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 two determine 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.

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, when calculating 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

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

[edit]

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 energy released 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]

[edit]

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

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 to be 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.

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 byproduct.

The relationship between health and fitness

There 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

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 a little '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

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 of understanding 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.

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 manage anxiety 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

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

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 branchedchain and increased concentrations of circulating aromatic amino acids with concomitantly altered amino 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 postabsorptive 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.

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].

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

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.

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 of known 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).

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

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

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. With diarrhea, 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 people want 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.

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 Goals IN 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

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:

Session Paper Marks Number of Question Duration First I 100 60 out of which 50 question to be attempted (09.30 A.M. to 10.45 A.M.) First II 100 12.00 NOON) 50 questions all are compulsory 1 Hours

1 Hours (10.45 A.M. to

Second III 150 P.M. to 4.00 P.M.)

75 questions all are compulsory

2 Hours (01.30

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.

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:

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 GENERAL PAPER II PAPER III 40 (40%) 40 (40%) 75 (50 %) 35 (35%) 60 (40 %) 67.5 (45 %) rounded off to 68

OBC(Non-creamy layer) 35 (35%) PWD/SC/ST 35 (35%) 35 (35%)

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.

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 the syllabus to individual candidates.

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 IGF levels. 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

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.