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排序方式: 共有2906条查询结果,搜索用时 15 毫秒
1.
Adriano Chiò Elena Herrero Hernandez Gabriele Mora Consuelo Valentini Gianluigi Discalzi Enrico Pira 《Amyotrophic lateral sclerosis and other motor neuron disorders》2004,5(3):188-191
A 34-years-old floor-layer developed optic neuropathy and motor neuron disease after being accidentally exposed to a solvent mixture containing methanol and other substances. Optic neuropathy is a complication of methanol poisoning, but the onset of a motor neuron disorder resembling amyotrophic lateral sclerosis after the exposure to these substances has not been previously described. The temporal onset of the clinical symptoms, biological plausibility, young age of the patient and absence of neurological disorders in the family history raises suspicion of a possible causative relationship. 相似文献
2.
Antonella d’Arminio Monforte Paola Cinque Luca Vago Aleandro Rocca Antonella Castagna Cristina Gervasoni Maria Rosa Terreni Roberto Novati Andrea Gori Adriano Lazzarin Mauro Moroni 《Journal of neurology》1996,244(1):35-39
Twenty patients with AIDS who had intracranial lesions underwent both brain biopsy and cerebro-spinal fluid (CSF) examination
to compare histological diagnosis with the polymerase chain reaction (CSF-PCR) for the identification of infectious agents.
CSF-PCR was performed for herpes simplex virus, varicella zoster virus, cytomegalovirus (CMV), JC virus (JCV), Epstein-Barr
virus (EBV), Toxoplasma gondii and Mycobacterium tuberculosis. A definitive diagnosis was obtained by brain biopsy in 14 patients (2 with astrocytoma, 12 with brain infection). CSF-PCR
was positive for EBV DNA in 3 of 3 cases of primary cerebral lymphoma, positive for JCV DNA in 6 of 7 biopsy-proven (and one
autopsy-proven) cases of progressive multifocal leukoencephalopathy (PML). CSF-PCR was positive for CMV DNA in one biopsy-proven
and one autopsy-proven case of CMV encephalitis (the former also had PML) and positive for M. tuberculosis DNA in one case of tuberculous encephalitis. None of the five toxoplasmic encephalitis cases (one definite, four presumptive)
were T. gondii DNA positive. There was close correlation between histology and CSF-PCR for CMV encephalitis, PML and PCL. Antitoxoplasma
therapy affected the sensitivity of both histological and CSF-PCR methods.
Received: 8 November 1995 Received in revised form: 9 July 1996 Accepted: 19 July 1996 相似文献
3.
Summary
The virological findings obtained during an outbreak of Bornholm disease which took place in the summer 1957 in Cermignano, in the province of Teramo, Italy, are described.
During this study it was possible to isolate 15 strains of a Goxsackie B2 type virus. 3 strains were isolated simultaneously from rectal and pharyn geal swabs, while 9 strains were isolated from pharyngeal swabs only. 相似文献
4.
5.
Ultrastructural Localization of Alpha-Naphthyl Acid Esterase in Human TM Lymphocytes 总被引:2,自引:0,他引:2 下载免费PDF全文
Antonio Zicca Annaldo Leprini Angela Cadoni Adriano T. Franzi Manlis Ferrarini Carlo E. Grossi 《The American journal of pathology》1981,105(1):40-46
The localization of alpha-naphthyl acid esterase (ANAE) activity in T lymphocytes with receptors for IgM (TM cells) have been studied at the electron microscope. The electron-opaque product of the cytochemical reaction was detected around, but never inside, single (or groups of) vesicles, which suggested a possible membrane localization of the enzyme activity. These same vesicles were found to contain acid phosphatase by both light- and electron-microscopic examination and were bound by unit membranes; this data indicates that they likely represent primary lysosomes. The presence of such lysosomes in a restricted paranuclear area is a distinctive feature of TM cells. 相似文献
6.
7.
Mesenteric lymph nodes are critical for the induction of high-dose oral tolerance in the absence of Peyer's patches 总被引:7,自引:0,他引:7
Spahn TW Weiner HL Rennert PD Lügering N Fontana A Domschke W Kucharzik T 《European journal of immunology》2002,32(4):1109-1113
We have previously demonstrated the loss of oral tolerance (OT) in lymphotoxinalpha-/- (LTalpha-/-) and TNFalpha / lymphotoxinalpha deficient (TNFalpha / LTalpha-/-) mice which have defective Peyer's patches (PP) and lymph node (LN) development. We have now studied OT in BALB / c mice with differential defects of the gut-associated lymphoid tissue (GALT) caused by inhibition of LTbetaR signaling during fetal development. Treatment of pregnant mice with LTbetaR-IgG (LTbetaRIgG) and TNFR I55-IgG (TNFR55IgG) abrogates the formation of PP (LTbetaRIgG) or of PP and mesenteric LN (MLN) (LTbetaRIgG / TNFRIgG) without genetically deleting the respective cytokine pathways. OT was readily induced in mice without PP but retaining MLN (PP null / LN +). In contrast, OTcould not be induced in mice lacking both MLN and PP (PP null / MLN null) as shown by the inability of these mice to suppress IFN-gamma secretion or DTH reactions. We next assessed OT in 129 x B6 LTalpha-/- mice with and without MLN. Timed treatment of pregnant LTalpha-/- mice with an agonist anti-LTbetaR mAb induces formation of MLN but not of PP in LTalpha-/- mice. LN + LTalpha-/- mice developed OT while LN LTalpha-/- mice were resistant to OT induction. Taken collectively, the data show that in the presence of MLN PP are not required for OT induction and that the presence of MLN is sufficient for OT induction in the LTalpha-/- model. 相似文献
8.
