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991.
目的探讨弥漫大B细胞淋巴瘤(DLBCL)患者血清血管内皮生长因子(VEGF)、碱性成纤维细胞生长因子(bFGF)的水平及临床意义。方法选取2019年2月至2020年2月我院收治的DLBCL患者140例及同期在我院进行体检的健康者70例为研究对象。采用环磷酰胺+阿霉素+长春新碱+泼尼松(CHOP)方案对患者进行化疗。比较DLBCL患者(治疗前)与健康者的血清VEGF、bFGF水平;比较不同临床分期DLBCL患者治疗前、治疗1个疗程后的血清VEGF、bFGF水平;比较治疗1个疗程后不同临床转归DLBCL患者的血清VEGF、bFGF水平及淋巴瘤国际预后指数(IPI)评分;对DLBCL患者治疗前的血清VEGF、bFGF水平与IPI评分的关系进行Pearson相关性分析。结果治疗前DLBCL患者的血清VEGF、bFGF水平均显著高于健康者,差异有统计学意义(P<0.05)。不同临床分期DLBCL患者的血清VEGF、bFGF水平比较差异有统计学意义,临床分期越高的患者治疗后其VEGF、bFGF水平的下降幅度越大(P<0.05)。治疗前、治疗1个疗程后,好转与恶化DLBCL患者的血清VEGF水平、bFGF水平、IPI评分比较差异有统计学意义,治疗后好转患者的血清VEGF水平、bFGF水平、IPI评分的降幅显著大于恶化患者(P<0.05)。Pearson相关性分析结果显示,DLBCL患者治疗前的血清VEGF、bFGF水平与其IPI评分均呈正相关。结论弥漫大B细胞淋巴瘤患者的血清VEGF、bFGF水平显著高于健康者,化疗后显著降低;患者的VEGF、bFGF水平与其治疗效果、病情、肿瘤侵袭情况等均存在较为密切的关系,对判断患者的病情、治疗效果及预后具有重要的临床意义。  相似文献   
992.

Aim

Kidney hypoxia can predispose to the development of acute and chronic renal failure in diabetes. Ischaemia–reperfusion injury (IRI) causes inflammation, and diabetes is known to exacerbate this inflammatory response in the kidney, whereas alarmin IL-33 could act as an innate immune mediator during kidney IRI. Thus, the present study examined the impact of genetic IL-33 receptor ST2 deficiency (ST2?/?) on renal IRI in euglycaemic and hyperglycaemic mice.

Methods

Hyperglycaemia was induced with streptozotocin (STZ) in adult male C57BL/6JRj wild-type (WT) mice and ST2?/? mice. Unilateral renal IRI was achieved 3 months after STZ treatment by left kidney nephrectomy (non-ischaemic control kidney) and clamping of the right renal artery for 32 min in STZ- and vehicle-treated animals. At 24 h after reperfusion, renal function and injury were determined by levels of plasma creatinine, blood urea nitrogen (BUN) and histological tubule scores. Also, in a complementary pilot clinical study, soluble ST2 concentrations were compared in diabetics and non-diabetics.

Results

Urinary albumin was significantly increased in STZ-induced hyperglycaemic mice, regardless of genotypic background. At 24 h post-ischaemia, plasma creatinine, BUN and tubular injury were significantly reduced in ST2?/? mice compared with vehicle-treated WT mice, but this protective effect was lost in the STZ-induced hyperglycaemic ST2?/? animals. Plasma concentrations of soluble ST2 were significantly greater in type 2 diabetes patients vs non-diabetics.

