全文获取类型
收费全文 | 1815852篇 |
免费 | 128003篇 |
国内免费 | 6777篇 |
专业分类
耳鼻咽喉 | 26100篇 |
儿科学 | 55239篇 |
妇产科学 | 50681篇 |
基础医学 | 265543篇 |
口腔科学 | 52950篇 |
临床医学 | 157161篇 |
内科学 | 345872篇 |
皮肤病学 | 40680篇 |
神经病学 | 138032篇 |
特种医学 | 70906篇 |
外国民族医学 | 526篇 |
外科学 | 278144篇 |
综合类 | 46851篇 |
现状与发展 | 21篇 |
一般理论 | 553篇 |
预防医学 | 129558篇 |
眼科学 | 43141篇 |
药学 | 139996篇 |
56篇 | |
中国医学 | 6830篇 |
肿瘤学 | 101792篇 |
出版年
2018年 | 17719篇 |
2016年 | 15622篇 |
2015年 | 17856篇 |
2014年 | 24631篇 |
2013年 | 36074篇 |
2012年 | 47874篇 |
2011年 | 51367篇 |
2010年 | 30618篇 |
2009年 | 29009篇 |
2008年 | 48106篇 |
2007年 | 52150篇 |
2006年 | 52668篇 |
2005年 | 50852篇 |
2004年 | 49020篇 |
2003年 | 47356篇 |
2002年 | 46525篇 |
2001年 | 83104篇 |
2000年 | 85648篇 |
1999年 | 72192篇 |
1998年 | 19761篇 |
1997年 | 17982篇 |
1996年 | 17539篇 |
1995年 | 16434篇 |
1994年 | 15368篇 |
1992年 | 55527篇 |
1991年 | 54782篇 |
1990年 | 54260篇 |
1989年 | 52784篇 |
1988年 | 49128篇 |
1987年 | 48397篇 |
1986年 | 46182篇 |
1985年 | 43955篇 |
1984年 | 32921篇 |
1983年 | 28024篇 |
1982年 | 16550篇 |
1981年 | 15147篇 |
1979年 | 31853篇 |
1978年 | 22910篇 |
1977年 | 19734篇 |
1976年 | 18227篇 |
1975年 | 20895篇 |
1974年 | 24762篇 |
1973年 | 23783篇 |
1972年 | 22962篇 |
1971年 | 21619篇 |
1970年 | 20336篇 |
1969年 | 19543篇 |
1968年 | 18332篇 |
1967年 | 16487篇 |
1966年 | 15168篇 |
排序方式: 共有10000条查询结果,搜索用时 15 毫秒
81.
82.
83.
84.
85.
Tianying Yang Jiawei Li Yichen Jia Chunchen Yang Ruirui Sang Tongyu Zhu Ming Xu Ruiming Rong Cheng Yang 《Translational andrology and urology》2021,10(1):204
BackgroundIn the field of transplantation, inducing immune tolerance in recipients is of great importance. Blocking co-stimulatory molecule using anti-CD28 antibody could induce tolerance in a rat kidney transplantation model. Myeloid-derived suppressor cells (MDSCs) reveals strong immune suppressive abilities in kidney transplantation. Here we analyzed key genes of MDSCs leading to transplant tolerance in this model.MethodsMicroarray data of rat gene expression profiles under accession number in the Gene Expression Omnibus (GEO) database were analyzed. Running the LIMMA package in R language, the differentially expressed genes (DEGs) were found. Enrichment analysis of the DEGs was conducted in the Database for Annotation, Visualization and Integrated Discovery (DAVID) database to explore gene ontology (GO) annotation and their Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. Their protein-protein interactions (PPIs) were provided by STRING database and was visualized in Cytoscape. Hub genes were carried out by CytoHubba.ResultsThree hundred and thirty-eight DEGs were exported, including 27 upregulated and 311 downregulated genes. The functions and KEGG pathways of the DEGs were assessed and the PPI network was constructed based on the string interactions of the DEGs. The network was visualized in Cytoscape; the entire PPI network consisted of 192 nodes and 469 edges. Zap70, Cdc42, Stat1, Stat4, Ccl5 and Cxcr3 were among the hub genes.ConclusionsThese key genes, corresponding proteins and their functions may provide valuable background for both basic and clinical research and could be the direction of future studies in immune tolerance, especially those examining immunocyte-induced tolerance. GSE28545相似文献
86.
