the HIVAN 1 locus. Comparing the gen-
otypes of three individual mice strains to the control FVB
strain on the SubIII region (subsection of the entire locus) of
the HIVAN 1 locus shows that the mutation for susceptibil-
ity to HIVAN does not exist as a single nucleotide polymor-
phism (SNP) but could still exist as an insertion/deletion.
Assessing DNA Transcription in an HPV 11 Upstream
Regulatory Region (URR) Using a Reporter Construct
Mutated in the AP1 Sites
By: Lubaina Haider
Recurrent Respiratory Papillomatosis (RRP) is a disease
caused by the human papilloma virus (HPV). The upstream
regulatory region (URR) of the HPV genome contains sev-
eral regulatory sites, which control transcription of specific
proteins that directly cause RRP. Our experiment attempts
to figure out whether the AP1d and/or the AP1p site are/is
important in HPV DNA transcription. To test the AP1 sites,
mutant plasmids were produced and transfected into HeLa
cells. A luciferase assay was used to determine whether the
AP1 sites promote or inhibit transcription of DNA. The
results showed that the AP1d site is a negative regulator of
E6 and E7 because the luciferase levels were higher in the
HeLa cells transfected with the AP1d mutant rather than the
HeLa cells transfected with the 311 DNA, which was not
mutated. These results are reliable because the same trend
was seen in four other HeLa cell transfections. To confirm
these results, the JNK pathway was inhibited to test for tran-
scription of DNA in HPV. The results from the inhibitor
research confirmed the results from the mutational study,
which means that the results presented in this report, are
valid; therefore, inhibition of the JNK pathway is not a good
therapeutic target.
Characterization of CD8 Regulatory T Cells in Umbili-
cal Cord Blood
By: Daniel Huang
Umbilical cord blood (CB) contains primitive hematopoietic
stem cells. It has become an alternative to bone marrow for
stem cell transplantation therapy to reconstitute the hemato-
poietic system in patients with malignant and non-
malignant, or other disorders. Success of bone marrow
transplantation is hampered by high rate of graft-versus-host
disease (GVHD) which may lead to death of patients. Find-
ing an appropriate donor to reduce chance of GVHD is very
hard, and waiting period is too long for some patients with
life threatening diseases. GVHD after CB transplantation is
lower partly due to immaturity of T cells and relatively
higher frequency of regulatory T cells (T regs) in CB. CD 4
T regs have been well studied, and their existence in CB has
been documented. CD8 T regs are less characterized; their
existence in CB has been suggested. In this study CD8 T
cells was first determined to have suppression function in
CB only after they are stimulated with allogeneic antigen
presenting cells (APC). Then CD8 T regs were molecularly
characterized CD8 from CB. It showed that CD8 T regs
from CB expressed higher level of BCL6 gene, which is a
molecular marker for CD8 T regs induced from adult pe-
ripheral blood (AB). It also further showed that the level of
micro-RNA (miRNA)-30b, which inhibits BCL6 gene, was
lower than the control. These results indicate that CD8 T
regs in CB may play a role in low rate of GVHD in CB
transplantation, and they may be used in cell therapy to fur-
ther reduce GVHD in CB transplantation if they can be ex-
panded in large quantity.
An Evaluation of Langerhans Cell Chimerism after Gen-
der-Mismatched Allogeneic Hematopoietic Stem Cell
Transportation
By: Martin John
For patients with hematologic and lymphoid malignancies,
allogeneic hematopoietic stem cell transplants (allo-HSCT),
also known as bone marrow transplants, often offer a cura-
tive treatment option beyond what chemotherapy alone can
provide. However, graft-versus-host disease (GVHD) is a
potentially serious complication that can occur when trans-
planted donor cells recognize host cells as foreign, despite
matching for the major human leukocyte antigens (HLA).
Doctors believe the recent success of donor T-cell depleted
allo-HSCT is the result of host antigen presenting cells
(APCs) changing to donor over time. Yet, mouse studies
have shown that precursors of host LCs are long-lived and
can self-renew in skin, unless the net egress of LCs to skin-
draining lymph nodes exceeds the capacity of local progeni-
tors to replenish them. Skin biopsy sections were used to
examine expression of donor sex chromosomes in recipient
Langerhans cells (LCs), a type of dendritic cell that resides
in the skin and is important for initiating immune responses
by donor T cells. Using fluorescence in situ hybridization
(FISH), sex chromosomes were highlighted in cells of skin
biopsy sections, which were co-stained with fluorescent
antibodies to distinguish LCs from other cells in the epider-
mis. The skin biopsies were collected from two patients
with GVHD and two patients without GVHD.
41
Results shown that mixed LC chimerism were examined in
the skin of all four patients, and a pattern can be seen be-
tween genders, rather than between those with GVHD and
those without. Furthermore, the mixed chimerism observed
suggest that not all host APCs in the patients are changing
into donor following allo-HSCT, though host cells are
changing into host only within the blood.
High Preservation of CpG Methylation Patterns in the
Liver of Aging Mus musculus musculus Mitochonadrial
Genome
By: Hyewon Kang
Epigenetic modification is heritable state of gene expression
that can contribute to age-related physical invalidity or dis-
eases such as cancer or depression. A significant aspect of
epigenetics is the methylation status of Cytosine-Guanine
(CpG) dinucleotides in the five position of the genomic
DNA regulation by interfering with the binding of transcrip-
tion factors to promoter regions in the gene. The mitochon-
drial DNA (mtDNA) is prone to mutation, single-nucleotide
mutation rate ranging from 2.7x10(-8) per mtDNA for brain
to 3.2x10(-9) per mtDNA for the liver. However, most of
the studies on methylation were done on the nuclear genome
while the mitochondrial DNA was not explored because the
mtDNA was believed to be unmethylated. Recently methyl-
ation sites were found in the mitochondrial genome in glob-
al assessment. To investigate the mouse liver at an epige-
netic level, the experiment aimed to find how unstable the
mtDNA in the mouse liver really is. Methylation in mtDNA
of the liver from young and old mice were analyzed using
noble sodium bisulfite conversion approaches which change
the DNA sequence depending on the methylation status of
cytosine residues. All the cytosine in the bisulfate treated
CG sites was converted into uracil, which showed up as
thymine in the PCR. The results indicate that the mitochon-
drial DNA is hypomethylated both in young and old mice
samples in the liver, and is surprisingly very stable in epige-
netic marks. The experiment thereby suggests that there
may be a repair system for epigenetic marks in the mito-
chondrial genome and may have further implications in
studying aging and its related diseases.
Using Lexical Features to Predict Winners of U.S. Presi-
dential and Vice-Presidential Debates
By: Ian Kaplan
An investigation of lexical, transcript based, features of
American Presidential and Vice-Presidential debates that
may correlate with personally appealing or politically per-
suasive language facilitates the discovery of the features of
personally appealing and politically persuasive language.
The investigation involved predictive models created that
attempted to, using the transcript of a Presidential or Vice-
Presidential debate, predict the winner of the debate as told
by polling. Chi-squared feature selection identified features
correlated with debate success. These features gave insight
into the distinct importance of discussing war and national
defense the modern American political system. Although
the extremely limited corpus size restricted both the training
and significance of the predictive models, with a set of sur-
face-level lexical features from historical debates the win-
ners of presidential debates can be predicted with 60-80%
accuracy.
