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1.
Objective To investigate the effect of rosiglitazone on p38 mitogen-activated protein kinase (p38MAPK) pathway in polycystic kidney cyst-lining epithelial cells. Methods The cyst-lining epithelial cells (PKD cells) from human polycystic kidney were treated with rosiglitazone (10 μmol/L), peroxisome proliferator-activated receptor-γ (PPARγ) inhibitor GW9662 (10 μmol/L), rosiglitazone (10 μmol/L) +GW9662 (10 μmol/L), p38MAPK specific inhibitor SB203580 (10 μmol/L), SB203580 (10 μmol/L)+ rosiglitazone(10 μmol/L) for 2 hours followed by epidermal growth factor (EGF) stimulation. Protein expressions of p38, phuspho-p38 (p-p38) and proliferating cell nuclear antigen (PCNA) were detected by Western blot. p38 mRNA was examined by RT-PCR. Expression of c-fos and c-jun was observed by immunocytochemistry. Results (1) EGF markedly up-regulated the expressions of p38, p-p38, PCNA, c-fos anti c-jun compared with control group (P<0.01). (2) Compared with EGF treated group, rosiglitazone significantly reduced p38 activation and mRNA expression (P<0.01, respectively). Rosiglitazone, rosiglitazone+SB203580 could significantly down-regulated p-p38, PCNA, c-fos and c-jun expression (P<0.01, respectively) with no significant difference between these two groups. (3) GW9662 partially reversed the reduction effect of rosiglitazone. Conclusions Rosiglitazone can inhibit proliferation of autosomal dominant polycystic kidney disease cyst-lining epithelial cells partially through down-regulating p38 activation and reducing c-fos, c-jun and PCNA expression. The above effect of rosiglitazone is in part PPARγ-independcnt. 相似文献
2.
Objective To investigate the effect of rosiglitazone on p38 mitogen-activated protein kinase (p38MAPK) pathway in polycystic kidney cyst-lining epithelial cells. Methods The cyst-lining epithelial cells (PKD cells) from human polycystic kidney were treated with rosiglitazone (10 μmol/L), peroxisome proliferator-activated receptor-γ (PPARγ) inhibitor GW9662 (10 μmol/L), rosiglitazone (10 μmol/L) +GW9662 (10 μmol/L), p38MAPK specific inhibitor SB203580 (10 μmol/L), SB203580 (10 μmol/L)+ rosiglitazone(10 μmol/L) for 2 hours followed by epidermal growth factor (EGF) stimulation. Protein expressions of p38, phuspho-p38 (p-p38) and proliferating cell nuclear antigen (PCNA) were detected by Western blot. p38 mRNA was examined by RT-PCR. Expression of c-fos and c-jun was observed by immunocytochemistry. Results (1) EGF markedly up-regulated the expressions of p38, p-p38, PCNA, c-fos anti c-jun compared with control group (P<0.01). (2) Compared with EGF treated group, rosiglitazone significantly reduced p38 activation and mRNA expression (P<0.01, respectively). Rosiglitazone, rosiglitazone+SB203580 could significantly down-regulated p-p38, PCNA, c-fos and c-jun expression (P<0.01, respectively) with no significant difference between these two groups. (3) GW9662 partially reversed the reduction effect of rosiglitazone. Conclusions Rosiglitazone can inhibit proliferation of autosomal dominant polycystic kidney disease cyst-lining epithelial cells partially through down-regulating p38 activation and reducing c-fos, c-jun and PCNA expression. The above effect of rosiglitazone is in part PPARγ-independcnt. 相似文献
3.
<正> 三点神经阻滞麻醉包括:股神经、股外侧皮神经、坐骨神经,本组于一九八三年中应用此麻醉方法对下肢十八例患者施行了手术,现介绍如下: 一、解剖复习:1、股神经:第二三四脊神经向下在第四腰椎横突处组成腰丛,股神经是腰丛中最大的分支,位于腰大肌及髂 相似文献
4.
