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41.
α adrenoreceptor 301–303 deletion polymorphism does not influence basal metabolic rate, insulin resistance or weight gain in Greek women with polycystic ovary syndrome.  相似文献   
42.
Insulin lispro is an insulin analogue that has the advantages of being fast-acting, convenient, and less likely to lead to hypoglycaemic episodes. Previous studies have proven its value in treating both Type 1 and Type 2 diabetes both alone and in combination with different treatment regimens.1,2 However, diabetes is heterogeneous and differs in etiology and clinical characteristics in different ethnic groups. Even with the same insulin treatment, different diets will produce different glycaemic profiles. Diet patterns differ between different ethnic groups. Traditional oriental foods are characterized by a higher proportion of carbohydrates and a lower proportion of fat compared to Caucasian diets. To date, there has been no study on the use of insulin lispro in Chinese diabetic patients. Whether the Chinese dietary pattern will affect the efficacy of insulin lispro treatment remains unknown. Therefore, we conducted this trial to assess the efficacy of insulin lispro treatment in Chinese patients.  相似文献   
43.
目的鉴定参与线虫衰老的神经内分泌调控的新基因。方法鉴于神经系统在衰老调控中的重要作用,通过寿命分析和脂褐质自发荧光的检测,从编码突触蛋白的遗传位点中筛选参与衰老调控的基因。我们还进一步检查了这些遗传位点相应的突变体的永久性幼虫形成情况,探讨它们是否可能受胰岛素样信号通路的调控。结果遗传位点 unc-10,syd-2,hlb-1,dlk-1,mkk-4,scd-2,snb-1,ric-4,nrx-1,unc-13,sbt-1,unc-64 可能参与线虫衰老的调控。而且在衰老的调控中,unc-10,syd-2,hlb-1,dlk-1,mkk-4,scd-2,snb-1,ric-4,nrx-1 的功能可能与unc-13,sbt-1,unc-64相反。肠道脂褐质自发荧光的检测进一步证明了筛选出的各基因对应突变体的长寿或短寿表型,是由减慢或缩短的组织衰老所致。在筛选出的基因中,syd-2,hlb-1,mkk-4,scd-2,snb-1,ric-4,unc-64 也参与了永久性幼虫形成的调控。另外,daf-2突变增强了syd-2和hlb-1的表达,降低了mkk-4,nrx-1,ric-4,sbt-1,rpm-1,unc-10,dlk-1,unc-13 的表达。daf-16突变提高了syd-2和 hlb-1 的表达,降低了mkk-4,nrx-1,sbt-1,rpm-1,unc-10,dlk-1,unc-13 的表达. 结论突触功能可能在个体寿命和永久性幼虫形成的调控机制中具有重要的作用。  相似文献   
44.
The characteristics of a glial Na+,K+-pump dependent on extracellular K+ within epileptogenic cortex were studied electrophysiologically, biochemically and histochemically in vitro using slices from cobalt-induced epileptogenic cortex of rat. When the extracellular K+ concentration ([K+]o) was varied between 4 and 40 mM, the mean slope of membrane potential plotted against [K+]o was about 57 mV in glia from the normal cortex (tissue A) and about 44 mV in glia from the epileptogenic cortex (tissue B); whereas no significant difference in the resting membrane potential of these tissues was observed. In glia from tissue B, a marked transient hyperpolarization above control level was caused by replacement of elevated [K+]o with the normal medium. Ouabain abolished these phenomena observed in glia from tissue B, but had no effect on the membrane potential during normal [K+]o. Reduction of extracellular Na+, Ca2+ and Cl did not significantly affect the membrane potential of glia from either tissue. In tissue A, the cells marked by intracellular injection of horseradish peroxidase after intracellular recording were protoplasmic astrocytes; in tissue B, fibrous astrocytes with abnormal processes predominated. K+-dependent stimulation of Na+,K+-ATPase activity of the astrocyte-enriched fraction and its membrane preparation from tissue B was much larger than that from tissue A. A certain amount of the reaction product of K+-pNPPase activity was seen on glial plasma membrane within tissue B but not on that from tissue A. The above findings suggest that a glial Na+,K+-pump within actively firing epileptogenic cortex may be modified to increase in its activity.  相似文献   
45.
目的:探讨非体外循环心脏不停跳冠状动脉搭桥术的安全性和早期临床效果。方法:自2000年7月至2002年3月51例冠心病患接受冠状动脉搭桥手术,按手术方式分为非体外循环组(n=21)和传统体外循环组(n=30)。将两组病人的术前临床资料,手术方式,术后并发症和疗效等进行对比分析。结果:两组术前临床资料无明显差异。非体外循环组手术时间,术后出血输血量,呼吸机辅助时间显少于体外循环组,并且术后心律失常的发生率明显降低(P均<0.05),其他重要器官的并发症发生率亦低于体外循环组。两组平均随访9.6个月,心绞痛均消失,心功能改善,活动量明显增加。结论:非体外循环冠状动脉搭桥术是安全可行的,并发症少,近期疗效满意。  相似文献   
46.
喂饲泵应用的临床观察及护理   总被引:7,自引:0,他引:7  
目的 探讨用喂饲泵行肠内营养摄入的临床应用价值。方法 实验组30例采用喂饲泵控制肠内营养液的滴入速度,对照组采用传统方法,用20ml或50ml注射器灌注营养液,观察两组并发症的发生情况,所得量化指标进行卡方检验。结果实验组其返流、呕吐、腹胀、吸入性肺炎的发生率明显低于对照组。结论应用喂饲泵行肠内营养的摄入,可有效预防并发症的发生。  相似文献   
47.
