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排序方式: 共有10000条查询结果,搜索用时 46 毫秒
991.
992.
Guixing Jiang Yunfu Cui Xin Yu Zhengrong Wu Guoping Ding Liping Cao 《Oncotarget》2015,6(11):9457-9466
Dysregulation of microRNAs (miRs) is involved in carcinogenesis. Deregulation of miR-211 has recently been observed in many tumors, but its function in hepatocellular carcinoma (HCC) is still unknown. Here we found that miR-211 was decreased in HCC cancer tissues compared with adjacent normal tissues. We also found that overexpression of miR-211 repressed proliferation and invasion in HepG2 and SMMC7721 cells. Luciferase reporter assays and western blot indicated that special AT-rich sequence-binding protein-2 (SATB2), is a direct target of miR-211. The expression of SATB2 was upregulated in HCC cancer tissues and cell lines and miR-211 levels inversely correlated with SATB2 levels in HCC. Importantly, SATB2 rescued the miR-211-mediated inhibition of cell invasion and proliferation. Finally, reintroduction of miR-211 repressed tumor formation of HCC in xenograft mice. This study provides insights into molecular mechanisms that miR-211 contributed to HCC. 相似文献
993.
Long Jiang Shanshan Jiang Dongrong Situ Yongbin Lin Han Yang Yuanfang Li Hao Long Zhiwei Zhou 《Oncotarget》2015,6(11):9542-9550
Metastatic soft tissue sarcomas (STS) represent enormous challenges to improve the low survival rate, which is almost the same as past 2 decades ago. Prognosis of cancer patients are based not only on tumor-related factors but also on host-related factors, particularly systemic inflammatory response. We evaluated the association among possible risk factors and survival for metastatic STS by reviewed a single-institution nearly 50-year experience. We found that both monocyte ratio and NLR ratio were significant prognostic predictors for OS and PFS of metastatic STS. And patients with monocyte ratio or NLR ratio > 1 should be screened out as candidates for more intensive or aggressive multimodality treatments and more aggressive follow-up. For this reason, this result could serve as a basis for future prospective study. 相似文献
994.
Qinhong Xu Pei Li Xin Chen Liang Zong Zhengdong Jiang Ligang Nan Jianjun Lei Wanxing Duan Dong Zhang Xuqi Li Huanchen Sha Zheng Wu Qingyong Ma Zheng Wang 《Oncotarget》2015,6(16):14153-14164
MicroRNAs are involved in the initiation and progression of pancreatic cancer. In this study, we showed that miR-221/222 is overexpressed in pancreatic cancer. MiR-221/222 overexpression significantly promoted pancreatic cancer cell proliferation and invasion while inhibiting apoptosis. The expression of the matrix metalloproteinases (MMPs) MMP-2 and MMP-9 was increased in miR-221/222 mimic-transfected pancreatic cancer cells. Validation experiments identified TIMP-2 as a direct target of miR-221/222. These data indicate that overexpressed miR-221/222 may play an oncogenic role in pancreatic cancer by inducing the expression of MMP-2 and MMP-9, thus leading to cancer cell invasion. 相似文献
995.
Zhiyuan Han Yanbin Zhang Qiaoyuan Yang Binbin Liu Jianjun Wu Yajie Zhang Chengfeng Yang Yiguo Jiang 《Oncotarget》2015,6(15):13149-13163
Cyclin E1, encoded by the CCNE1 gene, promotes G1/S transition, chromosome instability, and oncogenesis. Here, we show that miR-497 and miR-34a target the 3′-UTR of CCNE1. miR-497 and miR-34a are downregulated in cancer cells and their ectopic expression inhibited cell proliferation and colony formation in vitro, and inhibited tumor growth in a xenograft model. The effect of simultaneous overexpression of miR-497 and miR-34a on the inhibition of cell proliferation, colony formation, and tumor growth, and the downregulation of cyclin E1 was stronger than the effect of each miRNA alone. The synergistic actions of miR-497 and miR-34a partly correlated with cyclin E1 levels. When cells stably expressing CCNE1 were transfected with the Hi-miR-497/34a plasmid, there was no effect on colony formation, compared with that of cells transfected with either Hi-miR497 or Hi-miR34a. These results indicate cyclin E1 is downregulated by both miR-497 and miR-34a, which synergistically retard the growth of human lung cancer cells. 相似文献
996.
