Explain What Are Some Environmental Factors That Impact...

Explain What Are Some Environmental Factors That Impact...
Define Epigenetics  Epigenetics is the study of chemical reactions and factors that influence the
reactions controlling growth and development of an organism to be activated or deactivated in
specific locations of genome at specific times. 'Lick your Rats' interactive activity. 1. Explain how
this is an example of epigenetics. The mother rats that nurture their pups they grow up to be calm
adults, while the mother rats that neglect their pups they grow up to be anxious. The difference in
behaviour is an example of epigenetics, because the nurturing behaviour of a mother rat during the
first week of life shapes the pup's epigenomes. These epigenetic patterns that the mother established
remain even when the pups become adults. 2. Is an anxious mouse or a more relaxed mouse more
likely to ... Show more content on Helpwriting.net ...
The epigenetic tags are erased from the chromosomes of the parents. However, there are some
epigenetic tags remain on some genes known as imprinted genes. 3. What are some environmental
factors that can impact the epigenome? The environmental factors that impact the epigenome are
diet of the organism, involvement in physical activities and exposure to toxins and stress. 4.
Summarize the main point of the video – If two twins have identical genomes, what makes them so
different from one another? Twins are born with the same genome and epigenome but the
environmental factors that they are exposed to bring a difference in their epigenome. As twins grow
they experience different things and they make distinct life choices which can make twins so
different from each other. The 'Gene Control' activity 1. What are two different ways that changes in
the epigenome can lead to cancer? The abnormalities in the epigenome such as lower level of
methylation. Cancer cell DNA due to low methylation is highly active so it is more likely to be
... Get more on HelpWriting.net ...

Annotated Bibliography : Programmed Cell Death
By utilizing these two transgene expressions in a synchronized way, the adenovirus is granted the
ability to replicate, specifically when it is within a tumor cell. The promoter hTERT controls the
specificity of E1a's ability for viral replication. This assures that the adenovirus only replicates
within cancer cells because the gene marker is only triggered where the hTERT expression is
prevalent, which, as indicated earlier, is only within cancerous cells.
Another impressive dimension that adds to the efficacy of Ad–Apoptin–hTERT–E1a is the
adenoviruses' ability to attack tumor cells through the addition of the therapeutic transgene
expression Apoptin. Apoptin is a protein that is known to induce the process of apoptosis
specifically within malignant cells, but not in regular cells [3]. Apoptosis is often called
"programmed cell death" because it is a process in which cells that are no longer needed within an
organism are recognized and then destroyed. Inserting this transgene expression into the genome of
Ad–Apoptin–hTERT–E1a creates a cancer specific adenovirus equipped with dual threat potential.
With these transgene expressions inserted into the genome of an adenovirus, Ad–Apoptin–hTERT–
E1a, is a genetically modified oncolytic adenovirus that has been created which can theoretically
eradicate cancer cells through both lysis and apoptosis, but not negatively effect normal cells within
the host.
4. Case Study: Clinical Analysis of Oncolytic Adenovirus
A study by

Ischaemic Stroke: A Case Study
An ischaemic stroke occurs due to the restriction of blood supply to an area of the brain, thus
initiating a process called the ischaemic cascade (Deb, Sharma & Hassan, 2010). This begins with
the depletion of local oxygen stores, causing disruptions in the production of energy compounds
such as adenosine triphosphate (ATP). The depletion in energy may cause tissue death (infarction),
where occlusion for 5–10 minutes may lead to irreversible brain dysfunction (Karaszewski et al.,
2009). Inadequate energy supplies leads to a malfunction of cells ability to perform action
potentials, also resulting in the swelling of neuron and glial cells (). Cells at the core of the
ischaemia will die of necrosis (premature cell death), where apoptosis (programmed

Viral Manipulation Of Cell Death Lab
Geraldson D'Haiti
Doctor Susan McLaughlin
BI 201
March 22,2017 Viral Manipulation of Cell Death (Zakeri's Cell Death Lab) The cells of a
multicellular organism are members of a highly–organized community. The number of cells in this
community is regulated, not by controlling the rate of cell division, but also by controlling the rate
of cell death. If cells are no longer needed, they commit suicide by activating an intracellular death
program. This process is therefore called programmed cell death, although it is more commonly
called apoptosis. Cell death plays a role in development and the process is called, morphogenesis,
the biological process that causes an organism to develop its shape. It also plays a role in the
maintenance ... Show more content on Helpwriting.net ...
Mechanisms of dengue virus induces cell death by taking control of the machinery of the cell. It is
evident that dengue (DEN) viruses can trigger the host cell to undergo apoptosis in a cell–dependent
manner. Virally induced apoptosis contributes directly to the cytopathogenic effects of DEN virus in
cultured cells. The induction of apoptosis involves the activation of intracellular signaling systems.
The cellular factors that regulate cell death can adjust the outcome of DEN virus infection in
cultured cells. Apoptosis inhibitors delay DEN virus–induced apoptosis, thereby providing a suitable
environment for the virus. During DEN virus infection, cell death is also regulated by the harshness
of the infecting strains. Overall, the purpose this research provides information on the cellular
mechanisms and viral proteins associated with apoptosis in response to DEN

Impact Of Toxicity Of Commercial Sodium Salt On Kidney And...
Impact toxicity of commercial Sodium Chlorid Salt on Kidney and DNA of male mice Part 1
1*Aly, H. M. 2Gamela S.M. El–Saeed, 3Rizka K.Ali.
1Department of Cell Biology,
2Department of Medical Biochemistry,
3Department of Water Pollution Research,
Abstract: Sodium chloride is widely used in various industrial, medical and food applications that
increasing human exposure to it by excessive amount. However, almost all studies focused on its
nephrotoxicity and adaptation of kidney cells to high concentration salt and only few scientific
attentions were concerned on its cytoxicity. Hence, the oxidative DNA damage induction by
excessive salt intake in mice was investigated. mice were orally administrated with three different
concentrations commercial NaCl solution started with concentration at tap water. Second and third
concentrations were (50 & 100mg/L) orally administrated for 10 successive days then sacrificed 24
hour after the last orally administrated. Comet assays were used to evaluate the possible toxicity of
excessive salt on DNA levels. Also, some biochemical markers of kidney were assessed to shed
more light on salt mechanism of action. DNA damage induction by excessive intake of high salt was
evidenced by the statistical significant elevations in both two group. This was further evidenced by
appearance damage of DNA on agarose gel. Moreover, excessive NaCl caused significant elevation
in kidney function level in a dose dependent manner. It was also noticed that

