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41.
Cycloheximide Reduces the Effects of Anoxic Insult In Vivo and In Vitro   总被引:3,自引:0,他引:3  
In vivo and in vitro techniques were utilized to examine the influence of a protein synthesis blocker, cycloheximide (CHX), on the damaging effects of anoxia in the rat. CHX administered 1 h before transient (30 min) forebrain ischaemia increased the survival of animals, decreased body weight loss and reduced the occurrence of delayed degeneration in the CA1 pyramidal region. The same dose of CHX injected 1 h after ischaemia induced status epilepticus, a decrease in survival rate, and did not reduce weight loss or CA1 damage in any of the surviving rats. Electrophysiological techniques were then used to determine the effects of various periods of anoxia and aglycaemia (AA) on CA1 field excitatory postsynaptic potentials (EPSPs) in hippocampal slices incubated in the presence or absence of CHX. In CHX-treated slices, recuperation of EPSP amplitude (45±16%) was significantly greater than in control slices (9±9%) following an AA episode of 3 min 45 s. No difference was seen in the percent recuperation of EPSPs in the control and CHX-treated slices after shorter or longer episodes of AA. From these studies, it appears that CHX protects against the damaging effect of ischaemia in vivo or AA in vitro.  相似文献   
42.
We have studied outward currents of neurons acutely isolated from superficial layers of the entorhinal cortex with whole-cell patch-clamp recordings. If cells were held more negative than -50 mV, depolarizing voltage commands activated a transient A-type current together with a sustained outward current. Both currents were sensitive to 4-aminopyridine, while only the sustained current was blocked by tetraethylammonium. The sustained outward current showed a considerable rundown in amplitude over prolonged recording periods. At the same time its half-maximal inactivation shifted from -74 to -114 mV. Nystatin perforated patch recordings were used to minimize these perfusion effects. Under such conditions the amplitude and the steady-state inactivation properties of the sustained outward current remained stable for more than 1 h. Pharmacological investigations revealed that only a small part of the sustained outward current could be attributed to a calcium-activated potassium current. Therefore most of the rundown has to be due to changes in the delayed rectifier outward current. These results may suggest that the delayed rectifier current is under considerable metabolic control.  相似文献   
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44.
Abstract: Discordant xenotransplantation is complicated by delayed xenograft rejection (DXR). Previous studies have demonstrated that anti‐apoptotic genes are protective against DXR. This study examines the hypothesis that apoptosis plays a role in human anti‐xenograft responses. C57BL/6 mice and NOD SCID mice were given a single intravenous injection of either a lethal dose (LD, survival < 30 min) or a sublethal dose (SLD) of human serum, and isolated pig and mouse rod‐shaped cardiomyocytes were exposed to human serum in vitro. In situ detection of apoptotic cells in mouse hearts was assessed using a terminal deoxynucleotidyl transferase‐mediated dUTP nicked‐end labeling assay. Mice transfused with human serum had approximately a 10‐fold increased percentage of apoptotic cells after SLD 18 h post‐injection compared with animals given saline, and a fourfold increase over LD. Administration of cobra venom factor (CVF) decomplemented SLD 18 h did not significantly ( P  > 0.05) alter the percentage apoptosis. The addition of 20 mM Gal‐α‐1,3‐Gal to SLD 18 h significantly ( P  < 0.05) reduced percentage apoptosis to levels comparable to saline treated control animals. In vitro using mouse and pig cardiomyocytes demonstrated parallel results as in vivo experiments.
Human serum induces apoptosis of cardiomyocytes in immunocompetent and immunoincompetent mice in vivo, as well as mouse and pig cardiomyocytes in vitro. Further, this apoptotic response can be inhibited by the addition of Gal‐α‐1,3‐Gal without affecting the capacity of the serum to cause HAR. These results demonstrate that a putative human serum factor induces a delayed apoptotic injury of xenograft tissues, and supports the hypothesis that apoptosis may be an important mediator of DXR.  相似文献   
45.