Cigarette smoke prevents apoptosis through inhibition of caspase activation and induces necrosis 总被引:6,自引:0,他引:6
Wickenden JA Clarke MC Rossi AG Rahman I Faux SP Donaldson K MacNee W 《American journal of respiratory cell and molecular biology》2003,29(5):562-570
Emphysema is characterized by enlargement of the distal airspaces in the lungs due to destruction of alveolar walls. Alveolar endothelial and epithelial cell apoptosis induced by cigarette smoke is thought to be a possible mechanism for this cell loss. In contrast, our studies show that cigarette smoke condensate (CSC) induces necrosis in alveolar epithelial cells and human umbilical vein endothelial cells. Furthermore, study of the cell death pathway in a model system using Jurkat cells revealed that in addition to inducing necrosis, CSC inhibited apoptosis induced by staurosporine or Fas ligation, with both effects prevented by the antioxidants glutathione and dithiothreitol. Time course experiments revealed that CSC inhibited an early step in the caspase cascade, whereby caspase-3 was not activated. Moreover, cell-free reconstitution of the apoptosome in cytoplasmic extracts from CSC-treated cells, by addition of cytochrome-c and dATP, did not result in activation of caspases-3 or -9. Thus, smoke treatment may alter the levels of pro- and antiapoptogenic factors downstream of the mitochondria to inhibit active apoptosome formation. Therefore, unlike previous studies, cell death in response to cigarette smoke by necrosis and not apoptosis may be responsible for the loss of alveolar walls and inflammation observed in emphysema. 相似文献
9.
10.
Neuropathological Diagnostic Criteria for Creutzfeldt-Jakob Disease (CJD) and Other Human Spongiform Encephalopathies (Prion Diseases) 总被引:12,自引:0,他引:12
Herbert Budka Adriano Aguzzi Paul Brown Jean-Marie Brucher Orso Bugiani Filippo Gullotta Matti Haltia Jean-Jacques Hauw James W. Ironside Kurt Jellinger Hans A. Kretzschmar Peter L. Lantos Carlo Masullo Wolfgang Schlote Jun Tateishi Roy O. Weller 《Brain pathology (Zurich, Switzerland)》1995,5(4):459-466
Neuropathological diagnostic criteria for Creutzfeldt-Jakob disease (CJD) and other human transmissible spongiform encephalopathies (prion diseases) are proposed for the following disease entities: CJD - sporadic, iatrogenic (recognised risk) or familial (same disease in 1st degree relative): spongiform encephalopathy in cerebral and/or cerebellar cortex and/or subcortical grey matter; or encephalopathy with prion protein (PrP) immuno-reactivity (plaque and/or diffuse synaptic and/or patchy/perivacuolar types). Gerstmann-Sträussler-Scheinker disease (GSS) (in family with dominantly inherited progressive ataxia and/or dementia): encephalo(myelo)pathy with multicentric PrP plaques. Familial fatal insomnia (FFI) (in member of a family with PRNP178 mutation): thalamic degeneration, variable spongiform change in cerebrum. Kuru (in the Fore population). Without PrP data, the crucial feature is the spongiform change accompanied by neuronal loss and gliosis. This spongiform change is characterised by diffuse or focally clustered small round or oval vacuoles in the neuropil of the deep cortical layers, cerebellar cortex or subcortical grey matter, which might become confluent. Spongiform change should not be confused with non-specific spon-giosis. This includes status spongiosus (“spongiform state”), comprising irregular cavities in gliotic neuropil following extensive neuronal loss (including also lesions of “burnt-out” CJD), “spongy” changes in brain oedema and metabolic encephalopathies, and artefacts such as superficial cortical, perineuronal, or perivascular vacuolation; focal changes indistinguishable from spongiform change may occur in some cases of Alzheimer's and diffuse Lewy body diseases. Very rare cases might not be diagnosed by these criteria. Then confirmation must be sought by additional techniques such as PrP immunoblotting, preparations for electron microscopic examination of scrapie associated fibrils (SAF), molecular biologic studies, or experimental transmission. 相似文献