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91.
Alcoholism is a complex disease caused by a confluence of environmental and genetic factors influencing multiple brain pathways to produce a variety of behavioral sequelae, including addiction. Genetic factors contribute to over 50% of the risk for alcoholism and recent evidence points to a large number of genes with small effect sizes as the likely molecular basis for this disease. Recent progress in genomics (microarrays or RNA-Seq) and genetics has led to the identification of a large number of potential candidate genes influencing ethanol behaviors or alcoholism itself. To organize this complex information, investigators have begun to focus on the contribution of gene networks, rather than individual genes, for various ethanol-induced behaviors in animal models or behavioral endophenotypes comprising alcoholism. This chapter reviews some of the methods used for constructing gene networks from genomic data and some of the recent progress made in applying such approaches to the study of the neurobiology of ethanol. We show that rapid technology development in gathering genomic data, together with sophisticated experimental design and a growing collection of analysis tools are producing novel insights for understanding the molecular basis of alcoholism and that such approaches promise new opportunities for therapeutic development. 相似文献
92.
Evy Cleeren Johan Van der Heyden Angela Brand Herman Van Oyen 《Archives of Public Health》2011,69(1):8
The completion of the Human Genome Project triggered a whole new field of genomic research which is likely to lead to new
opportunities for the promotion of population health. As a result, the distinction between genetic and environmental diseases
has faded. Presently, genomics and knowledge deriving from systems biology, epigenomics, integrative genomics or genome-environmental
interactions give a better insight on the pathophysiology of common diseases. However, it is barely used in the prevention
and management of diseases. Together with the boost in the amount of genetic association studies, this demands for appropriate
public health actions. The field of Public Health Genomics analyses how genome-based knowledge and technologies can responsibly
and effectively be integrated into health services and public policy for the benefit of population health. Environmental exposures
interact with the genome to produce health information which may help explain inter-individual differences in health, or disease
risk. However today, prospects for concrete applications remain distant. In addition, this information has not been translated
into health practice yet. Therefore, evidence-based recommendations are few. The lack of population-based research hampers
the evaluation of the impact of genomic applications. Public Health Genomics also evaluates the benefits and risks on a larger
scale, including normative, legal, economic and social issues. These new developments are likely to affect all domains of
public health and require rethinking the role of genomics in every condition of public health interest. This article aims
at providing an introduction to the field of and the ideas behind Public Health Genomics. 相似文献
93.
Bliss C 《Social science & medicine (1982)》2011,73(7):1019-1027
This article examines the reflexive, biosocial nature of genomic meaning making around race, drawing on discourse analysis of 732 articles on genomics and race published from the years 1986-2010, in-depth interviews with 36 of the world's most elite genomics researchers, interviews with 15 critics, policymakers, and trainees involved in debates over race, and participant observation at a core genotyping facility that specializes in ancestry estimation. I reveal how biomedical researchers identify with, value, and make sense of the taxonomies they construct. My analysis goes beyond a consideration of instrumental rationales to analyze the experiential and political motivations that shape how researchers get involved in racial ethical dilemmas. I theorize taxonomic practice as a reflexive form of biosociality, a conscious shaping of social notions about biology and race to produce a future that researchers themselves want to live in. I demonstrate how reflexive biosociality paradoxically leads researchers to advance social explanations for race while investing in genomics as a solution to racial quandaries. 相似文献
94.
