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| Longer sleep linked with lower risk of heart disease factor |
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Sunday, November 08, 2009
Participants who slept an hour longer than others had a lower incidence of coronary artery calcification, linked with future heart disease.
Risk factors for coronary artery calcification (calcified plaques visible by computed tomography) include established heart disease risk factors like male sex, older age, glucose intolerance, tobacco use, high cholesterol levels and BP, obesity, raised inflammatory markers and the like.
Recent data suggest that sleep quantity and quality are connected to several of these risk factors. “However, some of these correlations have only been documented in studies in which sleep is measured by self-report, which may be biased or insufficiently accurate,” the authors write.
Christopher Ryan King, of the University of Chicago (UC) and colleagues tested whether objectively measured sleep duration predicted the development of calcification over five-years of follow-up.
The study included 495 participants from the Coronary Artery Risk Development in Young Adults (CARDIA) study, who were black and white men and women age 35-47 years.
At the start of the study in 2000-2001, the participants had no evidence of detectable coronary calcification on computed tomography scans. The incidence of calcification at five years was 12.3 percent. After adjusting for age, sex, race, education, smoking and apnea risk, the researchers found that one hour more of sleep per night decreased the estimated odds of calcification by 33 percent.
“We have found a robust and novel association between objectively measured sleep duration and 5-year incidence of coronary artery calcification,” the authors write.
“This study further demonstrates the utility of a simple objective measure of sleep that can be used at home. Future studies will be needed for crucial extensions to these results, said an UC release.
Cancer drug effectively treats kidney transplant rejections: Researchers have discovered that a cancer drug can effectively treat organ rejection.
Steve Woodle of University of Cincinnati (U-C) and colleagues found that the drug bortezomib, used to treat cancer of plasma cells, is effective in treating rejection episodes caused by antibodies that target transplanted kidneys and reversing rejection episodes that did not respond to standard therapies.
B-lymphocytes, or B cells, play a large role in human immune response by making immune proteins that attack transplanted organs.
“We found a body of literature demonstrating that bortezomib works well in suppressing transplant rejection in the laboratory,” said Woodle, co-author of the study and chief of transplant surgery at UC. “Moreover, it worked well in models of autoimmune diseases.”
T-lymphocytes, or T cells, are white blood cells that were commonly thought to cause the rejection of transplanted organs. Woodle and his team began searching for agents that targeted plasma cells in 2005.
“It has become clear that plasma cells and the antibodies they produce play a bigger role in rejection than previously thought, and the development of therapies targeting these cells has lagged,” he said.
“We realised that current therapies don’t target the plasma cells which may produce the antibody, in general.”
Researchers administered this drug to six kidney transplant recipients with treatment-resistant organ rejection, evaluating and recording their responses to the treatment, said a UC release.
In each case, treatment with the drug provided prompt rejection reversal, prolonged reductions in antibody levels and improved organ function with suppression of recurrent rejection for at least five months.
Jason Everly, a board-certified oncology pharmacist in the division of transplant surgery at UC and co-author of the study, says the toxicities associated with this drug were predictable and manageable and were much less than those associated with other anti-cancer agents.
UC researchers are currently conducting four industry-supported clinical trials to expand these findings.
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ISSN 1563-9479 
