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1.
 目的 评价尿中性粒细胞明胶酶相关脂质运载蛋白(NGAL)、肾损伤分子1(KIM-1)和N-乙酰-β-D氨基葡萄糖苷酶(NAG)在不同基础疾病导致急性肾损伤(AKI)儿童中的改变及其临床意义。方法 将在我院门诊和急诊进行肾功能检测且既往1年内曾因不同原因在我院进行过肾功能检测的无慢性肾脏疾病的患儿纳入本研究。入选患儿留取5 mL尿液。采用ELISA方法检测尿NGAL和KIM-1,记录患儿原发疾病、住院患儿的住院时间。以AKI pRIFLE为分期标准,将诊断为AKI的患儿分为AKI-R组、AKI-I组和AKI-F组。结果 共552名患儿纳入本研究,其中住院患儿316名,诊断为AKI的患儿59名。AKI组患儿尿NGAL、KIM-1和NAG值明显高于肾功能正常组(P<0.05),在血肌酐未升高前这3项指标均已升高,且随着肾损伤的加重升高更明显。住院AKI患儿中,AKI越严重,住院时间越长。结论 儿童AKI的发生不仅源于肾脏疾病本身,还可源于其他系统疾病。尿NGAL和KIM-1在AKI早期已经明显升高,在AKI诊断上较血肌酐敏感,尿NGAL和KIM-1较尿NAG值升高显著,可以作为儿童不同基础疾病导致AKI的早期诊断指标。  相似文献   
2.
水肿是小儿常见的症状及体征,除常见的肾性水肿外,还可由多病因引起,某些病因难以诊断易误诊或漏诊。介绍小儿水肿的鉴别诊断,以期对小儿水肿的临床诊断提供帮助。  相似文献   
3.
血尿是临床常见的症状,掌握科学的血尿诊断思路,合理地采用各种辅助检查,综合分析,才能正确地诊断血尿,减少漏诊和误诊。  相似文献   
4.
目的:通过观察谷氨酰胺(glutamine, Gln)对内毒素血症幼年大鼠肾脏信号转导通路ERK-2、p38及其mRNA表达的影响,探讨谷氨酰胺在大鼠内毒素血症中通过干预肾脏ERK-2以及p38信号转导途径来保护肾脏的机制。方法:选健康18日龄Wistar大鼠121只,按腹腔注射药物不同分为:0 h对照组(生理盐水,n=11), 内毒素组(LPS,n=55),谷氨酰胺组(Gln, n=55); 后两组又分为2,4,6,24及72 h共5个时间点,每个时间点11只,在各指定时间点分别将大鼠断头分离肾脏,8只用逆转录 聚合酶链反应(RT-PCR)方法测定ERK-2以及p38的mRNA的表达,另3只取肾组织后用甲醛固定,制成石蜡切片,用免疫组化方法确定ERK-2以及p38蛋白质的表达。结果:LPS组各时点ERK-2 mRNA, p38MAPK mRNA, ERK-2, p38MAPK表达均较对照组增强,最高点在 6 h,差异有显著性,P<0.01;Gln组各时点ERK-2 mRNA, p38MAPK mRNA, ERK-2, p38MAPK表达趋势与LPS组一致,但明显低于LPS组,P<0.05或P<0.01。结论:ERK及p38在内毒素血症表达均明显增强。谷氨酰胺可使其表达下调,从而减轻肾脏损伤。[中国当代儿科杂志,2009,11(4):301-305]  相似文献   
5.
