BrockPre-MedSociety&itsSubsidiariesPresents

Edition#2

MEDMAG
Brocks Premium Magazine

Dentistry
Physiotherapy
Pharmacy
Medicine

Presidents Statement
Dear Badger,
What you are holding is the efforts of roughly 40 students that have come together
to put MedMag #2 together. We have all worked together in bringing you another version
of the MedMag, a magazine that is dedicated to expanding the word of true science
amongst all students. As year 2 come to an end, we are proud to say that we have continued
our promise in empowering the student population with knowledge and leadership opportunities. We have witnessed the growth of Pre-Med and its Subsidiaries from a simple idea
into a powerhouse of excellent students, all in unison to learn, provide value, and leave
their footprints at Brock.
Nevertheless, a sincere thank you goes out to all of our sponsors and partners: Dr.
Salame of MapleWood Dental, Dr. Ramjist of MedCrashCourse, Dr. Ryan of SGU, Mrs.
Paterson of St. Catharines physiotherapy Center, Dr. Dudding of The Dudding Group &
BrockU, University of Torontos Pharmacy School, the Sutherland Chan School of
Massage Therapy, Princeton Review, The Hype, BioLinc, and BUSU/BUSAC. The contributions have been immense and have provided many Brock University students a chance
to educate themselves, network, and gain opportunities to advance themselves in their
respective fields. With that being said, thank you to all the wonderful Badgers that would
come out and fill our rooms to full capacity! With all of your love and support, we have
successfully established the roots for one of the largest student-body organizations at
Brock; it can be said with the utmost confidence that this will be one of the societies that
remain at Brock for many years to come.
As I graduate from this wonderful school, I am looking forward to seeing the
successes of our leaders of tomorrow. Brock University has easily been the best choice Ive
made; it had given me the opportunity to not only learn, but to innovate, create, and
educate. However, two short years later, it is time to let go of PreMed and the wonderful
people that Ive had the honour to work and succeed with. With that said, I would like to
present to you one last time the hard work that we have all put in and proudly call MedMag.
This is Edition #2, and undoubtedly, there are many more to come.
Yours Truly,

Iraj Zunair Afzal

Founding President of PreMed & MedMag Societies

TABLE OF CONTENTS
Pages 4 & 5

Vorinostat:A Potential Treatment Towards Metastatic Breast Cancer

Pages 6 & 7

Leucine A Potential Solution to Fat Loss

By Iraj Zunair Afzal

By Milin Patel

Gleevec: The Most Successful Cancer Treatment

Page 8

By Sachin Kaushal, Hari Selvan, & Malu Gupta

Potential Treatment for HIV-1 with Genvoya

Pages 9 & 10
Pages 11 & 12

By Danyal Mirza, Husnain Ali, and Adil Faruqui

Stem Cells: The upcoming regenerative future in dentistry

By Patrick Zaprzala

Page 13

Dental Fluorosis and Fluoridation in Drinking Water

Page 14

Stem Cells and Primary Teeth

By Anas Tareen, Andrew Seif, and Chandni Patel

By Bishoy Grgs and Anas Tareen

Pages 15 & 16
Page 17
Pages 18
Pages 20
Pages 22
Pages 24
Pages 26
Pages 28

High Fat Diets May Affect more than Just your Waistline
By Danial Behzad

Theranos and the Painless, Needleless Future

By Kirina Angrish, Veen Murali, Sim Summan, Pavleen Dhillon, Sukhi Mankhu, Suki Pannu, and Nikhil Ghandi
Constraint Induced Movement Therapy for Injured Limbs Post-Stroke
& 19
Constraint Induced Movement Therapy for Injured Limbs Post-Stroke
Repatha: Lowering Cholesterol 1 Person at a time
& 21
By Taylor MacIsaac
The Mirror Neuron Effect
& 23
TBy Sachin Kaushal
& 25 MAPK Kinase 3 Is a Tumor Suppressor with Reduced Copy Number in Breast Cancer
By Ivor Smajlagic
Applied Antibiotics
& 27
By Benjamin McArthur
The
Hype,
Events & Sponsors
& 29

Executive Circle of 2015

Pages 30 & 31

-3-

VORINOSTAT - A POTENTIAL
TREATMENT TOWARDS
METASTATIC BREAST
CANCER

By Iraj Zunair Afzal

Researchers have been

focusing very heavily on treating
cancers for many years and moving
away from the traditional methods that
usually involve a hail Mary type
treatment with chemotherapy &
radiation. A study done in 2009
examined the activity and effect of a new
drug, vorinostat, on breast cancers that
metastasize to the brain. Vorinostat, a
histone deacetylase inhibitor, is
comparably unique to other anti-cancer
drugs because it can diffuse across the
blood brain barrier (BBB) a barrier
that separates circulating blood from
the fluid outside of brain cells[1]. The
BBB has certain electrical, physical, and
chemical properties that inhibit many
drugs from entering but vorinostat
seems to meet all the criteria that allow
it to pass through like to a guard that
lets people pass if theyre on the VIP list.
The question that one may
ponder upon is does vorinostat even
work and the answer seems to be yes.
Researchers studied mice that were
injected with the cancer cells and found
that if vorinostat is administered within
the first 3 days post injection, there is a
reduction in large metastases by 62%
and micrometastases by 28%[1].
However, the efficiency of the

drug depends on the time of

administration. This is because when
the drug was administered 7 days post
injection, reduction of large metastases
reduced down to 35% - if the drug was
administered 14 days post injection,
reduction of large metastases was only
22% and deemed not statistically
significant (meaning that the drug was
likely inefficient and the reduction in
cancer size may have been due to
chance) [1]. Nevertheless, the fact that the
metastatic cancer reduced, it supported
the original belief that vorinostat can
cross the BBB. Another interesting
thing to note is that vorinostat was up
taken in the cancer cells three fold in
comparison to surrounding brain
tissue, indicating that its

-4-

Figure 1: Clonogenic Growth Responses to

Varying Quantities of Vorinostat compared
with Control Vehicle[1]

distribution is not homogenous[1]. However,

researchers found at the same time that there
are proteins in the brain that actively work to
remove vorinostat an d reduce its BBB
diffusion efficiency[1]. Using verapamil, a
drug that prevents these proteins from
removing vorinostat, researchers concluded
that vorinostat would more efficiently diffuse
and distribute among the brain and the
cancer if such proteins did not exist[1].
Knowing that vorinostat works is a
fantastic feat of modern science but as
always, an important question to ask is how
does this drug work? The reason for that is
because what is tested in a petri dish in the
lab (in vitro) is not always the same as what
happens in the body (in vivo) due to many
other factors[1]. For starters, vorinostat was
noted to cause apoptosis (cell death) in vitro
but during in vivo studies on the mice, this
wasnt detected. At the same time, in vitro
studies showed that histones were acetylated
because vorinostat is an inhibitor of histone
deacetylase, but, in vivo studies disagreed
with the in vitro results[1]. Researchers
attribute this to the fact that their
methods/equipment werent sensitive enough
to detect the acetylation. Nevertheless,
vorinostat still worked very well and this
may be due to two mechanisms that were
studied in vivo and agreed with in vitro
studies[1]. For starters, in vitro studies
showed that vorinostat caused the cell cycle
that leads to the expansion and growth of the
tumour to be halted when vorinostat was
administered(Figure 1)[1]. This is excellent,
especially for metastatic cancers, because the