87.
88.
Feasibility and Diagnostic Potential of Pulmonary Transit Time Measurement by Contrast Echocardiography: A Pilot Study
下载免费PDF全文
![点击此处可从《Echocardiography (Mount Kisco, N.Y.)》网站下载免费的PDF全文](/ch/ext_images/free.gif)
89.
Harit Kapoor Kush Raj Lohani Tommy H. Lee Devendra K. Agrawal Sumeet K. Mittal 《CTS Clinical and Translational Science》2015,8(6):841-847
Esophageal adenocarcinoma is the fastest rising cancer in the United States. It develops from long‐standing gastroesophageal reflux disease which affects >20% of the general population. It carries a very poor prognosis with 5‐year survival <20%. The disease is known to sequentially progress from reflux esophagitis to a metaplastic precursor, Barrett''s esophagus and then onto dysplasia and esophageal adenocarcinoma. However, only few patients with reflux develop Barrett''s esophagus and only a minority of these turn malignant. The reason for this heterogeneity in clinical progression is unknown. To improve patient management, molecular changes which facilitate disease progression must be identified. Animal models can provide a comprehensive functional and anatomic platform for such a study. Rats and mice have been the most widely studied but disease homology with humans has been questioned. No animal model naturally simulates the inflammation to adenocarcinoma progression as in humans, with all models requiring surgical bypass or destruction of existing antireflux mechanisms. Valuable properties of individual models could be utilized to holistically evaluate disease progression. In this review paper, we critically examined the current animal models of Barrett''s esophagus, their differences and homologies with human disease and how they have shaped our current understanding of Barrett''s carcinogenesis. 相似文献
90.
E. M. Peterman C. Sullivan M. F. Goody I. Rodriguez-Nunez J. A. Yoder C. H. Kim 《Infection and immunity》2015,83(1):430-440
Mitochondria are known primarily as the location of the electron transport chain and energy production in cells. More recently, mitochondria have been shown to be signaling centers for apoptosis and inflammation. Reactive oxygen species (ROS) generated as by-products of the electron transport chain within mitochondria significantly impact cellular signaling pathways. Because of the toxic nature of ROS, mitochondria possess an antioxidant enzyme, superoxide dismutase 2 (SOD2), to neutralize ROS. If mitochondrial antioxidant enzymes are overwhelmed during severe infections, mitochondrial dysfunction can occur and lead to multiorgan failure or death. Pseudomonas aeruginosa is an opportunistic pathogen that can infect immunocompromised patients. Infochemicals and exotoxins associated with P. aeruginosa are capable of causing mitochondrial dysfunction. In this work, we describe the roles of SOD2 and mitochondrial ROS regulation in the zebrafish innate immune response to P. aeruginosa infection. sod2 is upregulated in mammalian macrophages and neutrophils in response to lipopolysaccharide in vitro, and sod2 knockdown in zebrafish results in an increased bacterial burden. Further investigation revealed that phagocyte numbers are compromised in Sod2-deficient zebrafish. Addition of the mitochondrion-targeted ROS-scavenging chemical MitoTEMPO rescues neutrophil numbers and reduces the bacterial burden in Sod2-deficient zebrafish. Our work highlights the importance of mitochondrial ROS regulation by SOD2 in the context of innate immunity and supports the use of mitochondrion-targeted ROS scavengers as potential adjuvant therapies during severe infections. 相似文献