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L8/
University Department of
Biochemistry
Vol 2:2, July 2014
Editorial Board
Chief Editor Prof. G. B. Shinde
Head, Dept. Of Biochemistry
Advisors Prof. M. B. Patil
Prof. Swati Kotwal Prof.V.G. Meshram
Editor
Dr. Archana Moon
Circulation Incharge
Ms. Komal Talreja
Creative directors
Anuja Rai Drishti Singh
Email: [email protected]
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Vol 2:2, July 2014
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Vol 2:2, July 2014
STUDENTS ACTIVITIES DURING
JANUARY 2014 TO JULY 2014
13th-15th February - Workshop Cum Training on Animal
Use.
13th February - Guest Lecture by Dr. Sudhir Bhave on
Stress Management of current challenges before youth.
13th-14th February - Seminar by Dr. Vrinda Joglekar on
Biostatistics.
14th February - Guest Lecture by Mrs. Prafulata Rode on
Soft Skills.
28th March - Seminar on "Vesicle Transport - Nobel
Prize in Medicine and Physiology 2013 by Mr Kailash
Karale.
15th April 2014 - Valedictorial Ceremony of M. Sc. II
Batch 2014.
Student achievements
A)NET qualification 2013 December
1. Mr. Dinesh Wadikar
B) M. Sc. Project
100% students M. SC. II (Sem IV.): in house dissertation
Email: [email protected]
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PHOTO GALLERY
Email: [email protected]
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Page No.3
Workshop cum training program on research and soft skill development organized
by University Department of Biochemistry held from 13th
to 15th February 2014.
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Vol 2:2, July 2014
Email: [email protected]
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Dr. Sudhir Bhave addressed
the assembly on ‘Stress
Management of current
challenges before youth’ on
13th of February 2014.
Dr. Vrinda Joglekar
delivered lectures on
Biostatistics on 13th and 14
th
of February.
Mrs. Prafulata Rode gave a
talk on Soft Skill
development on 14th
of
February.
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Research in my lab is largely focused on the role of phytochemicals as an
anti-bacterial towards multidrug resistance bacterial strains and anti-cancer for treatment
and prevention of breast cancer metastasis to bone.
Recently, we have isolated the fourth and fifth antibiotic generation MDR bacterial
strains from UTI patients. We are investigating the antibiotic resistance at the molecular
level. The alteration in Penicillin Binding Proteins (PBP’s) is one of the mechanisms
towards emergence of resistance towards β-lactam antibiotics. The alteration in the
PBP structure in multidrug resistance (MDR) bacteria is our focus.
The combination of phytochemicals and nutrients for the prevention and treatment
of breast cancer metastasis to bones is being investigated. Presently, phytochemistry
and toxicity studies are being undertaken for the same. In-vitro and in-vivo studies are
envisaged in the project submitted to BRNS (DAE).
Ph.D. students:
Pallavi Sahare: Molecular studies on Penicillin Binding Proteins
(PBP) and development of In silco strategies for combating
multidrug resistance (MDR) by utilizing phytochemicals.
Komal Talreja: Anticancer bioactivities of phytochemicals and
nutrients for the prevention and treatment of breast cancer
metastasis to bone.
Dissertation students:
Allhad Acharya: Molecular analysis of PBP from MDR
uropathological bacteria.
Pallavi Sangolkar: Allelic differentiation of β-lactamase from
MDR bacteria.
Vidya Kondbattunwar: Phytochemical analysis of medicinal
plants.
Drishti Singh: Nicotine analysis from different tobacco samples.
Vol 2:2, July 2014
Dr. Archana Moon Associate Professor
LAB MEMBERS
Pallavi Sahare
Komal Talreja
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Nisha Singh: Analysis of Dihydrofolate reductase (DHFR) in MDR
bacteria.
Surbhi Shivhare: In vivo toxicity profile of Brassica oleraceae.
Anuja Rai: Age comparative study of serum bone biomarkers in
Albino Wistar rats.
Ravina Guriya: Phytochemical profiling of Brassica oleraceae
var. capitata and Brassica oleraceae var. italic.
Recent Publications:
Estimation of β-lactamase activity from multidrug
resistant uropathological bacteria.
