Animals And Locations Of Sprague Dawley Essay

Animals And Locations Of Sprague Dawley Essay
Animals and Locations Sprague Dawley (SD) Rats (8–11 weeks old and approximately 200–225 g in body weight at the beginning of the study) and
Swiss Albino Mice (6–8 weeks old and approximately 25–30 g in body weight at the beginning of the study), from the Animal Facilities of Central
Drug Research Institute, Lucknow, India, were used in the study. They were housed in a temperature controlled room with 12 h light/dark cycle at
Animal House, Faculty of Pharmacy, Integral University, Lucknow–India. Special inbreed pellets and autoclaved water were provided All of the
procedures using research animals were approved by Institutional Animal ethical committee of Integral University, Lucknow, India. Experimental
Design Development of Glycation Model in Sprague Dawley (SD) Rats Adult Male SD rats were procured from the Animal Facilities of Central Drug
Research Institute, Lucknow, India. All the animals' weights in between 200–225gm were housed in the Integral University animal house under
standard conditions. Mice were divided into four groups (each having five Rats). No treatment was done in group 1(GP1). In Group 2(GP2) all the
animals were injected with Alloxan (100mg/kg) and treated with 10% carbohydrate (added in drinking water). Group 3 (GP3) was the positive
control only animals were injected with alloxan (100mg/kg). Group 4(GP4) animals were only treated with 10% carbohydrate (added in drinking
water). The detail of the glycation model induction is given in Table 1. The
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How Does Geography Contribute To Diabetes?
Geography as a physical factor contributed to the Marshallese' population being prone to having diabetes. As mentioned earlier, prior to WWII, the
Marshallese' main staple were the products of the land and the surrounding ocean. Following WWII and after the U.S. detonated several atomic
(nuclear) bombs on the islands, the land and the surrounding ocean products became unsuitable for consumptions for many decades to come. The U.S.
government shipped in processed food that were easy to prepare resulting in the change in the population's diet and making them dependent on
imported processed goods. More often, these processed products are high in sodium, sugar, and fat, most of which contributes to diabetes and
cardiovascular diseases. According

How Does Sugar Affect Your Skin
Sugar, Not So Sweet For Your Skin
The highs and lows of artificial and regular sugar that impact your skin.
If the guarantee of a trimmer waistline hasn't reined your sweet tooth in, maybe the lure of smooth skin will. It's a tough pill to swallow, but experts
now think that a lifetime of gorging on sugar can make skin discolored, sagging and wrinkled.
With all of the negative evidence about sugar and its effects on heart health and obesity rates, it's time to break down its effects on appearance and
beauty, and let's just say the results aren't pretty.
Get the lowdown on what exactly sugar does to your skin and what you can do about it.
But why can't I eat a pint of Ben & Jerry's every day?
Let's begin with the basics. When you consume ... Show more content on Helpwriting.net ...
Artificial sweeteners are just one type of sugar substitute but there are many different kinds of sugar substitutes in products today.
Artificial sweeteners
Most artificial sweeteners are synthetic sugar substitutes that are derived from chemicals, such as aspartame and sucralose.
Aspartame is the ingredient found in NutraSweet, Equal, Spoonful, Equal Measure, AminoSweet, Benevia, NutraTaste, Canderel, and many popular
"diet" foods and beverages.
Sucralose is a synthetic chemical created in a laboratory which is found in Splenda.
But not all sweeteners that are harmful are comprised of chemicals. Take fructose for example, this natural ingredient is found in fruits but it can be
just as bad, if not worse for you than regular sugar. Especially if consumed in high quantities.

Natural sweeteners
As it has been established, refined sugar and chemical sweeteners are incredibly harmful. For this reason, people are looking for healthy alternatives.
There are natural sweeteners out there that are better for you, and one of them is stevia.
Stevia is a 100 percent natural, zero calorie sweetener with numerous health benefits that have been confirmed in human studies.
Reversing sugar–damaged

Saturated Fats Vs Cholesterol
The "F" word and the "C" word, two of the most offensive words especially when discussing heart health. Most people cringe at the thought of eating
saturated fats and cholesterol, it's become a mainstream mantra that eating saturated fat and cholesterol will make you fat and clog your arteries. It's all
thanks to Dr. Ancel Keys and his flawed 1953 epidemiological study comparing the saturated fat consumption and the prevalence of heart disease in 7
countries called the Seven Countries Study. Saturated fats and cholesterol are good for your body, it's sugar that's toxic to our health.
Cholesterol is needed by almost every cell in our bodies and is especially important for brain function. About 25% of our total body's cholesterol is
in our brain and the fatty myelin sheath that coats every nerve cell in our bodies is about 20% cholesterol. It is an important player in the production
of sex and stress hormones and helps skill cells stay hydrated and maintain elasticity. It is also used by the body as a raw material in the healing
process. In fact, the body will boost cholesterol production in response to a chronic infection or inflammation. The USDA removed the cholesterol
dietary recommendation in 2015, ... Show more content on Helpwriting.net ...
These sticky sugary coated proteins also called AEG's (advanced glycation end–products), damage cell walls leading to inflammation. Furthermore,
sugar metabolism, particularly fructose (sugar is 50% glucose/50% fructose) metabolism is responsible for a whole host of artery damaging
by–products including uric acid which causes gout, very low density lipoproteins (V–LDL) that contain the most triglycerides, reactive oxygen species
(ROS) that promote oxidation and it blocks the formation of NOx. NOx is responsible for arterial dilation, without it blood vessels constrict causing
high blood

Relationship Between Insulin And Leptin
Plasma leptin concentration has been increased due to high tail fat diet. Leptin is secreted by adipocytes that is implicated in nutrition and cognition
(Morrison 2009). Hyperleptinemia is induced by obesity and aging which is associated with dysregulation in leptin signaling; moreover, leptin
signaling is affected by diet manipulation. Low affinity leptin to its receptor (Ob–Rb) and inability of upregulation Ob–Rb proportional to leptin
concentration was developed by high fat diet (Mitchell et al. 2009). Also high fat diet decreased leptin receptors in cerebellum (Koros et al. 2009).
Insulin and leptin are signally interrelated as insulin resistance frequently associated with leptin resistance in high fat diet ingestion and obesity. There
is a positive relationship between insulin and leptin concentration and oxidative stress (MDA concentration) in plasma of overweight and obese
persons (Shaimaa Essa et al. 2016). Brain oxidative stress progress insulin and leptin resistance in endogenously generated oxidative stress model
(Yagishita et al. 2017). NO is a downstream signal of leptin and leptin inhibiting nitric oxide synthase activity (Calapai et al. 1999; Mehebik–Mojaat et
al. 2009).

