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41.
目的观察大气细颗粒物(PM2. 5)致大鼠气道黏液纤毛清除系统的损伤作用及标准桃金娘油干预的影响。方法将大鼠分成对照组(N组)、PM2. 5暴露组(PM组)、标准桃金娘油干预组(PM+CS组),分别予以吸入净化空气、暴露石家庄室外空气(PM2. 5浓度的范围29. 90 mg/m3~99. 65 mg/m3)、标准桃金娘油混悬液300 mg/(kg·d)灌胃。于3和6个月各处死大鼠8只,气管及肺组织行HE和AB-PAS染色;扫描电镜观察纤毛超微结构;计数BALF中细胞及分类; RT-qPCR测定黏蛋白(MUC) 5AC mRNA和水通道蛋白(AQP) 5 mRNA表达;免疫组化、Western blot测定MUC5AC蛋白表达。结果 PM组肺及气管组织炎性损伤及黏液细胞化生明显;气管纤毛黏连、倒伏及缺失、排列稀疏、紊乱,BALF中白细胞总数、中性粒细胞计数和中性粒细胞百分比显著高于N组(P<0. 05);MUC5AC mRNA相对表达量显著高于N组(P<0. 05); AQP5 mRNA相对表达量显著低于N组(P<0. 05...  相似文献   
42.
Serum and intracytoplasmic cytokines are mandatory in host defense against microbes, but also play a pivotal role in the pathogenesis of autoimmune diseases by initiating and perpetuating various cellular and humoral autoimmune processes.  相似文献   
43.
[摘要]目的观察参一胶囊(Rg3)对高转移人卵巢癌细胞系HO 8910PM的抑制作用。方法细胞分成6组:阴性对照组(A组):只加新鲜的全培养液;低浓度组(B组):含10 μg&#8226;mL 1 Rg3培养液;中浓度组(C组):含20 μg&#8226;mL 1 Rg3培养液;高浓度组(D组):含40 μg&#8226;mL 1 Rg3培养液;顺铂阳性对照组(E组):含10 μg &#8226;mL 1顺铂的培养液;顺铂+Rg3联合用药组(F组):含10 μg&#8226;mL 1顺铂+20 μg&#8226;mL 1 Rg3培养液。分别从台盼蓝活细胞计数法、细胞的增殖抑制(CCK 8法)进行观察。结果Rg3对人卵巢癌HO 8910PM细胞有明显的抑制作用,显示了较好的细胞毒活性作用(P<0.05)。Rg3与顺铂联合用药时,细胞毒作用与高浓度Rg3和顺铂组相似,但在微观结构上能造成更大的细胞形态结构损伤。结论Rg3对高转移人卵巢癌细胞有一定的抑制作用,Rg3与顺铂联合用药在细胞结构破坏上可能有相加或协同作用,这将为临床卵巢癌患者进行抗肿瘤治疗提供依据。  相似文献   
44.
Objectives: Published data obtained from outdoor stationary sampling stations cannot be applied directly to the exposure situation in vehicles. The aim of this study, therefore, was to assess the dust exposure relevant to passengers and drivers in public buses and trams. Method: In the years 1993 to 1996, PM10 samples were taken during 201 journeys of typically 4 h duration on 14 routes (nine bus routes, five tramways) which were representative for the overall Munich transportation system with respect to area characteristics and traffic density. The concentrations of the samples were compared with those collected at the same time at sampling stations of the Bavarian State Office for Environmental Protection (OEP). Dust exposure was continuously and synchronously recorded by means of a tyndallometric device. Traffic and passenger density, weather conditions, special events, etc. were noted by our personnel, travelling on every journey. Results: The average PM10 dust concentration for all rides was 155 μg/m3 (single journey max. 686 μg/m3, min. 13 μg/m3). Interior concentrations were 1.7 to 4.0 times above those collected at the static outdoor stations. We found only minor associations between dust concentrations and traffic density or time of day. During several journeys continuous recording disclosed anomalies, dependence on weather conditions and cyclic track characteristics. Conclusions: Interior PM10 particulate concentrations were comparable to those found elsewhere in truck drivers' cabs and are in the region of German regulative limits established for the general population's long term outdoor exposure. Indoor concentrations were well above the values found at stationary outdoor stations. Additional continuous recording of dust concentrations proved to be helpful in unveiling anomalies and dependencies on external effectors. Received: 10 August 1999 / Accepted: 20 November 1999  相似文献   
45.
