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   121167篇
  免费   7840篇
  国内免费   1795篇
耳鼻咽喉   1118篇
儿科学   3651篇
妇产科学   2623篇
基础医学   17164篇
口腔科学   4189篇
临床医学   11809篇
内科学   26283篇
皮肤病学   2844篇
神经病学   11261篇
特种医学   3084篇
外国民族医学   14篇
外科学   10734篇
综合类   2947篇
现状与发展   4篇
一般理论   51篇
预防医学   11568篇
眼科学   2086篇
药学   8997篇
  20篇
中国医学   1388篇
肿瘤学   8967篇
  2024年   129篇
  2023年   1204篇
  2022年   2771篇
  2021年   4469篇
  2020年   2888篇
  2019年   3633篇
  2018年   4078篇
  2017年   3178篇
  2016年   3555篇
  2015年   4118篇
  2014年   5380篇
  2013年   6606篇
  2012年   9988篇
  2011年   10489篇
  2010年   5827篇
  2009年   4858篇
  2008年   8186篇
  2007年   8091篇
  2006年   7502篇
  2005年   7048篇
  2004年   6185篇
  2003年   5536篇
  2002年   4956篇
  2001年   879篇
  2000年   741篇
  1999年   926篇
  1998年   985篇
  1997年   845篇
  1996年   728篇
  1995年   610篇
  1994年   571篇
  1993年   451篇
  1992年   389篇
  1991年   259篇
  1990年   280篇
  1989年   236篇
  1988年   216篇
  1987年   192篇
  1986年   193篇
  1985年   143篇
  1984年   162篇
  1983年   153篇
  1982年   164篇
  1981年   120篇
  1980年   127篇
  1979年   75篇
  1978年   80篇
  1977年   71篇
  1976年   63篇
  1974年   54篇
排序方式: 共有10000条查询结果,搜索用时 15 毫秒
1.
目的 观察结肠癌HCT116细胞健脾消癌方的条件培养液对HUVEC细胞管腔形成的影响,从PI3K/Akt生物轴调控角度探讨其作用机制。方法 培养HCT116细胞,细胞设3组:对照组,健脾消癌方组(加入15%健脾消癌方含药血清)及人参皂苷Rg3组;制备HCT116细胞健脾消癌方条件培养液(分组及制备方法见实验方法),用条件培养液干预HUVEC(脐静脉内皮细胞,Human Umbilical Vein Endothelial Cells),Matrigel基质胶法检测HCT116细胞健脾消癌方条件培养液对HUVEC小管形成的影响。随后采用蛋白免疫印迹法(Western blot)检测各组HCT116细胞磷脂酰肌醇3-激酶(PI3K)、蛋白激酶B(Akt)、p-Akt、VEGF(血管内皮生长因子,Vascular endothelial growth factor)蛋白表达。最后在结肠癌HCT116荷瘤小鼠中验证健脾消癌方对肿瘤生长速度的影响,并经瘤组织VEGF蛋白表达、CD31免疫组化染色检测肿瘤内血管生成情况。结果 模型组HUVEC细胞管腔形成较空白血清组显著增加(P<0.05);健脾消癌方组及人参皂苷Rg3组较模型组HUVEC细胞管腔形成显著减少(P<0.01)。p-Akt和VEGF蛋白表达水平模型组高于空白血清组(P<0.05),健脾消癌方组及人参皂苷Rg3组显著低于模型组(P<0.01);PI3K、Akt蛋白表达量组间差异无统计学意义。与对照组比较,模型组荷瘤小鼠肿瘤体积显著性增大,瘤组织内VEGF表达、CD31阳性面积显著性增加,差异有统计学意义(P<0.05);与模型组比较,健脾消癌方组及人参皂苷Rg3组荷瘤小鼠肿瘤体积显著减小,瘤组织内VEGF表达、CD31阳性面积降低,差异有统计学意义(P<0.05)。结论 健脾消癌方可抑制肿瘤的血管生成和生长,其作用机制可能与PI3K/Akt生物轴调控VEGF表达有关。  相似文献   
2.
Journal of Medical Ultrasonics - Chronic liver disease is still a major problem because disease progression will ultimately lead to liver cirrhosis. Portal hypertension is the hallmark in advanced...  相似文献   
3.

Background

Hyperglycaemia is common in patients with acute brain injury admitted to an intensive care unit (ICU). Many studies have found associations between development of hyperglycaemia and increased mortality in hospitalised patients. However, the optimal target for blood glucose control is unknown. We want to conduct a systematic review with meta-analysis and trial sequential analysis to explore the beneficial and harmful effects of restrictive versus liberal glucose control on patient outcomes in adults with severe acute brain injury.

Methods

We will systematically search medical databases including CENTRAL, Embase, MEDLINE and trial registries. We will search the following websites for ongoing or unpublished trials: http://www.controlled-trials.com/ , http://www.clinicaltrials.gov/ , www.eudraCT.com , http://centerwatch.com/ , The Cochrane Library's CENTRAL, PubMed, EMBASE, Science Citation Index Expanded and CINAHL. Two authors will independently review and select trials and extract data. We will include randomised trials comparing levels of glucose control in our analyses and observational studies will be included to address potential harms. The primary outcomes are defined as all-cause mortality, functional outcome and health-related quality of life. Secondary outcomes include serious adverse events including hypoglycaemia, length of ICU stay and duration of mechanical ventilation, and explorative outcomes including intracranial pressure and infection. Trial Sequential Analysis will be used to investigate the risk of type I error due to repetitive testing and to further explore imprecision. Quality of trials will be evaluated using the Cochrane Risk of Bias tool, and quality of evidence will be assessed using the Grading of Recommendations, Assessment, Development and Evaluations (GRADE) approach.

Discussion

The results of the systematic review will be disseminated through peer-reviewed publication. With the review, we hope to inform future randomised clinical trials and improve clinical practice.  相似文献   
4.
5.
6.
Clinical and Experimental Medicine - Recently, the use of novel targeted drugs significantly improved the overall response rate (ORR) and survival of patients with relapsed/refractory chronic...  相似文献   
7.
8.
The regulation of food intake is a complex mechanism, and the hypothalamus is the main central structure implicated. In particular, the arcuate nucleus appears to be the most critical area in the integration of multiple peripheral signals.Among these signals, those originating from the white adipose tissue and the gastrointestinal tract are known to be involved in the regulation of food intake.The present paper focuses on adiponectin, an adipokine secreted by white adipose tissue, which is reported to have a role in the control of feeding by acting centrally. The recent observation that adiponectin is also able to influence gastric motility raises the question of whether this action represents an additional peripheral mechanism that concurs with the central effects of the hormone on food intake. This possibility, which represents an emerging aspect correlating the central and peripheral effects of adiponectin in the hunger-satiety cycle, is discussed in the present paper.  相似文献   
9.
We report a Chinese family with members affected by epidermolytic ichthyosis (EI), caused by KRT gene mutations. The proband was a 14‐year‐old boy who had simultaneous appearance of nephroblastoma and epidermolytic ichthyosis (EI). Both the patient and his mother exhibited the specific clinical and pathological manifestations of EI. We analysed all exons and flanking sequences of the KRT1 and KRT10 genes using PCR, and found that the proband and his mother had a G>C transition at nucleotide position 1432 in exon 7 of KRT1, resulting in an amino acid substitution of glutamate (GAA) to glutamine (CAA) at codon 478 (E478Q). The KRT10 gene had no mutations.  相似文献   
10.
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