首页 | 本学科首页   官方微博 | 高级检索  
文章检索
  按 检索   检索词:      
出版年份:   被引次数:   他引次数: 提示:输入*表示无穷大
  收费全文   1104篇
  免费   121篇
  国内免费   91篇
耳鼻咽喉   1篇
儿科学   2篇
妇产科学   1篇
基础医学   35篇
口腔科学   11篇
临床医学   26篇
内科学   33篇
皮肤病学   6篇
神经病学   13篇
特种医学   6篇
外国民族医学   1篇
外科学   42篇
综合类   170篇
预防医学   57篇
眼科学   9篇
药学   427篇
  1篇
中国医学   432篇
肿瘤学   43篇
  2024年   50篇
  2023年   44篇
  2022年   65篇
  2021年   68篇
  2020年   54篇
  2019年   39篇
  2018年   41篇
  2017年   57篇
  2016年   67篇
  2015年   55篇
  2014年   55篇
  2013年   85篇
  2012年   88篇
  2011年   89篇
  2010年   57篇
  2009年   43篇
  2008年   48篇
  2007年   46篇
  2006年   31篇
  2005年   40篇
  2004年   19篇
  2003年   40篇
  2002年   21篇
  2001年   15篇
  2000年   21篇
  1999年   17篇
  1998年   11篇
  1997年   9篇
  1996年   12篇
  1995年   5篇
  1994年   6篇
  1993年   2篇
  1992年   5篇
  1991年   2篇
  1990年   2篇
  1988年   2篇
  1987年   2篇
  1986年   1篇
  1985年   1篇
  1979年   1篇
排序方式: 共有1316条查询结果,搜索用时 0 毫秒
1.
The aim of this study was to investigate the effects of quercetin and fish n‐3 fatty acids on the changes in testis induced by ethanol. Forty‐five rats divided into five groups, control, ethanol, ethanol+quercetin, ethanol+fish n‐3 fatty acids and ethanol+quercetin+fish n‐3 fatty acids. At the end of 8 weeks, all the rats were sacrificed. Degenerative changes in histopathological analyses, the decreased body weight gain and seminiferous tubule diameters in ethanol group have been observed. TUNEL assay also showed an increase in apoptotic cell number. The activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH‐Px), xanthine oxidase (XO) and testosterone levels were decreased as well as the levels of malondialdehyde (MDA) and nitric oxide (NO) were increased in ethanol group. Histopathological changes caused by ethanol have been improved by quercetin and fish n‐3 fatty acids. It was also found that protection was provided by increasing SOD, CAT and GSH‐Px activities in groups administered quercetin, fish n‐3 fatty acids and quercetin+fish n‐3 fatty acids, and by decreasing the levels of MDA and NO in groups administered both quercetin and fish n‐3 fatty acids together. These results suggest that quercetin and fish n‐3 fatty acids are beneficial agents to reduce testicular injury induced by ethanol except for testosterone levels.  相似文献   
2.
Renal cell carcinoma has become the most common subtype of kidney cancer, and has the highest propensity to manifest as metastatic disease. Because of lack of knowledge in events that correlated with tumor cell migration and invasion, few therapeutic options are available. Therefore, in current study, we explore the anti-tumoral effect of a potential chemopreventive natural product, quercetin, combined with anti-sense oligo gene therapy (inhibiting Snail gene). We found that either one of them had the remarkable effects in suppressing cell proliferation and migration, inducing cell cycle arrest and apoptosis in a ccRCC cell line, Caki-2 cells. The combination of both means provides even strong suppressive effects toward these ccRCC cells. Our study, for the first time, provides the possibility of using a novel treatment for renal cancer, by combining natural product and gene therapy.  相似文献   
3.
