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1.
LN Weinberger MJ Zirwas JC English III 《Journal of the European Academy of Dermatology and Venereology》2007,21(2):156-162
Male genital oedema can be defined as swelling or the appearance of swelling of the scrotum and/or the penile shaft and prepuce. Despite the various causes of genital oedema reported in the published work, a concise approach to the evaluation and management has not been sufficiently addressed. 相似文献
2.
Tolerance to self gangliosides is the major factor restricting the antibody response to lipopolysaccharide core oligosaccharides in Campylobacter jejuni strains associated with Guillain-Barré syndrome 下载免费PDF全文
Bowes T Wagner ER Boffey J Nicholl D Cochrane L Benboubetra M Conner J Furukawa K Furukawa K Willison HJ 《Infection and immunity》2002,70(9):5008-5018
Guillain-Barré syndrome following Campylobacter jejuni infection is frequently associated with anti-ganglioside autoantibodies mediated by molecular mimicry with ganglioside-like oligosaccharides on bacterial lipopolysaccharide (LPS). The regulation of antibody responses to these T-cell-independent antigens is poorly understood, and only a minority of Campylobacter-infected individuals develop anti-ganglioside antibodies. This study investigates the response to gangliosides and LPS in strains of mice by using a range of immunization strategies. In normal mice following intraperitoneal immunization, antibody responses to gangliosides and LPS are low level but can be enhanced by the antigen format or coadministration of protein to recruit T-cell help. Class switching from the predominant immunoglobulin M (IgM) response to IgG3 occurs at low levels, suggesting B1-cell involvement. Systemic immunization results in poor responses. In GalNAc transferase knockout mice that lack all complex gangliosides and instead express high levels of GM3 and GD3, generation of anti-ganglioside antibodies upon immunization with either complex gangliosides or ganglioside-mimicking LPS is greatly enhanced and exhibits class switching to T-cell-dependent IgG isotypes and immunological memory, indicating that tolerance to self gangliosides is a major regulatory factor. Responses to GD3 are suppressed in knockout mice compared with wild-type mice, in which responses to GD3 are induced specifically by GD3 and as a result of polyclonal B-cell activation by LPS. The anti-ganglioside response generated in response to LPS is also dependent on the epitope density of the ganglioside mimicked and can be further manipulated by providing secondary signals via lipid A and CD40 ligation. 相似文献
3.
R. G. Cutlip Dr. W. T. Stauber R. H. Willison T. A. McIntosh K. H. Means 《Medical & biological engineering & computing》1997,35(5):540-543
A dynamometer is designed and fabricated to measure the force output during static and dynamic muscle actions of the plantar
flexor muscles of anaesthetised rats in vivo. The design is based on a computer-controlled DC servomotor capable of angular
velocities in excess of 17.5 rad s−1. The system controls the range of motion, angular velocity and electrical stimulation of the muscles, while monitoring the
force output at the plantar surface of the foot. The force output is measured by a piezo-electric load cell that is rated
at 5 kg capacity. Angular velocity and position are measured by a DC tachometer and potentiometer, respectively. All measurement
devices are linear (r2=0.9998). The design minimises inertial loading during high-speed angular motions, with a variation in force output of less
than 0.2%. The dynamometer proves to be an accurate and reliable system for quantifying static and dynamic forces of rat plantar
flexor muscles in vivo. 相似文献
4.
Yang PY Almofti MR Lu L Kang H Zhang J Li TJ Rui YC Sun LN Chen WS 《第二军医大学学报》2006,27(6):637-637
Polygonum multiflorum stilbeneglycoside (PMS) is a water-soluble fraction of Polygonum multiflorum Thunb. , one of the most famous tonic traditional Chinese medicines, that has protective effects on the cardiovascular system. The purpose of the present study is to elucidate the effects of PMS on macrophage-derived foam cell functions and the reduction of severity of atherosclerosis in hypercholesterolemic New Zealand White (NZW) rabbits. NZW rabbits were fed for 12 weeks with a normal diet, a high cholesterol diet, or a high cholesterol diet associated with irrigation with different doses of PMS (25, 50, or 100 mg/kg). Treatment of NZW rabbits fed with high cholesterol diet with 100 mg/kg PMS attenuated the increase in plasma cholesterol, low-density lipoprotein cholesterol, very low-density lipoprotein cholesterol, and plasma triglyceride. Treatment with 50 and 100 mg/kg PMS caused 43% and 60% decrease in atherosclerotic lesioned area ratio to total surface area, respectively. In U937 foam cells, PMS could decrease the high expression of intercellular adhesion molecule (ICAM)-1 protein and the vascular endothelial growth factor (VEGF) protein levels in the medium induced by oxidized lipoprotein when analyzed by flow cytometry. The results proved that PMS is a powerful agent against atherosclerosis and that PMS action could possibly be through the inhibition of the expression of ICAM-1 and VEGF in foam cells. 相似文献
5.
