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BEIJING, Aug. 22 (Xinhuanet) -- Researchers have discovered how a human egg captures an incoming sperm for fertilization, paving the way to help couples suffering from infertility, according to media reports on Monday.An international team of researchers found that a sugar chain known as the sialyl-lewis-x sequence (SLeX) makes the outer coat of the egg “sticky,” which has proven to be helpful in binding the egg and the sperm.As a result, this observation has filled in a huge gap in the understanding of fertility and provides hope for ultimately helping couples who currently cannot conceive.Scientists and doctors know that a sperm identifies an egg when proteins on the head of the sperm match and bind to a series of specific sugars in the egg’s outer coating. With a successful match of proteins, the outside surfaces of the sperm and egg then bind together before merging, which is then followed by delivery of sperm’s DNA into egg.To identify this molecules, the researchers used ultra-sensitive mass-spectrometric imaging technology to observe and identify which molecules are most likely to be key in the binding process.They experimented with a range of synthesised sugars in the laboratory and found that it is SLeX that specifically binds sperm to an egg.According to the World Health Organisation, infertility affects about 15 percent of reproductive-aged couples around the world and almost one in every seven couples in Britain has problems conceiving a child for various reasons.

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."

LOS ANGELES, July 18 (Xinhua) -- U.S. scientists have proven that oncogenes can change normal cells into stem-like cells, paving the way to a safer and more practical approach to treating diseases like multiple sclerosis and cancer with stem cell therapy.In a collaborative study, researchers from the Keck School of Medicine of the University of Southern California (USC), and the Children's Hospital of Orange County (CHOC) in California and Good Samaritan Hospital Medical Center in New York have successfully converted human skin cells into brain cells by suppressing the expression of p53, a protein encoded by a widely studied oncogene. This suggests that p53 mutation helps determine cell fate -- good or bad -- rather than only the outcome of cancer.Oncogenes are generally thought to be genes that, when mutated, change healthy cells into cancerous tumor cells.Study findings were appearing Monday on the website of the American Association for the Advancement of Science (AAAS)."The reality may be more complicated than people think," said Jiang F. Zhong, Ph.D., assistant professor of pathology at the Keck School. "What is a stem cell gene? What is a cancer gene? It may be the same thing.""When you turn off p53, people think the cell becomes cancerous because we tend to focus on the bad thing," Zhong said. "Actually, the cell becomes more plastic and could do good things, too. Let's say the cell is like a person who loses his job (the restriction of p53). He could become a criminal or he could find another job and have a positive effect on society. What pushes him one way or the other, we don't know because the environment is very complicated."Stem cells can divide and differentiate into different types of cells in the body. In humans, embryonic stem cells differentiate into three families, or germ layers, of cells. The reasons why and how certain stem cells differentiate into particular layers are not clearly understood. However, from those layers, tissues and organs develop. The endoderm, for example, leads to formation of the stomach, colon and lungs, while the mesoderm forms blood, bone and heart tissue. In its study, Zhong's team examined human skin cells, which are related to brain and neural cells from the ectoderm.When p53 was suppressed, the skin cells developed into cells that looked exactly like human embryonic stem cells. But, unlike other man-made stem cells that are "pluripotent" and can become any other cells in the body, these cells differentiated only into cells from the same germ layer, ectoderm."IPSCs (induced pluripotent stem cells) can turn into anything, so they are hard to control," Zhong said. "Our cells are staying within the ectoderm lineage."Zhong said he expects that suppressing other oncogenes in other families of cells would have the same effect, which could have critical significance for stem cell therapy. Future research should focus on determining which genes to manipulate, Zhong said.The study is slated to appear in the Proceedings of the National Academy of Sciences later this month, according to AAAS.

BERLIN, June 17 (Xinhua) -- German authority said on Friday first case of human spreading deadly E. coli is detected, as death toll increases to 39 worldwide.A woman working in a kitchen of a catering company was infected by E. coli from sprouts, though she didn't fall ill immediately, said Harald Kehlborn, a spokesman for the consumer protection ministry of German state Hesse.Then she spread E. coli unconsciously to another 20 people through the food she prepared, said Kehlborn.The woman later developed serious complication of hemolytic- uremic syndrome (HUS), which causes failure of kidney and nervous system.According to the data of the Robert Koch Institute, Germany's national disease control centre, the number of people who are infected has reached 3,408 in Germany and 798 people have fallen into HUS, while the infection speed is slowing down.

BEIJING, Aug 4 (Xinhuanet) – A new urine test might help doctors detect prostate cancer and better evaluate a patient's treatment options, according to American reseachers Thursday."This is a tool that men and their physician can use to help them decide whether it's appropriate to get a biopsy now or delay that decision," said lead researcher Dr. Scott Tomlins, a pathology resident at the University of Michigan Health System.The test looks for two genetic markers associated with prostate cancer. The first, called TMPRSS2:ERG, is caused by two genes changing places and fusing together; it is thought to cause prostate cancer. Since the gene fusion is only seen in about half of cancer patients, the test also looks for another marker, called PCA3."We are exploiting some new bio-markers to try to refine the PSA (prostate-specific antigen) test," Tomlins said.