Three Components of Energy Expenditure

7/30/2019 Three Components of Energy Expenditure

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am student persuing bachelors of physiotherapy and i want to do

internship from ram manohar lohia hospital delhi .my result will be out

in july .so kindly guide the details for internship in physiotherapy what

all things i need to submit kindly guide me.

Three Components of Energy Expenditure

Energy expenditure concerns calories burned versus calories consumed. Imbalances between the twodetermine weight loss, gain or maintenance. Bodies that store too much energy become overweight.

One component of your expenditure is basal metabolic rate -- the energy you burn when inactive. The

other two components are activity thermogenesis, which are the calories burned during activity, and the

thermic effect of foods, which concerns calories used to digest foods you eat.

Percentages of Components

If you were to make a pie chart illustrating total energy expenditure, or TEE, the largest wedge would be

basal metabolic rate, or BMR, or the closely related resting metabolic rate. Both reflect energy

expended while inactive.The Food and Agriculture Organization of the United Nations says BMR can

range from 45 percent for people with a vigorous lifestyle to 70 percent for those who are sedentary.

The Colorado Clinical and Translational Sciences Institute, a health and education consortium, says

activity thermogenesis -- the burning of calories while moving -- is the second largest wedge of TEE. This

is energy expended during sports, exercise and nonexercise activity thermogenesis, or NEAT, which

encompasses activities of daily living including fidgeting. The remainder of TEE comes from the thermic

effect of food, the energy used during digestion, absorption and storage of nutrients.


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Basal Metabolic Rate

Basal metabolic rate has to be measured upon waking in a darkened room after 8 hours of sleep and 12

hours of fasting. It is more common to use the measure called resting metabolic rate, or RMR, whencalculating total energy expenditure, because RMR doesn't require sleeping overnight in a testing

facility. It can be calculated while you sit for a period of time; hwever, if you don't know your BMR or

RMR, you can still estimate daily calories needed for weight loss or maintenance by adding up caloric

estimates for all your activities in an average 24-hour period.

Activity Thermogenesis

Estimates of activity thermogenesis are based on energy use during vigorous activities as well as NEAT

activities throughout the day. Certified strength and conditioning specialist Jacob Wilson, who works

with body builders, notes that NEAT activities, such as standing and pacing during work, consume more

calories than sitting. James Krieger of Weightology Weekly says a decrease in NEAT is a bigger culprit in

weight gain than a decreasing metabolic rate. He notes that as people become more efficient at daily

tasks, they streamline movements and reduce energy expenditure. Both Krieger and Wilson say adults

can compensate by purposely increasing their nonexercise activities, such as climbing stairs instead of

using elevators. Wilson says even chewing gum increases activity thermogenesis.

Thermogenic Foods

The body uses lots of energy when it processes certain unrefined foods, including lean meats,

vegetables and whole grains. For some foods, including broccoli, celery, lemon water and salsa, this

process may burn more calories than they contain. In effect, they become zero-calorie foods that help

you stay full and healthy while losing or maintaining weight.

Energy systems

Adenosine triphosphate (ATP) is the usable form of chemical energy for muscular activity. It is stored in

most cells, particularly in muscle cells. Other forms of chemical energy, such as that available from the

foods we eat, must be transferred into ATP form before they can be utilized by the muscle

cells.[1]Contents [hide]

1 The Principle of Coupled Reactions


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2 Aerobic and anaerobic metabolism

3 ATP-PC: The phosphagen system

4 Anaerobic system

5 Aerobic system

6 How they work

7 References

8 Further reading

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The Principle of Coupled Reactions

Since energy is released when ATP is broken down, energy is required to rebuild or resynthesize ATP.

The building blocks of ATP synthesis are the by-products of its breakdown; adenosine diphosphate (ADP)

and inorganic phosphate (Pi). The energy for ATP resynthesis comes from three different series of

chemical reactions that take place within the body. Two of the three depend upon the food we eat,

whereas the other depends upon a chemical compound called phosphocreatine. The energy released

from any of these three series of reactions is coupled with the energy needs of the reaction that

resynthesizes ATP. The separate reactions are functionally linked together in such a way that the energyreleased by the one is always used by the other.[2]

There are 3 methods to resynthesize ATP:

ATP-PC system (Phosphogen system) - This system is used only for very short durations of up to 10

seconds. The ATP-PC system neither uses oxygen nor produces lactic acid if oxygen is unavailable and is

thus said to be alactic anaerobic. This is the primary system behind very short, powerful movements like

a golf swing, a 100 m sprint or powerlifting.

Anaerobic system (Lactic Acid system) - Predominates in supplying energy for exercises lasting less than

2 minutes. Also known as the Glycolytic System. An example of an activity of the intensity and duration

that this system works under would be a 400 m sprint.

Aerobic system - This is the long duration energy system. By 5 minutes of exercise the O2 system is

clearly the dominant system. In a 1 km run, this system is already providing approximately half the

energy; in a marathon run it provides 98% or more.[3]


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Aerobic and anaerobic metabolism

The term metabolism refers to the various series of chemical reactions that take place within the body.

