Henrietta Laks Lab Report

Henrietta Laks Lab Report
"By the early nineties, a scientist at Yale had used HeLa to discover that human cancer cells contain an enzyme called
telomerase that rebuilds their telomeres. The presence of telomerase meant cells could keep regenerating their telomeres
indefinitely. This explained the mechanics of HeLa's immortality: telomerase constantly rewound the ticking clock at
the end of Henrietta's chromosomes so they never grew old and never died."
– Rebecca Skloot, The Immortal Life of Henrietta Lacks
As our cells divide and our DNA replicates, our telomeres provide a start and an end point for the enzyme DNA
polymerase to attach to our chromosomes and replicate our DNA. By using a repeated, non–coding section of DNA as
the starting point for this replication, the telomeres allow our cells to replicate without damaging important genes at the
attachment point of the replicating enzyme. As this occurs though, our telomere begin to lose base pairs ... Show more
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Most telomere are no more that the simple repetition of the DNA nucleotide sequence TTAGGG – two thymine bases,
an adenine base, and three guanine bases. With a full length telomere containing more that 15,000 base pairs, telomeres
can perform their functions of preventing chromosome from losing coding regions of the genome during replication for
many replications before reaching what Dr. Jerry Shay describes as their "critical length" (Shay & Wright). When the
telomeres of a cell reach this critical length and can no longer replicate without damaging the base pair sequences of the
chromosomes themselves, programmed cell death occurs in the form of apoptosis. However, the length of a
chromosome's telomere is not only a linear function of erosion, but also a function of how often telomerase rebuilds the
strands by adding the TTAGGG base pair sequence. It is this way to "cheat" the critical point that provides medicine
with the possibility to extend our
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Scientific Literature Focused On Chromosomal Dna And Dna,...
Conglomeration of Scientific Literature Focused on Chromosomal Telomere Length (TL) In Blood Leukocytes,
Sputum, and Buccal Cells as It Relates to Cancer Occurrences by: Andy Barajas
Bio 490, Fall 2014
Department of Biological Sciences
California State Polytechnic University, Pomona
Abstract
This is a conglomeration of scientific literature as it relates telomere length in blood cells to the occurrence of cancer.
Telomeres are composed of repeating TTAGGG nucleotides and they are found at the ends of chromosomes. These
chromosomal caps are what protect the genetic material of a cell. Every time a cell replicates its DNA, its telomeres
become slightly shorter than the parent cell. Upon excessive shortening of the telomere, the chromosomal genetic
information begins to degrade upon replication which leads to instability. This eventually can cause cancer as the
studies discussed in this paper have shown. Individuals who have an inherited bone marrow condition known as
Dyskeratosis congenita (DC) have short telomeres and an 11–fold increase chance of getting cancer. Overall, cancer
patients were found to have shorter telomeres than usual in their leukocytes, sputum, or buccal cells. The cancers of
interest in this review include: head and neck, breast, gastric, lung, colorectal, ovarian, esophageal, prostate, skin
bladder, renal, endometrial, non–Hodgkin lymphoma, and liver cancer.
Introduction Chromosomes are usually capped by non–coding sequences known as telomeres. As

The Roles Of Telomeres And Chronic Disease
The Roles of Telomeres in Eukaryotic Cells During each and every cell replication, chromosomes shrink by a small, but
noticeable amount. Because of this, telomeres cap the ends to protect the coding regions of the chromosomes. With each
generation of DNA, more and more of the telomere disappears. An enzyme slowly rebuilds them, but it cannot keep up
with the degradation during chromosome replication. Eventually the shortened telomeres cause the cell to go through
apoptosis (Pierce 2014). Because telomeres are one cause of cell death, it is hypothesized that telomere size can
determine the health and age of an individual. Research has shown a correlation between telomere length and chronic
disease. Those with chronic diseases usually have significantly shorter telomeres. This raises the questions of what the
correlation means. Chronic disease could shorten the telomeres, or short telomeres could cause chronic disease. Another
hypothesis exists that shortened telomeres and chronic disease are both caused by another force; they occur
simultaneously, but one does not necessarily cause the other. Researchers have also seen a correlation between telomere
length and age. Physical age may be derived from the number of cells that have undergone apoptosis. There are a
number of things that we can do to prevent telomere reduction. Diet and exercise both play a key role in this. Things
that are "bad" for us, such as smoking and stress, increases the rate at which telomeres shorten. By

The Effects Of Meditation And Yoga
The whole concept might sound like the perfect idea for a science fiction film.
Even better, the gimmick in the last scene from an infomercial.
Meditation and yoga have been long praised for their never–ending mental and physical benefits: they decrease stress,
enhance your focus and attention and allow you to become more aware with your inner dialogue, helping you challenge
long–standing traumas and misconceptions that might be doing more bad than good.
Meditation and yoga have a truly transformative effect on your perception of the world and the way you react to it.
But according to recent studies, meditation and yoga might also have never before seen effects, in much deeper ways.
But, can meditation really change your DNA? Can it physically transform your genes?
According to several ... Show more content on Helpwriting.net ...
A 2013 study from the University of Wisconsin also showed that patients who engaged in yoga, meditation and
practices that encouraged mental and physical well–being showed genetic and molecular differences that gave way to
faster recovery from illnesses or stressful situations.
But this is not the first study that correlates telomere length with a healthier lifestyle.
In 2008, a study found that comprehensive life changes like a better diet, physical exercise and stress management
increased telomerase (the enzyme that produces telomeres) activity in men with prostate cancer.
The bottom line
But the findings didn't end there. One thing is to stop telomeres from shortening. Another is to actually lengthen them.
A study from Harvard University analyzed blood samples from both meditators and non–meditators and found that
those who meditate have longer telomeres, opening up the possibility that yoga and meditation might have the power to
physically enhance the telomere's

Biological Theories Of Aging Essay
No matter how many theories of aging psychologists, biologists, or doctors create and test, one foolproof method of
reducing aging is exercise. Being active whether you put forth ten minutes or two hours can help the bodies organs and
cells fight off the inevitable. A recent study performed by Dr. Mark Tarnopolsky provided new information about the
correlation between exercise and longevity to support the majority of biological theories of aging. According to the
Programmed aging theories an organism's life span is predetermined and built into their DNA. However, the study used
mice all with a specific lousy gene. This gene caused the mitochondria to fail at self repair, ultimately accelerating
aging and death all because of a shoddy powerhouse organelle. Even after the mice reached their reproductive peak, the
exercise group continued to thrive and show little to no aspects of aging. These supposed aging genes had no effect on
the exercising mice who still had healthy hearts, normal colored coats, and nearly the same amount of muscle mass and
brain volume. These normalities ... Show more content on Helpwriting.net ...
These proteins are responsible for continuing the replication of DNA. When an organism's telomeres become so
diminutive, DNA unravels and basically becomes game over for the organism. The mice study could lead to a better
understanding of telomeres and aspects that effect length. Until Dr. Tarnopolsky's research the studied characteristic was
stress and its affect on an individual's telomere length. Scientists knew that exercise had an effect on telomere length but
the experiment shed more light onto the subject. Like previously stated the mice had faulty mitochondrias this should
have led to their premature demise, but the exercising mice were able to out survive those mice who were sedentary.
The scientists in the experiment were able to keep the mice alive and keep their cells replicating by requiring physical

