郑州眼科近视手术(郑州哪里治疗眼镜斜视好) (今日更新中)

LOS ANGELES, June 17 (Xinhua) -- The size of low-oxygen zones created by respiring bacteria is extremely sensitive to changes in depth caused by oscillations in climate, thus posing a distant threat to marine life, a new study suggests."The growth of low-oxygen regions is cause for concern because of the detrimental effects on marine populations -- entire ecosystems can die off when marine life cannot escape the low- oxygen water," said lead researcher Curtis Deutsch, assistant professor of atmospheric and oceanic sciences at University of California, Los Angeles."There are widespread areas of the ocean where marine life has had to flee or develop very peculiar adaptations to survive in low- oxygen conditions," Deutsch said in the study to be published in an upcoming print edition of the journal Science.A team led byDeutsch used a specialized computer simulation to demonstrate for the first time that fluctuations in climate can drastically affect the habitability of marine ecosystems.The study also showed that in addition to consuming oxygen, marine bacteria are causing the depletion of nitrogen, an essential nutrient necessary for the survival of most types of algae."We found there is a mechanism that connects climate and its effect on oxygen to the removal of nitrogen from the ocean," Deutsch said. "Our climate acts to change the total amount of nutrients in the ocean over the timescale of decades."Low-oxygen zones are created by bacteria living in the deeper layers of the ocean that consume oxygen by feeding on dead algae that settle from the surface. Just as mountain climbers might feel adverse effects at high altitudes from a lack of air, marine animals that require oxygen to breathe find it difficult or impossible to live in these oxygen-depleted environments, Deutsch said.Sea surface temperatures vary over the course of decades through a climate pattern called the Pacific Decadal Oscillation, during which small changes in depth occur for existing low-oxygen regions, Deutsch said. Low-oxygen regions that rise to warmer, shallower waters expand as bacteria become more active; regions that sink to colder, deeper waters shrink as the bacteria become more sluggish, as if placed in a refrigerator."We have shown for the first time that these low-oxygen regions are intrinsically very sensitive to small changes in climate," Deutsch said in remarks published Friday by the American Association for the Advancement of Science on its website. "That is what makes the growth and shrinkage of these low-oxygen regions so dramatic."Molecular oxygen from the atmosphere dissolves in sea water at the surface and is transported to deeper levels by ocean circulation currents, where it is consumed by bacteria, Deutsch said."The oxygen consumed by bacteria within the deeper layers of the ocean is replaced by water circulating through the ocean," he said. "The water is constantly stirring itself up, allowing the deeper parts to occasionally take a breath from the atmosphere."A lack of oxygen is not the only thing fish and other marine life must contend with, according to Deutsch. When oxygen is very low, the bacteria will begin to consume nitrogen, one of the most important nutrients that sustain marine life."Almost all algae, the very base of the food chain, use nitrogen to stay alive," Deutsch said. "As these low-oxygen regions expand and contract, the amount of nutrients available to keep the algae alive at the surface of the ocean goes up and down. "Understanding the causes of oxygen and nitrogen depletion in the ocean is important for determining the effect on fisheries and fish populations, he said.

LONDON, Sept. 22 (Xinhua) -- A British publisher on Thursday issued an "unauthorized autobiography" of the founder of the controversial Wikileaks website Julian Assange.Assange became a global figure after he published 250,000 secret United States diplomatic cables on his Wikileaks website, which became a serious embarrassment to the American government.He was then accused by two women of rape when he was in Sweden. Swedish police said they wanted to question him, and issued a European Arrest Warrant in 2010 for him.Assange, 40, denies the allegations and surrendered himself to police in London at the end of 2010, and the Swedish authorities applied for his extradition to face questioning.Assange fought the extradition bid in the English courts, fearing that he could face further extradition from Sweden to the United States where he could face criminal charges related to the publishing of the secret cables, but failed.He appealed against the extradition ruling in July and a final decision on the case will be made by senior English judges, probably before Christmas.Assange agreed to cooperate with Edinburgh-based publisher Canongate in publishing an autobiography and had 50 hours of interviews with a ghostwriter between January and March this year, while he was on bail awaiting an outcome of the extradition hearings.He received a 500,000 pound advance (about 768,000 U.S. dollars) for the book.Publisher's spokesman Liz Sich told Xinhua Thursday, "It's an unauthorized autobiography -- it is his words. He was contracted to write his autobiography in December; a ghostwriter was assigned to it, approved by the publisher and Julian and an intense amount of work was done in the first three months of 2011. The first draft was delivered on schedule at the end of March. After that there was an hiatus and nothing happened; in June Julian decided he wanted to tear up the contract."Assange has opposed publication, but Sich said, "It is very much Julian's words, it is written in the first person. He didn't want it to be published but he was in breach of his contract. He couldn't pay the advance back because he had used it to pay his lawyers."The book is available only in English at the moment, but a Dutch publisher and a Turkish publisher said they would print translations in their languages, and other foreign language editions are also likely.

JIUQUAN, Gansu, Aug. 18 (Xinhua) -- China's experimental orbiter SJ-11-04, which was launched by a Long March II-C rocket Thursday, failed to enter the designated orbit due to a malfunction of the rocket.The rocket experienced malfunction during the flight following its launch from Jiuquan Satellite Launch Center at 5:28 p.m. Beijing Time in northwest Gansu Province.The specific cause of the failure is being analyzed.