Type 2 Diabetes Research Paper
Introduction Diabetes is a long–term metabolic condition characterized by high blood sugar levels.
There are three major categories of the disease, type 1 diabetes occurs when the body produces
minimal or no insulin, type 2 diabetes is when the body produces either little insulin or the cells are
unable to respond to insulin, gestational diabetes mainly occurs during pregnancy. Non–Insulin
Dependent Diabetes Mellitus, which is, type 2 diabetes is the most prevalent. The major
complication that is caused by Type 2 diabetes is unremitting hyperglycemia, which leads to
numerous changes in the body. There are several alterations in cellular, cardiovascular, and nervous
functioning, which contribute to complications such as neuropathies and heart ... Show more content
on Helpwriting.net ...
In adults, they include polydipsia, polyuria, poor vision, loss of weight, fatigue, severe gum
complications, burning sensations in extremities, vaginal infections in women, and erectile
dysfunction in men. Among children, there is obesity, mild polyuria and skin problems such as
acanthosis. Treatment of the disease includes not only drug therapy but also some lifestyle changes
such as proper diet, exercise and weight management. Biochemical and physiological changes
associated with type 2 diabetes are both as a result of the disease progress and therapy. Alterations in
mitochondrial functions and blood vessels lead to a high number of pathologies. The disorder is
linked to a high mortality rate due to complications developed such as heart disease (Barnett, 2011,
24). Biochemical and physiological changes in Type 2 Diabetes Biochemical and physiological
changes refer to those, which are associated with the chemical processes and normal functioning of
the body. The alterations in bodily functioning are highly caused by the effects of hyperglycemia.
Type 2 diabetes, therefore, causes changes in cellular, cardiovascular and nervous functions that
eventually lead to disorders such as heart failure, which increase morbidity and mobility. Any
alterations in the body affect several other biochemical and physiologic roles of the body, it is,
therefore, necessary to treat the significant changes that cause

Apoptosis And Suicide Synthesis Essay
The process of cell programming to commit suicide is also known as Apoptosis, it also is sometimes
characterized by different characteristics and energy mechanisms. Apoptosis is too be considered as
a very important part of different processes which mean proper development, cell–death, immune
system, and many other programs that are vital to the human body. Research will continue to focus
on the clearing up of the power of cell death. Also research will continue to seek how someone may
be able to control the process of Apoptosis. "Scientist are also at the moment trying to learn how to
modulate apoptosis, so they may be able to control programmed cell death"(2016).The process
normally will occur during the aging of someone or just natural ... Show more content on
Helpwriting.net ...
Anti–cancer drugs and radiation are an example that work by triggering programmed cell death in
diseased cells. I believe that understanding how to take control of apoptosis could become one of the
first steps to treating many different conditions. The past decade has witnessed tremendous advances
in the discovery and development of novel small–molecule inhibitors targeting apoptosis pathways
for cancer treatment, with some compounds now in clinical development. Early promising clinical
data have been reported with the new classes of anticancer drugs. This review covers the recent
advancements in the development of small–molecule inhibitors targeting three major classes of
antiapoptotic proteins: antiapoptotic B cell lymphoma 2, proteins, inhibitor of apoptosis proteins
(IAPs), and murine double–minute 2 (MDM2). A Lot of attention is given to those that have been
advanced into clinical trials. The challenges and future directions in the further preclinical and
clinical development of these new anticancer drugs are also talked

Research Paper On Apoptosis And Necrosis
Cell Death
Cell death is when a biological cell stops carrying out is function. Cell death can be due to the
natural process of replacing old cells with new ones, or may result from factors such as disease,
localized injury, or even death of the whole organism.
Apoptosis vs. Necrosis
Apoptosis is a form of cell death that is caused by normal processes of the human body, necrosis on
the other hand is a form of cell death that is caused by disease states or external inputs such as
infection or injury. Apoptosis also known as programmed cell death may also be used as a defence
mechanism for the body in the healing process and is usually normal and beneficial to the organism.
Necrosis is never normal or beneficial, but abnormal and harmful. Necrosis is regarded as an
unprogrammed death of the cell. Apoptosis almost never demands any medical treatment, on the
other hand if necrosis is left untreated it may result in critical injury or death Apoptosis Necrosis
Introduction Apoptosis, or programmed cell death, is a form of cell death that is generally triggered
by normal, healthy processes in the body. Necrosis is the premature death of cells and living tissue.
Though necrosis is being researched as a possible form of programmed cell death, it is considered
an "unprogrammed" cell death process at this time.
Natural Yes ... Show more content on Helpwriting.net ...
Degrading cellular components induces survival of cells during periods of starvation by conserving
cellular energy levels. In this process, certain constituents of the cytoplasm are isolated from the rest
of the cell within a double–membraned vesicle known as an autophagosome. The membranes of the
lysosome and autophagosome fuse and the autophagosome contents are degraded and recycled.
There are three different forms of autophagy that are commonly described, namely macroautophagy,
microautophagy and chaperone–mediated

Essay On Apoptosis
Given the vital role of caspase activation in apoptotic cell death, blocking their function is a useful
approach to find out whether apoptosis has a causal effect in triggering compensatory proliferation.
In various species tissue regeneration was impaired if cell death was blocked with pan–caspase or
effector caspase inhibitors (Fan and Bergmann 2008; Li et al. 2010; Ryoo and Bergmann 2012;
Tseng et al. 2007). This approach has also been shown to ameliorate loss of neuronal cells and
function after traumatic brain injury and retinal detachment (Hisatomi et al. 2001; Zacks et al.
2003). Following this approach we found that the pan–caspase inhibitor reduced the number of
cleaved CASP3+ cells in cultured retina explants, but not the overall ... Show more content on
Helpwriting.net ...
Following our gene expression data we further hypothesized that inhibition of RIPK1 in
combination with CASP8 might be even more specific and therefore similarly effective.
Two distinct signaling pathways trigger programmed apoptosis: the intrinsic pathway activated by
cellular damage and the extrinsic pathway induced by the binding of specific pro–apoptotic ligands,
like TNF, mediated by the initiator CASP8 activating executioner CASP3. CASP8 also has been
shown to negatively regulate necrosis by cleaving RIPK1 and RIPK3 (Festjens et al. 2007).
Apoptosis–induced compensatory proliferation has been shown to either induce generation of
different mitogenic cues, like WNT, SHH or TNF, via initiator or executioner caspases (Bergmann
and Steller 2010; Ryoo and Bergmann 2012). Previous work showed that dying photoreceptors in
fly eyes instruct cell death mediated compensatory proliferation via initiator caspases (Fan and
Bergmann 2008). And in the regenerating zebrafish retina dying photoreceptors, amacrines and
ganglion cells may express TNF that is required for the regeneration response (Nelson et al. 2013).
Inhibition of cell death and MG proliferation was