A Correlation Between Telomere Length And Chronic Disease
During each and every cell replication, chromosomes shrink by a small, but noticeable amount. Because of this,
telomeres cap the ends to protect the coding regions of the chromosomes. With each generation of DNA, more and
more of the telomere disappears. An enzyme slowly rebuilds them, but it cannot keep up with the degradation during
chromosome replication. Eventually the shortened telomeres cause the cell to go through apoptosis (Pierce 2014).
Because telomeres are one cause of cell death, it is hypothesized that telomere size can determine the health and age of
an individual. Research has shown a correlation between telomere length and chronic disease. Those with chronic
diseases usually have significantly shorter telomeres. This raises ... Show more content on Helpwriting.net ...
Telomeres are related to so many different aspects of our bodies because they play a key role in protecting our genetic
make–up. They are important structures in every cell of our body. Because of their role, their effect spreads well beyond
that of simply protecting chromosomes.
Structure and Function
Telomeres make up the tips of linear chromosomes and function to protect and stabilize the chromosomes from
degradation (Pierce 2014). There are other functions, but the primary one is protection. At each replication, DNA
shortens by just a few base pairs due to the nature of replication in eukaryotes (who have linear chromosomes). The two
strands of DNA are synthesized at different rates, creating a leading strand and a lagging strand. The leading strand is
replicated quickly and fluidly in a 5' to 3' direction, as seen in Image 1. The lagging strand is replicated in a backstitch
patter. Primers are placed along the DNA strand and DNA polymerase replaces them with segments of DNA. It can only
do this, though, if a 3'–OH group is present. The 3'–OH group precedes the primer, and would sit just to the right of the
green primers in Image 1. No 3'–OH group would be present at the end of the chromosome because it only exists on one
side of the primer. The area where the primer is sitting would not be replicated, and thus the DNA would shorten.
Tandem sequences of noncoding DNA sit at the ends of the

The Impact Of Advantages On Female Aging
For many women, a new study gives them a challenge that would test their character as a person and as a female. It is
because the research gave them two tempting choices in life that either way can make them happy in different ways.
The study by Bath University researchers discussed the impact of childbearing on female aging. It said that pregnancy,
breastfeeding, and childcare take a toll on the body. For every child that a woman bears, it increases the oxidative stress
in her body. It is a kind of chemical imbalance that can cause premature aging.
Younger–looking or more visitors?
Given the findings, the study suggested that if women will have only one or two children in their lifetime, they may
look younger and prettier. However, the trade–off is that a woman who has more children, when she reaches middle age
– even though she may own a saggier face – would have a larger family and more people who would visit her, The Sun
reported.
For the research, 500 people were asked to judge the photographs of women in their middle age. The authors, from the
Jagiellonian University in Poland, discovered that women who are post–menopausal and had fewer children were
considered by men and women as more attractive, younger, and healthier than the women who had more children.
Dr. Anthony Little, one of the authors of the study from the University of Bath, explained that becoming pregnant,
breastfeeding, and taking care of kids need a high expenditure of energy and higher nutrient

The Immortal Life of Henrietta Lacks by Rebecca Skloot
Rebecca Skloot's The Immortal Life of Henrietta Lacks presented an intriguing concept; cell immortality. Many have
pondered the idea that one day science will progress enough to make a human immortal. To this day, science has been
able to reveal the properties that make cells immortal yet research has not discovered a way to modify humans to give
them this incredible quality. It is known that a cell can undergo a series of replications before it reaches senescence,
known as cell death. In Chapter 27 "The Secret to Immortality" of The Immortal Life of Henrietta Lacks Rebecca
Skloot provided an explanation to why HeLa cells were "immortal" unlike other mortal cancer cells; the p53 tumor
suppressor gene had been "turned off" by the Human Papilloma Virus Lacks had. She mentions how according to the
Hayflick Limit, human cell's were able to replicate an average of fifty times. In addition, she explains how telomeres in
cells shrink slightly every time the cell divides. According to Aging Cell's 2004 article "The Cellular Lifespan and
Senescence Signalring in Embryonic Stem Cells," tumor cells "have high telomerase activity" yet they are not immortal.
HeLa cells, similarly to Embryonic Stem (ES) Cells have the tumor suppressor gene p53 turned off. This differentiates
HeLa from other tumor cells; while other tumor cells will replicated more than the average cell and eventually reach
senescence, HeLa continues to replicate to this day thanks to the HPV virus that turned off its

Exemplification Essay: Does Too Much Stress At Work
Have you ever heard the saying, too much stress can cause a person to go gray? Well it turns out there is more fact to
this than fiction. The past couple of months have been hard for you at your new job. The job requires you to work with
unfamiliar people, in an unfamiliar place, and to top it all off you are incredibly far behind on your monthly report,
which can cost you your job if not done correctly and on time. It is apparent to all your family and friends that this job
is causing heightened anxiety in you, and they are worried. You aren't as worried by the stress because you knew what
you were getting into with this job, that is until you looked in the mirror. After just a few weeks on the job, you notice a
couple gray hairs. Then ... Show more content on Helpwriting.net ...
There have been studies on the limit of how many times a cell can divide, and it was later shown that telomere
shortening was just slowly counting down to the deterioration of the cell (Okereke, Prescott, & Wong, 2012).
Telomeres are shortened due to the fact that DNA polymerase are not able to copy the end of the strands that it is
replicating. This causes it to shorten, then when it is duplicated once again it is shortened even more, and this process
just keeps continuing until the telomere is too short to complete its copying. When telomere lengths become too short, a
certain DNA defense goes into action, and this reaction leads to aging. So it is a proven fact that there is a significant
relationship between telomere length and the speeding up of physical aging (Prescott, Kraft, & Chasman, 2011).
Telomeres are directly correlated to the aging of a human body. Although some people might think that shorter telomere
lengths are detrimental, the natural shortening of these telomeres are essential to healthy and normal aging. It is natural
for cells to divide through mitosis, but each time cells are split telomeres are lost through the process. This is why the
telomere maintenance system was evolved to protect the ends of chromosomes (Prescott, Kraft, & Chasman, 2011).
Every time a cell is divided, its telomeres are weakened, and stress can accelerate this weakening, and biologically age
the person. As a

