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《Journal of cardiology》2014,63(6):449-459
BackgroundCells are naturally equipped with antioxidant defenses to counterbalance free radical production. Overproduction of free radicals is one of the reasons for a variety of diseases. The current investigation was planned to evaluate chronic alcohol- (for 30 days) induced oxidative stress in the cardiac tissue of rat and to explore the effectiveness of Thespesia populnea (TP)-induced cardio-protection in rat heart by utilizing an in vivo model of cardiac injury by alcohol.MethodsTen groups of rats were maintained and were divided into different groups. Alcohol 20% was administered and Thespesia leaf extracts (TPE) were administered at a dose of 250 mg/kg to chronic alcoholic rats for 30 days. The heart tissue was isolated and processed for further analysis, and also blood for estimation of blood alcohol level and serum creatine phosphokinase (CPK). The activities/levels of antioxidant enzymes, malondialdehyde (MDA), and protein carbonyls (PC) were estimated using established protocols. Histopathology was performed as evidence for the work and to establish the results.ResultsActivities of antioxidant enzymes like superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), and reduced glutathione content (GSH) showed a decrease, while glutathione-S-transferase (GST) activity, MDA, and PC recorded an elevation due to alcohol treatment in the cardiac tissue compared to the control rats. Alcohol-induced myocardial injury was observed, indicated by a significant increase in serum CPK, a well-known biomarker of myocardial injury, and histopathological evidence supported these observations by revealing predominantly extensive edema with vacuolization and severe necrosis.ConclusionTreatment with TPE confers protection on the heart tissue during alcohol-induced oxidative stress, and thereby minimizes oxidative damage to the cardiac tissue as clearly marked in histopathology.  相似文献   
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BACKGROUND: A wide variety of pathological conditions have been shown to result in cardiac remodelling and myocardial dysfunction. However, the mechanisms of transition from adaptive to maladaptive alterations, as well as those for changes in cardiac performance leading to heart failure, are poorly understood. OBSERVATIONS: Extensive studies have revealed a broad spectrum of progressive changes in subcellular structures and function, as well as in signal transduction and metabolism in the heart, among different cardiovascular disorders. The present review is focused on identifying the alterations in molecular and biochemical structure of myofibrils (myofibrillar remodelling) in hypertrophied and failing myocardium in different types of heart diseases. Numerous changes at the level of gene expression for both contractile and regulatory proteins have already been reported in failing hearts and heart diseases; these changes are potential precursors for heart failure such as cardiac hypertrophy and cardiomyopathies. Myofibrillar remodelling, as a consequence of proteolysis, oxidation, and phosphorylation of some functional groups in both contractile and regulatory proteins in hearts failing due to different etiologies, has also been described. CONCLUSIONS: Although myofibrillar remodelling appears to be associated with cardiac dysfunction, alterations in both contractile and regulatory proteins are dependent on the type and stage of heart disease.  相似文献   
