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Ethicists Debate New York State's Decision To Pay Egg Donors Who Aid Stem Cell Research
New York state"s decision last month to allow state-funded embryonic stem cell researchers to pay women for donating their eggs had drawn support from many scientists and doctors but fueled debate among some ethicists, Long Island Newsday reports. The state"s Empire State Stem Cell Board said that researchers can pay women up to $10,000 as compensation for their time and the invasive nature of the procedure.Scientists and research advocates say the decision could boost important research into cures of serious diseases while attracting investments and new jobs to the state. Opponents raise ethical concerns about using taxpayer money for research that some people find morally objectionable. Some also contend that payment might exploit low-income women, according to Newsday. The National Academy of Sciences and NIH do not permit payments to research participants beyond reimbursement.Thomas Berg -- director of the Westchester Institute for Ethics and the Human Person and a Roman Catholic priest opposed to embryonic stem cell research -- cast the sole dissenting vote in the stem cell board"s decision. Berg said the board ignored his suggestions to open the discussion to the public. However, Samuel Packer -- a member of the board and chair emeritus at the North Shore-Long Island Jewish Health System"s Department of Ophthalmology -- said the decision was made during a public meeting following a "long, lively debate." Packer said, "At some point the dissenting voice can"t stop the progress of science or anything else in society." He added, "There is a direct link between having better eggs and doing better research" (Ochs, Long Island Newsday, 7/9).
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Possible Link Between Pregnancy, The Flu And Schizophrenia
When mothers become infected with influenza during their pregnancy, it may increase the risk for schizophrenia in their offspring. Influenza is a very common virus and so there has been substantial concern about this association. A new study in the June 15th issue of Biological Psychiatry, published by Elsevier suggests that the observed association depends upon a pre-existing vulnerability in the fetus.
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New Culprit Behind Obesity's Ill Metabolic Consequences
Obesity very often leads to insulin resistance, and now researchers reporting in the July 8 issue of Cell Metabolism, a Cell Press publication, have uncovered another factor behind that ill consequence. The newly discovered culprit - a protein known as pigment epithelium-derived factor (PEDF for short) - is secreted by fat cells. They also report evidence to suggest that specifically blocking that protein"s action may reverse some of the health complications that come with obesity.
Endocrinology

Why Does Eczema Often Lead To Asthma?

Many young children who get a severe skin rash develop asthma months or years later. Doctors call the progression from eczema, or atopic dermatitis, to breathing problems the atopic march. In this week"s issue of PLoS Biology, scientists at Washington University School of Medicine in St. Louis report another step taken towards understanding the process of atopic march. Their findings show that a substance that is secreted by damaged skin can circulate through the body and trigger asthmatic symptoms in laboratory mice when exposed to eczema-causing or dermatitis-causing agents, also known as allergens . The researchers suggest that early treatment of skin rash and inhibition of the trigger substance might block asthma development in young patients with eczema. "Over the years, the clinical community has struggled to explain atopic march," says study author Raphael Kopan, Ph.D., professor of developmental biology and of dermatology. "So when we found that the skin of mice with an eczema-like condition produced a substance previously implicated in asthma, we decided to investigate further. We found that the mice also suffered from asthma-like responses to inhaled allergens, implicating the substance, called TSLP, as the link between eczema and asthma." The researchers found that cells in damaged skin can secrete TSLP (thymic stromal lymphopoietin), a compound capable of eliciting a powerful immune response. The skin is effective at secreting TSLP into the blood system, and therefore the substance is transported around the body. When it reaches the lungs, it renders them very sensitive to allergens, which is characteristic of asthma. Led by doctoral student Shadmehr (Shawn) Demehri, the researchers studied mice that had been engineered with a genetic defect in patches of their skin. In the affected areas, the typically ordered layers of skin cells were disrupted, creating a condition similar to eczema. The defective skin secreted TSLP as part of an alarm system that alerts the body that its protective barrier function has failed. Thus TSLP activates an immune response that fights invaders. Operating on the assumption that other barrier organs such as the lung will understand this alarm, the researchers tested what happened when the mice with skin defects inhaled an allergen. They found that their lungs reacted strongly - their breathing became labored and their lung tissue took on the traits that mark asthma in humans: mucous secretion, airway muscle contraction, invasion by white blood cells and conversion of lung cells from one type to another. Additional experiments showed that mice that had normal skin but were engineered to overproduce TSLP also developed the asthma-like symptoms. "We are excited because we"ve narrowed down the problem of atopic march to one molecule," Kopan says. "Now it will be important to address how to prevent defective skin from producing TSLP. If that can be done, the link between eczema and asthma could be broken." TSLP is also produced in lungs of asthma patients, and Kopan says that research in the skin could eventually lead to ways to interfere with TSLP made in the lungs and thereby ease asthma development even in cases that aren"t linked to eczema. Citation: "Skin-Derived TSLP Triggers Progression from Epidermal-Barrier Defects to Asthma." Demehri S, Morimoto M, Holtzman MJ, Kopan R (2009) PLoS÷ Biol 7(5):e1000067. doi:10.1371/journal.pbio.1000067 PLoS Biology


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