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131.
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对苯二胺氧化产物对小鼠经皮肤染毒的亚慢性毒性 总被引:1,自引:4,他引:1
[目的 ]研究氧化型染发剂主要成分对苯二胺 (PPD)氧化产物经皮吸收后对小鼠的亚慢性毒作用。 [方法 ]对苯二胺经双氧水氧化后的氧化产物为受试物 ,每隔 3d在小鼠背部皮肤染毒 1次 ,周期 1个月。整个过程中观察小鼠的一般生长情况 ,并于染毒 1个月后观察受试动物血生化指标、血常规、肝肾脾组织病理学改变和遗传毒性。 [结果 ]PPD氧化产物可影响小鼠的肝肾功能 ,随着PPD染毒剂量增加 ,ALT和BUN值逐渐增高 ,与对照组比较差异有显著性 (P<0 0 5或P <0 0 1)。PPD具有遗传毒性 ,能造成骨髓细胞染色体和DNA的损伤 ,并在受试剂量范围内存在剂量 效应关系。 [结论 ]频繁使用氧化型染发剂可能对机体具有潜在的危害 相似文献
134.
Xiaoyu Tang Kaixuan Cui Xi Lu Peiqi Wu Shanshan Yu Boyu Yang Yue Xu Xiaoling Liang 《Investigative ophthalmology & visual science》2022,63(6)
PurposeKC7F2 is a novel molecule compound that can inhibit the translation of hypoxia-inducible factor 1α (HIF1α). It has been reported to exhibit potential antiangiogenic effect. We hypothesized that KC7F2 could inhibit oxygen-induced retinal neovascularization (RNV). The purpose of this study was to investigate this assumption.MethodsOxygen-induced retinopathy (OIR) models in C57BL/6J mice and Sprague-Dawley rats were used for in vivo study. After intraperitoneal injections of KC7F2, RNV was detected by immunofluorescence and hematoxylin and eosin staining. Retinal inflammation was explored by immunofluorescence. EdU incorporation assay, cell counting kit-8 assay, scratch test, transwell assay, and Matrigel assay were used to evaluate the effect of KC7F2 on the proliferation, migration and tube formation of human umbilical vein endothelial cells (HUVEC) induced by vascular endothelial growth factor (VEGF) in vitro. Protein expression was examined by Western blot.ResultsKC7F2 treatment (10 mg/kg/d) in OIR mice significantly attenuated pathological neovascularization and decreased the number of preretinal neovascular cell nuclei, without changing the avascular area, which showed the same trends in OIR rats. Consistently, after the KC7F2 intervention (10 µM), cell proliferation was inhibited in VEGF-induced HUVEC, which was in agreement with the trend observed in the retinas of OIR mice. Meanwhile, KC7F2 suppressed VEGF-induced HUVEC migration and tube formation, and decreased the density of leukocytes and microglia colocalizing neovascular areas in the retinas. Moreover, the HIF1α–VEGF pathway activated in retinas of OIR mice and hypoxia-induced HUVEC, was suppressed by KC7F2 treatment.ConclusionsThe current study revealed that KC7F2 was able to inhibit RNV effectively via HIF1α–VEGF pathway, suggesting that it might be an effective drug for RNV treatment. 相似文献
135.