Negative Impact On Aging
America is aging. By 2033, people aged 65 and above – who comprise 14.5 percent of the US population in 2014 – will
more than double by 2060. However, as early as 2033, they will outnumber people younger than 18 for the first time in
the country's history.
However, the images celebrated in popular culture are almost all youthful, The Town Talk observed in an opinion piece.
The op–ed explained it to people seeing youth as beautiful and being old as something less desirable.
Changing the stereotype
The website pushed to change that stereotype because, in reality, America is aging. It laments the perception that old
age is not ideal because only the lucky ones get old. People who reach that age have lived and gained wisdom, while
their collective knowledge must be cultivated, appreciated, and used.
But because of the deep bias against aging, most people view their own aging as something to fight, deny, or dislike. At
a recent National Academies of Science Forum on Aging, Disability, and Independence, Becca Levy, a professor at Yale
University, shared a 2016 study.
The research had a positive subliminal message about aging shown to older adults in 15–minute weekly sessions. Levy
shared that after one month, all the seniors showed improved mobility and balance.
When people see aging solely about deterioration and loss, it becomes a self–fulfilling prophecy, a report by Kaiser
Health News, said. The tendency is for people who have that point of view tend to walk slower and

Devil Facial Disease
Tasmanian Devil facial cancer disease (DFCD) is a unique contagious cancer, which is transmitted among Devil
populations by biting, causing the cancer to present itself in tumours around the oral cavity. The cancer cells have
previously been found to be a rogue clonal cell line from a single Devil.
Aims
The aim of the two research papers was to investigate telomere length in Tasmanian Devils, the Devil Facial Tumour
Disease (DFTD), and in closely related marsupials. One of the articles focused on the striking dimorphism between the
homologous chromosomes of the Devils, and proposed possible explanations for this, while the other article focused
more closely on the telomere length and maintenance in the cancer cells, analysing the expression ... Show more content
on Helpwriting.net ...
This was completed with over 65 tissue samples from various locations. The analysis was performed with quantitative
PCR, using fluorescent signals.
Terminal restriction fragment analysis of the Devil telomeres was used to reveal that non–repeat sequences are present
between the telomeric repeats in the telomeres of the Devils (Bender et al., 2012). This technique involved the digestion
of the DNA with certain restriction enzymes, and the product was then run on an electrophoresis gel.
Semi–quantitative RT–PCR was used in both articles to examine the expression of the catalytic subunit of telomerase in
various cells from the Devil in order to detect the presence and activity of telomerase. Additionally a non–quantitative
telomere repeat amplification protocol (TRAP) was used to detect telomerase activity, this involved the use of PCR and
gel electrophoresis in order to visualise the results.

How Does Our Cells Divide
At the ends of our chromosomes are little 'caps' called telomeres. These caps protect our DNA and allow our cells to
divide. Some scientists now believe they hold the key to ageing, some even think it could be the 'fountain of youth'!
Every time a cell divides we lose a telomere, making it shorter. When it eventually gets too short the cell dies as it can
longer divide. Each time the telomere gets shorter the ageing process takes a step in one direction, our chance of cancer
goes up. This happens in all of our cells that regenerate, like the ones filled with fibers such as collagen and elastin, that
good stuff that keeps us looking young. So, the more years we are alive, the more times our cells divide shortening our
telomeres and before

Biological Theory Of Aging Essay
There are many factors that influence the aging process, and there are many theories and sub–theories that try to explain
the complex process of aging. Aging changes the biochemical and the physiological process. The theory that best aligns
with my view of aging is the biological theory because you can see these changes every day; maybe you see them in
yourself, possibly others. Cell and molecular biologist examine and propose theories to explain the aging process. There
are many biological theories that, in my opinion, do a great job at explaining outcomes and results of aging; they do so
in a way that is understandable, and these theories have much credible research behind it.
There are two main aging theory categories: programmed and error theories. Programmed theory assert that aging is an
essential and innate part of the biology of people, and that aging is programmed into our body systems; the three main
programmed theories are the programmed senescence theory, the endocrine theory, and the immune theory. These
theories explain changes over time, and these changes cause symptoms and signs of aging.
The programmed senescence theory is about the process in which a cell loses its ability to divide, grow and function;
loss of ... Show more content on Helpwriting.net ...
The stress theory of aging states that the biological system sustains damage from prolonged exposure to stress. Studies,
conducted by endocrinologist Hans Selye, show that when there is prolongs stress stress–related hormones are released
from the pituitary gland. Having been prolonged, stress causes high levels of these hormones continue to be released
and weaken the immunity system; the body becomes susceptible to physical symptoms of illness. In a groundbreaking
study that compared mothers of chronically ill children with mothers of healthy children, it was found that the stress
from the chronically ill children was inversely associated with telomere

Iv-1 Enzyme Telomorase
Throughout the past years, research of this unexpected instability has created a number of surprising discoveries. As a
matter of fact, it has led to the findings of a great enzyme named telomerase that acts on telomeres and is thought to be
required for the maintenance of many human cancers. Telomerase, the ends of the chromosomes, are eukaryotic
ribonucleoprotein complex, which contains both an essential RNA and a protein reverse transcriptase subunit. They are
meant to protect the chromosomal ends. They basically cap the ends of the chromosomes, thus protecting the ends.
Unlike viral or retroviral reverse transcriptase's, like the ones on HIV–1, the cellular enzyme telomerase focuses in
making the multiple short tandem repeats that are at

What Is The Alternative Lengthening Of Telomeres?
DNA replication results in the gradual shortening of telomeres over time, leading to the activation of senescence or
apoptosis. Therefore, telomere length is a key biological signal to limit the indefinite proliferation of somatic cells
(Roumelioti, et al., 2016). However, cancer cells can overcome telomere shortening by synthesising a new telomeric
DNA from an RNA template through the expression of telomerase (Roumelioti, et al., 2016). Alternatively, 10–15% of
human cancers utilise a DNA template in a homology–directed synthesis mechanism called alternative lengthening of
telomeres (ALT) (Cesare & Reddel, 2010). However, the process by which DNA damage such as telomeric shortening
results in the execution of homology–directed synthesis, ... Show more content on Helpwriting.net ...
However, ATR, Rad51 and Hop2 were not required for break–induced telomere synthesis in ALT cells and in fact,
knockdown of each gene increased the levels of nascent telomeres. To further support their findings, Dilley and
colleagues studied VA13 HOP2 CRISPR clones lacking Hop2 protein expression and found that no telomere shortening
took place. From these findings, the authors could therefore propose that break–induced telomere synthesis and ALT
telomere maintenance can occur independently of Rad51–Hop2 and ATR.
Dilley and co–workers subsequently determined that the replicative DNA polymerase Pol , including POLD3, POLD4
and POLD1 subunits, were instead required for break–induced telomere synthesis. Whereas Pol , Pol –primase and
MCM2–7 replicative helicase were found to be nonessential and were recruited at far lower levels. The POLD3 subunit
is also part of the Pol ζ complex involved in translesion synthesis. However, the REV3L catalytic subunit of Pol ζ was
not required for break–induced telomere synthesis, suggesting POLD3 primarily acts through Pol . This major role of
POLD3 has been supported in studies that revealed POLD3 depletion resulted in decreased frequency of replicated ALT
telomeres (Roumelioti, et al., 2016). Overall, the results by Dilley et al led to the suggestion that an alternative
replisome is required for ALT telomere synthesis.
Having proven that Pol is dominantly recruited to TRF1–FokI damage sites, Dilley et al set out

