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2.
Unidirectional fluxes of 45Ca, 36Cl, and of [3H]mannitol from blood into the sciatic nerve and cerebral cortex were determined from 5- and 15-min uptakes of these tracers after an intravenous (i.v.) bolus injection in awake rats. Rats were fed diets for 8 wk, that had either a low (0.01% wt/wt), normal (0.67%), or high (3%) Ca content. Plasma [Ca] was 32% less and 11% more in rats fed low (LOCA) and high Ca diets (HICA), respectively, than in rats fed a normal Ca diet (CONT). The mean permeability-surface area product (PA) of 45Ca at the blood-nerve barrier was about eightfold higher than at the blood-brain barrier in the same animals and did not differ significantly between groups (greater than 0.05). Mean PA ratios of 45Ca/36Cl for the blood-nerve and blood-brain barriers in CONT rats, 0.52 +/- 0.04 and 0.40 +/- 0.02, respectively, were not significantly different from corresponding ratios in LOCA and HICA groups, and corresponded to the aqueous limiting diffusion ratio (0.45). Our results show no evidence for concentration-dependent transport of Ca over a plasma [Ca] range of 0.8-1.4 mmol/liter at the blood-nerve barrier of the rat peripheral nerve, and suggest that Ca and Cl exchange slowly between nerve and blood via paracellular pathways.  相似文献   
3.
根据近几年来发表的与铁稳态有关的生物分子的研究文献 ,将这些生物分子根据其与铁的吸收、转运、储存以及对铁稳态的监控调节等方面的关系 ,对这些生物分子进行了分类。特别是对细胞膜载体、运铁蛋白受体、铁调蛋白及铁反应元件等作了较为详细地论述  相似文献   
4.
Human glioma cells obtained from established cell lines (Tp-276MG, Tp-301MG, Tp-378MG, Tp-483MG and U-251MG) were analyzed for the presence of ion channels with the tight-seal voltage clamp technique. The current-voltage relation revealed a marked inward rectification at hyperpolarizing voltages, due to the presence of inward rectifying K-channels in cells from all studied cell lines. These channels were conducting when the membrane potential was more negative than the K-equilibrium potential. The slope conductance for the inward K-currents (gKi) was affected both by [K+]i and [K+]0. gKi was proportional to [K+]0 raised to 0.35 or 0.50, of which the larger value was measured in the presence of low [K+]i (25mM). The rectification was not significantly different in cells perfused with Mg-free EDTA-buffered internal solution. Tl+ was 3.5 times more permaant than K+. gki was blocked by Cs+ (1 mM) in a voltage-dependent way (more effective in the hyperpolarized membrane), and by Na+ (154 mM) depending on voltage and time. From measurements of unitary current events in membrane patches (outside out or cell attached) the conductance of the single inward rectifying channel was estimated to be 27 ± 7 pS. This type of ion channel may be important for K-uptake by glial cells and hence for the K-homeostasis in the brain.  相似文献   
5.
利用人T淋巴母细胞(Jurkat)细胞系作为研究对象。企图探探索细胞外基质成份及肌醇磷脂细胞信息传递系统与细胞移动的关系。研究结果表明:当细胞被伏波醇酯(PMA)处理过后,其粘连性与移动件对纤维连结蛋白(FN)底物的反应在已是高水平的基础上有更进一步提高的作用。与FN刊相反的是,未经PMA处理处的Jurkat细胞对层粘连蛋白(Lm)底物却无明显的粘连性及移动性增加的反应,尽管在PMA处理过4小时内亦无任何的增强。但是,当PMA作用于细胞24一48小时后则明显池增加其Lm底物的粘连性及移动性反应,表明了其明显的协同作用。分别用抗FN、抗Lm及蛋白激酶C抑制剂Staurosprine(SP)时均起到特异性的抑制作用。可见,协同作用的产生是通过蛋白激酶C激活后的-段时间内,使细胞表面Lm受体密度增加而对底物Lm反应增强所致。  相似文献   
6.
Summary The high concentration of zinc in the bovine pineal gland prompted us to investigate the existence of a zinc-binding protein in this organ. In this study, we report that the subcellular distribution of zinc in the bovine pineal gland is nonuniform, with the crude nuclear, mitochondrial, microsomal, and supernatant fractions having 0.264±0.038, 0.160±0.019, 0.130±0.016, and 0.287±0.010 g zinc/mg protein, respectively. Furthermore, gel filtration studies using Sephadex G-75 and a 105,000 g supernatant fraction revealed two zinc binding protein peaks that bind 1.7 and 3.7 g Zn++/mg protein, respectively. Furthermore, purification of the protein peak with an elution volume (ve/vo) of 2.06 on anion exchange chromatography (DEAE-A 25) yielded a single protein peak which binds 10 g zinc/mg protein. The comparative high performance liquid Chromatographic (HPLC) profiles of the zinc-induced hepatic metallothionein isoform I (retention time=17.39 min) and of the bovine pineal metallothionein-like protein isoform I (retention time=17.49 min) are similar. Since zinc is a potent inhibitor of sulfhydryl-containing enzymes and receptor sites, we investigated the effects of zinc and found that it inhibited the binding of [3H]glutamate (IC 50=80 M) and of [3H]spiroperidol (IC 50=0.6 mM) to the pineal membranes. The results of these studies are interpreted to indicate that the bovine pineal gland possesses an active and dynamic zinc homeostatic mechanism, whose precise function(s) remain(s) to be delineated.  相似文献   
7.