Aerobic refers to the presence of oxygen, whereas anaerobic means with series of chemical reactions

that does not require the presence of oxygen. The ATP-PC series and the lactic acid series are anaerobic,

whereas the oxygen series, is aerobic.[4]

[edit]

ATP-PC: The phosphagen system

(A) Phosphocreatine, which is stored in muscle cells, contains a high energy bond. (B) When

phosphocreatine is broken down during muscular contraction, a large amount of energy is released. The

energy released is coupled with the energy requirement to re synthesize ATP.

PC is an abbreviation for phosphocreatine. PC, like ATP, is stored in the muscle cells, and when it is

broken down, a large amount of energy is released. The energy released is coupled to the energy

requirement necessary for the resynthesis of ATP.

The total muscular stores of both ATP and PC are very small. Thus, the amount of energy obtainable

through this system is limited. In fact, if you were to run 100 meters as fast as you could, the

phosphagen stores in the working muscles would probably be empty by the end of the sprint. However,

the usefulness of the ATP-PC system lies in the rapid availability of energy rather than quantity. This is

extremely important with respect to the kinds of physical activities that we are capable of performing.

[5]

[edit]

Anaerobic system

This system is known as anaerobic glycolysis. Glycolysis refers to the breakdown of sugar. In this

system, the breakdown of sugar supplies the necessary energy from which ATP is manufactured. When

sugar is only partially broken down, one of the by-products is lactic acid. Then, with enzymes, glucose is


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broken down to produce lactic acid; this process creates enough energy to couple with the energy

requirements to resynthesize ATP.

When H+ ions accumulate in the muscles causing the blood pH level to reach very low levels, temporary

muscular fatigue results. Another limitation of the lactic acid system that relates to its anaerobic quality

is that only a few moles of ATP can be resynthesized from the breakdown of sugar as compared to the

yield possible when oxygen is present. This system cannot be relied on for extended periods of time.

The lactic acid system, like the ATP-PC system, is extremely important to us, primarily because it too

provides for a rapid supply of ATP energy. For example, exercises that are performed at maximum rates

for between 1 and 3 minutes depends heavily upon the lactic acid system for ATP energy. Also, in some

performances, like running 1500 meters or a mile, the lactic acid system is used predominately for the

kick at the end of a race.[6]

[edit]

Aerobic system

Glycolysis

The Krebs Cycle

Oxidative Phosphorylation

Glycolysis - The first stage is known as glycolysis, which produces 2 ATP molecules, 2 reduced

molecules of NAD (NADH), and 2 pyruvate molecules which move on to the next stage - the Krebs cycle.

Glycolysis takes place in the cytoplasm of normal body cells, or the sarcoplasm of muscle cells.

The Krebs Cycle - This is the second stage, and the products of this stage of the aerobic system are a

net production of 1 ATP, 1 carbon dioxide Molecule, three reduced NAD molecules, 1 reduced FAD

molecule (The molecules of NAD and FAD mentioned here are electron carriers, and if they are said tobe reduced, this means that they have had a H+ ion added to them). The things produced here are for

each turn of the Krebs Cycle. The Krebs cycle turns twice for each molecule of glucose that passes

through the aerobic system - as 2 pyruvate molecules enter the Krebs Cycle. In order for the Pyruvate

molecules to enter the Krebs cycle they must be converted to Acetyl Coenzyme A. During this link

reaction, for each molecule of pyruvate that gets converted to Acetyl Coenzyme A, an NAD is also

reduced. This stage of the aerobic system takes place in the matrix of the cells' mitochondria.


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Oxidative Phosphorylation - This is the last stage of the aerobic system and produces the largest

yield of ATP out of all the stages - a total of 34 ATP molecules. It is called 'Oxidative Phosphorylation'

because oxygen is the final acceptor of the electrons and hydrogen ions that leave this stage of aerobic

respiration (hence oxidative) and ADP gets phosphorylated (an extra phosphate gets added) to form ATP

(hence phosphorylation).

This stage of the aerobic system occurs on the cristae (infoldings on the membrane of the

mitochondria). The NADH+ from glycolysis and the Krebs cycle, and the FADH+ from the Krebs cycle pass

down electron carriers which are at decreasing energy levels, in which energy is released to reform ATP.

Each NADH+ that passes down this electron transport chain provides enough energy for 3 molecules of

ATP, and each molecule of FADH+ provides enough energy for 2 molecules of ATP. If you do your math

this means that 10 total NADH+ molecules allow the rejuvenation of 30 ATP, and 2 FADH+ molecules

allow for 4 ATP molecules to be rejuvenated (The total being 34 from oxidative phosphorylation, plus

the 4 from the previous 2 stages meaning a total of 38 ATP being produced during the aerobic system).

The NADH+ and FADH+ get oxidized to allow the NAD and FAD to return to be used in the aerobic

system again, and electrons and hydrogen ions are accepted by oxygen to produce water, a harmless by-

product.

The relationship between health and fitnessThere is no doubt that health and fitness are related to each other. If you are fit, you ensure a healthy

life. Fitness is obtained by making all kinds of sports, even if it's just walking. Technology has brought us

many benefits and managed our time, but at the same time, we brought diseases and pains. Sedentary

life is not ours, nor have we created to sleep or sit all day. We were born to live our lives on the move

and be active, do all our stuff alone. Since you can not live without our cars, remote controls, elevators

and PDA, then you can practice any kind of sport to get the most out of it and be in good health

throughout life.