目的研究β-catenin异常表达、c-myc和Cyclin D1的高表达与胰腺癌发生、浸润、转移的关系。方法应用免疫组织化学方法检测5例正常胰腺组织和40例胰腺癌及13例相应癌旁组织中β-catenm、c-myc和Cyclin D1的表达。结果 5例正常胰腺组织及13例胰腺癌旁组织中β-catenin为正常表达,c-myc和Cyclin D1阴性表达,40例胰腺癌组织中25例有β-catenin的异常表达(25/40,62.5%),20例(20/40,50%)有c-myc的高表达,23例(23/40,57.5%)有Cyclin D1的高表达。β-catenin的异常表达率与淋巴结转移、浸润及病理分级相关(P<0.05),c-myc和Cyclin D1的高表达与分化程度,浸润,转移及病理分级无关,β-catenin的异常表达与c-myc的阳性表达不相关,而与Cyclin D1的阳性表达相关。结论β-catenin的异常表达可能主要是通过激活Cyclin D1引起细胞增殖,导致肿瘤的发生。 相似文献
6.
Ruppel KM Willison D Kataoka H Wang A Zheng YW Cornelissen I Yin L Xu SM Coughlin SR 《Proceedings of the National Academy of Sciences of the United States of America》2005,102(23):8281-8286
Toward identifying the roles of protease-activated receptor-1 (PAR1) and other G protein-coupled receptors important for vascular development, we investigated the role of Galpha13 in endothelial cells in the mouse embryo. LacZ inserted into Galpha13 exon 1 was highly expressed in endothelial cells at midgestation. Endothelial-specific Galpha13 knockout embryos died at embryonic days 9.5-11.5 and resembled the PAR1 knockout. Restoration of Galpha13 expression in endothelial cells by use of a Tie2 promoter-driven Galpha13 transgene rescued development of endothelial-specific Galpha13 knockout embryos as well the embryonic day 9.5 vascular phenotype in Galpha13 conventional knockouts; transgene-positive Galpha13-/- embryos developed for several days beyond their transgene-negative Galpha13-/- littermates and then manifested a previously uncharacterized phenotype that included intracranial bleeding and exencephaly. Taken together, our results suggest a critical role for Galpha13 in endothelial cells during vascular development, place Galpha13 as a candidate mediator of PAR1 signaling in this process, and reveal roles for Galpha13 in other cell types in the mammalian embryo. 相似文献
7.
Madeleine E. Cunningham Gavin R. Meehan Sophie Robinson Denggao Yao Rhona McGonigal Hugh J. Willison 《Journal of the peripheral nervous system : JPNS》2020,25(2):143-151
In mouse models of acute motor axonal neuropathy, anti‐ganglioside antibodies (AGAbs) bind to motor axons, notably the distal nerve, and activate the complement cascade. While complement activation is well studied in this model, the role of inflammatory cells is unknown. Herein we aimed to investigate the contribution of phagocytic cells including macrophages, neutrophils and perisynaptic Schwann cells (pSCs) to distal nerve pathology. To observe this, we first created a subacute injury model of sufficient duration to allow inflammatory cell recruitment. Mice were injected intraperitoneally with an anti‐GD1b monoclonal antibody that binds strongly to mouse motor nerve axons. Subsequently, mice received normal human serum as a source of complement. Dosing was titrated to allow humane survival of mice over a period of 3 days, yet still induce the characteristic neurological impairment. Behaviour and pathology were assessed in vivo using whole‐body plethysmography and post‐sacrifice by immunofluorescence and flow cytometry. ex vivo nerve‐muscle preparations were used to investigate the acute phagocytic role of pSCs following distal nerve injury. Following complement activation at distal intramuscular nerve sites in the diaphragm macrophage localisation or numbers are not altered, nor do they shift to a pro‐ or anti‐inflammatory phenotype. Similarly, neutrophils are not significantly recruited. Instead, ex vivo nerve‐muscle preparations exposed to AGAb plus complement reveal that pSCs rapidly become phagocytic and engulf axonal debris. These data suggest that pSCs, rather than inflammatory cells, are the major cellular vehicle for axonal debris clearance following distal nerve injury, in contrast to larger nerve bundles where macrophage‐mediated clearance predominates. 相似文献
8.
9.
