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排序方式: 共有4208条查询结果,搜索用时 15 毫秒
1.
目的研究急性支气管哮喘(BA)经特步他林并布地奈德治疗后白介素-5(IL-5)、白介素-10(IL-10)、肿瘤坏死因子-α(TNF-α)的变化。方法选取2016年1月至2020年12月商丘市中医院收治的122例急性BA患者的临床资料进行分析,根据不同治疗方法分为研究组(n=62,特步他林+布地奈德)和对照组(n=60,特步他林),比较两组临床疗效、肺功能[用力肺活量(FVC)、1秒用力呼气容器(FEV1)、1秒用力呼气容积占用力肺活量的百分比(FEV1/FVC%)、治疗前后IL-5、IL-10、TNF-α变化及不良反应情况。结果研究组总疗效(93.55%)高于对照组(81.67%),差异有统计学意义(P<0.05)。治疗后两组FVC、FEV1、FEV1/FVC%均较治疗前升高,且研究组高于对照组,差异具有统计学意义(P<0.05)。治疗后两组IL-5、TNF-α水平均降低,且研究组低于对照组,两组IL-10水平均上升,且研究组高于对照组,差异有统计学意义(P<0.05)。两组不良反应率比较差异无统计学意义(P>0.05)。结论特步他林与布地奈德联合治疗急性BA的效果显著,能够有效缓解患者的气道炎症反应,促进其肺功能的恢复,且联合用药无不良反应增加。  相似文献   
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PurposeThe variation in the immune response to Bartonella spp. infection in humans remains unclear. The present study compares the expression of selected interleukins, cytokines and cathelicidin (LL-37) in rheumatology clinic patients suffering from musculoskeletal symptoms with healthy blood donors. The patients had previously been tested for the presence of Bartonella henselae antibodies.MethodsGene expression of LL-37, interleukin (IL)-2, IL-4, IL-6, IL-12, interferon-(IFN)-γ, and tumor necrosis factor (TNF-α)-α was determined in blood samples using quantitative Polymerase Chain Reaction (qPCR). Statistical analysis was prepared with STATISTICA.ResultsStatistically significant differences in the mRNA levels of the tested cytokines (IFN-γ, TNF-α, IL-2, IL-4, IL-6, IL-12; p<0.0001) were observed between the healthy controls and patients; however, no difference was observed for LL37 mRNA (p ?= ?0.1974). No significant differences in mRNA expression were observed between IgG in anti-Bartonella seropositive and seronegative individuals (p>0.05). The only significant differences between the Bartonella spp. DNA positive and negative patients, indicated by PCR, were observed for TNF-α and IL-12 mRNA (p ?= ?0.0045 and p ?= ?0.0255, respectively).ConclusionA broadly similar immune response to the tested cytokines was observed among the participants irrespective of anti-Bartonella spp. IgG seropositivity. However, the Bartonella DNA-positive participants demonstrated significantly lower expression of IL-12 and TNF-α mRNA; this may indicate that these bacteria have a suppressive influence on the immune system.  相似文献   
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Objective: To evaluate the association of gene polymorphisms of the SNP of TNF-α gene -238G>A and IL-18 gene-607C>A with the development of hepatocellular carcinoma among Egyptian patients. Methods: One hundred and fifty patients were allocated to this study; eighty patients with hepatocellular carcinoma (Group A), seventy cancer-free HCV age, and sex-matched patients (Group B). We analyzed two Single nucleotide polymorphisms (SNPs) (TNF-α-238G>A and IL-18-607C>A) by real-time polymerase chain reaction using sequence-specific primers (PCR-SSP). Results: Significant higher risk of HCC was associated with genotype IL-18–607AA (p <0.001), OR: 5(2.188-11.47), allele