Determination of the Role of CBX3 in the Chemo-
resistance of Relapse Pediatric Acute Lymphoblastic
Leukemia
By: Rana Lamisa
Although there have been significant improvements in the
survival rate of childhood acute lymphoblastic leukemia
(ALL), the outcome for relapse patients is still poor. CBX3
is a missense mutation that could possibly change the func-
tion of a protein. CBX3 encodes for the heterochromatin
protein HP1y that is responsible for binding the trimethylat-
ed lysine 9 residues on histone H3. In previous research, it
has been shown that CBX3 is mutated in one pediatric re-
lapse ALL patient sample. One objective of this study is to
understand whether CBX3 binds to H3K9Me3, the protein
this gene encodes, and by what mechanisms. Another ob-
jective is to find the cellular functions CBX3 alters, and the
mechanisms it uses to do so. The third objective is to under-
stand whether CBX3 causes Chemoresistance. Of all the
experiments done, results showed that CBX3 mutant does
bind to the histone H3K9Me3 more readily than the CBX3
wild type does. All other results show that there is no
change between the mutant and the wild type. Our results
indicate that further experiments must be done to understand
the cellular activity of the cell when CBX3 is mutated. In
addition, CBX3 may be a passenger mutation and does not
play a major role in Chemoresistance of relapse ALL.
Comparing the Efficacies of Different Incubation Meth-
ods for Common Snapping Turtle (Chelydra Serpentina)
Eggs from the Bronx River
By: Candace Lee
As part of conservation efforts for common snapping turtles
(Chelydra serpentina), their eggs have traditionally been
collected from nests during the nesting period in late spring
and incubated in direct contact with vermiculite in sweater
boxes. Squamata Concepts LLC has standardized new Sus-
pended Incubation Method (S.I.M.) using suspended con-
tainers with vermiculite, but minimal research has been
done to compare S.I.M. containers with the traditional meth-
od for incubating the eggs of this species. The success of
traditional incubation was compared with that of the S.I.M.
container under various environmental conditions. Success
was measured in terms of the number of hatchlings, incuba-
tion period, hatchling mass, and size of the carapace and
plastron. Each clutch was divided into S.I.M. containers
42
and sweater boxes. Those collected in 2011 were placed in
two incubators (25°C and 30°C) in a nursery and those in
2012 were placed in an outside garage under fluctuating
temperatures that corresponded with the environment‘s
changing temperature. Weekly, lost water weight in sweater
boxes was compensated for by adding water to the vermicu-
lite and S.I.M. containers were aired. The S.I.M. containers
produced larger hatchlings after shorter incubation times
and were suggested to be better at producing more hatch-
lings than sweater boxes at constant temperatures in the
nursery. The sweater box produced hatchlings with greater
masses and larger sizes at fluctuating temperatures in the
garage, but at the expense of longer incubation times. The
results correspond with those of past studies done by scien-
tists such as Yntema, Spotila, Steyermark, Baumer, An-
drews, Bauwens, and Garel, who experimented on the ef-
fects of various factors during incubation on hatchlings of
reptile species, including snapping turtles.
Conditions for Turing Pattern Formation in Electrically
Coupled Networks of Neurons
By: Fred Lin
Neurons in the brain communicate by a combination of
chemical and electrical signals. Certain combinations of
these two types of signals could create Turing patterns, spa-
tially periodic oscillations, which are ubiquitous in biology.
However, the biological mechanism by which Turing pat-
terns could occur in a group of neurons is not well under-
stood. Gap junctions electrically couple many types of cells
in the brain and can coordinate inhibitory neuron firing.
Moreover, conductance through gap junctions depends on
neural activity and intracellular signaling. Here, we use a
computational model to show that gap junctions could link
chemical and electrical signaling in the brain to produce
Turing patterns. The strength of activity of gap junctions
required is biologically plausible.
The Ability of Color Recognition and Distinction in Ga-
lapagos Tortoises (Geochelone nigra microphyes)
By: Catherine Louie
The subspecies of Galapagos tortoises have morphological
characteristics that vary from different islands of the Gala-
pagos archipelago. These variations are the results of adap-
tations that may include certain visual abilities because of
the species‘ heavy reliance on their vision to forage. The
potential to see color and even differentiate between colors
has not been a subject of much research. Color vision and
differentiation is important because husbandry-training
methods can use colored targets for minimizing stress in the
animals during medical procedures. This experiment ex-
plored the visual capabilities of the Galapagos tortoise
(Geochelone nigra microphyes) and its application when
training. The hypothesis states that the color targets can be
utilized as a training tool.
Operant and classical conditioning were used alongside
clicker and target training to test color recognition and dif-
ferentiation. Individuals were conditioned to a specific col-
or (red, orange, black, or white) and assessed using trials in
which the color target each subject selected was recorded.
The results supported an inclination toward red colors in this
species and suggested that although differentiation between
colors is evident, differentiation between similar colors is
not. These findings can be applied to improve training ap-
proaches of zoo and medical staff when conducting standard
veterinary protocols, especially in cases where multiple ani-
mals are involved. It is also the onset of future research
regarding the natural selection and the conservation of the
renowned Galapagos tortoise species.
Investigation of Relationship Between Math Anxiety and
Math Ability in Different Ethnicities
By: Syeda Malliha
Although policies such as affirmative action aim to equalize
the disparity of educational opportunities in the United
States between different ethnicities, it is clear that contrasts
still exist. This study aims to identify how different ethnici-
ties perform with their respective math abilities and anxie-
ties, and if other prominent differences exist. It does so
through a questionnaire including measures for mathematics
anxiety, math ability, and relevant factors such as ethnicity.
The questionnaire was distributed among 160 students of
Hunter College and revealed a significant contrast between
the way Caucasians and Asians correlate math anxiety with
math ability and the way African Americans and Hispanics
correlate math anxiety with math ability, but none concern-
ing general anxiety and neuroticism. It has traditionally
been noted that math anxiety is negatively correlated with
math ability. However, through an ANOVA (using means
for math ability and math anxiety) it was found that math
ability has predictably a negative correlation with math anx-
iety in Caucasians and Asians (meaning the higher one‘s
math ability, the lower his math anxiety), whereas in Afri-
can Americans and Hispanics math ability has a positive
correlation with math anxiety (meaning the higher one‘s
math ability, the higher his math anxiety) - a very unex-
pected phenomenon. In essence, this implies that math anx-
iety cannot be blamed on math ability alone, and there is
another unknown factor that is essential in the causation of
math anxiety. This study highlights this critical difference
and opens the door to future research investigating why this
difference exists. The next steps entail lab experiments and
further questionnaires testing the accuracy of trends discov-
ered within this questionnaire and begin to delve into the
reasons as to why this trend exists. By discovering common
causes for math anxiety, methods of standard education can
be adjusted to prevent math anxiety among all races, and
thus produce a more mathematically able population.