Summary.  Background : The regulation of platelet function by pharmacological agents that modulate platelet signaling has proven a successful approach to the prevention of thrombosis. A variety of molecules present in the diet have been shown to inhibit platelet activation, including the antioxidant quercetin. Objectives : In this report we investigate the molecular mechanisms through which quercetin inhibits collagen-stimulated platelet aggregation. Methods : The effect of quercetin on platelet aggregation, intracellular calcium release, whole cell tyrosine phosphorylation and intracellular signaling events including tyrosine phosphorylation and kinase activity of proteins involved in the collagen-stimulated glycoprotein (GP) signaling pathway were investigated. Results : We report that quercetin inhibits collagen-stimulated whole cell protein tyrosine phosphorylation and intracellular mobilization of calcium, in a concentration-dependent manner. Quercetin was also found to inhibit various events in signaling generated by the collagen receptor GPVI. This includes collagen-stimulated tyrosine phosphorylation of the Fc receptor γ-chain, Syk, LAT and phospholipase Cγ2. Inhibition of phosphorylation of the Fc receptor γ-chain suggests that quercetin inhibits early signaling events following stimulation of platelets with collagen. The activity of the kinases that phosphorylate the Fc receptor γ-chain, Fyn and Lyn, as well as the tyrosine kinase Syk and phosphoinositide 3-kinase was also inhibited by quercetin in a concentration-dependent manner, both in whole cells and in isolation. Conclusions : The present results provide a molecular basis for the inhibition by quercetin of collagen-stimulated platelet activation, through inhibition of multiple components of the GPVI signaling pathway, and may begin to explain the proposed health benefits of high quercetin intake.  相似文献   
4.
佟宇  王晶 《中国公共卫生》2014,30(3):314-316
目的 探讨线粒体三磷酸腺苷(ATP)敏感性钾通道(mitoKATP)在槲皮素抑制乳大鼠心肌细胞肥大中的作用。方法 利用体外培养模型,以苯肾上腺素(PE)10 μmol/L诱导心肌细胞肥大,在mitoKATP通道阻断剂5-羟基癸酸(5-HD)存在情况下,槲皮素设25、50、100 μmol/L 3个剂量;用Lowry法检测心肌细胞蛋白质含量,消化分离法及计算机图像分析系统检测心肌细胞体积,逆转录-聚合酶链反应(RT-PCR)法检测心肌细胞心房钠尿肽(ANP)的mRNA 表达,Western印迹法测定KATP通道Kir6.2亚基表达。结果 与对照组比较,模型组大鼠心肌细胞总蛋白质含量[(27.45±2.45)μg]增加,细胞体积[(2 278±156)μm3]增大,ANP的mRNA 表达增多,Kir6.2表达无 明显变化;与模型组比较,槲皮素50、100 μmol/L组心肌细胞蛋白含量[分别为(21.15±1.39)、(19.28±2.23)μg]减少、细胞体积[分别为(1 656±230)、(1 398±298)μm3]减小,Kir6.2表达增加,呈剂量依赖性。而在加入5-HD后,槲皮素对PE诱导心肌肥大的抑制作用消失。结论 槲皮素可通过开放mitoKATP通道抑制 PE诱导的乳大鼠心肌细胞肥大。  相似文献   
5.
槲皮素对压力超负荷所致大鼠心肌肥厚的影响   总被引:12,自引:0,他引:12  
秦泰春  顾振纶  刘世增 《中草药》1999,30(4):275-277
大鼠腹主动脉部分狭窄5周后,形成实验性心肌肥厚模型,心肌和左心室重量明显增加,心肌过氧化脂质含量显著增加,SOD活性下降,心肌和主动脉Ca^2+含量明显增加。给槲皮素75,150mg/kg后均能明显降低心肌和左心室降低心肌LPO含量,增加SOD活性,降低心肌和主动脉Ca62+的含昨,提示槲皮素抗心肌肥厚作用与清除氧自由基和钙拮抗有关。  相似文献   
6.
