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1.
Background/objectiveObstructive sleep apnea (OSA) is independently associated with dyslipidemia, a surrogate marker of atherosclerosis. Low-density lipoprotein (LDL)-cholesterol is accepted as a major independent risk factor for cardiovascular disease. However, non-high-density lipoprotein (HDL)-cholesterol is a better marker of atherogenic dyslipidemia and recommended as a target of lipid lowering therapy. We aimed to assess the prevalence of atherogenic dyslipidemia, and relationship between OSA severity and serum LDL-cholesterol and non-HDL cholesterol levels in OSA patients.MethodsWe retrospectively evaluated treatment naïve 2361 subjects admitted to the sleep laboratory of a university hospital for polysomnography. All subjects’ lipid profile including total cholesterol, LDL-cholesterol, HDL-cholesterol, triglycerides, and non-HDL-cholesterol were measured.ResultsOut of 2361 patients (mean age 49.6 ± 11.9 years; 68.9% male, apnea-hypopnea index 36.6 ± 28.4/h), 185 (7.8%) had no OSA and 2176 (92.2%) had OSA. Atherogenic dyslipidemia prevalence was high (57–66%) in OSA patients, and especially increased in severe OSA compared to other groups (p < 0.05). Though total and LDL-cholesterol did not differ between those with and without OSA, non-HDL-cholesterol (p = 0.020), and triglycerides (p = 0.001) were higher and HDL-cholesterol levels (p = 0.018) were lower in OSA patients than non-OSA. Non-HDL-cholesterol was significantly correlated with OSA severity (p < 0.001) and hypoxia parameters (p < 0.01), whereas LDL-cholesterol showed no correlation.ConclusionsAtherogenic dyslipidemia is highly prevalent and non-HDL-cholesterol levels are significantly increased, predominantly in severe OSA patients. Non-HDL-cholesterol but not LDL-cholesterol, is significantly correlated with OSA severity and hypoxia parameters. Therefore, it could be better to use non-HDL-cholesterol, which is a guideline recommended target of lipid therapy, as a marker of atherosclerotic cardiovascular risk in OSA patients.  相似文献   
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不同性别的大学生心理健康调查研究   总被引:2,自引:0,他引:2  
目的:探讨不同性别的大学生心理状况的影响。方法:以260名大学生为研究对象,采用SCL-90对不同性别的大学生进行了评定。结果:女生在抑郁、焦虑和恐怖方面高于男生,两者均存在显著性差异(P〈0.01)。结论:大学生中女性学生存在一定的心理缺陷,应针对性地开展专业教育,帮助大学生建立稳定、乐观和积极进取的健康心理。  相似文献   
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目的 :探讨计算机专业人员的心理健康状况。方法 :以SCL 90为工具 ,对 71名计算机专业人员进行评估。结果 :计算机专业人员SCL 90总分和各因子显著低于全国常模 ;男性员工在躯体化、强迫、人际关系、焦虑、敌对、饮食和睡眠因子上得分显著高于女性员工 ;女性在恐怖因子得分显著高于男性。结论 :计算机专业人员心理症状较少 ,症状严重程度较低 ,男性员工自我感觉与自我评价方面低于女性员工。  相似文献   
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目的探讨内源性热休克蛋白90(HSP90)在缺氧心肌细胞丝氨酸苏氨酸蛋白激酶(AKT)相关信号通路中的作用。方法建立新生Wistar大鼠心肌细胞缺氧模型,将细胞分为正常组、缺氧组、加入HSP90特异性阻断剂格尔德霉素后再缺氧组(格尔德霉素+缺氧组)。于缺氧后1、3、6、12、24、48h用噻唑蓝法检测心肌细胞的活力;缺氧24h,原位缺口末端标记法检测心肌细胞凋亡指数(AI);缺氧1、3、6、12、24h,蛋白质印迹法检测大鼠心肌细胞中内源性HSP90及AKT表达水平。结果(1)缺氧24、48h,缺氧组、格尔德霉素+缺氧组细胞活力均较正常组明显下降(P〈0.05);格尔德霉素+缺氧组细胞活力缺氧12h即开始明显下降,缺氧48h时明显低于缺氧组(P〈0.05)。(2)缺氧24h,缺氧组细胞AI为(10.7±1.2)%,明显高于正常组[(1.9±0.3)%.P〈0.05];格尔德霉素+缺氧组细胞AI为(26、3±5.3)%,明显高于缺氧组(P〈0.01)。(3)缺氧12h,缺氧组心肌细胞内源性HSP90及AKT表达水平高于正常组与格尔德霉素+缺氧组;缺氧24h,缺氧组有所下降.格尔德霉素+缺氧组则下降更明显。结论内源性HSP90对维持心肌细胞的活力有重要作用.缺氧心肌细胞AKT表达水平可受内源性HSP90表达水平的影响。  相似文献   
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大学生心理健康教育干预研究   总被引:11,自引:2,他引:9  
