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Heike Nave Susanne Kuhlmann Georg Brabant Reinhard Pabst 《Experimental and toxicologic pathology》2003,55(1):45-49
Leptin, a potent anorectic, 16-kDa, adipose tissue-derived protein, predominantly acts in hypothalamic nuclei, signaling obesity and modulating ingestive behavior. To reach this brain area, leptin, probably has to cross the blood-brain barrier (BBB). In some cases of obesity, enhanced leptin levels in the blood do not result in anorectic effects, probably due to an altered leptin transport across the BBB. Therefore, we investigated the BBB in lean and diet-induced obese Lewis rats. To obtain information about the presence of microvessels with barrier dysfunction we examined three brain areas (hypothalamus, cortex, hippocampus) using a monoclonal antibody which detects intact microvessels of the BBB (anti-endothelial barrier antigen, anti-EBA). The results showed a significantly reduced EBA staining in the brain sections of the obese animals, except the hippocampus, compared to the control group. In a second step we injected I125-labeled leptin intravenously (i.v.) in permanent i.v.-cannulated, unrestrained Lewis rats (lean and obese). We measured the radioactivity in the cerebrospinal fluid after puncture of the cisterna magna, in the blood and brain tissue 90 min after injection. The leptin content in the cerebrospinal fluid and brain was not reduced in obese compared to lean rats, thus showing a similar transport capacity of the BBB in both experimental groups. Therefore, the results of the in vivo investigations do not indicate an impairment of the BBB in diet-induced obesity, despite the immunohistological findings. Further functional and morphological studies are necessary to evaluate the specific role of other organs and distinct forms of leptin (free and protein-bound) in the pathogenesis of diet-induced obesity. 相似文献
74.
David Baker Debra Butler Bernard J. Scallon Janet K. O'Neill John L. Turk Marc Feldmann 《European journal of immunology》1994,24(9):2040-2048
Tumor necrosis factor (TNF) activity was inhibited during the development of actively-induced, chronic relapsing experimental allergic encephalomyelitis (CREAE) in Biozzi AB/H mice, using a mouse TNF-specific (TN3.19.12) antibody and bivalent human p55 and p75 TNF receptor-immunoglobulin (TNFR-Ig) fusion proteins. The development of disease could be inhibited when repeated doses of antibody were administered prior to the anticipated onset. It has now also been shown that a therapeutic effect is evident even when antibody is administered after the onset of clinical signs, further indicating an important role for TNF in pathogenic effector mechanisms in CREAE. Although biologically-active TNF was not detected in the circulation, TNF-α was detected in lesions within the central nervous system (CNS). This suggested that the CNS may be the main site for TNF-specific immunomodulation and was supported by the observation that intracranial injection was significantly more potent than that administered systemically, for both antibody and TNFR-Ig fusion proteins. The fusion proteins were as effective as antibody at doses 10—100-fold lower than that used for antibody, reflecting their higher neutralizing capacity in vitro. Although treatment was not curative and relapse inevitably occurred in this model if treatment was not sustained, the data indicate that anti-TNF immunotherapy, especially within the CNS, can inhibit CREAE and may, therefore, be useful in the control of human neuroimmunological diseases. 相似文献
75.
ALBERT GJEDDE 《Acta physiologica (Oxford, England)》1980,108(4):331-339
A new kinetic analysis of blood-brain glucose transport is described, based on a steady-state model that takes account of cerebral blood flow, mean capillary glucose concentration, and cerebral metabolic rate. The maximal rate (Tmax) and half-saturation constant (Km) of glucose transport from blood to brain were determined in rats by measuring the rate of blood-to-brain glucose transfer at different blood glucose concentrations. Each determination lasted 20 seconds. For whole-brain, Tmax and Km averaged 258±33 (S.E.) μmol (100 g)-1 min-1 and 5.9±1.6 (S.E.) mmol 1-1, respectively. The regional variations were insignificant. The new approach permits kinetic parameters to be measured locally in brain in rapidly changing functional states. 相似文献
76.