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目的 对糖尿病仓鼠模型心肌中糜蛋白酶(chymase) mRNA水平及其酶活性进行检测,观察chymase mRNA水平、酶活性与心肌局部血管紧张素Ⅱ(Ang Ⅱ)水平的关系.方法 腹腔注射链脲菌素诱导糖尿病仓鼠模型,电镜观察心肌超微结构,链霉素-亲和素-生物素-过氧化物酶复合物法(SABC)检测心肌Ⅰ、Ⅲ型胶原水平,脱氧核糖核苷酸末端转移酶介导的缺口末端标记法(TUNEL)检测心肌细胞凋亡,反转录-聚合酶链反应(RT-PCR)检测chymase mRNA水平变化,放射免疫分析法测定心肌chymase和血管紧张素转换酶(ACE)活性、Ang Ⅱ含量.结果 (1)糖尿病组仓鼠心肌细胞线粒体肿胀明显,局部破裂,肌丝广泛溶解,核肿胀,Ⅰ、Ⅲ型胶原沉积、心肌细胞凋亡明显;(2)糖尿病组与对照组比较,心肌chyamse活性明显升高,分别为(0.88±0.07) U/mg组织和(0.54±0.04)U/mg组织(P<0.01),而ACE活性差异无统计学意义;Ang Ⅱ含量明显升高,分别为(95.8±16.0)pg/mg组织和(51.1±20.8)pg/mg组织(P<0.01);(3)糖尿病组心肌chyamse mRNA表达水平为0.810±0.026,较对照组0.490±0.087显著升高(P<0.01).结论 糖尿病仓鼠病变心肌的chymase mRNA表达水平和酶活性明显升高,并伴随心肌局部Ang Ⅱ含量的升高.  相似文献   
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目的 探讨左心室不同构型的甲状腺功能亢进症(简称甲亢)性心肌病兔血清肌钙蛋白I(cTn-I)水平及其与心功能的相关性。方法 对实验组兔(20只)腹腔注射左甲状腺素 建立甲亢动物模型,对照组兔(10只)每日腹腔注射生理盐水至实验结束。对两组兔行超声心动图检查,同时测定血清中cTn-I水平。实验组依据超声参数分为向心性肥厚(CH)亚组和离心性肥厚(EH)亚组。结果 与对照组比较,CH亚组二尖瓣环平均舒张期峰值速度(Ve)减低(P<0.01),EH亚组二尖瓣环平均收缩期峰值速度(Vs)、Ve明显减低(P均<0.01)。CH亚组和EH亚组血清cTn-I水平明显高于对照组(P均<0.01),EH亚组较CH亚组血清cTn-I水平进一步升高(P<0.01)。cTn-I与Vs及Ve呈负相关(P均<0.01)。结论 血清cTn-I浓度变化结合超声心动图可较敏感地反映甲亢性心肌病心肌损害的有无及其严重程度。  相似文献   
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目的 探讨实时三维超声心动图时间-位移参数及17节段时间-容积曲线参数指标在评价左室心肌致密化不全中的应用价值.方法 对10例左室心肌致密化患者(经磁共振证实)、20例正常者(对照组)行实时三维超声心动图检查.结果 左室心肌致密化不全组的17节段时间-容积曲线参数指标:左室16节段、12节段、6节段达最小收缩容积时间的标准差(Tmsv 16-SD,Tmsv 12-SD,Tmsv 6-SD),左室16节段、12节段、6节段达最小收缩容积时间的最大差值(Tmsv 16-Dif,Tmsv 12-Dif,Tmsv 6-Dif)以及左室16节段、12节段、6节段达最小收缩容积时间的标准差的校正值(Tmsv 16-SD%,Tmsv 12-SD%,Tmsv 6-SD%),左室16节段、12节段、6节段达最小收缩容积的时间最大差值的校正值(Tmsv 16-Dif%,Tmsv 12-Dif%,Tmsv 6-Dif%)较正常组显著增高,差异有统计学意义(P均<0.05),左室心肌致密化不全组的时间-位移参数中位移平均值、最小值低于正常对照组,差异有统计学意义(P<0.05).结论 实时三维超声心动图时间-位移参数显像及17节段时间-容积曲线参数指标能快速准确评价左室心肌致密化不全患者心肌节段功能及收缩同步性.
Abstract:
Objective To investigate the value of real-time three-dimensional echocardiography(RT-3DE) timing-excursion parametric index and 17 segment time-volume curves index in patients with leftventricular noncompaction(LVNC). Methods Ten patients with LVNC (proven by MRI) ,twenty subjects with normal LV function were examined by Philips iE33 with X3-1 probe. Results Parameter index (including Tmsv 16-SD,Tmsv 12-SD,Tmsv 6-SD,Tmsv 16-Dif,Tmsv 12-Dif,Tmsv 6-Dif,Tmsv 16-SD%,Tmsv 12-SD%, Tmsv 6-SD%, Tmsv 16-Dif%, Tmsv 12-Dif%, Tmsv 6-Dif%) of 17 segment time to minimal systolic volume was significantly higher in patients with LVNC than that in subjects with normal LV function( all P<0.05). Average and minimum value of excursion was significantly lower in patients with LVNC than that in subjects with normal LV function ( P<0.05). Conclusions RT-3DE with timeexcursion parameters and 17 segment of time- volume curve parameters can rapidly and accurately evaluate left ventricular systolic synchrony in patients with LVNC.  相似文献   
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目的:观察鞘氨醇激酶1(Sphk1)在糖尿病性心肌病(DCM)大鼠中的自噬作用,为DCM的防治寻求新的靶点。方法:雄性Wistar大鼠20只被随机分为正常对照组(n=10)、DCM组(n=10)。腹腔注射链脲佐菌素(STZ)70mg/kg建立DCM大鼠模型。每2周观察大鼠体重、空腹血糖,8周后,检测两组左室舒张末期内径(LVEDd)、左室收缩末期内径(LVESd)、左室射血分数(LVEF)等;取心脏组织,行HE染色观察心脏形态。应用蛋白质印迹法检测Sphk1、自噬相关蛋白LC3II/LC3I、自噬相关蛋白Beclin 1表达水平。结果:造模8周后,与正常对照组比较,DCM组体重[(351±27)g比(198±11)g]显著降低,血糖[(6.84±0.93)mmol/L比(32.45±4.27)mmol/L]显著升高(P均=0.001);LVEDd[(7.12±0.36)mm比(6.46±0.28)mm]显著减小、LVESd[(3.39±0.14)mm比(3.72±0.25)mm]显著增加,LVEF值[(82.69±3.37)%比(62.50±3.08)%]显著降低(P<0.05或<0.01);Sphk1[(0.30±0.02)比(1.12±0.20)]、LC3II/LC3I[(0.44±0.05)比(1.03±0.14)]、Beclin 1[(0.35±0.08)比(0.73±0.12)]蛋白表达显著升高(P<0.05或<0.01)。HE染色可见心肌细胞增生肥大、排列紊乱。结论:Sphk1通过自噬促使大鼠的糖尿病性心肌病的发生发展。  相似文献   
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