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41.
目的:建立鼠巨细胞病毒(MCMV)感染C57BL/6小鼠急性肝炎模型并对其感染特点进行分析及鉴定。方法:将24 只C57BL/6小鼠随机分为阴性对照组(n =12)及病毒感染组(n =12),病毒感染组腹腔注射1.0×106 PFU(200 μL)MCMV悬液,阴性对照组注射等体积小鼠胚胎成纤维细胞(MEF)悬液。于感染后第3天和第7天取外周血分离血清检测谷丙转氨酶(ALT)及谷草转氨酶(AST)。同时进行肝组织病毒分离、组织病理学及MCMV IE和M55基因、细胞因子白细胞介素-6(IL-6)、白细胞介素-1β(IL-1β)、肿瘤坏死因子α(TNF-α)的检测。结果:病毒感染组肝组织匀浆病毒分离均为阳性,肝炎发生率为100%。在感染后第3天即发生肝炎病理改变,病毒感染组血清ALT及AST较阴性对照组明显升高(P <0.01);病毒感染组肝脏HE染色第3天可见局灶性炎性细胞浸润及肝脏点灶状坏死,持续至第7天,Ishak评分较阴性对照组明显升高(P <0.01);在感染后第3天病毒感染组肝组织内可检测到MCMV IE及M55基因,且在感染后第7天仍可测得IE基因;感染后第3天及第7天病毒感染组炎性细胞因子IL-6、TNF-α及IL-1β mRNA表达水平明显升高(P <0.05)。 结论:成功建立MCMV感染C57BL/6小鼠急性动物肝炎模型,其感染表现主要集中在急性感染前期。 相似文献
42.
Miju Bae Sung Woon Chung Chung Won Lee Up Huh Min Su Kim Seung Hwan Song 《Asian journal of surgery / Asian Surgical Association》2019,42(1):235-239
Background
In Leriche syndrome, postoperative graft thrombosis remains one of the most significant clinical challenges.Methods
We reviewed 51 patients who underwent surgery for aortoiliac occlusive disease at our hospital from January 2007 to December 2014. The factors associated with graft patency were determined using the Cox proportional hazard model.Results
The 2-year prosthetic graft patency rate was 72.5%. Younger age (p = 0.017, Odd ratio (OR) = 1.112), postoperative uncontrolled hypertension (p = 0.044, OR = 3.797), and associated Trans Atlantic Inter-Society Consensus for the Management of Peripheral Arterial Disease II (TASC II) D femoropopliteal lesion (p = 0.008, OR = 11.139) were significantly related factors for prosthetic graft patency after surgical repair. The existing comorbidities of the patients that indicated the need for axillo-bifemoral bypass seemed to be related to lower graft patency or other complications.Conclusions
For better graft patency after an open surgical repair of Leriche syndrome, strict postoperative hypertension control and distal run-off resolution are necessary. 相似文献43.
44.
目的 探讨类风湿关节炎患者外周血miR-150-5p、细胞因子信号抑制因子1(suppressor of cytokine signaling 1,SOCS1)mRNA的表达及对类风湿关节炎(Rheumatoid Arthritis,RA)疾病诊断、中医证型判断的意义。方法 纳入符合诊断标准的RA患者57例及健康对照组19例,根据《22个专业95个病种中医诊疗方案》有关RA的中医证候诊断标准,判断RA的中医证型。qPCR检测RA患者及健康对照组miR-150-5p、SOCS1mRNA的相对表达水平,同时检测血常规、肝功能、肾功能等常规指标。双荧光素酶分析方法判断两者是否存在靶向关系。统计分析miR-150-5p、SOCS1 mRNA对RA疾病的诊断意义及其与中医证型的相关性。结果 RA患者外周血miR-150-5p的相对表达水平下调,低于正常人群(t = -19.019,P < 0.05);其表达水平随疾病活动度升高,有下降趋势;患者外周血SOCS1 mRNA的相对表达水平上调,低于正常人群(t = 5.333,P < 0.05);其表达水平随疾病活动度升高,有上升趋势。MiR-150-5p与SOCS1 mRNA有靶向结合关系(P < 0.05)。通过AUC曲线比较,miR-150-5p的相对表达水平区分RA的敏感性及特异性分别为98.1%、92.1%(AUC = 0.972,P < 0.05);SOCS1 mRNA的相对表达水平无法区分RA(AUC = 0.472,P > 0.05)。RA患者中miR-150-5p的相对表达水平低于3.06,RA患者风湿痹阻证、寒湿痹阻证的相对风险分别为8.33、250.00(P < 0.05)。结论 miR-150-5p、SOCS1 mRNA在RA患者中有差异性表达,且有靶向结合关系。miR-150-5p可能是RA的疾病诊断及中医风湿痹阻证、寒湿痹阻证证型诊断的潜在生物标志物。 相似文献
45.
