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排序方式: 共有1952条查询结果,搜索用时 15 毫秒
71.
Kirstin R. W. Matthews Ana S. Iltis Nuria Gallego Marquez Daniel S. Wagner Jason Scott Robert Inmaculada de Melo‐Martín Marieke Bigg Sarah Franklin Soren Holm Ingrid Metzler Matteo A. Mol Jochen Taupitz Giuseppe Testa Jeremy Sugarman 《The Hastings Center report》2021,51(1):47-51
It now seems technically feasible to culture human embryos beyond the “fourteen‐day limit,” which has the potential to increase scientific understanding of human development and perhaps improve infertility treatments. The fourteen‐day limit was adopted as a compromise but subsequently has been considered an ethical line. Does it remain relevant in light of technological advances permitting embryo maturation beyond it? Should it be changed and, if so, how and why? What justifications would be necessary to expand the limit, particularly given that doing so would violate some people's moral commitments regarding human embryos? Robust stakeholder engagement preceded adoption of the fourteen‐day limit and should arguably be part of efforts to reassess it. Such engagement could also consider the need for enhanced oversight of human embryo research. In the meantime, developing and implementing reliable oversight systems should help foster high‐quality research and public confidence in it. 相似文献
72.
Increased gene and protein expression of the novel eNOS regulatory protein NOSTRIN and a variant in alcoholic hepatitis 总被引:3,自引:0,他引:3
Mookerjee RP Wiesenthal A Icking A Hodges SJ Davies NA Schilling K Sen S Williams R Novelli M Müller-Esterl W Jalan R 《Gastroenterology》2007,132(7):2533-2541
BACKGROUND & AIMS: Increased intrahepatic resistance in cirrhosis is associated with reduced endothelial NO synthase (eNOS) activity and exacerbated by superimposed inflammation. NOSTRIN induces intracellular translocation of eNOS and reduces NO generation. Our aims were to quantify and compare hepatic expression of eNOS, NOSTRIN, NOSIP, and caveolin-1 in alcoholic cirrhosis with or without superimposed alcoholic hepatitis and in normal livers. METHODS: Biopsy specimens from 20 decompensated alcoholic cirrhotic patients with portal hypertension (10 with alcoholic hepatitis) and 6 normal livers were analyzed: real-time polymerase chain reaction for quantification of messenger RNA; Western blotting; and enzyme assays of eNOS in normal and diseased liver were performed. Localization and interaction of eNOS and NOSTRIN in liver was assessed by immunohistochemistry and co-immunoprecipitation. RESULTS: eNOS mRNA was significantly increased and eNOS activity decreased in alcoholic hepatitis patients, despite no differences in eNOS protein expression among the patients. Patients with alcoholic hepatitis had significantly higher hepatic levels of NOSTRIN and caveolin-1 mRNA compared with cirrhosis alone or normal biopsy specimens. A NOSTRIN splice variant, not present in normal tissue, was detected on mRNA and protein levels in all alcoholic patients. Coimmunoprecipitation demonstrated association among NOSTRIN, eNOS, and caveolin-1. CONCLUSIONS: An increase in mRNA and protein of NOSTRIN and its shortened variant in alcoholic hepatitis may partly account for the paradox of increased mRNA levels and normal protein expression but decreased enzymatic activity of eNOS in diseased liver. Such intracellular regulators of NO production may be important in the development of increased intrahepatic resistance in alcoholic hepatitis patients. 相似文献
73.
Kirstin Albers Christian Schlein Kirsten Wenner Peter Lohse Alexander Bartelt Joerg Heeren René Santer Martin Merkel 《Atherosclerosis》2014
Deficiency of apoprotein A-V (apoA-V) can cause hypertriglyceridemia. In an 11 months old boy presenting with a severe hypertriglyceridemia, a formerly unknown 24 nucleotide deletion in exon 2 of the APOA5 gene was detected. The homozygous mutation results in an eight amino acid loss in the signal peptide sequence (c.16_39del; p.Ala6_Ala13del). Screening of control persons proved that this deletion is a rare mutation. Hypertriglyceridemia in the patient was only found at the time when he was breast fed, while after weaning, triglyceride levels were close to normal. Under both dietary conditions, apoA-V protein was undetectable in plasma while post-heparin plasma lipoprotein lipase activity was normal. 相似文献
74.
75.
W J Morrow D A Isenberg R E Sobol R B Stricker T Kieber-Emmons 《Clinical immunology and immunopathology》1991,58(2):163-180
The acquired immune deficiency syndrome (AIDS) is a viral-induced disorder of humans that is reaching pandemic proportions. The etiologic agent responsible for AIDS is recognized as a retrovirus termed the human immunodeficiency virus (HIV). This virus is both cytotropic and cytopathic for T lymphocytes in vitro, and patients with AIDS and HIV-related conditions invariably have serious T cell abnormalities, notably a reduced number of the helper/inducer (CD4+) subpopulation. There is now a substantial body of evidence to suggest that the AIDS virus triggers a diverse range of autoimmune phenomena. The purpose of this article is to summarize the clinical and immunopathological manifestations of autoimmunity in HIV infection and to provide a perspective of the possible origins and roles autoimmune reactions play in HIV disease progression. 相似文献
76.
Marianne R. Spalinger Stephanie Kasper Claudia Gottier Silvia Lang Kirstin Atrott Stephan R. Vavricka Sylvie Scharl Tina Raselli Isabelle Frey-Wagner Petrus M. Gutte Markus G. Grütter Hans-Dietmar Beer Emmanuel Contassot Andrew C. Chan Xuezhi Dai David J. Rawlings Florian Mair Burkhard Becher Werner Falk Michael Fried Gerhard Rogler Michael Scharl 《The Journal of clinical investigation》2016,126(11):4388
77.
Ohne Zusammenfassung 相似文献
78.
Predictive value of the 2014 International Society of Urological Pathology grading system for prostate cancer in patients undergoing radical prostatectomy with long‐term follow‐up 下载免费PDF全文
79.
Medium‐term oncological outcomes for extended vs saturation biopsy and transrectal vs transperineal biopsy in active surveillance for prostate cancer 下载免费PDF全文
80.
Melanie E. Armitage Kirstin Wingler Harald H. H. W. Schmidt Mylinh La 《Journal of molecular medicine (Berlin, Germany)》2009,87(11):1071-1076
Cardiovascular diseases remain the leading cause of death in industrialised nations. Since the pathomechanisms of most cardiovascular
diseases are not understood, the majority of therapeutic approaches are symptom-orientated. Knowing the molecular mechanism
of disease would enable more targeted therapies. One postulated underlying mechanism of cardiovascular diseases is oxidative
stress, i.e. the increased occurrence of reactive oxygen species such as superoxide. Oxidative stress leads to a dysfunction
of vascular endothelium-dependent protective mechanisms. There is growing evidence that this scenario also involves impaired
nitric oxide (NO)-cyclic GMP signalling. Out of a number of enzyme families that can produce reactive oxygen species, NADPH
oxidases stand out, as they are the only enzymes whose sole purpose is to produce reactive oxygen species. This review focuses
on the clinically validated targets of oxidative stress, NO synthase (NOS) and the NO receptor, soluble guanylate cyclase
as well as the source of ROS, e.g. NADPH oxidases. We place recent knowledge in the function and regulation of these enzyme
families into clinical perspective. For a comprehensive overview of the biology and pharmacology of oxidative stress and possible
other sources and targets, we refer to other literature overviews. 相似文献