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LOS ANGELES, July 18 (Xinhua) -- At least 70 genetic mutations may be involved in the formation of colon cancer, far more than scientists previously thought, a new study suggests.The study by researchers at University of Texas (UT) Southwestern Medical Center contradicts previous thinking that only a few mutated genes may play a role in the development of colon cancer."The ways we've been treating patients up to now is to just go after one target when we should be going after three to four different pathways simultaneously," said Dr. Jerry W. Shay, vice chairman and professor of cell biology at UT Southwestern.The new study identified 65 candidate genes and at least five passenger genes whose mutations play significant roles in cancer development. Inactivating the function of any of these tumor- suppressing genes led to a key step in cancer development called anchorage-independent growth, meaning cells piled up on top of each other rather than aligning neatly.According to previous studies, there were 151 candidate genes and that mutations in just eight to 15 of them would lead to cancer. There were 700 other genes classified as passenger genes whose mutations were incidental to cancer growth.Current cancer treatments target just one or two known cancer- driver genes. While patients may get transient tumor burden reduction, almost universally tumor growth returns."Those numbers are dead wrong," Dr. Shay said, suggesting a new approach to colon cancer treatments targeting multiple genes and pathways simultaneously.The next step is further research to classify more accurately which genes drive cancer and which are merely passengers, the researchers said.Study findings were published in the July 2011 Cancer Research (Priority Reports).

BERLIN, June 8 (Xinhua) -- German health minister Daniel Bahr expressed cautious hope Wednesday for an end to the wave of E. coli infections as authorities reported two more deaths and more than 300 new cases."I can't give an all-clear, but after the analysis of the latest data we have reasons for hope, as the number of new infections is continuously dropping," Bahr told local public television ARD before an emergency meeting in Berlin with European Union Health Commissioner John Dalli."Unfortunately, there will be new cases and more deaths have to be expected, but overall new infections are clearly going down," he said.On the same day, Germany's national disease control center, the Robert Koch Institute, said the number of reported cases in Germany had risen by more than 300 to 2,648. Nearly 700 of those affected have been taken to hospital with a serious complication that can cause kidney failure.The Institute did not fully support Bahr's optimism. It said there was a declining trend in new cases but added it was not clear whether this was because the outbreak was truly waning or because consumers were staying away from the raw vegetables believed to be the source of the E. coli.The German government has faced increasing criticism from abroad and at home over its dealing with the crisis. It was twice wrong in naming the source of the outbreak and it has been criticized for a lack of coordination between research institutes.Dalli was quoted by local daily Die Welt as saying, "we have to rely on the experience and expertise across Europe, and even outside Europe."The Max Planck Institute for Infection Biology in Berlin also called for a federal government representative to coordinate the various government agencies dealing with the disease to eliminate mixed messages.

BERLIN, June 1 (Xinhua) -- Germany's disease control center reported on Wednesday 365 new cases of the fatal enterohemorrhagic E. coli (EHEC), which marked a sharp rise since its outbreak in the middle of May.Twenty-five percent of the new cases involved the hemolytic- uremic syndrome (HUS), a serious complication resulting from E. coli infection that affects the blood and kidneys, Germany's Robert Koch Institute said.Until now 17 people in Europe, one in Sweden, the other in Germany have been killed by the deadly disease, while the source of the infection was still not identified.According to the data of Robert Koch Institute, at present 470 patients are suffering from HUS due to the infection, raising concerns that the death toll could be even higher in the future.Germany's Agriculture and Consumer Protection Minister Ilse Aigner defended Germany's previous alert on cucumbers from Spain on Wednesday."The fatal strain of EHEC bacteria was indeed found on Spanish cucumbers. According to the European rules, a quick warning must be sent out," she told a local TV station.Laboratory tests in Hamburg on Tuesday overthrew the previous finding that Spanish cucumbers were the sources of the outbreak.As a result of the alert, Europe and Russia imposed bans on Spanish vegetables, leaving Spanish farmers a loss of 200 million euros (287.5 million U.S. dollars) a week.Spain has expressed its intention to take possible legal actions against authorities in Hamburg and ask for compensations from Germany and the European Union.

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."

WASHINGTON, Aug. 4 (Xinhua) -- Researchers have found a way to turn mouse embryonic stem cells into sperm and this finding opens up new avenues for infertility research and treatment, according to a study published Thursday in the online edition of journal Cell,A Kyoto University team coaxed mouse embryonic stem cells into sperm precursors, called primordial germ cells (PGCs), and shown that these cells can give rise to healthy sperm. The researchers say that such in vitro reconstitution of germ cell development represents one of the most fundamental challenges in biology.When transplanted into mice that were unable to produce sperm normally, the stem cell derived PGCs produced normal-looking sperm, which were then used to successfully fertilize eggs. These fertilized eggs, when transplanted into a recipient mother, produced healthy offspring that grew into fertile male and female adult mice. The same procedure could produce fertile offspring from induced pluripotent stem cells that are often derived from adult skin cells."Continued investigations aimed at in vitro reconstitution of germ cell development, including the induction of female primordial germ cell-like cells and their descendants, will be crucial for a more comprehensive understanding of germ cell biology in general, as well as for the advancement of reproductive technology and medicine," the researchers wrote.

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