-5-

spread of the cancer can be stopped if you

can stop its reproduction cycle[1]. At the same
time, in vivo research showed that vorinostat
actually caused damage to DNA by breaking
the DNA and creating two separate
fragments (also known as double stranded
breaks DNA or dsbDNA)[1].In vitro studies
showed that vorinostat caused the
production of nitric acid in the breast cancer
cells, which may be the cause for the
dsbDNA[1]. However, the cancer cells can
repair this damage through repair
machinery (RAD52 gene produces this
machinery)[1]. Heres where it gets better in
vivo vorinostat studies showed that the
RAD52 protein was not produced in the same
quantities as normal cells because vorinostat
was inhibiting its production, therefore, not
allowing the cancer cell to fix the damage
(Figure 2)[1]! Vorinostat works on other genes
as well (such as Hes1 a gene that suppresses
other genes from being expressed) and
therefore slows down the tumour cell
outgrowth[1]. Because of such powerful
effects, vorinostat may proceed into clinical
trials and would be closely studied as a
potential treatment to breast cancers that
can be metastasized to the brain.

Figure 2: Immunohistochemical validation of

decreased Rad52 in vivo[1]

Leucine A Potential
Solution to Fat Loss
By Milin Patel

Have you been trying to look for new exercises and

workouts for fat loss, but have not achieved success? Well, a
research experiment performed by Feifan Guo and his team
suggests that the solution may not necessarily be in the workout,
but in fact in the diet. To be more precise, it may be in leucine.
Leucine is an essential neutral pH, non-polar amino acid
that contains an isobutyl R group1. Guo and his team, in a
previous research experiment had found that mice maintained
on a leucine-deficient diet for 7 days experienced a dramatic
reduction in abdominal fat mass2. However, in a more recent
research experiment, they had confirmed these findings and
also determined the molecular and cellular mechanisms
underlying the rapid abdominal fat loss induced by the leucine
deprivation. They used a mouse model for this. 3 In this recent
experiment, they divided mice into three groups and assigned
each group a specific diet for 7 days: control diet, leucine
deficient diet, and pair fed diet. The control diet was not leucine
deficient, but the leucine deficient one was.3 Also, since their
earlier experiment had told them that mice fed on a leucine
deficient diet consume 15% less food than those on a control
diet, they wanted to see if reduction of leucine or reduction of
food intake was the actual cause of the abdominal fat loss.2 To
do this, they added a third diet, called the pair fed diet, in which
mice were fed 15% less food than the food in the leucine
deficient diet. 3
-6-

increased expression of uncoupling

protein 1 in brown adipose tissue,
suggesting increased thermogenesis and
therefore an increased internal body
temperature. 3
Although this experiment was
performed on mice, its results may be
applicable on humans as well. The
reason why you are still having trouble
shedding off your abdominal fat may, in
fact be your high leucine intake, more
than anything.

The results of this experiment

indicated that leucine deprivation for
7 days resulted in a 15% reduction in
food intake and body weight
compared with mice maintained on
the control diet (Figure 1A and 1B). 3
Also, there was significant abdominal
fat loss in mice fed the leucine deficient
diet (Figure 1C). However, body
weight was reduced <5% (Figure 1B)
and abdominal fat was not
significantly reduced (Figure 1C) in
pair-fed mice, compared with control
dietfed mice. 3 In addition, the total
body fat was significantly decreased
by leucine deprivation in comparison
with the control and pair-fed mice,
whereas there was no difference in the
proportion of lean mass among the
groups (Figure 1D and 1E).3 These
results suggest that the reduction of
leucine in the diet is in fact the reason
for abdominal fat loss, and that lean
mass is not affected by a leucine
deficient diet.
Guo and his team also found
that leucine deprivation for 7 days
increased oxygen consumption,
suggesting
increased
energy
expenditure. They also observed
increases in lipolysis and expression of
-oxidation genes and decreases in
expression of lipogenic genes and
activity of fatty acid synthase in white
adipose tissue, indicating increased
use and decreased synthesis of fatty
acids, respectively. Furthermore, they
observed that leucine deprivation

Figure 1: Body weight and

abdominal fat mass decreases in
leucine-deprived mice. Mice were
fed
a
control
diet,
leucine-deficient diet ((-)leu diet),
or pair-fed diet (pf diet) for 7
days. Body weight and food
intake were monitored daily. A.
Food intake change. B. Body
weight reduction. C. Adipose
tissue mass in proportion to body
weight. D. Fat mass composition
in body. E. Lean mass
composition in body.3

-7-

GLEEVEC
GLEEVEC
GLEEVEC
GLEEVEC
GLEEVEC
GLEEVEC
GLEEVEC
GLEEVEC
GLEEVEC
GLEEVEC
The Most Successful Cancer Treatment
By: Sachin K, Hari S & Malu G

Gleevec (Imatinib) is an actively

prescribed cancer treatment drug that was first
synthesized
by Novartis Pharmaceuticals in
1992[1]. Its synthesis was first created for its
purpose towards [2]
treating leukemia and other
forms of tumours . In 2001, Gleevec was FDA
approved for its treatment towards patients
suffering from Chronic Myeloid Leukemia
(CML) and in 2002 it was FDA approved for
patients suffering from
Gastrointestinal Stromal
Tumours (GISTs) [3].
With over 6000 Canadians being
diagnosed with leukemia each year, 10% of those
patients suffer from Chronic Myeloid Leukemia
(CML), at which 60% of those diagnosed
were
treated with the use of Gleevec[1]. Since then
Gleevec has risen in its potential to treat other
forms of disease such [2]as gastric tumours and
bone marrow disorders .
In 2015, Gleevec was labelled as being
the most successful cancer treatment drug to
date, which was purely due to the fact that it had
the least amount of side effects, along with its
ability to [5]
target cancer cells directly and cause
cell death . The only major issue with Gleevec's
use towards cancer treatment is the ability for
cancer cells to become resistant. Scientists today
are building resistance drugs as well as alternate
forms of Imatinib
to prevent cell resistance and
cell growth [4].
Leukemia is a type of cancer that
occurs when an abnormal amount of white blood
cells are produced in the bone marrow which
then accumulate within the blood and move to
other parts of the body. Gleevec (Imatinib) is a
BCR-ABL tyrosine kinase inhibitor, which
occurs in those who have chronic Mylogenous
leukemia and carry an abnormality on
chromosome [6]22 known as the Philadelphia
chromosome . Imatinib blocks cells containing

the BCR-ABL tyrosine kinase gene from

reproducing at a rapid rate. It prevents the
progression of leukemia by targeting abnormal
proteins that may promote the growth and
survival of cancer cells.
Dosages of Gleevec, just like any other
drug, varies according to many factors such as
age, body mass and the presence of impeding
conditions. Typically, doses should be
administered in 400 mg or 600 mg, once daily.
However, a dose of 800 mg is advised to be
administered as 400 mg twice a day. Some
common side effects of Gleevec include swelling
around the eyes and legs as well as diarrhea,
nausea, vomiting, muscle cramps, muscle or
bone pain, abdominal pain, fatigue, excessive gas
and rash. Long-term side effects include
musculoskeletal,
gastrointestinal,
and
respiratory irregularities. It should be noticed
that a positive evidence of risk has been noted
due to taking Gleevec, as the drug interacts with
and is absorbed by the skin and lungs increasing
the chances of affecting unborn babies. Gleevec
should be taken with close consideration to the
medical condition of the patient. While it serves
as a breakthrough method of second-line
treatment, much[7] care should be taken when
taking this drug .