If we took a walk for example, you will know someone who perseveres to walk every day for at least 1/2

hour, which are enjoying a healthy life, free from stress and illness. This is because of their perseverance

to walk improved his physical form, and thus, their health and mental well-being. In fact, you can ensure

a good and healthy life just to walk every day. You will have to do with your life stress, progress at work,

and even more, there will be more spiritual and religious. Simply because walking increases blood flow


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to the brain, therefore, increases the capacity for thought. So if you want to get smarter, then get on

foot.

Walking makes your body releases endorphins, which are natural hormones released within your body

to make you happy. This can be important when walking at a high speed. However, people who walk

slowly notice an improvement in their mood.

Almost all doctors recommend their patients to walk every day, or at least 3 times a week, and consider

it a natural treatment and an essential part of therapy. Many diseases are cured or improved on foot.

For example, hypertension, diabetes, arthritis, glaucoma, cataracts, depression, heart disease,

respiratory disease, lymphatic, circulatory and nervous systems.

As we said earlier that, while walking, your brain releases endorphins and thus achieve what many

medications and herbs try to get artificially, but in a natural way. This makes the treatment of

depression, a piece of cake. However, depression is a serious and life-threatening. In any case, you

should consult a physician in this case.

When you walk, you have much time to think and get away from any stress. This is because you can

breathe fresh air, look at nature and feel your body moving, which relieves tension in your body and

your mind, too.

Standing, you should wear comfortable clothes and shoes. Drinking enough water before, during and

after walking. Try to do it in a natural open-air place with trees and natural views around and the air

cool enough. Enjoy the view and breathe deeply as you can. Make sure you are away from any stressor.

Walking an hour after a meal, and do not walk on a full stomach. You can eat everything, but 1/2 hour

after your walk. Straighten your back, do not arch your back. Do not lean forward or backward. Look

ahead with his chin. Try to make your body relaxed, as far as possible, with your shoulders relaxed and alittle 'back. Pull the stomach inwards. Squeeze the glutes as you walk.

You can ask anyone you know to join you as you walk, because you do not feel bored because you talk

and laugh with them, and the time will pass by, leading many miles walked without noticing that the


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distance and time had passed . Go ahead from now on. Walk every day or at least 3 times a week, put it

on your schedule and never bounce.

Fatty acid mobilization from adipose tissue during exercise.

By far the largest energy reserve in the human body is adipose tissue triglycerides, and these reserves

are an important source of fuel during prolonged endurance exercise. To use this rich source of potential

energy during exercise, adipose tissue triglycerides must first be hydrolyzed and the resultant fatty acids

delivered to the working muscles. The aims of this review are to describe how exercise alters lipid

mobilization from adipose tissue, to identify alternative sources of lipids and to discuss some of the key

factors regulating fatty acid mobilization, uptake and oxidation during exercise. The impact ofunderstanding factors involved in the coordinated regulation of lipid mobilization and oxidation during

exercise goes far beyond its relevance for endurance exercise performance. A better understanding of

the regulation of these processes will facilitate the development of more effective treatment modalities

for obesity-related metabolic disorders.

Stress management

Stress management refers to a wide spectrum of techniques and psychotherapies aimed at controlling a

person's levels of stress, especially chronic stress, usually for the purpose of improving everyday

functioning.

In this context, the term 'stress' refers only to a stress with significant negative consequences, or

distress in the terminology advocated by Hans Selye, rather than what he calls eustress, a stress whose

consequences are helpful or otherwise positive.


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Stress produces numerous symptoms which vary according to persons, situations, and severity. These

can include physical health decline as well as depression. The process of stress management is named as

one of the keys to a happy and successful life in modern society.[1] Although life provides numerous

demands that can prove difficult to handle, stress management provides a number of ways to manageanxiety and maintain overall well-being.

Despite stress often being thought of as a subjective experience, levels of stress are readily measureable

using various physiological tests, similar to those used in polygraphs.

Many practical stress management techniques are available, some for use by health practitioners and

others for self-help, which may help an individual to reduce stress, provide positive feelings of being in

control of one's life and promote general well-being.

The effectiveness of the different stress management techniques can be difficult to assess, as few of

them have received significant attention from researchers. Consequently, the amount and quality of

evidence for the various techniques varies widely. Some are accepted as effective treatments for use in

psychotherapy, whilst others with less evidence favouring them are considered alternative therapies.

Many professional organisations exist to promote and provide training in conventional or alternative

therapies.

There are several models of stress management, each with distinctive explanations of mechanisms for

controlling stress. Much more research is necessary to provide a better understanding of which

mechanisms actually operate and are effective in practice.

traumatic brain injury can have wide-ranging physical and psychological effects.

Some signs or symptoms may appear immediately after the traumatic event,

while others may appear days or weeks later.

