全文获取类型
收费全文 | 748篇 |
免费 | 56篇 |
国内免费 | 33篇 |
专业分类
837篇 |
出版年
2023年 | 6篇 |
2022年 | 21篇 |
2021年 | 21篇 |
2020年 | 15篇 |
2019年 | 22篇 |
2018年 | 20篇 |
2017年 | 13篇 |
2016年 | 16篇 |
2015年 | 48篇 |
2014年 | 41篇 |
2013年 | 48篇 |
2012年 | 58篇 |
2011年 | 45篇 |
2010年 | 31篇 |
2009年 | 22篇 |
2008年 | 38篇 |
2007年 | 42篇 |
2006年 | 35篇 |
2005年 | 22篇 |
2004年 | 21篇 |
2003年 | 25篇 |
2002年 | 32篇 |
2001年 | 15篇 |
2000年 | 20篇 |
1999年 | 13篇 |
1998年 | 13篇 |
1997年 | 15篇 |
1996年 | 5篇 |
1995年 | 5篇 |
1994年 | 5篇 |
1993年 | 11篇 |
1992年 | 6篇 |
1990年 | 7篇 |
1989年 | 4篇 |
1988年 | 4篇 |
1987年 | 10篇 |
1986年 | 3篇 |
1985年 | 5篇 |
1984年 | 5篇 |
1983年 | 3篇 |
1981年 | 2篇 |
1976年 | 4篇 |
1975年 | 3篇 |
1974年 | 2篇 |
1973年 | 10篇 |
1972年 | 2篇 |
1970年 | 2篇 |
1968年 | 3篇 |
1967年 | 3篇 |
1966年 | 8篇 |
排序方式: 共有837条查询结果,搜索用时 8 毫秒
91.
为了解nm23-H1转染对全反式维甲酸诱导的人肝癌H7721细胞凋亡的影响,本研究通过质粒转染把nm23-H1导入人肝癌7721细胞,建立了nm23-H1过表达稳转细胞株。首先采用MTT法测定细胞生长曲线,再通过流式细胞术和丫啶橙染色法观察细胞凋亡,最后采用Western blot检测凋亡相关的信号通路分子bcl-2、PKB、PKB-Ser473、PKB-Thr308和p53的表达情况。研究发现,nm23-H1转染对人肝癌7721细胞的生长没有影响;但nm23-H1转染能明显促进全反式维甲酸诱导的细胞凋亡,nm23-H1转染细胞凋亡率为18.2%,而对照细胞凋亡率仅为1.0%;nm23-H1和对照细胞的过量表达对bcl-2的表达没有明显影响,但PKB的Ser473和Thr308位的磷酸化显著下调,抑癌基因p53的表达量上调。研究结果表明,nm23-H1的过量表达增加了人肝癌细胞对全反式维甲酸诱导的凋亡的敏感性,因此推测nm23-H1可作为肝癌治疗的有效靶点。 相似文献
92.
93.
Xiaodan Zhu Dong Yang Chunxue Bai Yuanlin Song Jun She 《Journal of cellular and molecular medicine》2014,18(6):1226-1235
Preservation or restoration of normal alveolar epithelial barrier function is crucial for pulmonary oedema resolution. Keratinocyte growth factor‐2 (KGF‐2), a potent epithelial cell mitogen, may have a role in preventing ventilator‐induced lung injury (VILI), which occurs frequently in mechanically ventilated patients. The aim of the study was to test the role of KGF‐2 in VILI in rats. Forty healthy adult male Sprague‐Dawley rats were randomly allocated into four groups, where rats in Groups HVZP (high‐volume zero positive end‐expiratory pressure) and HVZP+KGF‐2 were given intratracheally equal PBS and 5 mg/kg KGF‐2 72 hrs before 4 hrs HVZP ventilation (20 ml/kg), respectively, while PBS and KGF‐2 were administered in the same manner in Groups Control and KGF‐2, which underwent tracheotomy only with spontaneous breathing. Inflammatory cytokines (tumour necrosis factor‐α, macrophage inflammatory protein 2), neutrophil and total protein levels in bronchoalveolar lavage fluid and surfactant protein mRNA expression in lung tissue were detected; the number of alveolar type II cells, lung water content and lung morphology were also evaluated. The results indicate that pre‐treatment with KGF‐2 showed dramatic improvement in lung oedema and inflammation compared with HVZP alone, together with increased surfactant protein mRNA and alveolar type II cells. Our results suggest that KGF‐2 might be considered a promising prevention for human VILI or other acute lung injury diseases. 相似文献
94.