Figure 1: This figure illustrates the docking of

Gleevec (imatinib) in the ABL domain, which
inhibits
the reproduction of bone marrow stem
cells (1).
-8-

Potential Treatment for

HIV-1 with Genvoya

By: Danyal Mirza, Husnain Ali and Adil Faruqui

A biopharmaceutical company focuses on discovering and developing new

treatment for all types of diseases[1]. Gilead sciences developed Genvoya to treat Human
Immunodeficiency Virus-1 [HIV-1] and chronic hepatitis B, without the aid of other
antiretroviral medications[2]. Genvoya was recently FDA approved on November 5th,
2015[2]. Genvoya is an antiretroviral medicine used to slow down and prevent viral growth,
typically through inhibition[3]. Genvoya is composed of four antiretroviral medications:
Elvitegravir, Cobicistat, Emtricitabine and Tenofovir[2]. Each of these antiretroviral
medications work in different ways; Elvitegravir is an HIV-1 integrated strand transfer
inhibitor[4]. The reason why Genvoya is unique amongst all the other antiretroviral drugs is
because it contains Tenofovir Alafenamide [TAF]. Genvoya is on par with stribild for
treatment of HIV-1 however it's side effects are less demanding[2]. Due to TAF targeting
cells instead of going through bloodstream for the drug to take effect, less toxicity is being
released into the kidney and bone marrow[2].
Elvitegravir functions by blocking integrase activity of HIV virions thus preventing
the integration of the viral genome into the host cell[2]. The mechanism of action involves
Elvitegravirs Beta ketone and carboxylic moiety which assume a coplanar conformation
that binds to the viral integrase, inhibiting it[2]. By preventing the integration of viral and host
genomes, significant virus proteins cannot be translated and the virus particles cannot be
produced. Cobicistat is an essential drug that aids in HIV treatment but does not itself act on
any HIV particles[5]. Rather, Cobicistat increases the efficacy of other antiviral drugs by
reducing the activity of the liver metabolizing and eliminating anti-viral drugs[5]. Decreasing
the enzymatic activity of the liver allows for antiviral medication to remain within the body,
and boosts the effectiveness of Elvitegravir[5]. Cobicistat specifically targets and inhibits the
cytochrome P-450 3A isoforms, which are the proteins significant in the metabolism of
drugs such as Elvitegravir ultimately preventing the biotransformation of these drugs into
inactive metabolites[5]. Emtricitabine acts as an antiretroviral by inhibiting the function of
viral protein; reverse transcriptase[6]. Since HIV has single-stranded RNA as its initial
Table 1: Zidovudine [AZT], elvitegravir [EVG]
and L-870,810 antiviral activity compared to
different strains of HIV. This was measured by
EC50 which is the concentration required for half
the maximum inhibition of HIV replication, so
smaller value indicates more potent drug 4.

-9-

genome, it must be changed into DNA [cDNA] in order to be

integrated into the host genome[6]. If this activity can be
halted, integration of genomes and the synthesis of virions
and viral factors would also cease[6]. Emtricitabine utilizes a
mechanism which begins its phosphorylation by kinases
forming the active metabolite emtricitabine 5- triphosphate
which competes with the 2-deoxycitidine 5-triphosphate
substrate[6]. Since emtricitabine 5- triphosphate lacks a
hydroxyl group when incorporated into the HIV-DNA chain,
termination occurs and cDNA is not completely formed[6].
Tenofovir Alafenamide functions like Emtricitabine as a
reverse transcriptase inhibitor. The mechanism for this
involves the conversion of Tenofovir Alafenamide into
Tenofovir when entering the cell from blood plasma by
enzyme Cathepsin A[7]. Tenofovir is then further metabolized
into its active form Tenofovir diphosphate after being
phosphorylated which would then stop and terminate
formation of the cDNA by acting as a competitive inhibitor
of HIV-1 reverse transcriptase[7].

Figure 1: Structure of Tenofovir Alafenamide [left]

and Emtricitabine [right].

The dosage of Genvoya is dependent on the

healthcare provider, but generally it is taken once a
day. This medication should not be taken with any
other HIV- 1 medicines. The common side effects of
this drug include fluctuation of weight in the body,
increase in productivity of the immune system,
kidney problems including kidney failure, bone
problems and the most common would be nausea.
Individuals whom are interested in taking this drug
need to make sure they are not taking the following
drugs already: Alfuzosin hydrochloride,
Carbamazepine, Cisapride, and Ergot.
-10-

Stem Cells: The Upcoming

Regenerative Future In Dentistry
Stems cells offer new
potentials for treating diseases such
as diabetes and heart disease. New
research is now looking at the
potential use of stem cells in
dentistry. Stem cells are immature
cells that are able to divide and
mature into specialized cells that
perform a certain function in the
body. In humans there are two main
types of stem cells: embryonic stem
cells and adult stem cells. These cells
are able to act as repair mechanisms
in the body and are able to replenish
adult tissues [4]. There are three
known accessible sources of adult
stem cells in humans. They originate
in the bone marrow, adipose tissue,
blood and umbilical cord just after
birth. These stems cells are used
often in medical therapies, for
example in bone marrow
[2]
transplantation
.
Recently,
researchers have been able to grow
stem cells artificially and allow them
to mature into specialized cells.
One of the big issues with

By: Patrick Zaprzala

stem cells has been the accessibility to the

collection areas. However, dental pulp stem cells
have shown to be an answer to this problem.
Accesses to the dental pulp stem cells are easy,
highly efficient, have a low morbidity and are
able to mature extensively. Dental pulp is the
soft living tissue within a tooth (Figure 1). The
stem cells are located within this living soft
tissue. The particular types of stem cell scientists
have identified as the greatest future potential to
mature are the mesenchymal cells [6].

Figure 1. Model of dental pump within tooth [6]

DPSCs are obtained from adult teeth.