Mild traumatic brain injury


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The signs and symptoms of mild traumatic brain injury may include:

Loss of consciousness for a few seconds to a few minutes

No loss of consciousness, but a state of being dazed, confused or disoriented

Memory or concentration problems

Headache

Dizziness or loss of balance

Nausea or vomiting

Sensory problems, such as blurred vision, ringing in the ears or a bad taste in the mouth

Sensitivity to light or sound

Mood changes or mood swings

Feeling depressed or anxious

Fatigue or drowsiness

Difficulty sleeping

Sleeping more than usual

Moderate to severe traumatic brain injuries

Moderate to severe traumatic brain injuries can include any of the signs and symptoms of mild injury, as

well as the following symptoms that may appear within the first hours to days after a head injury:

Loss of consciousness from several minutes to hours

Profound confusion

Agitation, combativeness or other unusual behavior

Slurred speech

Inability to awaken from sleep

Weakness or numbness in fingers and toes

Loss of coordination

Persistent headache or headache that worsens


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Repeated vomiting or nausea

Convulsions or seizures

Dilation of one or both pupils of the eyes

Clear fluids draining from the nose or ears

Protein metabolism and liver disease.

In health, the liver orchestrates the metabolism of proteins and amino acids. When the liver is diseased,

the regulation of protein metabolism is frequently disturbed. The manifestations of disturbed protein

metabolism in liver disease are varied and change with disease aetiology and severity. The hallmarks of

protein and amino acid metabolism in liver disease are lowered concentrations of circulating branched-

chain and increased concentrations of circulating aromatic amino acids with concomitantly alteredamino acid kinetics. The changes in amino acid kinetics in liver disease are characterized by increased

endogenous leucine flux, an indicator of protein breakdown, and leucine oxidation in the post-

absorptive state (when calculated using a reciprocal-pool model and normalized for body cell mass). In

addition, the increase in whole-body protein synthesis in response to an amino acid infusion may be

attenuated in patients with cirrhosis. These changes are often accompanied by clinically apparent

muscle wasting, manifest as protein-calorie malnutrition, and associated low levels of hepatically

synthesized plasma proteins. While the pathogenesis of these changes in protein and amino acid

metabolism has not been elucidated, altered levels of circulating hormones, known to affect protein

metabolism, are probably important. Lowered levels of micronutrients and trace metals and elevated

levels of cytokines may also play a role.

Complications of heart disease include:

Heart failure. One of the most common complications of heart disease is heart failure. Heart failure

occurs when your heart can't pump enough blood to meet your body's needs. Over time, the heart can

no longer keep up with the normal demands placed on it. The ventricles may become stiff and don't fill

properly between beats. Also, the heart muscle may weaken, and the ventricles stretch (dilate) to the

point that the heart can't pump blood efficiently throughout your body. Heart failure can result from

many forms of heart disease, including heart defects, cardiovascular disease, valvular heart disease,

heart infections or cardiomyopathy.


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Heart attack. Coronary artery disease can cause a heart attack. Heart attacks usually occur when a

blood clot blocks the flow of blood through a coronary artery a blood vessel that feeds blood to a part

of the heart muscle. Interrupted blood flow to your heart can damage or destroy a part of the heart

muscle.

Stroke. Cardiovascular disease may cause an ischemic stroke, which happens when the arteries to

your brain are narrowed or blocked and too little blood reaches your brain. A stroke is a medical

emergency brain tissue begins to die within just a few minutes of a stroke.

Aneurysm. Cardiovascular disease can also cause an aneurysm, a serious complication that can occur

anywhere in your body. An aneurysm is a bulge in the wall of your artery. If an aneurysm bursts, you

may face life-threatening internal bleeding. Although this is usually a sudden, catastrophic event, a slow

leak is possible. If a blood clot within an aneurysm dislodges, it may block an artery at another point

downstream.

Peripheral artery disease. The same atherosclerosis that can lead to coronary artery disease can

also lead to peripheral artery disease (PAD). When you develop peripheral artery disease, your

extremities usually your legs don't receive enough blood flow to keep up with demand. This causes

symptoms, most notably leg pain when walking (claudication).

Sudden cardiac arrest. Sudden cardiac arrest is the sudden, unexpected loss of heart function,

breathing and consciousness. Sudden cardiac arrest usually results from an electrical disturbance in your

heart that disrupts its pumping action and causes blood to stop flowing to the rest of your body. Sudden

cardiac arrest almost always occurs in the context of other underlying heart problems, particularly

coronary artery disease. Sudden cardiac arrest is a medical emergency. If not treated immediately, it is

fatal, resulting in sudden cardiac death.

Lipid and glucose metabolism in HIV infection

Metabolic disturbances are a classic host response to infection, including HIV (Table 6)[57]. In men, high

density lipoprotein (HDL) cholesterol decreases early in HIV infection, followed by decreases in low

density lipoprotein (LDL) cholesterol (Table 6)[58,59]. At the time of transition to AIDS, triglycerides rise

due to increased very (V)LDL[58,59]. There is both a decreased clearance and an increased production of

triglyceride-rich particles[59,60]. The changes in triglycerides are related to interferon-agr; levels, the

host response to virally-infected cells[59-63].


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Studies of HIV-infected patients receiving PI have typically found increased triglyceride and cholesterol

levels ([21,35,36] K. Mulligan, C. Grunfeld, V. W. Tai, H. Algren, M. Pang, D.N. Chernoff, J.C. Lo, M.

Schambelan, unpublished data). In one study, fasting triglycerides were 106% higher in HIV-infected

patients on PI therapy compared with those not on PI therapy, which were in turn 33% higher than in

HIV-negative controls[21]. Cholesterol levels were 31% higher in those on PI, and HDL levels were

unchanged[21]. In another study, initiation of PI therapy was associated with an increase in fasting

triglycerides by 47%, in cholesterol levels by 23%, in calculated LDL cholesterol by 20%, and in directly

measured LDL by 27%; HDL cholesterol levels were unchanged (K. Mulligan, C. Grunfeld, V. W. Tai, H.

