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   3013篇
  免费   32篇
  国内免费   11篇
耳鼻咽喉   15篇
儿科学   211篇
妇产科学   24篇
基础医学   268篇
口腔科学   51篇
临床医学   502篇
内科学   442篇
皮肤病学   82篇
神经病学   172篇
特种医学   86篇
外国民族医学   2篇
外科学   399篇
综合类   244篇
预防医学   232篇
眼科学   65篇
药学   154篇
中国医学   28篇
肿瘤学   79篇
  2023年   8篇
  2022年   22篇
  2021年   69篇
  2020年   18篇
  2019年   350篇
  2018年   288篇
  2017年   161篇
  2016年   40篇
  2015年   51篇
  2014年   128篇
  2013年   80篇
  2012年   77篇
  2011年   130篇
  2010年   119篇
  2009年   106篇
  2008年   90篇
  2007年   66篇
  2006年   26篇
  2005年   34篇
  2004年   40篇
  2003年   33篇
  2002年   29篇
  2001年   32篇
  2000年   20篇
  1999年   19篇
  1998年   12篇
  1997年   22篇
  1996年   6篇
  1995年   16篇
  1994年   12篇
  1993年   9篇
  1992年   27篇
  1991年   25篇
  1990年   18篇
  1989年   9篇
  1988年   12篇
  1987年   8篇
  1986年   2篇
  1985年   134篇
  1984年   156篇
  1983年   82篇
  1982年   102篇
  1981年   91篇
  1980年   82篇
  1979年   83篇
  1978年   50篇
  1977年   35篇
  1976年   17篇
  1975年   6篇
  1973年   2篇
排序方式: 共有3056条查询结果,搜索用时 15 毫秒
1.
2.
27例肾上腺肿瘤及增生中皮质醇症8例、嗜铬细胞瘤16例、原发性醛固酮增多症、髓质增生症及无功能性肿瘤各1例。定位诊断主要为CT检查及腹膜后注气造影。皮质醇症术前应有效地控制血糖;嗜铬细胞瘤术前使用皮质激素有助于患者顺利地度过手术关。本组患者以手术治疗为主,并阐述了手术治疗的经验。  相似文献   
3.
5例强直性肌营养不良患者的腓肠肌活检标本超微结构研究结果发现,除肌纤维变性、萎缩和结缔组织增生外,毛细血管病变特别突出。血管壁严重增厚,基板呈多层性改变,周细胞增生。有些复层的毛细血管基板多达9层。内皮细胞外可有多层周细胞半包绕血管,有些周细胞又发出分支沿管壁延伸。周细胞一般位于内皮细胞下第一层基板之外,也可位于复层基板之中,周细胞与周细胞之间有多层基板。内皮细胞和周细胞内富含吞饮小泡。血管病变程度与肌纤维变性程度呈平行关系。  相似文献   
4.
本文对云南老山前、后方医院环境及战伤感染标本中绿脓杆菌(简称PA)进行调查,对所分离的333株PA进行血清学分型及药物敏感性测定。结果可看出除炸伤时创口易被泥土中PA污染外,前、后方医院环境也是感染源之一。提示各级医疗单位在战伤救治中对PA的监控十分重要。本文结果直接有益于前、后方医院对战创伤PA的防治。  相似文献   
5.
应用全血血小板聚集仪阻抗法对34例白血病患者的血小板聚集和 ATP 释放进行了同步测定。结果表明:白血病患者的血小板聚集和 ATP 释放明显低于正常。提示白血病患者不仅有血小板投量减少,亦存在其聚集及释放功能的障碍。  相似文献   
6.