They are grown on a media that has been
supplemented with growth factors. The initial
doubling time of media cultures is about 12 to 50
hours for the first 40 population doublings.
After it reaches about 50 population doublings
the growth rate is slowed and doublings take
about 60-90 hours.
-11-

The most common clinical

application of these dental pumps is
the regeneration of pulp within a
damaged tooth [3]. In a root canal
treatment the permanent molar stops
any continuous growth which leaves
the tooth as a thin egg shell and is at
high risk for fracture. With the
Figure 1 1. Prevalence of Moderate and Severe
harvested dental pulp they are able to
Periodontitis Among Adults Aged 45-74 in the
United States, 2009-2010
grow back the pulp of a severely
damaged tooth strengthening it. This allows the injured tooth to return to its normal,
heathy state.
Periodontal disease is the result of injury or defects that cause damage to the
periodontal ligaments and extremely prevalent in our society (Table 1). These stems
cells have also been a promising tool in repairing periodontal ligaments. These are the
connective tissue fibers that attach a tooth to the alveolar bone and are often referred to
as gums. Stems cells have shown the ability to create alveolar bone, periodontal
ligaments and cementum (surface layer of the root) in periodontal diseases [6].
[5]

Finally, stem cells have been found to be useful in regenerating

bone and correcting craniofacial defects due to cysts [1], tumors and
trauma. They are able to engineer bone grafts, joints and cranial
sutures using stem cell therapy. These aspects are useful in patients who
suffer from genetic defects or experience severe head injury.
In the future the regeneration of adult human teeth should be
possible with new advancements in stem cell therapy and tissue
engineering. These procedures would be a better alternative and
possibly replace the need for dental implants [6].
The future of dentistry is focusing more on the regenerative
aspects where patients will be able to treat their diseases using their own
cells. Stem cell therapy will to have a paramount role in the future
treatments and looks to have a bright future. Further research is need
with longer patient follow up to study the life time of these regenerated
tissues.

-12-

Dental Fluorosis and

Fluoridation in Drinking Water

By Anas Tareen, Andrew Seif, and Chandni Patel

Enamel on our teeth are the hardest and most mineralized substance in our body.
Every day it undergoes the processes of demineralization and remineralization [3]. Relative to
numerous minerals that help in the development of teeth, fluoride in particular has presented
some interesting benefits. In small doses, fluoride helps[3]strengthen and promotes the process of
remineralization, which
prevents risk of tooth decay . Fluoride has also shown effectiveness
in caries prevention [2]. But it is also important to note the drawbacks of fluoride. DenBesten
and Li (2011), found that high intakes of fluoride during tooth formation resulted in fluorosis
[4, 6]
.
Fluorosis first attracted attention in the early twentieth century. The severity of
fluorosis is related to the concentration of fluoride in the plasma [4, 5]. Plasma fluoride levels are
influenced by numerous factors including total fluoride[1]intake, renal func-tion, rate of bone
metabolism, metabolic activity as well as genetic factors . Based on a normal day life, we have
come across different products that contain recognizable levels of fluoride. Examples of these
products include fluoride supplements, fluori-dated-water and dental products, such as
toothpaste or mouth rinses.
According to the World Health Organization (2015), dental fluorosis is a
water-related disease [7].[7]Dental fluorosis is prevalent in less than one-quarter of people aged
6-49 in North America . It has been suggested that although moderate amounts can have
dental effects, long-term ingestion can lead to potentially severe skeletal problems and
Fluoride Modality

Low Caries Risk

High Caries Risk

Toothpaste

Starting at tooth emergence (smear of

paste until age 3 y, then pea-sized)

Starting at tooth emergence (smear of

paste until age 3 y, then pea-sized)

Fluoride varnish

Every 3-6 mo. starting at tooth

emergence

Every 3-6 mo. starting at tooth

emergence

Over-the-counter mouth rinse

Not applicable

Starting at age 6 y if the child can

reliably swish and spit

Community water fluoridation

Yes

Yes

Dietary fluoride supplements

Yes, if drinking water supply is not

fluoridated

Yes, if drinking water supply is not

fluoridated

Table 1: Summary of Fluoride

Modalities for
Low- and High-Risk Patients [3].

psychological distress
. The usual
cause of this problem is usually a result of
contaminated drinking water, which has
become a rising endemic in deve-loping
countries. Parental vigilance can play an
important role in preventing fluorosis.
Primary options is to find a supply of safe
drinking water with either safe fluoride
levels. Fluorosis can have a wide array of
symptoms, ranging from tiny white
specks to vivid dark brown stains and
[1, 7]

rough, pitted enamel

that is extremely
difficult to clean [1]. In some cases, mild
fluorosis that is untreated can diminish
over time, and further eliminated
from
the help of dental professionals [1]. Tooth
whitening is also an option for less severe
cases. Whereas, more severe cases may
require veneers, which are custom-made
shells that cover the front of the teeth to
improve their appearance.

-13-

By Bishoy Grgs and Anas Tareen

Stem Cells and

Primarily Teeth

Upon the opening of a

discussion related to stem cell research,
most people are under the assumption
that stem cells are obtained solely from
the bone marrow or the umbilical cord
of babies. Stem cell research presents an
opportunity for scientific evidence that
goes far beyond regenerative medicine [3].
Recent research has found that baby
teeth [2]can also be used as a source of stem
cells . The dental pulp in baby teeth
contain stem cells that can be regrown
with different types of cells like bone,
cartilage, neurons [2,and
some certain
types of cardiac cells 3]. This pulp is also
founds in childrens wisdom teeth if they
are not removed.
This only condition to this is
that it must be preplanned. The cells
should be living in[1, 2,order
to be alive
otherwise they die 3]. There if one is
planning on using their childs baby
teeth for stem cells, they must plan
ahead. In order for the cells to be alive,
they must have enough blood supply
within last 48 hours before being frozen.
Therefore the parents must order the
container from the lab with the
preservation
solution before the tooth
falls out [3]. So, the parents must put the
fallen tooth in the preservation solution
in the container and ship it to the lab
overnight.
By harvesting those stem cells,
in theory by using the desired extracts
from the primary teeth (baby teeth) a
variety of diseases can be treated, such as
Leukemia, inherited immune system
disorder [3] and various metabolic
disorders . The list of diseases that can
be treated using stem cells is largely
diverse, indicating that there is great
potential behind even the smallest of
primarily teeth. The human body is
compromised with roughly 200 different

kinds of specialized cells [1, 3]. Stem cells can be

pluripotent, which can specialize into every
cell in the body, and they can also be
multi-potent which
can become only certain
types of cells [3]. Stem cells are very
advantageous because they have the ability to
regenerate new tissues as well as repairing
damaged or old tissues. There is essentially no
limit to what stem cell can accomplish in the
human body from cellular level to tissues and
even organs. Within the next few years, these
cells will be used to restore the form and
function of the oral cavity using autologous
cells, thereby overcoming histocompatibility
mismatch and transmission of viral disease [3].
Similar to other scholars, we also recommend
that future research should address the issue
of associated ethical controversies, before
bringing this stem cell-based therapy for
clinical use.

Figure 1. Shown in the figure is the uses of

dental stem cells in the regeneration of
non-dental tissues [3].

