FDA Warns of Rare Acetaminophen Risk

Acetaminophen, a fever and pain reliever that is one of the most widely used medicines in the U.S., can cause rare but serious skin reactions, warns the Food and Drug Administration (FDA).

Although rare, possible reactions to acetaminophen include three serious skin diseases whose symptoms can include rash, blisters and, in the worst case, widespread damage to the surface of skin. If you are taking acetaminophen and develop a rash or other skin reaction, stop taking the product immediately and seek medical attention right away.

Diet affects sleep - Study

A new study from the University of Pennsylvania's Perelman School of Medicine shows an association between what one eats’ and how one sleeps,reported BBC health. "In general, seven to eight hours of sleep each night is most likely an experience of overall better health and well being.

Question that was asked in the study, `Are there differences in the diet of those who report shorter sleep, longer sleep, or standard sleep patterns?'" said study researcher Michael A. Grandner, Ph.D., of the Center for Sleep and Circadian Neurobiology at the university.

Researchers examined the daily calories and foods consumed - down to a glass of water. They also gathered information on the amount of time the study participants slept, putting them into four categories: "very short" sleepers, who slept fewer than five hours a night;"short" sleepers, who slept five to six hours a night; "standard" sleepers, who slept seven to eight hours a night; and "long" sleepers, who slept nine or more hours a night.

And researchers did find an association between the number of calories consumed and how long the study participants slept. Those who consumed the most were more likely to be "short" sleepers.

Interestingly, "normal" sleepers were the next type to consume a lot of calories, followed by "very short" sleepers and then "long" sleepers, researchers found.

The researchers also identified different associations between sleep time and the types of nutrients the participants ate.

Overall, researchers noted that the very short, short and long sleepers consumed a less varietal diet than those who were considered normal sleepers.

The question is now whether changing eating habits can actually affect sleep, as the study only showed an association.

KFC USES NO CHICKEN --- JUST A RUMOR OR A FACT?

KFC USES NO CHICKEN --- JUST A RUMOR OR A FACT?...................... Whats your opinion?


KFC has been a part of American traditions for many years. Many people, day in and day out, eat at KFC religiously. Do they really know what they are eating? During a recent study of KFC done at the University of New Hampshire, they found some very upsetting facts. First of all, has anybody noticed that just recently, the company has changed their name?

Kentucky Fried Chicken has become KFC. Does anybody know why? We thought the real reason was because of the "FRIED" food issue.
IT'S NOT!!

The reason why they call it KFC is because they can not use the word chicken anymore. Why? KFC does not use real chickens. They actually use genetically manipulated organisms. These so called "chickens" are kept alive by tubes inserted into their bodies to pump blood and nutrients throughout their structure. They have no beaks, no feathers, and no feet. Their bone structure is dramatically shrunk to get more meat out of them. This is great for KFC.

Because they do not have to pay so much for their production costs. There is no more plucking of the feathers or the removal of the beaks and feet. The government has told them to change all of their menus so they do not say chicken anywhere. If you look closely you will notice this.

A new type of malaria vaccine could beat all strains

JENNIFER REIMAN, GRIFFITH UNIVERSITY

A new type of malaria vaccine that has been shown to be safe in mice is about to start trials in humans.

This promising vaccine is different to other approaches to stopping the deadly disease because we use the whole malaria parasite in it. And it is able to protect against multiple strains of the illness.

Malaria and the need for a vaccine

Malaria is a mosquito-borne disease infecting nearly 250 million people each year across 109 countries. It causes approximately one million deaths each year, mostly among African children under the age of five.

The parasite has a complex life cycle with half of it lived within the female mosquito, and the other half in the human host (first within the liver and then by infecting red blood cells).

When the parasite bursts out of infected red blood cells, it destroys the cells and causes the symptoms of malaria.

Current preventive measures against malaria include those that act on the mosquito including insecticide-treated bed nets (physical barrier) and indoor residual spraying of chemicals (insecticides) to kill mosquitoes when they land on the walls.