Pallavi Sahare and Archana Moon*
J.of Advancement in Medical and Life Sciences, 1(4), 2014
Brassica oleracea:Phytochemical profiling for anticancer
compound.
Komal Talreja and Archana Moon*
Int. J. of Life Sciences and Pharma Research vol 4, Issue 4
Pg L1-L10, ISSN 2250-0480(online).
Cross talk between bones and bone protein markers.
Archana Moon*, Neha Bhale, Gangadhar Shinde, Pallavi Sahare
and Komal Talreja
International J. of Current Science 12:E20-38, ISSN 2250-1770
Combating uropathological multidrug resistant pathogens
with Soyamida febrifuga.
Vidya Kondbattunwar, Archana Moon*, Pallavi Sahare and GB
Shinde
Asiatic J. of biotechnology resources, 4(3), 8-12, 2014
Emergence of β-lactam resistance in clinical isolates of UTI
causing pathogens.
Pallavi Sahare and Archana Moon *
Int. J. of Science, Environment and Technology, 2014, vol 3 issue 4, Pg 1387-1392, ISSN:2278-3687
Vol 2:2, July 2014
Vol 2:2, July 2014
Vol 2:2, July 2014
Allhad Acharya
Vidya
Pallavi Sangolkar
Drishti Singh
Nisha Singh
Surbhi Shivhare Ravina Guriya Anuja Rai
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An untouched story behind occurrence of metabolic syndrome...
etabolic Syndrome (MS) is
a constellation of metabolic risk factors that
increase an individual’s predisposition
to atherosclerotic cardiovascular disease, type 2 diabetes and
hypertension.
Most of the metabolic and genetic
mechanisms behind the occurrence of MS in adults are already known. Here,
I will elaborate on how maternal nutritional stress programmes the offspring’s susceptibility to MS in their
adult life. Barker & Osmond at the
University Of Southampton, England, crystallized the concept of fetal
programming and early origin of adult diseases by suggesting that in utero stress as manifested by low birth
weight (LBW), increases the risk of cardiovascular disease and stroke in specific areas of England and Wales. In
simpler words, Hales & Barker’s hypothesis suggests that fetuses
exposed to suboptimal conditions during uterine life program the diseases that occur in their adult life.
Even if the postnatal conditions are optimal and nutrient resources are
abundant, the organism is ill-prepared to cope with the different environment and hence is more susceptible to
metabolic syndrome (MS). All we know about regulating our metabolism manually is by
regulating our lifestyle and nutritional habits for its proper functioning but
there is another mechanism that controls our metabolism
automatically, for instance the way B-cells work by producing antibodies against antigens as soon as they
enter our body. Did u eat a carrot or drink green tea immediately to make
B-cells work for u? No, the vaccine shots to which your mom exposed you at your early age has
programmed those memory cells to work whenever you need them to throughout your life. Similarly, when
mother exposes the fetus with adequate amount of nutrients, a
healthy life for the offspring is programmed.
What if mother herself is undernourished because of either macro or micronutrients scarcity?
Will the offsprings health be affected by that? Yes, this kind of
programming is called nutritional programming, where maternal under nutrition or nutritional stress
programmes poor health and susceptibility to metabolic syndrome
of her offsprings.
The programming starts right from
the preconception and preimplantation period, animal studies show that even stress limited
M
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Ms. Sona Sharma PhD student Agharkar Research Institute, Pune. Email: [email protected]
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to the preimplantation period (5 days)
can lead to impaired glucose intolerance. The different effects of stress during pregnancy can be
explained by the cellular events that occur during particular periods of
pregnancy. Stress in early gestation leads to a greater risk of an abnormal atherogenic lipid profile, obesity in
women, and coronary artery disease. Stress in the second trimester of
pregnancy, during which the number of nephrons increases rapidly, is associated with an increase in risk for
microalbuminuria. Finally, stress during the third trimester of pregnancy, when fat deposition occurs,
has a relatively higher effect in reducing birth weight (Fig.a). Abnormal
programming of the fetal pancreas may be a prime mechanism for adult-onset
of MS. Prenatal stress during
pregnancy can decrease both β-cell mass and β-cell function; such decreases may result in a decreased
insulin response to glucose.