Reactivity Of Hcl Acids With Cells Lab Report
Reactivity of the HOCl acids with cells
The reactivity of HOCl has been comprehensively assessed with in a wide range of cellular systems,
including yeast (Carmona–Gutierrez et al., 2013) and bacteria (Winterbourne and Kettle, 2013;
Winterbourne et al., 2006; Chapman et al., 2002), together with many studies focused on specific
mammalian cell types and tissues. It is clear from the numerous invitro studies that HOCl is highly
reactive and destructive, inducing cell death via both necrotic and programmed apoptotic pathways,
depending on the oxidant concentration and cell type under study.
HOCl–induced cell lysis
The a nucleate red blood cell (RBC) has been used extensively as a model system for investigating
mechanisms of MPO–mediated cell ... Show more content on Helpwriting.net ...
Perhaps somewhat paradoxically, the continued exposure of macrophages to HOCl has been shown
to exacerbate the inflammatory response in a number of disease settings, which is particularly
relevant with in the progression of atherosclerosis (Daugherty et al., 1994). It has been shown that
exposure of both murine macrophage cell lines and primary cultures of human monocyte–derived
macrophages (HMDMs) to physiologically relevant concentrations of HOCl results in the loss of
cell viability. In early studies employing the murine macrophage cell line P388D1 Schraufstätter and
co–workers (Schraufstätter et al., 1990) demonstrated a dose–dependent increase in the extent of
trypan blue uptake by the cells that was concurrent with the increased presence of lactate
dehydrogenase (LDH) in cellular supernatants. Both of these methods are indicative of disruption to
the cellular membrane and are used extensively as surrogate markers of cell death. In these studies,
it was shown that exposure of cells to HOCl concentrations as low as 25 µM decreased cell viability
by approximately 20% compared to controls, with 50 µM HOCl causing up to 50% cell death, and
complete cell lysis observed after exposure to 75 µM HOCl. Although these data were

The Static Storage Model
The following text considers the issues that arise from the static storage model. By looking at
mechanisms of death which occur in cells and taking human memory as an example of labile
storage, static memory is posited to be a problematic model. A link is traced between cellular death
mechanisms and memory transmission (mutations), and the new developments in synthetic DNA
storage. As the near future nature of truly embodied data stored in DNA is thought of within the
static storage model, I use this text to sketch the implications of this anachronism, and hope to
inspire thoughts on possible mutable memory models.
Static storage is understood here as a model, in the first instance, because it ranges across several
disciplines as a framework. In literature, static storage is a model in which memory is not altered
and representational. This notion has been challenged namely by Thomas Wägenbaur (1998) and
Kyle Pivetti (2015), accounting for amongst other factors, recent neuroscientific memory research.
In the sciences, neuroplasticity has replaced the notion of the immutable memory. Memory changes
every time it is recalled, transmission between neurons is highly mutable (Nader et al. 2000). In
computer science, static may refer to storage, variable allocation, or objects (to name but a few). ...
Show more content on Helpwriting.net ...
Though some thought is being put into DNA contamination, complex implications or possibilities
which could arise from synthetic DNA propagation are still unclear. Also, DNA is itself part of a
cycle of life that involves duplication, mutation and suicide. What happens if we try to impose a
static model upon a mutable format? Researchers at ETH have developed a sheath of silica glass to
encapsulate stored DNA data, which could allegedly survive a million years (Grass et al. 2015). This
literal example of impeded mutation begs the question, who does this contrived approach

What´s the Exact Cause of Cancer?
Cancer is a disease where there is uncontrolled cell division and surrounding tissues are invaded.
This invasion occurs by a process called metastasis; cells grow directly into surrounding tissues and
are transferred through the bloodstream or lymphatic system. These rapidly growing cells are
supported by angiogenesis, the growth of new blood vessels from old ones, which helps supply the
cells with nutrients.
Cancer results from cell mutations which stem from DNA damaged during the cell cycle. These
mutations are in genes that encode for proteins that control cell division. The uncontrolled division
of cells results in the growth of benign tumors or malignant tumors. Benign tumors do not undergo
the process of metastasis and are seldom life–threatening. Malignant tumors do undergo metastasis
and are very life–threatening. The exact causes of cancer are still undetermined, but there are many
things that raise the chances. Smoking and drinking has been linked to many cancers such as lung,
mouth throat, bladder, and kidney cancer. Radiation and too much exposure to sunlight can also lead
to cancer. It is known that changes in cells cause cancer but what causes these changes are unknown.
The cell cycle is the link between the unknown cause and cancer.
The cell cycle is the cycle of cell growth, replication of the genetic material and division into equal
daughter cells. The cell cycle consists of interphase and mitosis. Interphase has three steps; G1, S,
and G2

Gaining Control of the Gene Responsible for Apoptosis...
Gaining Control of the Gene Responsible for Apoptosis When we gain control of the gene
responsible for the phenomenon of apoptosis, we will be in control of aging. We are finding more
evidence every day, indicating genetic links to all sorts of factors in the human being. We are just
now beginning to scratch the surface of our own genetics. A landmark discover has just been
unveiled: In February [2001], the two groups charting the human genome published their results–the
entire 3 billion base pair sequence. The only definitive conclusion so far: Humans are far more
complicated than we thought. ...Eric Lander, director of the Whitehead Center for Genome Research
in Cambridge, Massachusetts ... adds: "within a decade, we will understand ... Show more content
on Helpwriting.net ...
Once this model of bone is complete, the cartilage cells are given the command to die. Osteoblasts,
or bone building cells, move in to the space formerly occupied by the Condrocytes, and replace the
cartilage matrix with a Calcium rich, rock hard, matrix, we know as bone (188). In the foregoing
example there are instances of cells being told to die, this is programmed death, and known as
apoptosis. During life, our cells carry out metabolic functions, producing digestive enzymes and
waste products, which are harmful to surrounding cells, if it spewed into the fluids among the cells.
These enzymes and toxins must be packaged in a way that is not harmful to the interstitial
environment, and in a manner in which appropriate cells in the region can readily absorb them. This
must be done without invoking an inflammatory response (Browder).
Aging, also known as Senescence, is a natural process, "beginning at reproductive fitness and
culminating in death," Observed in most living organisms, senescence is characterized by a gradual
reduction in "reserve capacity of organ systems", (Heydari). Supporting research by U. of Florida's
Aging Biochemistry Laboratory indicates an increased apoptotic rate of cardiomyocytes, T–
lymphocytes, and neurons, as age advances (Leeuwenburgh, par. 3.1). These factors manifest the
classic signs of aging as well as many age–associated diseases, such as reduced cardiac function,
susceptibility to illness and