Algren, M. Pang, D.N. Chernoff, J.C. Lo, M. Schambelan, unpublished data). In comparison, a group of

HIV-infected patients not receiving PI showed no such changes. Higher LDL levels have also been found

in patients taking PI therapy in other studies[17,35]. One study of women reported increases in total and

HDL cholesterol levels after PI therapy[11]. Another study found elevated serum triglyceride levels in 75

HIV-infected women when compared with 30 healthy controls, without relation to either PI use or body

weight[64]. However, this study did find a strong correlation between duration of PI use and triglyceride

levels. Additionally, triglyceride levels correlated positively with viral load, as might be predicted from

studies in the pre-PI era.

A previous study of initiating zidovudine in antiretroviral-nave patients showed decreased triglyceride

levels[62]; therefore, an increase in triglycerides in patients on PI is likely to be a direct effect of the PI,

rather than a result of improvement in health. Yet, given that LDL is low in HIV infection[58,59], the data

on increases in LDL levels ([35] K. Mulligan, C. Grunfeld, V. W. Tai et al. unpublished data) cannot

distinguish between restoration to health by PI-containing regimens with return-to-normal LDL levels

and increased formation of LDL from VLDL.

In the pre-PI era, HIV-infected subjects were generally found to have normal or decreased glucose

levels, without insulin resistance[63,65-68]. While several reports found hyperglycemia in patients on PI

therapy[8,29,69-74], most did not[21,34,36,75-77]. However, many of these studies involved chart

review of random glucose values. When fasting glucose levels are compared, there is little difference in

hyperglycemia between patients on PI therapy and those who are PI-nave ([21,35] K. Mulligan, C.

Grunfeld, V. W. Tai, H. Algren, M. Pang, D.N. Chernoff, J.C. Lo, M. Schambelan, unpublished data).

In contrast, insulin resistance, documented by high fasting insulin-to-glucose ratios, has been more

consistently reported in association with PI use ([21,34-36] K. Mulligan, C. Grunfeld, V. W. Tai et al.

unpublished data); such studies have predominantly analyzed male populations. Insulin resistance


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associated with PI therapy has been documented by provocative testing in two cohort studies. Oral

glucose tolerance testing showed impaired glucose tolerance accompanied by higher stimulated insulin

or C-peptide levels ([35] K. Mulligan, C. Grunfeld, V. W. Tai et al. unpublished data). Furthermore, a

study using insulin tolerance testing also demonstrated insulin resistance in patients taking PI[34].

However, a recent report comparing 75 HIV-infected women with 30 healthy weight-matched controls

found significant hyperinsulinemia in association with HIV infection that was independent of PI use[64].

In contrast, one study found that initiation of PI therapy in PI-nave subjects induces a small increase in

glucose levels (11%) and a larger increase in insulin levels (95%). Because their study compared values

before and after PI therapy in the same subjects, the results are not confounded by other potential

differences that may be found in cohort studies ([35], K. Mulligan, C. Grunfeld, V. W. Tai, H. Algren, M.

Pang, D.N. Chernoff, J.C. Lo, M. Schambelan, unpublished data). In all likelihood, therefore, the use of PI

is associated with insulin resistance. The prevalence and severity of this condition requires further

evaluation.

[Changes in carbohydrate metabolism in the HIV/AIDS patient].

Over the last few years, there has been a considerable reduction in the mortality and morbidity

associated with HIV patients, due to the use of protease inhibitors which have led to a true revolution in

the treatment of this infection. A new problem has arisen with the increased life expectancy: the onset

of a plurimetabolic syndrome characterized by hypertriglyceridaemia, hypercholesterolaemia and

hyperglycaemia; in addition to anomalies in composition and distribution of body fat (central obesity

and loss of peripheral fat) due to the associated lipodystrophy. As a result of the metabolic alterations,

there is an increase in the risk of cardiovascular disease. Hyperglycaemia is the result of insulin

resistance and is detected in between 13.6% and 46% of patients, possibly leading to type 2 diabetes

(diagnosed in between 2.4% and 7% of the patients). These alterations have been documented as

potentially related with the use of protease inhibitors and other drugs used in the handling of HIV

patients. The appropriate treatment of altered metabolism of carbohydrate requires: 1) a customized

dietary approach depending on individual BMI and lipid alterations; 2) a physical exercise programme; 3)

the use of insulin sensitization drugs: metformin and thiazolidinediones and, where the therapeutic

goals are not achieved or there is a contraindication for oral hypoglycaemic drugs; 4) insulin therapy

with regimens similar to other diabetic patients.


