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Obesity Heart Risk Underestimated: Study

December 24, 2009 By

obesity heart risk_The risk of dying from heart disease because of excess weight may be higher than thought. A study published in Wednesday’s issue of the British Medical Journal measured body mass index (BMI) and mortality among more than one million pairs of Swedish sons and their parents over 50 years.

The team from Bristol University and the Karolinska Institute in Sweden focused on offspring because the BMI of parents could be linked to illnesses they suffer rather than the extra weight itself.

The researchers found strong links between offspring BMI and parental mortality. For example, the risk of coronary heart disease for mothers increased by 1.15 times and 1.10 times for fathers depending on offspring BMI.

The link to heart-related deaths was much stronger than suggested by previous studies.

Using the father’s BMI measurements alone, the risk of heart deaths increased by 45 per cent for every three-point increase in BMI level. But using a measurement based on the child’s BMI, the risk increased by 82 per cent.

Unlike other studies of BMI in adults, the British and Swedish researchers found no link between a son’s low BMI and an increased risk of respiratory disease and lung disease for fathers.

There was a positive link between a mother’s risk of respiratory disease mortality and her son’s BMI, which the researchers said presumably reflects maternal smoking.

“These data suggest that the adverse influence of higher BMI and obesity in a population is of greater magnitude than previously thought,” George Davey Smith, a professor of clinical epidemiology at the University of Bristol and his colleagues concluded.

The findings also imply that programs to tackle obesity could offer major health benefits, they added.

Researchers have said that waist-to-hip ratio measurements are a better way of predicting obesity-related deaths than the standard BMI, since the distribution of fat also affects the risk of premature death. CBC News

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Testicular Cancer Found

July 1, 2009 By

testicular_cancer_foundScientists at the National Institutes of Health claim to have identified the second gene that can increase a man’s risk of familial, or inherited, testicular germ-cell cancer. Men with a family member who had a testicular germ cell cancer are at three-to six-fold greater risk than other men of developing testicular cancer. Although a family history of testicular cancer probably accounts for less than five percent of all testicular cancers, the careful study of rare familial cancer clusters has often led to important new understanding of the non-familial versions of the same cancer. “This study contributes to our understanding of why testicular germ cell cancer appears to run in families,” said Dr Raynard Kington, Acting NIH Director. “The findings may also lead to new ways to identify men at high risk, as well as more effective ways to prevent and treat testicular germ cell cancer,” Kington added.

According to researchers, the key pathway in this disease is the cyclic AMP pathway, which regulates how cells respond to such signals as hormones. Drugs that affect the cyclic AMP pathway are widely available, and, in theory, could affect progression of testicular cancer. The researchers found that seven different mutations in the gene in question, PDE11A, created abnormal versions of the PDE11A enzyme that slowed down the enzyme’s destruction of cyclic AMP. “The mutations don’t cause cancer directly, but instead appear to increase an individual’s susceptibility to developing a tumour,” said the study’s senior author, Dr Constantine Stratakis, D.Sc., chief of NICHD’s Section on Endocrinology and Genetics. “Almost one out of every five families we studied had a variation in the gene that affected its functioning,” Stratakis added.

Stratakis and his colleagues analyzed the portion of the DNA from 95 familial testicular cancer patients that contains the PDE11A gene. They found seven mutations in the cancer patients, and noted that the rate at which they were detected was much higher than that seen in the DNA of people without testicular cancer. Stratakis said that learning how disruptions in the PDE11A enzyme lead to an increased risk of tumor formation may help researchers identify other proteins that also play a role. The study appears in the Cancer Research.

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Transplant Of Pig Organs Into Humans

June 10, 2009 By

transplant_The prospect of using genetically modified pig organs to cut transplant waiting lists has moved forward with the creation of the first versatile pig stem cells. Scientists in China have successfully reprogrammed pig skin and bone marrow cells into an embryo-like state with the potential to form every type of body tissue. The achievement promises to provide a tool for breeding pigs that are genetically engineered to carry human immune system proteins so that their organs are less likely to be rejected for transplant. It also raises the possibility of modifying pigs to resist infections such as swine flu, and to grow pig tissues and organs as models for human diseases.

Lei Xiao, of the Shanghai Institute of Biochemistry and Cell Biology, who led the research, said: “Pig pluripotent stem cells would be useful in a number of ways, such as precisely engineering transgenic animals for organ transplantation therapies. The pig species is significantly similar to humans in its form and function, and the organ dimensions are similar to human organs. We could use embryonic stem cells or induced stem cells to modify the immune-related genes in the pig to make the pig organ compatible to the human immune system. Then we could use these pigs as organ donors to provide organs for patients that won’t trigger an adverse reaction from the patient’s own immune system.”

Several other important safety barriers remain before pig organs can be transplanted into human beings. Scientists remain concerned, for example, about exposing people to pig viruses. While embryonic stem cells have been derived from many animals, including human beings, attempts to culture these master cells from pig embryos have previously failed. In the research, published in the Journal of Molecular Cell Biology , the scientists have produced embryo-like stem cells by modifying several genes in adult tissue. The resulting induced pluripotent stem cells, or IPS cells, have similar properties to embryonic stem cells.

This would be useful to science because embryonic stem cells are important tools in genetic engineering. The main method of producing GM animals is to alter the DNA of embryonic stem cells and then add these to an embryo. The resulting animal will be a chimera containing some modified and some normal cells. If two chimeras breed with one another, some of their offspring will contain only the modified cells. Chris Mason, Professor of Regenerative Medicine at University College London, said that the research could have medical applications within ten years. “This potentially reinvigorates the quest to grow humanised pig organs such as pancreases for diabetics and kidneys for chronic renal failure,” he said.

“The clinical use of humanised porcine tissues and organs [xenografts] has moved a long way forward in recent months with successful small-scale clinical trials for the treatment of diabetes by Living Cell Technology in Australia. While the xenograft approach may not necessarily be the long-term solution, it may represent a step change in the treatment of organ failure, which could deliver real benefit to millions of patients within a decade.”

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