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81.
82.
目的研究周期性牵张肺泡Ⅱ型上皮细胞株A549细胞对Cyr61表达的影响。方法对肺泡Ⅱ型上皮细胞株A549细胞施加周期性机械牵张应力。加载频率0.5 Hz,加载时间2 h,加载应力分别为5%,15%,30%。加载应力为15%,加载频率0.5 Hz,加载时间分别0,15 min,30 min,60 min,120 min。每个实验均设立空白对照即不给予机械应力。用PCR法测定Cyr61 mRNA的表达,用western法测定Cyr61蛋白含量。结果随着加载应力的增加和加载时间的延长,Cyr61蛋白含量和mRNA表达均增加(P<0.05);施加不同加载幅度后,Cyr61蛋白含量和mRNA表达均增加(P<0.05)。结论肺泡Ⅱ型上皮细胞IL-8的产生和释放与周期性的机械牵张应力呈强度和时间依赖性。 相似文献
83.
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Donna M. Charponiere-Rickenberg Mukta M. Webber 《In vitro cellular & developmental biology. Plant》1983,19(5):373-375
Summary Adult human prostatic epithelium was cultured in a defined medium consisting of RPMI 1640 supplemented with transferrin, insulin,
epidermal growth factor, dexamethasone, and vitamin A. In the presence of insulin, stabilized with zinc, maximum epithelial
multiplication was obtained at an insulin concentration of 0.03 to 0.1 U/ml, corresponding to a zinc concentration of 1.4×10−7
M. At higher insulin concentrations, growth stimulation declined. Zinc-free insulin, on the other hand, stimulated cell multiplication
with an optimum concentration of 0.3 to 1.0 U/ml. At this concentration the maximum growth was twice that obtained with zinc-stabilized
insulin. Results demonstrate that growth inhibition caused by zinc limits the concentration of zinc-stabilized insulin, which
can be used in serum-free, defined culture media.
This work was supported by the Division of Cancer Cause and Prevention, National Cancer Institute, DHHS Grant No. CA-28279
to Webber. 相似文献
85.
86.
Ye Zhao Bing Yu Xiangbing Mao Jun He Zhiqing Huang Ping Zheng 《Archives of animal nutrition》2015,69(3):227-235
The study evaluated whether a 25-hydroxyvitamin D3 (25D3) supplementation decreases the replication of rotavirus by the retinoic acid-inducible gene I (RIG-I) signalling pathway in a porcine small intestinal epithelial cell line (IPEC-J2). The results show that IPEC-J2 cells express high baseline levels of 1α-hydroxylase (CYP27B1), which converts inactive 25D3 to the active 1,25-dihydroxyvitamin D3 (1,25D3). Porcine rotavirus (PRV) infection alone resulted in a significant increase in CYP27B1 mRNA, which augmented the production of active vitamin D. Physiological concentrations of 25D3 were found to decrease PRV replication in IPEC-J2 cells. RIG-I plays an important role in the recognition of double-stranded RNA virus by host cells. Upon recognition, RIG-I triggers a series of signalling molecules such as interferon-β (IFN-β) promoter stimulator 1 (IPS-1) leading to the expression of type I interferons (IFN-β). Active 25D3 that was generated by PRV-infected IPEC-J2 cells led to an increased expression of toll-like receptors 3 (TLR3), RIG-I, IPS-1, IFN-β and IFN-stimulated genes 15 (ISG15) with important innate immune functions. Inhibiting CYP27B1 also failed to increase RIG-I, IPS-1, IFN-β and ISG15 mRNA expression. These observations suggest that 25D3 can directly inhibit PRV in IPEC-J2 cells, which requires this active form of vitamin D. The anti-rotavirus effect of 25D3 is mediated at least in part by RIG-I signalling pathways in IPEC-J2 cells. 相似文献
87.