Genetic Determinants Of Hiv Infection
Genetic determinants of HIV infection:
HIV has two major types: HIV–1 and HIV–2. HIV–1 has four groups M, N, O and P. These groups
are further classified into subtypes. Group M is a major infecting group worldwide contributing to
90% of HIV–1 infections. Group M is classified into nine subtypes (A, B, C, D, E, F, G, H, J and K).
Subtype B is predominantly found in America and Western Europe. The susceptibility to HIV–1
infection, transmission of disease, and response to retroviral therapy depend on the genetic
determinants of the host cell. These genetic determinants vary in populations and among patients.
These genetic variants regulate chemokine co–receptors and ligands that involve in the entry of the
virus, major histocompatibility complex, killer cells Ig like receptor and cytokines, and TRIM5α
motif and apolipoprotein B mRNA–editing enzyme, catalytic polypeptide–like 3G (Kaur and
Mehra, 2009). In genome–wide association studies performed in European population, it was shown
that Human leukocyte antigen (HLA) class I variation (Eg. HLA–B*5701) is the major contributor
to viral set point and CD4+ T cell decline (Fellay et al., 2010). Cohort study of genetic
polymorphism in chemokine receptors in Indian population has shown that protective CCR5 Δ32
variant is rare and CCR5HHE carrying *59402A has the high likelihood of infections (Kaur and
Mehra, 2009). HIV Sequence Database contains annotated HIV sequences

Cancer: Uncontrolled Cell Division In The Body
Cancer is a universal term for a set of over 100 of diseases that affect can anyone. Cancer cells,
unlike somatic cells, divide at a quick and abnormal rate. Factors that may cause one to develop a
type of cancer include genetic links and aging; lifestyle factors such as physical activity, diet, and
tobacco or alcohol usage; and excessive environmental exposure to sunlight, ultraviolet light,
radiation, or certain chemicals or bacteria (American Cancer Organization). The most common way
one can develop cancer, however, is through uncontrolled cell division in the body.
The cells in the body either in one of two phases: interphase, during which cells grow, replicate
DNA, go about their routine functions, and prepare for mitosis or meiosis.

Why Ethanol Kills Cells
The reason that ethanol kills cells in plants is twofold. Firstly, ethanol is permeable to cell
membranes (Kinseth, 2006). Because of the nature of ethanol as a chemical is it able to get into the
cell very easily through passive transport(Koszler, 2013). This disrupts the balance of the cells'
aqueous environment (Morrow, 2009). It has also been shown that ethanol can disrupt the ion
channels in the plasma membrane (Karp, 2006). These channels in the cell membrane help pump
ions like calcium and potassium in and out of the cell which directly control how much water is
pumped in and out of the cell, therefore being responsible for the creation of the hypertonic
environment that causes programmed cell death (PCD) (Elbagoory, 2014). Secondly,

The Effects Of Genetic Mutations On Dna Repair Systems And...
Several decades of cancer research have identified thousands of mutation causing carcinogens,
genetic mutations in DNA repair systems and mutations that cause dysregulation in critical signal
pathways involved in cell cycle progression, cell growth and programmed cell death. Human
cancers cannot be classified as a single disease because they are each unique on the molecular level.
Often the same documented cancer type can inflict two patients with similar symptoms, but the
required treatment for each patient will be different because the molecular mechanisms causing the
symptoms must be treated differently. This is the primary reason why there is no "cure for cancer"
because we may have one word to describe all cancers; it is a classification of many diseases. (The
question is irrational and misinformed. If cancer were one disease with an underlying fundamental
mutation or pathogen that could be isolated, then we would have found the cure by now.) Each type
of cancer is inherently unique containing a minimum of 5 to 6 mutations that comprise the genotype,
which could result in similar phenotypes. However, they have similar properties for which they are
classified, called "hallmarks of cancer". The "hallmarks of cancer" include persistent signaling for
cell proliferation, circumventing growth/tumor suppressors, evading cell death, promoting endless
replication, activating angiogenesis, and triggering metastasis and invasive properties (Hanahan and
Weinberg 2011). The constant

A Study On The Beard Cells Essay
Rohon Beard cells (RBs) are transient neurons that are displayed in amphibians (Xenopus),
zebrafish (Danio rerio), and other teleosts early in embryonic development. These cells were first
described by two scientists independently of one another: Rohon (1894) and Beard (1896). RBs
develop on the border between the epidermis and the neuroectoderm because they are a component
of the peripheral nervous system. Along with their localization, RBs retain a number of
morphological attributes that distinguish them from other neurons (Reyes et al., 2004). Researchers
have studied RBs development in zebrafish for a variety of different reasons. First of all, zebrafish
are easy to handle and they breed quickly and efficiently. It is possible for one mating pair to
produce 200–300 embryos in one breeding session. Additionally, these embryos are relatively
transparent. Therefore, one can utilize an antibody stain to visualize the nervous system and the
images can be seen using a light microscope. When viewed under the microscope, zebrafish RBs
display a large soma (cell body), a large nucleus, and a granular cytoplasm. Additionally, they
display central and peripheral axons that extend into different areas of the nervous system (Reyes et
al., 2004). Generally, the central axon divides into a rostral axon that extends into the hindbrain, and
a caudal axon that extends into the dorsolateral tract. Conversely, peripheral axons of RBs innervate
the skin (Reyes et al., 2004).

Mitochondrial Pathway Of Mitochondrial And Mitochondrial...
1.2.2. Mitochondrial pathway
The mitochondrial pathway, also called intrinsic pathway, because it is initiated from inside the cell.
Various stimuli such as growth factors withdrawal, DNA–damage, hypoxia, and oxidative stress can
induce apoptosis through this cascade. These insults cause increasing permeability of the outer
mitochondrial membrane and opening of the mitochondrial permeability transition (MPT) pore
which is controlled by members of the Bcl–2 family proteins. This large family of proteins is
defined by the presence of conserved Bcl–2 homology domains (BH1 to BH4). Up to 30 Bcl–2
family genes have been identified in mammals, which have either pro–apoptotic or anti–apoptotic
functions. Some of the anti–apoptotic members include Bcl–2 itself, Bcl–XL, Bcl–w, BAG and
Mcl–1 which possess all domains of BH1 to BH4. The pro–apoptotic family proteins can be divided
into two subgroups: consists of Bak, Bax, and Bok with possess BH1 to BH3 domains, and Bad,
Bid, Bik, BNIP3, Bim, Bmf, Blk, Hrk, Noxa, Puma, and Spike) that only possesses BH3 domain
[Cory, 2002; Mund, 2003]. It is believe that BH3–only proteins interfere with the fine–tuned balance
of homo– or hetero–oligomerization between pro–apoptotic multidomains (eg., Bax/Bak) and anti–
apoptotic members (eg., Bcl–2/Bcl–XL) (Figure 3). In general, oligomers of Bak, Bax, and Bok
induce PMT, either by forming channels by themselves or by interacting with components of the
PMT [Antonsson, 2000]. Bad can also heterodimerize