采用 Mark-600型超声诊断仪测量了128例高血压病患者主动脉壁厚度(AWT),并同时检测了血脂指标,结果显示,高脂血症组血清 apoB 及 AWT 均显著高或厚于血脂正常组(P<0.01),其 apoAI/apoB 比值显著低于血脂正常组(P<0.01),临床合并冠心病的患病率亦显著高于血脂正常组(P<0.05)。相关性分析显示,AWT 与 apoB(r=0.338)呈直线正相关,与 apoAl(r=-0.385)及apoAl/apoB(r=-0.540),呈直线负相关,(P 均<0.01)。经逐步回归分析,筛选对 AWT 有显著作用的血脂指标,结果依次为 apoAl/apoB、apoB。  相似文献   
7.
我院1968~1984年间收治小儿肱骨髁上骨折并血循环障碍52例采用非手术治疗的方法如下:对无急性缺血者采取臂丛麻醉,手法整复,鹰嘴骨牵引1~2周后,小夹板外固定,功能煅炼等中西医结合的处理,均获得满意的功能恢复,无一例发生缺血性肌挛缩。  相似文献   
8.
The origins of the projections of the superior colliculus to the dorsal lateral geniculate nucleus and to the pulvinar in Dutch-belted rabbits were investigated using horseradish peroxidase (HRP) methods. Following injections of HRP in the dorsal lateral geniculate nucleus, retrogradely labeled neurons were found in the upper two-thirds of the stratum griseum superficiale of the ipsilateral superior colliculus. Most of the labeled somata were spindle-shaped, and their major axes tended to be perpendicular to the surface of the superior colliculus. In contrast, following injections of the pulvinar, labeled neurons were found in the lower third of the ipsilateral stratum griseum superficiale. In these cases, the labeled somata were larger than those labeled following dorsal lateral geniculate injections and were multipolar in shape.  相似文献   
9.
Eleven subjects demonstrating clinical, skin, and inhalation sensitivity to grass or ragweed pollen underwent serial inhalation challenges, with and without orally administered theophylline, terbutaline, and prednisone. Comparisons of antigen sensitivity and mediator release were made during these challenges. All three drugs significantly reduced antigen sensitivity (PD20 inhalation units increasing from 670 to ≧ 3,280). Peak plasma histamine levels after antigen challenge decreased from 11.4 ng/ml to ≦ 3.4 ng/ml during all drug administrations. Similarly, the percent increase in serum neutrophil chemotactic activity (NCA) also decreased, from 96% to ≦ 36% during drug administrations. However, even at antigen doses resulting in bronchospasm during drug administration the systemic appearance of NCA and histamine were reduced. We conclude that prednisone, theophylline, and terbutaline significantly reduce antigen-induced bronchospasm and mediator release. The occurrence of bronchospasm despite the inhibition of histamine and NCA suggests either that the local concentration of these mediators are critical or that other mediators produce the bronchospasm observed.  相似文献   
10.
Defective intestinal tight junction (TJ) barrier is an important pathogenic factor of inflammatory bowel disease. To date, no effective therapies that specifically target the intestinal TJ barrier are available. The purpose of this study was to identify probiotic bacterial species or strains that induce a rapid and sustained enhancement of intestinal TJ barrier and protect against the development of intestinal inflammation by targeting the TJ barrier. After high-throughput screening of >20 Lactobacillus and other probiotic bacterial species or strains, a specific strain of Lactobacillus acidophilus, referred to as LA1, uniquely produced a marked enhancement of the intestinal TJ barrier. LA1 attached to the apical membrane surface of intestinal epithelial cells in a Toll-like receptor (TLR)-2–dependent manner and caused a rapid increase in enterocyte TLR-2 membrane expression and TLR-2/TLR-1 and TLR-2/TLR-6 hetero-complex–dependent enhancement in intestinal TJ barrier function. Oral administration of LA1 caused a rapid enhancement in mouse intestinal TJ barrier, protected against a dextran sodium sulfate (DSS) increase in intestinal permeability, and prevented the DSS-induced colitis in a TLR-2– and intestinal TJ barrier–dependent manner. In conclusion, we report for the first time that a specific strain of LA causes a strain-specific enhancement of intestinal TJ barrier through a novel mechanism that involves the TLR-2 receptor complex and protects against the DSS-induced colitis by targeting the intestinal TJ barrier.