43
The Effect of Socioeconomic Enviroment on Birth Out-
comes of Women in the South Bronx: A Proposal
By: Maribel Maria
Preterm pregnancy is an enduring issue in the United States
despite the advances in technology geared towards aiding in
the delivery of children. The actual causes of preterm preg-
nancy remain unclear to this day. However, factors are
known to exist which influence the outcome of a pregnancy.
A potentially influential factor may be the socioeconomic
environment, such as the perceived safety in the community,
in which a woman lives in during the time of her pregnancy.
It could be predicted that African American and Hispanic
women in the South Bronx are negatively impacted by their
socioeconomic environment and are thus likely to give birth
prematurely. Further investigation into the issue would be
necessary to determine if socioeconomic environmental
factors do affect the pregnancy outcomes of African Ameri-
can and Hispanic women. This study proposes to investi-
gate and evaluate the causes of preterm birth in the popula-
tion of African American and Hispanic women, in the South
Bronx.
The Number of Cortical Neurons Used to See
By: Krisha Mehta
A neuron‘s receptive field is the area in the visual field in
which it responds to light. A neuron has one cell body and
many dendrites. Physiologically, the integration occurs as
the signals from the many dendrites converge on the cell
body. The integrated input signals cause the cell to fire, i.e.
produce an action potential. The cell firing stimulates the
dendrites of other neurons. The integration is linear
(weighted averaging) even though the cell firing depends
nonlinearly on that weighted average. The main nonlineari-
ty is a threshold. The cell does not fire if the weighted aver-
age is less than the neuron‘s threshold. Thus, although a
complete mathematical model of the neuron would include
the nonlinearity of the cell‘s response, the spatial integration
by the cell‘s receptive field (or dendrites) is a simple sum, a
linear weighted average. That weighted average is a sample
of the image in the visual field of the observer. The
weighting functions that produce these samples have been
extensively studied in individual neuraons in fish, cats, and
monkeys, but very little is known about how these animals
and people use multiple neurons to see. There are hundreds
of millions of neurons in the visual cortex, but so little is
known that previously studied performance of human ob-
servers might be accounted for by using a single cortical
neuron. Here a new technique, based on a new mathemati-
cal theorem, allows non-invasive visual tests to demonstrate
that people use a large number of neurons. More specifical-
ly, findings show that observers are using a maximum of
about 100 receptive fields, a new upper bound never before
found in neural studies. Saying how many neurons are used
is a significant step towards the ultimate goal of explaining
how these neurons do the visual computation that is seeing.
Molecular Identification and Functional Characteriza-
tion of fried, a Gene Required for Growth and Fertility
in Drosophila 2010-2013
By: Sharon Migdal
Fried is a mutant gene known to cause defects in the ovaries
and larvae of drosophila. Two alleles of the gene were iden-
tified and named fried150 and fried212. Using a genetic
trick known as the flp-FRT system, we were able to study
the physical and behavioral effects of the gene by producing
a homozygous mutant and observe the mutation in the eyes
of the drosophila. White stops indicated the fried allele.
Fried mutants demonstrated defective behaviors in compari-
son to wild type larvae, which include precocious wander-
ing, early lethality, extensive melanization and an overall
smaller body mass.
A Survey of Juvenile Horseshoe Crabs (Limulus poly-
phemus) along Plumb Beach, Brooklyn
By: Lawrence Moy
All organisms are part of a food web and play a unique role
in the ecosystem they live in. Like all organisms within a
food web, American horseshoe crabs are important and vital
for the survival of their ecosystem. American horseshoe
crabs exhibit spawning during the spring in areas such as
Plumb Beach in Brooklyn, New York. Unfortunately,
horseshoe crab populations are on the decline. These de-
clines could have an impact on local food webs and on spe-
cies that rely on horseshoe crabs to survive. In this study to
examine changes in spawning activity of horseshoe crabs,
Plumb Beach was used as the research site. The East and
West mudflats of the beach were surveyed in the experi-
ment. Transects were used to box off regions within the
areas. In each boxed off region, the top portion of the sand
was filtered and the contents left over were examined for
horseshoe crab hatchlings. No juvenile horseshoe crabs
were found in either location, but other marine wildlife was.
Sheddings of horseshoe crab juveniles and adult carcasses
were also found on the east side. None of these were found
on the west side. As expected, no juveniles were found in
the surveys since the spawning season has been over for
quite some time. Future research will examine changes in
juvenile counts during the spawning season along with
changes in horseshoe crab populations over a longer period
of time and the effect of these changes on local shorebirds.
Optimized Conditions of Genome-Wide Screening for
Genes Correlated with Regulatory B Cell Biogenesis
By: Ujwalla Murthy
The B cell is widely recognized for its role in producing
antibodies to protect the body from invaders and pathogens.
44
It is known also for its ability to present pathogens to killer-
or helper T cells. Recently, interest in a little understood
subset of B cells, regulatory B cells (Bregs), has emerged.
Bregs can secrete interleukin-10 (IL-10), an anti-
inflammatory cytokine involved in suppressing the inflam-
matory immune response, important in autoimmune diseases
and inflammatory disorders. How a B cell becomes a Breg
remains unknown. Identification of genes involved in Breg
formation would have therapeutic value in inflammatory
and autoimmune diseases. Here I describe the optimization
of conditions for a genome-wide screen of genes associated
with Breg formation. Employing a strategy in which target
genes in mammalian B cell lines and cultures are silenced,
activating B cells (Bregs) and measuring IL-10 production,
would enable identification of potential genes responsible
for Breg formation. The silenced genes would cause a de-
crease in IL-10 production. These genes would be identi-
fied as putative regulatory genes. Here, an appropriate cell
line, virus dilution, experimental design, and cell density
were determined in preparation for these future experiments.
I found that the CH12F3 cell line, 1:1000 virus dilution, and
a plating density of 2.92 × 105 cells/cm2 were conditions
suitable for genome-wide screens, through which genes in-
volved in Breg formation could be identified. As possible
therapeutic targets, the identified genes would facilitate the
effort to create novel therapies for autoimmune diseases and
inflammatory disorders.
Purification of Beta Cells in a Heterogeneous Population
for the Treatment of Diabetes Mellitus
By: Pratyusha Mutyala
Over 130 million people worldwide are afflicted with Dia-
betes mellitus. The current treatment for this disease in-
volves insulin-injection and glucose monitoring; however,
there is no cure. A cure for this disease can be achieved
through beta cell replacement therapy. A viable population
of beta cells can be acquired through differentiating human
embryonic stem cells. In this research, fluorescence stain-
ing, cell screening, and FACS were used to isolate beta cells
in a mixed human islet cell population. Highly fluorescent
cells were separated from less fluorescent cells on the cell
sorter. This helped us to identify several potential candi-
dates for cell surface markers among which, surface marker
CDXX held the most promise. CDXX was incubated with
single cells dissociated from human pancreatic islets and
identified to potentially recognize the insulin-positive cells.
The cells were tested for the expression of insulin using RT-
PCR and qRT-PCR. The highly fluorescent cell population
was enriched fifty-eight-fold for insulin-containing beta
cells, indicating that islet beta cells are relatively enriched in
CDXX antigen and can be partially purified in a heterogene-
ous stem cell population by this method. In the future, this
purification method can facilitate beta cell replacement ther-
apy to potentially cure patients with Diabetes mellitus.
