全文获取类型
收费全文 | 323650篇 |
免费 | 29690篇 |
国内免费 | 22795篇 |
专业分类
耳鼻咽喉 | 2982篇 |
儿科学 | 3421篇 |
妇产科学 | 4925篇 |
基础医学 | 39920篇 |
口腔科学 | 5490篇 |
临床医学 | 45267篇 |
内科学 | 49708篇 |
皮肤病学 | 3082篇 |
神经病学 | 18379篇 |
特种医学 | 11987篇 |
外国民族医学 | 213篇 |
外科学 | 33219篇 |
综合类 | 49873篇 |
现状与发展 | 76篇 |
一般理论 | 20篇 |
预防医学 | 19633篇 |
眼科学 | 9565篇 |
药学 | 32772篇 |
334篇 | |
中国医学 | 17402篇 |
肿瘤学 | 27867篇 |
出版年
2024年 | 996篇 |
2023年 | 4996篇 |
2022年 | 13021篇 |
2021年 | 16312篇 |
2020年 | 12032篇 |
2019年 | 10823篇 |
2018年 | 11412篇 |
2017年 | 9921篇 |
2016年 | 9363篇 |
2015年 | 14359篇 |
2014年 | 17808篇 |
2013年 | 15349篇 |
2012年 | 22812篇 |
2011年 | 25821篇 |
2010年 | 15919篇 |
2009年 | 12272篇 |
2008年 | 17040篇 |
2007年 | 17024篇 |
2006年 | 17063篇 |
2005年 | 16780篇 |
2004年 | 10675篇 |
2003年 | 9764篇 |
2002年 | 8439篇 |
2001年 | 7466篇 |
2000年 | 8280篇 |
1999年 | 9020篇 |
1998年 | 5475篇 |
1997年 | 5499篇 |
1996年 | 4332篇 |
1995年 | 3922篇 |
1994年 | 3213篇 |
1993年 | 2097篇 |
1992年 | 2827篇 |
1991年 | 2415篇 |
1990年 | 2117篇 |
1989年 | 1861篇 |
1988年 | 1563篇 |
1987年 | 1352篇 |
1986年 | 1107篇 |
1985年 | 912篇 |
1984年 | 526篇 |
1983年 | 373篇 |
1982年 | 242篇 |
1981年 | 238篇 |
1980年 | 188篇 |
1979年 | 221篇 |
1978年 | 82篇 |
1977年 | 89篇 |
1974年 | 102篇 |
1973年 | 83篇 |
排序方式: 共有10000条查询结果,搜索用时 15 毫秒
151.
目的分析25羟基维生素D[25(OH)D]水平对高血压合并冠心病患者心肌重构及左心室舒张功能的影响。方法选择80例高血压合并冠心病患者,根据左心室质量指数及左心室舒张功能分为心肌重构组和无心肌重构组、舒张功能障碍组和无舒张功能障碍组。Logistic回归分析影响高血压合并冠心病患者心肌重构及左心室舒张功能的独立危险因素,ROC曲线分析其诊断效能。结果与无心肌重构组比较,心肌重构组收缩压、总胆固醇(TC)、低密度脂蛋白胆固醇(LDLC)升高,25(OH)D降低(P<0.05)。与无舒张功能障碍组比较,舒张功能障碍组体质指数(BMI)、25(OH)D水平降低,LDLC升高(P<0.05)。25(OH)D是患者心肌重构及左心室舒张功能的危险因素(P<0.05)。25(OH)D水平对患者心肌重构、舒张功能障碍有较好的诊断效能。结论25(OH)D水平是影响高血压合并冠心病患者心肌重构及左心室舒张功能的独立危险因素,早期检测其水平有助于临床诊疗。 相似文献
152.
153.
154.
Sheng Zhang Yan Wang Jie Xu Bokyung Kim Wenbin Deng Fuzheng Guo 《The Journal of neuroscience》2021,41(2):251
The developing CNS is exposed to physiological hypoxia, under which hypoxia-inducible factor α (HIFα) is stabilized and plays a crucial role in regulating neural development. The cellular and molecular mechanisms of HIFα in developmental myelination remain incompletely understood. A previous concept proposes that HIFα regulates CNS developmental myelination by activating the autocrine Wnt/β-catenin signaling in oligodendrocyte progenitor cells (OPCs). Here, by analyzing a battery of genetic mice of both sexes, we presented in vivo evidence supporting an alternative understanding of oligodendroglial HIFα-regulated developmental myelination. At the cellular level, we found that HIFα was required for developmental myelination by transiently controlling upstream OPC differentiation but not downstream oligodendrocyte maturation and that HIFα dysregulation in OPCs but not oligodendrocytes disturbed normal developmental myelination. We demonstrated that HIFα played a minor, if any, role in regulating canonical Wnt signaling in the oligodendroglial lineage or in the CNS. At the molecular level, blocking autocrine Wnt signaling did not affect HIFα-regulated OPC differentiation and myelination. We further identified HIFα–Sox9 regulatory axis as an underlying molecular mechanism in HIFα-regulated OPC differentiation. Our findings support a concept shift in our mechanistic understanding of HIFα-regulated CNS myelination from the previous Wnt-dependent view to a Wnt-independent one and unveil a previously unappreciated HIFα–Sox9 pathway in regulating OPC differentiation.SIGNIFICANCE STATEMENT Promoting disturbed developmental myelination is a promising option in treating diffuse white matter injury, previously called periventricular leukomalacia, a major form of brain injury affecting premature infants. In the developing CNS, hypoxia-inducible factor α (HIFα) is a key regulator that adapts neural cells to physiological and pathologic hypoxic cues. The role and mechanism of HIFα in oligodendroglial myelination, which is severely disturbed in preterm infants affected with diffuse white matter injury, is incompletely understood. Our findings presented here represent a concept shift in our mechanistic understanding of HIFα-regulated developmental myelination and suggest the potential of intervening with an oligodendroglial HIFα-mediated signaling pathway to mitigate disturbed myelination in premature white matter injury. 相似文献
155.