IL-18 -607⁄A (P=0.001), OR: 2.1(1.32-3.3). A significant association was found between the size of HFL in the HCC group and different genotypes of IL18 genes (P=0.013) where 62.5% of patients with tumor size >5 cm carried the risky (AA) genotype on the other hand the SNP of TNF-α gene -238G>A showed no statistically significant association between the two groups. Conclusion: The SNP -607C>A in the IL18 gene was associated with increased HCC risk in Egyptian patients suggesting its use as a potential diagnostic non-invasive tool that allows to identify a new group of HCC patients at an earlier stage.  相似文献   
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目的探究心肌梗死合并肺部感染患者血清降钙素原(PCT)、白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)与心肌酶谱的关系及临床价值。方法选取2017年6月至2019年6月南阳市中心医院收治的急性心肌梗死患者160例(心梗组)作为研究对象,根据是否合并肺部感染分为合并感染组(n=42)和单纯心梗组(n=118),另选同期体检的健康人群80例作为对照组。检测所有受试者血清PCT、IL-6、TNF-α、谷草转氨酶(AST)、乳酸脱氢酶(LDH)、肌酸激酶(CK)及肌酸激酶同工酶(CKMB)水平,采用pearson相关分析急性心肌梗死合并肺部感染患者血清PCT、IL-6、TNF-α与心肌酶谱的关系,采用受试者工作特征(ROC)曲线分析血清PCT、IL-6及TNF-α水平对心肌梗死合并肺部感染患者的诊断价值。结果心梗组患者血清PCT、IL-6、TNF-α、AST、LDH、CK及CKMB水平均显著高于对照组,差异有统计学意义(P<0.05)。合并感染组患者血清PCT、IL-6、TNF-α水平明显高于对照组,差异有统计学意义(P<0.05)。pearson相关分析结果显示,在急性心肌梗死患者合并肺部感染患者体内,血清PCT、IL-6、TNF-α与AST、LDH、CK、CKMB均呈现显著正相关关系(P<0.05);ROC曲线分析结果显示,PCT、IL-6、TNF-α水平对于诊断急性心肌梗死患者合并肺部感染均有一定的价值(P<0.05),PCT+IL-6+TNF-α联合检测的AUC、灵敏度与准确度均高于PCT、IL-6及TNF-α单独检测(P<0.05)。结论急性心肌梗死合并肺部感染患者血清PCT、IL-6和TNF-α呈高表达水平,与血清心肌酶谱呈现一定正相关关系,且血清PCT、IL-6和TNF-α联合检测可提高急性心肌梗死患者的肺部感染检出率。  相似文献   
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BackgroundIschemia reperfusion (I/R) play an imperative role in the expansion of cardiovascular disease. Sinomenine (SM) has been exhibited to possess antioxidant, anticancer, anti-inflammatory, antiviral and anticarcinogenic properties. The aim of the study was scrutinized the cardioprotective effect of SM against I/R injury in rat.MethodsRat were randomly divided into normal control (NC), I/R control and I/R + SM (5, 10 and 20 mg/kg), respectively. Ventricular arrhythmias, body weight and heart weight were estimated. Antioxidant, inflammatory cytokines, inflammatory mediators and plasmin system indicator were accessed.ResultsPre-treated SM group rats exhibited the reduction in the duration and incidence of ventricular fibrillation, ventricular ectopic beat (VEB) and ventricular tachycardia along with suppression of arrhythmia score during the ischemia (30 and 120 min). SM treated rats significantly (P < 0.001) altered the level of antioxidant parameters. SM treatment significantly (P < 0.001) repressed the level of creatine kinase MB (CK-MB), creatine kinase (CK) and troponin I (Tnl). SM treated rats significantly (P < 0.001) repressed the tissue factor (TF), thromboxane B2 (TXB2), plasminogen activator inhibitor 1 (PAI-1) and plasma fibrinogen (Fbg) and inflammatory cytokines and inflammatory mediators.ConclusionOur result clearly indicated that SM plays anti-arrhythmia effect in I/R injury in the rats via alteration of oxidative stress and inflammatory reaction.  相似文献   
8.