A number of animal models have been established to try to understand the mechanism behind this programming,
but most of them considered only maternal macronutrients deficiency.
For example, maternal dietary restrictions of calories and protein, and umbilical artery ligation have all
been shown to cause fetal growth retardation, alter fat and glucose metabolism and elevate blood
pressure in the offspring. It is well recognized that micronutrients,
especially the minerals, play an important role in the structural and
Email: [email protected]
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Vol 2:2, July 2014
Fig. a. Critical windows of sensitivity during human pregnancy for the development of components
of metabolic syndrome later in life.
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metabolic activities of the organism.
For example, zinc, magnesium, manganese, iron and copper are known to modulate the synthesis, storage,
release and conformational integrity of insulin. Chromium increases insulin
binding due to an increase in insulin receptor number, activation of insulin receptor kinases and inhibition of
insulin receptor phosphatases .Vanadium shows insulin mimetic effects in vivo and in vitro when used in
pharmacologic doses. Recently, dietary iron and calcium restriction in rat
dams has been shown to increase hypertension and alter lipid metabolism in the offspring. Moreover,
mineral deficiencies and anemia are common in the developing world,
particularly during pregnancy and lactation. It is also known that maternal mineral deficiencies are
associated with low birth weight and increased rates of prenatal mortality and morbidity. Despite this and the
known effects of minerals per se on insulin synthesis/release/action, the
role of maternal mineral deficiencies in the etiology of insulin resistance in the offspring has not yet been explored.
Various studies on fetal
programming of MS are evidences for linking uterine stress and the offspring’s predisposition to
components of MS in their adult life. Undeniably, individual habits such as diet and exercise also affect one’s
predisposition to adult MS. Although, animal data provide multiple
biologically plausible mechanisms for fetal reprogramming, many questions remain unanswered. For example, the
mechanisms leading to adult disease need to be further studied so that novel strategies can be developed to
counteract the effects of in utero stress. In addition, the use of LBW as a
marker for in utero stress is of inadequate value, and new strategies to discover biomarkers of in utero stress
would be of great importance. In
developing countries like India these
findings have particular relevance, where the combination of poor nutrition in utero and over nutrition in
later life may drive the observed epidemics of metabolic syndrome.
Mother brings in our existence on earth,
MS is something for we shout “why on earth!!” Her fall in health is her
kid’s health fall, Cutting off her stress can
make a healthy baby crawl,
Just provide a mother open nutrition access, And imagine a world
without MS!
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DNA and Forensic Science
Forensic science is the scientific method of gathering and
examining information about the past. This is especially
important in law enforcement where forensics is done in
relation to criminal or civil law.
A branch of forensic science of great interest and under
constant research is the use of DNA in proving the guilt or
innocence of an accused in a crime.
How is forensic DNA typing done..??
Most of our DNA is identical to DNA of others. However,
there are inherited regions of our DNA that can vary from
person to person. Variations in DNA sequence between
individuals are termed "polymorphisms". As we will discover
in this activity, sequences with the highest degree of
polymorphism are very useful for DNA analysis in forensics
cases and paternity testing. This activity is based on analyzing
the inheritance of a class of DNA polymorphisms known as
"Short Tandem Repeats", or simply STRs.
Short Tandem Repeats (STRs) are DNA regions with
repeat units that are 2-6 base pair in length, also called
microsatellites or simple sequence repeats (SSRs); STRs are
scattered throughout the genome and occur on average every
10,000 nucleotides. STR sequences are named by the length of
the core repeat unit.
STRs are polymorphic in nature. They show both sequence
polymorphism and length polymorphism.
In forensic science, the property of length polymorphism is
applied to obtain an individual’s profile. STRs are inherited by
an individual as the rule is; from both his mother and father. In
order to take advantage of product rule, STR markers used in
forensic DNA typing are typically chosen from separate
chromosomes to avoid any problems with linkage between the
markers. A total of 16 STR alleles- 15 alleles and 1 allele to
The year 2013
marked 60 years of
elucidation of the
DNA structure by
Watson and Crick
and 30 years of
development of the
PCR technique.
These two
developments
played a
revolutionary role in
the field of Science.
Together they find a
major role in
forensic science.