Li-Yan Li Hong Jiang Yang-Min Xie Lian-Di Liao Hui-Hui Cao Xiu-E Xu Bo Chen Fa-Min Zeng Ying-Li Zhang Ze-Peng Du Hong Chen Wei Huang Wei Jia Wei Zheng Jian-Jun Xie En-Min Li Li-Yan Xu 《Oncotarget》2015,6(18):15940-15952
The paucity of new drugs for the treatment of esophageal squamous cell carcinoma (ESCC) limits the treatment options. This study characterized the therapeutic efficacy and action mechanism of a novel natural macrolide compound F806 in human ESCC xenograft models and cell lines. F806 inhibited growth of ESCC, most importantly, it displayed fewer undesirable side effects on normal tissues in two human ESCC xenograft models. F806 inhibited proliferation of six ESCC cells lines, with the half maximal inhibitory concentration (IC50) ranging from 9.31 to 16.43 μM. Furthermore, F806 induced apoptosis of ESCC cells, contributing to its growth-inhibitory effect. Also, F806 inhibited cell adhesion resulting in anoikis. Mechanistic studies revealed that F806 inhibited the activation of β1 integrin in part by binding to a novel site Arg610 of β1 integrin, suppressed focal adhesion formation, decreased cell adhesion to extracellular matrix and eventually triggered apoptosis. We concluded that F806 would potentially be a well-tolerated anticancer drug by targeting β1 integrin, resulting in anoikis in ESCC cells. 相似文献
997.
998.
Mengyang Zhao Weiyi Fang Yan Wang Suiqun Guo Luyun Shu Lijing Wang YiYu Chen Qiaofen Fu Yan Liu Shengni Hua Yue Fan Yiyi Liu Xiaojie Deng Rongcheng Luo Zhong Mei Qinping Jiang Zhen Liu 《Oncotarget》2015,6(17):15610-15627
ENO1 plays a paradoxical role in driving the pathogenesis of tumors. However, the clinical significance of ENO1 expression remains unclear and its function and modulatory mechanisms have never been reported in endometrial carcinoma (EC). In this study, ENO1 silencing significantly reduced cell glycolysis, proliferation, migration, and invasion in vitro, as well as tumorigenesis and metastasis in vivo by modulating p85 suppression. This in turn mediated inactivation of PI3K/AKT signaling and its downstream signals including glycolysis, cell cycle progression, and epithelial-mesenchymal transition (EMT)-associated genes. These effects on glycolysis and cell growth were not observed after ENO1 suppression in normal human endometrial epithelial cells (HEEC). Knocking down ENO1 could significantly enhance the sensitivity of EC cells to cisplatin (DDP) and markedly inhibited the growth of EC xenografts in vivo. In clinical samples, EC tissues exhibited higher expression levels of ENO1 mRNA and protein compared with normal endometrium tissues. Patients with higher ENO1 expression had a markedly shorter overall survival than patients with low ENO1 expression. We conclude that ENO1 favors carcinogenesis, representing a potential target for gene-based therapy. 相似文献
999.
Jiao Jian-tong Sun Jun Ma Jian-fen Dai Min-chao Huang Jin Jiang Chen Wang Cheng Cheng Chao Shao Jun-fei 《Journal of neuro-oncology》2015,124(3):475-484
Journal of Neuro-Oncology - Depression is found to be associated with up-regulation of inflammatory cytokines. However, the relationship in high grade glioma (HGG) patients is still unclear. In... 相似文献
1000.