Cancer Pathogenesis Of Cancer
There has been a spontaneous advancement in the understanding the pathogenesis of cancer over the
last two decades. Even though there has been a significant success in the knowledge of tumor, there
still a wide gap in the treatment of tumors. There is a little treatment information available on cancer
making it difficult to control it. Chemotherapy remains the only effective treatment method used.
This study aims at examining the possible roles of the p53 gene in leukemia and how that data can
be utilized for diagnosis and treatment of cancer.
Due to its potent tumor suppressive activity, a molecular understanding of p53 action will create
significant experiences into specific procedures that limit tumor growth and may identify key ...
Show more content on Helpwriting.net ...
There are essentially two pathways that transduce signs to start apoptosis in leukemia. The primary
route is the extrinsic pathway. It includes the trimerization of death factors like CD95/Fas/APO–1 or
TNF receptor one which initiates caspase 8, which initiates the apoptotic machinery. The second
pathway is the intrinsic pathway. This pathway involves the p53 gene and is subsequently of more
concern. The p53 gene initiates the arrival of cytochrome C from the mitochondrial intermembrane
space into the cytosol. The cytochrome C in the presence of ATP reasons the oligomerization and
activation of Apaf–1 and caspase 9 as per Schuler, (2000).
Therefore, then prompt caspase three and other effector caspases that cause apoptosis. By utilizing
this data, experiments have been carried out that try to induce apoptosis in cancer cells by activation
of the p53 gene. One particular examination was done on the human osteosarcoma cell line Saos–2,
which is deficient in p53. According to Schuler (2000), an introduction of the p53 gene led to
apoptosis through an intrinsic pathway. Subsequently subjecting p53 to gene treatment might be of
enormous importance in the battle against leukemia.
According to Liu (1994), it has additionally been discovered that p53 mutant tumors are more
unstable genetically and this state of instability may enable the tumors to become more rapidly
resistant to drug treatments.
Since p53

Arabidopsis: A Case Study
The immune system of Arabidopsis thaliana can be divided into two lines of defence. Initially,
pattern recognition receptors (PRRs) on the cell membrane detect pathogen–associated molecular
patterns (PAMPs), which leads to PAMP–triggered immunity (PTI) associated with basal resistance
that defends the plant cell from less adapted pathogens (Jones and Dangl 2006). Pathogens that are
able to surmount this initial immune response do so through the use of virulent effector molecules
that inhibit and suppress PTI, which, in turn, activates the second line of defence, effector–triggered
immunity (ETI) (Jones and Dangl 2006). ETI is achieved through the expression of numerous genes
involved in disease resistance (R genes) that subsequently encode nucleotide binding–leucine rich
repeat (NB–LRR) proteins that each recognizes specific effectors, which ultimately results in
increased basal resistance and possibly apoptosis in the case of a hypersensitive response (HR)
(Jones and Dangl 2006). The enhanced disease susceptibility1 (EDS1) gene is a crucial component
of ETI, as its gene product serves as a signaling intermediary between this initial ... Show more
content on Helpwriting.net ...
Nuclear EDS1 is directly involved in signalling SA–dependent transcriptional reprogramming of
genes that code for defensive proteins in addition to regulating apoptosis (García et al. 2010). An
increase in cytoplasmic EDS1 due to export from the nucleus, on the other hand, suppresses this
immune response and promotes apoptosis in an acute ETI response wherein EDS1 is unbound from
PAD4 and instead forms a complex with itself (García et al. 2010; Wagner et al. 2013). As a result,
proper EDS1 levels in different compartments of the cell are necessary for mounting the most
efficient immune response to different pathogenic microbes with respect to resistance and
programmed cell

Analysis Of The Film Blade Runner
The neo–noir film Blade Runner, directed by Ridley Scott, has become a classic example of a
futuristic dystopian society in which dominant humans develop a desensitized and barbaric attitude
toward a marginalized societal group: humanoid clones known as Replicants. This film is often
interpreted as the consequence of powerful corporate capitalism and a lack of ethics. When viewing
this film from a scientific immunological perspective however, a parallel between the film's
dystopian society and the function of the mammalian immune system can also be drawn. This
connection will be examined by viewing the Replicants as unwanted invaders, the specific markers
they exhibit that allow them to be easily identified, and their limited lifespan due to programmed
death.
Replicants are off–earth exiled humanoid slaves who will be killed if they ever come to earth as they
are viewed as threats to human society, much like a pathogen invading a host is a threat to the body.
The exile of Replicants is maintained by a government police force, specifically a special operations
police officer referred to as a "blade runner". The film follows his pursuit of four illegal Replicants
that have come to earth. If we view the earth as a cell functioning normally, and the four invading
Replicants as invading pathogens, the similarity between the pathogens' potential for invading the
body and Replicants' potential for invading earth become apparent. The four invading Replicants in
the film act as a

Nonspecific Immune Response Analysis
LO 2.28 I understand how to use representations or models to analyze quantitatively and
qualitatively the effects of disruptions to dynamic homeostasis in biological systems. Both models
and representations may be used to show the effects of changes in homeostasis. The main ways to
achieve homeostasis is through positive and negative feedback and disruptions can be viewed easily
through models or representations. (Campbell 644–645, 650–652)
LO 2.29 I understand how create representations and models to describe immune responses. There
are two main types of immune responses; primary and secondary. Primary is the first time a
response occurs in the presence of an antigen while secondary refers to a response after the initial.
Both may be modeled by showing examples of an antigen and the respective secondary/primary
response. (Campbell 719–720)
LO 2.30 I understand how to create representations or models to describe nonspecific immune
defenses in plants and animals. Animals and plants have some sort of immune response that protect
the organism from infection and that does not target any specific pathogen. Representations or
models may be created from this by detailing means by which the animal/plant can provide ... Show
more content on Helpwriting.net ...
Cell death is an essential part of a cell's life cycle in the three given situations. Apoptosis, a type of
programmed cell death, may be used as an example why death is useful. In development and
differentiation, it may be used to replace old cells that are either no longer functional/efficient or no
longer needed. For reusing molecules, cells may die so that the molecules within are released and
they may be used again. Finally, dynamic homeostasis uses cell death to either promote the
production of substance that is needed or as a means of negative feedback. (Campbell 313–315, 645,
and