CRISPR Pathway Analysis
The process in which the CRISPR pathway works contains a few steps that, after assembly of the RNA and nuclease
complex, will occur naturally in the cell. From this point forward, the RNA sequence that is engineered to bind
specifically to a target sequence will be referred to as guide RNA (gRNA). The assembly of the gRNA and Cas9
endonuclease complex binds to the target gene sequence and cleaves at a point just downstream of the protospacer
adjacent motif (PAM; Figure 1; Chang et al., 2013) The PAM is simply a sequence recognized by the Cas9 as 'non–self'
to allow for cleavage by the endonuclease (Chang et al., 2013). If this were not present, the bacteriophage sequences
incorporated into the host bacterial DNA initially, would be targeted by the bacteria's CRISPR system for cleavage. ...
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These breaks are then repaired by the cell in one of two manners: either utilizing non–homologous end joining or
homologous recombination directed repair (Figure 2; Hsu et al., 2014). Non–homologous end joining will cause the two
ends of the break to join together without the presence of the cleaved portion of DNA between them, resulting in a
frame shift mutation (Hsu et al., 2014). A frame shift mutation can be equated to reading a paragraph in a book with a
sentence or two missing. The appropriate proteins will no longer be synthesized for that gene, resulting in inactivation,
or what is referred to as 'knockout' of a gene (Hsu et al., 2014). The second repair mechanism utilizes homologous
recombination, during which the section that was broken can exchange DNA with a homologous section within the cell
to replace the cleaved sequence (Hsu et al., 2014). This is helpful in genomic manipulation and potential repair of
mutations, that otherwise would have led to

Taking a Look at DNA Supercoiling
DNA supercoiling is the over–winding or under–winding of a DNA strand. In general, most organisms' DNA is
negatively supercoiled. There are two types of supercoiling: positive and negative. Positive supercoiling means that the
DNA strands are twisted in the right direction; whereas negative supercoiling means that the DNA strands are twisted in
the left direction. The laws of Physics govern everything that happens in the world, including DNA coiling in living
beings. Some of the concepts in Physics that are involved in DNA coiling are quantum mechanics and statistical
mechanics.
Quantum physics is a branch of physics that explores certain units of energy, which are called quanta. These units of
energy are described by the Quantum Theory. The dictionary definition of the Quantum Theory is: "Any theory
predating quantum mechanics that encompassed Planck's radiation formula and a scheme for obtaining discrete energy
states for atoms, as Bohr theory." This definition means that Quantum Theory deals with Planck's radiation formula,
Bohr theory and indivisible units of energy. A great deal of research has been conducted in the field of quantum
mechanics and its connection with DNA supercoiling. Some Physicists have formed a theory, which states that quantum
entanglement holds DNA molecules together and prevents the DNA from falling apart. Quantum entanglement is the
relationship between any objects that deal with quantum mechanics. A Physicist named Elisabeth Rieper, from the

Aging And The Aging Process
Aging, it's something that as a species of life on this planet we are predisposed to and its results are an inevitable factor
that effects our bodies in several ways, from cataracts development to the progression of memory issues from such
diseases as Alzheimer's or Huntington's. The concepts of aging are broken down into two theories widely accepted by
several varying fields of studies such as gerontology, the study of the aging process, and oncology, the study of cancer
and tumor development. The Cellular theory, which focuses solely on the idea that a species and individual's lifespan
and condition in life is based on genetic and cellular factors that predispose us to a variety of diseases. The second
theory is known as Wear–and–Tear theory which heavily concentrates on the concepts of external factors in the aging
process. The studies behind this theory focuses on the physical condition of the body and the environmental
circumstances that result in the condition of the body as an individual is aging. The aging process is a unique aspect of
life that attributes to several varieties of diseases and conditions that affect the lifestyle of the individual both externally
and internally.
The concept that is become more appropriate among professional studies within the fields mentioned prior is a
combination of both cellular and physical theories. These studies are becoming more apparent as the population of 55 to
75 year olds is increasing both nationally across the United

Pathophysiology Of Ageing
Ageing, "the gradual decline in functions observed over time" (Rehman, 2016). Ageing is the result of genetic
mutations that build up over time and make it harder for the cell to copy DNA. Every three nucleotide base pairs code
for one amino acid, so by changing just one nucleotide can change the amino acid and the amino acid builds a different
protein and that protein does a different job than was intended before the base pair change. The DNA copying that takes
place in a cell during mitosis can be compared to a metaphor of a copying machine, one jam builds up and jams other
copies and the machine doesn't work as effectively. This paper jam is ageing, mitosis slows down and takes longer to
produce cells and thus intern causes a domino effect, ... Show more content on Helpwriting.net ...
These stem cells undergo a self–renewing cell division and maintain blood production for their lifetime. This means that
these stem cells are virtually capable of sustaining life until extinguished by external factors, rewriting the definition of
ageing and a normal lifespan. But maintaining this self–renewal process is crucial for homeostasis and the threat of
oxidative stress activates another protein called p38 MAPK in response to increasing levels of reactive oxygen species
thus limiting the lifespan of the HSCs. But by prolonging the treatment of the HSCs with antioxidants and inhibition of
p38 MAPK has shown to extend their lifespan. If these stem cells were able to live forever the production of red and
white blood cells as well as platelets would not slow down and the body would continue to function properly. Having
more white blood cells means the body could fight off infections and viruses more efficiently,

Telomerase Research Paper
Telomerase extends the telomeres of the chromosomes, and it is important during the development period. Although,
telomerase activates in 90% of tumors. The function of the enzyme telomerase is when the enzyme extends the
telomeres of the chromosomes. The enzyme is making the DNA using RNA as a template (Telomeres and Telomerase).
The binding of the enzyme goes to a special RNA molecule to contain a sequencing which is complementary to the
telomere repeat. It then extends an overhanging strand of the telomere DNA using the complementary RNA as a
template. The overhang then becomes long enough, and the matching strand is made by a normal DNA replication. This
finally produces a double–stranded DNA. Cancer can begin with a cell. The telomeres

