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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.

CANBERRA, Sept. 7 (Xinhua) -- A team of Australian and U.S. scientists on Wednesday said they discovered a genetic defect, which can lead to Leigh syndrome, a rare disorder which affects the central nervous syndrome.The scientists tested more than 1000 genes by encoding proteins active in two individuals who suffer from the illness. They used a new technique known as next-generation DNA sequencing to examine the genes.The gene they discovered encodes an enzyme which is found in the mitochondria which are subsets of cells. Without this enzyme the mitochondria do not translate proteins efficiently, and this then causes Leigh syndrome.According to David Thorburn, from the Murdoch Children's Research Institute in Melbourne, the discovery shows the enormous potential of the new technology."These findings demonstrate the ability of sequencing technologies to improve diagnosis," Professor Thorburn said in a statement released on Wednesday."Although it isn't clear in the case of Leigh syndrome whether the precise molecular diagnosis will necessarily lead to therapies, the current findings represent a meaningful service."He added that diagnosis of the disease along with its specific genetic cause can also be informative about the risk a couple has of having another affected child. The diagnostic information can help in decisions about whether and how to pursue alternative means of having children, for instance through the use of donor sperm or eggs.The research team consisted of scientists from Australia's Murdoch Institute as well as the Broad Institute in the U.S.In Leigh syndrome, infants are born apparently healthy only to develop movement and breathing disorders that worsen over time, often leading to death by the age of three. The problem is that the mitochondria responsible for powering their cells cannot keep up with the demand for energy in their developing brains.

WELLINGTON, Aug. 30 (Xinhua) -- Middle-aged women who wolf down their meals are much more likely to be overweight or obese than women who eat slower, New Zealand research has found.In what they claimed to be the first such nationwide study anywhere, Otago University researchers analyzed the relationship between self-reported speed of eating and body mass index (BMI) in more than 1,500 New Zealand women aged 40 to 50, an age group known to be at high risk of weight gain.The study by the university's department of human nutrition could lead to new and more successful methods of treating obesity, say the researchers.Study principal investigator Dr Caroline Horwath said that after adjusting for factors such as age, ethnicity, smoking, physical activity and menopause status, the researchers found that the faster women reported eating, the higher their BMI.Results from the two-year follow-up were expected to be published next year, and if analysis confirmed a causal relationship, the researchers would test interventions that focused on encouraging women to eat more slowly.

WASHINGTON, June 23 (Xinhua) -- NASA's next Mars rover has completed the journey from its California birthplace to Florida in preparation for launch this fall, the U.S. space agency said Thursday in a statement.The Mars Science Laboratory (MSL) rover, also known as Curiosity, arrived Wednesday at NASA's Kennedy Space Center aboard an Air Force C-17 transport plane. It was accompanied by the rocket-powered descent stage that will fly the rover during the final moments before landing on Mars.The rover's aeroshell -- the protective covering for the trip to the Red Planet -- and the cruise stage, which will guide it to Mars, arrived at Kennedy last month. The mission is targeted to launch from Cape Canaveral Air Force Station between Nov. 25 and Dec. 18. The car-size rover will land on Mars in August 2012.The rover and other spacecraft components will undergo more testing before mission staff stack them and fuel the onboard propulsion systems. Curiosity should be enclosed in its aeroshell for the final time in September and delivered to Kennedy's Launch Complex 41 in early November for integration with a United Launch Alliance Atlas V rocket.Curiosity is about twice as long and more than five times as heavy as any previous Mars rover. Its 10 science instruments include two for ingesting and analyzing samples of powdered rock delivered by the rover's robotic arm. During a prime mission lasting one Martian year -- nearly two Earth years -- researchers will use the rover's tools to study whether the landing region has had environmental conditions favorable for supporting microbial life and favorable for preserving clues about whether life existed.

LOS ANGELES, June 4 (Xinhua) -- Pregnant women who eat high-fat diet may be more likely to have a higher rate of stillbirth, a new study suggests.Researchers at Oregon Health & Science University (OHSH) came to the conclusion after observing 24 pregnant Japanese macaques that ate either a diet comprising 32 percent calories from fat or a control diet with 14 percent fat calories for at least four years.The researchers found the monkeys that ate a high-fat diet experienced a significant decrease in blood flow from the uterus to the placenta, a reduction of 38 percent to 56 percent, and a rise in placental inflammation.This was the case regardless of whether the monkeys were obese or slender. The risk of stillbirth was further compounded, however, when the monkeys were obese with hyper-insulinemia, or pre-diabetes.A large order of McDonald's french fries are shown May 22, 2008. McDonald's has switched to cooking oils free of trans fats in all of its restaurants in the United States and Canada, Chief Executive Jim Skinner said on may 23Eating a high-fat diet decreases blood flow from the mother to the placenta, the temporary organ that nourishes the unborn fetus, thus raising the risk of stillbirth, the researchers explained.Because the placental structure of the Japanese macaque is very similar to that in humans, cause and effect can be better established, the researchers said.Additional studies are needed to determine exactly how a high- fat diet decreases placental blood flow, the researchers noted.This is the first study to explain exactly how a fatty diet contributes to stillbirth, the researchers said in the study appearing in the June edition of the journal Endocrinology.The researchers hope their work will inform expectant moms and their physicians about the inherent dangers of a high-calorie, high- fat diet."This study demonstrates that maternal diet during pregnancy has a profound influence on both placental and fetal development," said Antonio Frias, M.D., principal investigator and assistant professor of obstetrics and gynecology (perinatology/maternal-fetal medicine) in the OHSU School of Medicine."The high-calorie, high-fat diet common in our society has negative effects on placental function and may be a significant contributor to adverse pregnancy outcomes, such as stillbirth."Previous studies have shown that nearly all adverse outcomes during pregnancy -- abnormal fetal growth, preeclampsia, preterm labor and stillbirth -- are in some way associated with an abnormally developed, or damaged, placenta, the temporary organ that nourishes the unborn fetus.In addition, maternal obesity has been associated with placental inflammation and dysfunction and an increased risk of stillbirth.Taking these findings into account, the researchers hypothesized that eating a diet high in fat during pregnancy also may increase the risk of placental inflammation and the risk of stillbirth.The researchers said they plan to conduct further studies on the impact of dietary changes and diet supplementation on improving outcomes in both monkeys and humans.