If you’re infected, anti-malaria drugs (artemisinin-based combination therapies) are used to kill the parasite, but not everyone has access to them.

What’s more, mosquitoes and malaria parasites are continually developing resistance to current chemicals and drugs, frustrating efforts to protect against the illness.

There is no licensed vaccine against malaria, and the most advanced experimental one in clinical trials, RTS,S is showing little protection.

Our vaccine

Researchers around the world have been working on a vaccine for malaria for over 80 years. The team I’m in has been working on the problem for over 20 years.

Based on previous results from our group showing that a vaccine containing low doses of the dead parasite protected against malaria, we decided to use the whole parasite while it is still inside the red blood cell (the second stage of malaria infection) in our vaccine.

Colleagues in North America had previously showed that treating sporozoites (the malaria parasite at the stage when it is transmitted from an infected mosquito) with a particular drug protected against infection with sporozoites of all strains.

We used this same drug to treat infected red blood cells. The drug binds to the parasite’s DNA and prevents it from multiplying.

We treated red blood cells from mice infected with malaria with the drug in a test tube, then washed away the excess drug and gave the remaining treated cells to mice. This is our vaccine.

Later, we infected the mice with malaria to see if they were protected. We found that mice given our vaccine before infection did not develop as many parasites in their blood. Some of the mice had so few parasites that we were unable to see them when we looked at the blood under a microscope.

And even though mice were immunised with only one strain of malaria and infected with a different strain, they were also protected by our vaccine. That means that our vaccine protects against all strains of malaria.

How our vaccine is different

Previous vaccines have been able to activate humoral immunity (protection mediated by antibodies). These vaccines stimulate to body to make antibodies that bind to proteins on the surface of the parasite and can prevent parasites from invading new red blood cells. Or they can make antibodies that bind to the surface of infected red blood cells and are important in their removal.

These vaccines have, for the most part, not been successful. Malaria can hide from these antibodies by making a new version of the protein that won’t be recognised by the antibodies.

People who live in malaria infected areas do eventually develop protection against malaria symptoms. But this protection doesn’t occur until they have been infected with multiple strains of malaria (and only if they don’t die from one of the infections first).

Unlike naturally acquired immunity to malaria, our vaccine works by turning on cell-mediated immunity which involves T lymphocytes (a type of white blood cell). These T lymphocytes are able to recognise all kinds of proteins including those hidden inside the malaria parasite.

The hidden proteins may be shared between the various strains of malaria and we suspect that’s why our vaccine protects not only against the strain given in the vaccine but all strains of malaria.

The next steps

The results from our studies in mice has prompted us to test our malaria vaccine in humans. Within the next few months, we will begin a human clinical trial testing the vaccine made in human red blood cells that are infected with the human malaria parasite.

If results of the study in healthy Australian volunteers is promising, the vaccine will progress onto studies in areas where malaria is present. We are very encouraged by the results so far and optimistic that our vaccine approach will aid the fight against this debilitating illness that affects so many people around the world.

Obesity can be inherited

New research from the University of Adelaide shows that the sperm of obese fathers could increase the risk of both their children and their grandchildren to inherit obesity.

In laboratory studies, researchers from the University's Robinson Institute have found that molecular signals in the sperm of obese fathers can lead to obesity and diabetes-like symptoms in two generations of offspring, even though the offspring are eating healthily.

The results of the research are published online inThe FASEB Journal.

"A father's diet changes the molecular makeup of the sperm. With obese fathers, the changes in their sperm - in their microRNA molecules - might program the embryo for obesity or metabolic disease later in life," says the lead author of the paper, Dr Tod Fullston, who is an NHMRC Peter Doherty Fellow with the University's Robinson Institute, based in Dr Michelle Lane's Gamete and Embryo Biology Group.

"For female offspring, there is an increased risk of becoming overweight or obese. What we've also found is that there is an increased chance of both male and female offspring developing metabolic disease similar to type 2 diabetes.

"This is the first report of both male and female offspring inheriting a metabolic disease due to their father's obesity," he says.