Enviroment Affects Cell Proliferation in Offspring
By: Chirilien Pang
There are many factors that may influence development in
offspring, including different proteins that are in the mother.
Previous studies have shown that maternal TNFa plays a
role in altering offspring memory. However, there still re-
mains a question about whether the effect on offspring
memory occurs prenatally, postnatally, or a combination of
the two. We found that foster mothers that express less or
no TNFa positively influence memory in offspring. Where-
as foster mothers that do have TNFa negatively influence
memory in offspring. Proliferation of cells in the dentate
gyrus of the hippocampus (as indicated by BrdU incorpora-
tion) was used as a measure of spatial memory. Our data
demonstrate how crucial and impressionable the postnatal
environment is to the offspring. Furthermore, we examined
whether the mother‘s milk was an underlying mechanism in
which the foster mother affected offspring memory. Our
data show that lactating mothers in whom TNFa was neu-
tralized fostered offspring with increased spatial memory as
measured by proliferation in the dentate gyrus of the hippo-
campus. These results are significant because they show the
effect of the postnatal environment on memory.
Initial In-silico Docking of M.Tuberculosis Beta-
Lactamase
By: Shivam Patel
Tuberculosis is a bacterial infection, which deals with the
lungs but has the ability to worsen and move throughout the
body. Currently, most cases of tuberculosis are able to be
treated with the regular strain; however there is a stronger
strain which is resistant to the penicillin. M. tuberculosis
beta-lactamase is the enzyme which will be used during this
experiment. This is because of the intrinsic resistance which
had developed for the enzyme to the illness; however the
enzyme does not always bind properly. The techniques may
be sufficient but the actual compound does not seem to ful-
fill the needed requirements. We are looking for a com-
pound which is able to destroy the strain which is at hand, as
well as keep the bacteria from leaving its dormant stage. If
no longer dormant or if present again, there can is strength
attained in the strain which will be able to cause more dam-
age to the person who is experiencing the bacteria. By using
in-silico doc king; we are using a cost effective method as
well as using a method which does not prove to be too tedi-
ous. The results which are attained here can be taken a step
further and put into experimentation. Certain compounds
have been proven to be better at this then others such as a
present carboxyl group, along with the presence of Clavu-
lanic acid and sulbactam. These specific components seem
to better the compounds affinity to bind with the enzyme.
45
Effect of Medial Dorsal Thalamic Lesions on the Devel-
opment of the Prefrontal Cortex
By: Ian Persaud
Gap junctions connect many types of cells, including neu-
rons. Diffusion of ions through gap junctions can coordi-
nate neuronal activity, hence influencing information propa-
gation and processing. However, exactly how diffusion
affects information processing remains poorly understood.
By modifying gap junctions, we examined how different
diffusion conditions affect sub-threshold oscillation in a 2
dimensional (2D) population of neurons. Here we describe
the derivation of those conditions under which diffusion of
ions through gap junctions allows Turing patterns- spatial
oscillations of ion concentration, which directly affects ac-
tion potential generation and other neuronal processes. We
derived these conditions for a sheet of neurons represented
by a system of linked reaction-diffusion equations. If gap
junctions slow the diffusion of inhibition below a critical
rate, Turing patterns cannot occur in sub-threshold neural
oscillations. At biologically plausible values of diffusion, if
the rate of diffusion is independent of space and time, Tu-
ring patterns occur. The spatial oscillations that Turing pat-
terns create occurs with a spatial frequency that depends on
the strength of diffusion. Our analysis show that recurrent
inhibitory neurons must scale to excitatory for Turing pat-
terns to occur. We also determined the effect of space, or
distance, between cells on Turing patterns of neuronal popu-
lations, a novel finding. We anticipate that our model will
lead to more sophisticated models of neural population in-
teraction. For example, modeling of neuron populations
with fluctuating thresholds or neuron populations with spik-
ing activity, even a 3D model of neuronal interaction are
plausible extensions of our model. Furthermore, since many
neurons perform functions in sub-threshold oscillation, an
understanding of the patterns associated with such functions
is essential to our understanding the neural system.
Immunostaining of UTF-1
By: Anjali Pillai
The purpose of this experiment is to use an immunostaining
method utilizing antibodies and antigen-retrieval to get the
best kind of staining of the marker UTF-1 (undifferentiated
embryonic cell transcription factor 1) that can be achieved.
UTF-1 is known for being a marker for pluripotency. It is
also known to be found to be expressed mainly in spermato-
gonia. Therefore, the hypothesis is that if properly stained,
UTF-1 will be expressed in the basement membrane of the
seminiferous tubules, where the spermatogonia are located.
The first part of the experiment involved going through the
typical protocol for immunostaining. This involves prepar-
ing the slides with testis samples for the antigen-retrieval
and addition of antibodies prior to the outcome of the stain-
ing itself. The slides were then stained to find where
exactly this transcription factor was seen. UTF-1 is thought
to be seen expressed in the spermatogonia of the testis. In
general, that would be the outline of the seminiferous tu-
bules (basement membrane). If this proved to work then
there would be proof of our hypothesis that there is a better
way to stain for this marker. The UTF-1 was expressed so
far with the basic protocol. The basis of this particular ex-
periment was to see the best staining. To find the best re-
sults, the experiment, and the protocol was to be optimized
so that the best possible results were produced. The idea
was to prove that there is a connection between UTF-1 and
spermatogonial self-renewal into various types of cells
(pluripotency). Overall then, that would mean that it was
expected that the marker is expected to work in the staining
but the following steps were taken take are to achieve the
best staining in the human testis samples.
The Interaction between the Ubiquitin/Proteasome Sys-
tem and the AMP-regulated Kinase Snf1
By: Anahi Potrero
The ubiquitin proteasome system (UPS) is the major proteo-
lytic system in the cytoplasm and nuclei of eukaryotic cells.
Many cellular functions are regulated via regulated turnover
of proteins by the proteasome and dysfunction of this sys-
tem is observed in many human diseases such as cancer and
in aging processes. To prevent unspecific protein degrada-
tion, proteasome activity is tightly controlled. Previous re-
ports indicate that the AMP regulated kinase Snf1/AMPK, a
regulator of energy levels in the cell, might functionally
interact with the UPS due to its UBA domain. In this work,
mutant and tagged Snf1 strains were created which allowed
the investigation of this interaction. The strains were puri-
fied and proteins that interact with the new strains will be
identified using mass spectrometry. This method will pre-
sent first evidence that the UPS interacts genetically with
SNF1 and that Snf1 itself is not a UPS target.
Pharmacological Dissociation of Smoking and Reward in
Schizophrenic Patients
By: Mousumi Reja
A high percentage of schizophrenics are smokers. This
study analyzes what happens in the brain when nicotine is
introduced in the brains of individuals, specifically schizo-
phrenics. When nicotine is introduced into the brain, there
is a large stimulation of receptor activity and large release of
acetylcholine. Glutamate is another neurotransmitter re-
leased in large amounts both because of the introduction of
nicotine in the brain and in schizophrenic patients. This
neurotransmitter is involved with memory, learning, and
enhances the reward system. This chemical activity within
the brain was studied in brains of schizophrenic smokers
and non-smokers. This study analyzed what happens in the
brains of schizophrenics when NMDA receptors are
blocked, a known consequence of nicotine use.