中心夜间透析和传统透析患者循环成纤维细胞生长因子23水平差异及影响因素 总被引:1,自引:1,他引:1
目的 比较中心夜间血液透析(INHD)和传统血液透析(CHD)患者循环成纤维细胞生长因子23(FGF23)水平差异并探讨影响患者FGF23水平的因素.方法 收集第二军医大学长征医院44例INHD及64例CHD患者空腹静脉血,测定患者钙、磷、全段甲状旁腺素(iPTH)、尿素清除指数(Kt/V)、25-羟维生素D、铁蛋白、血红蛋白、血脂、FGF23等指标并比较两组各指标的差异,采用多重线性回归分析探究FGF23的影响因素,Pearson相关性分析探究FGF23与血钙、血磷、钙磷乘积、iPTH、25-羟维生素D、Kt/V的相关性.结果 INHD患者血磷较CHD患者低(P<0.05),INHD透析充分性明显高于CHD,INHD患者循环FGF23水平低于CHD患者(P<0.05).FGF23与钙、磷、钙磷乘积相关(P<0.01),与iPTH及Kt/V不相关.结论 INHD比CHD更能有效改善慢性肾脏病-矿物质和骨异常(CKD-MBD)参数.钙磷乘积是血液透析患者FGF23水平的独立影响因素,INHD通过减少钙磷乘积降低血清FGF23水平可能是其改善患者临床预后的机制之一. 相似文献
5.
Objective To investigate the effect of rosiglitazone on p38 mitogen-activated protein kinase (p38MAPK) pathway in polycystic kidney cyst-lining epithelial cells. Methods The cyst-lining epithelial cells (PKD cells) from human polycystic kidney were treated with rosiglitazone (10 μmol/L), peroxisome proliferator-activated receptor-γ (PPARγ) inhibitor GW9662 (10 μmol/L), rosiglitazone (10 μmol/L) +GW9662 (10 μmol/L), p38MAPK specific inhibitor SB203580 (10 μmol/L), SB203580 (10 μmol/L)+ rosiglitazone(10 μmol/L) for 2 hours followed by epidermal growth factor (EGF) stimulation. Protein expressions of p38, phuspho-p38 (p-p38) and proliferating cell nuclear antigen (PCNA) were detected by Western blot. p38 mRNA was examined by RT-PCR. Expression of c-fos and c-jun was observed by immunocytochemistry. Results (1) EGF markedly up-regulated the expressions of p38, p-p38, PCNA, c-fos anti c-jun compared with control group (P<0.01). (2) Compared with EGF treated group, rosiglitazone significantly reduced p38 activation and mRNA expression (P<0.01, respectively). Rosiglitazone, rosiglitazone+SB203580 could significantly down-regulated p-p38, PCNA, c-fos and c-jun expression (P<0.01, respectively) with no significant difference between these two groups. (3) GW9662 partially reversed the reduction effect of rosiglitazone. Conclusions Rosiglitazone can inhibit proliferation of autosomal dominant polycystic kidney disease cyst-lining epithelial cells partially through down-regulating p38 activation and reducing c-fos, c-jun and PCNA expression. The above effect of rosiglitazone is in part PPARγ-independcnt. 相似文献
6.
7.
通心络胶囊治疗缺血性脑血管病35例 总被引:3,自引:0,他引:3
目的:观察通心络胶囊治疗缺血性脑血管病的临床观察。方法:将65例缺血性脑血管患者随机分为治疗组和对照组,其中治疗组35例,采用通心络胶囊(由石家庄以岭药业有限公司生产)治疗,口服每次4粒,日3次,对照组30例,给予尼莫地平片剂(由德国拜耳公司生产)治疗。口服每次30mg,日3次,均治疗4周为1疗程,采用单盲法给药。结果;通心络胶囊对缺血性脑血管病能明显改善临床症状及体征,治疗组显效17例(48.5%),有效15例(43.0%),无效3例(8.5%),总有效率91.5%;对照组显效12例(40%),有效12例(40%),无效6例(20%),总有效率80%;两组经统计学处理,有显著性差异,治疗组疗效明显优于对照组(P<0.05)。同时通心络胶囊可显著降低胆固醇,甘油三脂水平,改善血液流变学指标,并有91.5%的病例经过治疗后局部脑血流灌注显像(SPECT)显示局部脑血灌注损伤较治疗前明显改善。结论:通心络胶囊对缺血性脑血管病的气虚血瘀,脉络瘀阻等所致的半身不遂,口舌歪斜,语言不利,偏身麻木不仁等症状具有较好的疗效以及能降低血清胆固醇,甘油三酯,改善血液流变学指标和改善脑供血。 相似文献
8.