目的 观察原发性肾病综合征(PNS)患儿采用槐杞黄颗粒辅助治疗前后T调节细胞(Treg细胞)及IL-10水平的变化.方法 PNS患儿59例.随机将其分为泼尼松联合槐杞黄颗粒治疗组32例(A组),单纯泼尼松治疗组27例(B组).观察治疗前和治疗3个月其外周血CD4+CD25+Foxp3+Treg(Foxp3+Treg)细胞数量及IL-10的变化.同时选取体检健康儿童10名为健康对照组(C组).采用流式细胞仪检测PNS患儿外周血单核细胞中Foxp3+Treg细胞/CD4+细胞的百分比,结合血常规计算Treg细胞数量,采用酶联免疫吸附法测定其血浆IL-10水平.结果 1.Foxp3+Treg细胞:治疗前A、B组血Foxp3+Treg细胞/CD4+细胞百分比、Foxp3+Treg细胞数量均低于C组(Pa<0.01);治疗3个月A、B组Treg细胞/CD4+百分比较治疗前均明显升高(Pa<0.01),但仍低于C组(Pa<0.01),A、B两组间差异无统计学意义;治疗3个月A组Foxp3+Treg细胞数目较治疗前及B组治疗后明显升高(P<0.01),但仍显著低于C组(P<0.01),B组Foxp3+Treg数目较治疗前升高不明显(P>0.05).2.治疗前A、B组IL-10水平均低于C组(Pa<0.05),A组治疗3个月IL-10水平明显高于B组(P<0.01),仍未达C组水平.结论 Foxp3+Treg细胞数量下降及分泌IL-10减少可能参与PNS的发病,而槐杞黄颗粒可通过提高Foxp3+Treg细胞数量而发挥PNS患儿的免疫调节作用.  相似文献   
6.
目的探讨表没食子儿茶素没食子酸酯(EGCG)对肾小管上皮细胞转分化的作用机制。方法培养大鼠肾小管上皮细胞株NRK-52E,将其分成4组。1组:正常对照组(N),以DMEM培养液为空白对照。2组:转化生长因子(TGF-β1)诱导组;3组:EGCG200μg/L干预组;4组:EGCG400μg/L干预组。各细胞组在作用48 h后,应用免疫组化检测平滑肌肌动蛋白(α-SMA)和角蛋白(CK-18),Western-blot分析胞浆蛋白细胞周期素D1(Cyclin D1)、基质金属蛋白酶9(MMP9)含量,实时荧光定量PCR法测Cyclin D1、MMP9mRNA的相对表达量。结果 NRK细胞被TGF-β1诱导48 h后,胞浆中出现α-SMA蛋白高表达,CK-18蛋白表达明显减少;Cyclin D1、MMP9蛋白及其mRNA出现了高表达;EGCG干预组上述改变明显减轻。结论 EGCG以剂量依赖方式抑制TGF-β1诱导的NRK细胞的转分化,其机制可能是通过抑制Cyclin D1、MMP9蛋白及mRNA表达而实现的。  相似文献   
7.
Objective To investigate the mechanism of the kidney injure in the newborn rats with endotoxemia.Methods Eighty Wistar rats aged 7 days were randomly divided into 2 groups:control group (intraperitoneal injection of saline of 0.1 ml;n = 40),lipopolysaccharide(LPS) group(intraperitoneal injection of LPS of 5 mg/kg;n =40).The rats in either group were killed at 1 h,4 h,8 h and 12 hours after intraperitoneal injection,respectively.The expressions of NF-κB and TGF-β1 in the kidney were detected by using the immunohistochemical assay.Renal ultrastructural changes was observed with a CM100 Philips electron microscope.Results The NF-κB in control group had no expression.NF-κB in LPS group mainly expressed in the renal tubular epithelial cell,increased at 1 h after test and peaked at 8 h,and slightly descended at 12 h.The expression of TGF-β1 in control group was slight,and had not show significant difference from control group at 1 h,4 h and 8 h,but significantly higher than that in control group at 12 h.In LPS group,newborn rat renal glomerular basement membrane was complete,part epithelial cell foot processes were fused and renal tubules epithelial cell mild mitochondria vacuolization was found at 4 h.Renal glomeruli epithelial cell foot processes obvious confluenced,quantities of mesangial cells mitochondria vacuole,and renal tubules epithelial cell mitochondria expanded to bubbles at 12 h.Conclusion The NF-κB involves in the pathogenesis of kidney damage induced by endotoxemia,but TGF-β1 may help to repair the damaged kidney,and may repress the production of NF-κB.  相似文献   
8.