46
Ketamine, a phencyclidine hydrochloride derivative and
NMDA antagonist was used to block receptor activity. A
release of acetylcholine is accompanied with the release of
glutamate in smokers. When the level of glutamate increas-
es, so does the level of acetylcholine. Results showed that
in schizophrenics who were nicotine dependent, psychosis
was a response and patients had more cravings for nicotine.
Schizophrenics who were not nicotine dependent experi-
enced positive-like symptoms of schizophrenia, such as de-
lusions, thought disorders, and hallucinations. Healthy con-
trols experienced negative symptoms similar to those caused
by schizophrenia and were negatively affected by the in-
ducement of nicotine in their brains. This showed that keta-
mine blocks NMDA receptors from binding with glutamate
so that the reward system is not activated, but that schizo-
phrenic patients have more cravings for nicotine.
Prevalence of Parkinson’s Disease Mutation in Males
and Females: A Proposal
By: Martin Ridge
Parkinson's Disease is a neurodegenerative disorder that
affects over seven million people worldwide. The disease
ultimately leads to death, and can induce bradykinesia
(among other symptoms). Familial Parkinson's Disease is
an inherited form of the disease in which certain mutations
affect neural development. The most prevalent of these
mutations occurs in the Park8 gene, which encodes the pro-
tein Leucine-Rich Repeat-Kinase 2 (LRRK2). The mutation
creates a G2019S abnormality in the enzyme, causing it to
over-phosphorylate ERM Proteins in the dendrites. It has
been shown in mice that this over-activity of LRRK2 leads
to increased dendritic length and decreased dendritic
branching in early developmental milestones. In addition,
Parkinson's Disease has been shown repeatedly to have a
predilection for affecting males (in some studies, the rate of
incidence of Parkinson‘s Disease in males exceeded that of
females by over 90%). This project aims to ascertain the
relationship, if any, between the effects of LRRK2 G2019S
and gender. We expect to find lower rates of dendritic
branching in male mice compared to female G2019S mice
and control, along with lower dendritic lengths. The results
will show whether or not the increased prevalence of Park-
inson‘s Disease in males is correlated with the effects of
LRRK2 operation, or a more phenotypical set of stimuli. If
the results show that LRRK2 G2019S indeed affects den-
dritic branching in males more than in than females, then we
may proceed with testing the relationship between Parkin-
son's Disease and testosterone. A therapeutic method of
addressing this correlation would then be in reach.
The Modulating Effect of Pax5 on V(D)J Recombination
By: Amanda Ruiz
Acute lymphoblastic leukemia (ALL) is a cancer of the lym-
phocytes and is found to be prevalent in children.
Normally, lymphocytes fight bacterial and viral infections;
however, in all patients‘ newly developing lymphocytes do
not develop into mature cells, but stay as immature cells
called lymphoblasts. The immune system recognizes for-
eign substances via antigen receptors to elicit an antibody
response. The collection of antibody specificities an indi-
vidual has is known as the antibody or immunoglobulin
repertoire. The number of antibody specificities is limited
by the total number of B cells in an individual. V(D)J re-
combination is the process by which the variability and di-
versity of antigen receptors is generated. Since patients
with ALL do not properly develop B cells, their immuno-
globulin repertoire is very limited.
Lymphocytes have unique receptors, which enable recogni-
tion of almost any foreign substance. These receptors are
specialized and only match to one specific antigen. B lym-
phocytes develop in the bone marrow and produce receptors
via V(D)J recombination. This process increases the variety
of receptors of lymphocytes. V(D)J recombination, is a
mechanism of genetic recombination in the early stages of
immunoglobulin (Ig) and T cell receptor production. This
process primarily takes place in the primary lymphoid tis-
sue; the bone marrow for B cells, and Thymus for T cells.
The formation of an antigen receptor is categorized by the
combination of the Variable, Diverse, and Joining gene seg-
ments of vertebrates is a site-specific process. Since the
process of antigen receptor variability joins segments and
different genes almost randomly, the receptors produced are
able to diversely encode proteins to match antigens from
bacteria to tumor cells to pollen (Malu et al., 2012). V(D)J
recombination is initiated by the lymphoid-specific Rag1
and Rag2 proteins, which cooperate to make double-strand
breaks at specific recognition sequences (Gomez et al.,
2000).
Evidence of Hybrization in Camponotus pennsylvanicus
By: Sameer Sabharwal-Siddiqi
The purpose of the study was to test for the incidence of
hybridization in two species of hymenopterans: Dorylus
(Anomma) molestus and Dorylus (Anomma) wilverthi. This
study used morphometric and phylogenetic analysis to iden-
tify hybridization. Morphometric data was collected quanti-
tatively by measuring the posterior head lengths, and phylo-
genetic analysis was conducted through gene extraction,
PCR, and genotyping.
Youth-Generated Programs: Evaluating the Impact of
Project STEP-UP
By: Shyam Bhatt
Many adolescents in inner-city communities struggle in
school and in life, however, not much is done to help them.
Step-Up, a youth intervention stationed in two schools in
NYC, fills this void. The program assesses and addresses
mental health difficulties and provides opportunities
47
for increasing youths‘ social problem solving and life skills.
We hypothesized that Step-Up youth would evidence in-
creases in GPA and high school graduation rates that ex-
ceeded national and NYC rates of youth with mental health
difficulties, and that the more contextual stressors (i.e. race,
gender, who the youth live with, if they participate in out of
school activities) a Step-Up youth faces, the lower the GPA
and the more depressed he or she would be. All of the par-
ticipants completed surveys before and after the interven-
tion. The results from these surveys were analyzed using
SPSS. It was found that the program did not necessarily
increase the GPAs and decrease the CDI scores of the stu-
dents. However, it did maintain them (Mean GPA be-
fore=68.94, after=70.52; Mean CDI before=12.70, af-
ter=12.91). Since most of them were on a downward slope,
the fact that their situations did not become worse demon-
strates the success of the program. We also found that only
gender was a good predictor for post-intervention GPA, and
that none of the contextual stressors were good predictors
for post-intervention CDI results. This information can be
used to improve the Step-Up intervention and develop more
like it.
Toxoplasma gondii Genes Regulated by Apetala 2 Tran-
scription Factors Through Protein DNA Binding Motifs
and Transcription Start Sites
By: Lakshmi Devi Singh
vToxoplasma gondii, an Apicomplexan parasite carried by
cats, can infect humans and currently affects about one-third
of the world‘s population. The infection causes significant
brain inflammation, altered brain chemistry, and blindness,
which is of particular concern for susceptible populations
like AIDS, transplant and pregnant patients. Previous re-
search has found Apetala 2 (AP2) binding domains to be
prevalent in the genome of Apicomplexan parasites, includ-
ing Toxoplasma. This study focused on determining which
Toxoplasma genes have AP2 binding domains on their pro-
moter region. This was accomplished by creating a special-
ized computer program using two Bioconductor packages -
ChIPpeakAnno and Biostrings—to analyze the data of AP2-
GST fusion protein binding capabilities to DNA sequences
in Protein Binding Microarrays. The targeted approach of
the computer program was able to identify 116 genes in
Toxoplasma that have domains in their promoter region for
AP2 TF to initiate and promote transcription. These results
will facilitate in the understanding of gene regulation in
Toxoplasma gondii, which can be translated into advancing
the development of more effective treatments for infected
patients.
