全文获取类型
收费全文 | 5488篇 |
免费 | 563篇 |
国内免费 | 1059篇 |
专业分类
7110篇 |
出版年
2024年 | 29篇 |
2023年 | 66篇 |
2022年 | 164篇 |
2021年 | 267篇 |
2020年 | 206篇 |
2019年 | 250篇 |
2018年 | 225篇 |
2017年 | 174篇 |
2016年 | 275篇 |
2015年 | 358篇 |
2014年 | 475篇 |
2013年 | 472篇 |
2012年 | 595篇 |
2011年 | 491篇 |
2010年 | 364篇 |
2009年 | 344篇 |
2008年 | 376篇 |
2007年 | 377篇 |
2006年 | 287篇 |
2005年 | 256篇 |
2004年 | 226篇 |
2003年 | 182篇 |
2002年 | 160篇 |
2001年 | 77篇 |
2000年 | 62篇 |
1999年 | 84篇 |
1998年 | 62篇 |
1997年 | 27篇 |
1996年 | 32篇 |
1995年 | 21篇 |
1994年 | 24篇 |
1993年 | 17篇 |
1992年 | 16篇 |
1991年 | 12篇 |
1990年 | 5篇 |
1989年 | 5篇 |
1988年 | 4篇 |
1987年 | 5篇 |
1986年 | 6篇 |
1985年 | 4篇 |
1984年 | 2篇 |
1982年 | 5篇 |
1981年 | 3篇 |
1977年 | 2篇 |
1972年 | 2篇 |
1967年 | 1篇 |
1961年 | 1篇 |
1950年 | 4篇 |
1925年 | 1篇 |
1915年 | 1篇 |
排序方式: 共有7110条查询结果,搜索用时 15 毫秒
121.
Genome assembly provides insights into the genome evolution and flowering regulation of orchardgrass
122.
123.
Xiangcheng Qin Aimei Lu Meilin Ke Weizhi Zhu Xiaolei Ye Gang Wang Guobin Weng 《Cell biology international》2020,44(4):937-946
The regulation of DJ‐1 on AR signaling plays an important role in the pathogenesis of prostate cancer (PCa). DJ‐1 could alter autophagy and regulate Beclin1‐involved autophagy response through JNK‐dependent pathway. JNK is known to mediate autophagy through Bcl2–Beclin1 complex. Therefore, this study aimed to investigate the significance of autophagy in DJ‐1‐modulated PCa cells. The current studies showed that DJ‐1 overexpression in LNCaP decreased LC3 transformation and autophagosome formation. However, DJ‐1 knockdown exerted the opposite effect. Moreover, DJ‐1 silencing inhibited survival and promoted death in LNCaP, which was recovered by autophagy inhibition with 3‐MA. In addition, DJ‐1 overexpression inhibited the phosphorylation of JNK and Bcl2, and the dissociation of Beclin1 and Bcl2; while the effect of silencing DJ‐1 was completely opposite. More important, JNK activated by anisimycin inhibited the proliferation and promoted death of DJ‐1‐overexpressed LNCaP while increasing LC3 transformation and LC3‐puncta formation, but these results were reversed by the decrease of Beclin1 (by spautin‐1). In contrast, when DJ‐1 was silenced, the death of LNCaP, LC3 transformation, and LC3‐puncta formation were inhibited by JNK inhibitor SP600125, which promoted cell proliferation. However, Bcl2 inhibition (by ABT737) reversed all the effects of SP600125. Our results suggested that DJ‐1 in PCa cells could promote the growth of PCa through autophagy inhibition, and JNK–Bcl2–Beclin1 signaling played an important role in it. The study provided new insights into the role of DJ‐1 in the development of PCa. 相似文献
124.
125.