目的 观察当归补血汤对糖尿病肾病(DKD)大鼠足细胞线粒体分裂及凋亡的影响,探讨当归补血汤对DKD大鼠肾脏保护作用及机制。方法 SD大鼠随机分为造模组65只,喂养高糖高脂饲料;正常组10只,喂养普通饲料;6周后,造模组大鼠予腹腔注射链脲佐菌素(STZ)制备2型糖尿病(T2DM)模型。将制备成功的T2DM大鼠随机分为模型组、厄贝沙坦组(0.014 g·kg-1)、当归补血汤低、中、高剂量组(0.36、0.72、1.44 g·kg-1)。连续灌胃16周。治疗第16周末检测各组大鼠空腹血糖(FBG)、24 h尿蛋白(24 h UTP);苏木素-伊红(HE)、马松(Masson)染色观察大鼠肾组织病理;透射电镜(TEM)观察足细胞线粒体;二氢乙锭(DHE)法检测大鼠肾组织活性氧簇(ROS)表达水平;原位末端标记法(TUNEL)检测各组大鼠肾细胞凋亡情况;免疫组化法(IHC)检测大鼠肾组织中足细胞标志蛋白突触足蛋白(Synaptopodin)、膜蛋白(Podocin)及切割型胱天蛋白酶-3(cleaved Caspase-3)表达水平;蛋白免疫印迹法(Western blot)检测肾组织激酶锚定蛋白1(AKAP1)、磷酸化动力相关蛋白1(p-Drp1)、线粒体融合蛋白2(Mfn2)、B细胞淋巴瘤-2(Bcl-2)、Bcl-2相关X蛋白(Bax)蛋白表达。结果 与正常组比较,模型组大鼠FBG、24 h UTP表达升高;可见肾小球内系膜增生,基底膜增厚;电镜下足细胞线粒体肿胀,线粒体嵴断裂、紊乱;ROS表达增加,TUNEL阳性细胞明显增多,Synaptopodin、Podocin表达降低,cleaved Caspase-3表达增加,AKAP1、p-Drp1表达增加,Mfn2、Bcl-2/Bax表达降低(P<0.01);与模型组比较,当归补血汤高剂量组能降低FBG、24 h UTP水平,肾组织病理损伤及足细胞线粒体损伤明显改善,ROS表达减少,肾组织TUNEL阳性细胞数明显减少,Synaptopodin、Podocin表达升高,cleaved Caspase-3表达降低,AKAP1、p-Drp1表达降低,Mfn2、Bcl-2/Bax表达增加(P<0.05,P<0.01)。结论 当归补血汤可通过调控AKAP1/Drp1通路抑制足细胞线粒体分裂及凋亡,减少蛋白尿,从而延缓DKD进展。 相似文献
136.
改良晶状体切除术在眼外伤晶状体玻璃体联合术中的应用 总被引:1,自引:1,他引:0
目的:探求一种安全有效、并发症少且更适合眼外伤时晶状体玻璃体联合手术的晶状体切除术方式.方法:对27例(27眼)眼外伤行晶状体玻璃体联合手术者进行回顾性研究.所有患者均由睫状体平坦部巩膜切口行改良晶状体切除术,保留晶状体囊,并联合玻璃体视网膜手术.结果:所有患者均成功地切除了晶状体并最大限度保留有用的晶状体囊,患者术后视力均有不同程度的提高.继发性青光眼术后眼压得到控制.结论:该改良晶状体切除术是一种安全有效、并发症少且更适合眼外伤时晶状体玻璃体联合手术的手术方式. 相似文献
137.
目的:探讨儿童先天性白内障手术后无晶状体眼或人工晶状体眼的平均中央角膜厚度(CCT)的改变,并与同年龄组健康人群的中央角膜厚度进行对照研究。方法:该实验包括随机抽样的先天性白内障术后的45个无晶状体眼及人工晶状体眼患者共45眼,同时有46个健康的进行性别和年龄配比的志愿者作为对照研究,对他们进行包括中央角膜厚度及眼压(Goldmann眼压计及Tonopen眼压计)的全面的眼部检查。将测得的眼压与角膜中央厚度结果进行分组比较。结果:研究对象的45眼中包括35只无晶状体眼与10只人工晶状体眼,其角膜厚度中位数为626μm(范围为523~870μm),而正常对照组的中央角膜厚度为556.0μm(范围为490~640μm)其差异有统计学意义(P<0.05);先天性白内障患儿术后无晶状体眼与手术时一期植入人工晶状体的眼之间的中央角膜厚度的差异有统计学意义(P=0.011)。但先天性白内障术后的患儿中二期植入人工晶状体眼与无晶状体眼之间中央角膜厚度的差异则不具备统计学意义(P=0.847)。患者的年龄中位数为36mo(年龄从1wk到10岁不等),且其年龄与CCT之间呈负相关(r=-0.485,P=0.001)。结论:儿童先天性白内障术后无晶状体眼与人工晶状体眼的患者显著比正常对照组的角膜变厚。这种差异对解释术后眼内压升高有重要的作用,同时对儿童先天性白内障无晶状体眼患者术后最常见的继发青光眼的并发症的解释有重要的作用。 相似文献
138.
