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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."

JIUQUAN, Gansu, Sept. 26 (Xinhua) -- Engineers are conducting the final preparations before launching China's first space laboratory module at the end of this week at a launch center in northwest China.The unmanned Tiangong-1 module was originally scheduled to be launched into low Earth orbit between Sept. 27 and 30. However, a weather forecast showing the arrival of a cold air mass at the Jiuquan Satellite Launch Center forced the launch to be rescheduled for Sept. 29 or 30, depending on weather and other factors."This is a significant test. We've never done such a thing before," said Lu Jinrong, the launch center's chief engineer.A full ground simulation was conducted on Sunday afternoon to ensure that the module and its Long March 2F carrier rocket are prepared for the actual launch.Cui Jijun, commander-in-chief of the launch site system and director of Jiuquan Satellite Launch Center, told Xinhua that they developed a new target spacecraft for the mission and made more than 170 technical improvements to the Long March 2F, China's manned orbital carrier rocket.Engineers have also made more than 100 updates at the launch site in order to make it compatible with the Tiangong-1, Cui added.The module will conduct docking experiments after entering orbit, which is the first step in China's space station program.Cui said the launch site has an updated computer center and command monitoring system and increased ability to adapt to changes in mission conditions, as well as the resources to handle both the launch and command duties. An integrated simulation training system for space launching has also been developed for the docking mission.The mission comes just one month after the Long March 2C rocket malfunctioned and failed to send an experimental satellite into orbit. The Tiangong-1 mission was subsequently rescheduled in order to allow engineers to sort out any problems that might occur during the launch.Cui said that engineers conducted a two-month comprehensive technical check on equipment at the launch site from March to May. The safety and reliability of all the instruments have been significantly improved."[The launch site] has the full conditions to conduct the Tiangong-1 mission," said Cui.The Tiangong-1 will remain in orbit for two years. During its mission, it will dock with China's Shenzhou-8, -9 and -10 spacecrafts.Unmanned docking procedures will be an essential step toward China achieving its goal of establishing a manned space station around 2020.

WASHINGTON, Sept. 14 (Xinhua) -- Controlling diabetes may someday involve mining stem cells from the lining of the uterus, Yale School of Medicine researchers report in a new study published Wednesday in the journal Molecular Therapy. The team treated diabetes in mice by converting cells from the uterine lining into insulin-producing cells.The endometrium or uterine lining, is a source of adult stem cells. These cells generate uterine tissue each month as part of the menstrual cycle. Like other stem cells, however, they can divide to form other kinds of cells.Led by Yale Professor Hugh Taylor, the researchers bathed endometrial stem cells in cultures containing special nutrients and growth factors. Responding to these substances, the endometrial stem cells adopted the characteristics of beta cells in the pancreas that produce insulin. Over the course of a three- week incubation process, the endometrial stem cells took on the shape of beta cells and began to make proteins typically made by beta cells. Some of these cells also produced insulin.After a meal, the body breaks food down into components like the sugar glucose, which then circulates in the blood. In response, beta cells release insulin, which allows the body's cells to take in the circulating glucose. In this study, Taylor and his team exposed the mature stem cells to glucose and found that, like typical beta cells, the cultured cells responded by producing insulin. The team then injected diabetic mice with the mature, insulin-making stem cells. The mice had few working beta cells and very high levels of blood glucose.Mice that did not receive the stem cell therapy continued having high blood sugar levels, developed cataracts and were lethargic. In contrast, mice that received the cell therapy were active and did not develop cataracts, but the animals' blood sugar levels remained higher than normal.The Yale team's findings suggest that endometrial stem cells could be used to develop insulin-producing islet cells, which are found in the pancreas. These islet cells could then be used to advance the study of islet cell transplantation to treat people with diabetes.Taylor said in a statement that the next step in the research will be to verify how long this treatment remains effective.

WASHINGTON, June 21 (Xinhua) -- A new study from Harvard School of Public Health (HSPH) and University of California, San Francisco, researchers suggests that men with prostate cancer who smoke increase their risk of prostate cancer recurrence and of dying from the disease. The study will be published Wednesday in the Journal of the American Medical Association."In our study, we found similar results for both prostate cancer recurrence and prostate cancer mortality," said Stacey Kenfield, lead author and a research associate in the HSPH Department of Epidemiology. "These data taken together provide further support that smoking may increase risk of prostate cancer progression."Kenfield and her colleagues conducted a prospective observational study of 5,366 men diagnosed with prostate cancer between 1986 and 2006 in the Health Professionals Follow-Up Study. The researchers documented 1,630 deaths, 524 (32 percent) due to prostate cancer, 416 (26 percent) due to cardiovascular disease, and 878 prostate cancer recurrences.The researchers found that men with prostate cancer who were current smokers had a 61 percent increased risk of dying from prostate cancer, and a 61 percent higher risk of recurrence compared with men who never smoked. Smoking was associated with a more aggressive disease at diagnosis, defined as a higher clinical stage or Gleason grade (a measure of prostate cancer severity). However, among men with non-metastatic disease at diagnosis, current smokers had an 80 percent increased risk of dying from prostate cancer.Compared with current smokers, men with prostate cancer who had quit smoking for 10 or more years, or who had quit for less than 10 years but smoked less than 20 pack-years before diagnosis, had prostate cancer mortality risk similar to men who had never smoked. Men who had quit smoking for less than 10 years and had smoked 20 or more pack-years had risks similar to current smokers."These data are exciting because there are few known ways for a man to reduce his risk of dying from prostate cancer," said senior author Edward Giovannucci, professor of nutrition and epidemiology at HSPH. "For smokers, quitting can impact their risk of dying from prostate cancer. This is another reason to not smoke."Prostate cancer is the most frequently diagnosed form of cancer diagnosed in the United States and the second leading cause of cancer death among U.S. men, affecting one in six men during their lifetime. More than two million men in the U.S. and 16 million men worldwide are prostate cancer survivors.

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).

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