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排序方式: 共有1197条查询结果,搜索用时 781 毫秒
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Mizuki Kobayashi Shintaro Narita Yoshiyuki Matsui Souhei Kanda Yu Hidaka Hiroyasu Abe Toyonori Tsuzuki Katsuhiro Ito Takahiro Kojima Minoru Kato Shingo Hatakeyama Yuto Matsushita Sei Naito Masanobu Shiga Makito Miyake Yusuke Muro Shotaro Nakanishi Yoichiro Kato Tadamasa Shibuya Tetsutaro Hayashi Hiroaki Yasumoto Takashi Yoshida Motohide Uemura Rikiya Taoka Manabu Kamiyama Satoshi Morita Tomonori Habuchi Osamu Ogawa Hiroyuki Nishiyama Hiroshi Kitamura Takashi Kobayashi the Japan Urological Oncology Group 《BJU international》2022,130(2):226-234
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Ayano Doi Kosuke Ishikawa Nao Shibata Emi Ito Jiro Fujimoto Mizuki Yamamoto Hatsuki Shiga Hiromi Mochizuki Yoshifumi Kawamura Naoki Goshima Kentaro Semba Shinya Watanabe 《Molecular oncology》2015,9(2):355-364
The early steps of mammary tumorigenesis include loss of epithelial cell polarity, escape from anoikis, and acquisition of proliferative capacity. The genes responsible for these processes are predicted to be early diagnostic markers or new therapeutic targets. Here we tested 51 genes coamplified with ERBB2 in the 17q12–21 amplicon for these tumorigenic activities using an MCF10A 3D culture‐based screening system. We found that overexpression of retinoic acid receptor α (RARA) disrupted normal acinar structure and induced epithelial‐to‐mesenchymal transition (EMT). The mRNA levels of known EMT‐inducing factors, including SLUG, FOXC2, ZEB1, and ZEB2, were significantly increased upon RARA overexpression. Knockdown of ZEB1 suppressed the RARA‐mediated EMT phenotype. These results suggest that overexpression of RARA enhances malignant transformation during mammary tumorigenesis. 相似文献
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Koji Mizuhashi Mizuki Nagata Yuki Matsushita Wanida Ono Noriaki Ono 《Journal of bone and mineral research》2019,34(8):1387-1392
The growth plate provides a substantial source of mesenchymal cells in the endosteal marrow space during endochondral ossification. The current model postulates that a group of chondrocytes in the hypertrophic zone can escape from apoptosis and transform into cells that eventually become osteoblasts in an area beneath the growth plate. The growth plate is composed of cells with various morphologies; particularly at the periphery of the growth plate immediately adjacent to the perichondrium are “borderline” chondrocytes, which align perpendicularly to other chondrocytes. However, in vivo cell fates of these special chondrocytes have not been revealed. Here we show that borderline chondrocytes in growth plates behave as transient mesenchymal precursor cells for osteoblasts and marrow stromal cells. A single-cell RNA-seq analysis revealed subpopulations of Col2a1-creER-marked neonatal chondrocytes and their cell type–specific markers. A tamoxifen pulse to Pthrp-creER mice in the neonatal stage (before the resting zone was formed) preferentially marked borderline chondrocytes. Following the chase, these cells marched into the nascent marrow space, expanded in the metaphyseal marrow, and became Col(2.3 kb)-GFP+ osteoblasts and Cxcl12-GFPhigh reticular stromal “CAR” cells. Interestingly, these borderline chondrocyte-derived marrow cells were short-lived, as they were significantly reduced during adulthood. These findings demonstrate based on in vivo lineage-tracing experiments that borderline chondrocytes in the peripheral growth plate are a particularly important route for producing osteoblasts and marrow stromal cells in growing murine endochondral bones. A special microenvironment neighboring the osteogenic perichondrium might endow these chondrocytes with an enhanced potential to differentiate into marrow mesenchymal cells. © 2019 American Society for Bone and Mineral Research. 相似文献
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Mizuki Kuramochi Takeshi Izawa Munmun Pervin Alexandra Bondoc Mitsuru Kuwamura Jonathan LaMarre Jyoji Yamate 《Experimental and toxicologic pathology》2017,69(8):589-597
The liver is the primary organ participating in the metabolism of xenobiotics and is therefore an important target in the safety assessment of drugs, chemicals and environmental toxins. Drug-induced liver injury (DILI) has recently become widely recognized in human medicine as an adverse event. The progression of DILI often involves “damage-associated molecular patterns” (DAMPs) of gene and protein expression such as high-mobility group boxes (HMGBs), S100 proteins and heat shock proteins (Hsp). DAMPs are released from injured or necrotic cells and are bound to Toll-like receptors (TLRs) and modulate inflammatory reactions. Previously, in thioacetamide (TAA; 300 mg/kg body weight, single injection)-induced rat liver, we demonstrated that the expressions of DAMPs, TLR4 and major histocompatibility complex (MHC) class II were simultaneously increased, accompanied with progression of hepatocellular injury and inflammation. Here we investigated the association of DILI and DAMPs, TLRs and MHC class II by using rat livers repeated injections with TAA (100 mg/kg body weight, once, three times). Two days after TAA single injection, centrilobular hepatocellular necrosis with infiltration of mononuclear cells was observed, being paralleled with increase in serum levels of aspartate transaminase (AST), alanine transaminase (ALT) and alkaline phosphatase (ALP). However, two days after duplicate and triplicate injections, only mild degenerative change of hepatocytes and slight infiltration of mononuclear cells were seen in the affected centrilobular area. Serum levels of AST, ALT and ALP were also decreased to the same levels of control. mRNA expressions of DAMPs (HMGBs, S100A4 and Hsp 70-2), TLR4 and MHC class II tended to be increased only on single injection, although the number of MHC class II-positive cells in the centrilobular area was still increased on each examination point. The analysis of enzymes (CYP2E1 and Flavin monooxygenase (FMO) 3), which metabolize TAA in hepatocytes, showed a significant decrease in FMO3 on the duplicate and triplicate injections. Autophagy and regulatory T cells were not significantly changed for the attenuation of hepatocyte injury. Collectively, these results suggest that hepatocytes may adapt accumulation of the toxicant by changing their enzyme functions; furthermore, MHC class II cells, which still showed increased number in the duplicate and triplicate injections, may be related with protection from the toxicant. 相似文献
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Delay of treatment change after objective progression on first‐line erlotinib in epidermal growth factor receptor‐mutant lung cancer
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