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1.
目的 研究金芪玉泉方治疗气阴两虚夹瘀型糖尿病肾病(DN)的疗效及其可能的机制。方法 82例辨证为气阴两虚夹瘀型糖尿病肾病患者随机分为治疗组、对照组各41例,均给予控制饮食、适量运动、降糖、降压等基础治疗,治疗组在此基础上加用金芪玉泉方,治疗周期为12周。比较2组治疗前后血糖、血脂谱、血压、肾功能、尿蛋白、血清胱抑素C(CysC)、尿足细胞标志蛋白(PCX)的变化。结果 2组患者治疗前后血糖、血脂、血压无明显变化;治疗组有效率60.97%,对照组有效率29.26%,2组比较差异有统计学意义(P<0.01);治疗组治疗后的尿白蛋白排泄率(UAER)、24 h尿蛋白定量、估算肾小球滤过率(eGFR)、CysC、PCX较治疗前显著改善(P<0.01),组间比较治疗组优于对照组(P<0.01)。结论 金芪玉泉方能通过保护足细胞功能显著减少气阴两虚夹瘀型糖尿病肾病患者的尿蛋白,改善肾脏功能。  相似文献   
2.
目的:分析肾脏足细胞特异蛋白podocalyxin(PCX) 的表达和尿足细胞数在紫癜性肾炎(Henoch-Schönlein purpura nephritis,HSPN) 病理进展过程中的变化。方法:56 例HSPN 患儿为病例组,根据肾脏病理改变分为4 组:HSPN II (IIa+IIb) 级组(n=10),III (IIIa+IIIb) 级组(n=21),Ⅳ级组(n=16) 和Ⅴ级组(n=9);另取非肾脏疾病死亡病例尸检切取的肾脏标本4 例作为正常肾组织对照组;同时收集8 例健康儿童的晨尿作正常尿液对照组。应用免疫荧光方法检测PCX 在4 例正常肾组织及56 例HSPN 肾组织中的表达,并对其结果进行定量分析;同时检测8 例健康儿童及56 例HSPN 患儿尿足细胞阳性的发生率和尿足细胞数。结果:在正常对照组和HSPN II (IIa+IIb) 级组的肾组织中,PCX 表达完整,2 组之间肾组织PCX 阳性面积占肾小球面积的百分比差异无统计学意义(P>0.05);在HSPN III(IIIa+IIIb) 级﹑Ⅳ级和Ⅴ级组的肾组织中,PCX 表达均有不同程度缺失,从III (IIIa+IIIb)~V 级其表达依次下降,各组间比较差异有统计学意义(P<0.01);病理分级在III (IIIa+IIIb)级以上的HSPN,尿中有PCX 的阳性表达,提示尿中有足细胞存在;肾组织PCX 荧光阳性面积占肾小球的百分比与尿中足细胞数呈负相关(r=-0.637,P<0.01)。结论:足细胞损伤在儿童HSPN 病理进展中发挥一定作用;可以在一定程度上反映HSPN 的病理损伤程度。  相似文献   
3.
目的探讨糖尿病患者尿足细胞标志蛋白(PCX)、血清胱抑素C(CysC)和高敏C反应蛋白(hs-CRP)的变化对早期糖尿病肾病的诊断价值。方法对糖尿病患者(110例)和正常人(45例)尿PCX、血清CysC、hs-CRP和肌酐(Cr)水平进行联合检测,观察上述指标与病程和病情的关系。结果糖尿病患者尿PCX、血清CysC和hs-CRP水平显著高于正常人,而血Cr水平与正常人比较无显著性差异。随着糖尿病病程的延长和肾脏病变的加重,上述各项指标增加更为明显。结论联合检测糖尿病患者尿PCX、血清CysC和hs-CRP有助于糖尿病肾病的早期诊断。  相似文献   
4.
