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Editorial Calls Supreme Court's Pregnancy Leave Decision 'Not Just'
"The Supreme Court keeps finding ways to deny women equal pay and benefits," a New York Times editorial states in response to the court"s 7-2 ruling on Monday that employers are not required to award women credit toward pension benefits for pregnancy leave taken before Congress passed the 1978 Pregnancy Discrimination Act. According to the Times, the ruling reflects reasoning similar to the court"s 2007 decision in which it denied former Goodyear employee Lilly Ledbetter"s "claim for equal pay because it thought she waited too long to file it." In Monday"s decision, the majority "reasoned mainly that the pregnancy leaves predated the 1978 law, and since the law was not retroactive, the discrepancy in benefits was the product of "past completed events that were entirely lawful at the time they occurred,"" the editorial states. It notes that the majority included "two generally reliable votes for equality, Justices John Paul Stevens and David Souter." The editorial continues, "This may sound logical, but it is not just." The editorial says that Justice Ruth Bader Ginsburg, in writing the dissent, "quite correctly" recognized a company"s "ongoing denial of equal benefits not as past discriminatory behavior that started and ended decades ago, but as a current violation of the act." In a similar way, "Goodyear discriminated against Lilly Ledbetter by maintaining her unequal pay for years, not merely the first time the company underpaid her." The Times calls on Congress to "write corrective legislation" on pregnancy leave (New York Times, 5/21).

Green Tea Chemical Shows Potential As Low-Cost Intervention Against Sexual HIV Transmission, Study Says
A chemical found in green tea might be an effective tool against the sexual transmission of HIV, according to a study conducted by researchers at the University of Heidelberg in Germany and published online in the Proceedings of the National Academy of Sciences, AFP/Google.com reports. According to the study, green tea polyphenol -- called epigallocatechin-3-gallete, or EGCG -- neutralizes a protein in sperm that aids in the transmission of HIV during sex. The researchers noted that they "recently identified a peptide fraction in human semen that consistently enhanced HIV-1 infection." The study found that EGCG is able to neutralize the sperm protein, known as a semen-derived enhancer of virus infection, or SEVI. The researchers said that SEVI is "an important infectivity factor of HIV." According to the researchers, EGCG "appears to be a promising supplement to antiretroviral microbicides to reduce sexual transmission of HIV-1." The researchers said that because a majority of people living with HIV contract the disease through heterosexual transmission and that 96% of new cases are reported in developing and impoverished nations, the use of green tea in topical creams could be a "simple and affordable prevention method" (AFP/Google.com, 5/19).
News of the day
Genomes Of Parasitic Flatworms Decoded
Two international research teams have determined the complete genetic sequences of two species of parasitic flatworms that cause schistosomiasis, a debilitating condition also known as snail fever. Schistosoma mansoni and Schistosoma japonicum are the first sequenced genomes of any organism in the large group called Lophotrochozoa, which includes other free-living and parasitic flatworms as well as segmented roundworms, such as the earthworm.
Mental Health

Scientists Out A Gene For Gout

Having partnered last year with an international team that surveyed the genomes of 12,000 individuals to find a genetic cause for gout, Johns Hopkins scientists now have shown that the malfunctioning gene they helped uncover can lead to high concentrations of blood urate that forms crystals in joint tissue, causing inflammation and pain the hallmark of this disease. The ABCG2 gene, they found, makes a protein that normally transports urate out of the kidney and into urine before the waste product does any harm. In studies using frog egg cells genetically engineered with human DNA, the Hopkins researchers established the role of the ABCG2 gene as a cause of gout, lending credence to suspicions that metabolic deficiencies, in addition to too much rich food and alcohol, are mostly to blame for this painful type of arthritis that affects 3 million Americans. The gene, they believe, may be responsible for some 10 percent of gout in Caucasians. A report on the research, funded by the National Institutes of Health, was published June 8 in the online Early Edition PNAS. The research began with a "genome-wide association study" that involved participants of the Artherosclerosis Risk in Communities Study, originally initiated two decades ago to examine the roots of heart disease. Over the course of that research, blood was collected from the study participants and analyzed for a variety of chemical elements, including uric acid. Subjects also reported whether they had ever been diagnosed with gout, enabling researchers to link information from DNA, uric acid levels and gout. By analyzing associations between blood uric acid levels and genotypes, the researchers identified the gene known as ABCG2 and specifically a certain mutation as a candidate for causing the joint inflammation and pain that are symptoms of gout. Because animal models for gout are not representative of humans all mammals except for higher primates have an enzyme that efficiently breaks down uric acid the researchers turned to genetic engineering to figure out just how the human ABCG2 gene might work to regulate uric acid levels, and how its mutation may lead to gout. First, the team injected both normal and the mutant versions of the human ABCG2 gene into frog eggs which served as the live "factories" for producing the protein made by the gene. A couple of days later, after the egg cells produced lots of ABCG2 protein, the researchers bathed them in a radioactive-tagged uric acid bath. Using the tag to identify and measure how much urate accumulated in the cells, the investigators then measured how quickly the urate left the cell. Comparing these so-called "efflux rates" to rates in control cells injected with the normal ABCG2, the scientists found that the cells with the mutant ABCG2 protein excreted uric acid at a rate just half of normal. "We were able to show for what we believe is the first time that the ABCG2 protein is vital for transporting urate out of cells,"says Owen Woodward, Ph.D., a postdoctoral fellow in physiology in the Johns Hopkins University School of Medicine. The researchers further showed that the ABCG2 protein is located in the kidney at a location where urate exretion takes place. They suggest that a lack of efficiency in removing urate from the blood leads to its increased concentration and crystallization. In humans, these crystals get caught in joint tissues, leading to painful inflammation. "As the first major gene identified to cause gout, we believe that ABCG2 also represents an attractive new drug target," says Michael Kottgen, M.D., a biological chemistry research associate in the Johns Hopkins University School of Medicine. One strategy is to identify a drug that makes excretion faster and more efficient by activating the "urate transporter" protein. "Instead of trying to limit urate production the major current approach to gout treatment newer treatments could focus on getting urate out of the bloodstream," Kottgen says. "We anticipate that activation of ABCG2 with a drug may help to promote excretion of urate." "It"s exciting that a finding from genome-wide association studies has been directly translated into better understanding physiology and perhaps will help us find better clinical therapies", says Anna Kottgen, M.D., M.P.H., an epidemiologist in the Johns Hopkins University Bloomberg School of Public Health. Authors of the paper, in addition to Michael Kottgen, Owen Woodward and Anna Kottgen are Josef Coresh and William Guggino, also of Johns Hopkins University, and Eric Boerwinkle of the University of Texas. Johns Hopkins Medicine


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