-14-

By: Danial Behzad

It Affects More Than

Just Your Waistline,
It Affects Your Brain!

Everyone is aware of the health risks associated with a

high fat diet, yet on a day to day basis we continue to indulge in fried
foods, cakes, pastries, chips, chocolate, and the list goes on. Even
many common ingredients such as margarine, butter, cooking oils,
mayonnaise, and cream contain a high amount of fat. Most people
are aware that high fat diets play a key role in obesity, heart disease,
and type 2 diabetes. What many people dont recognize is that aside
from the weight gain, a high fat diet can also harm your brain. 1
There is recent evidence that suggests that short-term
exposure to a high fat diet may result in cognitive deficits. It was
reported that healthy adults who ate a high fat diet for 5 days
performed worse on tasks measuring attention and speed of
retrieval than they had prior to the diet.2
There are various reports in rodent models that indicate
that high fat diet induced obesity impairs cognitive function. 3 One
of the major discoveries in these rodent studies is that a long-term
high fat diet results in cognitive deficits, especially in spatial tasks
involving the hippocampus.4 The hippocampus is thought to be the
center of emotion, memory, and the autonomic nervous system.
These studies suggest that the changes in the hippocampus mediate
the link between obesity and cognitive defects. These changes
include neuroinflammation, oxidative stress, and/or decreased
levels of neurotrophins.5
Dr. Stranahan and his team at Georgia Regents
University conducted a rodent model study, which demonstrated
that dietary obesity impairs hippocampal function, which may
result in synaptic stripping by microglia.6 Synapses are essential in
our body as they are the structures that facilitate electrical and

Figure 1: HFD impairs spatial recognition memory,

based on reduced alternation in the Y-maze. HFD/LFD
mice alternate at rates that are similar to LFD/LFD
mice, consistent with reinstatement6 of spatial
recognition memory with diet reversal.

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chemical signals from neuron to neuron.7 To understand

stripping, it is important to recognize that any pathologic event
may lead to the activation of microglia, the immunocompetent
cell of the central nervous system that helps form its primary
immune defense. Microglia usually rid the brain of harmful
agents, but excess fat impairs this process. Normally, microglia
are constantly moving around, but with obesity, they stop
moving. They essentially sit there removing synapses instead,
which is referred to as synaptic stripping.8 Referring back to Dr.
Stranahans experiment, the researchers discovered that after 12
weeks of a high fat diet, the mice were obese and the excess fat in
their body resulted in chronic inflammation, which triggered an
autoimmune response from microglia. This is what eventually
leads to memory and learning impairments.6

Figure 2: Confocal micrographs

of IBA1/MHCII fluorescence, with DAPI
nuclear counterstain. 6

These findings are further backed

by the research of Dr. Morris and her
research team at the University of New
South Wales. Also performing a high fat diet
test on mice, they discovered an association
between deficits in hippocampal-dependent
recognition
tasks
and
increased
hippocampal markers of inflammation and
oxidative stress.9 Upon further study, they
discovered that this resulted in impaired
memory retention. Whereas Kanoski and
Davidson discovered that rats on a high fat
and glucose diet performed worse on spatial
tasks than chow fed control rats after only 3
days. Although it took over 30 days of a high
fat diet for non-spatial memory
impairments.10 The good news though is
that the experiment showed that switching
back to a low fat diet, returned the mice to
normal within 8 weeks. Therefore,
suggesting that a low fat diet may indeed
offset any neurological damage caused by a
high fat diet.1

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Theranos and the Painless,

Needleless Future

By Mohamed Hamade

In the past decade, the biotech

industry is regarded as one of the most
innovative industries that pools in
relatively large investments due to its
ever-growing markets and public need.
Much like Steve Jobs to computer
technology, the Bio Tech industry has a
Steve Jobs of its own: Elizabeth Holmes.
The young Stanford dropout is now worth
an estimated $4.5 Billion, running a
company that grew to $9 Billion in just a
few years. Her innovative business,
Theranos, was born out of dire need to
improve the decades old blood-testing
system . Theranos doesnt only provide you
with the results to over 32 to 240 different
medical variables, but it also only requires
a few milliliters of blood from a
finger-prick in just a few minutes, accuracy
is yet to be verified. Theranos Edisons
innovation will shorten the time required
for blood tests; hasten the availability of
results potentially saving many lives in the
process . As futuristic and revolutionary as
this may seem, it did not end there. The
Biotech industry is an incredibly
competitive space with many willing
financial backers.
Google has recently jumped at the
scene of a potentially estimated at $140
billion by developing its own needleless
blood testing technology, the details of such
technology are yet to be released.
According to a patent application by

Google, it seems to be a wearable watch for

a needle-free blood draw system.
2015 has witnessed further
innovating blood-testing solutions; with
Tasso releasing a device they claim to be
more
efficient
than
traditional
blood-testing because it is almost nearly
painless. Perhaps the thought of how
that Tasso plans to undergo this process is
enough source of mental pain. To acquire
the fluids needed for the blood-test, Tasso
will require you to jab the devices needle
into your shoulder, as illustrated in the
picture . Tasso aims to send this
technology to the FDA to have the product
ready for launch by 2016.
While new biotechnologies flood
the market, Ms. Holmes of Theranos seems
to be fighting a more internal battle . The
company reported having a shake-up in its
board of directors, and another multiple
encounters with legislative branches
regarding the legitimacy of its claims and
the accuracy of the Edison technology.

-17-

Figure 1: Theranos CEO holding the patented

nanotainer that is only 1.29cm in length and draws
less blood than the standard method [v].

Effects of Constraint Induced

Movement Therapy in Stroke
Patients
By: Kirina Angrish, Nikhil Gandhi, Pavleen Dhillon, Sukhi
Manku, Suki Pannu, Veen Murali and Sim Summan

There are various types of

therapies that are used to help with the
rehabilitation of injured limbs after a
stroke. One that has gained a lot of
popularity for its large improvements
in motor function for the affected
limbs is termed constraint induced
movement therapy. This therapy
forces the use of the affected area
while restraining the unaffected side in
the efforts to heal the affected side
more efficiently and effectively1. For
example a method of constrained
therapy would involve the restriction
of movement of the intact upper
extremity by placing it within a sling
for 90% of waking hours for 12 days
and training the affected extremity for
7 hours on the weekdays during that
period3. This type of therapy is most
common in chronic and acute stroke
patients3. It is understood that this is a
well-used technique for more efficient
and effective recovery but many
wonder how effective it actually is. We
will look into this shortly.
The purpose of a Constraint
Induced Movement Therapy is to force
movement involving the ipsilesional
limb by performing repetitive tasks
and activities, conduced and
monitored by a clinician1. The
Extremity
Contained
Induced
Therapy Evaluation (ECITE), is the
first national randomized study to test
the neurorehabilitation therapy in
patients who have suffered a stroke for
the first time but have some ability to
extend their fingers, three to nine
months prior to enrolment in the
study1. The study had hypothesized
that patients who had suffered a
stroke, would be able to improve

upper extremity function in the nine month of

CIMT, compared to patients who would have
received usual and customary care.

