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51.
56例Ⅲ度房室传导阻滞和病窦综合征病人根据起搏部位分为:右室心尖部起搏组(RVA组),右室高位室间隔起搏组(RHVS组)。起搏后3个月左室射血分数、每搏输出量明显高于RVA组,B型脑利钠肽、QRS波时限明显低于RVA起搏。结论:HRVS起搏对心功能的影响优于RVA组,可能是一个较为理想的起搏部位。  相似文献   
52.
大柴胡汤对急性坏死性胰腺炎大鼠模型的影响   总被引:1,自引:0,他引:1  
目的:研究大柴胡汤对急性坏死性胰腺炎(ANP)大鼠的作用.方法:54只雄性SD大鼠随机分为假手术组、ANP组和大柴胡汤组,制模后3 h、6 h、12 h时间点分别处死6只.记录腹水量,测定血清淀粉酶,HE染色观察胰腺、肺、肠壁组织病理改变;按Schmidt方法对组织病理改变进行严重度评分.伊文思蓝(EB)染料血管外渗法检测组织毛细血管通透性.结果:大柴胡汤组腹水量明显低于ANP组(P<0.05);各时间点ANP组血清淀粉酶水平高于假手术组(P<0.01);ANP组胰腺、肺、肠壁组织EB含量均显著高于假手术组(P<0.05);大柴胡汤组血清淀粉酶水平较ANP组显著降低(P<0.05);大柴胡汤组胰腺、肺、肠壁组织病理改变较ANP组减轻;胰腺、肺、肠壁组织EB含量均显著低于ANP组(P<0.05).结论:大柴胡汤预处理可以改善ANP大鼠模型的疾病严重程度,其机理可能与降低毛细血管通透性有关.  相似文献   
53.
目的探讨老年高脂血症性急性胰腺炎(HLAP)的临床特点,同时考察C反应蛋白(CRP)、降钙素CT以及降钙素原(PCT)在HLAP严重程度评价中的作用及其对HLAP预后评估的临床价值。方法选取上海中医药大学附属普陀医院2012年7月至2015年7月收治的148例老年胰腺炎患者,其中,76例HLAP患者为观察组,72例胆源性急性胰腺炎(BAP)患者为对照组。对两组患者的临床特征进行比较分析;同时,总结收治的76例HLAP患者,按诊断标准分为急性轻症胰腺炎组(MAP)和急性重症胰腺炎组(SAP)两组,比较两组患者降脂前后Ranson和CT评分,以及两组患者血脂和CRP水平。结果在临床评分相同的情况下,与BAP患者比较,HLAP患者糖尿病发生率、脂肪肝发生率和血脂水平均较高,肝功能受损程度和血清淀粉酶水平较低,差异均有统计学意义(P<0.05)。与MAP组比较,SAP组患者的CRP、甘油三脂均显著增高(P<0.05)。结论与一般急性胰腺比较,老年HLAP具有血脂高、病情重、复发率高、并发症多、血清淀粉酶低等特点,CRP联合高血脂可作为评判HLAP严重程度的评价指标。CRP、CT以及PCT对老年HLAP的预后评估具有方便、可行、可较早诊断等临床价值。  相似文献   
54.
本研究探讨miR-16在T淋巴母细胞淋巴瘤/急性淋巴母细胞白血病(T-LBL/ALL)中的表达及其与预后的关系.应用免疫组织化学法对宜共市人民医院血液科有详细随访资料的38例T-LBL/ALL石蜡标本进行CD3、cCD3、CD10、CD20、CD34、CD43、CD99、TdT、PAX-5、BCL-2和Ki67免疫组织化学标记检测,采用real-time RT-PCR方法检测miR-16的表达水平,以15例淋巴结反应性增生作为对照.结果表明:38例T-LBL/ALL中TdT阳性率最高(94.7%),CD34阳性最低(22.1%),PAX-5及CD20为阴性.在39.5%病例中Ki67大于80%.与淋巴结反应性增生相比较,miR-16在T-LBL/ALL中表达上调,其表达量是淋巴结反性增生的4.87倍(P<0.05).T-LBL中miR-16高表达组总体生存率下降(P<0.05).BCL-2蛋白表达阳性组预后优于阴性组预后(P<0.05).miR-16表达与BCL-2蛋白存在相关性(r=0.51,P<0.05).结论:在T-LBL/ALL中miR-16的高表达组总体生存率明显高于低表达组,提示miR-16可能与预后有相关性,而BCL-2蛋白表达阳性组预后好于阴性组,可能也是一种影响预后的因素.  相似文献   
55.