Essay on Telomeres: Implications and Current Research
At the core of every organism lies a particular cellular alphabet which encodes the information for the lifelong
development and maintenance of that organism. This genetic library, or genome, of an organism is located in the
nucleus and consists of the complete set of DNA segments that are packaged into chromosomes. Each chromosome has
one long twisted DNA molecule which is made up of hundreds to thousands of genes that encode genetic information in
the specific sequence of the four types of nucleotides: Adenine, Thymine, Cytosine and Guanine. The deoxyribonucleic
acid of all organisms is composed of the four kinds of nucleotides but the differences in their sequencing is what
distinguishes one organism from another. Hence, all life forms ... Show more content on Helpwriting.net ...
This phenomenon, called the "end replication problem", was pointed out by James Watson in 1972. Eukaryotic
chromosomal DNA molecules overcome this problem by the molecular mechanism of telomeres. Telomeres are
appendages of non–coding, repetitive sequences of nucleotides located at the ends of linear DNA molecules such as
those in eukaryotic cells. These protective "caps" found at chromosomes ends prevent the shortening of genes during
DNA replication, make it possible for our cells to divide without the erosion of genetic units and ensure that genetic
material is successfully passed down from one generation to the next. They also protect the chromosomes from fusing
and connecting DNA with each other. Recent studies have also shown that telomeres correlate to aging and that
telomeres play a significant role in the immortality of cancer cells. As previously noted, eukaryotes have repeated
nucleotide sequences on the ends of their chromosomes. For example, the repeated unit in human telomeres is
TTAAGGG. Now as the DNA replicates, the enzyme telomerase catalyzes the elongation of telomeres at chromosome
ends. Through this telomerase activity, telomeres prevent chromosomes from losing base pair sequences that can code
for an organism's genes. Ultimately, telomeres suspend the erosion of genes at chromosome ends. This

Biology Summative: Telomeres, Telomerase, and Cancer Essay
In current society, cancer is one of the most fatal and prevalent diseases to exist. However, new research being
conducted on telomeres and telomerase provides insight on not only the aging process and mortality of cells, but also on
how the idea of cell death connects to cancer cells. By gaining knowledge on the supposed immortality of cancer cells,
researchers are acquiring a higher understanding of the subject, and attempting to work on alternate techniques to
provide treatment for the illness. The connection between telomeres and cancer and the momentous discoveries being
made on them is revolutionizing the world through potential current and future applications that have significant
implications for cancer treatment, and society, the ... Show more content on Helpwriting.net ...
Another study conducted on human melanoma suggested the link between telomerase activity and cancer; it was
discovered that a mutation on the promoter region of a telomere length regulating gene acts as a cancer drivers6, 7.
Thus, there is a definite connection between telomeres, telomerase, and cancer. Secondly, the knowledge of this link led
to significant implications and applications for cancer treatment, which are highlighted through recent and important
discoveries. First of all, current methods of cancer treatment are unreliable; both chemotherapy and radiotherapy have
dangerous side effects, including second cancers12, 13. As a result, vigorous research is being conducted in using the
connection between telomeres and cancer to treat the illness. One potential solution that scientists discovered is the use
of telomerase inhibitors, which would actively inhibit the enzyme10. An experimental anticancer technique that Geron
researchers tested is a mixture of the drug Alkeran and an anti–telomerase agent GRN163L10. The drugs hindered the
development precancerous cells, and even fought real cancers10. In another experiment, scientists inhibited telomerase
activity in a cancer by building complementary RNA strands of the telomerase production gene, which would attach to
the telomerase mRNA and obstruct the process9. The

Telomere Length Essay
Currently one of the worlds most discussed about biological issues is ageing, and how we can stop it or even more
reverse it. Ageing is defined as the deterioration of bodily function and organs necessary for living and fertility over
time. A large multitude of theories that explain the causes of ageing exists but one worth going more depth in is
telomere length. Telomere is an area of repetitive nucleotide at each end of a chromatid that protects the chromosome
from deterioration or fusing with neighboring chromosomes. It is believed that telomere shorting complements human
aging as well as premature aging syndromes. Those two points are the key hypothesis to the specific research article
that telomere length direct affects longevity. If proven true this would mean homeostasis would play an important part
in the variation of longevity in the human population. Homeostasis being the regulation of a system in order to maintain
a regulated ... Show more content on Helpwriting.net ...
In particular telomere length has become a required biomarker for anyone analyzing the effect of and variables into
human fitness. Telomere length has been related to obesity, bone demineralization and other aging indexes, including
high risk of premature death and development of cancer. It has been found believable that the presences of short
telomeres trigger cell senescence in vivo, in consequence affecting organ and tissue function. Their observation strongly
support that telomere shorting is a major cause of cell senescence in organs with high proliferative potential, detectable
in aged human individuals. Which causes the degeneration of organs and bones that lead to the age related diseases that
are shorting the lifespan of humans. Telomere length has become an excellent predictive measure for some of these age
related disease because of its close correlation to the

Telomere Length Lab Report
I.13. Methods to Determine Telomere Length:
The standard method to measure average of chromosome telomere lengths is the and impractical for high–throughput
screening. Cautious interpretation is cautioned when evaluating with controls, due to the fact telomere length varies
with ethnicity.
These techniques are sufficient at measuring the telomere content but insensitive to detect individual chromosome
telomere lengths which might be more relevant to pathogenesis due to the fact that the. Single telomere length assay is a
PCR based technique that measures chromosome specific telomere length from very small quantities of DNA (as few as
50 cells) with the caveat of low throughput and has been utilized in research laboratories.
In a study found that mean telomere content measured by flow–FISH in peripheral blood lymphocytes was less than the
primary percentile compared with age–matched controls, patients correctly identified with telomerase gene mutations in
the event that they have classical dyskeratosis congenita. In cohorts of children and adults lacking typical features of
dyskeratosis congenita, the sensitivity and specificity are much less established. The most effective 1 of the 7 patients
with adult–onset AA originally identified as having a mutation in TERT had telomere lengths measured below the 1st
percentile (maximum had been between the 1st and 10th percentile). ... Show more content on Helpwriting.net ...
Telomere length may be normal, despite a strong suspicion primarily based on the clinical findings. As yet unidentified
genes that have an effect on telomerase expression would possibly mildly impair telomere repair or have off–target
pathologic

The Creation Of Telomerase
The cell is busier than the streets of New York, and when it splits, it must have everything go perfectly. If the
chromosomes were to break down, the DNA it is holding could be damaged. That could be catastrophic for the cell.
This is where telomere comes in. Telomere is a small area of nucleotides that repeat at the end of every chromosome to
keep the chromosome from falling apart and breaking down. But, the telomere doesn't just appear out of nowhere. It is
created just like everything else, with DNA. Nobel Prize winner cell biologist Carol W. Greider discovered the enzyme
telomerase. Telomerase is what creates the DNA found in telomere.
In 1961, the nobel prize winner Carol W. Greider was born in San Diego, California. Her father, Kenneth

Telome Fusion
Telomere loss can initiate CIN through chromosome fusion., The loss of telomere function can be a signal for cell
senescence, chromosome fusion is common in cells that are deficient in the senescence pathway. The importance of
telomeres in preventing chromosome fusion is demonstrated by the extensive chromosome fusion observed in cells
when telomeres become critically short (Yaswen and Stampfer, 2002). Also the loss of telomere function brought about
by expression of dominant–negative TRF2 which results in extensive chromosome fusion and cell death (van Steensel
et al., 1998). The type of fusions that occur due to telomere loss depends on which ends of the chromosome lack
telomeres. Loss of telomeres from both ends of the same chromosome result in the formation of ring chromosome,
while the loss of telomeres from the ends of two different chromosomes result in the formation of dicentric
chromosomes. Both these types of chromosome aberrations are visible at metaphase and are common in cells in which
telomere function has been severely compromised, such as in cells deficient in TRF2 (John P. Murnane, 2007). ... Show
more content on Helpwriting.net ...
Although fusion between two different chromosomes will not occur, following DNA replication but the loss of a single
telomere can result in fusion of sister chromatids (Sabatier et al., 2005). This type of chromosome rearrangement is
more difficult to monitor than ring or dicentric chromosomes, because sister chromatid fusions are not detectable by
routine cytogenetic analysis. As first described by McClintock, sister chromatid fusion can result in prolonged CIN
involving breakage/fusion/bridge (B/F/B) cycles. B/F/B cycles occur when the fused sister chromatids form a bridge
during anaphase and then break when the sister chromatids are pulled toward the daughter cells during cytokinesis
(John P. Murnane,