Many studies have shown that CIMT

improves function in the ipsilesional side by
increasing the cortical reorganization of the
injured limb in the brain, in patients who have
suffered a stroke2. A particular study by Liepert
et al, found that CIMT, increases the
recruitment of neurons and its innervation for
movements in people who have suffered
cerebrovascular accidents. The finding shows
that there can be a permanent increase in
function in the affected limbs, due to the fact that
there is an increase representation in the brain2.

Figure 1: WMFT Performance Times and MAL Amount

of Use Score

Also from baseline to 12 months, the

CIMT group demonstrated greater growth than
the control group in the MAL Amount of Use
(increasing from 1.21 to 2.13 vs. only 1.15 to 1.65
on a scale from 0-5). Similarly, in the MAL
Quality of Movement, the number rose from
1.26 to 2.23 whereas; the control group had a
small increase from 1.18 to 1.66. When focusing
on self-perceived hand function difficulty, the
CIMT had a greater decrease, 19.5 versus only
10.1 for the control group.
The results of this study may have
varied due to limitations; one such limitation is
by the number of participants with
low-functioning
capabilities.
Whereas
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higher-functioning participants results showed

significant improvement at all post treatments,
lower-functioning participant sample size was
reduced for generalized results
at two time points:
2 weeks and 12 months1. A second limitation
referred to the treatment was given
to the 48.9%
of the control group participants1. Monitoring the
intensity of treatments was also challenging and
may have compromised the results. Lastly, there
was insufficient amount of information regarding
medication usage of participants and considering
the influences of these variables.
Results can be improved overall with
recruiting a larger number of participants with
low-functioning capabilities to minimize the
variance and collect more precise information.
Gathering more data on the intensity of the
treatments would have given more accurate and
precise outcomes. Future researchers may need to
consider investing more time to monitor
treatment intensities. Also a more detailed
personal profile which consisted of stroke
location, intensity, duration, medication history,
family history and the influences of these on the
participant would have narrowed down the
relationship between 1CIMT and the progress
much more specifically .
Overall, the Constraint Induced
Movement Therapy is much more effective than
other techniques to date. Allowing the survivor to
use his or her affected arm repetitively and
intensively for two weeks after stroke will help
improve the upper extremity function.
Participants of the CIMT group have proven to be
more successful in completing the WMFT items in
120 seconds, with a retention rate of 76.1% for the
trial. The experimental group also showed
significantly greater improvement in grip force
after the experiment. All in all, CIMT produced
significant and clinically relevant improvements
in arm motor function after a stroke.

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Repatha: Lowering

Cholesterol 1 Person at a time

By Taylor MacIsaac

Heart disease remains one of the largest medical burdens in

Canada and the world, with an estimated 1.6 million Canadians7
currently living with heart disease or disabled due to a stroke.
However, with new medications like Repatha on the market,
hopefully these sobering statistics can be turned around.
Repatha belongs to a revolutionary new class of cholesterol
lowering drugs called PCSK9
inhibitors that have recently been
approved by the FDA1. PCSK9 (Proprotein convertase
subtilisin/kexin type 9) inhibitors are the first ever
human-antibodies designed specifically
to lower low-density
lipoprotein cholesterol (LDLc). 1,2 Repatha is for use in patients
showing levels advanced atherosclerosis or homo/heterozygous
familial hypercholesterolemia (HeFH/HoFH)
conditions causing
abnormally high LDLc levels.3 HeFH/HoFH are genetically
inherited conditions with a global frequency of 1/500 (HeFH) which
is thought to significantly contribute
to the global prevalence of
atherosclerosis and heart disease.4
LDLc is often referred to as the bad cholesterol. This is
because unlike high-density lipoprotein (HDL), LDLc contributes
largely to the formation of cholesterol plaques along arterial
walls,
which eventually leads to their narrowing (atherosclerosis).4,5 This is
a major risk factor for heart disease and stroke, as these plaques are
prone to rupture, a process that results in the formation of a blood5
clot at the site of the rupture, leading to a blockage in the artery.
Having a genetic susceptibility to high levels of LDLc in the blood
can lead to premature atherosclerosis
and increased likelihood of an
early-onset heart condition.4
Statins, or HmG CoA reductase inhibitors have long been
the drug that doctors turn to for the reduction of cholesterol; they
include such brands as Lipitor and Crestor. Along with the
reduction of total cholesterol in the blood (including LDL), they have
been linked to decreased mortality rates and likelihood of coronary
artery disease (CAD) in people with and without a history of heart
disease.6 These drugs lower cholesterol by inhibiting a key player in
cholesterol synthesis: an enzyme called HMG-CoA reductase.
However for some people, this reduction is not enough. In clinical
trials, PCSK9 inhibitors outperformed statins in every category
tested; (39 to 62% cholesterol reduction for alirocumab and 47 to
56% for Repatha.) suggesting they can be used in conjunction with
statins in patients showing a serious need for cholesterol reduction
and in patients who arent responding to standard treatment.1, 2,3
The action of PCSK9 takes place in the liver, where LDLc
metabolism occurs. LDL binds to the LDL receptor (LDLr) on the
surface of 1,hepatic
liver cells, where it is imported into the cell to be
destroyed. 2 PCSK9 controls the LDLr expression in the liver cells

-20-

Figure 1: Mechanism of action of PCSK9 inhibiors.Nature Reviews Cardiology.8

by binding to LDLr, and marking it for degradation or

destruction.1, 2 This prevents the LDLr from being recycled
and removing more LDL from the blood.1,2 By inhibiting this
regulatory protein, PCSK9, the LDLr is able to be recycled to
the surface of the cell, where it can remove more LDL from
the blood. This drug actually works by mimicking a loss of
function mutation a genetic defect that lowers the activity of
a protein - in the PCSK9 gene. This is seen in ~1-3% of the
total population who also show low LDL cholesterol.1
Patients with HeFH/HoFH are recommended
bi-weekly injections of 140-mg/mL/280-mg/mL, respectively,
however monthly injection with a double concentration dose
is also available. 3 Side effects of Repatha include bruising at
the site of injection, nausea, back paint and respiratory
infection. Repatha may cause an allergic reaction and is not
for use in children under the age of 13. 3

-21-

The Mirror
Neuron Effect

What are Mirror Neurons?

