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221.
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AMP-activated protein kinase (AMPK) is indispensable for the development and maintenance of brown adipose tissue (BAT),and its activity is inhibited due to obes... 相似文献
223.
Lei Chen Ghassan K. Abou-Alfa Bo Zheng Jing-Feng Liu Jian Bai Lu-Tao Du Yun-Song Qian Rong Fan Xiao-Long Liu Lin Wu Jin-Lin Hou Hong-Yang Wang The PreCar Team 《Cell research》2021,31(5):589-592
Dear Editor,
Hepatocellular carcinoma (HCC) is the second most deadly cancer worldwide.1 Cirrhosis of different causes predisposes patients to HCC,increasing th... 相似文献
224.
Yunqing Gu Jun Cao Xinyu Zhang Hai Gao Yuyan Wang Jia Wang Juan He Xiaoyi Jiang Jinlan Zhang Guanghui Shen Jie Yang Xichen Zheng Gaowei Hu Yuanfei Zhu Shujuan Du Yunkai Zhu Rong Zhang Jianqing Xu Fei Lan Di Qu Guoliang Xu Yun Zhao Dong Gao Youhua Xie Min Luo Zhigang Lu 《Cell research》2022,32(1):24-37
Host cellular receptors play key roles in the determination of virus tropism and pathogenesis.However,little is known about SARS-CoV-2 host receptors with the e... 相似文献
225.
Xiaorong Hu Ruisong Ma Jianlei Cao Xianjin Du Xinyong Cai Yongzhen Fan 《Journal of cellular and molecular medicine》2022,26(6):1776
Hypoxia/reoxygenation (H/R)‐induced myocardial cell injury is the main cause of acute myocardial infarction (AMI). Many proofs show that circular RNA plays an important role in the development of AMI. The purpose of this study was to investigate the role of circSAMD4A in H/R‐induced myocardial injury. The levels of circular SAMD4A (circSAMD4A) were detected in the heart tissues of AMI mice and H/R‐induced H9C2 cells, and the circSAMD4A was suppressed in AMI mice and H/R‐induced H9C2 cells to investigate its’ function in AMI. The levels of circSAMD4A and miR‐138‐5p were detected by real‐time quantitative PCR, and MTT assay was used to detect cell viability. TUNEL analysis and Annexin V‐FITC were used to determine apoptosis. The expression of Bcl‐2 and Bax proteins was detected by Western blot. IL‐1β, TNF‐α and IL‐6 were detected by ELISA kits. The study found that the levels of circSAMD4A were up‐regulated after H/R induction and inhibition of circSAMD4A expression would reduce the H/R‐induced apoptosis and inflammation. MiR‐138‐5p was down‐regulated in H/R‐induced H9C2 cells. circSAMD4A was a targeted regulator of miR‐138‐5p. CircSAMD4A inhibited the expression of miR‐138‐5p to promote H/R‐induced myocardial cell injury in vitro and vivo. In conclusion, CircSAMD4A can sponge miR‐138‐5p to promote H/R‐induced apoptosis and inflammatory response. 相似文献
226.
In this study,a human-chair model was developed as the basis for a wearable-chair design.Aprototype chair,HUST-EC,based on the model was fabricated and evaluate... 相似文献
227.
Lu Qiao Lili Men Shanshan Yu Junjie Yao Yu Li Mingming Wang Ying Yu Ning Wang Liyuan Ran Yingjie Wu Jianling Du 《Cell death & disease》2022,13(3)
Nonalcoholic fatty liver disease (NAFLD) is closely associated with insulin resistance (IR) and type 2 diabetes mellitus (T2DM), which are all complex metabolic disorders. Selenoprotein S (SelS) is an endoplasmic reticulum (ER) resident selenoprotein involved in regulating ER stress and has been found to participate in the occurrence and development of IR and T2DM. However, the potential role and mechanism of SelS in NAFLD remains unclear. Here, we analyzed SelS expression in the liver of high-fat diet (HFD)-fed mice and obese T2DM model (db/db) mice and generated hepatocyte-specific SelS knockout (SelSH-KO) mice using the Cre-loxP system. We showed that hepatic SelS expression levels were significantly downregulated in HFD-fed mice and db/db mice. Hepatic SelS deficiency markedly increased ER stress markers in the liver and caused hepatic steatosis via increased fatty acid uptake and reduced fatty acid oxidation. Impaired insulin signaling was detected in the liver of SelSH-KO mice with decreased phosphorylation levels of insulin receptor substrate 1 (IRS1) and protein kinase B (PKB/Akt), which ultimately led to disturbed glucose homeostasis. Meanwhile, our results showed hepatic protein kinase Cɛ (PKCɛ) activation participated in the negative regulation of insulin signaling in SelSH-KO mice. Moreover, the inhibitory effect of SelS on hepatic steatosis and IR was confirmed by SelS overexpression in primary hepatocytes in vitro. Thus, we conclude that hepatic SelS plays a key role in regulating hepatic lipid accumulation and insulin action, suggesting that SelS may be a potential intervention target for the prevention and treatment of NAFLD and T2DM.Subject terms: Metabolic syndrome, Obesity 相似文献
228.
阿尔采末病与免疫炎症反应的相关性 总被引:11,自引:0,他引:11
阿尔采末病(Alzheimer’sdisease,AD)可能是中枢神经系统内免疫活性细胞过程激活而导致的免疫炎症反应,其病灶周围存在大量激活的小胶质细胞和星形细胞,可产生大量补体,炎性细胞因子,急性期反应物等导致神经细胞损伤,破坏和死亡。同时体内寂体调节剂和抑制性细胞因子的水平明显长高,虽然不足以保护神经元免遭破坏,但却提示抑制或阻断中枢神经系统的免疫炎症反应的药物可能在AD的防治中具有重要作用。 相似文献
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The mismatch repair proteins, MutS and MutL, interact in a DNA mismatch and ATP-dependent manner to activate downstream events in repair. Here, we assess the role of ATP binding and hydrolysis in mismatch recognition by MutS and the formation of a ternary complex involving MutS and MutL bound to a mismatched DNA. We show that ATP reduces the affinity of MutS for mismatched DNA and that the modulation of DNA binding affinity by nucleotide is even more pronounced for MutS E694A, a protein that binds ATP but is defective for ATP hydrolysis. Despite the ATP hydrolysis defect, E694A, like WT MutS, undergoes rapid, ATP-dependent dissociation from a DNA mismatch. Furthermore, MutS E694A retains the ability to interact with MutL on mismatched DNA. The recruitment of MutL to a mismatched DNA by MutS is also observed for two mutant MutL proteins, E29A, defective for ATP hydrolysis, and R266A, defective for DNA binding. These results suggest that ATP binding in the absence of hydrolysis is sufficient to trigger formation of a MutS sliding clamp. However, recruitment of MutL results in the formation of a dynamic ternary complex that we propose is the intermediate that signals subsequent repair steps requiring ATP hydrolysis. 相似文献