Cancer : A Serious Problem Around The World With No Real...
Cancer is a serious problem around the world with no real cure. So much money and time are being
put into studies and trials to try to make progress towards a cure. As of right now lung cancer is the
leading cause of cancer death in the United States.1 Most patients who are diagnosed with
metastatic lung cancer have a survival rate of less than 5%.1 Chemotherapy is the first intervention
taken to fight lung cancer. Even though eighty percent of patients are responsive to this first line of
chemotherapy treatment, most still relapse, for which there is no approved therapies beyond the
second line.1 However, it is now being shown that the immune system is able to create an antitumor
response. Recently studies have shown that immunotherapy could become a viable therapeutic
approach in fighting lung cancer. Immunotherapy itself is using the body's own immune system to
help fight cancer cells. These cells are constantly rapidly–dividing and frequently mutate to trick the
immune system. Immunotherapy drugs are ment to help the immune system locate and destroy the
cancerous cells.2 Cancer cells are not normally recognized as foreign because they are normal self–
cells that have mutated, which causes them to no longer behave like normal cells.2 The immune
system cannot recognize this occurring which allows the cells to grow and divide. Cancerous cells
stay hidden by sending signals to the PD–1 CTLA–4 receptors on immune cells.2 Those signals are
what trick the body into

Caenorhabditis Elegans
I. Introduction
All throughout the body, cells are reproducing then dying. It is a part of life in which we maintain
homeostasis. This is what scientists know as programmed cell death. The cell turnover within the
body depends on what type of cell and what it is used for. These mechanisms take place over and
over within the bodies of many animals, including humans. In fact, human began life as just "one
fertilized egg cell." Genetic regulation of programmed cell death and organ development was a
concern for Sydney Brenner, Robert Horvitz, and John Sulston. Their scientific discoveries have
enhanced biological and medical research by allowing scientists to understand how these processes
are regulated. In this essay I will explore Caenorhabditis elegans, cell lineage, and programmed cell
death in which the article goes in depth with.
II. C. elegans ... Show more content on Helpwriting.net ...
This worm made it fairly easy for them to examine under a microscope to pick out changes that may
have occurred to it when introduced to mutations that may affect organ formation. Sulston always
took part in this as well. He took notice of the cell divisions while studying the cell lineage of the
worm and that gave other scientists insight into how organs and tissues develop and die. This worm
earned them the Nobel Peace Prize by enabling them to grasp the knowledge of how bacteria and
viruses invade cells. The benefits from this research also allowed Horvitz to come to the conclusion
to that there were death genes in the worm that triggers certain

Why Is Mitochondria Important?
Mitochondria: a word many people have used in their vocabulary, but one that most people fail to
understand. Why is the mitochondria famously known as the powerhouse of the cell? It is because of
its energy production. The mitochondria is responsible for the large majority of the production of
ATP(adenosine triphosphate for those who actually care). ATP is the molecule that provides energy
for most of the body's functions. This organelle also aids in the processes of cellular
differentiation(the changing of one cell type to another) and cell death(literal programmed,
predetermined death of a cell). The mitochondria is made up of several different regions that help
the organelle to function properly. These regions include the outer membrane,

The Cradle And The Grave And How We Are Affected By Our Genes
Ever thought about why or even how we age? That has been one of the greatest questions science
has ever had. There are so many different things that can affect the way all living organisms live and
die. In this paper, I will discuss the time that is between the cradle and the grave and how we are
affected by our genes, free radicals, and everyday choices. The term "Aging" refers to in specific
human beings, many animals, and fungi. Organisms such as bacteria, recurrent plants and some
simple animals are theoretically immortal. Ageing can refer to single cells within an organism which
have ceased dividing, also known as cellular senescence. Many don't consider the everyday choices
and how their bodies will respond. Whether it's going to the beach with no sunscreen or going to a
BBQ and eating a big greasy burger. The littlest things will cause our bodies to react in our own
ways. In humans, ageing represents the buildup of changes in an individual over time, including
physical, psychological, and social change. Response time may slow with age, while experiencing
world events, our wisdom may expand, but our bodies will slow down. Ageing is comparable to risk
factors for most human diseases, approximately 150,000 people die each day globally, about two
thirds die from age–related causes. The causes of ageing are still uncertain, some theories place
blame on the damage concept, this means it's the accumulation of damage, such as DNA breaks or
oxidized DNA. This

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

Apoptosis
Kerr, Wyllie, and Currie first used the term apoptosis in a paper in 1972 to describe a
morphologically distinct form of cell death, although certain components of the apoptosis concept
had been described years previously. Our understanding of the mechanisms involved in the process
of apoptosis in mammalian cells transpired from the investigation of programmed cell death that
occurs during the development of the nematode Caenorhabditis elegans (Horvitz, 1999). In this
organism 1090 somatic cells are generated in the formation of the adult worm, of which 131 of these
cells undergo apoptosis or "programmed cell death." These 131 cells die at particular points during
the development process, which is invariant between worms, demonstrating the ... Show more
Necrosis is an uncontrolled and passive process that usually affects large fields of cells whereas
apoptosis is controlled and energy–dependent and can affect individual or clusters of cells. Necrosis
is caused by factors external to the cell or tissue, such as infection, toxins, or trauma that result
unregulated digestion of cell components
Some of the major morphological changes that occur with necrosis include cell swelling; formation
of cytoplasmic vacuoles; distended endoplasmic reticulum; formation of cytoplasmic blebs;
condensed, swollen or ruptured mitochondria; disaggregation and detachment of ribosomes;
disrupted organelle membranes; swollen and ruptured lysosomes; and eventually disruption of the
cell membrane. This loss of cell membrane results in the release of the cytoplasmic contents into the
surrounding tissue, sending chemotatic signals with eventual recruitment of inflammatory cells.
Because apoptotic cells do not release their cellular constituents into the surrounding tissue and are
quickly phagocytosed by macrophages or normal cells, there is essentially no inflammatory reaction.
It is also important to note that pyknosis and karyorrhexis are not exclusive to apoptosis (Kurosaka
et al., 2003).
Mechanisms of Apoptosis
The mechanisms of apoptosis are highly complex involving an energy dependent cascade of
molecular events. Research