目的 研究高校心理健康干预模式 ,提高大学生心理健康水平。方法 采取分层整群抽样的方法 ,运用SCL - 90自评量表对该院学生测试评分 ,分别进行实施心理健康干预模式 (心理教育、心理预防、心理训练 )前后状况调查 ,比较学生心理测试总体水平。结果 学校心理健康教育干预实施后一年 ,学生心理测试 8项因子分均值低于心理健康干预实施前 ,其中强迫、人际关系、焦虑、恐怖、偏执因子分实施前后有显著性差异 (P <0 0 5 )。结论 学校实施心理健康教育干预能有效地维护大学生心理健康 ,促进大学生心理发展 ,提高大学生心理素质  相似文献   
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In a prospective study the results of a pterygium excision in 54 patients (57 eyes) who underwent a superficial free conjunctival autograft (FCG) were compared to those of patients who were treated with postoperative90Sr-irradiation. In 51 cases the minimum follow-up was six months, the maximum follow-up seven years. We divided the study up into a randomized part and an open part. In the randomized part, surgery of a primary pterygium was performed in 25 eyes, of which 16 were treated with a FCG and compared with 9 eyes with primary pterygium surgery and postoperative90Sr beta-irradiation. In the same period 16eyes were treated because of a recurrent pterygium: 8 with FCG and 8 with90Sr-irradiation. In the open part of the study16 eyes with primary pterygium were successively treated with FCG alone. The results showed in the randomized, as well as in the open study on primary surgery with a minimum follow-up of six month, one recurrence in each of the FCG-groups (2 out of 31 eyes =6.4%), and no recurrences in the 90Sr-group(0%). In the randomized group of patients treated for a recurrent pterygium one recurrence developed in the FCG group (1 out of 8 eyes =12.5%) and one in the 90Sr-group (1 out of 7 =14.6%). Analysis of other clinical parameters showed that postoperative treatment with corticosteroids, nonsteroidal anti-inflammatory drugs, and artificial tears was necessary for a longer period in the FCG group than in the90Sr-group. This revised version was published online in August 2006 with corrections to the Cover Date.  相似文献   
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The hypothesis that benzodiazepine-induced hyperphagia is due to a specific enhancement of the palatability of foods has been supported by previous ‘taste reactivity’ studies of affective (hedonic and aversive) reactions to taste palatability. Diazepam and chlordiazepoxide enhance hedonic reactions of rats (rhythmic tongue protrusions, etc.) to sweet tastes in a receptor-specific fashion. A role for brainstem circuits has been indicated by a previous demonstration of the persistence of the taste reactivity enhancement by diazepam after midbrain decerebration. The present study examined whether benzodiazepine brainstem receptors are the chief substrates for palatability enhancement even in intact brains. We compared the effectiveness of benzodiazepine microinjections to elicit feeding and enhance hedonic reactions when delivered into either the lateral ventricle (forebrain) or the fourth ventricle (brainstem) of rats. The results show diazepam is reliably more effective at eliciting feeding and enhancing positive hedonic reactions to oral sucrose when microinjections are made in the fourth ventricle than in the lateral ventricle. We conclude that brainstem neural systems containing benzodiazepine-GABA receptors are likely to be the chief substrates for benzodiazepine-induced palatability enhancement.  相似文献   
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