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Vol 2:2, July 2014
By Ms. Neha Bhale Assistant Chemical Analyzer Forensic Laboraotry, Nagpur
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determine gender- are PCR amplified and detected to obtain a profile. The quantity of
the STR markers of interest being low, PCR technique is used to amplify the number of
copies of the STR markers from the DNA sample of an individual. These amplified
PCR products are separated using capillary electrophoresis, ultimately giving an
electrophoretogram. This electrophoretogram is unique for each individual, so much so
that a different allele at even a single locus will imply a different individual.
A Single-nucleotide polymorphism (SNP) is a DNA sequence variation occurring
when a Single Nucleotide — A, T, C or G — in the genome (or other shared sequence)
differs between members of a biological species or paired chromosomes.
a) Sequence Polymorphism:
two sequenced DNA fragments from different individuals,
AAGCCTA
AAGCTTA
contain a difference in a single nucleotide.
b) Core repeat unit – (AAGT)
AAGT-AAGT-AAGT-AAG
Repeated 4 times given the allele no.4.
Types of cases solved using forensic DNA typing:
1) Disputed Paternity- cases where paternity of father-child is under suspicion. Samples
collected from the child, mother and putative father are STR typed, profiles matched
and reported as paternity proved or not.
2) Identity of a dead unknown body- Samples from the unknown body are profiled and
later matched with relatives who claim the body, ultimately proving its identity.
3) Murder and Rape cases- Prove the presence of deceased blood on evidence collected
from the accused in murder cases and presence of semen of accused on victim
proving rape; by profiling the biological material collected on samples and matching
them.
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he result of HIV infection is
relentless destruction of the
immune system leading to onset of the
acquired immunodeficiency syndrome
(AIDS). The AIDS epidemic has already
resulted in the deaths of over half its
victims. All HIV-infected persons are at
risk for illness and death from
opportunistic infections and neoplastic
complications as a consequence of the
inevitable manifestations of AIDS (Moss
and Bacchetti, 1989).
Human immunodeficiency virus
(HIV) is a lentivirus (slowly-replicating
retrovirus) that causes acquired
immunodeficiency syndrome (AIDS), an
infectious disease in which progressive
failure of the human immune system leads
to life-threatening opportunistic infections
and/or other biochemical
consequences. HIV infects vital cells in
the human immune system such as
helper T cells (specifically CD4+ T
cells), macrophages, and dendritic cells.
HIV infection leads to low levels of
CD4+ T cells through three main
mechanisms: First, direct viral killing of
infected cells; second, increased rates of
apoptosis in infected cells; and third,
killing of infected CD4+ T cells by
CD8 cytotoxic lymphocytes that
recognize infected cells. When CD4+ T
cell numbers decline below a critical
level, cell-mediated immunity is lost,
and the body becomes progressively
more susceptible to opportunistic
infections. Once this virus enters a host
cell, it removes its coat and produces
another kind of genetic material –the
dsDNA, known as the provirus. This
provirus then gets incorporated into
T
Vol 2:2, July 2014
HIV/AIDS Current status and future prospects
KailashKarale
University Department of Biochemistry, Nagpur
(MS),
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human DNA, hijacks the host cell
apparatus and starts producing hundreds
and hundreds of new virion particles.
Since the whole life cycle of this virus
passes inside the host cell, it becomes
really challenging to find an appropriate
treatment. The scientific community,
however, has found some suitable drugs
against HIV, which target the different
stages of its proliferation and
multiplication. Presently, seven groups of
anti-HIV drugs targeting different stages
of its life cycle are being used: nucleoside
reverse transcriptase inhibitors (NRTIs),
nucleotide reverse transcriptase inhibitors
(NtRTIs), non-nucleoside reverse
transcriptase inhibitors (NNRTIs),
protease inhibitors (PIs), fusion inhibitors
(FIs), co-receptor inhibitors (CRIs) and
integrase inhibitors (INIs), and these drugs
have proved their usefulness also in
halting the HIV from reproducing.
However, a unique phenomenon was
noticed with HIV. Unlike other viruses, it
was found capable of showing different
behavior not only from cell to cell but also
from person to person. This was because
of mutation in its genetic material and as a
result, different strains of viruses were
developed. These mutated viruses
developed resistance to the drugs being
used. At this critical junction, a
combination therapy known as HAART
(Highly Active Antiretroviral Therapy)
was introduced to stop HIV from
reproducing and it has greatly reduced the
high morbidity and mortality rate.
