Vol 2 - Nagpur University

Transcription

Vol 2:2, July 2014
University Department of
Biochemistry
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
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Email: rtmnubiochem@gmail.com
e-BioResource: An e-Newsletter of University Department of Biochemistry
L8/
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Vol 2:2, July 2014
STUDENTS ACTIVITIES DURING
 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
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JANUARY 2014 TO JULY 2014
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No.2
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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PHOTO GALLERY
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Vol 2:2, July 2014
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 14th
of February.
Mrs. Prafulata Rode gave a
talk on Soft Skill
development on 14th of
February.
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Vol 2:2, July 2014
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.
LAB MEMBERS
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.
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Dr. Archana Moon
Associate Professor
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.
 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
Vidya
Pallavi Sangolkar
 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
Drishti Singh
Nisha Singh
Surbhi Shivhare
Ravina Guriya
Anuja Rai
Allhad Acharya
Recent Publications:
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Vol 2:2, July 2014
An untouched story behind occurrence
of metabolic syndrome...
M
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
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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
Ms. Sona Sharma
PhD student
Agharkar Research Institute, Pune.
Email: sonastud@gmail.com
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Vol 2:2, July 2014
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.
Fig. a. Critical windows of sensitivity during human pregnancy for the development of components
of metabolic syndrome later in life.
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
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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
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
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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!
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
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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.
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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
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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.
By Ms. Neha Bhale
Assistant Chemical Analyzer
Forensic Laboraotry, Nagpur
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Vol 2:2, July 2014
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:
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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two sequenced DNA fragments from different individuals,
1
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HIV/AIDS Current status and future prospects
T
he result of HIV infection is
consequences. HIV infects vital cells in
relentless destruction of the
the human immune system such as
immune system leading to onset of the
helper T cells (specifically CD4+ T
acquired immunodeficiency syndrome
cells), macrophages, and dendritic cells.
(AIDS). The AIDS epidemic has already
HIV infection leads to low levels of
resulted in the deaths of over half its
CD4+ T cells through three main
victims. All HIV-infected persons are at
mechanisms: First, direct viral killing of
risk
from
infected cells; second, increased rates of
opportunistic infections and neoplastic
apoptosis in infected cells; and third,
complications as a consequence of the
killing of infected CD4+ T cells by
inevitable manifestations of AIDS (Moss
CD8
and Bacchetti, 1989).
recognize infected cells. When CD4+ T
for
Human
illness
and
death
immunodeficiency
cytotoxic
lymphocytes
that
virus
cell numbers decline below a critical
(HIV) is a lentivirus (slowly-replicating
level, cell-mediated immunity is lost,
retrovirus)
and the body becomes progressively
that
causes
acquired
immunodeficiency syndrome (AIDS), an
more
susceptible
to
opportunistic
infectious disease in which progressive
infections. Once this virus enters a host
failure of the human immune system leads
cell, it removes its coat and produces
to life-threatening opportunistic infections
another kind of genetic material –the
and/or other biochemical
dsDNA, known as the provirus. This
KailashKarale
University Department of Biochemistry, Nagpur
(MS),
provirus then gets incorporated into
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DNA, hijacks the host
cell
used.
At
this
critical
junction,
a
apparatus and starts producing hundreds
combination therapy known as HAART
and hundreds of new virion particles.
(Highly Active Antiretroviral Therapy)
Since the whole life cycle of this virus
was
passes inside the host cell, it becomes
reproducing and it has greatly reduced the
really challenging to find an appropriate
high
treatment.
community,
However, this therapy too cannot cure
however, has found some suitable drugs
AIDS and patients are destined to undergo
against HIV, which target the different
life-long treatment and use of this therapy
stages
and
has several limitations, like toxicity,
multiplication. Presently, seven groups of
development of drug resistanceand poor
anti-HIV drugs targeting different stages
tolerability (S.J. Little, et al 2002). The
of its life cycle are being used: nucleoside
stepping-stones