紧密连接是维持黏膜上皮机械屏障和通透性的重要结构.claudin是紧密连接的骨架蛋白,形成屏障且构成特定的孔道,调节紧密连接的密封性和选择性通透,对维持细胞内外稳态起着至关重要的作用.近年来研究发现,急性胰腺炎与claudin异常表达和结构破坏密切相关.因此,阐明claudin蛋白与急性胰腺炎之间的关系,对揭示胰腺炎病理基础,以及疾病的诊断和治疗都有重要意义.  相似文献   
56.
蕲蛇汤治疗结节性皮肤血管炎42例临床观察   总被引:1,自引:0,他引:1  
结节性皮肤血管炎是皮肤科常见病多发病。该病多反复发作,迁延不愈,给患者带来很多痛苦。本组选用蕲蛇汤治疗结节性皮肤血管炎42例,取得较好疗效,报告如下。1 资料和方法1.1 病例 42例为门诊病人,根据临床表现及病理变化确诊  相似文献   
57.
Objective To study the expression of aquaporin 1 ( AQP1 ) in pancreas and its pathogenic role in rats with experimental acute necrotizing pancreatitis (ANP). Methods Forty-eight male Sprague-Dawley rats were randomly divided into two groups : control group ( n = 24 ) and ANP group ( n = 24). Six rats in each group were sacrificed at 3,6,12 and 18 h after induction of experimental models. Quantity of ascites and levels of serum amylases were measured at each time point. Serum AQPI was determined by ELISA. Pathological changes of pancreatic tissues were examined. Capillary permeability in pancreatic tissues was tested by Evans Blue (EB) extravasation method. AQPI expression in pancreatic tissues was detected by immunohistochemieal staining, Western blot and fluorescence quantitative polymerase chain reaction (FQ-PCR). Results (1) Serum amylase level at 3,6,12, and 18 h in control group was (1308±759) ,(1077±508), (1325±761),(1328±762) U/L,and that in ANP group was (9102± 2199), (8799±1634), (9398±1473), (9484±862) U/L respectively. The concentration of EB in pancreatic tissues at each time point in control group was (205.61±32.99), (141.46±27.18 ), (96.94± 26.79), (61.43±24.82) mg/L, and that in ANP group was ( 273.59±23.47 ), ( 253.51±31.68 ), (221.15±73.68 ), (185.28±42.35) ,respectively. There was significandy difference between two groups. Serum AQP1 level in control group at each point was ( 74.08±11.80), (78.49±9.06 ), (75.77± 7.37 ), ( 72.75±13.87 ) mg/L, and that in AN P group was (73.29±9.61 ), ( 62.85±7.28 ), (62.07± 4.39 ), (46.33±11.91 ) mg/L, respectively ( P < 0.01 ). ( 2 ) Protein expression of AQPI in pancreatic tissues detected by immunohistochemical staining in control group at each time point was 114.13±7.92, 122.39±7.99,145.98±6.48,113.98±6.48, and that in ANP group was 80.07±14.89,110.54± 4.45,103.77±10.48,99.18±6.95;Protein expression of AQP1 in pancreatic tissues detected by Western blot in control group at each time point was 1.19±0.33,1.02±0.25,0.90±0.33,1.06±0.20,and that in ANP group was 0.83±0.11,0.96±0.21,0. 58±0.28,0.72±0.14, respectively ( P < 0.05 ). ( 3 ) The mRNA level of AQP1 gene expressed in pancreas in control group at each time point was 0.91±0.22,1.01±0.83,0.48±0.23,0.61±0.51,and that in ANP group was 2.13±0.63,2.02±1.40, 2.07±0.86,2.49±2.47,respectively (P<0.01).Condusion The expression of AQP1 wasdown-reg-ulated in pancreas in rats with ANP,which might could play an important role in the pathogenesis of capil-lary leak syndrome.  相似文献   
58.
