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   995262篇
  免费   112834篇
  国内免费   396篇
  2018年   9087篇
  2016年   11737篇
  2015年   15326篇
  2014年   18466篇
  2013年   26514篇
  2012年   29631篇
  2011年   30495篇
  2010年   20711篇
  2009年   19099篇
  2008年   27128篇
  2007年   28254篇
  2006年   26523篇
  2005年   25657篇
  2004年   25340篇
  2003年   24630篇
  2002年   24057篇
  2001年   41867篇
  2000年   42166篇
  1999年   33628篇
  1998年   12099篇
  1997年   12706篇
  1996年   12074篇
  1995年   11457篇
  1994年   11344篇
  1993年   11258篇
  1992年   29039篇
  1991年   28891篇
  1990年   28154篇
  1989年   27770篇
  1988年   25770篇
  1987年   24756篇
  1986年   23209篇
  1985年   23503篇
  1984年   19590篇
  1983年   17034篇
  1982年   13014篇
  1981年   11824篇
  1980年   11263篇
  1979年   19141篇
  1978年   15004篇
  1977年   13860篇
  1976年   13208篇
  1975年   14779篇
  1974年   15557篇
  1973年   15335篇
  1972年   14130篇
  1971年   12717篇
  1970年   11045篇
  1969年   10483篇
  1968年   9624篇
排序方式: 共有10000条查询结果,搜索用时 15 毫秒
1.
2.
We have identified mouse and human FKBP60, a new member of the FKBP gene family. FKBP60 shares strongest homology with FKBP65 and SMAP. FKBP60 contains a hydrophobic signal peptide at the N-terminus, 4 peptidyl-prolyl cis/trans isomerase (PPIase) domains and an endoplasmic reticulum retention motif (HDEL) at the C-terminus. Immunodetection of HA-tagged FKBP60 in NIH-3T3 cells suggests that FKBP60 is segregated to the endoplasmic reticulum. Northern blot analysis shows that FKBP60 is predominantly expressed in heart, skeletal muscle, lung, liver and kidney. With N-succinyl-Ala-Ala-Pro-Phe-p-nitroanilide as a substrate, recombinant GST-FKBP60 is shown to accelerate effectively the isomerization of the peptidyl-prolyl bond. This isomerization activity is inhibited by FK506. mFKBP60 binds Ca2+ in vitro, presumably by its C-terminal EF-hand Ca2+ binding motif, and is phosphorylated in vivo. hFKBP60 has been mapped to 7p12 and/or 7p14 by fluorescence in situ hybridization (FISH).  相似文献   
3.
4.
A patient with chronic anemia is presented who radiologically showed prominent rugae of the stomach. Angiography demonstrated an arteriovenous malformation with a large feeding artery and prominent draining veins.  相似文献   
5.
6.
A conceptual model is proposed, describing potential Zostera marina habitats in the Wadden Sea, based on reported data from laboratory, mesocosm and field studies. Controlling factors in the model are dynamics, degree of desiccation, turbidity, nutrients and salinity. A distinction has been made between a higher and a lower zone of potential habitats, each suitable for different morphotypes of Z. marina. The model relates the decline of Z. marina in the Wadden Sea to increased sediment and water dynamics, turbidity, drainage of sediments (resulting in increased degree of desiccation) and total nutrient loads during the twentieth century. The upper and lower delineation of both the higher and the lower zone of potential Z. marina habitats appear to be determined by one or a combination of several of these factors. Environmental changes in one of these factors will therefore influence the borderlines of the zones. The lower zone of Z. marina will be mainly affected by increased turbidity, sediment dynamics, degree of desiccation during low tide and nutrient load. The higher zone will be affected by increases in water and sediment dynamics, desiccation rates and nutrient loads. Potential Z. marina habitats are located above approx. –0.80 m mean sea level (when turbidity remains at the same level as in the early 1990s) in sheltered, undisturbed locations, and preferably where some freshwater influence is present. At locations with a high, near-marine, salinity, the nutrient load has to be low to allow the growth of Z. marina. The sediment should retain enough water during low tide to keep the plants moist. Our results suggest that the return of Z. marina beds within a reasonable time-scale will require not only suitable habitat conditions, but also revegetation measures, as the changes in the environment resulting from the disappearance of Z. marina may impede its recovery, and the natural import of propagules will be unlikely. Furthermore, the lower zone of Z. marina may require a genotype that is no longer found in the Wadden Sea. Received: 26 April 1999 / Received in revised form: 15 October 1999 / Accepted: 16 October 1999  相似文献   
7.
8.
9.
10.
Based on its proven anabolic effects on bone in osteoporosis patients, recombinant parathyroid hormone (PTH1-34) has been evaluated as a potential therapy for skeletal repair. In animals, the effect of PTH1-34 has been investigated in various skeletal repair models such as fractures, allografting, spinal arthrodesis and distraction osteogenesis. These studies have demonstrated that intermittent PTH1-34 treatment enhances and accelerates the skeletal repair process via a number of mechanisms, which include effects on mesenchymal stem cells, angiogenesis, chondrogenesis, bone formation and resorption. Furthermore, PTH1-34 has been shown to enhance bone repair in challenged animal models of aging, inflammatory arthritis and glucocorticoid-induced bone loss. This pre-clinical success has led to off-label clinical use and a number of case reports documenting PTH1-34 treatment of delayed-unions and non-unions have been published. Although a recently completed phase 2 clinical trial of PTH1-34 treatment of patients with radius fracture has failed to achieve its primary outcome, largely because of effective healing in the placebo group, several secondary outcomes are statistically significant, highlighting important issues concerning the appropriate patient population for PTH1-34 therapy in skeletal repair. Here, we review our current knowledge of the effects of PTH1-34 therapy for bone healing, enumerate several critical unresolved issues (e.g., appropriate dosing regimen and indications) and discuss the long-term potential of this drug as an adjuvant for endogenous tissue engineering.  相似文献   
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