目的:研究一氧化碳及其限速酶(血红素氧合酶-1)对局灶性缺血脑组织血脑屏障通透性的影响。方法:将SD大鼠随机分为3组(n=6),使用血红素氧合酶诱导剂及抑制剂腹腔注射,用等量生理盐水腹腔注射作为对照组,12h后复制MCAO模型。梗塞后24h后检测血液中一氧化碳浓度、血脑屏障通透性。结果:诱导剂组一氧化碳浓度明显高于对照组(P<0.01),血脑屏障通透性明显低于对照组(P<0.05),而抑制剂组一氧化碳浓度明显低于对照组(P<0.01),血脑屏障通透性明显高于对照组(P<0.05)。血红素氧合酶诱导剂、抑制剂对非梗塞侧的血脑屏障通透性没有影响(P>0.05)。结论:一氧化碳作为一种信使分子,脑缺血时浓度升高具有保护血脑屏障的作用。 相似文献
77.
Mais V.; Ajossa S.; Piras B.; Guerriero S.; Marongiu D.; Melis G.B. 《Human reproduction (Oxford, England)》1995,10(12):3133-3135
To evaluate the effectiveness of the oxidized regenerated celluloseabsorbable barrier (Interceed®, TC7) in the prevention ofde-novo adhesion formation after laparoscopic myomectomy, aprospective and randomized study was performed at the Departmentof Obstetrics and Gynaecology of the University of Cagliari,Cagliari, Italy. A total of 50 pre-menopausal non-pregnant women,aged 2342 years, who submitted to laparoscopic myomectomyfrom January 1993 to June 1994, were randomized to surgery alone(control group, n = 25) or surgery and oxidized regeneratedcellulose barrier (Interceed group, n = 25). Neither group receivedany other treatment for adhesion prevention. A second-look laparoscopywas performed 1214 weeks after laparoscopic myomectomy.The incidence of adhesion-free patients was assessed at second-looklaparoscopy by an investigator not informed of the treatment.The numbers of adhesion-free patients were three out of 25 (12%)in the control group and 15 out of 25 (60%) in the treatmentgroup (P < 0.05). In conclusion, the oxidized regeneratedcellulose absorbable barrier significantly reduced de-novo adhesionformation after laparoscopic myomectomy. 相似文献
78.
早、中、晚孕期胎盘因子体外抗HIV-1的研究 总被引:1,自引:0,他引:1
目的 探讨早、中、晚孕期胎盘因子(PF)体外抗人免疫缺陷病毒-1(HIV-1)及在HIV-1垂直传播中的作用.方法 荧光染料Calcien-AM标记的H9/HIV-1ⅢB分别与早、中、晚孕期不同稀释浓度的PF作用后,与MT2细胞培养,荧光显微镜下观察合胞休的形成;用HIV-1ⅢB感染MT2细胞,并分别与早、中、晚孕期不同稀释浓度的PF作用后,用MTT法检测HIV-1感染细胞的存活率,用ELISA方法检测细胞培养上清中p24抗原水平.结果 各孕期PF并不能抑制MT2和H9/HIV-1ⅢB细胞的融合,但可以增加HIV-1感染细胞的存活率及减少HIV-1 p24抗原的表达,且效应以早孕期PF最大,中孕期PF其次晚孕期PF最小,并与剂量呈正相关.结论 PF在体外具有抗HIV-I的作用,并呈现孕期和剂量相关性,可能在阻断HIV-1垂直传播中具有一定作用. 相似文献
79.
Dysfunction of the blood–cerebrospinal fluid barrier (BCB) has been implicated in the pathogenesis of Parkinson's disease (PD) and other neurodegenerative disorders. Therefore, we assayed serum and cerebrospinal fluid (CSF) from 30 parkinsonian patients and 30 controls for concentrations of albumin and IgG. The CSF/serum ratio for albumin (AQ), IgG (GQ), IgG-index as well as determination of oligoclonal bands were used to evaluate BCB function and to quantify humoral immune response within the central nervous system (CNS). Levels of AQ, GQ and IgG-index did not significantly differ in both groups. We found no dysfunction of the blood–CSF barrier or signs of local synthesis of IgG in the central nervous system of parkinsonian patients. Our data do not support the hypothesis of a dysfunctional BCB that contributes to pathophysiological mechanisms underlying PD. 相似文献
80.