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主题:给无力者力量

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  发贴心情 Post By:2003/9/24 17:52:51

我们在为自己服务,何必言谢

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  发贴心情 Post By:2003/9/24 18:44:21

在关节部位,除了按摩之外,建议还要做屈伸运动。要尽可能保持关节不变形,光靠按摩还不够,关节的屈伸更加重要。患者每天应让所有的关节都得到活动,自己能做关节屈伸的就自己做,自己不能做,则由家人帮助做被动的关节屈伸。次数不需要很多,只要活动开就行。

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  发贴心情 Post By:2003/9/26 18:58:29

有可能出现治疗DMD的药物 RESEARCHERS BLOCK MOLECULAR WASTE DISPOSAL SYSTEM, SAVE MUSCLE CELLS TUCSON, Ariz., Sept. 22, 2003 — Blocking a molecular waste disposal system that normally degrades incomplete or abnormally made proteins is a new pathway toward treatment for a common childhood muscular dystrophy, the Muscular Dystrophy Association (MDA) announced today. MDA grantee Michael Lisanti of Albert Einstein College of Medicine in New York was part of a U.S. and Italian research group that blocked “proteasomes” — molecular garbage disposal units — in the muscle cells of MD-affected mice. The team published its results in the October issue of the American Journal of Pathology. (An online preview was published today at http://ajp.amjpathol.org.) “Many strategies to correct muscular dystrophy rely upon replacing muscle proteins,” said Sharon Hesterlee, MDA director of Research Development. “This approach is unique because it attempts instead to save flawed proteins before they’re discarded.” The researchers blocked the proteasomes with a compound they injected first into a leg muscle and later delivered via a continuous pump into the muscles of mice with Duchenne muscular dystrophy (DMD), the most common childhood form of the disease. The underlying problem in DMD is any of a large number of genetic mutations in the gene for dystrophin, with different mutations leading to different types of abnormal dystrophin protein molecules. Cellular waste disposal mechanisms are presumed to get rid of abnormally formed dystrophin molecules, even some that might be useful to the muscles. In DMD, dystrophin is missing from its normal place in the cell membrane. The disease causes progressive muscle weakness and wasting and usually results in death by the 20s or 30s from respiratory or cardiac muscle failure. With their proteasomes disabled, the DMD-affected mice, which make short forms of dystrophin, benefited from their dystrophin even though it wasn’t normal. The short dystrophin pieces inserted into the cell membrane, probably similarly to the way full-length dystrophin molecules normally do. Other proteins, missing from the membrane in DMD because of dystrophin’s absence, also assembled properly after the anti-proteasome treatment. The dystrophin and associated proteins restored the structure and function of the cell membranes and the appearance of the muscle tissue under the microscope, the researchers say. “This is a very exciting development, as it may open the way toward a new drug treatment for Duchenne and Becker muscular dystrophy, as well as for related muscle diseases,” Lisanti commented. 这是一个令人振奋的进步,它可能会打开一条用药物治疗DMD和BMD,甚至其他肌病的道路。 He said his group used a proteasome-blocking compound that’s only approved for laboratory research but that he knows of a similar drug that’s used in cancer treatment. 他的小组研究的药物只允许在实验室中使用,但是他知道有相同的药物被用于癌症治疗。

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  发贴心情 Post By:2003/9/26 18:59:41

这是一条多么振奋人心的消息,想一想每天三顿口服药就能够治好我们的肌病,那前景是多么美妙。现在我更坚信人类攻克肌病的日子不会遥远,让我们一起等待。

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  发贴心情 Post By:2003/9/27 10:04:52