reverse transcriptase inhibitors (NRTIs),
achievement of long-term virus control
nucleotide reverse transcriptase inhibitors
are
(NtRTIs),
reverse
improvement of patient adherence and
(NNRTIs),
minimization of drug resistance. Thus,
protease inhibitors (PIs), fusion inhibitors
the challenge still present before the
(FIs), co-receptor inhibitors (CRIs) and
scientific community all over the world
integrase inhibitors (INIs), and these drugs
is
have proved their usefulness also in
compounds with new mechanisms of
halting
action, accepted toxicity and resistance
The
of
transcriptase
the
scientific
its
proliferation
non-nucleoside
inhibitors
HIV
from
reproducing.
However, a unique phenomenon was
introduced
morbidity
to
stop
and
to
develop
mortality
towards
simplification
HIV
of
novel
from
rate.
the
therapy,
anti-HIV
profile.
noticed with HIV. Unlike other viruses, it
was found capable of showing different
Drug targets
behavior not only from cell to cell but also
During its proliferation inside the host
from person to person. This was because
cell, the virus is exposed to various
of mutation in its genetic material and as a
types of interventions, which can prove
result, different strains of viruses were
detrimental to its multiplication and, in
developed.
turn, its existence. These possible
These
mutated
viruses
developed resistance to the drugs being
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targets and agents for intervention have
of drugs that target various stages in the
been summarized in Table 1.
life cycle of HIV. These are
Table 1.
1. Nucleoside reverse transcriptase
Stage of HIV life Potential
inhibitors (NRTIs)
cycle
2. Nucleotide reverse transcriptase
Binding to the host Antibodies
cell
to
inhibitors (NtRTIs)
the virus or cell
3. Non-nucleoside reverse transcriptase
receptor
inhibitors (NNRTIs)
Entry to the host Drugs blocking
4. Protease inhibitors (PIs)
cell
fusion
5. Fusion inhibitors (FIs)
Reverse
Reverse
It is doubtless that new anti-HIV drugs
transcription
transcriptase
are needed with novel mechanisms of
inhibitors
action
Integration
of Integrase
DNA into the host
inhibitors
as
towards
these
the
would
contribute
broadening
of
the
combinations used in HAART. A
genome
number of such drugs undergoing
Expression of viral Inhibitors of the
clinical trials.
genes
Challenges on the way to successful
tat protein
Production
and Myristoylation,
HAART
The challenges before the present
assembly of viral
glycosylation
Components
and
treatment can be summarized as:
protease
1. Minimizing drug resistance
inhibitors
2. Simplification of regimens
Budding
of
the Interferons
Reduction of side effects
virus
The use of anti-HIV drugs can lead
to various toxicities, which, though not
Treatment: current status
combination
life threatening, can eventually affect
therapy – HAART utilizes seven classes
the quality of life and the willingness of
The
present
day
the patients to adhere to their regimens.
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intervention
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No.14
In some cases, patients may need to
change their initial drug combination
because of adverse affects. Besides, longterm 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.
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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
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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 hormonereleasing 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.
Vol 2:2, July 2014
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No.15
Vol 2:2, July 2014
and
supporting
agencies
for
HIV/AIDS research.
Department of AIDS Control, Ministry of Health
and Family Welfare, Government of India
(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
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.
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)
***
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 disoproxil fumarate,
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
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ESTB
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Funding
1
Page6
No.16
Vol 2:2, July 2014
Vol 2:2, July 2014
Believe in yourself
Friend
You find them before you seek,
Believe in yourself,
For you who is always meek.
To the depth of your being.
To hear them is always your pleasure,
Nourish the talents,
The one who becomes your treasure.
Your spirit is freeing.
Whom you think can understand you better,
Know in your heart,
From whom you never hide any matter.
From the simplest to your deepest feelings.
That your faith in yourself,
Whom you can approach anytime,
Will continue to grow.
In every situation they make you feel fine.
Don’t forfeit ambition,
Whom you know better than yourself,
When others may doubt.
Whom you believe in, more than, in yourself.
It’s your life to live,
With whom you enjoy yourself and even sigh,
you must live it throughout.
In each moment who stands by.
Learn from your errors,
Who remains with you even when they are away,
Don’t dwell in the past.
Who helps you out in every possible way.
Never withdraw,
Who is there for you forever and always,
From a world that is vast.
Who is selfless for you, no matter what others say.
Believe in yourself
Find the best that is you
Who is perfect and an ideal person,
Your being together has infinite reasons.
Who relieves you from your tensions,
Let your spirit prevail
By giving you all needed attention.
Steer a course that is true.
The one whom you are fond of now and then,
Is no one else but your real friend.
Kumari Amrita
M.Sc. 2nd year, Semester III 2014-15,
Department of Biochemistry, RTMNU
With whom you share everything,
When the going gets slow,
1
7

Vol 2 - Nagpur University

Transcription

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