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991.
Darren Ming‐Chun Poon 《Asia-Pacific Journal of Clinical Oncology》2020,16(Z3):18-23
For advanced and metastatic urothelial carcinomas (UCs), platinum (preferably cisplatin)‐based chemotherapy has been the standard treatment for many years. However, many patients are ineligible for cisplatin‐based chemotherapy because of poor performance status and/or other age‐related conditions. At the other end of the spectrum, patients with localized non‐muscle–invasive bladder cancer who are unresponsive to intravesical Bacillus Calmette‐Guérin (BCG) treatment often face radical cystectomy as the only option. In recent years, the application of immunotherapy in the form of immune‐checkpoint inhibitors has provided viable alternatives in the second‐line postplatinum and first‐line cisplatin‐ineligible settings. Recent and ongoing clinical trials are also assessing the safety and efficacy of immunotherapy for neoadjuvant and adjuvant uses before/after cystectomy, for BCG‐unresponsive cases, and for combination treatments that include the newer indoleamine 2,3‐dioxygenase‐1 inhibitors and/or BCG. This review summarizes recent developments in immunotherapy for UCs. 相似文献
992.
综合医院急诊科护理风险管理体会 总被引:25,自引:2,他引:23
目的探讨急诊科护理风险管理措施,提高急诊护理质量。方法总结并分析以老年病为中心的急诊科风险问题,加强风险管理,完善规章制度,实施安全管理措施,关注老年急诊病人急救护理工作中的不安全因素。结果护士风险意识明显提高,自觉落实安全管理措施,减少了护理缺陷的发生。结论实施风险管理十分重要,直接关系到抢救护理质量和病人的满意度。 相似文献
993.
994.
目的研究固定矫治器治疗前后牙釉质脱矿牙数,好发部位及影响因素.方法对照组治疗前检查记录:酒精擦拭牙面后吹干,有白垩色损害者为脱矿.分析组治疗后记录.结果固定矫治可增加脱矿牙数,部位多为牙颈部,邻面,托槽及带环周缘. 相似文献
995.
996.
细胞外基质(extracellularmatrix,ECM)降解是肿瘤发生浸润转移过程中的关键一步,肿瘤细胞分泌的多种丝氨酸蛋白酶包括基质金属蛋白酶(matrixmetallopoteinases,MMPs)参与细胞外ECM降解。组织因子途径抑制物2(tissuefactorpathwayinhibitor-2,TFPI-2)是一种具有32000丝氨酸蛋白酶抑制物,可抑制包括纤溶酶、胰蛋白酶、MMPs在内的多种蛋白酶。越来越多的研究表明,TFPI-2通过降解MMPs等抑制肿瘤转移、降低肿瘤的侵袭转移能力。TFPI-2在抑制肿瘤细胞迁徙及浸润转移过程中发挥重要作用,可作为一种潜在的基因治疗靶点。 相似文献
997.
目的:探讨氟伐他汀单用及与醛固酮拮抗剂安体舒通联用对兔颈动脉粥样硬化的影响及其机制。方法:高脂饲养建立兔颈动脉硬化斑块模型。96只雄性新西兰兔分为对照组、高脂饮食组、氟伐他汀处理组(氟伐他汀组)以及氟伐他汀与安体舒通联合处理组(联合处理组),每组24只。用免疫组织化学法检测MMP-9表达,TONEL法检测细胞凋亡,HE染色观察颈动脉粥样硬化斑块结构变化。结果:(1)MMP-9在高脂饮食组表达水平高于对照组(P〈0.01),且8周、12周时高于4周时(P〈0.01)。氟伐他汀组12周时MMP-9表达低于4周时(P〈0.01)。联合处理组8周和12周时MMP-9表达低于4周时(P〈0.01)。氟伐他汀组和联合处理组MMP-9表达低于对照组和高脂饮食组(P〈0.01)。联合处理组8周和12周时MMP-9表达低于氟伐他汀组各对应时间点(P分别〈0.05和0.01)。(2)高脂饮食组TUNEL阳性细胞数多于对照组(P〈0.01),且8周、12周时多于4周时(P〈0.01)。氟伐他汀组和联合处理组8、12周时TUNEL阳性细胞数少于4周时(P〈0.01)。氟伐他汀组和联合处理组TUNEL阳性细胞数少于对照组、高脂饮食组各时间点(P〈0.01);联合处理组8周和12周时TUNEL阳性细胞数少于氟伐他汀组(P〈0.01)。结论:随着高脂饲养时间的延长,动脉斑块中MMP-9表达增加,凋亡细胞数增多;他汀类药物可通过降低MMP-9表达和抑制细胞凋亡延缓动脉粥样硬化形成.联用醉固酮桔抗剂这一效应得到增强. 相似文献
998.
