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WASHINGTON, July 15 (Xinhua) -- Researchers at Mount Sinai School of Medicine have found that grape seed polyphenols -- a natural antioxidant -- may help prevent the development or delay the progression of Alzheimer's disease.The research, led by Giulio Pasinetti, was published online Friday in the Journal of Alzheimer's Disease, which causes brain changes that gradually get worse.This is the first study to evaluate the ability of grape- derived polyphenols to prevent the generation of a specific form of amyloid (A) peptide, a substance in the brain long known to cause the neurotoxicity associated with Alzheimer's disease.In partnership with a team at the University of Minnesota, Pasinetti and collaborators administered grape seed polyphenolic extracts to mice genetically determined to develop memory deficits and A neurotoxins similar to those found in Alzheimer's disease. They found that the brain content of the A*56, a specific form of A previously implicated in the promotion of Alzheimer's disease memory loss, was substantially reduced after treatment.Previous studies suggest that increased consumption of grape- derived polyphenols, whose content, for example, is very high in red wine, may protect against cognitive decline in Alzheimer's. This new finding corroborates those theories."Since naturally occurring polyphenols are also generally commercially available as nutritional supplements and have negligible adverse events even after prolonged periods of treatment, this new finding holds significant promise as a preventive method or treatment, and is being tested in translational studies in Alzheimer's disease patients," said Pasinetti.In Alzheimer's disease, brain cells degenerate and die, causing a steady decline in memory and mental function.

BEIJING, Aug. 3 (Xinhuanet) -- The first man in Britain who received a complete plastic heart is allowed to leave hospital and live a relatively normal life at home.Matthew Green, 40, who was dying from arrhythmogenic right ventricular cardiomyopathy, was awaiting a transplant when his condition became so bad that the doctors at Papworth Hospital, the world renowned heart center near Cambridge, decided to give him Britain’s first ever full artificial heart.During a six-hour operation on June 9, 2011, surgeons replaced Mr Green's damaged heart with the device which will serve the role of muscles and ventricles.Unlike previous artificial hearts, they have usually only replaced parts of the organ, the new one is powered by a pump which sits outside the body and can be held in a backpack or shoulder bag.All Mr Green has to do is replace the batteries in the pump every few hours and the heart should last up to three years.Transplant milestones1964 US National Institutes of Health starts artificial heart programme.1966 First transplant of partial mechanical heart, to assist pumping of ventricle.1969 Texas man receives first total artificial heart transplant. After 64 hours on the mechanical device received a donor organ, but died within two days.1982 Artificial heart designed by Utah University doctor Robert Jarvik implanted into man who survived for 112 days.2001 First surgical implant of internally powered artificial heart, which was charged via transduction through skin.

CANBERRA, June 10 (Xinhua) -- Going to work when you are feeling sick can make you sicker in the long run, an expert told Australia's media on Friday.New Zealand sociologist Professor Kevin Dew from the Victoria University in Wellington, has assessed more than 40 papers about " presenteeism".He defined presenteeism as: "People that are turning up at work when they feel that they should be at home sick.""People feel compelled to go to work because someone else would have to take up the workload (and they have a) feeling of responsibility for not being able to care properly for patients (if they don't show up)," he told the Australia Associated Press on Friday.He said that evidence suggested people who go to work when they are sick can have long term negative effects on health and productivity.Evidence shows that presenteeism increases illness, including musculoskeletal pain, fatigue, depression, and serious coronary events. It also leads to exhaustion which, in turn, leads to more presenteeism.Prof. Dew said certain medical conditions like depression and migraine are also linked with presenteeism because they are not seen as legitimate reasons for absence.He has written an editorial in the latest issue of the British Medical Journal about his findings.

SAN FRANCISCO, Aug. 9 (Xinhua) -- Nokia is planning to stop selling its low-end phones and smartphones in the United States, instead focusing on products using Microsoft's Windows Phone platform, U.S. media reported on Tuesday.The Finnish handset maker will end sales of its low-end Series 40 phones and smartphones based on the Symbian mobile operating system in the United States and Canada, as it needs to put all of its efforts into the Windows Phone products which are due out later this year, Chris Weber, head of Nokia's U.S. subsidiary, told technology news site All Things Digital."When we launch Windows Phones we will essentially be out of the Symbian business, the S40 business, etc.," Weber said.Staff members speak to trade visitors at the Nokia booth at the CommunicAsia expo in Singapore June 21, 2011.In February, Nokia and Microsoft announced plans to form a broad strategic partnership, under which Nokia agrees to adopt Windows Phone as its principal smartphone strategy.North America is a priority for Nokia, Weber noted, in part because it is a key market for Microsoft and also because Nokia sees it as a key to winning in the smartphone battle globally."We'll develop for North America and make the phones globally available and applicable," Weber said.In another development, technology blog Engadget and other U.S. media on Tuesday reported that Nokia will not bring N9, its first smartphone running the Linux-based mobile operating system MeeGo, to the U.S. market."After the very positive reception to the launch of the Nokia N9, the product is now being rolled out in countries around the world. At this time we will not be making it available in the U.S., " Nokia said in a statement.

WASHINGTON, Aug. 2 (Xinhua) -- The weakness of aging is associated with leaky calcium channels inside muscle cells and a drug already in Phase II clinical trials for the treatment of heart failure might plug those leaks, according to a report published Tuesday in the online edition of Cell Metabolism.Earlier studies by the research team led by Andrew Marks of Columbia University showed the same leaks underlie the weakness and fatigue that come with heart failure and Duchenne muscular dystrophy."It's interesting, normal people essentially acquire a form of muscular dystrophy with age," Marks said. "The basis for muscle weakness is the same." Extreme exercise like that done by marathon runners also springs the same sort of leaks, he added, but in that case damaged muscles return to normal after a few days of rest. A microscopic view shows smooth muscle cells derived from human embryonic stem cells showing the nuclei (blue) and proteins of the cytoskeleton (green) in this handout photo released to Reuters by the California Institute for Regenerative Medicine, March 9, 2009The leaks occur in a calcium release channel called ryanodine receptor 1 (RyR1) that is required for muscles to contract. Under conditions of stress, those channels are chemically modified and lose a stabilizing subunit known as calstabin1.Calcium inside of muscle cells is usually kept contained. When it is allowed to leak out into the cell that calcium itself is toxic, turning on an enzyme that chews up muscle cells. Once the leak starts, it's a vicious cycle. The calcium leak raises levels of damaging reactive oxygen species, which oxidize RyR1 and worsen the leak.The researchers made their discovery by studying the skeletal muscles of young and old mice. They also showed that 6-month-old mice carrying a mutation that made their RyR1 channels leaky showed the same muscular defects and weakness characteristic of older mice.When older mice were treated with a drug known as S107, the calcium leak in their muscles slowed and the animals voluntarily showed about a 50 percent increase in the amount of time spent wheel running. Now in clinical trials for patients with heart failure, the drug is known to work by restoring the connection between costabilin and RyR1.Despite considerable effort to understand and reverse age- related muscle wasting, there are no established treatments available. The new work suggests there may be hope in approaching the problem from a different angle."Most research has focused on making more muscle mass," Marks said. "What's different here is that we are focused not on muscle mass but on muscle function. More muscle doesn't help if it is not functional."