Diabetes : A Metabolic Disorder
Diabetes mellitus, commonly known as diabetes, is a metabolic disorder characterized by chronic high blood sugar levels. It is caused by an absolute
or functional deficiency of circulating insulin, resulting in an inability to transfer glucose from the bloodstream into tissues where it is needed as fuel
(Ahmed, Laing and Yates 2011). The disruption in the metabolism of carbohydrates, fats and proteins interferes with the secretion or action of insulin,
which plays a vital role in the metabolism and utilization of energy from the nutrients especially carbohydrates. Insulin is produced in the pancreas and
secreted in the gastrointestinal tract in the response to high blood sugar levels after ingestion of a substance (REFERENCE).
The ... Show more content on Helpwriting.net ...
Diabetes can be diagnosed and monitored by either a random or fasting blood sugar test, oral glucose tolerance test and using HBA1c. The oral glucose
tolerance test, which is considered as a gold standard, has proven to be more useful, especially in clarifying the diagnosis and considering impaired
glucose tolerance and impaired fasting glycaemia (Blann, 2013). In addition, it may also be diagnosed by noticeable symptoms which arise from
high blood sugar. These includes polyuria (urination), polydipsia (thirst) and weight loss (despite adequate consumption of food), visual disturbances
and at times frequent recurrent infection and exhaustion (REFERENCES). Where there is presence or absence of symptoms known as
asymptomatic, the clinician will then request for a urine sample to check for the presence of glucose and a fasting plasma glucose level in your
blood to confirm a clear diagnosis.The finger prick test is an appropriate test for all patients, it has been approved and backed up by the national
quality assurance scheme. It enables health professionals to carry out finger–prick Hb/c tests by matching the results found in the laboratory to the
quality assurance results. Laboratory venous HbA1c must be done to confirm the finger prick test in an accredited laboratory.
The table below shows the summaries the 2006 WHO recommendations for the diagnostic criteria for Diabetes

Types Of Collagen Type I Collagen
Since the beginning of 20th century, collagen has been reviewed extensively in studies and researches. Collagen is the most abundant protein in
vertebras and signifies 30% of the proteins in the body. The composition of collagen is manifested in various parts of the body like bone, skin,
cartilage and blood vessel. Collagen fibre is the main structure in extracellular matrix contributing great assistance in maintaining the integrity of cells
and tissues structures. The major functions of collagen include the provision of strength and elasticity, along with maintaining rigidity. Till date, 28
types of collagen have been identified and they are classified into few sub–group. A number of factors distinguish a collagen from another such as
morphological characteristics, molecular compositions, distributions, and functions. Of all types of collagen, type I collagen is the most abundant
form and is responsible for substituting 90% of the body's collagen. In view of the important of collagen type I collagen in human body structures and
functions, the aim of this paper is to provide in–depth information about type I collagen post–translational modification process, and diseases that are
governed by it.
Collagen has few subgroups and fibril forming collagen is the largest group in the human body. Type I collagen is found in most of the connective
tissues, especially bone, tendon, ligament, cornea and skin. It provides tensile strength to these structures. The interaction of fibrils

The Effects Of STZ On О’-Cells Of Pancreas
The stimulation of experiment in animals using chemicals mainly destroys ОІ cell of pancreas, is very convenient and easy to use. Strptozotocin and
alloxan monohydrate are most common substances to induction diabetes in animals. The effects of STZ on ОІ–cells of pancreas consists of so many
processes such as oxidation of essential SH groups, glucokinase inhibitors, free radical generation and alteration in intracellular calcium homeostasis
(Szkudelski, 2001). It is observed that STZ causes massive reduction of the pancreatic ОІ cells and finally produced hyperglycemia. Several studies
described that a significant increase in lipid peroxidation were noted in diabetic rats (Limaye et al., 2003). The present findings are in accordance also
with previous report indicated significant increase in TBARS in STZ diabetic rats (Murugan and Pari, 2006). The lipid peroxidation may attribute to
the hypoinsulinemia caused by STZ progressive deterioration of normal pancreatic ОІ–cell function. This hypoinsulinemia induced an increase in the
activity of fatty acyl Co–A oxidase that initiate the ОІ–oxidation of fatty acids resulting in lipid peroxidation (Baynes and... Show more content on
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This study showed that, administration of E. jambolana significantly recovered the hepatic TBARS level in untreated diabetic rats. These results are
underlined by the

Catcher In The Ryethyllysine
Fasting glucose may fail to explain the positive relationship between HbA1c and CVD and mortality (Selvin et al.,2010).Correction for classical risk
factors (including smoking, dyslipidaemia, inflammation) explain the relationship better (van't Riet et al., 2012), suggesting that a shared mechanism
may drive the increase in HbA1c levels. In the glycation pathway, oxidative stress can increase glycation in two ways, by promoting glucose
aut–oxidation or by fructosamine oxidation leading to increased AGEs production (mainly CML). The first mechanism, the Wolff pathway, suggests
that in the presence of oxidative stress, especially transition metal ions, glucose can get 'autoxidised' and produce a–oxoaldehydes (like methylglyoxal).
The oxoaldehyde ... Show more content on Helpwriting.net ...
The second pathway is not completely independent from the first,as in this, the Amadori product (fructosamine) reacts with oxidative agents, like
hydroxyl radicals, and undergoes modifications that lead to the formation of carboxymethyllysine (CML), one of the main AGEs (Ahmed et al., 1986,
Booth et al., 1997, Thorpe and Baynes, 2003). The hydroxyl radicals can be produced either by transition metal–catalysed oxidation or by glucose
autoxidation (Hunt and Wolff, 1991). This close interaction between glycation and oxidation leads to the development of the term glycoxidation, which
describes the fact that AGEs are produced mostly from the interaction of these two processes (Baynes, 1991). Although indications and potential
mechanisms are in place to suggest an active involvement of oxidative stress in protein glycation in normoglycaemia and hence the increase in the risk
of chronic diseses, so far little evidence is available to support such a hypothesis.
MECHANISM OF AGES
AGEs mediate their tissue effects through three main mechanisms: (1) Cross linking extracellular (matrix) proteins thereby affecting tissue mechanical
properties (Zieman et al., 2004) (2) Cross linking intracellular proteins thus altering their physiological functions(Bidasee et al., 2004) and (3) binding
to their cell surface receptor rage to inducing multiple intracellular signalling cascade (Neeper et

Aging- Living Organisms
Aging is a fundamental truth and an inevitable aspect of every living organism in the world. There are more than four hundred theories on 'how' and
'why' we age. None of them stands out as a single winner in explaining everything about 'aging' but in fact, they are all interconnected and together
they explain the possible process of aging. This assignment attempts to explore the research based avenues which could possibly help Mickey live
significantly longer than Minnie, based on the assumption that Mickey and Minnie inherit the same genetic programme but follow different life
styles. Different authors and researchers define aging differently. Aging has been defined by Balducci(2007) as a loss of "entropy and fractality."
Loss of entropy implies a progressive reduction in an individual's functional reserve, whereas loss of fractality implies a progressive reduction in the
ability to coordinate different activity and negotiate the environment". Yet another definition which would encapsulate the wider meaning of the term
aging is "aging as a multifaceted phenomenon associated with decrements in cellular and physiological functions, increases in the incidence of
numerous degenerative diseases and diminished capacity for responding to stress (Beckman and Ames, 1998). The theories on aging can broadly be
classified as programmed and damage based. While the former argues that the complex process of aging is primarily pre–programmed by genes and
not due to any random or