LOS ANGELES, June 5 (Xinhua) -- U.S. researchers have developed two new drugs that can prolong the lives of patients with advanced melanoma, it was announced on Sunday.Research on both drugs was presented at the on-going annual meeting of the American Society of Clinical Oncology in Chicago, according to HealthDay News.This is the first big news in years for treatment of melanoma, one of the deadliest forms of skin cancer and one that is notoriously difficult to treat, let alone cure, the report said.The first treatment, vemurafenib, inhibits a gene mutation harbored in half of all melanoma patients, but is not yet approved by the U.S. Food and Drug Administration.The other drug, Yervoy (ipilumumab), is an immune system therapy that won approval in March."The March FDA approval of ipilumumab (Yervoy) was the first new drug approval for melanoma in 13 years," said Tim Turnham, executive director of the Melanoma Research Foundation.The two drugs were developed by researchers at Memorial Sloan- Kettering Cancer Center in New York City, the report said."This is really a huge step toward personalized care in melanoma," Dr. Paul Chapman, lead author of the first study and the attending physician in the melanoma/sarcoma service at Memorial Sloan-Kettering, said in a statement. "This (vemurafenib) is the first successful melanoma treatment tailored to patients who carry a specific gene mutation in their tumor, and could eventually become one of only two drugs available that improves overall survival in advanced cancers.""Having two trials that show a benefit in survival in patients with melanoma, both of these in first-line settings -- we weren't here just a few years ago," said Dr. Stephen Hodi, director of the Melanoma Center at Dana Farber Cancer Institute in Boston. "These are huge, paradigm-shifting results for the field."In the vemurafenib trial, sponsored by the drug's makers, researchers randomly assigned 675 patients with advanced, inoperable melanoma to receive either the chemotherapy drug dacarbazine or vemurafenib. Vemurafenib targets the V600E mutation in the BRAF gene.At the three-month mark, patients taking vemurafenib were 63 percent less likely to die and 74 percent less likely to die or see their cancer return, compared to patients taking dacarbazine alone.Few patients had side effects in the vemurafenib group, although some did develop squamous cell carcinoma, a less dangerous form of skin cancer.This is the first drug that has been proven superior to chemotherapy in this group of hard-to-treat patients, the researchers said."There was such a substantial benefit that we recommended that patients cross over," Chapman said at a Sunday news briefing. "It' s unprecedented to report a trial this early. The median follow-up time was three months." Yet the differences between the two groups became evident almost immediately.Dr. Lynn Schuchter, co-moderator of the briefing and division chief of hematology-oncology at Abramson Cancer Center of the University of Pennsylvania in Philadelphia, said symptoms subsided in some patients almost immediately, enabling them to cut back on pain medication in just 72 hours."The median time to progression with dacarbazine was 1.6 months versus three months with vemurafenib, which is a huge difference," said Chapman.In the second study, about 500 patients were randomly picked to receive Yervoy plus dacarbazine or dacarbazine alone.Those taking both drugs lived a median of 11.2 months compared to 9.1 months for those taking dacarbazine alone. Time to recurrence of disease was about the same for both groups: 2.8 months and 2.6 months, respectively.Almost half of those taking the combination therapy were alive after one year, compared to 36.3 percent in the other group. After two years, the rates were 28.5 percent and 17.9 percent, respectively.By three years out, 20.8 percent of those in the combination group were alive compared with 12.2 percent of those taking chemotherapy alone.This is the first study to combine chemotherapy and immunotherapy both safely and effectively.A study to test vemurafenib in combination with Yervoy has already begun, according to HealthDay News.

WASHINGTON, Sept. 12 (Xinhua) -- An enzyme that appears to play a role in controlling the brain's response to nicotine and alcohol in mice might be a promising target for a drug that simultaneously would treat nicotine addiction and alcohol abuse in people, U.S. researchers find.Over the course of four weeks, mice genetically engineered to lack the gene for protein kinase C (PKC) epsilon consumed less of a nicotine-containing water solution than normal mice, and were less likely to return to a chamber in which they had been given nicotine. In contrast, normal mice steadily increased their consumption of nicotine solution while the mice lacking PKC epsilon did not.The study conducted by researchers at the Ernest Gallo Clinic and Research Center, affiliated with the University of California, San Francisco, appeared Monday in the online edition of the Proceedings of the National Academy of Sciences.In normal mice, as in humans, nicotine binds to a certain class of nicotinic receptors located on dopamine neurons, which causes dopamine to be released in the brain. Dopamine creates a feeling of enjoyment, and thus prompts a sense of reward. Researchers found that mice lacking PKC epsilon are deficient in these nicotinic receptors.The finding complements earlier research in which researchers found that mice genetically engineered to lack the PKC epsilon enzyme drank less alcohol than normal mice and were disinclined to return to a chamber in which they had been given alcohol."This could mean that these mice might not get the same sense of reward from nicotine or alcohol," said Gallo senior associate director and investigator Robert Messing. "The enzyme looks like it regulates the part of the reward system that involves these nicotinic receptors."The reward system is a complex of areas in the brain that affect craving for nicotine, alcohol and other addictive substances.The next step in the research, said Messing, would be to develop compounds that inhibit PKC epsilon. The ultimate goal, he added, would be medications that could be used "to take the edge off of addiction by helping people get over some of their reward craving."

来源：资阳报