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1.
背景糖尿病心脏自主神经病变(DCAN)是糖尿病常见且严重的慢性并发症之一,但目前关于甲状腺功能与DCAN关系的研究报道较少。目的探讨亚临床甲状腺功能减退症(SCH)对DCAN的影响。方法选取2019年10月至2020年10月在首都医科大学附属北京友谊医院住院及门诊就诊的2型糖尿病患者564例。所有患者均完成Ewing试验。收集患者一般资料、体格检查结果、实验室检查结果,并依据Ewing试验评估并筛查DCAN。相关性分析采用Pearson相关分析和Spearman秩相关分析,采用多因素Logistic逐步回归分析探究2型糖尿病患者并发DCAN的影响因素。结果564例2型糖尿病患者中,129例并发DCAN(DCAN组),435例未并发DCAN(对照组),DCAN发生率为22.9%。2型糖尿病患者中合并SCH者84例(14.9%),DCAN组患者中合并SCH者36例(28.0%),对照组患者中合并SCH者48例(11.0%),DCAN组患者合并SCH患病率高于对照组(χ2=22.346,P<0.001)。2型糖尿病并发DCAN患者Valsalva试验动作期间最大R-R间距与最小R-R间距比值(VAL R-R比值)与糖尿病病程、糖化血红蛋白(HbA1c)、空腹血糖(FBG)、低密度脂蛋白胆固醇(LDL-C)、三酰甘油(TC)、超敏C反应蛋白(hs-CRP)、促甲状腺激素(TSH)、尿微量白蛋白/肌酐(UACR)呈负相关,与舒张压(DBP)呈正相关(P<0.05)。多因素Logistic逐步回归分析结果显示,SCH〔OR=1.717,95%CI(1.246,2.365)〕是2型糖尿病患者并发DCAN的独立影响因素(P<0.05)。结论2型糖尿病患者TSH水平与DCAN相关,且SCH是2型糖尿病患者并发DCAN的独立影响因素。  相似文献   
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目的探讨糖尿病足溃疡(DFU)患者中性粒细胞淋巴细胞比值(NLR)与其病变严重程度的相关性及对预后的预测价值。方法回顾性分析2016年6月—2020年6月收治的DFU 176例的临床资料。收集入院时NLR、C反应蛋白(CRP)等指标,分析不同DFU病情、下肢缺血及感染程度NLR水平。根据随访6个月时转归分为预后良好组和预后不良组,应用多因素Logistic回归分析DFU患者预后不良的危险因素,并采用受试者工作特征(ROC)曲线评估NLR对DFU患者预后不良的预测价值。结果随病情严重程度、下肢缺血程度、感染程度加重NLR水平逐渐升高(P<0.01)。176例随访6个月后溃疡预后不良60例(34.09%)。NLR>6.58、CRP>58.35 mg/L是DFU患者预后不良的危险因素。NLR以7.17为临界值预测DFU患者预后不良的曲线下面积高于CRP(P<0.01)。结论DFU患者短期预后不良风险高,NLR能反映其病变程度,且早期预测预后不良的价值高于CRP。  相似文献   
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Diabetic macular ischaemia (DMI) is traditionally defined and graded based on the angiographic evidence of an enlarged and irregular foveal avascular zone. However, these anatomical changes are not surrogate markers for visual impairment. We postulate that there are vascular phenotypes of DMI based on the relative perfusion deficits of various retinal capillary plexuses and choriocapillaris. This review highlights several mechanistic pathways, including the role of hypoxia and the complex relation between neurons, glia, and microvasculature. The current animal models are reviewed, with shortcomings noted. Therefore, utilising the advancing technology of optical coherence tomography angiography (OCTA) to identify the reversible DMI phenotypes may be the key to successful therapeutic interventions for DMI. However, there is a need to standardise the nomenclature of OCTA perfusion status. Visual acuity is not an ideal endpoint for DMI clinical trials. New trial endpoints that represent disease progression need to be developed before irreversible vision loss in patients with DMI. Natural history studies are required to determine the course of each vascular and neuronal parameter to define the DMI phenotypes. These DMI phenotypes may also partly explain the development and recurrence of diabetic macular oedema. It is also currently unclear where and how DMI fits into the diabetic retinopathy severity scales, further highlighting the need to better define the progression of diabetic retinopathy and DMI based on both multimodal imaging and visual function. Finally, we discuss a complete set of proposed therapeutic pathways for DMI, including cell-based therapies that may provide restorative potential.  相似文献   
5.