Ever wonder why when

someone is about to get punched in
the face we react to it before it
happens. Ever see someone get into
a car crash and we feel for the
person's pain as it if were us being
injured. Our central nervous
system reacts to these actions as if
it were us in those situations,
because our CNS is built in a way
where it cannot differentiate
observation from experience, and
only recognizes it as either painful
or rewarding. This means our
central nervous system cannot
dictate the different between
imagination and reality and simply
responds to its environment, based
on what it senses [3]. Whether we
are the one feeling pain or the one
observing someone in pain our
central nervous system reacts to
both situations in a similar way.
The mirror neuron effect
has such a huge impact on humans
adapt and develop, that it has some
neuroscientists saying it is the
"single
most
important
unpublicized stories of the decade"
which clearly emphasizes its
potential [1].
So what exactly is a
'mirror neuron effect'. A mirror
neuron effect is defined as the
reaction living systems have
towards the intention behind every
action [3]. Just like the example
given above, when we see someone
about to get hurt we react to it
before it happens because as
humans we understand the
"intention behind the action".
When you see someone slip and fall
we react towards it because we feel
their pain which has been
recognized by previous experiences

By: Sachin Kaushal

or observation, and so we understand that it is an

action that causes pain. As humans are adaptive
creatures we avoid pain but seek pleasure, and it
is the mirror neurons that might be the
explanation for why humans respond in this way
[4]

Although the mirror neuron effect is a

fairly new topic based on current scientific
research, what scientists know for sure is that it
allows humans to observe and copy actions
based on perception [2]. This observation and
copying based on perception could possibly be a
method towards learning [5]. Learning as an
infant is the best example because when humans
are first born, it is our minds that seek for as
much knowledge and experience as possible, so it
can adapt and mold around the individuals
current environmental conditions [5]. Whether
we learn through observation or through
experience mirror neurons might hold the
responsibility for this explanation. When a child
is observing his father hitting a nail with a
hammer and he accidently hits his finger, he
immediately screams in pain. The kid at first
might laugh at the situation but overtime
through more and more experience he or she will
start to correlate this action as painful and so he
will learn at an unconscious level that hitting
your finger with hammer is painful. Like all
neurons, the more mirror neurons that become
activated the stronger it becomes, meaning that
what is observed or experienced eventually
becomes habitual.
Although most of this is based on limited
research and speculation, it holds the answers to
understanding why mirror neurons work, and
why they might be responsible for why humans
are able react to what we see versus what
actually happens to us.

Personal Experience:

Do you ever remember coming out of a

movie theater and the main character of that
movie intrigued you because he or she was
someone you admired or respected in a sense
-22-

that you wanted to be like them? Have you've

ever noticed your character and body language
start to change and follow that of the character
in which you admired in that movie? Again this
is mere speculation, but mirror neurons might
be the answer to this cause and it is shown that
you as a person will behave and perform specific
actions that were similar to that observed. The
reason this works is because we as humans
constantly adapt and we adapt better when we
have a clear focus or goal to whatever it is that
we want. So when we see someone who
replicates that end goal, our minds are more
persuaded to that individual which makes us
much more easily influenced by the character's
level of status.

First Proven Study: Macaque Monkey

A research experiment was conducted

at the University of Parma where an accidental
discovery was found. A group of neuroscientists
were working with macaque monkeys where
they hooked scanners to the monkeys brain and
saw a certain noise frequency was made through
the activation of specific neurons every time the
monkey grabbed for a peanut and thus the
emphasis of motor neurons was proven.
One day by accident a neuroscientist
walks into the lab and decides to grab one of the
peanuts, and had heard a frequency noise again
even though the monkey had not grabbed the
peanut himself. This proved that the specific
neurons that were being measured could not
detect perception from reality. This emphasized
the idea of monkey see monkey do'. This
brought the idea of mirror neurons, as the same
part of the brain was activated as if the monkey
was grabbing the peanut, even though he was
merely observing it happen.
As this noise was only tested, further
fMRI scans were produced and showed that the
expected result and observed results produced
the same activation in certain parts of the brain.

-23-

Figure 1:6 macaque monkeys were used to

measure its response to both observation and
expectation results. The measuring of the
pre-motor area F5 and the inferior parietal area
PFG are both measured. (a) The experiment on
the left is the expectation where specific neurons
are activated in response to carrying the object.
An Example of a monkey responding during
observation and execution of a grasping action.
(c) The experiment on the right is the monkey's
observation of the object being picked up by the
researcher. The little bars indicated below the (a)
and (c) image indicate single action potential in
different sections of the brain. Arrows indicate
the grasping onset [1]

MAPK Kinase 3 Is a Tumor Suppressor with

Reduced Copy Number in Breast Cancer

By Ivor Smajlagic

Breast
cancer
is
recognized as the silent killer
and is considered to be the
second-leading
cause
of
cancer-related deaths. The
reasoning behind this is because
of the asymptomatic development
of this cancer that occurs in the
majority
of
women.
Understanding the importance of
the MKK3 gene and its role in
cancer is essential. This will lead
to the development of potential
therapeutic medication, which
will improve survival and quality
of life for women that are at risk at
developing breast cancer. The
purpose of this is to investigate the
properties of the MKK3 gene and
determine how this gene
influences the development of
breast cancer through the analysis
of an experimental mouse model
that mimics human breast cancer.
The majority of cancers
develop because of errors that
occur within DNA. DNA is
located within a cell, which is the
basic structural and functional unit
of life. DNA is normally able to
encode proteins through the
stimulation of genes. These
proteins have a wide array of
functions. An important gene of
interest that is involved in the
cancer [1]response is the MKK3
gene . The MKK3 gene is
characterized as a tumor
suppressor gene that prevents the

formation of cancer [1]. Tumor

suppression occurs through cell
signaling, which leads to the
activation of two important proteins
[1]
. These proteins interfere with the
early stages of the cell cycle, which
then prevent
the cancerous cells from
dividing [1]. Tumor suppression is not
witnessed in an altered MKK3 gene
that was observed through the use of a
mouse model. Normally, individuals
have two copies of every gene present
in their DNA. The authors of this
article show that people that have
breast cancer only have one copy of
the MKK3 gene and
it is not
completely functional [1].
Two types of datasets were
analyzed. First, the authors detected
the presence of a molecule (mRNA)
that is made from the MKK3 gene
within DNA, in human tumor tissues
and then they [1]compared this to
healthy tissue . This was done
outside of the body in a laboratory
setting using sample breast cancer
tissue. It was determined that there
was a decreased amount of mRNA
and protein in various cancers and a
significant
decrease in breast and liver
cancer [1]. These results were obtained
through a series of scientific tests
that
helped determine these ratios [1]. The
main finding that caused this
decreased expression was due to the
presence of only one[1] MKK3 gene in
breast cancer tissue .
The other method was
performed to determine if there would
-24-

be a change in the regulation of tumor growth using a mouse model [1]. A human breast
cancer cell line
was used since it closely resembles the MKK3 gene content in human
breast cancer [1]. This cell line was then used as a control in some mice. In other mice, this
cell line was modified with either an inactive MKK3 gene or an[1]active MKK3 gene
where the protein it codes for is inactive or active, respectively . Over a span of a
couple of weeks, they noticed that the tumor grew the slowest in the active MKK3 gene
cell line; followed by [1]the control and lastly, the tumor grew the fastest in the inactive
MKK3 gene cell line . This experiment also confirms that the normal MKK3 gene
participates in tumor suppression [1].
The goal of the normal MKK3 gene is to indirectly suppress cancer cell division
through cell regulation [1]. MKK3 signaling will activate a specific protein, which will
then activate another factor that
regulates the expression of two important proteins that
is independent of two
interfere with the cell cycle [1]. This process is unique since it [1]
pathways that are normally expressed to fight and prevent cancer[1] . These pathways are
not expressed because they are mutated in this specific cell line .

