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81.
82.
Long-term effects of physiologic concentrations of dexamethasone on human bone-derived cells 总被引:2,自引:0,他引:2
M M Wong L G Rao H Ly L Hamilton J Tong W Sturtridge R McBroom J E Aubin T M Murray 《Journal of bone and mineral research》1990,5(8):803-813
Bone cells derived from human trabecular explants display osteoblastic features. We examined the modulation of alkaline phosphatase activity and cAMP production as the result of exposing trabecular explants to physiologic concentrations of dexamethasone for 4 weeks during cellular outgrowth and subculture. Cells treated with dexamethasone were observed to grow generally more slowly than control cells. Cells appeared larger and more polygonal, and staining for alkaline phosphatase was more intense in the dexamethasone-exposed cultures. There was a progressive increase in cellular PTH responsiveness with increasing duration of exposure of cells to dexamethasone. Cells grown for 6 weeks in 3 x 10(-8) M dexamethasone had a 10-fold increase in PTH-stimulated cyclic AMP accumulation. Dexamethasone-treated cells also had a significantly increased alkaline phosphatase activity. 1,25-(OH)2D3-stimulated alkaline phosphatase activity was increased approximately 20-fold. cAMP responses were significantly increased to PTH (21.7-fold), PGE1 (2.67-fold), and forskolin (4.81-fold), but not to cholera toxin. Dexamethasone-treated cells also had a mean decrease in 1,25-(OH)2D3-stimulated osteocalcin production to 26.2% of control values (p less than 0.001). Hydrocortisone treatment gave rise to similar effects but of smaller magnitude than those of dexamethasone. Testosterone did not have a significant effect on alkaline phosphatase activity or cAMP production. Skin fibroblasts showed a significant enhancement of alkaline phosphatase activity in response to dexamethasone, but of a much smaller magnitude than in bone cells. The phenotypic changes induced by long-term culture in dexamethasone are consistent with the promotion of a more differentiated osteoblastic phenotype. 相似文献
83.
84.
海岛纤恙螨经卵传递恙虫病立克次体的研究 总被引:1,自引:0,他引:1
1985年8月~1986年11月,作者以我国发现的恙螨新种海岛纤恙螨子代幼虫656只,分为21组,叮咬健康小鼠,从子1代到子4代幼虫叮咬过的小鼠中,连续分离出7株恙虫病立克次体,证明海岛纤恙螨能够经卵传递恙虫病立克次体至少4代.同时在该螨的卵、幼虫、若虫、成虫组织细胞内发现有恙虫病立克次体寄生,并发现有分裂增殖形态的立克次体,证明海岛纤恙螨各变态期内均保有恙虫病立克次体,这些立克次体能在恙螨体内大量增殖,连续传代.此项研究结果,对于确认海岛纤恙螨为浙江沿海地区恙虫病的传染媒介和宿主,提供了重要的科学依据. 相似文献
85.
腹茧症16例诊治体会 总被引:4,自引:1,他引:3
目的 探讨腹茧症的诊断及治疗方法。方法 回顾性分析l6例腹茧症的临床资料及随访结果。结果 16例腹茧症均经手术治疗并确诊。术前11例误诊为机械性肠梗阻2~l0年,4例为误诊慢性阑尾炎,l例误诊为腹部肿块。术后并发症2例,全部患者均临床治愈。并获随访1~l0年,2例分别因反复发作肠梗阻于1年和5年死亡,2例反复发作不完全性肠梗阻合并营养不良,12例情况良好。结论 腹茧症术前诊断困难,上消化道造影和B超及CT对诊断可能有帮助;包膜切除,肠粘连松解是治疗本病的有效方法。 相似文献
86.
作者对15例贲门癌患者行根治术同时,采用食管残胃间插入带蒂空肠并附加贲门再造术,通过SPECT胃食管返流指数测定、食管下端pH检测及返流症状评定方法,并与单纯食管胃套叠吻合术进行随机对比分析,证明该术式具有单向住屏障作用,能有效地预防返流性食管炎的发生。 相似文献
87.
CA von Arnim R Spoelgen ID Peltan M Deng S Courchesne M Koker T Matsui H Kowa SF Lichtenthaler MC Irizarry BT Hyman 《The Journal of neuroscience》2006,26(39):9913-9922
The beta-amyloid (Abeta) precursor protein (APP) is cleaved sequentially by beta-site of APP-cleaving enzyme (BACE) and gamma-secretase to release the Abeta peptides that accumulate in plaques in Alzheimer's disease (AD). GGA1, a member of the Golgi-localized gamma-ear-containing ARF-binding (GGA) protein family, interacts with BACE and influences its subcellular distribution. We now report that overexpression of GGA1 in cells increased the APP C-terminal fragment resulting from beta-cleavage but surprisingly reduced Abeta. GGA1 confined APP to the Golgi, in which fluorescence resonance energy transfer analyses suggest that the proteins come into close proximity. GGA1 blunted only APP but not notch intracellular domain release. These results suggest that GGA1 prevented APP beta-cleavage products from becoming substrates for gamma-secretase. Direct binding of GGA1 to BACE was not required for these effects, but the integrity of the GAT (GGA1 and TOM) domain of GGA1 was. GGA1 may act as a specific spatial switch influencing APP trafficking and processing, so that APP-GGA1 interactions may have pathophysiological relevance in AD. 相似文献
88.
Several hormones, neurotransmitters, and neuropeptides were screened for the ability to stimulate inositol phosphate formation in cultured human retinal epithelial (RPE) cells. Carbachol, vasopressin and thrombin were found to be effective. Treatment of RPE cells with all three agents produced increases in inositol monophosphate, inositol bisphosphate and inositol trisphosphate in the presence of 10 mM LiCl. Carbachol stimulated a 4-fold increase in the total of inositol phosphates at 1 mM. Studies with cholinergic antagonists showed a rank order of 4 DAMP greater than QNX greater than pirenzepine greater than methoctramine, suggesting the presence of M3 muscarinic receptors. Vasopressin gave a 2.5-fold stimulation at 10 microM. Agonists of vasopressin were also tested and gave differential responses. Studies using a V1 agonist (PIOVP) and a V2 agonist (DAVP) showed DAVP matching the level of stimulation elicited by vasopressin whereas treatment with PIOVP only reached 50% of the vasopressin response. These data suggested the presence of V2 receptors in the RPE cells. Several proteases were tested for their ability to stimulate RPE inositol phosphates. Thrombin caused a 7-fold increase in inositol phosphate formation at 1 U/ml, whereas trypsin and plasmin elicited smaller responses (approximately 2-fold). The thrombin effect was blocked by the thrombin-specific inhibitor, hirudin, but not by other protease inhibitors. Several mediators of inflammation such as bradykinin, histamine and serotonin were also tested, and they were ineffective in stimulating inositol phosphate turnover in the RPE cells. 相似文献
89.
90.
报告以DPH作为膜标记探剂,用荧光偏振法测定烧伤后淋巴细胞膜流动性变化。将小鼠背部造成11%~12%体表面积Ⅲ度烧伤,于伤后第6天取脾淋巴细胞,测其膜流动性。结果表明:烧伤后淋巴细胞膜流动性明显下降(P<0.001),同时淋巴细胞增殖反应及ConA刺激的IL-2生成亦下降;淋巴细胞功能受抑制的程度与淋巴细胞膜流动性呈负相关;脾淋巴细胞膜流动性与脾组织过氧化脂质水平呈负相关。结果提示烧伤后淋巴细胞膜流动性下降可能是烧伤后淋巴细胞功能抑制的原因之一,膜流动性降低与脂质过氧化亢进有关 相似文献