Puerarin (PR), a natural isoflavone isolated from Chinese traditional plant pueraria lobata, has attracted considerable attention due to its important biological and pharmacological activities. However, its effects on lesion of peri-implant and related mechanism of action are still not clear, which require further investigation. In this study, we evaluated the effects of PR on polymethylmethacrylate (PMMA)-induced lesion of peri-implant in vitro and in vivo, and explored its possible mechanism of action. Our results indicated that PR could inhibit PMMA-induced osteoclastogenesis in RAW264.7 cells with a dose-dependent manner in vitro and effectively down-regulate mRNA and protein expressions of matrix metalloprotein 9 (MMP-9), tumor necrosis factor (TNF)-α, interleukin (IL)-6, and receptor activator of nuclear factor (NF)-κB (RANK), primarily via the suppression of NF-κB signaling. Furthermore, we found that PMMA induction could directly cause the phosphorylation of IκB and significantly promote the nuclear translocation of p65 in RAW264.7 cells. In other words, PR was able to dose-dependently attenuate the PMMA-induced nuclear translocation of p65 in RAW264.7 cells. In vivo, PR was observed to attenuate PMMA-induced osteoclastogenesis, osteolysis, mRNA expressions of receptor activator of nuclear factor (NF)-κB ligand (RANKL) and RANK, as well as protein levels of MMP-9, TNF-α, IL-6, and p65 in a murine calvarial osteolysis model. These findings suggested that PR might be a potential therapeutic drug to lesion of peri-implant, and provided new insights for understanding its possible mechanism.  相似文献   
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《Diabetes & metabolism》2019,45(5):473-479
AimThe association of non-alcoholic fatty liver disease (NAFLD) with insulin resistance (IR) is well established, yet little is known of their possible relationship with intrahepatic iron and serum tumour necrosis factor (TNF)-α concentrations in adults without diabetes. Thus, this study looked at the relationship of intrahepatic iron and serum TNF-α with intrahepatic triglycerides and IR in non-diabetic adults.MethodsIn this cross-sectional study of 104 healthy non-diabetic Caucasians, a quantitative magnetic resonance (MR) imaging T2 gradient-echo technique was used to measure hepatic iron, with 1H-MR spectroscopy used to measure hepatic triglycerides. HOMA-IR was calculated to determine IR.ResultsThe prevalence of hepatic iron overload (HIOL) was 26.6% in individuals with NAFLD vs. 0% in those without. IR was present in 87.5% of subjects with both NAFLD and HIOL, in 45.4% of those with NAFLD but not HIOL, and in 4.5% of those with neither. HOMA-IR was positively correlated with hepatic triglycerides (r = 0.56, P < 0.001) and hepatic iron (r = 0.52, P < 0.001), whereas serum TNF-α concentrations correlated with intrahepatic triglyceride levels (r = 0.28, P < 0.04), but not with intrahepatic iron. Hepatic triglycerides, serum TNF-α and age were the only significant determinants of IR in regression analyses.ConclusionIR is closely associated with intrahepatic triglycerides and, to a lesser extent, intrahepatic iron, with some interplay between them. High serum TNF-α concentrations may contribute to the association between NAFLD and IR, while increased hepatic triglycerides appear to be a determinant of the development of HIOL in non-diabetic subjects without haemochromatosis.  相似文献   
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BackgroundAutoimmune hepatitis is a chronic inflammatory disease, the abnormal immunological function is the main pathogenesis. Interleukin-34 is a newly identified cytokine that shares the same receptor as colony stimulating factor-1.MethodsWe used interleukin-34 knockout and wild-type mice in a Con A-induced hepatitis model and cocultured RAW264.7 macrophage cells with interleukin-34. We then detected associated inflammatory cytokine and chemokine levels to elucidate the role of interleukin-34.ResultsIn this study, we found that the loss of interleukin-34 resulted in higher sensitivity to Con A-induced hepatitis. RAW264.7 macrophage cells were able to differentiate to the M2 phenotype upon interleukin-34 stimulation.ConclusionsWe conclude that interleukin-34 may protect the liver from Con A-mediated hepatitis by driving M2 macrophage polarization and suppressing inflammation.  相似文献   
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