The Effects Of Alzheimer 's And Dementia Among Elderly...
Introduction:
Alarming statistics project that by the year 2050, an estimated 115 million people globally will be diagnosed with Alzheimer's disease. In 2011, the
cost of Alzheimer's care in the United States exceeded $130 billion (Trivedi, Bijal, 2012). Approximately 90% of older nursing home residents are
estimated to have a psychiatric disorder which includes Alzheimer 's disease (Curlik, SM, et al, 1991). In 2003, the report on the President's New
Freedom Commission on Mental Health, Achieving the Promise: Transforming Mental Health Care in America, recommended that mental health must
be addressed with urgency in light of the prevalence of increasing diagnoses of Alzheimer's and dementia among elderly populations ( "President 's New
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Type 2 diabetes is associated with poor sensitivity to insulin. This had led some some researchers to suggest that Alzheimer's disease may in fact be
another type of diabetes (Trivedi, Bijal, 2012).
Discussion:
Alzheimer's disease is characterized by the development of plaque or protein deposits in the brain, especially areas associated with memory. Brain
neurons collapse, crumble, and lose connections with other neurons which causes disorientation, confusion, erratic behavior, and partial to complete
memory loss. (Trivedi, Bijal, 2012). While a poor sensitivity to insulin is associated with type 2 diabetes, some researchers including Dr. Suzanne
de la Monte, a neuropathologist at Brown University in Providence, Rhode Island, have suggested that Alzheimer's disease may in fact be another
type of diabetes. If these scientists are correct in their suppositions about diabetes and dementia, immediate and troubling concerns are going to
present overwhelming challenges to the medical and senior care systems. Ewan McNay, of the University of Albany in New York states that "if the
epidemic of type 2 diabetes continues on its current trajectory, it is likely to be followed by an epidemic of dementia" (Trivedi, Bijal, 2012).
Alzheimer 's disease is increased in individuals with diabetes. Higher glucose levels in individuals without diabetes has also been associated with
elevated occurrences of Alzheimer 's disease. These findings

Relation Between Sarcopenia And Functional Disabilities...
Relation between sarcopenia and functional disabilities and increase risk of falls
Several cross–sectional, observational studies have related sarcopenia to decline of functional status, such as mobility performance, self–reported
functional limitations, and disability, it is well established that the aging process itself is associated with numerous changes in the human body. One of
the most significant age–related anatomical changes is that which happens to the skeletal muscle mass (Visser and Schaap, 2011).
"Sarcopenia" is used to indicate progressive reduction in muscle mass, muscle strength and function that affect older people (Pathy et al., 2006).
Sarcopenia results in unfavorable and detrimental effects on an older person's physical function. Muscle mass decrease is probably the single most
frequent cause of late–life disability among older people. It is directly responsible for functional impairment with loss of strength, and increased
likelihood of falls and fractures, as muscles account for 60% of the body protein stores, the reduction in lean body mass has other health effects
independent of its functional consequences (Rolland et al., 2008).
A number of physiological functions that take place within the muscle tissues have an essential role in human metabolism. For example, muscles are
important body protein reserves and energy that can be used in extreme conditions such as stress or malnutrition; amino–acids can be mobilized during
acute infections and are

Atherosclerotic Plaque Formation
3) In 4–6 sentences, describe the process of atherosclerotic plaque formation. 6 pts for response, 2 pt for source: To begin with, cells create
atherosclerotic deposits, and these deposits arise on vessel walls. This is formed when LDL deposits tend to become stuck in the matrix, and they
undergo oxidation and glycation. Macrophages then feast on LDL's, becoming fueled with fatty droplets. If there is an inflammatory disease, this can
cause more growth of plaque, and a fibrous cap or the lipid core is established. Then, foam cells weaken the caps by digesting matrix molecules,
which then leads to the damage of smooth muscle, resulting in the inability to repair the cap. If a clot is big enough, the flow of blood will be interrupted
resulting ... Show more content on Helpwriting.net ...
HDL helps to the body to get rid of cholesterol.
Citation:
Sugerman, Deborah Tolmach. "Blood Lipids." Jama Patient Page Hyperlipidemia. N.p., 23 Oct. 2013. Web. 15 Nov. 2016.
c) Hypertension: Hypertension is just a synonym for high blood pressure. "Hypertension is called the "silent killer." It is called the "silent killer"
because a lot of people do not know that they have high blood pressure.
Citation:
Torpy, J. M. (2010, May 26). Hypertension. Retrieved November 15, 2016, from http://jama.jamanetwork.com/
d) Cardiac Arrest: Cardiac arrest happens when the heart stops functioning correctly. During cardiac arrest, "blood flow ceases, organs begin to shut
down, resulting in the person dying." When people have this identified at an early time, it can prevent damage to body organ and death.
Citation:
Torpy, J. M. (2006, January 4). Cardiac Arrest. Retrieved November 15, 2016, from http://jama.jamanetwork.com/
e) Myocardial infarction: Myocardial infarction is a heart attack. "Myocardial infarction occurs when blood supply to a part of the myocardium is
interrupted. This can be caused by a lack of blood flow, obstruction by a clot, or a rupture of plaque build up."

Wrinkles And Aging Signs Research Paper
What Causes Wrinkles & Aging Signs? One of the main causes of wrinkles and other outward aging signs is free radical damage. The primary cause
of free radical damage and a prematurely aged appearance is overexposure to the sun. Sun Exposure EXPOSED Knowing that more people are being
cautious about their exposure to sunlight, researchers have begun to look more closely at other contributing factors. Vitamin D is Vital The average
person's exposure to sunlight has decreased enough in the past few decades to have caused an increased incidence in vitamin D deficiency among the
general population. The body produces vitamin D due to exposure to sunlight. There are few naturally occurring dietary sources. The type found in
supplements is not

Herbs And Spices That Can Help Manage Your Diabetes
5 Herbs and Spices That Can Help Manage Your Diabetes
Meal planning is one of the most important (and sometimes frustrating) things for those with diabetes. It can be challenging to create dishes that
provide sound nutrition, limit sugar and carbohydrates, AND taste good. But, by focusing on whole foods that incorporate a variety of herbs and
spices, you'll find you not only develop tastier dishes, but ones that can bolster your fight against diabetes.
The five herbs and spices on this list have been shown to assist in managing blood glucose levels as well as reduce inflammation in the body, which
can lead to insulin resistance and diabetes (along with a whole host of other chronic diseases!)
Herbs and Spices Have Historically Been Used as Medicine
Herbs and spices have been used for thousands of years for their health benefits. Papyri from Ancient Egypt spoke of fennel, juniper, coriander, cumin,
garlic and thyme as health promoting spices. [1] Ancient cuneiform records noted spice and herb use in Mesopotamia, where many aromatic plants
were traditionally used; and Sumerian medical literature dating from the 3rd millennium BC mention various odoriferous plants, including thyme. [2]
Modern medicine is finally catching up to the ancients in realizing the health promoting benefits of myriad herbs and spices. For instance, a study by
the University of Georgia revealed that many herbs and spices are a rich source of the antioxidant phenol, which can prevent inflammation and