The Effect of CF-301 and Daptomycin on Polymicrobial
Biofilms
By: Elias Strizower
Staphylococcus aureus and Enterococcus faecalis are
pathogens that are leading causes of nosocomial infections
in humans. Each bacterium has unique abilities to adapt and
become resistant to conventional antibiotics, making treat-
ment difficult for clinicians. This is evident in the rise of
antibiotic-resistant strains of both bacteria. It is believed
that besides resistance via genotypic changes, the ability of
both of these bacteria to form complex communities that
function to prevent antimicrobial treatment is key in their
virulence. Biofilms, defined by J.W. Costerton to be a mi-
croniche of bacteria enveloped in an exopolysaccharide ma-
trix, pose a threat because of their shield- like properties to
bacteria. It is also a problem that biofilms do not usually
exist as single species because this makes them more diffi-
cult to treat. Polymicrobial infections are commonly found
in humans and often the culprits are combinations of S. au-
reus and E. faecalis. Current therapies have been shown to
be limited in combating these poly- microbial threats. The
treatment of S. aureus and E. faecalis biofilms by Daptomy-
cin and CF- 301is focused on in this paper. Daptomycin is a
broad- spectrum antibiotic most commonly used on forms of
S. aureus and E. faecalis that are not in biofilms. CF-301 is
a lysin, which has been shown to break through the cell
membrane through the process of lysis and has been shown
to have anti-biofilm properties and successfully kill bacteria
grown in biofilms. The results of this experiment show that
the use of Daptomycin and CF- 301 together can successful-
ly treat Polymicrobial biofilms.
An Intervention to Control Vasomotor Symptoms for
Advanced Prostate Cancer Patients on Hormone Thera-
py
By: Maliha Sultana
The research conducted in this study attempts to use modern
technology to propose a treatment for one of the side effects
resulting from androgen deprivation therapy, paced breath-
ing, for prostate cancer patients. Because vasomotor symp-
toms yielded a significant decrease in hot flash episodes
with menopausal women with similar experiences, it was
hypothesized that perhaps prostate cancer patients with sim-
ilar episodes would have similar results. In order to facili-
tate these trials, researchers in this study used iPods, inte-
grating modern technology in the research; this is different
from other oncological research in not only does it incorpo-
rate modern technology as a form of individual treatments,
but it focuses on current ways of dealing with those with the
disease already rather than depending on molecular sciences
to prevent the disease. The results have shown that patients
appreciated this program and that further improvements in
the final version would most likely be successful.
Suppression of Prion Toxicity in Yeast by Deletion of
Ubiquitin Ligases Correclates with Decreased Sizes of
Protein Aggregates
By: Sarah Sutto-Plunz
48
Neurodegenerative disorders such as Alzheimer‘s, Parkin-
son‘s, and Huntington‘s disease affect millions of people
worldwide. Each of these disorders has in common the in-
tracellular accumulation of misfolded and aggregated pro-
teins that are insoluble and are associated with cell toxicity.
These toxic compounds are known as prion proteins. Simi-
lar toxic accumulated proteins are found in the model eukar-
yotic organism yeast. RNQ1 is a yeast protein that, in its
prion form, leads to cell death. Toxicity is thought to be due
to a failure or overloading of protein quality control path-
ways in the cell. This idea is supported by the observation
that overexpressing a second protein that misfolds, Ste11?
NK444R, in the RNQ1 prion background further increases
protein aggregation and toxicity. The purpose of the experi-
ments presented here was to investigate the effects of Ste11?
NK444R expression on RNQ1 toxicity in yeast toward bet-
ter understanding the role of different protein quality control
pathways in protecting cells. In a cell viability assay, it was
found that loss of the Ubr1 and Ltn1 ubiquitin ligases that
target misfolded proteins to the proteasome suppressed tox-
icity. As shown by Western blot analysis and microscopy,
reduced toxicity in the ubr1? strains correlated with reduced
number and size of protein aggregates, despite the total
amount of Ste11?NK444R RNQ1 protein in the cell being
the same as compared to wild type. Furthermore, the results
of a semi-denaturing gel suggested that there is a relation-
ship between a decrease in toxicity and decrease in polymer
size in the aggregates. This suggests that the yeast strains
surviving exposure to the toxic aggregates may have sur-
vived by altering polymer and aggregate size. This work
has important implications for possibly finding a drug that
would aid quality control pathways to eliminate the toxic
compounds, or even prevent their formation, and using it to
cure the aforementioned neurodegenerative diseases, help-
ing save millions of lives.
Phosphodiesterase Inhibitors Reduce Proliferation in
Malignant Gliomas
By: Philip To
Malignant Gliomas are a deadly form of cancer with very
poor prognosis. Current available chemotherapies for treat-
ing malignant Gliomas result in significant adverse effects
indicating the necessity of novel less toxic treatments. Pre-
vious studies have shown that activation of the Protein Ki-
nase A/ Cyclic AMP responsive element binding protein
(PKA/CREB) pathway results in a decrease in proliferation
of Gliomas cells due to the induction of cellular differentia-
tion state. The PKA/CREB pathway is activated by increas-
es in levels of the small second messenger cyclic AMP
(cAMP). In this project, the effects of specific inhibitors on
Phosphodiesterase (PDEs), the enzymes that degrade
cAMP, on CREB activation are computationally modeled
and then experimentally validated to determine their ability
to prevent proliferation of Gliomas cells. First, an ordinary
differential equation based model of the kinetic reactions of
the PKA/CREB pathway was constructed to predict the
contribution of each individual PDE to PKA/CREB activa-
tion. Next, the effect of targeting specific PDEs with inhibi-
tors was measured experimentally via a CREB activation
assay and expression of a glial cell differentiation marker in
a Gliomas cell line. These data were used to refined the
computational model, and improve its predictive power.
Based on the simulation results, predictions on the anti-
proliferation potential of single PDE inhibitors and combi-
nations of PDE inhibitors were made. Lastly, the anti-
proliferating effects of PDE inhibitors in Gliomas cells were
tested experimentally. It was found that targeted inhibition
of PDE3, PDE4, and PDE7 in the Gliomas cell line U87
results in increased activation of CREB and decreased cell
proliferation. The targeted single PDE3 inhibitor displayed
the most pro-differentiation and anti- proliferation potential
in U87 cells. This is the first systematic study comparing
the contribution of multiple PDEs to the differentiation pro-
cess in Gliomas cells, and highlighting PDE3 inhibition as a
novel therapeutic approach to treat malignant Gliomas.