目的 探讨原发性高血压患者不同高血压类型、脉压、脉压指数与早期肾损害的关系.方法 将原发性高血压患者182例作为高血压组,另选取体检健康者30例作为对照组.收集各组清晨首次清洁中段尿,测定尿微量白蛋白(mALB)、尿足细胞标志蛋白podocalyxin (PCX),计算比较高血压组和对照组及不同类型高血压组[单纯收缩期高血压(ISH)组,单纯舒张期高血压(IDH)组,收缩期高血压合并舒张期高血压(SDH)组]、不同脉压组(≤50 mmHg组、51 ~60 mmHg组、>60 mmHg组)、不同脉压指数组(<0.4%组、0.4% ~0.5%组、>0.5%组)mALB、PCX阳性率.结果 高血压组mALB、PCX阳性率较对照组高(P<0.05或<0.01);且高血压组PCX阳性率较mALB阳性率高(P<0.01).高血压类型中ISH组、SDH组mALB、PCX阳性率较IDH组高(P均<0.01);且ISH组、SDH组PCX阳性率较mALB阳性率高(P均<0.01).脉压>60 mmHg组mALB、PCX阳性率较≤50 mmHg组高(P均<0.01),且各不同脉压组PCX阳性率较mALB阳性率高(P均<0.05).脉压指数0.4% ~0.5%组、>0.5%组mALB、PCX阳性率较<0.4%组高(P<0.05或<0.01);且不同脉压指数组PCX阳性率较mALB阳性率高(P<0.01).结论 原发性高血压患者ISH、SDH比IDH更易发生肾损害,脉压和脉压指数越大肾损害的发生率越高,所以联合检测尿中mALB、PCX有利于早期诊断高血压肾损害.  相似文献   
5.
胡小云  张碧丽 《山东医药》2011,51(40):57-60,F0003
目的 探讨阿霉素肾病(ADN)大鼠肾组织nephrin及podocalyxin蛋白表达及泼尼松的干预作用。方法 24只雄性Wistar大鼠随机分成ADN组、泼尼松组、对照组,于0、4、8周测定大鼠24h尿蛋白(24hUP)、血清胆固醇(Cho)及白蛋白(Alb)。实验8周取肾组织观察病理形态改变,计算肾小球细胞外基质面积与肾小球面积之比(ECM/GA),评估肾脏病理积分。用免疫组织化学法观察肾小球nephrin、podocalyxin表达。结果 实验4周时,ADN组较之对照组24hUP、Cho升高(P〈0.05),Alb下降(P〈0.01)。实验8周时,泼尼松组较ADN组24hUP、Cho下降,ECM/GA及肾脏病理积分降低,nephrin、podoralyxin表达增多,Alb升高(P〈0.01)。ADN组nephrin、podlocalyxin表达与24hUP、Cho、ECM/GA及肾小球病理积分均呈负相关,与Alb呈正相关;nephrin与podocalyxin呈正相关。结论 nephrin、podocalyxin与蛋白尿的发生及发展密切相关。泼尼松能减轻ADN大鼠的蛋白尿及肾脏病理损害,其机制可能通过上调nephrin、podoralyxin表达来发挥肾保护作用。  相似文献   
6.
The leukocyte adhesion molecule, L-selectin, mediates the recruitment of lymphocytes to secondary lymphoid organs via interactions with specific ligands presented on high endothelial venules (HEV). Although the HEV-derived ligands for L-selectin are still incompletely defined, they share a common sialomucin-like structure which is thought to present clustered oligosaccharides to the lectin domain of L-selectin. Podocalyxin-like protein (PCLP) is a transmembrane sialomucin that is similar in structure to the well-characterized L-selectin ligand CD34. PCLP has been shown previously to be expressed on the foot processes of podocytes in the kidney glomerulus as well as on vascular endothelium at some sites. We have determined that PCLP is present on HEV, where it binds to both recombinant L-selectin and the HEV-specific monoclonal antibody MECA-79. Furthermore, purified HEV-derived PCLP is able to support the tethering and rolling of lymphocytes under physiological flow conditions in vitro. These results suggest a novel function for PCLP as an adhesion molecule and allow the definition of conserved structural features in PCLP and CD34, which may be important for L-selectin ligand function.  相似文献   
7.
