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91.
背景:自体富血小板血浆激活后可释放多种生长因子,可以促进骨髓间充质干细胞的增殖与分化。目的:观察自体激活富血小板血浆对体外培养的兔骨髓间充质干细胞向成软骨细胞分化的影响。方法:取兔股骨骨髓,全骨髓贴壁法分离培养骨髓间充质干细胞;取第3代骨髓间充质干细胞,分别应用体积分数10%自体激活富血小板血浆和体积分数10%胎牛血清培养液进行体外培养,观察其向成软骨细胞分化情况。结果与结论:分离培养的兔骨髓间充质干细胞呈长梭形,传代后细胞生长迅速。流式细胞仪检测发现第3代细胞高表达CD29、CD44,而低表达CD45。免疫荧光细胞化学染色显示经自体激活富血小板血浆诱导的骨髓间充质干细胞表达Ⅱ型胶原;实时荧光定量PCR检测发现经自体激活富血小板血浆诱导的骨髓间充质干细胞Ⅱ型胶原α1链基因和聚集蛋白聚糖基因表达明显高于经胎牛血清诱导的骨髓间充质干细胞(P〈0.01)。可见自体激活富血小板血浆具有促进兔骨髓间充质干细胞向软骨细胞方向分化的潜能。  相似文献   
92.
目的 分析不同病理分型、不同临床分期的肺癌患者中促血管生成素-2(Ang-2)的表达水平,进一步探讨该病的发病机理,为临床诊断提供依据.方法 对112例肺癌患者,16例健康体检者进行血清Ang-2检测,同时进行血清中其他相关肿瘤标志物检测.比较不同病理分型、临床分期及远处转移患者血清Ang-2的不同.结果 非小细胞肺癌患者血清Ang-2水平高于正常对照组(与鳞癌比较Sig 值为0.049,P<0.05;与腺癌比较Sig值为0.011,P<0.05);非小细胞肺癌Ⅲ、Ⅳ期患者血清Ang-2水平高于对照(与Ⅲ期比较Sig值为0.013,P<0.05;与Ⅳ期比较Sig值为0.000,P<0.001);远处转移患者血清Ang-2水平非常显著高于非远处转移者(Sig值为0.008,P<0.01);结论 分析血清Ang-2水平对肺癌患者的临床诊断、预测转移和预后判断均有临床价值,应用Ang-2与其他肿瘤标志物联合检测可提高患者诊断阳性率.  相似文献   
93.
This meta-analysis evaluates the efficacy of imagery rehearsal as a treatment for nightmares, general sleep disturbance, and symptoms of post-traumatic stress. Bibliographic databases and cited references were searched to identify clinical trials of imagery rehearsal in individuals with post-trauma nightmares. Thirteen studies met inclusion criteria and reported sleep and post-traumatic stress outcomes in sufficient detail to calculate effect sizes. Results indicate that imagery rehearsal had large effects on nightmare frequency, sleep quality, and PTSD symptoms from the initial to post-treatment assessments. These effects were sustained through 6 to 12months follow-up. Furthermore, interventions that included both imagery rehearsal and cognitive behavioral therapy for insomnia resulted in greater treatment-related improvement in sleep quality than imagery rehearsal alone. Combined treatment did not improve outcomes for PTSD or nightmares. Notably, effect sizes were small in the single study that included an active-treatment control condition. Future research should identify necessary and sufficient components of interventions for trauma-related sleep disturbance and post-traumatic stress (e.g., exposure, cognitive reappraisal, sleep and circadian regulation).  相似文献   
94.
目的腹腔注射卡介苗(BCG),建立炎症相关抑郁模型,明确栀子、首乌对炎症诱导抑郁模型的抗抑郁作用和机制。方法小鼠腹腔注射卡介苗200 mg.kg-1,吗氯贝胺组和栀子首乌组同时分别给予吗氯贝胺75 mg.kg-1和栀子首乌500 mg.kg-1水溶液灌胃,观察药物对动物体重、自主活动和强迫游泳实验中不动时间的影响。同时,使用ELISA法检测脑组织吲哚胺-23,-过氧化酶(IDO)和N-甲基-D-天冬氨酸受体(NMDAR1)含量。结果与模型组比较,栀子首乌药不能对抗BCG引起的小鼠体重下降(P〉0.05),对小鼠的自主活动没有明显影响(P〉0.05),但能明显缩短BCG模型小鼠强迫游泳不动时间(P〈0.05),同时降低了脑组织中IDO和NMDAR1含量(P〈0.05或P〈0.01)。结论 BCG腹腔注射能引起动物抑郁样行为,栀子、首乌选择性增加小鼠不动时间,显示出一定的抗抑郁作用,其作用机制与抑制IDO活性减少五羟色胺(5-HT)代谢,下调NMDAR1减轻神经元毒性损伤有关。  相似文献   
95.
Wheat is a common cereal in the Western diet and an important source of protein as well as fiber. However, some individuals develop adverse reactions to a wheat-containing diet. The best characterized is celiac disease which develops after intake of gluten in individuals with genetic predisposition. Other wheat-related conditions are less well defined in terms of diagnosis, specific trigger and underlying pathways. Despite this, the overall prevalence of wheat-related disorders has increased in the last decades and the role of microbial factors has been suggested. Several studies have described an altered intestinal microbiota in celiac patients compared to healthy subjects, but less information is available regarding other wheat-related disorders. Here, we discuss the importance of the intestinal microbiota in the metabolism of wheat proteins and the development of inflammatory or functional conditions. Understanding these interactions will open new directions for therapeutic development using bacteria with optimal wheat protein degrading capacity.  相似文献   
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Non-vitamin K antagonist (VKA) oral anticoagulants (NOACs) have several advantages over VKAs that render them an attractive option for adults with congenital heart disease (CHD). Efficacy and safety data specific to the adult CHD population are emerging. Herein, we synthesize the growing literature regarding NOACs in adults with CHD and attempt to identify subgroups for which it appears reasonable to extrapolate data from populations without CHD. Small observational studies suggest that NOACs are safe and effective in selected adults with CHD. NOACs are contraindicated in patients with a mechanical valve, in those with mitral or tricuspid valve stenosis with enlarged and diseased atria, with or without a mitral or tricuspid bioprosthesis, and after recent cardiac surgery (< 3 months). There is currently insufficient evidence to recommend NOACs in patients with a Fontan circulation or cyanotic CHD. Growing literature supports the use of NOACs in patients without CHD who have various forms of valvular heart disease. Therefore, when an indication for oral anticoagulation is established, it appears reasonable to consider a NOAC instead of a VKA in adults with CHD lesions analogous to isolated mitral regurgitation, tricuspid regurgitation, or aortic regurgitation or stenosis. The NOAC agent selected and the prescribed dose should be tailored according to bleeding risk, body weight, renal function, and comedications, especially antiepileptic drugs. The decision to initiate a NOAC should be shared between the patient and care provider. Large-scale research studies are required to further assess safety and efficacy in selected patient subgroups.  相似文献   
100.

