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BEIJING, Sept. 8 (Xinhuanet) -- Middle-aged white women drinking alcohol moderately are more likely to stay healthy than nondrinkers, according to a new study from Harvard.The study has followed about 14,000 mostly white women since 1976.As a result, compared with teetotalers, those who had 3 to 15 alcoholic drinks weekly in their late 50s were 28 percent higher of being free from physical disability, chronic illness, mental health problems, and cognitive decline at the age of 70.Even having just one or two drinks per week increased a woman's odds of good health by 11 percent.However, women should be aware that even moderate drinking has been linked to an increased risk of breast cancer, said Qi Sun, M.D., a lead author of the study and a nutrition researcher at the Harvard School of Public Health.These findings don't necessarily apply to men or to nonwhite women. But they reinforced the evidence for the health benefits of moderate drinking.

BEIJING, Sept. 1 (Xinhua) -- Medicine prices at public clinics have been notably reduced thanks to a policy that promotes basic medicine, an office of the State Council said Thursday.Current price levels of basic medicine used by government-funded township hospitals and community clinics have been reduced an average of 25 percent from the levels two years ago when the policy started, according to a statement from the State Council office in charge of reforming the country's healthcare program.China has introduced a state list of basic medicine used by government-funded township hospitals and community clinics, which includes roughly 300 types of commonly-used Western and traditional Chinese medicine.Provincial governments will purchase basic medicine through public bidding and distribute them to local clinics.These clinics must not raise the prices of listed medicine and in return, the government will provide them with subsidies.The policy has been implemented at all township and community clinics in all the 31 provinces, municipalities and autonomous regions in the Chinese mainland, the statement said. 

WASHINGTON, Sept. 12 (Xinhua) -- An enzyme that appears to play a role in controlling the brain's response to nicotine and alcohol in mice might be a promising target for a drug that simultaneously would treat nicotine addiction and alcohol abuse in people, U.S. researchers find.Over the course of four weeks, mice genetically engineered to lack the gene for protein kinase C (PKC) epsilon consumed less of a nicotine-containing water solution than normal mice, and were less likely to return to a chamber in which they had been given nicotine. In contrast, normal mice steadily increased their consumption of nicotine solution while the mice lacking PKC epsilon did not.The study conducted by researchers at the Ernest Gallo Clinic and Research Center, affiliated with the University of California, San Francisco, appeared Monday in the online edition of the Proceedings of the National Academy of Sciences.In normal mice, as in humans, nicotine binds to a certain class of nicotinic receptors located on dopamine neurons, which causes dopamine to be released in the brain. Dopamine creates a feeling of enjoyment, and thus prompts a sense of reward. Researchers found that mice lacking PKC epsilon are deficient in these nicotinic receptors.The finding complements earlier research in which researchers found that mice genetically engineered to lack the PKC epsilon enzyme drank less alcohol than normal mice and were disinclined to return to a chamber in which they had been given alcohol."This could mean that these mice might not get the same sense of reward from nicotine or alcohol," said Gallo senior associate director and investigator Robert Messing. "The enzyme looks like it regulates the part of the reward system that involves these nicotinic receptors."The reward system is a complex of areas in the brain that affect craving for nicotine, alcohol and other addictive substances.The next step in the research, said Messing, would be to develop compounds that inhibit PKC epsilon. The ultimate goal, he added, would be medications that could be used "to take the edge off of addiction by helping people get over some of their reward craving."

WASHINGTON, July 15 (Xinhua) -- Coastal communities along the U. S. East Coast may be at risk to higher sea levels accompanied by more destructive storm surges in future El Nino years, according to a new study published Friday by the U.S. National Oceanic and Atmospheric Administration (NOAA).The study was prompted by an unusual number of destructive storm surges along the East Coast during the 2009-2010 El Nino winter.The study, led by Bill Sweet, from NOAA's Center for Operational Oceanographic Products and Services, examined water levels and storm surge events during the "cool season" of October to April for the past five decades at four sites representative of much of the East Coast: Boston, Atlantic City, Norfolk and Charleston.From 1961 to 2010, it was found that in strong El Nino years, these coastal areas experienced nearly three times the average number of storm surge events (defined as those of one foot or greater). The research also found that waters in those areas saw a third-of-a-foot elevation in mean sea level above predicted conditions."High-water events are already a concern for coastal communities. Studies like this may better prepare local officials who plan for or respond to conditions that may impact their communities," said Sweet. "For instance, city planners may consider reinforcing the primary dunes to mitigate for erosion at their beaches and protecting vulnerable structures like city docks by October during a strong El Nino year."El Nino conditions are characterized by unusually warm ocean temperatures in the Equatorial Pacific that normally peak during the Northern Hemisphere "cool season." They occur every three to five years with stronger events generally occurring every 10-15 years. El Nino conditions have important consequences for global weather patterns, and within the U.S., often cause wetter-than- average conditions and cooler-than-normal temperatures across much of the South.

WASHINGTON, June 16 (Xinhua) -- Cells in the human body are constantly being exposed to stress from environmental chemicals or errors in routine cellular processes. While stress can cause damage, it can also provide the stimulus for undoing the damage. New research by a team of scientists at the University of Rochester has unveiled an important new mechanism that allows cells to recognize when they are under stress and prime the DNA repair machinery to respond to the threat of damage.Their findings will be published Friday in journal Science. Cells in the human body are constantly being exposed to stress from environmental chemicals or errors in routine cellular processes. While stress can cause damage, it can also provide the stimulus for undoing the damage.The scientists, led by biologists Vera Gorbunova and Andrei Seluanov, focused on the most dangerous type of DNA damage -- double strand breaks. Unrepaired, this type of damage can lead to premature aging and cancer. They studied how oxidative stress affects efficiency of DNA repair. Oxidative stress occurs when the body is unable to neutralize the highly-reactive molecules, which are typically produced during routine cellular activities.The research team found that human cells undergoing oxidative stress synthesized more of a protein called SIRT6. By increasing SIRT6 levels, cells were able to stimulate their ability to repair double strand breaks. When the cells were treated with a drug that inactivated SIRT6, DNA repair came to a halt, thus confirming the role of SIRT6 in DNA repair. Gorbunova notes that the SIRT6 protein is structurally related to another protein, SIR2, which has been shown to extend lifespan in multiple model organisms."SIRT6 also affects DNA repair when there is no oxidative stress," explains Gorbunova. "It's just that the effect is magnified when the cells are challenged with even small amounts of oxidative stress."SIRT6 allows the cells to be economical with their resources, priming the repair enzymes only when there is damage that needs to be repaired. Thus SIRT6 may be a master regulator that coordinates stress and DNA repair activities, according to Gorbunova.