A randomised controlled trial of intravenous immunoglobulin in IgM paraprotein associated demyelinating neuropathy 总被引:3,自引:0,他引:3
Comi G Roveri L Swan A Willison H Bojar M Illa I Karageorgiou C Nobile-Orazio E van den Bergh P Swan T Hughes R Aubry J Baumann N Hadden R Lunn M Knapp M Léger JM Bouche P Mazanec R Meucci N van der Meché F Toyka K;Inflammatory Neuropathy Cause Treatment Group 《Journal of neurology》2002,249(10):1370-1377
This multicentre randomised double blind crossover trial tested the short term efficacy of intravenous immunoglobulin (IVIg)
2.0 g/kg given over 24 or 48 hours in patients with paraproteinaemic demyelinating neuropathy (PDN). Twenty-two patients were
randomised and completed the trial. After 2 weeks, the overall disability grade decreased during both IVIg treatment and placebo
but neither change was significant nor was the mean difference between the treatment effects. After 4 weeks the overall disability
decreased by a mean of 0.55 [0.67] grades during the IVIg period (p = 0.001) while it was substantially unmodified during
the placebo period. The mean difference between the treatment effects was significant (p = 0.05). Overall during the IVIg
period 10 patients improved and 11 were stable and one got worse. During the placebo period 4 patients improved, 4 deteriorated
and 14 were stable. Many secondary outcome measures, including Rankin scale, time to walk 10 metres, grip strength, sensory
symptoms score were significantly better during IVIg treatment. Two serious adverse events occurred during the trial, both
during placebo treatment. In conclusion the trial showed some short-term benefit of IVIg in about half of the patients confirming
previous observation.
Received: 6 August 2001, Received in revised form: 6 March 2002, Accepted: 12 March 2002
RID="*"
ID="*"The other members of the INCAT group are Jacques Aubry PhD, Institut de Biologie, INSERM Unit 463, 9 Quai Moncousu,
44 035 Nantes, France; Nicole Baumann MD, InSERM Unit 495, Salpetriere Hospital, 75 651 Paris, Cedex 13 France; Robert Hadden
PhD, Michael Lunn, MD, Department of Neuroimmunology, Guy's, King's and St. Thomas' School of Medicine, Guy's Hospital, London
SE1 9 UL, UK; Martin Knapp Phd, Personal Social Services Research Unit, London School of Economics and Political Science,
Houghton Street, London WC2A 1AE, UK; Jean-Marc Léger MD, Pierre Bouche MD, Service d'Eplorations Functionelles de la Salpetriere,
47 Boulevard de l'Hospital, 75 651 Paris, Cedex 13, France; Radim Mazanec CSc, Charles University, 2nd Medical School, University Hospital, V uvalu 84, Prague 5, Czech Republic; Nicoletta Meucci MD, Institute of Clinical Neurology,
University of Milan, Ospedale Maggior-Policlinico, via Sforza, 20 122 Milan, Italy; Frans van der Meché PhD, Department of
Neurology, Erasmus Medical Center Rotterdam, dr. Molewaterplein 40, 3015 GD Rotterdam, The Netherlands; and Klaus Toyka PhD,
Universitat Würzburg, Josef-Schneider Strasse 2, 97 080 Würzburg, Germany
Correspondence to Giancarlo Comi, MD 相似文献
10.
Willison HJ 《Revue neurologique》2002,158(123):16-20
Recent years have seen major progress in our understanding of the clinical pathophysiology of autoimmune neuropathies particularly with the identification and analysis of antibodies to gangliosides and related glycolipids in the serum of patients. Anti-glycolipid antibodies react with epitopes on the carbohydrate region of glycolipid molecules and can be routinely measured by standard immunoassays. In multifocal motor neuropathy, IgM anti-GM1 antibodies that cross react with GD1b and asialo-GM1 are detectable in around 50p. 100 of cases. This condition may clinically resemble certain forms of lower motor neurone disease. IgM anti-GD1b antibodies are found in IgM paraproteinaemic neuropathy characterised by profound sensory ataxia. In the anti-myelin associated glycoprotein (anti-MAG) IgM paraproteinaemic neuropathy, antibodies also react with the acidic glycolipids, sulphated glucuronyl paragloboside and its higher lactosaminyl homologue (SGPG and SGPLG). Thus a variety of chronic syndromes can be defined by their anti-glycolipid antibody profile. In Guillain-Barré syndrome, anti-GM1, GM1b, GD1a and GalNAc-GD1a antibodies are found in patients with acute motor axonal neuropathy (AMAN) and anti-GQ1b IgG antibodies are a very sensitive and specific marker for the Miller Fisher syndrome. Many other anti-glycolipid antibodies are being increasingly identified in other neuropathy subtypes. The article will summarise existing clinical and serological information in this field. 相似文献