目的:观察白虎加桂枝汤对尿酸性肾病(HN)大鼠的治疗效果,并从肾小管损伤角度探讨其作用机制。方法:将60只无特定病原体(SPF)级SD雄性大鼠随机分为正常对照组、模型组、白虎加桂枝汤高剂量组(BHJGZ高组)、白虎加桂枝汤中剂量组(BHJGZ中组)、白虎加桂枝汤低剂量组(BHJGZ低组)、别嘌醇组,每组10只。采用腺嘌呤灌胃联合腹部皮下注射氧嗪酸钾构建大鼠尿酸性肾病模型,连续造模18 d。造模成功后,正常对照组及模型组给予等体积蒸馏水灌胃,其余各组给予对应药物灌胃,连续干预8周。观察大鼠体质量、活动能力、精神状态及毛色,检测大鼠血清尿酸(UA)、血清尿素氮(BUN)、血清肌酐(Scr)、24 h尿蛋白定量(24 h UTP),通过HE染色、过碘酸希夫(PAS)染色和Masson染色,观察高尿酸血症(HUA)大鼠肾脏组织形态学、肾小球系膜增生以及肾间质纤维化情况。结果:与模型组比较,治疗6周后,白虎加桂枝汤各剂量组大鼠体质量增加,活动能力、精神状态及毛色好转(P<0.05)。BHJGZ中组可显著降低大鼠血清Scr水平(P<0.01),BHJGZ中组、BHJGZ高组可明显降低大鼠血清BUN水平(P<0.01);白虎加桂枝汤各剂量组均可明显降低HUA大鼠血清UA、24 h UTP水平并改善肾组织形态学、肾小球系膜增生及肾间质纤维。结论:白虎加桂枝汤可能通过抑制肾小球系膜基质增生、减少肾小管损伤及肾间质纤维化,延缓HN进展。  相似文献   
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ObjectiveTo explore the protective effect and potential mechanisms of danshen root (Salvia miltiorrhiza Bge., S. miltiorrhiza) and its extracts for the treatment of diabetic nephropathy (DN).MethodsPreclinical studies of S. miltiorrhiza and its extracts on DN were systematically searched in nine databases. The primary outcomes were blood glucose, kidney function, proteinuria, and renal histopathology. The secondary outcomes included the related mechanisms. The methodological quality of animal studies was assessed based on the risk of bias tool of the Systematic Review Centre for Laboratory Animal Experimentation (SYRCLE) for animal studies. Meta-analysis was performed using R software (version 4.1.2).ResultsTwenty-nine animal experimental studies that met the eligibility criteria were included in this study. Compared to the control group, S. miltiorrhiza reduced the serum creatinine, blood urea nitrogen, 24-h urine protein, 24-h urine albumin, blood glucose, and kidney index (kidney weight/body weight), and alleviated renal pathological damage. In terms of the mechanism of action, compared to the control group, S. miltiorrhiza reduced the levels of transforming growth factor β1, collagen IV, malondialdehyde, tumor necrosis factor α, interleukin-6, and monocyte/macrophage (ED-1), and increased the levels of superoxide dismutase, glutathione peroxidase, nuclear factor E2–related factor 2, and heme oxygenase-1.ConclusionThe existing evidence shows that S. miltiorrhiza has beneficial effects on the animal model of DN, and its mechanism is mainly related to improving kidney fibrosis, oxidative stress, and inflammatory response.  相似文献   
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目的 探讨益气活血通络方对糖尿病神经病理性疼痛(diabetic neuropathic pain,DNP)的影响及其作用机制。方法 高脂喂养大鼠4周后,35 mg/kg链脲佐菌素(streptozotocin,STZ)腹腔注射复制2型糖尿病大鼠模型,通过观测大鼠机械痛阈和热缩足反应时间作为判定DNP模型复制成功的标准。将DNP大鼠随机分为模型组,益气活血通络方高、中、低剂量组和阳性对照组(甲钴胺),另设空白对照组。Western blot法和免疫荧光双标检测脊髓中补体受体- 3的单克隆抗体(monoclonal antibody of complement receptor type 3,OX42)和P2X7(purinergic 2X7)的表达水平;ELISA法检测血清肿瘤坏死因子- α(tumor necrosis factor- α,TNF- α)、白细胞介素- 1β(interleukin- 1β,IL- 1β)和趋化因子配体3(CC- chemokine ligand 3,CCL3)水平。结果 益气活血通络方干预后,DNP大鼠的机械痛阈和热缩足反应时间均得到显著的改善;大鼠血清TNF- α、IL- 1β和CCL3水平显著降低(P<0.05);脊髓组织中OX42和P2X7表达水平均显著降低(P<0.05)。结论 益气活血通络方对DNP大鼠具有显著的治疗作用,其作用机制可能是通过抑制脊髓小胶质细胞活性,调节P2X7的表达,从而减轻神经炎症反应。  相似文献   
9.