Yuanqing Tan Lei Wang Gang Chen Wenjing Liu Zhongwen Li Yukai Wang Liu Wang Wei Li Jun Wu Jie Hao 《Cell proliferation》2020,53(12)
IntroductionEnormous progress has been made in cardiac regeneration using human embryonic stem cell‐derived cardiomyocyte (hESC‐CM) grafts in pre‐clinical trials. However, the rate of cell survival has remained very low due to anoikis after transplantation into the heart as single cells. Numerous solutions have been proposed to improve cell survival, and one of these strategies is to co‐transplant biocompatible materials or hydrogels with the hESC‐CMs.MethodsIn our study, we screened various combinations of biomaterials that could promote anoikis resistance and improve hESC‐CM survival upon co‐transplantation and promote cardiac functional recovery. We injected different combinations of Matrigel, alginate and hyaluronate with hESC‐CM suspensions into the myocardium of rat models with myocardial infarction (MI).ResultsOur results showed that the group treated with a combination of hyaluronate and hESC‐CMs had the lowest arrhythmia rates when stimulated with programmed electrical stimulation. While all three combinations of hydrogel‐hESC‐CM treatments improved rat cardiac function compared with the saline control group, the combination with hyaluronate most significantly reduced pathological changes from left ventricular remodelling and improved both left ventricular function and left ventricular ejection fraction by 28 days post‐infarction.ConclusionHence, we concluded that hyaluronate‐hESC‐CM is a superior combination therapy for promoting cardiac regeneration after myocardial infarction. 相似文献
126.
Yaxing Chen Chen Qin Jianhan Huang Xin Tang Chang Liu Keru Huang Jianguo Xu Gang Guo Aiping Tong Liangxue Zhou 《Cell proliferation》2020,53(3)
Central nervous system (CNS) maintains a high level of metabolism, which leads to the generation of large amounts of free radicals, and it is also one of the most vulnerable organs to oxidative stress. Emerging evidences have shown that, as the key homeostatic cells in CNS, astrocytes are deeply involved in multiple aspects of CNS function including oxidative stress regulation. Besides, the redox level in CNS can in turn affect astrocytes in morphology and function. The complex and multiple roles of astrocytes indicate that their correct performance is crucial for the normal functioning of the CNS, and its dysfunction may result in the occurrence and progression of various neurological disorders. To date, the influence of astrocytes in CNS oxidative stress is rarely reviewed. Therefore, in this review we sum up the roles of astrocytes in redox regulation and the corresponding mechanisms under both normal and different pathological conditions. 相似文献
127.
催乳素受体通过结合催乳素,能调节鱼体渗透压。为研究催乳素受体1(PRLR1)在高盐水体和低盐水体中对军曹鱼(Rachycentron canadum)的渗透调节作用,利用cDNA末端快速扩增(RACE-PCR)技术,获得了军曹鱼PRLR1全长cDNA序列。该基因全长为2629 bp,包含1953 bp的开放阅读框ORF,可编码650个氨基酸。氨基酸序列包含了2个纤维连接蛋白3型结构域(FN3)、保守的WS区和box1。采用qRT-PCR技术,检测不同盐度(10‰、30‰和35‰)条件下鳃、肠、体肾中PRLR1基因mRNA表达情况。结果显示,PRLR1基因在军曹鱼的各个组织中均有表达,其中鳃表达量最高,其次是肌肉、体肾和肠,而在胃、脾、脑和心脏中则微量表达。低盐组、正常组和高盐组中,PRLR1基因的表达量均为鳃最高;肠次之;体肾最低。随着盐度提高,PRLR1基因的鳃、肠和体肾组织表达量变化规律均呈逐步下降趋势。以上结果反映了军曹鱼PRLR1在渗透压器官中的功能差异性,说明PRLR1在军曹鱼渗透压调节上具有重要作用。 相似文献
128.
Xiaolian Ye Gang Zou Jinxing Hou Huiru Bi Cuihua Zhou Runmin Wang Yun Xu Chun Wang Guiquan Chen Zhenyu Yin Jinping Zhang Chaoli Huang 《Biochemistry and Biophysics Reports》2020
Prolonged neuroinflammation is a driving force for neurodegenerative disease, and agents against inflammatory responses are regarded as potential treatment strategies. Here we aimed to evaluate the prevention effects on gliosis by dexamethasone (DEX), an anti-inflammation drug. We used DEX to treat the nicastrin conditional knockout (cKO) mouse, a neurodegenerative mouse model. DEX (10 mg/kg) was given to 2.5-month-old nicastrin cKO mice, which have not started to display neurodegeneration and gliosis, for 2 months. Immunohistochemistry (IHC) and Western blotting techniques were used to detect changes in neuroinflammatory responses. We found that activation of glial fibrillary acidic protein (GFAP) positive or ionized calcium binding adapter molecule1 (Iba1) positive cells was not inhibited in nicastrin cKO mice treated with DEX as compared to those treated with saline. These data suggest that DEX does not prevent or ameliorate gliosis in a neurodegenerative mouse model when given prior to neuronal or synaptic loss. 相似文献
129.