Background

Multiple quantitative trait loci for blood pressure (BP) have been localized throughout human and rodent genomes. Few of them have been functionally identified especially in humans, and little is known about their pathogenic directionality when identified. We focused on Chrm3 encoding the muscarinic cholinergic receptor 3 (M3R) as the causal gene for C17QTL1 in the Dahl salt-sensitive rat model.

Methods and Results

Congenic knock-ins, gene-specific knockout, and ex vivo and in vivo function studies were applied in the Dahl salt-sensitive rat model of polygenic hypertension. A Chrm3 missense T1667C mutation in the last intracellular domain functionally correlated with a rise in BP increased the M3R signalling and resensitization, and adrenal epinephrogenesis. Gene targeting that abolished the M3R function without affecting any of noncoding Chrm3 variants caused a decrease in BP, indicating that the M3R-mediated signalling promotes hypertension. In contrast, removing 8 amino acids from the M3R first extracellular loop had no effect on BP.

Conclusions

The M3R-specialized signalling constitutes a new pathway of hypertension pathogenesis within the context of a polygenic and quantitative trait. Increased epinephrine in the circulation and secreted from the adrenal glands are suggestive of a molecular mechanism partially mediating M3R to promote hypertension. The structure-function relationships for various M3R domains in their effects on BP pave the way for identifying missense mutations that impact functions on BP as potential diagnostic targets.  相似文献   
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