The study also extended into the second generation of progeny, which showed signs of similar metabolic disorders, including obesity, although it was not as severe as the first generation.

Dr Fullston says even if the obese father does not show any signs of diabetes, metabolic disease similar to diabetes was being seen in two generations of their descendants.

"It's been known for some time that the health of a mother before, during and after pregnancy can impact on her child's health, but the father's health during this period is often overlooked," Dr Fullston says.

"If our laboratory studies are translatable to humans, this could be a new and as yet unexplored intervention window into the epidemic of childhood obesity.

"A focus on the mother's health is extremely important, but we're seeing that the father's health is also important for conception. It's possible that by showing additional attention to diet and exercise in the father, this could have a positive impact on his future children and grandchildren."

Facts about Kidney Disease

1. The incidence kidney failure (or chronic Kidney disease) has doubled the last 15 years.

2. It is estimated that currently there are over 1 million people worldwide who are alive on dialysis or with a functioning graft.

3. Diabetes is an important cause of kidney failure and diabetes is five times more common in the Asians when compared to the white population

4. Another lifestyle related disorder - hypertension is an important cause of kidney failure and it too has seen a global increase in its incidence. Asians again are twice more prone to develop this condition in comparison to the white population.

5. Almost 66% kidney failure occurs due to hypertension or diabetes.

6. There are approximately 7.85 million people suffering from chronic kidney failure in India.

7. It is estimated that there are between 11 to 30 million people with chronic Kidney disease or other evidence of kidney disease in USA.

8. In the United States the cost of treating patients with renal replacement therapy will be US $28 billion by the year 2013. It is estimated that over 600 000 patients will require treatment.

9. In India 90 % patients suffer from kidney disease are not able to afford the cost of treatment.

10. The crisis of kidney shortage is a global phenomenon and it is worst in Asian countries.

Peptic Ulcer Disease- A review

RECEPTORS

RECEPTORS

 

 

 

 

CONTENTS

1- ENZYME-LINKED RECEPTORS
2- LIGAND GATED ION CHANNELS
3- VOLTAGE GATED ION CHANNELS
4- G PROTEIN COUPLED RECEPTORS
5- NUCLEAR RECEPTOR


 

 

 

 

ENZYME-LINKED RECEPTORS

 

These receptors are themselves enzymatic proteins. The agonist binding site lies on the outer, while the catalytic site lies on the inner face of the plasma membrane. These two domains are interconnected through a single trans- membrane stretch of peptide chain.
Most Enzyme-Linked receptors have tyrosine kinase as the enzyme. e.g. Insulin, epidermal growth factor, platelet derived growth factor & certain interleukins. The intracellular events are triggered by phosphorylation of relevant proteins. The receptor itself gets autophosphorylated on tyrosine residues which promote association of several receptor molecules, organizing the complex signaling mechanisms.

 

LIGAND GATED ION CHANNELS

They regulate the flow of ions across the membranes. Ligand binds and regulates their activity. They are fast acting receptors, respond in sub-milliseconds.
Natural ligands include Ach, Serotonin, GABA & Glutamate.
Neurotransmitter binds to the receptor, altering its concentration to open or close the channel to the flow of Na+, K+, Cl- or Ca++ ions across the membrane.
These receptors mediate neurotransmission, cardiac conduction and muscle contraction.


 


VOLTAGE GATED ION CHANNELS

They transport ions across the membrane and are regulated by the electrical potential difference near the channel. Some are composed in a way that they have a central pore through which ions travel down their electrochemical gradients.
Change in potential induces a conformational change in the channel, it opens admitting the ion influx or efflux to occur across the membrane down the electrochemical gradient.
Example include Na+ and K+ Voltage gated channels
They play role in the generation and propagation of nerve impulse across the membrane.