External Causes Of Aging
There are many reasons why your skin ages. The number one reason is aging. It is simply natural for skin to become thinner, produce less collagen,
elastin, and decrease cellular regeneration as you get older. There is not much you can do about these internal causes of aging, but there are external
causes of aging skin that you can control to some extent.
The number one external reason skin ages is exposure to the ultraviolet (UV) rays of direct sunlight over extended periods. Ultraviolet rays break down
elastin and collagen and hamper the production of new collagen, which the skin naturally produces to repair the damage. Prolonged exposure to the sun
also significantly increases the risk of skin cancer. This is true for tanning beds and indoor tanning equipment. Fortunately,... Show more content on
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A sedentary lifestyle will slow circulation, and over time contribute to prematurely aging skin. Exercise will also help you have more energy, which
will make you look and feel younger.
Cold weather contributes to aging skin, especially cold wind. It dries out the skin causing wrinkles. When you need to go outside in cold weather,
you can protect your face with a good moisturizer. Indoors the air may be heated and dry. This is also not good for the skin. A humidifier can reduce
the dryness in the air its aging effects on the skin.
Regular consumption of alcohol will gradually dilate the small blood vessels in the skin and increase the blood flow near the surface of the skin,
especially on the face. This condition can become permanent and create a flushed appearance caused by broken blood vessels. Alcohol also dehydrates
the skin causing wrinkles.
A healthy diet with lots of fruits and vegetables as well as Omega–3 fatty acids will go a long way to protect the skin against premature aging.
Regularly eating too much sugar may cause glycation, which will harm collagen and eventually cause a loss of elasticity and

Endothelial Cells Contribute Inflammation in Key Diseases
Endothelial cells are originated from embryonic mesoderm. It is a thin layer of cells found in the body like in the blood vessels, heart and
coverings of organs. It regulates permeability of blood flow all around the body and maintain vascular homeostasis. If the body is not well taken care
of due to stressful lifestyle and not taking proper meals, endothelial cells can be inflamed and damaged leading to key disease such as artherosclerosis,
heart disease, diabetes, kidney disease and Alzheimer's disease.
Atherosclerosis is a lipid storage disease where too much of lipid is deposited in endothelial of arteries causing narrowing to prevent blood to flow. It
is triggered by daily diet of consuming highly saturated fat, hypertension and smoking. In healthy endothelial cells, leukocytes do not stick on to the
endothelial cells. During early phases of inflammation in endothelial cells, the leukocytes attach to the arteries cell wall with the help of vascular cell
adhesion–1 (VCAM–1) and penentrate into the endothelial layer. VCAM–1 binds monocytes and T lymphocytes, the types of leukocytes found in
early atherosclerotic plaques. ( Libby P., 2006:456S) Atherosclerosis lesion is a foam cells whereby macrophages engulf lipid particles. The lesion
secretes cytokines and growth factors to promote proliferation of smooth muscle. The increased of inflammatory markers like interleukin 6 (IL–6) and
interleukin 1 (IL–1) accumulated in the endothelial cells accerlate the progess of

Essay about Chronic Inflammation and Glycation
Inflammation is a natural body reaction in response to infection or tissue injury, which helps man to boost immune defenses and overcome stress. Acute
inflammatory responses are often triggered by trauma or invasive microorganisms such as bacteria and viruses, but if well–controlled these immune
responses may help prevent further damage and assist in body repair processes. On the other hand, prolonged cellular stress caused by certain stimuli
such as pollution, poor diet, lack of exercise and other lifestyle factors can cause chronic inflammation, which can lead to premature aging and chronic
disease. Chronic Inflammation and Glycation Chronic cellular stress often leads to cell dysfunction and many mechanisms for how these processes...
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It is a natural chemical reaction in which a simple sugar or carbohydrate molecule attaches to another bio molecule such as a protein, lipid, or nucleic
acid without the help of enzymes. Unlike glycosylation, which is a similar metabolic process that is catalyzed by an enzyme, glycation usually
disrupts normal cellular processes and are usually associated with oxidative damage. During glycation process, simple sugars like glucose and fructose
act as reducing sugars, which become attached to proteins, nucleic acids or lipids, forming glycation adducts called Schiff base over a few hours.
Healthy cells can eliminate these byproducts, but with chronic inflammation, these compounds can rearrange to become more stable compounds called
Amadori products. Over months, accumulation of these compounds can lead to a series of chemical reactions that result in irreversible formation of
highly stable substances called advanced glycation end products (AGEs). AGEs and Mitochondrial Dysfunction AGEs normally form at slow but
constant rates in the cells and may accumulate with time. The accumulation of AGEs occurs when there is an increase in their production and/or a
decrease in their elimination. With aging, low protein turnover, for example, results in the accumulation of extracellular AGEs on collagen, resulting in
wrinkles. In diabetics, high plasma levels of glycosylated hemoglobin (HbA1c) increase as a result of high blood glucose levels. Studies show

Neonatal Epilepsy
Epilepsy is one of the most common neurodegenerative disorders that affect around 1% of the global population worldwide. Although the optimal use
of the 24 approved anti–epileptic drugs in The United States has successfully treat some of the symptoms–related epilepsy, but not the underlying
epileptogenesis processes, particularly in neonatal epilepsy. Newborn are more subjected to early–onset of epilepsy because of the common
complications of labor in human, such as hypoxia–ischemia and pre–eclampsia. Such complications may cause major damage in the neonates' brain,
including inflammation, neuronal degeneration and other types of damage–related brain injuries. In recent years, great number of evidence point to
inflammation as a potential pathway ... Show more content on Helpwriting.net ...
It is a well–known biomarker of brain injury associated with Alzheimer's disease, concussion and epilepsy. Based on literature review, an
overproduction of soluble S100B from the astrocytes binds to the receptor for advanced glycation end products (RAGE) leading to various responses
including increased reactive oxygen species (ROS) formation, release of pro–inflammatory markers, and activation of stress response kinases resulting
in neuronal cell death. The ongoing neuronal injury and inflammation further promotes cellular apoptosis and impairs neurogenesis in epileptic brain.
Identification of this mechanistic relationship between acquired epilepsy and inflammation will provide an important therapeutic target pathway for
prevention of

This Is What Happens To Your Brain On Sugar Essay
Title: THIS Is What Happens To Your Brain On Sugar
Category: Health
Tags: Alzheimer's disease, too much sugar, sugar addict, sugar brain
Teaser: Too much sugar in your diet can damage a protein that is essential in fighting Alzheimer's disease, in its early stages.
Article:
It's no secret; sugar, when consumed in excess leads you down the road to obesity and diabetes. Still, sugar–loaded foods and beverages have become a
way of life for many Americans. So much so, that the average person consumes about 20 teaspoons of sugar a day! That's about 14 teaspoons or 60
grams more than is recommended for a healthy diet. All that sugar not only makes you fat, but now experts agree it may also lead to Alzheimer's.
Here's what happens to your brain ... Show more content on Helpwriting.net ...
This figure is thought to rise to over 125 million by 2050. This amounts to hundreds of billions of dollars spent on medical and social care because of
the cognitive effects of the disease.
Dr. Omar Kassaar, also from the University of Bath, further added that "excess sugar is well known to be bad for us when it comes to diabetes and
obesity, but this potential link with Alzheimer's disease is yet another reason that we should be controlling our sugar intake in our diets."
Why we crave the white stuff
Your brain has built–in evolutionary mechanisms that drive your cravings. Many of these mechanisms are meant for survival, one of the which is
eating. And of course, the release of hormones is also involved according to Tufts. When you eat something sweet and delicious, the good feeling of
the experience is determined in part by hormone receptors. Over time, these receptors become less sensitive to the hormones produced when we enjoy
a particular food – like chocolate cake. So, you'll need to consume more and more chocolate cake to have the same pleasant experience.
We're addicted and we may not know it!
But it's not just the obvious treats like sugary soda, candy, cookies and cakes that turn us into sugar addicts. Today's modern diet is so loaded with
hidden sugars and sweeteners that we