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Liver failure

Liver failure is the inability of the liver to perform its normal synthetic and metabolic function as part of

normal physiology. Two forms are recognised, acute and chronic.[1]

Acute

Acute liver failure is defined as "the rapid development of hepatocellular dysfunction, specifically

coagulopathy and mental status changes (encephalopathy) in a patient without known prior liver

disease".[2]:1557

The diagnosis of acute liver failure is based on physical exam, laboratory findings, patient history, and

past medical history to establish mental status changes, coagulopathy, rapidity of onset, and absence ofknown prior liver disease respectively.[2]:1557

The exact definition of "rapid" is somewhat questionable, and different sub-divisions exist which are

based on the time from onset of first hepatic symptoms to onset of encephalopathy. One scheme

defines "acute hepatic failure" as the development of encephalopathy within 26 weeks of the onset of

any hepatic symptoms. This is sub-divided into "fulminant hepatic failure", which requires onset of

encephalopathy within 8 weeks, and "subfulminant", which describes onset of encephalopathy after 8

weeks but before 26 weeks.[3] Another scheme defines "hyperacute" as onset within 7 days, "acute" as

onset between 7 and 28 days, and "subacute" as onset between 28 days and 24 weeks.[2]:1557

Chronic

Chronic liver failure usually occurs in the context of cirrhosis, itself potentially the result of many

possible causes, such as excessive alcohol intake, hepatitis B or C, autoimmune, hereditary and

metabolic causes (such as iron or copper overload, Steatohepatitis or non-alcoholic fatty liver disease).


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Liver transplantation

Liver transplantation or hepatic transplantation is the replacement of a diseased liver with a healthy

liver from another person (allograft). The most commonly used technique is orthotopic transplantation,

in which the native liver is removed and replaced by the donor organ in the same anatomic location as

the original liver. Liver transplantation nowadays is a well accepted treatment option for end-stage liver

disease and acute liver failure. Typically three surgeons and two anesthesiologists are involved, with up

to four supporting nurses. The surgical procedure is very demanding and ranges from 4 to 18 hours

depending on outcome. Numerous anastomoses and sutures, and many disconnections and

reconnections of abdominal and hepatic tissue, must be made for the transplant to succeed, requiring

an eligible recipient and a well-calibrated live or cadaveric donor match. By any standard, hepatic

transplantation is a major surgical procedure with an appreciable degree of risk.[citation needed]

Nutrition and HIV/AIDS

Nutrition is a key component in managing the condition of HIV/AIDS

People living with HIV/AIDS face increased challenges in maintaining proper nutrition. Despite

developments in medical treatment, nutrition remains a key component in managing this condition. The

challenges that those living with HIV/AIDS face can be the result of the viral infection itself or from the

effects of anti-HIV therapy (HAART).[1]

Some of the side effects from HAART that may affect how the body absorbs and utilizes nutrients

include fatigue, nausea, and poor appetite.[2] As well, the nutritional needs of people with HIV/AIDS are

greater due to their immune system fighting off opportunistic infections that do not normally cause

disease in people with healthy immune systems.[3] Medication along with proper nutrition is a major

component of maintaining good health and quality of life for people living with HIV/AIDS.Contents

[hide]

Energy requirements

Monitoring caloric intake is important in ensuring that energy needs are met. For people with HIV/AIDS,

energy requirements often increase in order to maintain their regular body weight.[4] A classification


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system revised by the Centers for Disease Control and Prevention (CDC), categorizes HIV-infection into 3

clinical stages and addresses the suggested caloric requirements for each stage.[5]

1. Clinical Category A: Asymptomatic HIV

This stage is characterized by Acute HIV. People in this category have estimated needs of 30-35 kcals/kg.

2. Clinical Category B: Symptomatic HIV

This stage is characterized by complications that arise from HIV symptoms. People in this category have

estimated needs of 35-40 kcals/kg.

3. Clinical Category C: Presence of AIDS condition

This stage is characterized by having a T-cell count under 200, signaling the presence of an AIDS defining

condition and/or an opportunistic infection. People in this category have estimated needs of 40-50

kcals/kg and are at an increased risk of malnourishment.

Micronutrient requirements

Multivitamins and supplementation

There is no consensus regarding the effects of multivitamins and nutrient supplementation on HIV

positive individuals. This is partly due to a lack of strong scientific evidence that would support the

supplementation of any particular micronutrient.

Some studies have looked into the use of implementing daily multivitamins into the diet regimens of

HIV/AIDS patients. One study done in Tanzania involved a trial group with one thousand HIV positive

pregnant women. Findings showed that daily multivitamins benefited both the mothers and their

babies. After four years, the multivitamins were found to reduce the womens risk of AIDS and death by

approximately 30%.[6] Another trial in Thailand revealed that the use of multivitamins led to fewer

deaths, but only among people in advanced stages of HIV.[7] However, not all studies have provided a

positive correlation. A small trial done in Zambia found no benefits from multivitamins after one month

of use.[8]

Regarding individual vitamin and mineral supplementation, research shows mixed results. Vitamin A

supplementation has been shown to reduce mortality and morbidity rates among African children

suffering from HIV. The World Health Organization (WHO) recommends vitamin A supplements for all

young children 6 to 59 months old that are at high risk of vitamin A deficiency every 4 to 6 months[9] . In

contrast, a trial from Tanzania found that the use of vitamin A supplements increased the risk of


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mother-to-child transmission by 40%.[10][11] With the inconsistency of these results, scientists have not

reached a consensus regarding Vitamin A supplementation and its possible benefits for HIV/AIDS

patients.