Conclusion

Our data suggest that the IL-33/ST2 pathway exerts differential effects depending on the glucose environment, opening-up new avenues for future research on alarmins and diabetes in ischaemia-related diseases.  相似文献   
993.
霉酚酸酯抑制内皮细胞表面粘附分子的表达   总被引:3,自引:2,他引:3  
目的 :观察霉酚酸酯 (MMF)对炎症因子刺激下内皮细胞表面粘附分子ICAM 1表达的影响。  方法 :以TNFα(2 0 μg/L)刺激内皮细胞 ,细胞表面的ICAM 1蛋白表达以流式细胞术检测 ,内皮细胞ICAM 1mRNA表达采用逆转录 半定量PCR法进行测定。  结果 :TNFα(2 0 μg/L)刺激内皮细胞 2 4h ,内皮细胞表面的粘附分子ICAM 1的蛋白和mRNA表达明显上升。MMF可以抑制内皮细胞的ICAM 1蛋白和mRNA的表达 ,这一抑制作用随着MMF剂量的增加而增强。  结论 :MMF可以抑制内皮细胞粘附分子ICAM 1的表达  相似文献   
994.
目的研究血管内皮细胞生长因子(VEGF)基因多态性与糖尿病肾病(DN)的关系。方法单纯2型糖尿病(DM)组76例,DN组81例,健康对照(NC)组60例。UNIQ-10柱提取全血基因组DNA。标本基因型的判断用聚合酶链反应-限制性酶切片断长度多态性技术。Hardy-Weinberg平衡法检验各组基因频率的群体代表性。结果(1)DN组VEGF-460和+405CC基因型频率和C等位基因频率明显高于DM组和NC组。(2)-460位点CC基因型DN患病率明显高于CT和TT基因型。+405位点CC基因型DN患病率明显高于CG和GG基因型。(3)显示VEGF-460和+405基因多态性均为DN发生的独立危险因素。结论(1)VEGF-460C/T基因多态性与DN发生有关。C等位基因可能是DN易感基因。(2)VEGF+405G/C基因多态性与DN发生有关。C等位基因可能是DN的易感基因。  相似文献   
995.
目的为制备组织工程学血管随时提供种子细胞,对人脐静脉内皮细胞分离、体外培养、传代及鉴定方法进行研究,并研究其冻存技术,探讨建立脐带血管内皮细胞库的可能性.方法新鲜脐带49务,脐静脉内灌注消化酶消化,获得内皮细胞,进行体外培养,相差显微镜下观察酶消化结果及所获内皮细胞贴壁生长规律;采用VⅢ因子免疫荧光染色,鉴定所获内皮细胞及其纯度;加入冻存液,置于液氮进行保存,复苏后,分别进行台酚蓝拒染试验及MTT还原试验,绘制细胞生长曲线.结果血管内灌注消化液法可获得取高纯度的内皮细胞,胰酶和胶原酶混合灌注法消化结果优于单纯胰酶及胰酶和EDTA组,各组消化时间均以10~15min为佳;混合酶消化组细胞获得率及贴壁结果均较其他二组为优.与未冻存细胞相比,复苏的细胞活力保持在95%以上.复苏后的内皮细胞的生长曲线与未冻存细胞的生长曲线无差异.结论脐静脉灌注酶消化法可获取足够数量及纯度的内皮细胞,混合酶消化法消化效果最佳,经体外培养扩增后,可提供足够数量及纯度的内皮细胞.冻存的内皮细胞复苏后仍保持较高的活力及体外增殖能力,能及时提供制备组织工程学血管的种子细胞来源.  相似文献   
996.
We report the case of a 76-year-old man diagnosed with angioimmunoblastic T-cell lymphoma (AITL) with high serum vascular endothelial growth factor (VEGF) preceded by Remitting seronegative symmetrical synovitis with pitting edema syndrome. He suffered respiratory discomfort caused by large amounts of pleural effusion. Interestingly, changes in serum VEGF measured over time were similar to changes in pleural effusion. Whether VEGF is related to the pathological condition of AITL is a very important question.  相似文献   
997.
Endothelial cell damage causes massive hepatic necrosis as a result of fibrin deposition in the hepatic sinusoids. When a stable analog of prostaglandin I2, beraprost sodium, was administered to rats given either dimethylnitrosamine, carbon tetrachloride, or endotoxin followingCorynebacterium parvum administration, the hepatic necrosis produced in each was attenuated, but to a greater extent in the dimethylnitrosamine and endotoxin/Corynebacterium parvum models, where fibrin deposition in the hepatic sinusoids occurs, as compared to the carbon tetrachloride model, where such fibrin deposition does not occur. Beraprost sodium reduced the expected increase of portal venous pressure in the endotoxin/Corynebacterium parvum model without affecting plasma thrombin-antithrombin III complex levels. Beraprost sodium also significantly reduced cell killing of both isolated rat hepatocytes and hepatic sinusoidal endothelial cells exposed totert-butyl hydroperoxide when compared to controls. Beraprost sodium could prove to be a therapeutic candidate for the treatment of hepatic necrosis, particularly in cases associated with fibrin deposition in the hepatic sinusoids because of its fibrin clot-clearning action.  相似文献   
998.
血管内皮生长因子的表达与胃癌浸润和转移的关系   总被引:3,自引:1,他引:3  