Teloomerase Research Paper
Telomerase (TERT) is an enzyme responsible for maintaining the ends of telomeres and reversing the process of
telomere shortening in humans by adding a "TTAGGG" polynucleotide to the 3' end of the telomere. The addition of the
"TTAGGG" compensates for inefficiencies in replication of the ends of DNA in eukaryotes. Telomerase is limited to
highly proliferative cells such as germ cells and lymphocytes where the telomerase is necessary to maintain telomere
length, and the telomeres themselves are not sufficiently long to facilitate such rapid cell division without incurring
damage to the DNA. Most somatic cells exhibit no telomerase activity and in cells where telomerase is present
telomerase activity is strictly regulated. In cells that exhibit

How Can Save Your Life With Stress Relief?
How To Save Your Life With Stress Relief
By Matthias K. Maas | Submitted On September 16, 2014
Recommend Article Article Comments Print Article Share this article on Facebook Share this article on Twitter Share
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Expert Author Matthias K. Maas
How often do you feel on the edge? Frustrated... anxious... tense... angry...
Whether it 's from arguing with your teenager or getting stuck in traffic, stress is an inevitable part of life. With so much
on our schedules and so little time to get things done, we feel stretched to our ... Show more content on Helpwriting.net
...
"People think of stress as something that keeps them up at night or something that makes them yell at their kids," says
Dr. Carol Shively, Ph D., a professor and medical researcher at Wake Forest School of Medicine,"But if you asked me
what stress is, I 'd say it 's this huge plaque in your artery. This is stress."[1]
As Dr. Shively and other researchers have demonstrated, the physical changes our body goes through in response to
stress may be helpful over the short term.
But over the long term they 're deadly, linked to higher blood pressure, cholesterol levels and plaque build–up in your
arteries.[2]
And it gets worse...
Stress ' fatal impact isn 't just felt in your heart and blood vessels. It works its deadly fingers deep into your very cells,
impacting your lifespan at the genetic level.
One landmark study demonstrated this like no other. University of San Francisco researchers tracked 58 mothers aged
twenty to fifty. About 40 of these mothers had a chronically ill children, the remaining group had healthy children.
The mothers who had enormous caretaking burdens on them due to their child 's illness reported much more stress,
understandably, than the control group who had healthy children.
The scientists then decided to look at the mother 's DNA. What they found was shocking...
See, each strand of DNA is protected by little shields called telomeres. Telomeres are kind of like

Dark Matter In The Human Genome Essay
The new revelation in the human genome that scientists have developed an understanding of the useless junk are
actually noncoding DNA, also known as dark matter. The understanding of the dark matter focus on genetics,
deoxyribonucleic acid; also known as DNA, especially non coding DNA in the human genome. During the Human
Genome Project, the first establish genome sequence shows that there were a lack of use of DNA in our body. Only a
certain amount of the human genome's DNA encode protein sequences while the rest are non coding DNA. The non
coding DNA serves a purpose in the body, but without proof they were announced as dark matter, thus signifying that
the dark matter in the human genome are useful not useless. The new revelation of the ... Show more content on
Helpwriting.net ...
The telomerase carry its own RNAs molecule as a template to restoring the telomere back to its proper length after the
cell division. Since the telomere is consist of dark matter that helps protect the cell from losing any important DNA.
The DNA that which is located in the cell nucleus. Telomere, "a region of repetitive nucleotide sequences at each end of
a chromosome" ("What Is a Telomere?), which protects the end of the chromosome from deterioration, from combining
with neighboring chromosomes. However, if the telomere is shortened the enzyme telomerase will do its best to fix
itself and the telomere can not be fix regardless of how hard the telomerase tries to restore its length. Once the telomere
is shortened the "SOS response, and the cell will do one of two things: stop replicating by turning itself off, becoming
what is known as senescent; stop replicating by dying, called apoptosis" ("What Happens When DNA Becomes
Damaged?"). If the telomere decides to continue to divide, becoming abnormal and potentially dangerous for the human
body it can lead to having cancer. Overall, if understanding the gene expression of the enzyme telomerase restoring a
dark matter shows that dark matter are the instructor that gives instruction to encoding

Immortality Gene
Ehrenstein, D. (1998). Immortality gene discovered. Science, 279(5348), 177. Retrieved from
https://portal.lib.fit.edu/login?url=http://go.galegroup.com.portal.lib.fit.edu/ps/i.do?
id=GALE%7CA20159125&v=2.1&u=melb26933&it=r&p=AONE&sw=w&asid=2d4170234ecf72507d4a14c7ad6192e4
Cells with a genetic defect can become immortal and never stop dividing. At Baylor College of Medicine in Houston, a
group of researchers have found a gene that may determine whether a cell will stop dividing or continue to divide. The
group had cloned a gene that makes some types of cells immortal when it is mutated. The gene, called MORtality
Factor from chromosome 4 (MORF4), makes a protein that controls the activities of other genes. The researchers are
hoping that it ... Show more content on Helpwriting.net ...
Telomeres are the repeating end caps of chromosomes. As a cell divides and duplicates, the telomere genes began to
shorten. The shortening of the genetic end caps is considered a biological clock which counts down to a cellular death,
also known as apoptosis. Aging is accompanied by telomere shortening and it has been discovered in age related
diseases, such as premature aging syndromes. The consequences of a telomere dysfunction are very diverse and can
include nail dystrophy, abnormalities in skin pigmentation, aplastic anemia, pulmonary fibrosis, and a rapidly
expanding list of other diseases. The erosion of the telomere genes is meant to suppress malignant transformations. In
exceptional cases, it can cause chromosomal instability and promote the formation of tumors. Telomerase is the enzyme
which can replace telomere genes lost through cellular senescence. Unregulated expression of telomerase has been seen
in a majority of cancers. Telomerase is a double edged sword as it allows cancerous cells to divide without regulation.
The accumulated evidence on telomere genes would suggest that they have the ability to maintain telomere length and
to mask them from recognition as damaged DNA. Understanding telomerase regulation and telomere length
maintenance will uncover many mysteries in the control of aging and