Thus, further research is required to determine the relationship between supplements and HIV/AIDS in

order to develop effective nutritional interventions

Nutrition Guidelines for AIDS

The AIDS Information Network defines "Good Nutrition" as getting enough macronutrients and

micronutrients. Macronutrients contain calories (energy): proteins, carbohydrates, and fats. They help

maintain body weight. Micronutrients include vitamins and minerals. They keep cells working properly,

but will not prevent weight loss.

Good nutrition can be a problem for many people with HIV. When the body fights any infection, it uses

more energy and the patient needs to eat more than normal. But when one feels sick, they eat less than

normal.

Some medications can upset the stomach, and some opportunistic infections can affect the mouth or

throat. This makes it difficult to eat. Also, some medications and infections cause diarrhea. Withdiarrhea, the body actually uses less of what you eat.

With weight lose, they might be losing fat, or they might be losing lean body weight like muscle. If they

lose too much lean weight, the body chemistry changes. This condition is called wasting syndrome or

cachexia. Wasting can kill.26

First, eat more. Extra muscle weight will help fight HIV. This is very important. Many peoplewant to lose weight, but for people with HIV, it can be dangerous.

Make sure they eat plenty of protein and starches, with moderate amounts of fat. Protein helps build and maintain muscles. Meats, fish, beans, nuts, and seeds are good sources.

Carbohydrates give energy. Complex carbohydrates come from grains, cereals, vegetables, and fruits.

They are a "time release" energy source and are a good source of fiber and nutrients. Simple

carbohydrates, or sugars give quick energy. Sugars are in fresh or dried fruit, honey, jam, or syrups.


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Fat gives extra energy. The patient needs some - but not too much. The "monounsaturated" fats in nuts,

seeds, canola and olive oils, and fish are considered "good" fats. The "saturated" fats in butter and

animal products are "bad" fats.

A moderate exercise program will help the body turn food into muscle. Take it easy, and work exercise

into daily activities.

Drinking enough liquids is very important when the person has HIV. Extra water can reduce the side

effects of medications. It can help avoid a dry mouth and constipation. Be aware that drinking tea,

coffee, colas, chocolate, or alcohol can actually make a person lose body liquid.

Guidelines for Meeting Nutritional GoalsIN HEPATIC FAILURE PATIENT. In 1997, the

European Society for Clinical Nutrition and Metabolism created guidelines for meeting nutritional goals

in patients with end-stage liver disease.[53] They recommend initiation of enteral feeding when oral

intake is inadequate. In patients with compensated cirrhosis, the guidelines recommend that patients

consume 25-35 kcal/kg body weight per day of nonprotein energy and 1-1.2 g/kg body weight per day of

protein or amino acids. In patients with complicated cirrhosis associated with malnutrition, nonprotein

energy should be increased to 35-40 kcal/kg body weight per day and protein intake should increase to

1.5 g/kg body weight per day. According to the guidelines, protein intake should decrease to 0.5-1.5

g/kg body weight/day if stage I or II encephalopathy is present, and to 0.5 g/kg body weight/day if stage

III or IV encephalopathy is present. More recent evidence suggests that protein restriction should not be

recommended, even in the setting of episodic hepatic encephalopathy.[56]

Distribution of Calorie Intake

The distribution of calorie intake throughout the day has also been studied. It has been proposed that

eating a late evening snack could alleviate the shift towards lipid oxidation by reducing the length of

time a patient fasts overnight. Indeed, a late evening meal has been shown to improve the nitrogen

balance[57] and raise the nonprotein respiratory quotient.[58] A typical recommendation for patients

with advanced liver disease is to consume four to five small meals per day, as well as a late evening

snack


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National Eligibility Test

Important Dates:- June 2013

Last date for Applying Online & generation of filled Bank Challan for Fee. :

Friday; May 03, 2013

Last date of submission of Fee through online generated Bank Challan, at any

branch of State Bank of India (SBI). : Monday; May 06, 2013

Last date of taking printout of Application Form,Attendance Slip and Admit Card

from UGC website (www.ugcnetonline.in) : Thursday; May 09, 2013

Last date for receiving the printout of online Application Form (one copy) and

Attendance Slip (one copy) at the respective Coordinating University opted by

the candidate (with fee receipt & category certificate(s) ) : Monday;

May 13, 2013

SCHEME AND DATE OF TEST :

i) The Test will consist of three papers. All the three papers will consist of

only objective type questions and will be held on 30th June, 2013 (SUNDAY) in

two separate sessions as under:


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Session

Paper

Marks

Number of Question

Duration

First I 100 60 out of which 50 question to be attempted 1 Hours

(09.30 A.M. to 10.45 A.M.)

First II 100 50 questions all are compulsory 1 Hours (10.45 A.M. to

12.00 NOON)

Second III 150 75 questions all are compulsory 2 Hours (01.30

P.M. to 4.00 P.M.)

Paper-I shall be of general nature, intended to assess the teaching/research

aptitude of the candidate. It will primarily be designed to test reasoning ability,

comprehension, divergent thinking and general awareness of the candidate.

Sixty (60) multiple choice questions of two marks each will be given, out of

which the candidate would be required to answer any fifty (50). In the event of

the candidate attempting more than fifty questions, the first fifty questions

attempted by the candidate would be evaluated.


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Paper-II shall consist of 50 objective type compulsory questions based on the

subject selected by the candidate. Each question will carry 2 marks.