舒普深与头孢哌酮治疗小儿肺炎疗效对比分析   总被引:2,自引:0,他引:2  
观察舒普深与头孢哌酮对68例小儿肺炎的治疗效果.患者随机抽样分为两组,分别用舒普深或头孢哌酮治疗.舒普深组治疗小儿肺炎有效率为94.1%,头孢哌酮组为79.4%,两组差异显著.舒普深在治疗小儿肺炎中疗效高于头孢哌酮.  相似文献   
9.
Objective To investigate the mechanism of the kidney injure in the newborn rats with endotoxemia.Methods Eighty Wistar rats aged 7 days were randomly divided into 2 groups:control group (intraperitoneal injection of saline of 0.1 ml;n = 40),lipopolysaccharide(LPS) group(intraperitoneal injection of LPS of 5 mg/kg;n =40).The rats in either group were killed at 1 h,4 h,8 h and 12 hours after intraperitoneal injection,respectively.The expressions of NF-κB and TGF-β1 in the kidney were detected by using the immunohistochemical assay.Renal ultrastructural changes was observed with a CM100 Philips electron microscope.Results The NF-κB in control group had no expression.NF-κB in LPS group mainly expressed in the renal tubular epithelial cell,increased at 1 h after test and peaked at 8 h,and slightly descended at 12 h.The expression of TGF-β1 in control group was slight,and had not show significant difference from control group at 1 h,4 h and 8 h,but significantly higher than that in control group at 12 h.In LPS group,newborn rat renal glomerular basement membrane was complete,part epithelial cell foot processes were fused and renal tubules epithelial cell mild mitochondria vacuolization was found at 4 h.Renal glomeruli epithelial cell foot processes obvious confluenced,quantities of mesangial cells mitochondria vacuole,and renal tubules epithelial cell mitochondria expanded to bubbles at 12 h.Conclusion The NF-κB involves in the pathogenesis of kidney damage induced by endotoxemia,but TGF-β1 may help to repair the damaged kidney,and may repress the production of NF-κB.  相似文献   
10.
Objective To investigate the mechanism of the kidney injure in the newborn rats with endotoxemia.Methods Eighty Wistar rats aged 7 days were randomly divided into 2 groups:control group (intraperitoneal injection of saline of 0.1 ml;n = 40),lipopolysaccharide(LPS) group(intraperitoneal injection of LPS of 5 mg/kg;n =40).The rats in either group were killed at 1 h,4 h,8 h and 12 hours after intraperitoneal injection,respectively.The expressions of NF-κB and TGF-β1 in the kidney were detected by using the immunohistochemical assay.Renal ultrastructural changes was observed with a CM100 Philips electron microscope.Results The NF-κB in control group had no expression.NF-κB in LPS group mainly expressed in the renal tubular epithelial cell,increased at 1 h after test and peaked at 8 h,and slightly descended at 12 h.The expression of TGF-β1 in control group was slight,and had not show significant difference from control group at 1 h,4 h and 8 h,but significantly higher than that in control group at 12 h.In LPS group,newborn rat renal glomerular basement membrane was complete,part epithelial cell foot processes were fused and renal tubules epithelial cell mild mitochondria vacuolization was found at 4 h.Renal glomeruli epithelial cell foot processes obvious confluenced,quantities of mesangial cells mitochondria vacuole,and renal tubules epithelial cell mitochondria expanded to bubbles at 12 h.Conclusion The NF-κB involves in the pathogenesis of kidney damage induced by endotoxemia,but TGF-β1 may help to repair the damaged kidney,and may repress the production of NF-κB.  相似文献   
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