上海肺部4个小结节,小于5毫米(上海毛玻璃结节浸润性) (今日更新中)

WASHINGTON, Oct. 13 (Xinhua) -- U.S. researchers have corrected sickle cell disease in adult laboratory mice that had been bred to have the inherited blood disorder by activating production of a special blood component, according to a study published online Thursday in the journal Science.Sickle cell disease results from an abnormality in hemoglobin, the protein found in red blood cells that is responsible for transporting oxygen throughout the body. People living with sickle cell disease have two copies of an altered gene that produces sickle hemoglobin instead of normal adult hemoglobin. Sickle hemoglobin changes shape after releasing its oxygen, causing the red blood cell to become stiff, misshapen and sticky, and slowing blood flow to tissues. This process damages organs and causes pain.The study tested a new approach to increasing the production of a third form of hemoglobin -- fetal hemoglobin. Production of fetal hemoglobin predominates before birth, but turns off thereafter as adult hemoglobin production takes over. People with sickle cell disease are unable to make normal adult hemoglobin, and instead make sickle hemoglobin starting in infancy.An elevated level of fetal hemoglobin within the red blood cell reduces the tendency of sickle hemoglobin to change the shape of red blood cells. Considerable research has shown that the drug hydroxyurea increases production of fetal hemoglobin and reduces the number of pain crises and other complications of sickle cell disease in adults and children. However, not all patients respond well to hydroxyurea, and adverse side effects are a concern.The current study explores a more targeted approach to increasing fetal hemoglobin production. It builds upon earlier studies that discovered a protein called BCL11A normally suppresses the production of fetal hemoglobin soon after birth. The researchers viewed the BCL11A protein as a target for therapy and decided to see what would happen if they blocked production of the protein.The paper details how the research team silenced the mouse gene that produces the BCL11A protein in mice with sickle cell disease. Silencing the gene turned off production of the BCL11A protein and allowed the adult mice to continue to produce fetal hemoglobin. It appears to have eliminated disease symptoms without affecting other aspects of blood production."This discovery provides an important new target for future therapies in people with sickle cell disease," said Susan Shurin, acting director of the U.S. National Heart, Lung, and Blood Institute, which co-funded the study. "More work is needed before it will be possible to test such therapies in people, but this study demonstrates that the approach works in principle."Approximately 100,000 Americans live with sickle cell disease. It is most prevalent in people of African, Hispanic, Mediterranean, and Middle Eastern descent. There is no widely available cure for sickle cell disease. Bone marrow transplants have cured some patients, but the treatment is not without risk and most patients do not have relatives who can donate compatible and healthy bone marrow to them.

WASHINGTON, Sept. 30 (Xinhua) -- At least 15 people have been killed amid 84 sickened in 19 states in listeria outbreak traced to Colorado cantaloupes, making it the most deadly U.S. outbreak of food-borne infection since 1998, the Centers for Disease Control and Prevention (CDC) said Friday.Of the 15 victims, five were in New Mexico, three in Colorado, two in Texas, and one each in Kansas, Maryland, Missouri, Nebraska and Oklahoma. Health departments in Wyoming and Kansas have said they are investigating additional deaths that may be connected to the outbreak.The previous toll announced on Tuesday was 13 dead and 72 sick.The Food and Drug Administration on Sept. 14 warned consumers not to eat cantaloupes from Colorado's Rocky Ford region shipped by Jensen Farms. The cantaloupes with the brand name Rocky Ford were distributed from July 29 to Sept. 10 in at least 17 states."Even if some of the cantaloupe has been eaten without becoming ill, dispose of the rest of the cantaloupe immediately. Listeria bacteria can grow in the cantaloupe at room and refrigerator temperatures," the CDC said.Listeria is a common bacterium that typically causes mild illness in healthy people, but can cause severe illness in older people and those with compromised immune systems. It also can cause miscarriages and stillbirths in pregnant women and severe infections in new babies.Listeria infections lead to about 1,600 serious illnesses each year and about 260 people die, according to the CDC.The CDC estimates that about 48 million people in the U.S. each year get sick from tainted food, with about 128,000 hospitalized and 3,000 deaths.

BEIJING, Oct. 13 (Xinhuanet) -- Scientists have decoded the genome of Black Death which caused one of the worst plagues in human history.The finding was published Wednesday in the scientific journal Nature.A team of German, Canadian and American scientists collected the bacteria's DNA from ancient plague victims' teeth and bones, which were excavated from the burial ground in London.With a careful NDA comparison between the ancient bacteria and the modern strains, scientists found the direct variant of the medieval bacteria still exist today.Black Death's descendants kill around 2,000 people a year, mostly in the developing world, the scientist said."This will provide us with direct insights into the evolution of human pathogens and historical pandemics," said Johannes Krause Of Germany's University of Tubingen, who worked on the study.Black Death, the fatal plague of medieval Europe, wiped out some 30 million people -- about 50 percent of the population on the continent, within just five years, between 1347 and 1351.

WASHINGTON, Jan. 2 (Xinhua) -- A hormone derived from visceral fat called adiponectin may play a role as a risk factor for development of all-cause dementia and Alzheimer's disease (AD) in women, according to a study published on Monday in online issue of the Archives of Neurology.Thomas van Himbergen, from Human Nutrition Research Center on Aging at Tufts University, and colleagues measured levels of glucose, insulin, and glycated albumin, as well as C reactive protein, lipoprotein associated phospholipase A2, and adiponectin in the plasma of patients at the 19th biennial examination (1985 -- 1988) of the Framingham Heart Study.The 840 patients (541 women, median age of 76 years) were followed-up for an average of 13 years and evaluated for signs of the development of AD and all-cause dementia. During that time, 159 patients developed dementia, including 125 cases of AD. After adjustment for other dementia risk factors (age, low plasma docosahexaenoic acid, weight change) only adiponectin in women was associated with an increased risk of all-cause dementia and AD."It is well established that insulin signaling is dysfunctional in the brains of patients with AD, and since adiponectin enhances insulin sensitivity, one would also expect beneficial actions protecting against cognitive decline," the authors write. "Our data, however, indicate that elevated adiponectin level was associated with an increased risk of dementia and AD in women."

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