Paper-III will consist of 75 objective type compulsory questions from the subject

selected by the candidate. Each question will carry 2 marks.

All questions of Paper-II and Paper-III will be compulsory, covering entire

syllabus (including all electives, without options).

The candidate will have to mark the responses for questions of Paper-I, Paper-II

and Paper-III on the Optical Mark Reader (OMR) sheet provided along with the

Test Booklet.

The detailed instructions for filling up the OMR Sheet will be uploaded on UGC

website (www.ugcnetonline.in or www.ugc.ac.in) in the last week of May, 2013.

It may noted that instructions to candidates will not be sent to the candidate by

post.

PROCEDURE & CRITERIA FOR DECLARATION OF RESULT:


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This will comprise of following steps:

Step I: Minimum marks to be obtained in NET for considering a candidate for the

award of JRF and eligibility for lectureship:

The candidates are required to obtain following minimum marks separately in

Paper-I, Paper-II and Paper-III as given below:

CATEGORY Minimum Marks (%) to be obtained

PAPER I PAPER II PAPERIII

GENERAL 40 (40%) 40 (40%) 75 (50 %)

OBC(Non-creamy layer) 35 (35%) 35 (35%) 67.5 (45 %) rounded off to 68

PWD/SC/ST 35 (35%) 35 (35%) 60 (40 %)

Step II: Amongst those candidates who have cleared step I, a merit list will be

prepared subject-wise and category-wise using the aggregate marks of all the

three papers secured by such candidates.

Step III: Top 15% candidates (for each subject and category), from the merit list

mentioned under step II, will be declared NET qualified for eligibility for

lectureship only.


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Step IV: A separate merit list for the award of JRF will be prepared from

amongst the NET qualified candidates figuring in the merit list prepared under

step III.

It may be noted that the above qualifying criteria decided by UGC is final and

binding.

ii) For Persons with Disability (Visually Challenged candidates) thirty

minutes extra time shall be provided separately for paper-I and Paper-II. For

paper-III, forty five minutes extra time shall be provided. They will also be

provided the services of a scribe who would be a graduate in a subject other

than that of the candidate. Those Persons with Disability (Physically Challenged)

candidates who are not in a position to write in their own hand-writing can also

avail these services by making prior request (at least one week before the date

of UGC-NET) in writing to the Co-ordinator of the NET Coordinating University.

Extra time and facility of scribe would not be provided to other Persons with

Disability (Physically Challenged) candidates.

iii) Syllabus of Test: All questions of Paper-II and Paper-III will be compulsory,

covering entire syllabus (including all electives, without options). Syllabi for all

NET subjects can be downloaded from the UGC Website www.ugc.ac.in and are

also available in the libraries of all Indian Universities. UGC will not send thesyllabus to individual candidates.


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iv) In case of any discrepancy found in the English and Hindi versions, the

questions in English version shall be taken as final.

NOTE : PRINTOUT OF ONLINE APPLICATION FORM SENT DIRECTLY TO THE UGC

OFFICE WILL NOT BE ENTERTAINED.

Metabolic Aspects of Cancer

Tumor development is influenced by the endocrine and metabolic environment.

This section reviews the potential role of hyperglycemia and the insulin/IGF axis.

Cancers rely on anaerobic glycolysis for their energy needs, but are normally able

to extract all the glucose they need at normoglycemic levels. Consistent with this,

glucose control has not been shown to modify cancer risk in diabetes. Both

diabetes and obesity are associated with hyperinsulinemia and increased IGFlevels. Many cancers overexpress receptors for insulin, including the insulin

receptor A (normally found only in fetal life), together with the IGF-1 receptor and

hybrid insulin/IGF-1 receptors. Increased insulin/IGF signalling harnesses the

proproliferative actions of the two hormones to maximize cell reproduction.

Insulin is not required for glucose entry or utilization in cancer tissues, but


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anaerobic glycolysis allows glucose to be used as a substrate for synthesis of (e.g.)

nucleotides as well as meeting the energy requirents of the cell. Cancer cells thus

hijack metabolic pathways needed for growth and reproduction and use glucose

as a substrate as well as a fuel. The high levels of insulin and IGFs seen in diabesity

are thought to play an important role in promoting cancer development;

hyperglycemia appears less important.

Metabolic aspects of HIV: associated wasting

Despite recent progress in the treatment of human immunodeficiency virus (HIV)

infection, wasting syndrome (WS) is now one of the major aspects of acquired

immunodeficiency syndrome (AIDS). Malnutrition in HIV infected patients is

characterised by a predominant loss of body cell mass (BCM), the amount of

functional protoplasm in non-adipose tissue. This loss of BCM is correlated with a

higher risk of AIDS events and a greater risk of mortality. If anorexia plays a major

role in the development of the WS, some abnormalities in the metabolism drive

the predominant loss of BCM. In the stable state, the resting energy expenditure

(REE) is increased by about 10%. The REE is significantly correlated with the whole

body protein turn over as measured by C13 leucine. This particular and only

metabolic situation is associated with an increased insulin sensitivity and a high

level in de novo hepatic lipogenesis. During periods of secondary infections,patients had a striking average weight loss, resulting from the combination of

anorexia and dramatic elevated REE.

Documents

Three Components of Energy Expenditure