139.
Jinghui Peng Shengbin Pei Yangyang Cui Yiqin Xia Yue Huang Xiaowei Wu Mingjie Zheng Miaomiao Weng Xu Han Hongtao Fu Lili Yang Wenbin Zhou Ziyi Fu Shui Wang Hui Xie 《Oncology Letters》2022,24(2)
In patients with triple-negative breast cancer (TNBC), high tumour mutation burden and aberrant oncogene expression profiles are some of the causes of poor prognosis. Therefore, it is necessary to identify aberrantly expressed oncogenes, since they have the potential to serve as therapeutic targets. Transient receptor potential channel 5 opposite strand (TRPC5OS) has been previously shown to function as a novel tumour inducer. However, the underlying mechanism of TRPC5OS function in TNBC remain to be elucidated. Therefore, in the present study TRPC5OS expression was first measured in tissue samples of patients with TNBC and a panel of breast cancer cell lines (ZR-75-1, MDA-MB-453, SK-BR-3, JIMT-1, BT474 and HCC1937) by using qRT-PCR and Western blotting. Subsequently, the possible effects of TRPC5OS on MDA-MB-231 cells proliferation were determined using Cell Counting Kit-8 and 5-Ethynyl-2′-deoxyuridine assays after Lentiviral transfection of MDA-MB-231. In addition, potential interaction partners of TRPC5OS were explored using liquid chromatography-mass spectrometry (LC-MS)/MS. Gene expression patterns following TRPC5OS overexpression were also detected in MDA-MB-231 cells by using High-throughput sequencing. Gene Ontology (GO) and Kyoto Encyclopaedia of Genes and Genomes (KEGG) analysis were then used to systematically verify the potential interactions among the TRPC5OS-regulated genes. The potential relationship between TRPC5OS-interacting proteins and gene expression patterns were studied using Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) analysis. TRPC5OS expression was found to be significantly higher in TNBC tumour tissues and breast cancer cell lines compared with luminal tumour tissues and ZR-75-1. In addition, the overexpression of TRPC5OS significantly increased cell proliferation. High-throughput sequencing results revealed that 5,256 genes exhibited differential expression following TRPC5OS overexpression, including 3,269 upregulated genes and 1,987 downregulated genes. GO analysis results indicated that the functions of these differentially expressed genes were enriched in the categories of ‘cell division’ and ‘cell proliferation’ regulation. KEGG analysis showed that the TRPC5OS-regulated genes were associated with processes of ‘homologous recombination’ and ‘TNF signalling pathways’. Subsequently, 17 TRPC5OS-interacting proteins were found using LC-MS/MS and STRING analysis. The most important protein among interacting proteins was ENO1 which was associated with glycolysis and regulated proliferation of cancer. In summary, data from the present study suggest that TRPC5OS overexpression can increase TNBC cell proliferation and ENO1 may be a potential target protein mediated by TRPC5OS. Therefore, TRPC5OS may serve as a novel therapeutic target for TNBC. 相似文献
140.
目的 探讨正念减压疗法对老年淋巴瘤患者疲乏症状及睡眠质量的影响。方法 选取老年淋巴瘤患者100例,随机分为对照组和观察组,每组50例,对照组采用常规疗法,观察组采用正念减压疗法,观察2组干预效果、疲乏症状及睡眠质量。结果 观察组总有效率90.0%,高于对照组的50.0%;干预后焦虑自评量表(SAS)、抑郁自评量表(SDS)评分方面,观察组分别为(35.54±2.65)分、(34.56±3.46)分,低于对照组的(46.38±2.95)分、(43.36±3.74)分;干预后,观察组癌因性疲乏量表(CFS)、匹兹堡睡眠质量指数量表(PSQI)各项评分均低于对照组,费城老年中心信心量表(PGC-CS)各项评分均高于对照组,差异有统计学意义(P<0.05)。结论 正念减压疗法可以有效改善老年淋巴瘤患者抑郁、焦虑及疲乏症状,提高了患者的睡眠质量和幸福感。 相似文献