Investigating The Aetiology And Pathophysiology Of Renal...
There have been a number of manuscripts reporting on the association of complications in type 2 diabetes with high glucose blood levels, high levels
of C–Peptide, high advanced glycation end products (AGEs) and vascular cell adhesion molecule–1 (VCAM–1) and oxidative stress. In order to further
investigate the aetiology and pathophysiology of renal microvascular complications in type 2 diabetes, papers were reviewed through 2000 using the
NIH PubMed Literature Search System. Inclusion criteria were that manuscripts 1) be primary peer–review research article; 2) concisely explained, or
investigated, the pathophysiology of renal microvascular complications in type 2 diabetes; 3) be published in English. High blood glucose levels and...
Enhanced oxidative stress and changes in antioxidant capacity, found in both clinical and experimental diabetes, are thought to be the main cause of
chronic diabetic complications, in particular at a microvascular level (Moussa 2008). Excessively high levels of free radicals cause damage to vital
cellular components such as proteins, membrane lipids, and nucleic acids, and finally lead to cell death (Maritim, Sanders & Watkins 2003). The
formation of advanced glycation end products (AGEs), is another factor to be considered in diabetes type 2 microvascular nephropathy (Motawi et al.,
2013). Interaction of AGEs with their cellular receptors (RAGE) has an important role in the pathogenesis of diabetic complications via enhanced
expression of adhesion molecules, including vascular cell adhesion molecule–1 (VCAM–1), and intercellular adhesion molecule–1 (ICAM–1), both
markers of vascular injury (Motawi et al., 2013). Motawi et al. (2013) advanced the hypothesis that tight glycemic control may restore plasma levels of
sRAGE, VCAM–1 and oxidative stress parameters near the normal level in type 2 diabetic patients, reported as a decoy receptor for AGEs. Motawi
et al. (2003) demonstrated that poor glycemic control decreases plasma sRAGE and increases VCAM–1 levels while good glycemic control improves
these abnormalities which provides benefit to diabetic patients. Many other studies (Nakamura et al., 2008;

Theories Of Brain Aging
Aging is a process of becoming older. It is among the largest known risk factors for most human diseases and most common neurodegenerative
disorders. The multisystem deВ¬cline is associated with increasing pathology. Aging process is associated with several structural, chemical, and
functional changes in the brain as well as neurocognitive changes. Brain aging may occur in several forms, such as progressive loss of specific
neuronal populations and connections, behavioral and memory deficits, increased oxidative stress (Maynard et al., 2015). In the brain, the most
sensitive regions to oxidative stress include the cerebral cortex, the hippocampus, and the striatum. Brain aging has many theories, oxidative stress
hypothesis is one of these theories

Four Theories Of Aging
In this week's assignment, I've learned several things about how aging affects you physically and mentally. With my personal growth, this week's
assignment it made me realize why we age and we get older. It is a mystery and there are many theories about how we age. This expanded my
knowledge because it forced me to look into why our bodies and minds age. I did not know about the theories of aging and how we age, this a new
concept and something I did not have an understanding about. I believed it was the way life evolved. You're born as an infant that develops into a
young person that matures into an adult. The most valuable lesson I've learned, there are four theories of aging. The theories are 1. Oxidative stress –
the body inability

Paleo Pros And Cons
"Vegan vs Paleo" has been an ongoing, emotionally charged feud in the health community for quite some time, especially between youtube
personalities.
It's important to acknowledge that Vegans, Vegetarians, Paleo and Primal eaters alike make conscious decisions about their diets, which is always
going to be superior to making no decisions (eating refined carbs with sick animals.)
We commend people for taking responsibility for themselves and their impact on the world.
That being said, the truth is that this ongoing food feud isn't fruitful for the overwhelming majority of us. Most people's ideal diet falls somewhere
between Veganismand Paleo, or High Carb and Low Carb, because we're living in the melting pot.
Most of us are very genetically ... Show more content on Helpwriting.net ...
Paleo
The Good: Paleo, Primal, and other low carb diets address the chronic carbing that has become an issue for our society.
The Bad: A lot of Paleo diet recommendations underplay the importance of plant foods.
The Reality: Americans are eating an absurd amount of carbohydrates, and most of the time these carbohydrates (White Flour, White Sugar, etc. ) have
been 'predigested' by machinery and processing, leaving them a demineralized blood sugar bomb. They spike insulin and send you on a roller–coaster
of energy highs and lows.
The Science:
When you eat carbohydrates, your pancreas secretes Insulin into the bloodstream. Insulin shuttles nutrients into cells and stores excess energy as fat.
A lot of bad stuff happens when you spike Insulin with high–glycemic foods like grains or sugar. These foods are considered high GI because they're

very easily digestible, and so they affect your blood sugar rapidly. Even more so when they're refined with processes that strip the minerals and other
nutrients, leaving plain sugars or starches. These fast–acting carbs have been shown to be even more addictive than

Hba1c's Role In Diabetic Analysis
Glycated haemoglobin is a measure of blood glucose levels over the previous 120 days and reflects the time averaged blood glucose over the preceding
1–3 months, depending on the rate of change of blood glucose levels. HbA1c, or glycosylated haemoglobin, is formed through the non–enzymatic
binding of circulating glucose to haemoglobin (glycation). HbA1c is measured as the ratio of glycosylated to non glycosylated haemoglobin (Sacks et
al, 2002). Higher levels of glucose in the blood contribute to more binding and consequent higher levels of glycosylated haemoglobin. Glycation occurs
over the entire 90–120 day life span of the red blood cell. HbA1c can consequently be interpreted as an average of the blood glucose present over the
past 3–4 months. Measurement of HbA1c is accepted as a... Show more content on Helpwriting.net ...
Decisions regarding treatment are often based on HbA1c. Although the American Diabetes Association 2003 does not currently recommend HbA1c
measurement for the diagnosis of diabetes, studies have shown frequency distributions similar to those of fasting plasma glucose (FPG) used in
diagnosing diabetes, HbA1c is a more comprehensive measure of total glycaemic exposure than FPG due to the representation of blood glucose in the
postprandial state in