Sleep deprivation (SD) increases extracellular adenosine levels in the basal forebrain, and pharmacological manipulations that increase extracellular adenosine in the same area promote sleep. As pharmacological evidence indicates that the effect is mediated through adenosine A1 receptors (A1R), we expected A1R knockout (KO) mice to have reduced rebound sleep after SD. Male homozygous A1R KO mice, wild-type (WT) mice, and heterozygotes (HET) from a mixed 129/C57BL background were implanted during anesthesia with electrodes for electroencephalography (EEG) and electromyography (EMG). After 1 week of recovery, they were allowed to adapt to recording leads for 2 weeks. EEG and EMG were recorded continuously. All genotypes had a pronounced diurnal sleep/wake rhythm after 2 weeks of adaptation. We then analyzed 24 h of baseline recording, 6 h of SD starting at light onset, and 42 h of recovery recording. Neither rapid eye movement sleep (REM sleep) nor non-REM sleep (NREMS) amounts differed significantly between the groups. SD for 6 h induced a strong NREMS rebound in all three groups. NREMS time and accumulated EEG delta power were equal in WT, HET and KO. Systemic administration of the selective A1R antagonist 8-cyclopentyltheophylline (8-CPT) inhibited sleep for 30 min in WT, whereas saline and 8-CPT both inhibited sleep in KO. We conclude that constitutional lack of adenosine A1R does not prevent the homeostatic regulation of sleep.  相似文献   
8.
肌醇磷脂介导缺血脑损伤信号传导作用的研究进展   总被引:4,自引:0,他引:4  
肌醇磷脂途径作为一种重要的细胞内信号传导通路,在神经系统特别是中枢神经系统发挥重要作用。本文旨在综述其在中枢神经系统的生理性作用。从而进一步探讨在脑缺血发生后这一通路的生理性代偿机制及病理生理机制。  相似文献   
9.
目的探讨妊娠高血压患者血清ALT、AST、LDH、Ca2+、BILI T、血脂、凝血项目检测与妊高征发生及进展的关系。方法对2006年1月至2007年12月入住我院孕妇,进行上述项目的回顾性分析。结果1.子痫前期组、妊娠高血压组BILI T比正常妊娠对照组低,有显著性差异(P<0.01);2.子痫前期组的Ca2+、血浆凝血酶原时间(PT)、活化部分凝血酶时间(APTT)比正常妊娠对照组低,有显著性差异(P<0.01);3.重度子痫前期FIB、ALT、AST、LDH、TG、CHO、LDL-C、比正常妊娠对照组高有显著性差异(P<0.01);4.轻度子痫前期组、妊娠高血压组的PT、APTT、HDL-C、UA、TG、CHO、ALT、AST、LDH之间无明显差异,但前三者低于正常妊娠对照组有明显差异(P<0.05);而后者则高于正常妊娠对照组有明显差异(P<0.05)。凝血酶时间(TT)在各之间无显著性差异(P>0.05)。结论妊娠20w后进行生化项目检测可以协助早期诊断,为及早预防妊高症发生、发展,为母婴健康提供有用依据,同时指导孕妇在怀孕期间补充营养同时,注意补助钙、维生素C、维生素E,可以有效预防妊高症发生及发...  相似文献   
10.
Acute liver failure was induced in rats by CCl4 administration and its effects on the hepatic Krebs cycle and gluconeogenic fluxes were evaluated in situ by 13C NMR isotopomer analysis of hepatic glucose following infusion of [U-13C]propionate. In fed animals, CCl4 injury caused a significant increase in relative gluconeogenic flux from 0.80+/-0.10 to 1.34 +/-0.24 times the flux through citrate synthase (p<0.01). In 24-h fasted animals, CCl4-injury also significantly increased relative gluconeogenic flux from 1.36+/-0.16 to 1.80+/-0.22 times the flux through citrate synthase (p<0.01). Recycling of PEP via pyruvate and oxaloacetate was extensive under all conditions and was not significantly altered by CCl4 injury. CCl4 injury significantly reduced hepatic glucose output by 26% (42.8+/-7.3 vs 58.1+/-2.4 micromol/kg/min, p=0.005), which was attributed to a 26% decrease in absolute gluconeogenic flux from PEP (85.6+/-14.6 vs 116+/-4.8 micromol/kg/min, p<0.01). These changes were accompanied by a 47% reduction in absolute citrate synthase flux (90.6+/-8.0 to 47.6+/-8.0 micromol/kg/min, p<0.005), indicating that oxidative Krebs cycle flux was more susceptible to CCl4 injury. The reduction in absolute fluxes indicate a significant loss of hepatic metabolic capacity, while the significant increases in relative gluconeogenic fluxes suggest a reorganization of metabolic activity towards preserving hepatic glucose output.  相似文献   
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