原文摘要: Treatment of mdx Mice Rescues the Expression and Membrane Localization of Dystrophin and Dystrophin-Associated Proteins Gloria Bonuccelli*, Federica Sotgia*, William Schubert*, David S. Park*, Philippe G. Frank*, Scott E. Woodman*, Luigi Insabato, Michael Cammer, Carlo Minetti¶ and Michael P. Lisanti* From the Department of Molecular Pharmacology and The Albert Einstein Cancer Center,* Albert Einstein School of Medicine, Bronx, New York; the Division of Hormone-Dependent Tumor Biology, The Albert Einstein Cancer Center, Albert Einstein College of Medicine, Bronx, New York; the Department of Biomorphological and Functional Sciences, Section of Pathology, Faculty of Medicine, University of Naples Federico II, Naples, Italy; the Department of Anatomy and Structural Biology, The Analytical Imaging Facility, Albert Einstein College of Medicine, Bronx, New York; and Servizio Malattie Neuro-Muscolari,¶ Università di Genova, Istituto Gaslini, Genova, Italy Dystrophin, the protein product of the Duchenne muscular dystrophy (DMD) gene, is absent in the skeletal muscle of DMD patients and mdx mice. At the plasma membrane of skeletal muscle fibers, dystrophin associates with a multimeric protein complex, termed the dystrophin-glycoprotein complex (DGC). Protein members of this complex are normally absent or greatly reduced in dystrophin-deficient skeletal muscle fibers, and are thought to undergo degradation through an unknown pathway. As such, we reasoned that inhibition of the proteasomal degradation pathway might rescue the expression and subcellular localization of dystrophin-associated proteins. To test this hypothesis, we treated mdx mice with the well-characterized proteasomal inhibitor MG-132. First, we locally injected MG-132 into the gastrocnemius muscle, and observed the outcome after 24 hours. Next, we performed systemic treatment using an osmotic pump that allowed us to deliver different concentrations of the proteasomal inhibitor, over an 8-day period. By immunofluorescence and Western blot analysis, we show that administration of the proteasomal inhibitor MG-132 effectively rescues the expression levels and plasma membrane localization of dystrophin, ß-dystroglycan, -dystroglycan, and -sarcoglycan in skeletal muscle fibers from mdx mice. Furthermore, we show that systemic treatment with the proteasomal inhibitor 1) reduces muscle membrane damage, as revealed by vital staining (with Evans blue dye) of the diaphragm and gastrocnemius muscle isolated from treated mdx mice, and 2) ameliorates the histopathological signs of muscular dystrophy, as judged by hematoxylin and eosin staining of muscle biopsies taken from treated mdx mice. Thus, the current study opens new and important avenues in our understanding of the pathogenesis of DMD. Most importantly, these new findings may have clinical implications for the pharmacological treatment of patients with DMD. --------------------------------------------------------------------------------

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  发贴心情 Post By:2003/9/28 21:08:30

前一段时间一直在表姐家,所以没能上网。我是昨天才看到黄海华记者的报道的,真有些相见恨晚的感觉。我开心了一整天,那激动、幸福、感激之情不以言表…… 很久以来,我的内心被一种无形的痛苦压抑着、煎熬着,我想,不仅是我,和我同命相连的朋友们也一定有着同样的感受。我们曾经无忧无虑稚嫩的心,被一次次泪水打湿、淹没;我们曾经美丽的幻想、五彩的梦,被残酷的现实击破、打碎。可恶的病魔时刻纠缠着我们,不给我们一刻喘息的机会。它日复一日年复一年的吞噬着我们的生命,扼杀着我们的意志。我们希望去了解世界,希望在社会的某个角落找到自己的位置,希望被亲人和朋友所需要。我们渴望友情、亲情、爱情,但我们又害怕这些情感的到来,我们怕给爱我们的人带来悲伤和负担。我们的内心是那么的无助、无奈! 尽管如此,我们仍热爱生活,也更珍惜这有限的生命。社会对我们“无力家族”知道的太少,了解的太少。任何叹息的言语在我们看来都是那么苍白无力,我们不需要惋惜与怜悯,我们只渴盼世人的理解与帮助。你们的关心是我们生命中的一缕缕阳光,他将温暖我们阴冷的心。《解放日报》的同仁们让我们又一次看到了久违的阳光,感觉到了早已陌生的温暖。但愿这光亮能更加强烈,可以持久,可以普照大地!让我们怀着一颗感恩的心面对生活、面对世人,感谢所有关心帮助我们的人们! 愿好人幸福、平安——
[此贴子已经被作者于2003-9-28 21:12:16编辑过]

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  发贴心情 Post By:2003/9/29 9:39:43

Why?为什么? 为什么要求社会关注时,门庭若市;要大家写信时,却门可罗雀。中残联是我们残疾人的娘家,我们都不敢写信,还怎样向更高的权利部门呼吁呢? 病友们啊!我们不要做光说不练的假把式,要做能说敢干的真把式。 我再次大声疾呼,为了我们的未来,积极响应达人的建议,把信寄到中残联,把我们心中积郁的渴望告诉娘家人。
[此贴子已经被作者于2003-9-29 9:48:00编辑过]

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  发贴心情 Post By:2003/9/29 11:32:26

中残联地址 地址:北京东城区北池子大街44号 中国残疾人联合会收 邮编100006

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  发贴心情 Post By:2003/9/29 16:00:55

我也曾想要给残联写信,只是不知道该怎么下笔. 我相信,在我们每个人心中一定都有很多话想说.可多写怕别人不耐烦看下去,写的少又担心不能把我们内心的渴望表达清楚,不够诚恳. lzx老师,您说我们应该写些什么?
[此贴子已经被作者于2003-9-29 16:10:23编辑过]

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  发贴心情 Post By:2003/9/29 16:48:08

水心写写吧,你文笔那么好。加上你是以一个女孩的身份写,比我们这几个小子有优势,嘿嘿:) 内容上,想说什么就说什么呗!你要拿不准的话,写好后可电邮给LZX老师来“把把关”。呵呵,我想LZX冲着你这个“老师”的称呼也会很乐意的,嘿嘿。。。图片点击可在新窗口打开查看
[此贴子已经被作者于2003-9-29 16:54:43编辑过]

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