 


 
G PROTEIN COUPLED RECEPTORS

 
These are a large family of cell membrane receptors which are linked to the effector through one or more GTP-activated proteins.
These receptors comprise a α helical peptide which has seven membrane spanning regions.
The extracellular domain contains a ligand binding area, intracellularly, these are linked to a G protein (Gs,Gq,Gi) having 3 subunits α,β,ϒ, that binds GTP.
Binding of ligand to receptor activates the G protein, which releases GDP & binds GTP.
ADENYLYL CYCLASE (c AMP) PATHWAY
Turned on by Gsà activation of Adenylyl Cyclase àintracellular accumulation of
c AMP à increased Ca++ influx and enzyme activity

 

 
PHOSPHOLIPASE C (IP3-DAG) PATHWAY

Turned on by Gq à activation of Phospholipase C à Generation of IP3 & DAG à

Increased intracellular Ca++ and protein kinase activity

 



NUCLEAR RECEPTOR

 
These receptors work with other proteins to regulate the expression of specific genes.
Ligands include thyroid hormone, heme, cholesterol, Vitamin A & D
Ligand binding to the receptors à translocation from cytoplasm to cell nucleus à binding to nuclear hormone response elementsà resulting in up regulation or down regulation of gene expression
There are 48 known human nuclear receptors, e.g. Thyroid hormone receptor, Retinoic acid receptor, Estrogen receptor

 

Gout

Definition:

Gout is a form of arthritis which is caused by the accumulation of uric acid crystals in joints. In this condition, due to a metabolic dysfunction, there is deposition of uric acid in and around the joints causing severe painfulness, swelling and restricted mobility of the affected joint. 

Gout is a disease that results from an overload of uric acid in the body. This overload of uric acid leads to the formation of tiny crystals of urate that deposit in tissues of the body, especially the joints. When crystals form in the joints, it causes recurring attacks of joint inflammation arthritis. Gout is considered a chronic and progressive disease. Chronic gout can also lead to deposits of hard lumps of uric acid in the tissues, particularly in and around the joints and may cause joint destruction, decreased kidney function, andGout has the unique distinction of being one of the most frequently recorded medical illnesses throughout history. It is often related to an inherited abnormality in the body's ability to process uric acid.

Symptoms:
Gout is an intensely painful condition, which mostly affects only one joint (monoarthritis) at a time, most commonly the big toe. However, Gout may also affect elbows, knees, ankles, wrists or small joints of the hands and feet. The classic history in a patient suffering from Gout is of excruciating and sudden pain, swelling, redness, warmth and stiffness of the joint. Low-grade fever may also be present. The skin overlying the joint can also be swollen, tender and sore if it is touched even lightly. Patients with longstanding hyperuricemia (high levels of uric acid in blood) can have uric acid crystal deposits called tophi in other tissues as well, e.g. the helix of the ear.

Causes of Gout:

Hereditary

Improper function of kidney which results in decreased excretion of urates in urine.

Reaction to alcohol. Reaction to certain drugs, including antibiotics.

Enzyme deficiencies.

Lead poisoning.

Disorder is often associated with an injury or surgical procedure.

Highly proteinous diet.

Unidentified causes—Idiopathic causes.

Starvation—diminished renal excretion of uric acid.

Psoriasis—due to over production of uric acid.

Toxaemia of pregnancy—due to diminished excretion of uric acid. May also occur in some cases of tumors or cancers.

Gout has four distinct stages     

 Asymptomatic: High levels of Uric acid in blood but no joint complaints

Acute phase: Acute complaints described above occur for a brief period

Intercritical phase: There is no pain or swelling of joints in this phase, the patient is relatively symptom-free.

Chronic: Gout attacks may become frequent during this phase and the condition may affect many joints at a time (polyarticular). Tophi formation may also be seen.        

FINGER CLUBBING -- DIAGNOSIS

SCHAMROTH SIGN 

Absence of a closed triangular space described by the nails of two index 

fingers when their distal phalanges are held in dorsal opposition

PHALANGEAL DEPTH RATIO 

In normal fingers, the distal phalangeal depth should be smaller than the 

interphalangeal depth; this relationship is reversed in the finger with clubbing
.
Since calipers may not be readily available, physicians may estimate the 

phalangeal depth ratio

ANS REVIEW

GALL BLADDER