目的 研究血管内皮生长因子165(VEGF)mRNA在胃癌中的表达 ,探讨VEGF与胃癌浸润和转移的关系。方法 采用RT PCR方法 ,对 31例胃癌及非癌组织手术标本中VEGF165mRNA的表达进行相对定量研究。结果 胃癌组织中VEGF165mRNA表达的平均相对量 (1.12 5± 0 .35 6 )明显高于非癌组织的表达量 (0 .76 0± 0 .2 78,P <0 .0 5 ) ,其中淋巴结转移组 (1.2 19± 0 .377)和Ⅲ、Ⅳ期组 (1.2 6 2±0 .386 )分别高于无淋巴结转移组 (0 .92 7± 0 .2 0 5 )和Ⅰ、Ⅱ期组 (0 .934± 0 .194 ,P均 <0 .0 5 )。VEGF高表达者中淋巴结转移率为 83.3% ,Ⅲ和Ⅳ期占 77.8% ,均明显高于VEGF低表达者的 4 6 .2 %和 33.8%(P <0 .0 5 )。结论 胃癌组织中有VEGF的高表达 ,VEGF的表达在胃癌浸润和转移过程中发挥重要作用。  相似文献   
999.
Introduction: Patients with persistent atrial fibrillation (AF) have hemodynamic changes, which impair endothelial cell function resulting in decreased nitric oxide (NO) production. The aim of this work was to assess endothelial function in AF patients before and at various time points after cardioversion. Methods: Forty-two patients with AF and 21 normal and age-adjusted healthy controls were studied. Nitrites and nitrates (NO x ) and von Willebrand factor (vWf) concentrations were measured on blood samples taken just before cardioversion and over a 30 day period after the procedure. Results: Plasma levels of NO x in AF were significantly lower compared to healthy controls (p < 0.001), but after cardioversion gradually increased to approach to those of the healthy controls by the end of the first month of sustained sinus rhythm (p = 0.004). Interestingly plasma levels of NO x were negatively correlated to left atrial volume measured by ultrasonography (r = –0.34, p < 0.05). Plasma levels of vWf in AF patients were significantly higher compared to the healthy controls (p < 0.01) but with sustained sinus rhythm decreased (p = 0.02). Conclusion: The parallel normalization of the NO x titers and vWf levels suggests that vascular endothelial function improves after 30 days of normal sinus rhythm.  相似文献   
1000.
AIM: To investigate effects of ischemic pre-conditioning on the liver endogenous oxidant-antioxidant system during ischemia/reperfusion injury. METHODS: Twenty-four male Sprague-Dawley rats were randomly divided into sham-operated (Sham), ischemia/ reperfusion (I/R), ischemic pre-conditioning plus ischemia/ reperfusion (IPC) groups. Serum ALT, AST and hyaluronic acid levels were assayed and pathologic alterations observed. Liver malondialdehyde (MDA) contents, endogenous antioxidant enzymes, superoxidase dismutase (SOD), catalase (CAT), gultathionine peroxidase (GSH-Px) activities, neutrophils accumulation marker, myeloperoxidase (MPO) activities were measured respectively. RESULTS: Compared with I/R group, sinusoidal endothelial cells as well as hepatocytes damages, as assessed biochemically and histochemically, were improved significantly in IPC group; neutrophils infiltration was also markedly reduced. In IPC group, liver peroxidation, as measured by MDA contents, was significantly decreased when compared with I/R group; endogenous antioxidant enzymes, SOD, CAT and GSH-Px activities were markedly higher than that in I/R group. CONCLUSION: Ischemic pre-conditioning exerts protective effects on both hepatic sinusoidal endothelial cells and hepatocytes during liver I/R injury. Its mechanisms may involve dimunition of neutrophils infiltration and modulation of the imbalance of endogenous oxidant-antioxidant system in the organism.  相似文献   
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