Vazhaikkurichi M. Rajendran Navalpur S. Nanda Kumar Chung M. Tse Henry J. Binder 《The Journal of biological chemistry》2015,290(42):25487-25496
Diarrhea associated with ulcerative colitis (UC) occurs primarily as a result of reduced Na+ absorption. Although colonic Na+ absorption is mediated by both epithelial Na+ channels (ENaC) and Na-H exchangers (NHE), inhibition of NHE-mediated Na+ absorption is the primary cause of diarrhea in UC. As there are conflicting observations reported on NHE expression in human UC, the present study was initiated to identify whether NHE isoforms (NHE2 and NHE3) expression is altered and how Na+ absorption is regulated in DSS-induced inflammation in rat colon, a model that has been used to study UC. Western blot analyses indicate that neither NHE2 nor NHE3 expression is altered in apical membranes of inflamed colon. Na+ fluxes measured in vitro under voltage clamp conditions in controls demonstrate that both HCO3−-dependent and butyrate-dependent Na+ absorption are inhibited by S3226 (NHE3-inhibitor), but not by HOE694 (NHE2-inhibitor) in normal animals. In contrast, in DSS-induced inflammation, butyrate-, but not HCO3−-dependent Na+ absorption is present and is inhibited by HOE694, but not by S3226. These observations indicate that in normal colon NHE3 mediates both HCO3−-dependent and butyrate-dependent Na+ absorption, whereas DSS-induced inflammation activates NHE2, which mediates butyrate-dependent (but not HCO3−-dependent) Na+ absorption. In in vivo loop studies HCO3−-Ringer and butyrate-Ringer exhibit similar rates of water absorption in normal rats, whereas in DSS-induced inflammation luminal butyrate-Ringer reversed water secretion observed with HCO3−-Ringer to fluid absorption. Lumen butyrate-Ringer incubation activated NHE3-mediated Na+ absorption in DSS-induced colitis. These observations suggest that the butyrate activation of NHE2 would be a potential target to control UC-associated diarrhea. 相似文献
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89.
4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is a carcinogenic compound of cigarette smoke that generates electrophilic
intermediates capable of damaging DNA. Recently, we have shown that NNK can modulate mediator production by alveolar macrophages
(AM) and bronchial and alveolar epithelial cells, suggesting that cigarette smoke can alter lung immune response. Thus, we
investigated the effect of NNK and cigarette smoke extract (CSE) on AM capacity to eliminate tumoral cells. Rat AM cell line,
NR8383, was treated with NNK (500 μM) or CSE (3%) and stimulated with lipopolysaccharide (10 ng/ml). The release of cytotoxic
mediators, tumor necrosis factor (TNF) and reactive oxygen species (ROS), was measured in cell-free supernatants using ELISA
and superoxide anion production. TNF- and ROS-dependent cytotoxicity were studied using a 51Chromium-release assay and WEHI-164 and P-815 cell lines. Treatment of AM with NNK and CSE for 18 h significantly inhibited
AM TNF release. CSE exposure resulted in a significant increase of ROS production, whereas NNK did not. TNF-dependent cytotoxic
activity of NR8383 and freshly isolated rat AM was significantly inhibited after treatment with NNK and CSE. Interestingly,
although ROS production was stimulated by CSE and not affected by NNK, CSE inhibited AM ROS-dependent cytotoxicity. These
results suggest that NNK may be one of the cigarette smoke components responsible for the reduction of pulmonary cytotoxicity.
Thus, NNK may have a double pro-carcinogenic effect by contributing to DNA adduct formation and inhibiting AM cytotoxicity
against tumoral cells. 相似文献
90.
肺炎链球菌(Streptococcus pneumoniae,SP)普遍定植于呼吸道,是人类重要的侵袭性病原菌之一,是社区获得性肺炎、中耳炎、脑膜炎、菌血症、鼻窦炎的主要病原菌。肺炎链球菌粘附和毒力因子A(pneumococcal adherence and virulence factor A,PavA)是肺炎链球菌早期感染和侵袭过程中关键的毒力因子。体外试验表明,缺失PavA的肺炎链球菌的突变株其粘附和侵入上皮细胞和内皮细胞的能力明显下降。作为一种保护性抗原,其诱导的细胞和体液免疫可以有效的抵抗肺炎链球菌的感染,是肺炎链球菌新一代疫苗的候选蛋白。但是,PavA在肺炎链球菌与人肺上皮细胞交互对话中作用机制的研究尚属空白,本文就肺炎链球菌粘附和毒力因子A得最新研究进展作一综述。 相似文献