Boyang Wei Wei Kong Xiaoyang Mou Shuaiqun Wang 《Pathology, research and practice》2019,215(1):159-170
Cancer immunotherapy has achieved unprecedented success in the treatment of cancer. However, different patients have different responses to immunotherapy. More and more studies have shown that tumor immune heterogeneity has an important influence on the prognosis of cancer. Therefore, understanding the clinical impact of tumor immune infiltration and the regulatory mechanism of RNA molecules is crucial for exploring the pathogenesis of lung adenocarcinoma (LUAD) and the development of immunotherapy protocols.The endogenous competitive RNA hypothesis provides new ideas for studying immune heterogeneity. Therefore, by using the method of immune genomics, this article explores the relationship between immune infiltration and prognosis of patients with lung adenocarcinoma, and found that B-cell immune infiltration highly affects the survival of patients. Through differential analysis, differential mRNAs, lncRNAs and miRNAs were extracted, and 318 differentially expressed mRNAs related to B cell immunity were screened by correlation analysis, and prognosis of patients with COX risk regression model was predicted and analyzed. Through multiple database searches, an immune-related ceRNA regulatory network was constructed, containing 3 key mRNAs, 4 miRNAs, and 50 lncRNAs. Three mRNAs and most miRNAs, lncRNAs, are significantly associated with LUAD prognosis. Bioinformatics analysis of the network showed that LINC00337 may up-regulate the expression of PBK and KIF23 through competitive binding of has-mir-373 and has-mir-519d. The competitive binding of has-mir-373 and has-mir-372 can up-regulate the expression of SLC7A11. The interaction between these RNAs may have an important regulatory role in the immune infiltration in lung adenocarcinoma, thereby affecting the patient's prognosis and immunotherapy efficacy. 相似文献
95.
Cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC) is the fourth commonest female malignancy worldwide. CESC progresses in immune-microenvironment mainly composed of infiltrating immune and stromal cells. Here, we performed an integrated analysis incorporating the expression profiles from the Cancer Genome Atlas (TCGA) database and scores of immune and stromal cells calculated by Estimation of Stromal and Immune cells in Malignant Tumours using Expression data (ESTIMATE) algorithm. A two-gene signature (CD1C and CD6 genes) was established to predict the prognosis of CESC. Based on this signature, patients were divided into the high- and low-risk groups, and this signature showed good prognostic performance according to the results of Kaplan-Meier analysis and receiver operating characteristic (ROC) analysis in train set and two validation sets. A nomogram was built for evaluating the clinical applicability of this signature. In addition, based on Tumor Immune Estimation Resource (TIMER) database, 2 hub genes showed negative correlations with tumor purity and positive correlations with infiltrating levels of immune filtrating cells. What’s more, we propose new treatment strategies for the two prognostic subtypes. Low- risk patients were found presenting with a higher level of immune checkpoint molecules and showing higher immunogenicity in immunophenoscore (IPS) analysis, which indicated a better response for immunotherapy. Meanwhile, estimated by Genomics of Drug Sensitivity in Cancer (GDSC) database, the high-risk patients showed sensitive responses to five chemotherapy drugs. Finally, 10 candidate small-molecule drugs for CESC were defined. In summary, the CD1C-CD6 signature can accurately predict the prognosis of CESC. 相似文献
96.
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98.
《International journal of medical microbiology : IJMM》2021,311(7):151534
Salmonella enterica serovar Typhimurium DT160 was the predominant cause of notified human salmonellosis cases in New Zealand from 2000 to 2010, before it was superseded by another S. Typhimurium strain, DT56 variant (DT56v). Whole genome sequencing and phenotypic testing were used to compare 109 DT160 isolates with eight DT56v isolates from New Zealand animal and human sources. Phylogenetic analysis provided evidence that DT160 and DT56v strains were distantly related with an estimated date of common ancestor between 1769 and 1821. The strains replicated at different rates but had similar antimicrobial susceptibility profiles. Both strains were resistant to the phage expressed from the chromosome of the other strain, which may have contributed to the emergence of DT56v. DT160 contained the pSLT virulence plasmid, and the sseJ and sseK2 genes that may have contributed to the higher reported prevalence compared to DT56v. A linear pBSSB1-family plasmid was also found in one of the DT56v isolates, but there was no evidence that this plasmid affected bacterial replication or antimicrobial susceptibility. One of the DT56v isolates was also sequenced using long-read technology and found to contain an uncommon chromosome arrangement for a Typhimurium isolate. This study demonstrates how comparative genomics and phenotypic testing can help identify strain-specific elements and factors that may have influenced the emergence and supersession of bacterial strains of public health importance. 相似文献
99.
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