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31.
32.
Central precocious puberty and abnormal chromosomal patterns 总被引:1,自引:0,他引:1
Central precocious puberty (PP) can be caused by chromosomal aberrations. We report three patients presenting with central
PP in whom karyotype analysis demonstrated abnormal chromosomal patterns. The first patient was affected by the triple-X syndrome,
commonly characterized by premature ovarian failure. The second patient, a girl with inv dup(15)(pter→q12::q12→pter), had
a chromosomal aberration involving an imprinted region of the human genome, whose deletion is commonly associated with Prader-Willi
syndrome (PWS) and hypogonadotrophic hypogonadism. The third patient was a boy carrying a rare chromosome abnormality, the
duplication of chromosome 9 (q22→qter). All patients had mental retardation, which was mild in patient 1, moderate in patient
2, and severe in case 3. They underwent treatment with luteinizing hormone releasing hormone (LHRH) analogs, which were able
to stop the progression of the sexual development. We confirm that chromosomal aberrations are an important cause of central
PP, and that karyotype analysis in patients with PP and mental retardation, even if mild, is necessary because chromosomal
abnormalities can be present. 相似文献
33.
Iréne?LundEmail author Thomas?Lundeberg Louise?Sandberg Cecilia?Norrbrink?Budh Jan?Kowalski Elisabeth?Svensson 《BMC medical research methodology》2005,5(1):31
Background:
Rating scales like the visual analogue scale, VAS, and the verbal rating scale, VRS, are often used for pain assessments both in clinical work and in research, despite the lack of a gold standard. Interchangeability of recorded pain intensity captured in the two scales has been discussed earlier, but not in conjunction with taking the influence of pain etiology into consideration. 相似文献34.
Paola Origone Carlo Bellini Debora Sambarino Barbara Banelli Guido Morcaldi Carmen La Rosa Franco Stanzial Claudio Castellan Domenico A. Coviello Cecilia Garrè Eugenio Bonioli 《Human mutation》2003,22(4):341-341
In the original version of this article, the title was incorrect. Please find the correct title given here. The publisher deeply regrets this error. The original article to which this Erratum refers was published in Human Mutation 22:179–180 Human Mutation(2003) 22(2) 179–180 相似文献
35.
36.
The Yin-Yang of tumor-associated macrophages in neoplastic progression and immune surveillance 总被引:5,自引:1,他引:5
Paola Allavena Antonio Sica Cecilia Garlanda Alberto Mantovani 《Immunological reviews》2008,222(1):155-161
Summary: An intrinsic (oncogene-driven) pathway and an extrinsic (microenvironment-driven) pathway connect inflammatory reactions and cancer. M2-polarized tumor-associated macrophages and the related myeloid-derived suppressor cells are key prototypic components of smoldering inflammation driving neoplastic progression. However, mononuclear phagocytes can exert anti-tumor activity by killing tumor cells and eliciting tissue disruptive reactions (M1), a likely scenario in the early phases of carcinogenesis of immunogenic tumors and following therapeutic intervention. Shifting the macrophage balance represents a viable therapeutic target. Herein, the 'macrophage balance' is discussed in the context of the apparent paradox of tumor promotion by innate immunity-driven inflammation and the seemingly opposed tumor surveillance by adaptive immune responses. 相似文献
37.
D'Adamo P Welzl H Papadimitriou S Raffaele di Barletta M Tiveron C Tatangelo L Pozzi L Chapman PF Knevett SG Ramsay MF Valtorta F Leoni C Menegon A Wolfer DP Lipp HP Toniolo D 《Human molecular genetics》2002,11(21):2567-2580
Non-specific mental retardation (NSMR) is a common human disorder characterized by mental handicap as the only clinical symptom. Among the recently identified MR genes is GDI1, which encodes alpha Gdi, one of the proteins controlling the activity of the small GTPases of the Rab family in vesicle fusion and intracellular trafficking. We report the cognitive and behavioral characterization of mice carrying a deletion of Gdi1. The Gdi1-deficient mice are fertile and anatomically normal. They appear normal also in many tasks to assess spatial and episodic memory and emotional behavior. Gdi1-deficient mice are impaired in tasks requiring formation of short-term temporal associations, suggesting a defect in short-term memory. In addition, they show lowered aggression and altered social behavior. In mice, as in humans, lack of Gdi1 spares most central nervous system functions and preferentially impairs only a few forebrain functions required to form temporal associations. The general similarity to human mental retardation is striking, and suggests that the Gdi1 mutants may provide insights into the human defect and into the molecular mechanisms important for development of cognitive functions. 相似文献
38.
Lack of association between angiotensin converting enzyme polymorphism and sporadic Alzheimer's disease 总被引:3,自引:0,他引:3
Monastero R Caldarella R Mannino M Cefalù AB Lopez G Noto D Camarda C Camarda LK Notarbartolo A Averna MR Camarda R 《Neuroscience letters》2002,335(2):147-149
Epidemiological and pathogenetic evidences suggest a strong association between vascular risk factors and sporadic Alzheimer's disease (sAD). In agreement with the vascular hypothesis of AD, the role of various candidate genes for atherosclerosis has been investigated, leading to conflicting results. In order to clarify the significance of angiotensin-converting enzyme (ACE) gene insertion (I)/deletion (D) polymorphism in a group of patients with sAD, we conducted a case-control study including 149 cases and 149 age and sex matched controls. All subjects were genotyped for ACE and Apolipoprotein E (APOE). There were no significant differences in ACE genotype or allele frequencies between cases and controls, even after stratification for APOE4 carrier status. Our data suggest that the ACE I/D polymorphism is not associated to genetic susceptibility in sAD patients. 相似文献
39.
Immune regulatory mechanisms influence early pathology in spinal cord injury and in spontaneous autoimmune encephalomyelitis 下载免费PDF全文
Marcondes MC Furtado GC Wensky A Curotto de Lafaille MA Fox HS Lafaille JJ 《The American journal of pathology》2005,166(6):1749-1760
Injuries to the central nervous system (CNS) trigger an inflammatory reaction with potentially devastating consequences. In this report we compared the characteristics of the inflammatory response on spinal cord injury (SCI) caused by a stab wound between the T7 and T9 vertebrae and spontaneous experimental autoimmune encephalomyelitis (EAE). SCI and EAE were compared in two types of myelin basic protein Ac1-11-specific T-cell receptor transgenic mice: T/R+ mice harbor regulatory T cells, and T/R- mice lack regulatory T cells. Our results show that 8 days after SCI, T/R- mice developed a strong T-cell infiltrate in the spinal cord, with remarkable down-modulation of CD4 expression that was accompanied by a local increase in Mac-3+ and F4/80+ reactivity and diffuse local and distal astrogliosis. In contrast, T/R+ mice exhibited a modest increase in CD4+ cells localized to the site of injury, without CD4 down-modulation; focal astrogliosis was restricted to the site of the lesion, although Mac-3+ and F4/80+ cells were also present. Similarly to T/R- mice that underwent SCI, T cells displaying down-modulated CD4 expression were found in the CNS of older T/R- mice afflicted by spontaneous EAE. Overall, our results suggest that common mechanisms regulate T-cell accumulation in CNS lesions of different causes, such as mechanic lesion or autoimmune-mediated damage. 相似文献