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角膜移植为治疗角膜盲的主要手段,而角膜移植排斥则是决定角膜植片存活时间和病人术后视力的关键。角膜得益于其特殊的眼前节“免疫赦免”状态,使得角膜移植能够在众多器官移植中享有极低的排斥率,然而排斥反应发生的风险依然存在。当机体处于遗传物质异常的特殊状态时,宿主将通过宏观调控“免疫赦免”状态对植片的保护作用或受体对移植物排异产生的有害作用,延迟或促进角膜移植排斥反应的发生,进而影响移植物的存活时间和透明度。该文综述与角膜移植排斥相关的多种全身性遗传疾病,总结全身性遗传疾病对角膜移植排斥的影响,浅析其发生的病理生理学机制以及诊疗的特殊性。 相似文献
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BackgroundTuberculosis meningitis (TBM) is the most severe form of tuberculosis, and currently lacks efficient diagnostic approaches. Metabolomics has the potential to differentiate patients with TBM from those with other forms of meningitis and meningitis-negative individuals. However, no systemic metabolomics research has compared the cerebrospinal fluid (CSF) of these patients.Methods1H nuclear magnetic resonance (NMR) was used for CSF metabolic profiling. Principal component analysis and orthogonal signal correction-partial least squares-discriminant analysis (OPLS-DA) were used to screen for important variables. The Human Metabolome Database was used to identify metabolites, and MetaboAnalyst 4.0 was used for pathway analysis and over-representation analysis.ResultsOPLS-DA modeling could distinguish TBM from other forms of meningitis, and several significantly changed metabolites were identified. Additionally, 23, 6, and 21 metabolites were able to differentiate TBM from viral meningitis, bacterial meningitis, and meningitis-negative groups, respectively. Pathway analysis indicated that these metabolites were mainly involved in carbohydrate and amino acid metabolism, and over-representation analysis indicated that some of these pathways were over-represented.ConclusionsThe metabolites identified have the potential to serve as biomarkers for TBM diagnosis, and carbohydrate and amino acid metabolism are perturbed in the CSF of patents with TBM. Metabolomics is a valuable approach for screening TBM biomarkers. With further investigation, the metabolites identified in this study could aid in TBM diagnosis. 相似文献
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A high salt diet (HSD) is among the most important risk factors for many diseases. One mechanism by which HSD aggravates cerebral ischemic injury is independent of blood pressure changes. The direct role of HSD in inflammation after cerebral ischemia is unclear. In this research, after twenty-one days of being fed a high salt diet, permanent focal ischemia was induced in mice via operation. At 12 h and 1, 3 and 5 days postischemia, the effects of HSD on the lesion volume, microglia polarization, aldose reductase (AR) expression, and inflammatory processes were analyzed. We report that in mice, surplus dietary salt promotes inflammation and increases the activation of classical lipopolysaccharide (LPS)-induced microglia/macrophages (M1). This effect depends on the expression of the AR protein in activated microglia after permanent middle cerebral artery ligation (pMCAL) in HSD mice. The administration of either the AR inhibitor Epalrestat or a p38-neutralizing antibody blocked the polarization of microglia and alleviated stroke injury.In conclusion, HSD promotes polarization in pro-inflammatory M1 microglia by upregulating the expression of the AR protein via p38/MAPK, thereby exacerbating the development of ischemia stroke. 相似文献
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目的:观察调神针刺法治疗不安腿综合征及其伴发睡眠障碍、焦虑情绪的临床疗效,为调神法在临床上的应用提供理论依据。方法:将60例患者随机分为观察组和对照组,每组30例。对照组予常规针刺治疗,穴取足三里、阳陵泉、悬钟等下肢局部腧穴;观察组在对照组取穴基础上加用百会、神庭、本神。两组均每日治疗1次,每周6d,1周为一疗程,连续治疗3个疗程。观察两组患者治疗前后国际不安腿综合征评定量表(IRLS)、匹兹堡睡眠质量指数(PSQI)和汉密尔顿焦虑量表(HAMA)评分变化。结果:治疗后两组患者IRLS评分、PSQI和HAMA总评分均较治疗前下降(P<0.05),且观察组治疗后各评分改善均优于对照组(P<0.05)。结论:在常规针刺基础上,调神针刺法可明显减轻不安腿综合征患者的下肢不适感,改善其睡眠障碍和焦虑情绪,疗效优于单纯常规针刺。 相似文献
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胃肠道间质瘤(gastrointestinal stromal tumor,GIST)是起源于胃肠道间叶组织的肿瘤,由于GIST存在恶性潜能,且多数GIST患者无明显临床症状,所以GIST的早期发现、诊断和治疗显得尤为重要。GIST通常在内窥镜、超声内镜(endoscopic ultrasound,EUS)检查中发现。GIST的诊断取决于形态学和免疫组织化学染色,因此组织样本的充足性是其关键。近年来,新的成像技术的应用和分子生物学的发展提高了GIST的诊断准确率,并为GIST的预后及辅助治疗提供了依据。 相似文献
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目的:探讨脂肪和肥胖相关基因(FTO)对异位子宫内膜间质细胞(eESCs)纤维化的影响及其机制。方法:采用实时定量聚合酶链反应(qRT-PCR)检测子宫内膜异位症(EMs)患者病变组织中m6A相关基因的表达;通过慢病毒载体过表达FTO,在eESCs中检测纤维化相关基因的表达;通过m6A2 Target数据库和MeRIP-qPCR预测和验证eESCs中FTO与Toll样受体2(TLR2)的关系;Western blot法检测p38的蛋白表达变化。结果:FTO在EMs中表达下调(P <0.05);FTO过表达促进eESCs纤维化并抑制其增殖(P <0.05);在eESCs中,FTO通过TLR2 的m6A修饰途径上调其蛋白水平(P <0.05);FTO在eESCs中经TLR2/p38 信号通路促进细胞纤维化(P <0.05)。结论:FTO在EMs中低表达,上调FTO可能通过TLR2/p38信号通路促进eESCs纤维化。 相似文献