Co-immunoprecipitation Reveals an Interaction between
Human Factor P53 and Dengue Viral Protease NS2B/3
By: Pablo Vasquez
Dengue Virus is the most common mosquito-borne viral
disease in the world, with about 50 million cases of infec-
tion each year and is usually isolated in tropical environ-
ments where mosquitoes thrive. Because dengue virus
evades the innate immunity of the body, it can lead to sever-
al severe manifestations such as Dengue Hemorrhagic Fever
(DHF) or Dengue Shock Syndrome (DDS). Not all manifes-
tations of dengue virus are as severe, however. There are no
vaccines or antibiotics for dengue and treatment focuses on
treating symptoms. For instance, if dengue is diagnosed
early, it can be treated for by administering electrolytes. The
non-structural dengue protein NS2B/3 has been implicated
in interactions with host-cell proteins and it is possible that
those interactions help the Dengue virus evade the innate
immunity of the body. NS2B/3 has been shown to prefer
cleaving quartets of amino acids with the P1 site being ei-
ther Arginine or Lysine. The quartet follows the pattern of
two basic amino acids, followed by two small amino acids.
A pull down assay of NS2B/3 in a transfected cell revealed
over 300 potential specific binding partners. Proteins select-
ed fulfilled three criteria: 1.The proteins were present in the
initial pull down assay. 2. The proteins are involved in the
immune system in some way. 3. The protein has a potential
NS2B/3 cleavage site. Likely host-protein candidates in-
clude human proteins: PI3K, NIRF, DDX (17/39/60), P53
and the TRIP. Understanding which proteins, both viral and
human immune cell proteins, interact with which, is neces-
sary in order to understand how the dengue virus evades the
innate immune response. This study will use transfections,
and if necessary, co-immunoprecipitation to determine if the
given proteins interact with the NS2B/3 and further our un-
derstanding of the innate immune response evasion.
49
AMPure beads: Size-Selection of DNA
By: Navya Voleti
DNA Sequencing has become evident over the years, and
scientists have even been successful in sequencing the
whole human genome. In order for the DNA to be prepared
before it is sequenced, depending on the size of the DNA
fragments, because certain types of sequencing must be
done. In order to select the size of the DNA, gel electropho-
resis is used. However, it is very time-consuming and re-
quires techniques that are more complex than that of using
AMPure beads, which are magnetic beads that attach to the
DNA, so that the DNA that is attached can be taken out,
using a magnet. However, the use of AMPure beads is very
new and had to be tested in order to find an effective con-
centration that would yield the best results. The testing of
AMPure beads was done in order to find a better concentra-
tion of the beads that would yield a higher amount of the
target DNA size. AMPure beads are magnetic beads that
bind to the DNA. When these magnetic beads bind to the
DNA, it allows us to separate the DNA from the enzymes
and reagents. This is more efficient than running gel electro-
phoresis, since this takes about an hour, versus 3 hours for
gel electrophoresis. It was concluded that the concentration
of 1.5X would yield the highest amount of the target size of
DNA. Knowing this increases efficiency because it lets us
know the correct concentration at which we can use these
magnetic beads to obtain the DNA fragments that we need.
Regulation of Root Plasticity in Arabidopsis thaliana
By: Vinesh Vora
A major problem that we face today is a shortage of food
due to the decrease in crop output. This inadequate food
supply is the result of the changing climate that causes unfa-
vorable environments for the plants to thrive in. Plant root
system has major impact on plant survival, and it is regulat-
ed by myriads of internal and external factors. Understand-
ing how the root plasticity is regulated in different environ-
ments would be beneficial in crop production. Here we in-
tend to apply a combinatorial method utilizing 5 different
signals, known to regulate root plasticity, two Nitrogen sig-
nals (NO3-, NH4+) and three hormone signals (Auxin-IAA,
Cytokinins-CK and Abscisic Acid-ABA), to quantify root
development (Trait) and gene expression (Gene). We then
correlate Trait-to-Gene and use network analysis to identify
novel candidate genes regulating root plasticity. Finally, we
validate our hypothesis and identified a protein, the K+ pro-
tein channel that has a direct role in regulating the move-
ment of the stomata and transpiration rate, and potential
regulator of root development. We tested knockout mutant
line of this gene, and identified root phenotype in six root
traits. Potential application of this finding could be genetic
manipulation of this gene, thus allowing the plants to sur-
vive in the harsh environments.
Characterization of Novel Stem Cell Population
By: Phoebe Wong
Cartilage and tendons are one of the most difficult tissues to
repair due to lower metabolic rates and tearing post-repair.
A new look at therapy reveals stem cells, cells capable of
differentiating into various tissues, may be the key to repair.
This study focuses on comparing stem cell populations from
gingival and dermal sources, cultured with and without
transforming growth factor beta-3 (TGF-?3), to determine
the extent of chondrogenesis or tendogenesis in an in vitro
culture. TGF-?3 is a growth factor used for studies of Mes-
enchymal stem cells (MSCs), due to its proliferative and
differentiative effect on cells. Rabbit gingival and dermal
fibroblasts were cultured with/without TGF-?3. They were
examined with Safranin O/Fastgreen stains and qRT-PCR
with Collagen I, Collagen II, and Aggrecan, Decorin, and
Tenomodulin gene markers. Results showed TGF-?3 in-
creased proliferation and gene expression (except tenomod-
ulin) of both cell types. In addition, all samples were more
inclined for chondrogenesis than tendogenesis, because all
genes except tenomodulin (the only marker for tendogene-
sis) were expressed. The gingival MSCs were larger, had
higher levels of extracellular matrix, and attained more sig-
nificant gene expression values than that of the dermal fi-
broblasts. All qualitative and quantitative results indicated
that gingiva is a finer source than dermal for harvesting
stem cells, and that TGF-?3 effectively enhances cartilage
tissue formation of MSCs.
Various Agents Induce Encystment in the Protozoan
Parasite Giaradia
By: Jeffrey Wu
Giardia intestinalis, a protist that causes the diarrheal dis-
ease giardiasis, kills 1.8 million people each year, world-
wide. Giardia has two forms: trophozoite and cyst. Tropho-
zoites feed and reproduce in the intestine, causing disease,
and are shed in feces. Trophozoites do not exist long out-
side hosts. Cysts develop from trophozoites in the host, are
shed in feces, and can survive hardily outside. Cysts are
responsible for rapid spread of the parasite from host to
host. Bile, produced by the liver and an emulsifier of fats, is
an inducement factor of cysts in the host. It was hypothe-
sized that the ability of bile to induce cysts is due to its de-
tergent-like properties. The effect of detergent on cyst for-
mation in Giardia was tested in vitro. This research is im-
portant because it will help people understand how to con-
trol the spread of giardiasis. Inhibiting cyst formation
would help prevent host shedding of cysts in feces. If the
host only sheds trophozoites that cannot survive outside the
host long, the Giardia would likely die before reaching an-
other host.