Functions And Relationship With Age And The Mutations...
Telomeric Functions and Relationship with Age and the Mutations Affecting Children with Hutchinson–Gilford
Progeria Syndrome (HGPS)
Author: Monica Peña
Introduction
Telomeres function as a means of protection for chromosomes. In DNA replication, the telomeres of a chromosome
cannot be replicated, resulting in chromosomes becoming shortened over time (Vidak, 2016). This characteristic of
telomeres gives great insight to the importance of functions of telomerase and telomeres on chromosomes, the impact
telomeres have on aging, and the origin of RNA in telomerase. Telomere functionality and defects in regulation can also
give great understanding to aging diseases in children such as Hutchinson–Gilford progeria syndrome (HGPS).
Functions of ... Show more content on Helpwriting.net ...
When telomeric length reaches a level where it is too short, the cell undergoes senescence and/or apoptosis (Pierce,
2012). Telomerase prevents this cell death from occurring.
During DNA replication, DNA polymerase is unable to replicate the 3' end of linear chromosomes because replication
can only proceed in the 5' to 3' direction and requires a primer (Garavis, 2013). Telomerase is able to recognize the
presence of the G–rich repeat sequence. It elongates he strand in the 5' to 3' direction and adds additional repeats, using
the RNA template in the enzyme as it moves past the template strand. DNA polymerase, which carries a DNA primase
as one of its subunits, completes the lagging strand. This step successfully completes original information at the ends of
linear chromosomes (Garland Science, 2009). Without telomerase, telomeres would shorten, resulting in aging. The
shortening of telomeres as a person ages leads to higher likelihood of heart disease, bone problems, cancer, and the
more obvious, aged skin (Chojnowski, 2015). This process can be observed in Figure 1. Figure 1: Represents a step by
step process of the function of telomerase in DNA replication. In the first step, the G–rich strand can be seen.
Telomerase uses its RNA component

Carol W. Greider: A Brief Biography
Carol W. Greider was born in San Diego on april 15 1961.(54 years old).She hasn't died and she's a bloomberg
distinguished professor. she discovered enzyme telomerase in 1984 one year Greider then completed her postdoctoral
work, and also held a faculty position, at the Cold Spring Harbor Laboratory, Long Island, New York. During this time,
Greider, in collaboration with Ronald A. DePinho, produced the first telomerase knockout mouse, showing that
although telomerase is dispensable for life, increasingly short telomeres result in various deleterious phenotypes,
colloquially referred to as premature aging. In the mid–1990s, Greider was recruited by Michael D. West, founder of
biotechnology company Geron (now CEO of BioTime) to join the company's

Theories Of Aging
Over the years there have been many theories on how aging works. For example, The Entropic theory of Aging, The
Vitalist theory, The Hormonal Theory, The Free Radical Theory, The Nutritional Theory, and the Genetic Theory. Most
of these listed theories give insight into parts of the aging process. But, yet none of these theories give a complete
understanding of how aging works. To fully understand how aging works we need to look at the cell's telomeres. To see
how telomere lengths impact the aging process. The Telomere theory of aging puts all the pieces of the puzzle together
on how aging works.
With this new way of thinking, the telomere theory of aging ties together the contradictory view points from past
theories. Making a single theory ... Show more content on Helpwriting.net ...
For instance, young mitochondrial cells produce a lot of energy in the form of ATP. With this energy production, we are
also creating free radicals which damage our cells. Young mitochondrial cells produce a lot of energy and few free
radicals. They are also better at containing the free radicals not allowing them to escape from the mitochondria. For the
ones that do escape there are scavenger molecules that capture and destroy them. In young cells the rate at which the
cells are replaced and DNA repaired is much higher than the production of free radicals. However, as we age telomeres
shorten and gene expression changes causing changes to occur. Older mitochondria become less efficient at producing
energy while creating more free radicals. This occurs because aging cells lose their ability to supply the mitochondria
with the needed proteins. Which causes the mitochondria to fail. As we age, mitochondria lose their ability to contain
the free radicals within their membrane. Allowing for more free radicals to escape causing even more damage. With
age, mitochondrial scavenger molecules begin to fail, so we aren't able to capture and destroy them as well. Lastly, as
we age the rate at which cells are turned over decreases. With these changes in gene expression there are more free
radicals being produced causing more damage to cells. Since the rate at which these damaged cells are replaced/repaired
slows down, we start to have more damaged cells than functioning ones. Due to the decrease in turnover rate damage
begins to accumulate within the cells. The rate at which the molecules are replaced can't keep up with the rate at which
the molecules become damaged. Which eventually leads to cells becoming dysfunctional and no longer able

Extending Lives--But at What Cost?
Even though the prospect of extending life indefinitely via the philosopher's stone has been around since the ancient
Greeks and has also been mentioned in the Bible, modern–day biochemists and biomedical engineers are much closer to
achieving the ideal of immortality. Life extension has also had its role in popular culture in movies such as Logan's Run.
The movie depicts American society in 2274 when a totalitarian government is in power. Due to the limited resources,
the dystopian government dictates that all citizens must die when they reach age thirty, and all the citizens of this
government live with a watch that ticks down the time they have left to live (talk about a literal biological clock). This
is a darkly humored film that can be viewed as an interpretation of Malthusian theory (described in 1798), which states
that while resources like arable land, food, and natural oils grow linearly, the human population grows exponentially.
Although life extension is an intriguing idea for some people, the potential problems it would likely cause, in addition
to the existing problems that it would exacerbate, would greatly outweigh the benefits. Specifically, there are drawbacks
behind extending the average human's lifespan by a considerable amount, like extending the individual's life past his or
her health span and functionality. People could be sustained through biotechnology past their prime just to live in pain
due to the tissues not integrating themselves correctly into

Telomere Research Paper
Time is of the essence! By the end of this research paper the reader will know the reasoning behind time itself. A
telomere is quite significant because it can detect cancer, diseases, and aging. The telomer was discovered around the
1960's by Dr. Leonard Hayflick he discovered it by learning about how long a cell can live. There are billions of cells
through plants, animals, and humans it's how an organism operates. A telomer is at the end of each chromosome inside a
eukaryote cell (Plant and Animal Cell) and its importance is copying DNA (Deoxyribonucleic Acid). DNA is the
genetics that we obtain through our parents. If we could preserve the telomer to be continuous then organisms can
become eternal. A telomer holds the true meaning of ... Show more content on Helpwriting.net ...
Telomere can be described as a weight lifting bar, telomers are at the end of each chromosome like two weights on both
ends of a bar. A chromosome is an organelle inside the eukaryotic cell (animal and plant cell), chromosomes obtain
genetic information forming genes. Plants, animals, and humans contain trillions of cells throughout their anatomy.
How does a telomere relate to genetics? A telomere helps the cell reproduce DNA. Without copying DNA, it is
impossible for a cell to live. In 2009 a Noble Prize was won by three experts on heredity discovered the telomere
genetic code. One of their significant pieces of this research was in the 1970's when they did a critical research paper on
isolating the sequence of telomeres. They quickly discovered a telomer is used many times each use the telomere breaks
off when the DNA is replicated that's when the length of the telomer shrinks. Before a telomere was discovered Dr.
Leonard Hayflick discovered how long a cell can live and his results come out to be 50 to 60 cycles. His results were
not understood by scientist but they had faith in his research they quickly understood once the telomer was discovered
scientist concluded with a hypothesis if they can control the length of a telomer than I cell can be indestructible it would
live forever. Somehow if a discovery came along to uphold a telomer than it could cure cancer, diseases, and provide
longer life for a