This is a case of priapism (21 h) following an intracavernosal injection of vasoactive intestinal polypeptide (VIP) 25 mcg with phentolamine mesylate (PM) 1 mg responding to venesection and intracavernosal injection of 1 mg metaraminol.  相似文献   
46.
Epidemiologic studies have shown associations between ambient particulate matter (PM) and adverse health outcomes including increased mortality, emergency room visits, and time lost from school and work. The mechanisms of PM-related health effects are still incompletely understood, but a hypothesis under investigation is that many of the adverse health effects may derive from oxidative stress, initiated by the formation of reactive oxygen species (ROS) within affected cells. While the adverse effects from PM have historically been associated with the airborne concentration of PM and more recently fine-particle PM, we considered it relevant to develop an assay to quantitatively measure the ability of PM to catalyze ROS generation as the initial step in the induction of oxidative stress. This ability of PM could then be related to different sources, chemical composition, and physical and spatial/temporal characteristics in the ambient environment. The measurement of ROS-forming ability in relation to sources and other factors will have potential relevance to control of redox-active PM. If oxidative stress represents a relevant mechanism of toxicity from PM, the measurement of redox activity represents a first step in the elucidation of the subsequent downstream processes. We have developed an assay for PM redox activity, utilizing the reduction of oxygen by dithiothreitol which serves as an electron source. We have found that PM will catalyze the reduction of oxygen and have examined the distribution and chemical characteristics of the redox activity of PM fractions collected in different sites in the Los Angeles Basin. Samples of concentrated coarse, fine, and ultrafine PM, obtained with aerosol concentrators, were studied with regard to their chemical properties and redox activity. Redox activity was highest in the ultrafine fraction, in agreement with results indicating ultrafines were the most potent toward inducing that heme oxygenase expression and depleting intracellular glutathione, which has relevance to induction of oxidative stress. Comparison of the redox activity with chemical composition showed a reasonable correlation of redox activity with elemental carbon (r(2)=0.79), organic carbon (r(2)=0.53), and with benzo[ghi]perylene (r(2)=0.82), consistent with species typically found in mobile emission sources.  相似文献   
47.
Redox regulation is important for the modulation of cytosolic Ca(2+) concentration. Hence, we have investigated the effect of H(2)O(2) on store-mediated Ca(2+) entry (SMCE). In fura-2-loaded human platelets treatment with H(2)O(2) resulted in a concentration-dependent increase in Ca(2+) release from intracellular stores, while the effect on Ca(2+) entry was biphasic. In addition, 1mM H(2)O(2) reduced SMCE induced by agonists. The inhibitory effect of 1mM H(2)O(2) was prevented by inhibition of actin polymerization with cytochalasin D. Consistent with this, we found that 10microM H(2)O(2) and store depletion by treatment with thapsigargin plus ionomycin induced a similar temporal sequence of actin reorganization, while exposure to 1mM H(2)O(2) shifted the dynamics between polymerization and depolymerization in favor of the former. One millimolar H(2)O(2)-induced polymerization was reduced by treatment with methyl 2,5-dihydroxycinnamate and farnesylthioacetic acid, inhibitors of tyrosine kinases and Ras superfamily proteins, respectively. Finally, exposure to 1mM H(2)O(2) significantly increased store depletion-induced p60(src) activation. We conclude that H(2)O(2) exerted a biphasic effect on SMCE. The inhibitory role of high H(2)O(2) concentrations is mediated by an abnormal actin reorganization pattern involving both Ras- and tyrosine kinases-dependent pathways.  相似文献   
48.