50
Identifying Novel Function of Let-7 miRNA in Promot-
ing Nephron Formation
By: Carly (Yue) Yu
Kidney failure, one of the most severe health disorders to-
day, afflicts over 26 million American adults. The ultimate
cure is kidney transplantation. However, as recorded by the
U.S Renal Data System, approximately twelve patients die
every day amongst 100,000 others while waiting for an or-
gan donor. Therefore, widely available bio-artificial kid-
neys, which require a comprehensive understanding of kid-
ney development to build, will become crucial in future
treatment. Previous research has acknowledged that Mesen-
chymal Epithelial Transition (MET), in which the mesen-
chyme differentiates into divergent cell types to form neph-
ron, is essential during kidney growth. One regulator of
epithelial development is miRNA, which are small genes
that modulate organogenesis. We hypothesize that miRNA
may function in the MET process during which essential
internal structures of the kidney develop. To test our hy-
pothesis, the miRNA expression profile during MET was
screened, and 20 up regulated miRNA including the Let-7
family were found. Through Let-7f targeting by antagomir,
we have discovered that down regulation of Let-7f inhibits
ureteric bud branching and greatly reduces nephron growth,
which allows us to draw the conclusion that Let-7f miRNA
is a key player during kidney development. Thus, under-
standing the mechanism of Let-7f miRNA in a functional
kidney promotes groundbreaking advancement in engineer-
ing a feasible, replacement bio-artificial transplant kidney.
Assessment of Effect of Exercise on Body Composition
Changes Following Spinal Cord Injury
By: Zejia Yu
Persons with spinal cord injury (SCI) may become wholly
or partially paralyzed. Muscle atrophy, because of immobi-
lization and lack of exercise induces dramatic changes in
body composition. In the able-bodied population, exercise
programs are crucial in the prevention and control of many
metabolic syndrome-related disorders, such as carbohydrate
and lipid metabolism. To date, no standard guidelines have
been developed about exercise in the SCI population. In
addition, there have been no studies that examine the exist-
ing literature in order to summarize the relationship between
insulin sensitivity and exercise in those with spinal cord
injury. The goal of this comprehensive review was to exam-
ine the existing literature in the field of SCI medicine and
rehabilitation and to determine the variables reported that
may be associated with insulin resistance in the SCI popula-
tion. It is hypothesized that there will be a direct relation-
ship identified between body composition changes, duration
of exercise, type and intensity of exercise and the degree of
insulin sensitivity, or conversely lack of exercise, increased
fat mass, and/or loss of lean mass with insulin resistance.
The review study thus implicates that activity training with
duration from 8-52 weeks using the functional electrical
stimulation (FES) aerobic training method increases glucose
metabolism and insulin sensitivity, as well as prevents the
progression of insulin resistance to diabetes mellitus and
other associated metabolic disorders in patients with SCI.
WNT Signaling Protein LEF1 in Prostate Cancer Metas-
tasis
By: Valerio Zhang
?-catenin is a cadherin and a transcription co-factor that
plays a large role in the growth, invasion, and metastasis of
prostate cancer (PCa). ?-catenin during the Wnt signaling
pathway can be either degraded or partake as a downstream
effector for lymphoid binding-enhancer factor (LEF)1.
LEF1 in previous research has been identified as a mediator
in the Wnt/?-Catenin pathway (coordinating with Androgen-
Receptor (AR)) and regulator for cell growth and fate.
In this project we cultured PCa cell lines LNCaP, LNCaP-
AI, LNCaP-Lef1OE, LNCaP-AI-Lef1KD. The cells were
run through a 4% acrylamide gel electrophoresis detecting
for ?-catenin and 14-3-3?. A cell fractionation of the four
lines was run through a 10% acrylamide gel electrophoresis
detecting changes in the expression of ?-catenin and 14-3-3?
The results showed 14-3-3? to have higher concentrations in
the cytoplasm of the four cell lines and ?-catenin to be found
more concentrated in the nucleus than the cytoplasm with
the presence of 14-3-3?. When 14-3-3? was knocked down
with siRNA, ?-catenin had a significantly lower concentra-
tion in the nucleus than the cytoplasm. To confirm these
results, we used immunofluorescence microscopy with fluo-
rescent-dyes specific to ?-catenin, LEF1, and 14-3-3?.
In this experiment, we identified 14-3-3? as a chaperone
for ?-catenin and aids translocation of ?-catenin to and from
the nucleus. In addition, we will determine the cellular lo-
calization of both ?-catenin and 14-3-3? in multiple prostate
cancer cell lines
Reactive Oxygen Species Elicit Renin Release from Mast
Cells
By: Qinru Zou
Mast cells are present in myocardial tissue in close vicinity
to myocytes and nerve endings. Though these cells are best
known for their role in allergic reactions, research has
shown these cells are pivotal in the activation of a local car-
diac renin angiotensin system, a hormone system that is best
known for its regulation of blood pressure and water bal-
ance. Evidence suggests that mast cells constitute an addi-
tional source of renin in the heart. Human mastocytoma
cells and murine bone marrow-derived mast cells were incu-
bated with H2O2 to mimic ischemic conditions in the heart.
As a function of its concentration, H2O2 elicited mast cell
degranulation, as evidenced by the release of hexosamini-
dase, which was associated with a release of renin.
51
Award Winners in Biology 2012
American Academy of Neurology Neuroscience Prize
Vincent Shieh
Intel Science Talent Search Semi-Finalists Award
Sahil Agrawal, Bhargava Chitti, Olivia Munk, Talal Syed, Qian Kun Tan, Catherine Wang
ISEF Finalists
Shu Hui Liu, Talal Syed, Tongzhu Xu
Junior Science and Humanities Symposium (JSHS) Finalists
Bhargava Chitti, Christina Liao, Qian Kun Tan, Tongzhu Xu
New York City Science and Engineering Fair Finalists
Sahil Agrawal, Yuwen Cheng, Bhargava Chitti, Florence Dasrath, Matthew Eakle, Gabrielle
Frenkel, Michela Garabedian, Enkhmend Gereltogtokh, Vivek Gupta, Andreas Hadjigeorgiou,
Anthony Hagouel, John Hong, Tahsina Islam, Christina Liao, Shu Hui Liu, Anton Morozov,
Yaseen Morshed, Olivia Munk, Anne Qiu, Brianna Saunders, Andrew Shakalis, Vincent Shieh,
Talal Syed, Diptesh Tailor, Qian Kun Tan, Matias Tong, Tongzhu Xu
Siemens-Westinghouse Contest
Finalist: Yuwen Cheng
Semi-finalists: Anthony Hagouel, Vincent Shieh
Award Winners in Biology 2013
Intel Science Talent Search Semi-Finalists Award
Yashaswini Chittampalli, Daniel Donenfeld, Amanda Ruiz
ISEF Finalists
Uri Rosenshine
Junior Science and Humanities Symposium (JSHS) Finalists
Lubaina Haider
New York City Science and Engineering Fair Finalists
Tyler Bell, Daniel Donenfeld, Ekramul Gofur, Daniel Huang, Ian Kaplan, Rana Lamisa, Fred
Lin, Pratyusha Mutyala, Chirlien Pang, Ian Persaud, Elias Strizower, Maliha Sultana, Philip To
Siemens-Westinghouse Contest Semifinalist
Sarah Sutto-Plunz
52
Photo Credit: : Shutterstock / Sebastian Kaulitzki
The Journal of Biology is published annually by the
Students of the Bronx High School of Science.
The Bronx High School of Science
The Journal of Biology, Rm 329D
75 West 205th Street
Bronx, NY, 10468