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Diagnonistic Test

Lower GI Series

Endoscopic image of colon cancer identified in...
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A lower gastrointestinal (GI) series uses x rays to diagnose problems in the large intestine, which includes the colon and rectum. The lower GI series may show problems like abnormal growths, ulcers, polyps, diverticuli, and colon cancer.

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Before taking x rays of your colon and rectum, the radiologist will put a thick liquid called barium into your colon. This is why a lower GI series is sometimes called a barium enema. The barium coats the lining of the colon and rectum and makes these organs, and any signs of disease in them, show up more clearly on x rays. It also helps the radiologist see the size and shape of the colon and rectum.

You may be uncomfortable during the lower GI series. The barium will cause fullness and pressure in your abdomen and will make you feel the urge to have a bowel movement. However, that rarely happens because the tube used to inject the barium has a balloon on the end of it that prevents the liquid from coming back out.

You may be asked to change positions while x rays are taken. Different positions give different views of the colon. After the radiologist is finished taking x rays, you will be able to go to the bathroom. The radiologist may also take an x ray of the empty colon afterwards.

A lower GI series takes about 1 to 2 hours. The barium may cause constipation and make your stool turn gray or white for a few days after the procedure.

Preparation
Your colon must be empty for the procedure to be accurate. To prepare for the procedure you will have to restrict your diet for a few days beforehand. For example, you might be able to drink only liquids and eat only nonsugar, nondairy foods for 2 days before the procedure; only clear liquids the day before; and nothing after midnight the night before. A liquid diet means fat-free bouillon or broth, gelatin, strained fruit juice, water, plain coffee, plain tea, or diet soda. To make sure your colon is empty, you will be given a laxative or an enema before the procedure. Your physician may give you other special instructions.

National Digestive Diseases Information Clearinghouse
2 Information Way
Bethesda, MD 20892–3570
Phone: 1–800–891–5389
TTY: 1–866–569–1162
Fax: 703–738–4929
Email: nddic@info.niddk.nih.gov
Internet: www.digestive.niddk.nih.gov

The National Digestive Diseases Information Clearinghouse (NDDIC) is a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). The NIDDK is part of the National Institutes of Health of the U.S. Department of Health and Human Services. Established in 1980, the Clearinghouse provides information about digestive diseases to people with digestive disorders and to their families, health care professionals, and the public. The NDDIC answers inquiries, develops and distributes publications, and works closely with professional and patient organizations and Government agencies to coordinate resources about digestive diseases.

Sources: http://digestive.niddk.nih.gov/ddiseases/pubs/lowergi/index.htm

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Western Diet Ups Heart Attack Risk

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Diets that are rich in fried and salty foods increase heart attack risk, while eating lots of fruit, leafy greens and other vegetables reduces it, a groundbreaking study showed.
Western diet boosts colon cancer risk by 300 per cent .

6/12/2008 – (NaturalNews) People who eat a typical “Western diet” or drink diet soda have a higher risk of developing metabolic syndrome and cardiovascular disease, according to a study published in the journal Circulation. “This is a red-alert wake-up call,”…

Green’s The Way: People who ate a ‘Prudent Diet’ — high in fruits and vegetables — had a 30% lower risk of heart attack…..CLICK & SEE

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The study, called Interheart, looked at 16,000 heart attack patients and controls between 1999 and 2003 in countries on every continent, marking a shift from previous studies which have focussed on the developed world.

The patients and controls filled in a “dietary risk score” questionnaire based on 19 food groups, which contained healthy and unhealthy items and were tweaked to include dietary preferences of each country taking part in the study.

The researchers found that people who eat a diet high in fried foods, salty snacks, eggs and meat — the “Western Diet” — a 35% greater risk of having a heart attack than people who consumed little or no fried foods or meat, regardless of where they live.

People who ate a “Prudent Diet” — high in leafy green vegetables, other raw and cooked vegetables, and fruits — had a 30% lower risk of heart attack than those who ate little or no fruit and veg, the study showed.

The third dietary pattern, called the “Oriental Diet” because it contained foods such as tofu and soy sauce which are typically consumed in Asian societies, was found to have little impact on heart attack risk.

Although some items in the Oriental diet might have protective properties such as vitamins and anti-oxidants, others such as soy sauce have a high salt content which would negate the benefits, the study said. The study was groundbreaking in its scope and because previous research had focused mainly on developed countries, according to Salim Yusuf, a senior author of the study.

“We had focussed research on the West because heart disease was mainly predominant in western countries 25-30 years ago,” Yusuf, who is a professor of medicine at McMaster University in Canada, said.

“But heart disease is now increasingly striking people in developing countries. Eighty percent of heart disease today is in low- to middle-income countries” partly because more people around the world are eating western diets, he said.

“This study indicates that the same relationships that are observed in western countries exist in different regions of the world,” said Yusuf, who is also head of the Population Health Research Institute at Hamilton Health Sciences in Ontario.