95.
噪声习服对听觉损伤的保护作用机制探讨 总被引:2,自引:0,他引:2
目的:探讨噪声习服对听觉损伤的保护作用机制.方法:建立噪声习服实验动物模型.采用免疫组织化学、激光扫描共聚焦显微镜(LSCM)及图像分析等技术,定量研究噪声习服后毛细胞内纤维状肌动蛋白(F-actin)、钙调蛋白(CaM)、热休克蛋白70(HSP70)的表达及游离Ca2 浓度的变化.结果:噪声暴露后毛细胞中F-actin、CaM及HSP70的表达均呈增加趋势.与噪声损伤暴露组(H组)比较,噪声习服后损伤暴露组(CH组)中F-actin和HSP70的表达均明显增多,CaM的表达具有增加趋势.声暴露后毛细胞内游离Ca2 浓度升高,噪声损伤暴露组毛细胞内游离Ca2 浓度明显高于噪声习服组(C组)和习服后损伤暴露组.结论:噪声习服使毛细胞对于其后声刺激的保护性反应增强,毛细胞内细胞骨架系统的加强及胞内钙稳态的维持在噪声习服的保护机制中具有重要意义. 相似文献
96.
Jin Wang Ping Liu Mary F.H. She Saeid Nahavandi Abbas Kouzani 《Biomedical signal processing and control》2013,8(6):634-644
Automatic analysis of biomedical time series such as electroencephalogram (EEG) and electrocardiographic (ECG) signals has attracted great interest in the community of biomedical engineering due to its important applications in medicine. In this work, a simple yet effective bag-of-words representation that is originally developed for text document analysis is extended for biomedical time series representation. In particular, similar to the bag-of-words model used in text document domain, the proposed method treats a time series as a text document and extracts local segments from the time series as words. The biomedical time series is then represented as a histogram of codewords, each entry of which is the count of a codeword appeared in the time series. Although the temporal order of the local segments is ignored, the bag-of-words representation is able to capture high-level structural information because both local and global structural information are well utilized. The performance of the bag-of-words model is validated on three datasets extracted from real EEG and ECG signals. The experimental results demonstrate that the proposed method is not only insensitive to parameters of the bag-of-words model such as local segment length and codebook size, but also robust to noise. 相似文献
97.
98.
本文研究了白芨中的萜类化合物对血管生成的抑制作用.及其抑制血管生成的可能机制。采用萃取和色谱法从白芨中分离和纯化了该萜类化合物。通过鸡胚绒毛囊膜(CAM)和人脐静脉内皮细胞(HUVEC)研究了白芨中萜类化合物及其粗提物对血管及血管内皮细胞的抑制作用。结果表明,含该萜类的粗提物显著抑制鸡胚绒毛尿囊膜血管生成;该萜类纯品能明显抑制HUVEC增殖,且可诱导HUVEC凋亡,包括细胞体积缩小,细胞膜起泡,细胞核裂解,染色质浓缩和边集,出现凋亡小体,DNA降解。因此.白芨萜类化合物的抗血管生成作用与诱导血管内皮细胞凋亡有关。 相似文献
99.
100.
Jie Sun Tao Tao Wei Zhao Lisha Wei Fan She Pei Wang Yeqiong Li Yanyan Zheng Xin Chen Wei Wang Yanning Qiao Xue-Na Zhang Min-Sheng Zhu 《遗传学报》2019,46(3):109-118
Several factors have been implicated in obesity-related hypertension, but the genesis of the hypertension is largely unknown. In this study, we found a significantly upregulated expression of CPI-17(C-kinasepotentiated protein phosphatase 1 inhibitor of 17 kDa) and protein kinase C(PKC) isoforms in the vascular smooth muscles of high-fat diet(HFD)-fed obese mice. The obese wild-type mice showed a significant elevation of blood pressure and enhanced calcium-sensitized contraction of vascular smooth muscles. However, the obese CPI-17-deficient mice showed a normotensive blood pressure, and the calcium-sensitized contraction was consistently reduced. In addition, the mutant muscle displayed an abolished responsive force to a PKC activator and a 30%-50% reduction in both the initial peak force and sustained force in response to various G protein-coupled receptor(GPCR) agonists. Our observations showed that CPI-17-mediated calcium sensitization is mediated through a GPCR/PKC/CPI-17/MLCP/RLC signaling pathway. We therefore propose that the upregulation of CPI-17-mediated calcium-sensitized vasocontraction by obesity contributes to the development of obesity-related hypertension. 相似文献