Symptoms And Treatment Of Crohn 's Disease
Crohn's disease is an inflammatory condition that is immunologically mediated. Even though the
etiology of the disease is not yet determined, results from different researches such as human
genetics, clinical tests and basic science have given significant insights in the inflammatory disease
pathogenesis. In addition, the studies reports that Crohn's disease is heterogeneous disease that is
characterized by different genetic abnormalities that results to T cells responses. The research paper
has highlighted various signs of the disease that indicates that T cells usually response to the
environment. For instance, the paper states that T cells are important to an individual's immunity and
has both protective and harmful immune response. The research paper has a purpose statement that
provides the theme or the question that is being examined in the paper. The paper also reviews both
the Crohn's mechanism and the assumed pathophysiological mechanisms. Assumed
pathophysiological mechanisms include intestinal permeability, infectious agents, pro–inflammatory
moles and the abnormal immunological response. On the other hand, signs and symptoms of the
Crohn's disease include diarrhea, weight loss, abdominal pain and fever. Introduction Crohn's
disease is usually defined as a chronic inflammatory bowel disorder that affects the digestive track
lining. The disease is categorized in the group of Inflammatory Bowl Diseases conditions. It is
commonly known to affect the ileum

Programmable Cell Cancer
Cancer has been ascertained as a leading cause of morbidity and mortality among individuals
worldwide. It occurs in the body when cells grow uncontrollably and no longer die. In regular cells a
programmed cell death called apoptosis will occur before a neoplasm can be formed; however in
carcinoma cells, this programmable cell death is broken and invasive, metastatic tumors can form.
Metastatic tumors are cancer cells that have spread throughout the body using the bloodstream
making detection even more difficult and potentially lead to death [1]. These cancer cells can
interfere with normal functioning cells by up taking nutrients and resources by invading into the
normal cells and tissues; this development is called metastasis. Death

What Is Myelin Gene Regulatory Factor ( MRF )?
Recently, it has been demonstrated by DNA microarray analysis that myelin gene regulatory factor
(MRF) expression is specific to terminally differentiated oligodendrocytes (Cahoy et al., 2008;
Heiman et al., 2008). Importantly, knockdown of MRF in oligodendrocytes by RNA interference
downregulates expression of the majority CNS myelin genes (Emery et al., 2009). In contrast,
overexpression of MRF in in vitro cultured OPCs can promote myelin gene expression.
Oligodendrocyte lineage–specific MRF knockout mice show normal premyelinating
oligodendrocytes but they display severe myelin gene expression deficits and subsequently fail to
myelinate axons. In addition, these knockout mice die early due to severe seizures.
Oligodendrocyte ... Show more content on Helpwriting.net ...
Ye et al., 2009).
In addition to transcriptional regulation and epigenetic mechanisms, posttranscriptional regulation
by microRNAs is also critically involved in the intracellular signaling of oligodendrocyte
differentiation. Studies using transgenic mice in which microRNA processing is specifically
disrupted in the oligodendrocyte lineage by way of Dicer enzyme knockout have shown that
microRNA processing is indispensible for normal CNS myelination (Dugas et al., 2010), and that in
vitro OPCs also fail to differentiate in the absence of mature microRNAs. Specifically, three
microRNAs including miR–219, miR–138, and miR–338 are found to be elevated by 1–2 orders of
magnitude during OPC differentiation into oligodendrocytes, and that miR–219 when induced
alone, is sufficient to promote the differentiation (Dugas et al., 2010). The downstream target of
miR–219, ELOVL7, is also identified as a main molecular component involved in the development
of the Dicer mutant phenotype (Shin, Shin, McManus, Ptacek, & Fu, 2009), and that overexpression
of ELOVL7 results in lipid accumulation, which is in turn suppressed by co–overexpression of
miR–219. Other important target genes of the above mentioned microRNAs include PDGFRa,
Sox6, and Hes5 (Dugas et al., 2010; X. Zhao et al., 2010), all of which serve to

Cancer : An Uncontrollable Division Of Cells
INTRODUCTION TO CANCER
What is Cancer?
Cancer is described as an uncontrollable division of cells. According to the National Cancer
Institute, cancer is one of the leading causes of death in the world, with an estimated 595,690 deaths
and 1,685,210 new cases in 2016 alone (NIH 2015). Cancer can develop from almost every organ of
the body, with the most common organs affected being the breasts, lungs, prostate, colon, and
bladder (NIH 2015). As the disease progresses, it may become metastatic, where the cancer cells
migrate from their point of origin to other parts of the body. Cancer can spread in three ways:
through tissue, through the lymph system, and through the blood (NIH 2015). When cancer
progresses to a metastatic state, it is ... Show more content on Helpwriting.net ...
While the overall cancer death rate has declined, the war continues today as we are still plagued
with the complicated disease, cancer.
Hallmarks of Cancer (Hanahan and Weinberg 2011)
During tumor development and progression, cells develop/acquire six hallmark capabilities as they
transform from normal cells to neoplastic tumor cells. These hallmarks are developed at various
times throughout cancer cell progression are thought to promote the growth and metastasis of
tumors. These hallmark qualities, as outlined by Hanahan and Weinberg, are thought to be fostered
by underlying genomic instability, referring to mutations in the genome, and inflammation, usually
brought on by the immune system. The six hallmark capabilities include: sustaining proliferative
signaling, evading growth suppressors, resisting cell death, enabling replicative immortality,
inducing angiogenesis, and activating invasion and metastasis.
1. Proliferative Signaling
Cell growth and division is controlled by the production and release of growth promoting signals.
While normal cells carefully regulate the release of these signals, these signals are deregulated in
cancerous cells. Cancer cells are believed upregulate the cell cycle and cell growth through growth
factors which bind to cell–surface receptors and release signals. Other mechanisms for sustaining
proliferative signaling in cancer cells include: autocrine stimulation, where the cancer cells emit
growth factors and then respond to those same

Lung Cancer Research Paper
Cancer is due to uncontrollable growth of cells. Cancer cells differ from normal cells as it alters
from a systematic cell growth, division and apoptosis. Cancer forms when apoptosis fails to begin.
Unlike normal cells, cancer cells do not experience programmed cell death. Hence, cancer cells will
continue to multiply and segregate. This in turn, triggers a magnitude of abnormal cells that grow
without limitation. Lung cancer occurs when abnormal cells develop within the lungs, causing
disruption to the functions of normal lung cells. Lung cancers are highly due to the consequence of
inhaling carcinogenic substances, such as tobacco and arsenic. These carcinogenic substances have
damaging effects to DNA. Lung cancer is the leading cause of