Dfus: A Case Study Essay
As of all other DCWs, DFUs develop due to a disruption in the healing process, which in turns, hinders the normal acute ulcers from healing [9]. The
factors that are involved in the development of DFUs can be categorised mainly into causative and contributing factors [13].
The most common causative factor is profound peripheral neuropathies, which often inhibits nociception as aforementioned. Peripheral neuropathies
occur due to the sustained hyperglycemic state of a diabetic patient which generate oxidative stress and glycosylate nerve cells. Consequently, the risk
of developing DFUs increases as the patients are more vulnerable to physical and thermal trauma [13] Moreover, damage to the motor neurons that
innervate foot musculature can also lead to excessive plantar pressure, which is another causative factor for the increased risk of DFUs [13].
Apart from the causative factors, numerous contributing factors also play a role in increasing the risk of developing DFUs, one of which is chronic
inflammation. Diabetic patients generally suffered a persistent inflammatory response following injury which impede proper wound healing [9]. In
particular, there is an elevated number of neutrophils and macrophages ... Show more content on Helpwriting.net ...
Impaired angiogenesis and vasculogenesis are often observed in diabetic patients and when coupled with chronic inflammation, it impairs endothelial
progenitor cells (EPCs) migration and thus, hinders blood vessels regrow [9] [14]. Furthermore, hyperglycaemia can also cause the production of
advanced glycation end (AGE) products which hinders the proper wound healing by decreasing the solubility of the extracellular matrix and
propagating altered inflammatory responses associated with diabetes [9]

List And Describe The Signs And Symptoms Of Ad
List and Describe the Signs and Symptoms of AD? Alzheimer's Disease (AD) affects individuals and families mentally, emotionally and physically.
The signs and symptoms are progressive in nature, and can significantly impact the quality of life of those who are affected. Early symptoms of AD
are often not detected, and therefore may lead to delayed treatment and support. In the early stages of the disease, patients often try to conceal their
symptoms, in hopes that family members, friends and coworkers will not detect signs of deficits. Early symptoms of AD include: forgetfulness, subtle
memory loss, mild speech impairments as well as onset of depression (Pellico, 2013, p. 2013). According to Pellico (2013), early signs and symptoms...
1238), losing or misplacing valuable objects as well as difficulty with planning or organization (Alzheimer's Association, n.d). As imagined, detection
may be challenging for healthcare providers as well, as patients may not discuss their symptoms, due to beliefs that symptoms are strictly associated
with the aging process. Moderate AD, which is known to be the longest lasting stage, can last for many years (Alzheimer's Association, n.d). Behaviors
associated with the middle–stage of the disease include progressive forgetfulness of events or about one 's own personal history, withdrawnness
especially in socially or mentally challenging situations, poor mood regulation, confusion about where they are or what day it is, inability to recall
personal address or telephone number or the high school or college from which they graduated, requiring assistance with choosing proper clothing for
the season or the occasion, interruptions in sleep patterns such as sleeping during the day and becoming restless at night, increased wandering and
becoming lost, as well as difficulty with controlling bladder and bowels in some individuals (Alzheimer's Association, n.d). Progressive personality
changes are also often associated with middle–stage AD, and include suspiciousness and delusions or compulsiveness (Pellico, 2013, p. 1238). Lastly,
as the disease progresses into the

Process Essay: The History Of Aging
History of Aging There have been multiple disputes over whether our aging depends on the time our genes were programed to deteriorate, or
whether aging solely depends on different factors that effect the way we will age over time. A very early theory of aging was from Leslie Orgel in
1963, he believed that errors in transcription from DNA lead to errors in proteins which build–up over time and cause more errors in transcription,
creating an amplifying loop that eventually kills the cell and leads to aging (Orgel, 1973). The first idea is that our genes control how long we live, this
means that we have genes that tell us how long we live. Many scientists believe that if you find the gene that determines our life span, we could
possibly alter how long we live. The second idea is based on a theory that over time we damage our body and our DNA causing us to ... Show more
content on Helpwriting.net ...
Telomeres are at the ends of our chromosomes, they shorten with each round of cell division. Telomere shortening limits stem cell function,
regeneration, and organ maintenance, causing aging to take place. Chronological age is the individuals age based on the day they were born.
Oxidative stress is an imbalance between the production of free radicals and the ability of the body to counteract or detoxify their harmful effects
through neutralization by antioxidants (Dr. Ananya Mandal, 2015). Oxidate stress leads to Parkinson's and Alzheimers disease, gene mutations,
cancers, heart disorders, and other organ failures. Glycation is a process where sugar in your blood attaches to proteins to form advanced glycation
end products that are harmful and cause aging. The amount of glycation a person has determines how resistant their skin will be to wrinkling. Because
glycation causes wrinkles, diabetics are known to age earlier because of their high blood sugar

HMGB1 And Alzheimer's Disease Analysis
HMGB1 is a prototypic damage–associated molecular pattern (DAMP) protein highly secreted by activated macrophages and monocytes as a cytokine
mediator of inflammation. This DNA–binding nuclear protein is released both passively during cell death and actively following cytokine stimulation.
It is also implicated in both infectious and sterile inflammatory disorders [32–36] affecting the central nervous system (CNS) such as in Parkinson's
disease (PD) [37], multiple sclerosis (MS) [38,39], ischemic stroke [40], traumatic brain injury (TBI) [41] and Alzheimer's disease – AD [42–44].
HMGB1 activates cells by differential engagement of several membrane receptors including advanced glycation end products (RAGE), toll–like
receptor 2 (TLR2), and TLR4 which are primarily responsible for HMGB1 pro–inflammatory activity and BBB impairment [45,46]. Specific to the
proposed work, several studies have clearly outlined the role of OS in the development of microvascular and cardiovascular complications of 2DM [47].

Diabetes Affects The Body
Diabetes is a disease that affects the use of insulin in the body. According to the Merriam Webster Online Dictionary diabetes mellitus is a " disorder of
carbohydrate metabolism caused by a combination of hereditary and environmental factors and usually characterized by inadequate secretion or
utilization of insulin, by excessive urine production, by excessive amounts of sugar in the blood and urine, and by thirst, hunger, and loss of weight" ("
Diabetes Mellitus"). This disease not only impacts the amounts of sugar in the blood, it also has lasting effects on the rest of the body. Diabetes
impacts the body and its systems negatively if the body's blood sugar levels are not treated or maintained properly.
In the body there are twelve different ... Show more content on Helpwriting.net ...
Type one is characterized as an autoimmune disease, because the body targets it's own beta cells in the pancreas. The beta cells are cells that produce
insulin for the entire body. The body stops making insulin, causing people to become insulin dependent. An insulin dependent person would use
insulin injections or an insulin pump ordinarily to manage their sugar levels. Type two diabetes is different. The body of a type two diabetic no longer
responds to the body made insulin. Beta cells destroy themselves from the overproduction of insulin because the cells themselves try to compensate for
the deficiency of insulin. Type two is either treated without medications like exercise and diet or with insulin tablets. But, there are some occurrences
in which insulin injections would be needed ("Differences Between Type 1 and Type 2"). Both types are dangerous if not monitored, and cause the
circulatory system to