However, this therapy too cannot cure
AIDS and patients are destined to undergo
life-long treatment and use of this therapy
has several limitations, like toxicity,
development of drug resistanceand poor
tolerability (S.J. Little, et al 2002). The
stepping-stones towards the
achievement of long-term virus control
are simplification of therapy,
improvement of patient adherence and
minimization of drug resistance. Thus,
the challenge still present before the
scientific community all over the world
is to develop novel anti-HIV
compounds with new mechanisms of
action, accepted toxicity and resistance
profile.
Drug targets
During its proliferation inside the host
cell, the virus is exposed to various
types of interventions, which can prove
detrimental to its multiplication and, in
turn, its existence. These possible
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targets and agents for intervention have
been summarized in Table 1.
Table 1.
Stage of HIV life
cycle
Potential
intervention
Binding to the host
cell
Antibodies to
the virus or cell
receptor
Entry to the host
cell
Drugs blocking
fusion
Reverse
transcription
Reverse
transcriptase
inhibitors
Integration of
DNA into the host
genome
Integrase
inhibitors
Expression of viral
genes
Inhibitors of the
tat protein
Production and
assembly of viral
Components
Myristoylation,
glycosylation
and
protease
inhibitors
Budding of the
virus
Interferons
Treatment: current status
The present day combination
therapy – HAART utilizes seven classes
of drugs that target various stages in the
life cycle of HIV. These are
1. Nucleoside reverse transcriptase
inhibitors (NRTIs)
2. Nucleotide reverse transcriptase
inhibitors (NtRTIs)
3. Non-nucleoside reverse transcriptase
inhibitors (NNRTIs)
4. Protease inhibitors (PIs)
5. Fusion inhibitors (FIs)
It is doubtless that new anti-HIV drugs
are needed with novel mechanisms of
action as these would contribute
towards the broadening of the
combinations used in HAART. A
number of such drugs undergoing
clinical trials.
Challenges on the way to successful
HAART
The challenges before the present
treatment can be summarized as:
1. Minimizing drug resistance
2. Simplification of regimens
Reduction of side effects
The use of anti-HIV drugs can lead
to various toxicities, which, though not
life threatening, can eventually affect
the quality of life and the willingness of
the patients to adhere to their regimens.
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In some cases, patients may need to
change their initial drug combination
because of adverse affects. Besides, long-
term toxicities occur as a result of
treatment discontinuation or regimen
switching due to adverse effects. Hence
new alternatives with better tolerance and
convenient dose schemes are needed.
New options are now being
searched that can alleviate the side
effects and reduce compliance. The
growth hormone releasing factor analog
tesamorelin has shown reduction of
adipose tissue in HIV patients being
treated with HAART (J. Falutz, et. al.
2007). Clinical trials are going on to
study the effect of uridine, pravastatine
and their combination on the recovery of
HAART-associated lipoatrophy.
However, minimal benefit has been
found in this approach.
References
1. S.J. Little, S. Holte, J.P. Routy, E.S. Daar, M.
Markowitz, A.C. Collier, R.A. Koup, J.W.
Mellors, E. Connick, B. Conway, M. Kilby, L.
Wang, J.M. Whitcomb, N.S. Hellmann, D.D.
Richman, Antiretroviral-drug resistance among
patients recently infected with HIV, N. Engl. J.
Med. 347 (2002) 385–394.
2. M. Popovic, M.G. Sarngadharan, E. Read,
R.C. Gallo, Detection, isolation and continuous
production of cytopathic retroviruses (HTLV-III)
from patients with AIDS and pre-AIDS, Science
224 (1984) 497–500.
3. S. Broder, The development of antiretroviral
therapy and its impact on the global HIV-1/AIDS
pandemic, Antiviral Res. 85 (2010) 1–18.
4. H. Mitsuya, K.J. Weinhold, P.A. Furman, St.
M.H. Clair, S.N. Lehrman, R.C. Gallo, D.