999.
Rihwa Choi Gayoung Chun Unyeong Go Sang Gon Lee Eun Hee Lee 《Journal of clinical laboratory analysis》2022,36(4)
BackgroundLimited data are available with regard to biological variations of the Mac‐2–binding protein glycosylation isomer (M2BPGi), a liver fibrosis biomarker.MethodsLong‐term biological variation of M2BPGi was investigated using longitudinally measured M2BPGi test results from healthy Korean adult subjects. One‐way analysis of variance (ANOVA) tests were used to calculate the reference change value (RCV) of M2BPGi based on biological variation estimates. Furthermore, asymmetric RCV was calculated according to a recent publication of the European Federation of Clinical Chemistry and Laboratory Medicine Working Group on Biological Variation and Task Group for the Biological Variation Database (EFLM TG‐BVD).ResultsA total of 363 test results from 174 Korean subjects undergoing general health checkups were requested from 13 local clinics and hospitals during a 38‐month period. The within‐subjects biological variation (CVI), between‐subject biological variation (CVG), analytical variation (CVA), RCV, and individuality index (II) values for serum M2BPGi were 23.3%, 30.0%, 4.3%, 65.6%, and 0.78, respectively. Asymmetric RCV calculated using formulae by a recent EFLM TG‐BVD publication ranged from −41.9 to 72.0%. Desirable analytical performance specifications for M2BPGi derived from biological variation were as follows: imprecision 11.6%, bias 9.6%, and total allowable error 28.7%.ConclusionsRCV based on biological estimates may be helpful for evaluating and interpreting serial M2BPGi measurements by physicians and in clinical laboratories. 相似文献
1000.
BackgroundHepatocellular carcinoma (HCC) is a common malignancy with high morbidity. The current study aimed to explore the molecular mechanism of lncRNA SLC16A1‐AS1 in the tumorigenesis of HCC.Material and methodsThe expression of SLC16A1‐AS1 and miR‐411 was examined in clinical HCC tissues. HCC cell lines Hep3B and Huh‐7 were employed and transfected with si‐SLC16A1‐AS1. The correlation between SLC16A1‐AS1 and miR‐411 was verified by luciferase reporter assay. Cell viability was detected by CCK‐8 assay. Cell migration and invasion capacity were examined by transwell assay. The protein level of MITD1 was analyzed by western blotting.ResultsThe expression of SLC16A1‐AS1 markedly increased in HCC tissues and cell lines. Subsequent studies identified SLC16A1‐AS1 as a downstream target of miR‐411. In addition, SLC16A1‐AS1 knockdown and miR‐411 overexpression significantly stagnated the progression of HCC cells. SLC16A1‐AS1 knockdown also downregulated MITD1 levels.ConclusionOur findings showed that SLC16A1‐AS1 was overexpressed in HCC cells and tissues. SLC16A1‐AS1 promoted the malignant characteristics of HCC cells and acted as an oncogene. Its regulatory effect may be associated with miR‐411/MITD1 axis. Therefore, SLC16A1‐AS1 has the potential to be used as a biomarker or therapeutic target for the treatment of HCC. 相似文献