Intraperitoneal administration of quercetin (6.25–50 mg/kg) significantly (p<0.5-0.01) reduced intestinal transit in mice and this effect was antagonized by yohimbine and phentolamine but not by atropine or naloxone. Quercetin (12.5–50 mg/kg) reduced also (p<0.05-0.01) intraluminal accumulation of fluid and diarrhoea induced by castor oil and these effects were antagonized by yohimbine. Finally quercetin (12.5–50 mg/kg) reduced the area of gastric ulcer but not the number. It is suggested that α2-adrenergic receptors mediate the effect of quercetin on intestinal motility and secretion.  相似文献   
7.
目的 建立TLC及HPLC法定性定量测定尖瓣过路黄中槲皮素和山柰酚.方法 TLC法确定黄酮类化合物的种类,HPLC法测定山柰酚、槲皮素的含量.结果 槲皮素在0.081 6-0.571 2μg范围内线性关系良好(R2=0.999 4);平均回收率101.88%,RSD=1.572 4%,n=6.山柰酚在0.069 6-0...  相似文献   
8.
目的通过槲皮素灌胃阻断热休克蛋白(HSP)70表达,观察艾灸预处理对大鼠急性胃黏膜损伤指数及细胞凋亡的影响,以进一步探明艾灸的细胞保护作用及其与HSP70的关系。方法40只大鼠随机分为捆绑对照组(A组)、模型组(B组)、艾灸+模型组(C组)、槲皮素+艾灸+模型组(D组)、槲皮素+模型组(E组)。D、E组每日采用槲皮素灌胃。C、D组每日艾灸足三里、梁门,以上处理共8 d。第9日,B、C、D、E组均采用无水乙醇灌胃制作大鼠急性胃黏膜损伤模型。采用western-blot方法检测胃黏膜HSP70蛋白表达;TUNEL法检测胃黏膜细胞凋亡指数(AI)。结果与A组比较,模型组大鼠胃黏膜AI明显增高(P〈0.05),胃黏膜HSP70表达升高(P〈0.01)。与B组相比,C组大鼠AI明显降低(P〈0.05),HSP70表达显著升高(P〈0.01);D组大鼠胃黏膜AI值明显增加(P〈0.01),HSP70表达未见上调。与C组相比,D组大鼠胃黏膜AI值升高明显(P〈0.01),HSP70表达明显下调。结论艾灸预处理上调胃黏膜HSP70表达,急性病胃黏膜损伤所致的细胞凋亡被抑制。槲皮素阻断HSP70合成后,艾灸预处理抑制急性胃黏膜...  相似文献   
9.
A 22-month-old boy, who regularly consumed the oral dietary supplement, quercetin, was suspected erroneously of having a catecholamine-producing tumor, based on elevated serum and urine levels of the dopamine metabolite, homovanillic acid (HVA). Subsequent studies of healthy adult volunteers showed that significant elevations in plasma HVA are a consequence of quercetin ingestion.  相似文献   
10.
高效液相色谱法测定金线莲中黄酮含量   总被引:6,自引:0,他引:6  
目的:研究金线莲黄酮母核类型,测定各类型苷元的含量及比例,为金线莲种的鉴别和人工栽培研究提供依据。方法:建立 HPLC-水解法,测定福建产金线莲黄酮苷元含量,计算主要苷元含量之和及比例,将其与云南金线莲比较。采用 SymmetryC_(18)色谱柱(3.9 mm×150 mm,5 μm),流动相为乙腈-0.03%磷酸水溶液(24:76),流速为1.0 mL·min~(-1),检测波长为370nm,柱温35℃。结果:福建金线莲主要黄酮苷元总含量为0.086%,RSD 为2.2%(n=5),槲皮素、山柰素、异鼠李素3种主要苷元比例为4.3∶1.0∶6.1;云南金线莲中黄酮主要苷元的类型与福建金线莲相同,苷元总含量为0.134%,RSD 为2.1%(n=5),3种苷元比例为:1.0∶1.0∶10.0。结论:HPLC-水解法可用于金线莲中黄酮母核类型的鉴定,测定各苷元的含量,计算苷元总含量以及比例,从化学成分角度为不同品种和产地的金线莲鉴别提供依据。  相似文献   
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号