The Effect Of Glucose On Food And Chemistry
Morgan Thiel
General Chemistry
National Chemistry
10/20/14
Glucose Introduction: What influence does Glucose have within food and chemistry itself? We all know that Glucose itself is a simple
monosaccharide that we normally call Sugar, however what does it all really cover within the basis of food? So let's get down to the bottom of this
and discover what role Glucose plays within the chemistry of food.
Background: Glucose, which is also called D–glucose or Dextrose is a monosaccharide within one of the carbohydrate groups known as simple sugars.
Originally based off of the Greek word, "glukus", which is translated to the word, "Sugar," Glucose is found the most in fruits and honey. Its molecular
formula is C6H12O6 and is the most common simple sugar regulated in the blood of animals. Glucose was first discovered within raisins in 1747 by
the German chemist Andreas Marggraf. Since glucose is a core necessity of many living creatures, a basic understanding of its chemical makeup and
structure contributed immensely to the growth of organic chemistry.
Search Findings: All forms of glucose are void of color and soluble in water, acetic acid, and several other solvents. They are only semi soluble in
methanol and ethanol. Glucose is the main source of energy in cell function comes primarily from carbohydrates which then break down into simple
sugars, and the regulation of metabolism. It is one of the three monosaccharides

Reaction Of The Maillard Reaction
Introduction
The non–enzymatic reaction of reducing sugars with amino groups of amino acids, peptides and proteins is called as non–enzymatic glycosylation or
simply glycation. This non–enzymatic reaction ultimately results in the formation of complex brown pigments and protein–protein crosslinks that were
first studied under defined conditions by Maillard in the early 1900s (Maillard and Gautier, 1912) and the reaction came to known as the Maillard
reaction. There is a condensation reaction between reducing sugar and free amino acids at the amino terminus or susceptible Оµ–amino group of lysine
residues of proteins producing labile N–substituted glycosylamine (Schiff base) that may undergo two sequential rearrangements, forming a stable
Amadori product (Fayle & Gerrard, 2002). The reducing sugars namely, glucose, fructose, galactose, mannose, ribose and certain carbohydrate
relatives are inherently reactive toward nucleophilic groups. Glucose is the least reactive among common sugars because it exists in least concentration
in the open chain form (Paulsen and Pflughaupt, 1980). Amadori rearrangement was a key early step in the Maillard reaction (Hodge, 1955). Early
glycation directs the formation of Schiff's bases and Amadori products that further oxidized to advanced glycated end products (AGEs) (Chetyrkin et
al., 2008). Studies have shown that the glycation process (in the early stage where the interaction of sugars, such as glucose, with free amino groups of
lysine and

Pediatric Sepsis
Receptor for Advanced Glycation End Products in Pediatric Sepsis : A pilot study
Abstract
BACKGROUND: Sepsis in pediatric patients still a leading cause of morbidity and mortality. AIM: To determine whether serum level of receptor for
advanced glycation end products (RAGE) could be used as a potential diagnostic and prognostic marker in septic child.
METHODS: A pilot study on pediatric intensive care unit patients over a 1year period with clinical evidence ofsepsis. Forty patients were enrolled in
the study within the first 24 h after onset of sepsis; they were classified according to 28 day mortality into survivors and non–survivors. CBC,ESR,
CRP and sRAGE were measured . Bacterial cultures from suitable body fluids in septic patients were carried out. ... Show more content on
Helpwriting.net ...
Also, we recommend more researches with larger scale on pediatric subjects to confirm the results of our study and clarify the functional role of
sRAGE in sepsis and its putative role as a new sepsis marker.
References
1.Larosa SP. Sepsis: menu of new approaches replaces one therapy for all.Cleve Clin J Med. 2002; 69(1):65–73. 2–Randolph AG. The purpose of the
1st international sepsis forum on sepsis in infants and children. Pediatr Crit Care Med 2005; 6[Suppl.]:S1–S2.
3.Raucci A, Cugusi S, Antonelli A et al . A soluble form of the receptor for advanced glycation end products (RAGE) is produced by proteolytic
cleavage of the membrane–bound form by the sheddase a disintegrin and metalloprotease 10 (ADAM10). FASEB J. 2008;22(10):3716–27.
4.Yamagishi S, Matsui T. Soluble form of a receptor for advanced glycation end products (sRAGE) as a biomarker. Front Biosci (Elite Ed). 2010; 2:
1184–95.
5.Van Zoelen MA, van der Poll T. Targeting RAGE in sepsis. Critical
Care.

High Fructose Ry Sweeteners
Sugar–it is that deliciously sweet white substance that we just can't seem to resist. It is a guilty pleasure that is known by almost everyone to be
unhealthy, but is sugar actually a chronic toxin? Is it slowly killing us from the inside out? In recent years, more and more research seems to suggest
so. With the increasing epidemic of obesity and diabetes, scientists are looking for answers, and their findings are quite disturbing. If sugar is a toxin,
then people need to know because health and lives are at stake and the sugar industry could fall apart. To answer the question about the toxicity of
sugar, one must be clear about what type of sugar is being discussed because there are many different types. This essay will discuss high fructose...
According to L. Bell, studies show that the sugar fructose in high fructose corn syrup messes up the appetite controls, causing a person to not realize
that they are full even though they ate the energy–dense fructose (L. Bell, 2013). This overeating can lead to weight gain, which can in turn lead to
other serious health problems. According to a study published in the International Journal of Obesity (2013) "High SSB [fructose–rich
sugar–sweetened beverages] consumption has a notable effect on increased levels of BMI [body mass index] and SUA [serum uric acid]" (W.T.
Lin, H.L. Huang, M.C. Huang, T.F. Chan, S.Y. Ciou, C.Y. Lee, Y.W. Ciou, T.H. Duh, P.L. Lin, T.N. Wang, T.Y. Liu, and C.H. Lee, 2013, p. 532). In
other words, the consumption of beverages sweetened with high fructose corn syrup significantly increases levels of body mass index and the
production of uric acid. Uric acid is harmful because it can lead to kidney disease and gout, the painful inflammation of the joints because of all of
the extra uric acid circulating in the blood. Another concern about fructose is how it effects the liver. Every cell in the body can use glucose to make
energy, but only the liver can break down fructose. When fructose is eaten, it must pass through the liver to be broken down. According to R. Lustig,
once it gets to the mitochondria, the power plant of the cell,

Osteoarthritis Research Paper
Osteoarthritis is a condition that affects the bones. This degenerative condition can cause the bones to become brittle and fragile, which puts a
person at a greater risk for a fracture. Fortunately, you can ease osteoarthritis symptoms by changing your diet. There are foods that you will need to
avoid. Below is a list of foods that you need to avoid if you are suffering from osteoarthritis: Processed And Fried Foods Processed and fried foods
trigger inflammation. Inflammation can worsen osteoarthritis symptoms. Processed and fried foods are also high in fat and calories. On the other
hand, studies have shown that reducing one's intake of processed and fried foods can actually improve osteoarthritis. Meat Meat is not something you
have