BACKGROUND: We previously reported urinary podocytes to be a marker of glomerular injury. The aim of the present study was to determine whether cerivastatin, a newly developed, potent synthetic statin, affects proteinuria and urinary podocyte excretion in patients with chronic glomerulonephritis (CGN). METHODS: We randomly assigned 40 normotensive hypercholesterolemic patients with CGN to receive either cerivastatin 0.15 mg/day (n=20) or placebo (n=20). Subjects comprised 24 men and 16 women, with a mean age of 40.8+/-14.4 years; 27 had IgA nephropathy and 13 had non-IgA proliferative glomerulonephritis. Treatment was continued for 6 months. Plasma total cholesterol, HDL-cholesterol, LDL-cholesterol and triglycerides, urinary protein excretion and the number of podocytes were measured before treatment and at 3 and 6 months after treatment. RESULTS: After 6 months, a significant reduction in total cholesterol (P<0.001), LDL-cholesterol (P<0.001) and triglycerides (P<0.05), and a significant increase in HDL-cholesterol (P<0.001) were observed in the group treated with cerivastatin. Urinary protein excretion decreased from 1.8+/-0.6 to 0.8+/-0.4 g/day, (P<0.01) in this group, and urinary podocyte excretion decreased from 1.6+/-0.6 to 0.9+/-0.4 cells/ml (P<0.01). However, placebo showed little effect on these lipid levels, urinary protein excretion and urinary podocyte excretion. The differences between the cerivastatin group and the placebo group were significant (cholesterol, P<0.001; LDL-cholesterol, P<0.001; triglycerides, P<0.05; HDL-cholesterol, P<0.001; urinary protein, P<0.01; and urinary podocytes, P<0.01). CONCLUSION: Statins such as cerivastatin may be beneficial for restoration of injured podocytes in patients with CGN and hypercholesterolaemia.  相似文献   
8.
In the 24 October 2006 issue of PNAS, Alexander and colleagues[1] describe the results of a systematic search for thrombocytopenicmice generated by large-scale mutagenesis. Amongst 3523 mice,one pedigree indeed exhibited 50% reduction in platelet counts.Apart from thrombocytopenia, the only other notable featureof these mice was prominent renal disease (albuminuria/proteinuria,glomerulosclerosis and tubulointerstitial inflammatory infiltration)leading to uraemia and death at around 200 days after birth.This renal disease was not immune mediated, since it persistedin mutant mice crossed to  相似文献   
9.
目的:探讨来氟米特对慢性肾小球肾炎患者尿足细胞标志蛋白( PCX)排泄的影响。方法选取慢性肾小球肾炎患者63例和健康体检者30例,将慢性肾小球肾炎患者随机分为来氟米特组和常规组,健康体检者为对照组,采用双抗体夹心酶联免疫吸附法( ELISA)测定尿液中PCX水平,分别检测治疗前、治疗后4周及治疗后12周尿PCX水平的变化,并结合24小时尿蛋白定量( UTP)、血肌酐、尿素氮、血白蛋白、血脂等指标进行统计学分析。结果来氟米特组和常规组治疗前尿PCX水平与对照组比较差异均有统计学意义( P<0.05)。2组治疗前尿PCX水平与UTP无相关性,治疗后尿PCX水平均较治疗前下降;来氟米特组较常规组治疗4周后PCX水平差异无统计学意义,治疗12周后差异有统计学意义。结论慢性肾炎患者尿中PCX的表达较正常人明显增多,与UTP无相关性。来氟米特可以减少肾脏足细胞的损伤,起到保护肾脏的作用。  相似文献   
10.
Epithelial–mesenchymal transition (EMT) plays an important role in the progression of lung carcinoma. Podocalyxin (PODXL), which belongs to the CD34 family and regulates cell morphology, has been linked to EMT in lung cancer, and PODXL overexpression is associated with poor prognosis in several different classes of cancers. The aim of this study was to clarify the role of PODXL overexpression in EMT in lung cancer, and to determine the prognostic value of PODXL overexpression in tumors from lung cancer patients. The morphology, EMT marker expression, and migration and invasion abilities of engineered A549 PODXL‐knockdown (KD) or PODXL‐overexpression (OE) lung adenocarcinoma cells were examined. PODXL expression levels were assessed by immunohistochemistry in 114 human clinical lung adenocarcinoma specimens and correlated with clinical outcomes. PODXL‐KD cells were epithelial in shape, whereas PODXL‐OE cells displayed mesenchymal morphology. Epithelial markers were upregulated in PODXL‐KD cells and downregulated in PODXL‐OE cells, whereas mesenchymal markers were downregulated in the former and upregulated in the latter. A highly selective inhibitor of phosphatidylinositol 3‐kinase‐Akt signaling attenuated EMT of PODXL‐OE cells, while a transforming growth factor inhibitor did not, suggesting that PODXL induces EMT of lung adenocarcinoma cells via the phosphatidylinositol 3‐kinase pathway. In lung adenocarcinoma clinical specimens, PODXL expression was detected in minimally invasive and invasive adenocarcinoma, but not in non‐invasive adenocarcinoma. Disease free survival and cancer‐specific survival were significantly worse for patients whose tumors overexpressed PODXL. PODXL overexpression induces EMT in lung adenocarcinoma and contributes to tumor progression.  相似文献   
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