Intestinal epithelial tight junctions (TJs) are the apical-most junctional complexes and act as a functional and structural barrier against the paracellular permeation of harmful luminal antigens, which promote intestinal inflammation.1 The increased intestinal permeability caused by defective intestinal epithelial TJ barrier or a leaky gut is an important pathogenic factor that contributes to the development of intestinal inflammation in inflammatory bowel disease (IBD) and other inflammatory conditions of the gut, including necrotizing enterocolitis and celiac disease.2,3 Clinical studies in patients with IBD have found that a persistent increase in intestinal permeability after clinical remission is predictive of poor clinical outcome and early recurrence of the disease, whereas normalization of intestinal permeability correlates with a sustained long-term clinical remission.4, 5, 6 Accumulating evidence has found that a defective intestinal TJ barrier plays an important role in exacerbation and prolongation of intestinal inflammation in IBD. Currently, no effective therapies that specifically target the tightening of the intestinal TJ barrier are available.Intestinal microbiota play an important role in modulating the immune system and in the pathogenesis of intestinal inflammation.7 Patients with IBD have bacterial dysbiosis in the gut, characterized by a decrease in bacterial diversity and an aberrant increase in some commensal bacteria, which are an important factor in the pathogenesis of intestinal inflammation.8,9 Normal microbial flora of the gastrointestinal tract consists both of bacteria that are known to have beneficial effects (probiotic bacteria) on intestinal homeostasis and bacteria that could potentially have detrimental effects on gut health (pathogenic bacteria).10 The modulation of intestinal microflora affects the physiologic and pathologic states in humans and animals. For example, fecal transplantation from healthy, unaffected individuals to patients with refractory Clostridium difficile colitis is curative in up to 94% of the treated patients, and transfer of stool microbiome from obese mice induces obesity in previous lean mice, whereas transfer of microbiome from lean mice preserves the lean phenotype.11, 12, 13 The beneficial effects of gut microbiota are host and bacterial species-specific.14 Although multiple studies indicate that some commensal bacteria play a beneficial role in gut homeostasis by preserving or promoting the intestinal barrier function, because of conflicting reports, it remains unclear which probiotic species cause a persistent predictable enhancement in the TJ barrier and could be used to treat intestinal inflammation by targeting the TJ barrier. For example, some studies suggest that Lactobacillus acidophilus, Lactobacillus casei, Lactobacillus plantarum, or Lactobacillus rhamnosus cause a modest enhancement in the intestinal epithelial TJ barrier, whereas others have found minimal or no effect of these probiotic species on the intestinal TJ barrier.15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25 The major aim the current study was to perform a high-throughput screening of Lactobacillus and other bacterial species to identify probiotic species that induce a rapid, predictable, and marked increase in the intestinal epithelial TJ barrier and protect against the development of intestinal inflammation by preserving the intestinal TJ barrier.In the studies described herein, most of the probiotic species tested (>20 species or strains) had a modest or minimal effect on intestinal TJ barrier function. L. acidophilus uniquely caused a rapid and marked increase in intestinal TJ barrier function. Further analysis indicated that the effect of L. acidophilus was strain-specific, limited to a specific strain of L. acidophilus, and did not extend to other L. acidophilus strains. The L. acidophilus enhancement of the intestinal TJ barrier was mediated by live bacterial-enterocyte interaction that involved Toll-like receptor (TLR)-2 heterodimeric complexes on the apical membrane surface of intestinal epithelial cells. Our animal studies also found that L. acidophilus causes a marked enhancement in mouse intestinal barrier function and protects against the dextran sodium sulfate (DSS)–induced colitis by preserving and augmenting the mouse intestinal barrier function in a strain-specific manner.  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