Bolognesi, D.W. Barry, S. Broder, 3_-Azido-3_-
deoxythymidine (BW A509U): an antiviral agent
that inhibits the infectivity and cytopathic effect
of human T-lymphotropic virus type
III/lymphadenopathy-associated virus in vitro,
Proc. Natl. Acad. Sci. U.S.A.U. S. A. 82 (1985)
7096–7100.
5. J.R. Arribas, A.L. Pozniak, J.E. Gallant, E.
Dejesus, B. Gazzard, R.E. Campo, S.S. Chen, D.
McColl, C.B. Holmes, J. Enejosa, J.J. Toole,
A.K. Cheng, Tenofovir
disoproxilfumarate, emtricitabine, and
efavirenz compared with zidovudine/
lamivudine and efavirenz in treatment-naive
patients: 144-week analysis, J. Acquir. Defic.
Syndr. 47 (2008) 74–78.
6. R.A. Domaoal, L.M. Demeter, Structural
and biochemical effects of human
immunodeficiency virus mutants resistant to
non-nucleoside reverse transcriptase
inhibitors, Int. J. Biochem. Cell Biol. 36
(2004) 1735–1751.
7. T. Matthews, M. Salgo, M. Greenberg, J.
Chung, R. DeMasi, D. Bolognesi, Enfuvirtide:
the first therapy to inhibit the entry of HIV-1
into host CD4 lymphocytes,
Nat. Rev. Drug Discov. 3 (2004) 215–225.
8. J. Falutz, S. Allas, K. Blot, D. Potvin, D.
Kotler, M. Somero, D. Berger, S. Brown, G.
Richmond, J. Fessel, R. Turner, S. Grinspoon,
Metabolic effects of a growth hormone-
releasing factor in patients with HIV, N. Engl.
J. Med. 357 (2007) 2359–2370.
9. R.W. Buckheit, K.M. Watson, K. Moorrow,
A.S. Ham, Development of topical
microbicides to prevent the sexual
transmission of HIV, Antiviral Res. 85 (2010)
142–158.
10 C.J. Elias, L.L. Heise, Challenges for the
development of female-controlled vaginal
microbicides, AIDS 8 (1994) 1–10.
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Department of AIDS Control, Ministry of Health
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(http://www.naco.gov.in/NACO/)
National Medicinal Plant Board, Department of
AUSH, Ministry of Health and Family Welfare,
Government of India (http://nmpb.nic.in/)
Department of Biotechnology (DBT),
(http://dbtindia.nic.in)
Indian Council of Medical Research
(ICMR).(http://icmr.nic.in/)
Office of AIDS Control, National Institute of
Health, USA,
(http://www.oar.nih.gov/oarac/members.asp)
HIV research trust, UK
(http://www.hivresearchtrust.org.uk/home.htm)
***
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Vol 2:2, July 2014
Email: [email protected] ESTB
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Vol 2:2, July 2014
Believe in yourself
Believe in yourself,
To the depth of your being.
Nourish the talents,
Your spirit is freeing.
Know in your heart,
When the going gets slow,
That your faith in yourself,
Will continue to grow.
Don’t forfeit ambition,
When others may doubt.
It’s your life to live,
you must live it throughout.
Learn from your errors,
Don’t dwell in the past.
Never withdraw,
From a world that is vast.
Believe in yourself
Find the best that is you
Let your spirit prevail
Steer a course that is true.
Friend
You find them before you seek,
For you who is always meek.
To hear them is always your pleasure,
The one who becomes your treasure.
Whom you think can understand you better,
From whom you never hide any matter.
With whom you share everything,
From the simplest to your deepest feelings.
Whom you can approach anytime,
In every situation they make you feel fine.
Whom you know better than yourself,
Whom you believe in, more than, in yourself.
With whom you enjoy yourself and even sigh,
In each moment who stands by.
Who remains with you even when they are away,
Who helps you out in every possible way.
Who is there for you forever and always,
Who is selfless for you, no matter what others say.
Who is perfect and an ideal person,
Your being together has infinite reasons.
Who relieves you from your tensions,
By giving you all needed attention.
The one whom you are fond of now and then,
Is no one else but your real friend.
Vol 2:2, July 2014
Kumari Amrita
M.Sc. 2nd year, Semester III 2014-15,
Department of Biochemistry, RTMNU