随着对肿瘤热疗和肿瘤免疫微环境(TIME)的深入研究,近年来热疗对TIME的作用越来越受到学者们的重视。本文就目前国内外研究进展,对热疗与TIME中几类主要免疫细胞和免疫相关细胞因子的影响及作用机制作一综述。全面而透彻的了解热疗对TIME的调控作用,有助于为肿瘤治疗提供新的思路和方法。 相似文献
156.
157.
Ling Zhang Xue-Jun Shang Hong-Fei Li Yu-Qin Shi Wei Li Maria E Teves Zhi-Qiong Wang Gao-Feng Jiang Shi-Zhen Song Zhi-Bing Zhang 《Asian journal of andrology》2015,17(1):86-93
Mammalian spermatogenesis is a well-organized process of cell development and differentiation. Meiosis expressed gene 1 (MEIG1) plays an essential role in the regulation of spermiogenesis. To explore potential mechanisms of MEIG1''s action, a yeast two-hybrid screen was conducted, and several potential binding partners were identified; one of them was membrane occupation and recognition nexus repeat containing 3 (MORN3). MORN3 mRNA is only abundant in mouse testis. In the testis, Morn3 mRNA is highly expressed in the spermiogenesis stage. Specific anti-MORN3 polyclonal antibody was generated against N-terminus of the full-length MORN3 protein, and MORN3 expression and localization was examined in vitro and in vivo. In transfected Chinese hamster ovary cells, the antibody specifically crossed-reacted the full-length MORN3 protein, and immunofluorescence staining revealed that MORN3 was localized throughout the cytoplasm. Among multiple mouse tissues, about 25 kDa protein, was identified only in the testis. The protein was highly expressed after day 20 of birth. Immunofluorescence staining on mixed testicular cells isolated from adult wild-type mice demonstrated that MORN3 was expressed in the acrosome in germ cells throughout spermiogenesis. The protein was also present in the manchette of elongating spermatids. The total MORN3 expression and acrosome localization were not changed in the Meig 1-deficient mice. However, its expression in manchette was dramatically reduced in the mutant mice. Our studies suggest that MORN3 is another regulator for spermatogenesis, probably together with MEIG1. 相似文献
158.
借力医院文化环境探索传染病专科医院研究生医德培养的方法及途径 《医学教育管理》2021,7(4):402-405
新医改环境下,临床医学人才的医德培养愈发重要,也越来越引起管理层重视。而医院文化环境对研究生医德培养可以起着潜移默化的引领作用,优秀的医院文化,能塑造并铸就研究生良好信念,强化研究生医德养成。结合传染病专科医院自身文化环境特点,探索传染病学研究生医德培养方式,对于传染病专科医院研究生医德培养具有一定理论指导意义。 相似文献
159.
160.
Feng He Yuanjun Ma Shi Li Haozhe Ren Qian Liu Xiaohua Chen Hui Miao Tao Ye Qian Lu Zuge Yang Tianle Li Xin Tong Hongxu Yang Mian Zhang Helin Wang Yazhou Wang Shibin Yu 《Journal of bone and mineral research》2022,37(5):1044-1055
Temporomandibular joint osteoarthritis (TMJOA) is a chronic degenerative disease for which the underlying mechanism still remains unclear. Compared with apoptosis and autophagy, necroptosis causes greater harm to tissue homeostasis by releasing damage-associated molecular patterns (DAMPs). However, the role of necroptosis and downstream key DAMPs in TMJOA is unknown. Here, rodent models of TMJOA were established by the unilateral anterior crossbite (UAC). Transmission electron microscopy (TEM) and immunohistochemistry of receptor interacting protein kinase 3 (RIPK3)/phosphorylation of mixed lineage kinase domain-like protein (pMLKL) were conducted to evaluate the occurrence of necroptosis in vivo. The therapeutic effects of blocking necroptosis were achieved by intra-articularly injecting RIPK3 or MLKL inhibitors and using RIPK3 or MLKL knockout mice. In vitro necroptosis of condylar chondrocyte was induced by combination of tumor necrosis factor alpha (TNFα), second mitochondria-derived activator of caspases (SMAC) mimetics and carbobenzoxy-valyl-alanyl-aspartyl-[O-methyl]- fluoromethylketone (z-VAD-fmk). The possible DAMPs released by necroptotic chondrocytes were screened by quantitative proteomics and blocked by specific antibody. Translucent cytosol, swollen organelles, and ruptured cell membranes, features of necroptosis, were frequently manifested in chondrocytes at the early stage of condylar cartilage degeneration in TMJOA, which was accompanied by upregulation of RIPK3/pMLKL. Inhibiting or knocking out RIPK3/MLKL significantly prevented cartilage degeneration. DAMPs released by necroptotic condylar chondrocytes, such as syndecan 4 (SDC4) and heat shock protein 90 (HSP90), were verified. Furthermore, blocking the function of SDC4 significantly attenuated the expression of TNFα in cartilage and synovium, and accordingly increased cartilage thickness and reduced synovial inflammation. Thus, the necroptotic vicious cycle of TNFα-SDC4-TNFα contributes to cartilage degeneration and synovitis, and can serve as a potential therapeutic target for treating TMJOA. © 2022 American Society for Bone and Mineral Research (ASBMR). 相似文献