Stereochemical Dependence for dSp
Interestingly, studies from our laboratory and others have demonstrated a stereochemical dependence for dSp
processing by enzymes in ODNs. The first instance of a dSp diastereomer difference was reported from our laboratory
when Klenow Fragment (exo–) was allowed to insert dATP opposite the isomers for which dSp1–containing ODNs
were found to be the more favorable substrate for insertion and bypass.32 This study was extended to in vivo
experiments by Neeley, et al. to include pol II and pol IV, also showing more favorable bypass kinetics for dSp1.34 As
further evidence for in vivo stereochemical dependency in dSp processing, Henderson, et al. utilized the restriction
endonuclease and postlabeling assay (REAP) to determine the mutation profiles for dSp1 and dSp2 in Escherichia
coli.28 In the sequence context 5'–d(GSpA)–3', they found a strong stereochemical dependence in the relative amounts
of dG→dT and dG→dC transversion mutations for dSp1 and dSp2. In subsequent experiments, Delaney, et al. showed a
somewhat different dependence of mutation profiles on the dSp diastereomers in the sequence context 5'–(TSpG)–3'
using the REAP and competitive replication of adduct bypass assays (CRAB).29,30 An additional observation from our
laboratory quantified the digestion kinetics of dSp isomers in the dinucleotides 5'–d(Np[Sp])–3' (N = A, T, G or C) by
nuclease P1 that showed dSp1 was the kinetically preferred substrate in all sequence combinations.33 Lastly, in
collaboration

Reference Values
The specific aim of the project is original as no detailed reference values for telomere length in children are available.
However, the probable impact of the reference values will be low because telomere length is a biomarker of
questionable value. The association of telomere attrition with mortality and morbidity has been widely reported, but it
has many limitations. An important limitation is the technical variability and dependence on laboratory procedures. It is
important to remark that the project aims to determine telomere length with qPCR, a method of known sensitivity to
differences in technique or equipment. Therefore, the reference values will be of limited validity beyond the specific
laboratory where they are developed. In addition, ... Show more content on Helpwriting.net ...
The PA has experience in the role of project leader. He counts with a paper on telomere length shortening associated
with prenatal exposure to tobacco. However, his area of expertise is focused in social and psychological factors on child
development, wellbeing and accomplishment through epidemiological research. The team includes statisticians, another
member with experience in telomerase activity, and members providing their experience and access to the Hong Kong
Child Health Survey, which is the source of samples and information.
Budget is commensurate with the required laboratory studies.
It seems that all the ethical and safety requirements are adequately addressed.
Strong points of this project are the availability of samples from an epidemiological survey, the participation of
researchers with relevant experience in several aspects of the project, the large sample size intended, the availability of
preliminary data and the original aim of defining telomere length reference ranges adjusted for age and gender.
Weak points of the proposal are the too optimistic view about the potential of telomere length as a biomarker of utility
for the individual subject, the transversal design of the validation step of the study, and the reliance on the information
obtained from parents for this validation

Titanium Essay
1. INTRODUCTION:
Titanium has played a successful biomaterial in biomedical application especially for orthopedics (bone–anchoring
systems), dentistry, drug delivery, and nanotherapeutics in treating bone cancer and arthritis. One of the treatments of
bone cancer patients is the replacement of cancerous bone with implant material. The current implant materials have
implemented coating technology (such as Calcium phosphate or hydroxyapatite) which gives good cytocompatibilty but
over the time it gets encapsulated with the surrounding bone cells and lead to poor osseointegration. An augment of
current implant material, we used nanotechnology application tailoring nanoscale topography on conventional implant
material into TNA by anodization ... Show more content on Helpwriting.net ...
This indicate the TNA may result in modification of the cellular protein lead to clustering or aggregation and this could
explain the variations in the cells shape and spreading behaviours that we observed earlier. Our preliminary result
suggested the interaction of the TNA surfaces with bound cells may induce structural and cellular changes could be due
to the surface roughness, chemistry and wettability that may count as the cell interaction factors. Therefore, we would
like to suggest further detail study of genomic and proteomic test that can help us to explain this phenomenon. We
would also like to screen several oncogene and tumor suppressor gene expression in order to study the potential
carcinogenesis effect of this material.
2. OBJECTIVES
2.1 To evaluate the differential in telomere length of the cells grown on the TNA and the test–control materials.
2.2 To measure the expression of telomerase activity in the cells that grown on the TNA and test–control materials.
2.3 To study the TNA effect on the genetic changes using metaphase spread technique and immunoblot for the protein
changes in looking the potential anticancer properties.
2.4 To screen the possible oncegene expression or tumor suppressor gene product of the cells grown on the TNA
compared with the test–control.
3. LITERATURE

Schizophreni A Preliminary Study From Australia
Blake Nuttall
MMBIO 240
Prof. Poole
15 March 2017
Shorter Telomere Length in People with Schizophrenia: A Preliminary Study from Australia
Journal: Schizophrenia Research March 2017
Authors: Cherrie Galletly, Varinderpal S. Dhillon, Dennis Liu, Ryan P. Balzan, Lisa A. Hahn, Michael F. Fenech
Hypothesis: Since those with schizophrenia have lower life expectancy, scientists have often wondered if schizophrenia
was connected to telomere The authors were only testing for a correlation between telomere length and schizophrenia
diagnosis. Experimental Techniques: They had a control group of 51 males from Australia who did not have
schizophrenia. Their experimental group consisted of 48 males also from Australia who were diagnosed with ... Show
more content on Helpwriting.net ...
For this reason, they ask them the questionnaire about their lifestyle.
Results: The control group had a mean telomere length of 6140.43±175.67 base pairs while the experimental group had
a mean length of 5171.74±145.39 base pairs. Therefore, the null hypothesis is rejected. However, the questionnaire
given to both groups revealed other significant differences. The schizophrenics had less education and less routine
exercise; they had more medical conditions, smoked more and more likely to live alone; and overwhelming majorities
of them were unemployed, single, and received welfare. Yet there was not a difference in BMI and alcohol
consumption.
Conclusions: There is a difference in telomere length between those with and without schizophrenia. Despite the other
differences, they concluded that those would have no or negligible effects on telomere length.
Justification: They got the data and they got the math. I learned about standard error of the mean in PDBIO. There is no
overlap between the control and experimental means plus or minus the SEMs. There's about a 1000 base pair difference
when with SEMs of only 145 and 175 base pairs. Ultimately, the scientists got what they tested for. What could
potentially discredit these numbers is the major differences between the groups. The ones they have given in the data
are significant, but do not effect telomere size. However, they mention that there were a

Henrietta Laks Lab Report

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