The main countries in the study were Argentina, Brazil, Chile and Colombia in South America; Canada and US in North America; Sweden in western Europe; and Egypt, Iran and Kuwait for the Middle East. Nearly all of South Asia — India, Pakistan, Bangladesh, Nepal and Sri Lanka — took part.

Sources: The Times Of India

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The Unfolding Mystery of Scleroderma

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Scleroderma, an autoimmune disease, tends to afflict middle-age women and can affect many parts of the body, inside and out.

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Lung disease, the biggest killer of scleroderma patients, is the main focus of research today..

Doctors have a growing arsenal of proven and potential treatments, some of which are risky and the subjects of current research, including stem cell transplants and powerful but toxic cancer drugs.

Like many autoimmune ailments, scleroderma remains a great unknown. Despite decades of research, the cause of this rare and complicated disease has yet to be discovered. But the good news is that doctors have a pretty clear understanding of how scleroderma progresses — a natural history, they call it — and are better than ever at extending and easing their patients’ lives.

“Lots of patients and lots of doctors used to consider it a ‘black box’ disease, a complete mystery, with little that could be done,” said Dr. Philip J. Clements of the University of California, Los Angeles, who is a scleroderma specialist. “Now there’s a body of evidence that tells us what to watch out for, and when.”

Experts now know, for example, that the gradual hardening of tissues and blood vessels that is a hallmark of scleroderma usually starts on the hands and face, with skin thickening, pitted scars and cool, pale fingertips among the earliest symptoms. Damage can then progress inward to internal organs, though the course varies widely from patient to patient. Of the 10,000 cases diagnosed among Americans each year, mainly women, a small subset will die quickly. But many others are able to manage their condition with a variety of treatments and have normal life expectancies.

Doctors also now know that if a patient’s internal organs are going to be affected as well as the skin, that is likely to happen in the first four or five years of the disease. So early diagnosis and close monitoring of the heart, lungs and kidneys are vitally important.

They have also learned that steroids, once viewed as a cure-all for immune disorders, can worsen the effects of scleroderma, especially in the kidneys, and should be used with caution.

“Learning which drugs to avoid was itself a big step,” said Dr. John Varga, the Gallagher Professor of Medicine at Northwestern University and chairman of the Medical Advisory Board for the Scleroderma Foundation, a nonprofit group that sponsors research and support for patients and families.

Kidney disease used to cause 90 percent of scleroderma-related deaths until the advent of a class of blood pressure drugs called angiotensin-converting enzyme, or ACE, inhibitors in the 1980s. ACE inhibitors prevent kidney damage by slowing down the chemicals that cause the muscles surrounding blood vessels to contract. Complications in the kidneys now account for only 14 percent of scleroderma deaths, Dr. Steen said.

The lungs are still a challenge. About 80 percent of scleroderma patients develop some form of lung problem — either pulmonary hypertension, due to hardening of the veins and arteries in the lung, or pulmonary fibrosis, in which the lung tissue becomes inflamed and then thickened with scarring. Some patients develop both. Either way, breathing becomes more difficult as the lungs become less pliable.

“If you die of a scleroderma-related problem, half of those deaths are from lung disease,” said Dr. Virginia Steen, a professor at Georgetown University and director of the Rheumatology Fellowship Program there. She wrote a seminal 2007 article that documented the shift from kidney disease to pulmonary disease as the biggest cause of death among scleroderma patients.

One successful remedy called Revatio, routinely prescribed since 2005, came from an unexpected source: Viagra. Repackaged from a little blue diamond to a round white tablet and renamed for marketing, dosage and insurance purposes, the drug works by relaxing the blood vessels and improving blood flow, whether for erectile or lung dysfunction.

“No one could understand why all these women were taking it four times a day,” said Frannie Waldron, chief executive of the Scleroderma Foundation.

Doctors also have a growing arsenal of experimental treatments and potential cures, some of which are risky.

Among them is cyclophosphamide, or Cytoxan, a powerful but highly toxic cancer drug that acts on the immune system. The drug decreases the inflammation that causes pulmonary fibrosis and has been used on scleroderma patients for the last 10 years.

But cytoxan has dangerous side effects, including an increased risk of bladder cancer, and usually is not given for more than a year. Moreover, the fibrosis seems to start again once drug treatments stop. Several studies involving the medication are under way, as well as efforts to find alternative treatments, many of them sponsored by drug companies.

Another big push involves stem cell transplant, an extremely risky process in which doctors try to reset the patient’s immune system and bypass the glitch that causes scleroderma. The procedure is the subject of a National Institutes of Health study called the SCOT trial, for Scleroderma: Cyclophosphamides or Transplantation?

Similar to a bone marrow transplant, doctors first draw the patient’s blood and extract the stem cells, the highly malleable building blocks that are thought to be free of the seeds of scleroderma. The patient is then subjected to high doses of radiation or chemotherapy with Cytoxan to kill the bone marrow. The last step is to reinfuse the stem cells, in the hopes that they replicate themselves in a healthy form free of disease.