北京市某区餐厅室内空气细颗粒物浓度水平现况研究   总被引:2,自引:0,他引:2  
目的了解餐厅室内空气细颗粒物(PM2.5)的污染现状,揭示各影响因素的作用,为卫生标准及政策法规的制定提供科学依据。方法采用分层抽样方法选择北京市某区42家餐厅,使用AM-510智能防爆粉尘仪进行餐厅室内外细颗粒物浓度的检测,同时记录餐厅内人员数量、吸烟者数量等情况,比较不同类别餐厅、室内外细颗粒物浓度的差异,分析影响因素与室内细颗粒物浓度的关系。结果 42家餐厅室内、外PM2.5平均浓度分别为194μg/m3、76μg/m3,室内比室外高155.26%;有吸烟的餐厅室内PM2.5平均浓度高于室外206μg/m3(228.89%)且差异有统计学意义,无吸烟的餐厅室内与室外水平基本相当;中式正餐厅吸烟比例、PM2.5浓度水平高于中式快餐厅和西式快餐厅且差异有统计学意义,而中式快餐厅和西式快餐厅室内外PM2.5浓度水平相当;大、中、小型餐厅吸烟比例、PM2.5浓度水平差异无统计学意义;餐饮业量化分级管理的A、B、C级餐厅吸烟比例、PM2.5浓度水平差异亦无统计学意义;经Spearman非参数相关分析,室内与室外PM2.5浓度存在正相关且有统计学意义,室内无吸烟的餐厅该相关关系更为紧密,而有吸烟的餐厅室内与室外PM2.5浓度无相关关系,以无吸烟餐厅的PM2.5浓度为应变量(y),其室外PM2.5浓度为自变量(x)进行一元线性回归分析,回归方程为y(μg/m3)=0.828x+9.456(R2=0.862,F=100.327,P〈0.001);餐厅室内PM2.5浓度与吸烟支数密度存在正相关关系(r=0.814,P〈0.001)。结论餐厅内细颗粒物污染严重;吸烟和室外空气PM2.5浓度是影响餐厅室内PM2.5浓度的主要因素。  相似文献   
49.
目的综合分析国内外可吸人大气颗粒物(PM10)短期暴露与人群死亡关系的流行病学资料,以获取大气PM10污染与居民死亡的暴露一反应关系。方法在计算机联机检索文献和手工检索的基础上,对近十年来发表的相关研究文献采用meta分析的方法进行综合评价,并检验、校正可能存在的发表偏倚,从而准确、定量地确定PM10污染与居民死亡的暴露一反应关系。结果建立了居民短期接触大气PM10污染的暴露一反应关系,即在未考虑发表偏倚的情况下,大气中PM10每增加100μg/m^3,居民死亡的相对危险度增加3.87%(95%CI:2.84%~5.02%),在校正了发表偏倚后大气中PM10每增加100p.μg/m^3,死亡的相对危险度增加下降为1.41%(95%CI:0.30%-2.43%),与考虑偏倚前相比下降了63.6%。结论该研究建立的暴露-反应关系较早注意到发表偏倚的影响,具有一定的代表性与科学性,可用于大气颗粒物暴露健康危险度评价工作参考,为制定相关环境决策提供科学依据。  相似文献   
50.
目的 探讨大气细颗粒物PM2.5对小鼠主动脉Toll样受体(Toll-like receptors,TLRs)信号通路的影响及阿魏酸的干预作用。方法 采用气管滴注方法以10,20 mg·kg-1PM2.5处理小鼠,并用40,80 mg·kg-1的阿魏酸对部分20 mg·kg-1 PM2.5处理后的小鼠进行治疗。2周后处死小鼠,血液细胞分析仪检测小鼠血液中炎症细胞水平,ELISA检测血清中IL-1β和IL-6的含量,并用荧光定量PCR检测主动脉中IL-1β和IL-6的mRNA水平,Western blot检测各组小鼠主动脉组织中TLR2、TLR4、MyD88、NF-κB p65蛋白的表达,免疫组化技术观察TLR2和TLR4在小鼠主动脉中的水平。结果 PM2.5能提高血液中NEUT、EOS的数量及其在总细胞中的比率,增加血液和主动脉组织中炎症因子IL-1β、IL-6的含量,上调主动脉组织中的TLRs通路相关分子TLR2、TLR4、MyD88、NF-κB p65的表达;而用阿魏酸干预后,血液中白细胞数量、EOS数量、NEUT与EOS的比率明显降低,IL-1β、IL-6水平下降。同时主动脉组织中的TLRs通路相关分子的表达下调。结论 PM2.5可能通过TLRs通路诱导小鼠主动脉炎症的产生,而阿魏酸可能通过抑制TLRs通路相关因子的表达而发挥抑制PM2.5诱导的小鼠主动脉炎症的作用。  相似文献   
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