Peperomia pellucida (L.) Kunth is a medicinal plant used to manage inflammatory illnesses such as conjunctivitis, and gastrointestinal and respiratory tract disorders in tropical and subtropical regions. However, little is known about its pharmacological mechanism of action against eye diseases. This review aims to critically discuss the phytochemistry, pharmacology and toxicology of P. pellucida as well as its roles in the treatment of cataract, glaucoma and diabetic retinopathy. Recent developments in the uses of P. pellucida for healthcare and nutraceutical products by the pharmaceutical industry are also covered in this review. For this review, a literature search was performed with PubMed, ScienceDirect, SciFinder Scholar and Scopus databases, using relevant keywords. Among the various phytochemicals identified from P. pellucida, β-caryophyllene, carotol, dillapiole, ellagic acid, pellucidin A, phytol and vitexin exhibit strong pharmacological activities within the mitogen-activated protein kinase and nuclear factor-κB signalling pathways in inflammatory eye diseases. The antihypertensive, anti-inflammatory, antioxidant, antihyperglycemic and anti-angiogenic activities displayed by P. pellucida extracts in many in vitro, in vivo and clinical studies suggest its potential role in the management of inflammatory eye diseases. P. pellucida extract was non-toxic against normal cell lines but displayed mild toxicity in animal models. The growing public interest in P. pellucida has inspired the nutraceutical and pharmaceutical industries to process the plant into health products. Although the potential pharmacological mechanisms against eye diseases have been summarized, further studies of the interactions among constituent phytochemicals from P. pellucida within various signalling pathways shall support the use of the plant as an alternative therapeutic source.  相似文献   
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Whether the underlying mutations are homozygous, heterozygous, or co-inherited with other hemoglobinopathies, sickle cell disease is known to afflict the kidneys, leading to the clinical entity known as sickle cell nephropathy (SCN). Although common, SCN remains diagnostically elusive. Conventional studies performed in the context of renal disorders often fail to detect early stage SCN. This makes the quest for early diagnosis and treatment more challenging, and it increases the burden of chronic kidney disease-related morbidity among patients. Novel diagnostic tools have been employed to overcome this limitation. In this study, we discuss various biomarkers of SCN, including those employed in clinical practice and others recently identified in experimental settings, such as markers of vascular injury, endothelial dysfunction, tubulo-glomerular damage, and oxidative stress. These include kidney injury molecule-1, monocyte chemoattractant protein-1, N-acetyl-B-D-glucosaminidase, ceruloplasmin, orosomucoid, nephrin, and cation channels, among others. Furthermore, we explore the potential of novel biomarkers for refining diagnostic and therapeutic approaches and describe some obstacles that still need to be overcome. We highlight the importance of a collaborative approach to standardize the use of promising new biomarkers. Finally, we outline the limitations of conventional markers of renal damage as extensions of the pathogenic process occurring at the level of the organ and its functional subunits, with a discussion of the expected pattern of clinical and biochemical progression among patients with SCN.  相似文献   
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