Figure 1: MKK3 activity is tumor

suppressive in MDA-MB-468 cells
which
enhance
p21
and
p27-mediated G cell-cycle arrest.
A, MKK3 activity enhances
cell-cycle arrest. MKK3 activity as
a
p53-independent
tumor
suppressor regulating p21 and
p27 expression and subsequently
leading to G1 cell-cycle arrest
and inhibited breast cancer tumor
growth [1].

-25-

By Benjamin McArthur

APPLIED
ANTIBIOTICS

In November of 2015, 39 Americans residing in the Pacific Northwest reported symptoms that could
be loosely identified as that resulting of food poisoning [1]. The victims of a Shiga toxin-producing E. coli O26
(STEC O26) all recent visited a Chipotle Mexican Grill Restaurant, and at the time of this magazines
publication 53 individuals had fallen ill to the same strain of bacteria, with 20 illnesses resulting in
hospitalization. The contaminated menu item has yet to be identified.
Figure 1: The results of the initial outbreak
of E. coli O26, by date of illness onset [2]

As the CDC continues to track the outbreak of STEC O26, the centers advise
against the use of antibiotics in the remediation of the STEC-induced illness [2] since the
diarrheal symptoms associated with STEC O26 tend to pass in a week anyway. Ignoring
this advice bears serious consequence that may result in antibiotic resistance in the bacteria
being treated. Antibiotic resistance is the appropriate term for this consequence because the
infection in question
is bacterial: antimicrobial treatment instead focuses on fungi, viruses,
and parasites [3]. Shiga toxin-producing E. coli acquired their toxin-producing mechanism
through horizontal gene transfer, where a Shigella dysenteriae bacterium died and an E.
coli bacterium successfully [4][5]
incorporated a portion of the Shigella genome into its own
circular genome (a plasmid) .
Should one bacterium be borne of antibiotic resistance, it needs only to
successfully reproduce to show threat to its host organism because of the accelerated rate

-26-

obtained a gene through horizontal gene

transfer called mcr-1, which [8]supports
of bacterial growth. The alternative consequence of resistance to the antibiotic Colistin . Of the
abusing antibiotics is an opportunistic infection, the 523 samples of raw meat tested in this study,
result of an antibiotic drug intentionally killing 15% contained E. coli SHP45.
endosymbiotic bacteria and allowing harmful
While The Lancet Infectious
environmental bacteria like C. difficile to multiply [6].
While opportunistic infections are more often Diseases indicates that the bacterium is
observed at an elderly age, the understanding of currently constrained to China, and there is no
an allegory
antibiotic resistance should be instilled in all school immediate fear of transmission,
plays out in Canada [8]. A CBC Marketplace
children.
report in 2011 tested 100 samples of
According to the online abstract from which supermarket chicken in Vancouver, Toronto,
[11]
the headline originated, one antibiotic (Colistin) no and Montreal for antibiotic resistance .
longer works against [8]an E. coli strain found in five Every bacterial culture obtained was resistant
provinces in China . Colistin was discovered in to at least one antibiotic, with some bacteria
1952, medically approved by the end of the decade, resistance to more than six different drugs.
and then [9][10]
outlawed by the 1980s due to apparent The explanation identifies poor livestock
toxicity
. In the case where beta-lactams, hygiene and accelerated agricultural demand
aminoglycosides, or quinolone antibiotics do not serve as an excuse for overuse of antibiotics,
their purpose, doctors
turn to Colistin, dubbed the whereas advocacy groups identify the
last-resort drug [7]. Colistin (polymyxin E) is not like prescription as judicious. Without
the beta-lactam penicillin [10]
in its method of eradicating consequence the Canadian government may
gram-negative bacteria , polymyxin antibiotics see no need to revise policy, while several
modify the lipopolysaccharides of bacterial cell governing bodies across the globe have taken
in
regulating
antibiotic
membranes by inducing phosphate substitution and initiative
thus weaken the structural integrity of gram-negative consumption. The result of the Chinese study
bacteria. The strain in question: E. coli strain SHP45 spurred immediate voluntary restriction of
Colistin use by the UK farming sector, as the
Responsible Use of Medicines in Agriculture

Alliance (RUMA) announced the change

while the EU performs a risk assessment [12].
The CDC are currently investigating
a second strain of STEC O26 that was
distributed by Chipotle Mexican Grill
Restaurant, affecting five Americans between
North Dakota, Oklahoma, and Kansas [1]. Had
either of these outbreaks been of antibiotic
resistant bacteria, America would see a
outbreak like none other. The average
consumer can do their part to limit the
development of antibiotic resistance by being
more wary of the risk that comes with
purchasing industrially farmed meats,
proactively monitoring their personal hygiene
during social interactions, and only
consuming antibiotics as instructed by a
healthcare professional. This including the
fact of finishing a full cycle of antibiotics as
prescribed by medical professionals when one

Figure 2: The number of publications that have

used either Colistin or Colistin resistance,
measured across time.

is ill or else resistance towards that antibiotic

drug can be perceived. It may be another
decade before microbiologists develop an
antibiotic prescription that does not fall
victim to natural selection, meanwhile we
must be wise in using the drugs we are
prescribed.
-27-

Hey, what kind of work do you people do?

We do creative advertising.

Okay. So you do marketing.

No. We are advertisers.

Marketing, advertising, same thing.

Uh... no its not.

Whats the difference?

The difference is that were
advertisers. Hell, you can even
call us creatives. But never
Marketers.

Okay... What does an advertiser do?

An advertiser makes this boring
dialogue into something that
people are going to read.

Thats stupid.
We know.
BrockHype

The Successes of 2015/2016

Sponsors:

-29-

2015-2016 EXEC
Pre-Med Parent Branch

Pre-Pharmacy Subsidiary

Founder/President
Iraj Zunair Afzal

President
Sachin Kaushal

Vice-Presidents
Saad Hanan
Wisdom Dickson

Vice-President
Danyal Mirza
Finance Manager
Adil Faruqui

Finance Manager
Alina Jaglanian

Secretary
Taylor MacIsaacs

Secretary
Alina Jaglanian

Public Relations Manager

Manny Singh

Public Relations Managers

Anmol K. Nandha
Pavleen Dhillon
Merna Suleiman

Marketing Manager
Taylor MacIsaacs
Husnain Ali

Marketing Managers
Sonia Aksamit
Danial Behzad

MedMag
Founder/President
Iraj Zunair Afzal
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Ravinder Singh
-30-

CUTIVE CIRCLE
Pre-Physio Subsidiary

Pre-Dentistry Subsidiary

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Simranjit Summan

President
Bishoy Suleiman

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Suki Pannu

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Mike Gianceterino

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Veen Murali

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Anas Tareen

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Pat Zaprzala
Ivor Smajlagic
Mohamed Hamade
Sachin Kaushal
Danyal Mirza
-31-

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