开幕式挺有振动和声学特点，安排弦乐四重奏表演。正式开会前，是英国作曲家爱德华·埃尔加 ( Edward Elgar ) 爵士的作品，他是英国国歌的作曲者。开幕式上演奏英国作曲家和小提琴演奏家埃里克·科茨 (Eric Coates) 的《伦敦组曲 ( London Suite ) 》。我都没有听出什么名堂，到底是研究振动的，不研究声学。 开幕式的发言都比较简短。去年雅典会议真是繁文缛节，难怪希腊要破产了。总主席介绍，有近千名代表来自 54 个国家和地区。共收到 1265 个摘要，最后录用了 932 篇，包括 135 个墙报。参会人数最多的前三个国家是中国、英国和德国。 大会报告共有 6 个。第一个报告人是哈佛的一位物理学家，他研究声学有些玩票的性质，写了本书， Why You Hear What You Hear 。这次的报告是， The Miracle of Resonance and Formants ，从声学角度给出共振非常广泛的定义。列举一些声学现象，做了较为直观的解释。不是我熟悉的报告类型，公式很少。 第二个报告也是声学方面， The Ear beyond the Hearing: From Smart Earplug to in-Ear Brain Computer Interfaces 。报告风格很独特，开始放了 10 多分钟视频，解释背景。总体上也上偏技术，我兴趣不大。 第三位报告人是胡海岩院士， Advances in Flutter Analysis and Control of Aircraft Structures ，讲飞机结构颤振分析和控制的进展。结构振动我相对熟悉，这种进展性报告，我听着也更习惯些。 第四个报告又是听觉的声学， Reading the World with Two Ears 。仍然不太懂。 第五个报告，也是声学的。忙着准备自己的报告，没有去听。 最后一个报告是结构振动方面。海洋结构的振动，考虑流体作用，但似乎还不是真正的流固耦合。还考虑了冰山撞击，模型似乎有些过于简单。 我的报告排在第 3 天下午。事情比较多，也没有准备。原来打算当天上午准备，遇到些事情，只是大致看看，想想表达和词汇。内容也比较单薄，说明结构用 NES 减振可能出现分岔和混沌。都是计算结果，也不太好讲。因为这个会振动同行不多，所以把更合适报告的题目留给别的会议了。原计划参加 4 个国际会议。不过，准备 PPT 时，增加些我们实验的工作作为背景，又扩充些解析的内容。估计能讲 15 分钟。 现场发挥还可以。有计时器，便于掌握时间。最后是超时半分钟。报告后，没有人提问题。主持人也懒得捧场，就退场了。 出来后，有位中国工程物理研究院总体工程研究所的年轻同行与我讨论。他对我们的分析方法及其数值实现比较有兴趣。邀请我到绵阳给他们讲讲。我原则上同意，细节以后另行安排。 与他交流期间，有位洋人想打招呼。开始介绍是某某的学生。我还没有反应过来某某是谁。差点儿要问了。突然意识到，他说的是 Ali Nayfeh 。搞非线性振动，如果不知道真是太失礼了。他的问题倒是简单，我解释几句，就搞定了。 闭幕式时人已经很少了。只是在茶歇的走廊里，总主席讲几句话，就算结束了。 明年的会议，将在日本大阪举行。如果没有意外，我还是会参加。
原文如下 Microbiologists continue to compile examples of microorganisms being associated with chronic diseases in humans or in animals serving as models for studying human diseases. Sometimes those links are one-on-one, and other times they involve microbial communities, particularly the microbiota of the gut (Microbe, June 2011, p. 259; July 2011, p. 300 and p. 301). Here are several examples described during the 111th ASM General Meeting (GM) last May in New Orleans. "We're walking bioreactors, and changes in the gut microbiome can change our health," says Liping Zhao of Shanghai Jiao Tong University in Shanghai, China. He spoke during the GM opening session, "Microbes among Us: Marvel or Menace," about how that microbial population could be an important factor affecting the epidemic of obesity in the United States, China, and many other countries. "In microbiology, the chronic diseases are also part of our battlefield," he says, a reminder that microorganisms do more to impair health than cause short-term infections. "Let's go for it." Zhao and his collaborators are doing just that in studying obesity. "Can we identify key players in the gut microbiome as new targets for controlling obesity?" he asks. Changes in diet can shift the makeup of that microbiota, with a high-fat diet leading to sharp increases in sulfate-reducing bacteria in the gut microbiota of mice, he and his collaborators find. Keeping such rodents on a low-calorie, low-fat regimen can extend the lengths of their lives by about 50%, he points out. Moreover, the longest-lived animals also have the lowest levels of a bacterially derived, lipopolysaccharide (LPS)-binding protein circulating in the bloodstream, perhaps leading to a lower degree of host inflammatory responses and better health in general. Similar changes among gut microbiota can also occur in obese humans who switch to radically reduced-fat, low-caloric diets, Zhao says, cautioning that these observations are anecdotal and thus in contrast to those obtained through systematic experiments involving mice. "We can't say it's causal, but this work is increasing the plausibility," he says. There is "evidence of the gut microbiota being part-time players for any disease at which we looked," says Elaine Holmes of Imperial College in London, England, following a broadly similar line of research as Zhao. She spoke during the symposium "Metabolomics and Microbes in Health and Disease" about how she and her collaborators are studying the microbiota of obese rats, searching for metabolites that could serve as markers of that condition. "We're starting to address the potential of modulating gut microbiota while looking for health-related signatures," she says. A bit higher in the gastrointestinal tract, Helicobacter pylori bacteria of the stomach can cause ulcers and are a risk factor for stomach cancer. Now these bacteria also appear to contribute to Parkinson's disease, based on experiments involving mice, according to Traci Testerman of Louisiana State University in Shreveport and her collaborators. She spoke during the GM poster session "Host Cell Responses to Microbial Attachment/Internalization." For example, when "older" mice, equivalent in age to middle-aged humans, are infected with such bacteria, regions of the brains of those infected mice produce lower-than-usual levels of dopamine, the neurotransmitter that becomes reduced in Parkinson's patients, Testerman says. Moreover, the movements of the infected mice are impaired in ways that resemble what happens in humans with the disease. H. pylori produce a modified, sugar-containing cholesterol compound that apparently is "trafficked to the brain" where it acts as a neurotoxin. This modified version of cholesterol resembles a chemical made by cycad plants that is similarly damaging to the central nervous system, she points out. Meanwhile, Chlamydia pneumoniae bacteria appear responsible for increasing the severity of asthma among some population groups, according to Eduard Drizik of the University of Massachusetts, Amherst, where he works with Wilmore Webley. Drizik spoke during the GM symposium "The Best and Brightest in Diagnostic Microbiology and Epidemiology." C. pneumoniae bacteria are more prevalent in lungs of adults and children with severe asthma than in comparable nonasthmatic populations, he says. Moreover, children with asthma also produce higherthan- usual levels of IgE antibodies against those bacteria, referring to a class of antibodies that typically trigger allergic responses and also symptoms of asthma. Treating such patients long-term with antibiotics eliminates C. pneumoniae, reduces airway inflammation, and reduces IgE antibody levels-while also bringing significant relief in terms of their asthma symptoms, he says. Jeffrey L. Fox pdf 链接
标签: 大会报告
