首页 | 本学科首页   官方微博 | 高级检索  
文章检索
  按 检索   检索词:      
出版年份:   被引次数:   他引次数: 提示:输入*表示无穷大
  收费全文   206篇
  免费   28篇
  国内免费   1篇
  235篇
  2021年   3篇
  2018年   5篇
  2017年   4篇
  2016年   3篇
  2015年   3篇
  2014年   5篇
  2013年   7篇
  2012年   8篇
  2011年   7篇
  2010年   8篇
  2009年   10篇
  2008年   7篇
  2007年   8篇
  2006年   5篇
  2005年   13篇
  2004年   10篇
  2003年   4篇
  2002年   3篇
  2001年   8篇
  2000年   2篇
  1999年   4篇
  1998年   2篇
  1997年   6篇
  1996年   4篇
  1995年   5篇
  1994年   3篇
  1993年   3篇
  1992年   3篇
  1991年   5篇
  1990年   6篇
  1989年   4篇
  1988年   2篇
  1987年   5篇
  1986年   4篇
  1985年   5篇
  1984年   2篇
  1979年   3篇
  1978年   2篇
  1977年   3篇
  1976年   2篇
  1975年   6篇
  1974年   2篇
  1973年   3篇
  1971年   4篇
  1970年   3篇
  1969年   3篇
  1966年   3篇
  1947年   2篇
  1912年   1篇
  1892年   1篇
排序方式: 共有235条查询结果,搜索用时 0 毫秒
231.
A cross-over trial of pancreatic enzyme replacement therapy has been conducted on 12 children with cystic fibrosis using Pancrex V forte and Nutrizym tablets in equivalent dosage. No differences were found in the effectiveness of these products as measured by stool volume, number of bowel actions, faecal fat excretion, and urine urea excretion. Neither product eliminated the steatorrhoea. Though there was no laboratory evidence to support their choice nine patients expressed a preference for Nutrizym at the conclusion of the trial. This preference was based partly on the smaller number of tablets which are required.  相似文献   
232.
D. J. Goodchild  C. Miller 《Protoplasma》1997,198(3-4):130-134
Summary Immunocytochemical localisation of hemoglobin on sections ofFrankia-infecledCasuarina glauca nodule tissue confirmed its presence in nitrogen-fixing infected cells. Using colloidal gold as the marker, hemoglobin was shown to be restricted to the cytoplasm and nucleus of infected cells. None was associated with endophyte hyphae or uninfected cells. As infection developed, with its associated thickening and modification of host cell walls, the level of label, and by implication, the level of hemoglobin increased.Abbreviations SPL semi-permeable layer - GA glutaraldehyde - PFA paraformaldehyde  相似文献   
233.
234.
The adhesion of artificially generated lipid membrane vesicles to Chinese hamster V79 fibroblasts in suspension was used as a model system for studying membrane interactions. Below their gel-liquid crystalline phase transition temperature, vesicles comprised of dipalmitoyl lecithin (DPL) or dimyristoyl lecithin (DML) absorbed to the surfaces of EDTA- dissociated cells. These adherent vesicles could not be removed by repeated washings of the treated cells but could be released into the medium by treatment with trypsin. EM autoradiographic studies of cells treated with[(3)H]DML or [(3)H]DPL vesicles showed that most of the radioactive lipids were confined to the cell periphery. Scanning electron microscopy and fluorescence microscopy further confirmed the presence of adherent vesicles at the cell surface. Adhesion of DML or DPL vesicles to EDTA-dissociated cells modified the lactoperoxidase-catalyzed iodination pattern of the cell surface proteins; the inhibition of labeling of two proteins with an approximately 60,000- dalton mol wt was particularly evident. Incubation of cells wit h (3)H-lipid vesicles followed by sodium dodecyl sulfate (SDS)- polyacrylamide gel electrophoresis showed that some of the (3)H-lipid migrated preferentially with these approximately 60,000-mol wt proteins. Studies of the temperature dependence of vesicle uptake and subsequent release by trypsin showed that DML or DPL vesicle adhesion to EDTA- dissociated cells increased with decreasing temperatures. In contrast, cells trypsinized before incubation with vesicles showed practically no temperature dependence of vesicle uptake. These results suggest two pathways for adhesion of lipid vesicles to the cell surface-a temperature-sensitive one involving cell surface proteins, and a temperature-independent one. These findings are discussed in terms of current models for cell-cell interactions.  相似文献   
235.
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号