Diabetic Neuropathy Essay
Diabetic peripheral neuropathy is among the chronic microvascular complications of diabetes mellitus due to hyperglycemia. Prevalence of diabetic
neuropathy is high, affecting more than 60% of diabetics (Boulton et al., 2005). The clinical manifestation of diabetic neuropathy include numbness,
tingling sensation in toes, feet, legs, arms, hands and fingers (Kumar et al.). It leads to significant morbidity, impact on quality of life of patients
(Zychowska et al.) and increases the risk of infections leading to the foot ulcers and non traumatic amputations (Bansal et al.). In diabetic neuronal
cells, hyperglycemic flux activates four cellular pathways: the polyol, advanced glycation end–product, protein kinase C, and hexosamine pathways
increasing... Show more content on Helpwriting.net ...
It leads to the reduced coupling efficiency in mitochondria and increased superoxide radical generation damaging both nuclear DNA and mitochondrial
DNA leading to activation of poly ADP ribose polymerase enzyme (PARP) (Fernyhough et al.Brownlee, 2001; Nishikawa et al., 2000b, to be added).
PARP activation leads to inactivation of AMPK which facilitates mitochondrial biogenesis. Thus, PARP activation compromises the cellular
mitochondrial genesis which leads to accumulation of damaged mitochondria in the cell. Molecular studies have revealed the involvement of
transcriptional regulators such as Nrf2, NF–ОєB, and COX–2 inflammatory cascade in the pathology of diabetic neuropathy. The Nuclear factor 2
erythroid related factor (Nrf2) is a redox transcription factor for the production of endogenous antioxidant defenses and detoxifying enzymes. Nuclear
factor–kappa light chain enhancer of ОІ–cells(NF–ОєB) is a transcription factor, involved in pro inflammatory cytokine production (Negi et al.). Both
Nrf2 and NF– ОєB regulation are co–ordinated in order to maintain redox homeostasis in healthy cells. However, during pathological conditions this
regulation is disturbed offering an opportunity for therapeutic intervention. Diabetic neuropathy is a condition , in which change in expression pattern
of Nrf2 and NF–ОєB has been reported(Koriyama et

What Is The Free Amino Groups Of Nucleobases?
Parallel to proteins, the free amino groups of nitrogen bases of nucleosides and nucleotides under alkaline pH conditions are also prone to the
Maillard reaction (Reihl, O. et al, 2004). DNA reacts with reducing sugars (glucose, fructose, ribose etc.) and advances via Amadori reaction leading to
the formation of irreversible complexes known as DNA–advanced glycation end products (DNA–AGEs) (Bidmon, C. et al 2007; Frischmann, M. et al
2005). Various report suggested that nucleobases possessing amine groups are susceptible to glycation. Thus, guanine and guanine derivatives was
found to be the most reactive of all the nucleobases (Dutta et al 2005, 2006). The conformation of each nucleobase (G > A > C) is affected upon
binding with sugar ... Show more content on Helpwriting.net ...
3A). However, other nucleotides like deoxycytidine (Fig. 3A) are glycated at high О±–oxoaldehyde concentrations forming 5–glycolylcytidine
(Frischmann, M. et al 2005; Kasai, H. et al 1998; Krymkiewicz, N. 1993). Inter–strand cross–links in duplex DNA (Seidel W and Pischetsrieder M
1998; Kasai, H. et al 1998) and DNA–protein cross–links in human keratinocytes were reported at higher MG concentrations. A recent in vitro study
has demonstrated that CEdG (Fig. 3B) formation in DNA can hinder the Klenow fragment–mediated DNA synthesis (Cao, H. et al 2007). Due to AGEs
the hydrogen–bonding property of the modified guanine is affected, resulting efficient incorporation of purine than pyrimidine nucleotides (Cao, H. et
al 2007). Addition of bulky AGEs groups on the N2 position of guanine altered the Watson
–Crick base pairing characteristic of these nucleobases
resulting in destabilization of duplex DNA. The presence of dGTP–AGEs in DNA may change DNA structure, leading to the formation of abasic sites
and DNA strand breaks (Pischetsrieder, M. et al 1999; Seidel W and Pischetsrieder M 1998; Cao, H. et al 2007). DNA glycation generates several
nucleotide adducts that increases oxidative stress by the generation of hydrogen peroxide, superoxide, and hydroxyl radicals (Mistry, M. et al 2003;
Thornalley, P.J. 1996). Recently a study demonstrated an accumulation of

Renal Microvascular Complications Of Type 2 Diabetes Essay
Renal Microvascular Complications of Type 2 Diabetes: Aetiology and Pathogenesis
Abstract
There have been a number of manuscripts reporting on the association of complications in type 2 diabetes with high glucose blood levels, high levels
of C–Peptide, high advanced glycation end products (AGEs) and vascular cell adhesion molecule–1 (VCAM–1) and oxidative stress.
In order to further investigate the aetiology and pathophysiology of renal microvascular complications in type 2 diabetes, papers were reviewed
through 2000 using the NIH PubMed Literature Search System. Inclusion criteria were that manuscripts 1) be primary peer–review research article; 2)
concisely explained, or investigated, the pathophysiology of renal microvascular complications in type 2 diabetes; 3) be published in English.
High blood glucose levels and enhanced oxidative stress, found in both clinical and experimental diabetes, are thought to be the main cause of chronic
diabetic complications.
Advanced glycation end products (AGEs) resulted to be strongly correlated to renal microvascular complications via enhanced expression of adhesion
molecules, including vascular cell adhesion molecule–1 (VCAM–1).
Renal Microvascular Complications of Type 2 Diabetes: Aetiology and Pathogenesis
Diabetes mellitus type 2 is a complex disease with

Thermodynamics: What Is Aging?
What is Aging?
From the physical point of view, human aging is a process of cumulative changes, both morphological and physiological, resulting in a progressive
diminution of our body and organs ability to defend from external aggression and to adapt to changing conditions.
There are many factors contributing to aging, but I will discuss three that are inherent to our body functioning. They are a natural outcome of our normal
metabolism.
Free Radicals.
Free radicals are highly reactive molecules with an imbalance on their number of electrons. They are a sub–product of the energy generation process
within our cells. This imbalance makes them react with our cells modifying their normal functioning.
Energy generation is a fundamental ... Show more content on Helpwriting.net ...
If you take a human fibroblast ( a type of cell) belonging to a child, it will divide itself around 60 times and it will stop proliferating. The same type of
cell from a 40–year–old man will only divide around 40 times while in an 80–year–old man it will only divide around 30 times.
At that moment the fibroblast is detected as a damaged cell and it dies. It is a defense mechanism stopping damaged cells to reproduce, thus increasing
tumor and cancer risk, but in the long run there is a progressive diminution of this response and the body will support an increasing number of
malfunctioning cells.
Healthy Aging.
As we have just seen, stronk aging factors work from the inside. The way it looks, chances are science will not be able to to stop the process. So
what can we do about it. The answer is Healthy Aging, a lifestyle allowing us to grow old while maintaining the best possible health condition.
It is only reasonable to think that if we decrease the aging factors the result will be a slower aging so let's discuss some ways to achieve that.

Free Radicals
A good way to slow down the aging process is to restrict the ingest of calories by eating more fruits and vegetables. This is a very effective method
mainly

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