Summary To define the glucose to insulin dose-response relationship before the onset of diabetes, we studied 22 nondiabetic co-twins of patients with Type 1 (insulin-dependent) diabetes mellitus and nine control subjects. All had intravenous glucose tests at 0.02, 0.1 and 0.5 g/kg and were followedup prospectively for at least 6 years. Seven twins developed diabetes a mean of 7 months later; the remaining 15 are now unlikely to develop diabetes. The seven pre-diabetic twins had higher fasting insulin levels than control subjects (4.2±2.0 vs 1.8±1.8 nmol/l; p<0.05); but lower glucose clearance (1.0±0.5 vs 1.9±0.7 %/min; p<0.05), first phase insulin response at 0.5 g/kg (21.1±23.2 vs 143±50 nmol/l; p<0.0001), and total insulin responses at 0.1 g/kg (p<0.05) and 0.5 g/kg (p<0.00005). Using a curve-fitting programme, the normal glucose to insulin relationship was lost in prediabetic twins who had lower coefficient of determination (R2) than control subjects (p<0.01). In contrast, 15 low-risk twins and their nine control subjects had similar fasting glucose and insulin levels, glucose clearance, R2 and insulin secretory responses to different glucose loads. The positive predictive values of subnormal R2 and subnormal first phase insulin response were 67 % and 58 % respectively. These observations demonstrate an altered glucose to insulin dose-response relationship and loss of maximum insulin secretory response to glucose before the onset of Type 1 diabetes.  相似文献   
48.
目的:探讨儿童甲亢患者糖代谢紊乱的特点。方法:用SUPER GLUCOCARD^TM血糖仪和放射免疫方法检测29例甲亢患儿餐前、餐后60min、120min血糖和餐前、餐后60min胰岛素、C肽、胰高糖素、皮质醇及T3、T4、TSH、TGA、TMA(其中10例糖耐量减低为甲亢1组,另19例糖耐量正常为甲亢2组),并与20例健康儿童进行比较。结果:(1)34.5%甲亢患儿出现糖代谢紊乱,病程大于1年和小于1年糖代谢紊乱发生率为50%,9%(P<0.05)。(2)甲亢1组餐后60min胰岛素、胰岛素/血糖、胰岛素/胰高糖素显著升高(P<0.05)。结论:甲亢儿童存在糖代谢紊乱现象,表现为葡萄糖耐量减低和胰岛素拮抗,其发生与病程有关,病程较长,发生率较高。糖代谢紊乱可能与自身免疫、胰岛β细胞功能受损及胰岛素拮抗有关。  相似文献   
49.
Summary The involvement of nitric oxide as an intracellular messenger in the control of insulin secretion from pancreatic Beta cells was studied in rat islets of Langerhans by measuring: (i) nitric oxide generation in response to physiological insulin secretagogues; (ii) the effects of inhibitors of nitric oxide synthesis on insulin secretory responses to physiological secretagogues, and on insulin synthesis; (iii) changes in islet cyclic guanosine monophosphate in response to secretagogues; (iv) the effects of exogenous cyclic guanosine monophosphate and dibutyryl cyclic guanosine monophosphate on insulin secretion from electrically permeabilised islets and from intact islets, respectively. These studies produced no evidence that nitric oxide generation is required for the initiation of insulin secretion by common secretagogues. However, the results of our experiments suggest that the generation of nitric oxide may be involved in long-term, glucose-dependent increases in cyclic guanosine monophosphate content of islet cells, although the physiological relevance of these changes requires further investigation.  相似文献   
50.
Summary Insulin resistance and a defective insulin activation of the enzyme glycogen synthase in skeletal muscle during euglycaemia may have important pathophysiological implications in Type 2 (non-insulin-dependent) diabetes mellitus. Hyperglycaemia may serve to compensate for these defects in Type 2 diabetes by increasing glucose disposal through a mass action effect. In the present study, rates of whole-body glucose oxidation and glucose storage were measured during fasting hyperglycaemia and isoglycaemic insulin infusion (40 mU·m–2min–1, 3 h) in 12 patients with Type 2 diabetes. Eleven control subjects were studied during euglycaemia. Biopsies were taken from the vastus lateralis muscle. Fasting and insulin-stimulated glucose oxidation, glucose storage and muscle glycogen synthase activation were all fully compensated (normalized) during hyperglycaemia in the diabetic patients. The insulin-stimulated increase in muscle glycogen content was the same in the diabetic patients and in the control subjects. Besides hyperglycaemia, the diabetic patients had elevated muscle free glucose and glucose 6-phosphate concentrations. A positive correlation was demonstrated between intracellular free glucose concentration and muscle glycogen synthase fractional velocity insulin activation (0.1 mmol/l glucose 6-phosphate: r=0.65, p<0.02 and 0.0 mmol/l glucose 6-phosphate: r= 0.91, p<0.0001). In conclusion, this study indicates an important role for hyperglycaemia and elevated muscle free glucose and glucose 6-phosphate concentrations in compensating (normalizing) intracellular glucose metabolism and skeletal muscle glycogen synthase activation in Type 2 diabetes.  相似文献   
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