The study will compare the benefits of the stem cell transplant with giving patients just monthly doses, but high ones, of Cytoxan. Preliminary results have been promising, several experts said.

“You’d think you’d have trouble recruiting for this,” said Dr. Arthur C. Theodore of Boston University, one of the investigators in the project. “But scleroderma patients are desperate.”

Sources: The New York Times

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Six Tribes of Bacteria Live in Your Inner Elbow

The crook of your elbow is a special ecosystem that provides a bountiful home to six tribes of bacteria. Even after you wash, there are still 1 million bacteria living on every square centimeter.

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These bacteria are what biologists call commensals, helpful rather than harmful organisms. They moisturize your skin by processing the raw fats that it produces.

The bacteria were discovered as part of the human microbiome project, a study researching all of the various microbes that live in people. The project is in its early stages, but has already established that the bacteria in the human microbiome collectively possess at least 100 times as many genes as the 20,000 or so in the human genome.

The bacterial cells also outnumber human cells by 10 to 1.

Humans depend on their microbiome for essential functions, including digestion, leading microbiologists to conclude that a person should really be considered a superorganism.

You may click to see :->The multitudinous world inside your elbow

Sources:

* New York Times May 23, 2008

* Genome Research May 23, 2008

* Science May 22, 2008

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The Long and Short of it


 

Scientists have discovered genes that influence height but are yet to explain the gap between the tallest and shortest of people:

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A meeting between two ordinary men in a remote locale in Mongolia hit the headlines all over the world in July last year. But neither Bao Xishun, 56, nor He Pingping, 19, holds a position of eminence. Nor are they film or sports celebrities. The encounter grabbed world attention because of the two men’s contrasting statures. While Xishun, at 2.36m, is the world’s tallest living man, the 74-cm Pingping claims he is the shortest.

Modern science may not be able to explain the yawning gap between the heights of these two men — both hailing from Inner Mongolia — but it has gained some genetic insight into the varying stature of billions of others who fall between Xishun and Pingping in terms of height.

For nearly a century, scientists have believed that genes handed down from parents are responsible for 90 per cent of the normal variation in human height in a population. And it is not just one gene but probably a few hundred that contribute towards making a person tall or short. But until last year, scientists were clueless about their location on the human genome, which consists of more than 3 billion DNA base pairs.

In September 2007, researchers from both sides of the Atlantic, while foraging through DNA from 35,000 people, stumbled upon a difference in a gene called HMGA2, which plays a decisive role in making people taller or shorter, albeit marginally. They found that if a person had two copies of a longer variant of HMGA2, he or she would be 1cm taller than one who has two shorter versions of it.

The HMGA2 gene thus became the first reliable genetic link to human height. Later, scientists zeroed in on yet another gene, GDF5, which makes for an average height difference of 0.4cm.

What made the discovery of such genes possible is what scientists call genome-wide association studies. This is a relatively new way of identifying genes involved in human diseases. Made possible by advances in genetics and sophistication in scientific tools, this method searches the genome for small variations, called single nucleotide polymorphisms (SNPs). The tools are so advanced that researchers can search for hundreds or thousands of SNPs simultaneously. Such studies pinpoint genes that may contribute to a person’s risk of developing a certain disease or those associated with a trait such as height or eye colour.

If 2007 saw a beginning in understanding the role played by genes in deciding how tall a person will be, 2008 has so far proved to be a watershed. The same consortium of scientists who discovered the HMGA2 and GDF5 genes, now split into two groups, recently discovered 40 more genetic locations. Combined, they may be able to explain a height difference of up to 6cm, or 5 per cent of the population variation in height.

The number and variety of genetic regions discovered so far show that height is determined not just by a few genes operating in the long bones, notes Thomas Frayling of Peninsula Medical School in the UK. Frayling is the lead author of the one of the two studies that appeared in Nature Genetics last month.

Joel Hirschhorn, a paediatric endocrinologist at Broad Institute in the US, who led the other study, says that the new findings account for only a small fraction of the variation in height among people and that there is a lot more to discover. “This is much more than we had even last year. But we are not close to predicting adult height,” Hirschhorn told Knowhow.

The study of genes involved in determining adult height stems from more than sheer curiosity. By identifying which genes affect normal growth, it is easy to understand the processes that lead to abnormal growth, the scientists say. “There appears to be a definite correlation between height and some diseases,” says Michael Weedon, a colleague of Frayling. Weedon was not only part of the original team that discovered the HMGA2 gene but was also instrumental in the latest discovery of 20 new genetic locations linked to height. For instance, there is a strong association between shortness and a slightly increased risk of conditions such as heart disease. Similarly, tall people are more prone to certain cancers and, possibly, osteoporosis.

A predominant factor that determines one’s height may be heredity, but diet too has a role to play. In fact, improved nutrition means that each generation gets successively taller, as has been shown by a recent study on Indians.

That said, Indians still have some catching up to do: an average Indian man (165.3cm) is two centimetres shorter than an average Czech woman who stands 167.3cm tall.

Sources: The Telegraph (Kolkata, India)

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