Xue Yao Yan Zhang Jian Hao Hui-Quan Duan Chen-Xi Zhao Chao Sun Bo Li Bao-You Fan Xu Wang Wen-Xiang Li Xuan-Hao Fu Yong Hu Chang Liu Xiao-Hong Kong Shi-Qing Feng 《中国神经再生研究》2019,(3)
Ferroptosis is an iron-dependent novel cell death pathway. Deferoxamine, a ferroptosis inhibitor, has been reported to promote spinal cord injury repair. It has yet to be clarified whether ferroptosis inhibition represents the mechanism of action of Deferoxamine on spinal cord injury recovery. A rat model of Deferoxamine at thoracic 10 segment was established using a modified Allen's method. Ninety 8-week-old female Wistar rats were used. Rats in the Deferoxamine group were intraperitoneally injected with 100 mg/kg Deferoxamine 30 minutes before injury. Simultaneously, the Sham and Deferoxamine groups served as controls. Drug administration was conducted for 7 consecutive days. The results were as follows:(1) Electron microscopy revealed shrunken mitochondria in the spinal cord injury group.(2) The Basso, Beattie and Bresnahan locomotor rating score showed that recovery of the hindlimb was remarkably better in the Deferoxamine group than in the spinal cord injury group.(3) The iron concentration was lower in the Deferoxamine group than in the spinal cord injury group after injury.(4) Western blot assay revealed that, compared with the spinal cord injury group, GPX4, xCT, and glutathione expression was markedly increased in the Deferoxamine group.(5) Real-time polymerase chain reaction revealed that, compared with the Deferoxamine group, mRNA levels of ferroptosis-related genes Acyl-CoA synthetase family member 2(ACSF2) and iron-responsive element-binding protein 2(IREB2) were up-regulated in the Deferoxamine group.(6) Deferoxamine increased survival of neurons and inhibited gliosis. These findings confirm that Deferoxamine can repair spinal cord injury by inhibiting ferroptosis. Targeting ferroptosis is therefore a promising therapeutic approach for spinal cord injury. 相似文献
46.
Clinical clues for differential diagnosis between verruca plana and verruca plana‐like seborrheic keratosis
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Won‐Jeong Kim Won‐Ku Lee Margaret Song Hoon‐Soo Kim Hyun‐Chang Ko Byung‐Soo Kim Moon‐Bum Kim 《The Journal of dermatology》2015,42(4):373-377
Sometimes the clinical differentiation between verruca plana (VP) and VP‐like seborrheic keratosis (SK) could be challenged. However, there have been no studies on this issue to date. The aim of this study was to elucidate clinical and dermoscopic differences between these two diseases, and also to suggest a diagnostic algorithm of VP and VP‐like SK without skin biopsy. The patients who had lesions clinically considered as VP or VP‐like SK were the target of our study. We took clinical and dermoscopic photos with informed consent and conducted a questionnaire. All patients had their diagnoses confirmed by biopsy. Thirty‐three patients were enrolled in our study. Seventeen patients were finally diagnosed with VP (51.5%) and 16 patients with VP‐like SK (48.5%). In clinical findings, VP‐like SK showed significantly more scattered distribution than VP (P = 0.039), which exhibited more clustered or grouped distribution (P = 0.039). In dermoscopic findings, brain‐like appearance was more commonly observed in VP‐like SK (P = 0.003) whereas VP showed more red dots or globular vessels (P = 0.017) and even‐colored light brown to yellow patch (P < 0.001). Sex, onset age, the size of each lesion, location, color and shape showed no significant differences between them (P > 0.05). Based on our results, we suggest a diagnostic algorithm using Koebner's phenomenon, dermoscopic findings, distribution of each lesion and biopsy for multiple VP‐like lesions in adults, and we think it will be a very useful diagnostic tool in daily clinical dermatological practice. 相似文献
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49.
Ling Zhang Xue-Jun Shang Hong-Fei Li Yu-Qin Shi Wei Li Maria E Teves Zhi-Qiong Wang Gao-Feng Jiang Shi-Zhen Song Zhi-Bing Zhang 《Asian journal of andrology》2015,17(1):86-93
Mammalian spermatogenesis is a well-organized process of cell development and differentiation. Meiosis expressed gene 1 (MEIG1) plays an essential role in the regulation of spermiogenesis. To explore potential mechanisms of MEIG1''s action, a yeast two-hybrid screen was conducted, and several potential binding partners were identified; one of them was membrane occupation and recognition nexus repeat containing 3 (MORN3). MORN3 mRNA is only abundant in mouse testis. In the testis, Morn3 mRNA is highly expressed in the spermiogenesis stage. Specific anti-MORN3 polyclonal antibody was generated against N-terminus of the full-length MORN3 protein, and MORN3 expression and localization was examined in vitro and in vivo. In transfected Chinese hamster ovary cells, the antibody specifically crossed-reacted the full-length MORN3 protein, and immunofluorescence staining revealed that MORN3 was localized throughout the cytoplasm. Among multiple mouse tissues, about 25 kDa protein, was identified only in the testis. The protein was highly expressed after day 20 of birth. Immunofluorescence staining on mixed testicular cells isolated from adult wild-type mice demonstrated that MORN3 was expressed in the acrosome in germ cells throughout spermiogenesis. The protein was also present in the manchette of elongating spermatids. The total MORN3 expression and acrosome localization were not changed in the Meig 1-deficient mice. However, its expression in manchette was dramatically reduced in the mutant mice. Our studies suggest that MORN3 is another regulator for spermatogenesis, probably together with MEIG1. 相似文献
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