目的:探讨神经松动术结合常规康复训练对卒中后不同阶段偏瘫患者手功能恢复的疗效。方法:脑卒中偏瘫患者102例,根据卒中后时间分为1月组(46例),2月组(32例),3月组(24例);3组均行神经松动术结合常规康复训练3个月。于治疗前、训练1、3个月分别采用Fugl-Meyer上肢运动量表(FMA-U)、偏瘫上肢功能测试(FTHUE)、改良Barthel指数(m BI)和日常生活活动能力(ADL)评价偏瘫手精细动作、运动协调能力、感觉功能、日常生活能力等。于治疗后1、3月部分患者行静息状态下fMRI扫描检测中央前回第一运动区激活情况。结果:治疗前,3组各量表评分差异无统计学意义(P0.05)。治疗1、3个月后,各组FMA、FTHUE、MBI和ADL评分均较同组治疗前改善(P0.05);其中,1月组各评分统计学差异最显著(P0.01)。治疗1、3个月后,中央前回第一运动区信号强度明显升高,1月组最明显(P0.01)。结论:神经松动术结合常规康复训练能有效的促进脑卒中偏瘫患者手运动功能的恢复,对卒中早期患者疗效更好。 相似文献
9.
目的 研究syndecan-4对碱性成纤维细胞生长因子(bFGF)诱导人肾小球系膜细胞(HMC)增殖及细胞外基质(ECM)分泌的影响,并探讨syndecan-4-蛋白激酶Cα(PKCα)途径在其中的作用。 方法 免疫荧光方法观察syndecan-4在HMC上的表达。筛选有效的syndecan-4-siRNA转染HMC,噻唑蓝(MTT)比色法检测HMC在bFGF不同作用时间下的增殖差异;ELISA法检测细胞上清液中的Ⅰ、Ⅳ型胶原和纤连蛋白(FN)含量;荧光定量PCR观察syndecan-4和PKCα含量的变化。 结果 syndecan-4蛋白在HMC有表达。bFGF可促进HMC的增殖及FN、Ⅳ型胶原的分泌,使得每百万看家基因中PKCα拷贝数明显增加。转染syndecan-4 siRNA后,显著降低了HMC的增殖速度(48~60 h时点,P < 0.01)、ECM分泌(FN:24 h时点,P < 0.01,48~96 h,P < 0.05;Ⅳ型胶原:72~96 h时点,P < 0.05)及PKCα含量 (0 h时点,P < 0.05,12 ~48 h时点,P < 0.01)。 结论 syndecan-4参与调控bFGF诱导HMC的增殖及ECM分泌过程。syndecan-4-PKCα途径可能在其中扮演重要作用。 相似文献
10.
Objective To investigate the effect of rosiglitazone on p38 mitogen-activated protein kinase (p38MAPK) pathway in polycystic kidney cyst-lining epithelial cells. Methods The cyst-lining epithelial cells (PKD cells) from human polycystic kidney were treated with rosiglitazone (10 μmol/L), peroxisome proliferator-activated receptor-γ (PPARγ) inhibitor GW9662 (10 μmol/L), rosiglitazone (10 μmol/L) +GW9662 (10 μmol/L), p38MAPK specific inhibitor SB203580 (10 μmol/L), SB203580 (10 μmol/L)+ rosiglitazone(10 μmol/L) for 2 hours followed by epidermal growth factor (EGF) stimulation. Protein expressions of p38, phuspho-p38 (p-p38) and proliferating cell nuclear antigen (PCNA) were detected by Western blot. p38 mRNA was examined by RT-PCR. Expression of c-fos and c-jun was observed by immunocytochemistry. Results (1) EGF markedly up-regulated the expressions of p38, p-p38, PCNA, c-fos anti c-jun compared with control group (P<0.01). (2) Compared with EGF treated group, rosiglitazone significantly reduced p38 activation and mRNA expression (P<0.01, respectively). Rosiglitazone, rosiglitazone+SB203580 could significantly down-regulated p-p38, PCNA, c-fos and c-jun expression (P<0.01, respectively) with no significant difference between these two groups. (3) GW9662 partially reversed the reduction effect of rosiglitazone. Conclusions Rosiglitazone can inhibit proliferation of autosomal dominant polycystic kidney disease cyst-lining epithelial cells partially through down-regulating p38 activation and reducing c-fos, c-jun and PCNA expression. The above effect of rosiglitazone is in part PPARγ-independcnt. 相似文献