Histone Research Paper
Histones are the basic proteins that wrap DNA into nucleosomes. Each histone has a flexible N–
terminal tail, which carry the sites for modification. Histones fall into five protein families, the core
histones H2A, H2B, H3 and H4, and the linker histone family H1.
They play a few important roles:
– Structural
Histones are sets of small basic proteins. They are found inside the nucleus. Their purpose is to
package DNA into structural units called nucleosomes. They are the main proteins in chromatin.
Nucleosomes are made of DNA wrapped around eight histone proteins and they are called a histone
octamer. Each histone octamer has two copies of the histone proteins H2A, H2B, H3, and H4. The
chain of nucleosomes is then wrapped into a 30 nm spiral called a solenoid, where additional H1
histone proteins are associated with each nucleosome to maintain the chromosome structure.
– Transcription
All of the histones are linked to the free groups of amino acids. Acetylation and methylation occur
on the free amino group of lysine. Acetylation of the lysine residues at the N terminus of histone
proteins makes the electrostatic interactions between histones and DNA weaker. This process allows
the chromatin to be able to adopt more ... Show more content on Helpwriting.net ...
Chromatin rearrangement takes place during repair to increase accessibility of damage to repair
proteins. Activity of histone acetyltransferases and chromatin remodeling complexes seems to be
essential for nucleosome rearrangement during repair. Once repair is completed, reconstitution of
nucleosomes is required to recover primary chromatin structure. Such chromatin assembly is
coupled to repair DNA synthesis. DNA damages induce some modifications to chromatin structure
(e.g. phosphorylation of a histone H2A variant in response to DNA double–strand breaks). Such
chromatin modifications may serve as signals recognized by DNA repair

Literature Review On Lung Cancer
1.0 Literature review
1.0.1 Lung Cancer
Lung cancer is a dangerous health problem which affects many people (Thomas, 2013). It becomes
the top killer among other types of cancers in the world (Molina, Yang, Cassivi, Schild & Adjei,
2008). According to the statistics made by National Institute of Health, more than 161, 000 cases
were reported in U.S. involving death caused by lung cancer in 2008 (Samet, Tang, Boffetta,
Hannan, Marston, Thun et, al., 2009). Despite the decreasing trends of lung cancer incidence rates
for men in the 1980s and for women in the late 1990s, still the lung and bronchus cancer remain the
significant cause of cancer mortality in the United States, with an estimation of 87,750 and 72,590
deaths to occur in men and women, respectively, in 2012 (Field & Withers, 2012) American Lung
Association (2015) has defined lung cancer as a growth of abnormal cells in the lungs without
control, which ... Show more content on Helpwriting.net ...
This may occur to the old cells, to be replaced by new ones. This is denoted as a natural process.
Cell death may also occur due to localized injury and disease (Martes, 2014). There are two ways a
cell death can occur which are necrosis and apoptosis.
Necrosis occurs due to the harm caused by an external force, such as bodily injury, poison and
infection. When the body cells die due to necrosis, it causes serious inflammation and further injury
in the body (Martes, 2014). The other way of cell death is apoptosis. It is also called as programmed
cell death. It follows a predictable and control routine (Kogel & Prehn, 2013).
Abnormal apoptosis, either too much or too little of it can cause many serious diseases in human
such as neurodegenerative diseases, autoimmune disorders, ischemic damage and many types of
cancer (Elmore, 2007). Therefore, the field of apoptosis is gaining attention in the research to
analyze the signaling pathways of

Essay On Distracted Driving
Saving Lives Is Important
A distraction is anything that takes your mind off your primary task. Becoming a driver is very
exciting, but with a new license a person has certain responsibilities on the road. One of them is not
to be distracted while operating a vehicle. It is reasonable to assume that distracted drivers are an
issue. We can deduce that distracted drivers can injure someone. It is unreasonable to assume that
people who text and drive will be completely focused on the road. Hence, cell phones should be
programmed not to work in a moving car. The claim that driving while using a cell phone is safe is
fallacious.
First, manipulating a car requires taking care of the passenger lives as a primary responsibility.
Multitasking ... Show more content on Helpwriting.net ...
Calling or texting while driving is very dangerous that can lead to tragedies. For example, some
tragedies can be deaths or physical impairment. Also, reducing the use of electronic devices while
behind the wheel is a benefit that can lower car crashes on the road. Finally, taking a ride or driving
without cell phones gives an advantage to be more focus on the road, and to be more aware about
the surrounding. It is important to emphasize that distracted drivers on the road can be really
hazardous for everyone that is driven around them. Calling or texting while driving can cause a
serious accidents that can have a devastating effect on a person on his or her family. Eliminating the
cell phone use while behind the wheel makes people to be more safer and confident while driving or
taking a ride. It seems evident that cell phones use while driving are a distraction because it takes
away the visual, manual and cognitive focused on the road. People should avoid using their cell
phones while

Pectin Essay
The assay measured the ability of pectin to cause cell death. Both pectin samples induced necrotic
cell death in HT–29 cells, both pectin concentration and pectin type had a significant (p < 0.0001)
effect on cell cytotoxicity. 400W treated pectin at 0.75 mg/ml concentration induced 14.41±1.64%
LDH activity while 0.1mg/ml resulted in 6.40± 0.59% cytotoxicity, on the other hand the 200W
treated pectin at 0.1mg/ml concentration induced 3.09±0.28% while 0.75mg/ml induced 6.83 ± 0.80
% cell cytotoxicity. The ability of modified pectin to induce cell cytotoxicity was recently reported
[23], 3mg/ml of heat modified citrus pectin induced over approximately 20% and 15% cell
cytotoxicity in HepG2 cells and A549 cells respectively after 24hours exposure. ... Show more
400W sonicated pectin had small molecular weight pectin fractions compared to 200W pectin,
which could have enhanced its transportation into the cells, hence higher concentration of 400W
sonicated pectin entered the cells leading to its higher activity than high molecular weight 200W
treated pectin. Moreover, 400W sonicated pectin had higher galactose and arabinose content which
are known to play a role in pectin induced cell death. It was reported that galactose rich pectin has
higher biological activity than low galactose content pectin, for instance MCP is rich in galactose
and galacturonic acid which are attributed to its activity [16,42]. Measuring the release of the
intracellular enzyme lactate dehydrogenase (LDH) enzyme by cells after exposure to a compound is
a reliable measure of compounds cytotoxicity to

Explain What Are Some Environmental Factors That Impact...

Recommended

Recommended

More Related Content

Similar to Explain What Are Some Environmental Factors That Impact...

Similar to Explain What Are Some Environmental Factors That Impact... (6)

More from Mindi Schneider

More from Mindi Schneider (20)

Recently uploaded

Recently uploaded (20)

Explain What Are Some Environmental Factors That Impact...