急性脑肿胀去大骨瓣减压术后迟发性血肿   总被引:1,自引:0,他引:1  
目的探讨外伤后急性脑肿胀去大骨瓣减压术后迟发性血肿的发病机制及临床表现,以提高该类病人的手术疗效。方法回顾性分析28例急性脑肿胀去大骨瓣减压术后迟发性颅内血肿病人的临床表现。结果外伤后急性脑肿胀去大骨瓣术后迟发性血肿的发生率为19.56%,术区继发硬膜外血肿10.87%。死亡率为32.12%。结论急性脑肿胀去大骨瓣术后迟发性血肿的发生率较高,多见于脑肿胀缓解病例,对术中出现的急性脑膨出和术后病情恶化应考虑到迟发性血肿的可能,早期的诊断是提高疗效的关键。  相似文献   
46.
顺铂缓释剂局部植入药代动力学的实验研究   总被引:1,自引:0,他引:1  
目的 研究局部植入顺铂缓释剂 (DDPSRP)在大鼠和狗体内的药代动力学。方法 用原子吸收分光光度法 (灯电流 12 5mA ,波长 2 6 5 9nm)测定血浆顺铂 (DDP)的浓度。结果 大鼠皮下植入DDPSRP后 ,DDP可持续缓慢释放 ;狗静脉注射DDP 4mg·kg-1,其时间 -浓度曲线呈二室模型 ;狗肌肉植入 2mg·kg-1DDPSRP后 ,其有效血浆浓度 -时间曲线呈一室模型特点 ,但其维持有效血浆浓度时间 (0 1mg·L-1)长达 16 8~ 2 6 4h。结论 DDPSRP有显著的缓释作用  相似文献   
47.
目的:研究中药穴位贴敷法的全身免疫调节作用,探讨其防治小儿哮喘的机理.方法:采用幼龄哮喘豚鼠模型,在迟发相哮喘反应阶段,观察中药穴位贴敷对血清SOD、MDA的影响.结果:中药穴位贴敷可使豚鼠血清MDA含量下降而SOD升高.结论:中药穴位贴敷法具有全身免疫调节作用,从而可阻断气道炎症和气道高反应性的发生.  相似文献   
48.
目的研究心脏M3受体/M3受体介导的钾通道与心律失常的关系,寻找抗心律失常药物的新靶点。方法 分别以结扎大鼠左冠状动脉前降支所致急性心律失常模型和膜片钳技术为基础,观察M3受体的干预作用及作用机制。结果M3受体阻断剂4DAMP(4-diphenylacetoxy-n-methylpiperidine-methiodide)加重结扎大鼠冠状动脉前降支所致心律失常,而M3受体激动剂胆碱能明显对抗其作用。其他亚型受体阻断剂,M1受体阻断剂(prienzepine)、M2受体阻断剂(methotramine)和M4受体阻断剂(tropicamide)对结扎大鼠左冠状动脉前降支所致急性心律失常无影响。在膜片钳实验中发现,胆碱可激活一种延迟整流钾电流(IKM3),此电流可被M3受体阻断剂4DAMP明显抑制。而M1,M2和M4受体阻断剂对胆碱介导的电流无作用。结论胆碱通过激动心肌M3受体诱发一外向钾电流(IKM3),并在维持心脏离子通道平衡中起重要作用。M3受体/IKM3可能是抗心律失常新靶点。  相似文献   
49.
肠安康胶囊对小鼠炎症和免疫功能的影响   总被引:2,自引:0,他引:2  
王献坤  郑晓鹤  邢建峰  侯家玉 《中成药》2004,26(12):1043-1045
目的:研究肠安康胶囊(黄芪、黄连、金银花等)对小鼠急性炎症和免疫功能的影响.方法:观察肠安康对二甲苯致小鼠耳肿胀和醋酸致毛细血管通透性增高急性炎症的影响;以二硝基氟苯诱发小鼠迟发型超敏反应(DTH),观察耳肿胀度、淋巴细胞增殖能力,同时检测血清中肿瘤坏死因子-α(TNF-α)、白细胞介素1-β(IL-1β)的变化.结果:肠安康胶囊能明显抑制小鼠急性炎症,抑制DTH小鼠耳肿胀,抑制T、B淋巴细胞增殖,降低血清中TNF-α的含量,但对IL-1β的含量无明显影响.结论:肠安康胶囊有明显的抗炎和对DTH的抑制作用,降低TNF-α的含量可能是其作用途径之一.  相似文献   
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