Objective To study the expression of aquaporin 1 ( AQP1 ) in pancreas and its pathogenic role in rats with experimental acute necrotizing pancreatitis (ANP). Methods Forty-eight male Sprague-Dawley rats were randomly divided into two groups : control group ( n = 24 ) and ANP group ( n = 24). Six rats in each group were sacrificed at 3,6,12 and 18 h after induction of experimental models. Quantity of ascites and levels of serum amylases were measured at each time point. Serum AQPI was determined by ELISA. Pathological changes of pancreatic tissues were examined. Capillary permeability in pancreatic tissues was tested by Evans Blue (EB) extravasation method. AQPI expression in pancreatic tissues was detected by immunohistochemieal staining, Western blot and fluorescence quantitative polymerase chain reaction (FQ-PCR). Results (1) Serum amylase level at 3,6,12, and 18 h in control group was (1308±759) ,(1077±508), (1325±761),(1328±762) U/L,and that in ANP group was (9102± 2199), (8799±1634), (9398±1473), (9484±862) U/L respectively. The concentration of EB in pancreatic tissues at each time point in control group was (205.61±32.99), (141.46±27.18 ), (96.94± 26.79), (61.43±24.82) mg/L, and that in ANP group was ( 273.59±23.47 ), ( 253.51±31.68 ), (221.15±73.68 ), (185.28±42.35) ,respectively. There was significandy difference between two groups. Serum AQP1 level in control group at each point was ( 74.08±11.80), (78.49±9.06 ), (75.77± 7.37 ), ( 72.75±13.87 ) mg/L, and that in AN P group was (73.29±9.61 ), ( 62.85±7.28 ), (62.07± 4.39 ), (46.33±11.91 ) mg/L, respectively ( P < 0.01 ). ( 2 ) Protein expression of AQPI in pancreatic tissues detected by immunohistochemical staining in control group at each time point was 114.13±7.92, 122.39±7.99,145.98±6.48,113.98±6.48, and that in ANP group was 80.07±14.89,110.54± 4.45,103.77±10.48,99.18±6.95;Protein expression of AQP1 in pancreatic tissues detected by Western blot in control group at each time point was 1.19±0.33,1.02±0.25,0.90±0.33,1.06±0.20,and that in ANP group was 0.83±0.11,0.96±0.21,0. 58±0.28,0.72±0.14, respectively ( P < 0.05 ). ( 3 ) The mRNA level of AQP1 gene expressed in pancreas in control group at each time point was 0.91±0.22,1.01±0.83,0.48±0.23,0.61±0.51,and that in ANP group was 2.13±0.63,2.02±1.40, 2.07±0.86,2.49±2.47,respectively (P<0.01).Condusion The expression of AQP1 wasdown-reg-ulated in pancreas in rats with ANP,which might could play an important role in the pathogenesis of capil-lary leak syndrome.  相似文献   
59.
目的:比较原发性骨髓增生异常综合征(MDS)患者WHO(2001)分型与FAB分型的IPSS染色体核型分析及预后的相关性分析。方法:经FAB标准确诊的原发MDS的患者重新按WHO标准分型,对2种结果的IPSS及染色体异常与各亚型的关系进行分析。结果:按FAB分型各亚型的IPSS及染色体异常无显著性差异,按WHO分型的难治性细胞减少伴多系增生异常(RCMD)与难治性贫血(RA)患者染色体异常率有统计学意义(66.6%,41.7%,P<0.01),RAEB-2高危组比例明显高于RAEB-1组(25%,0%,P<0.01)。结论:原发MDS的WHO分型与FAB分型相比,前者与预后的相关性更好。  相似文献   
60.
目的 探讨水通道蛋白1( aquaporin 1,AQP1)对急性坏死性胰腺炎(acute necrotizing pancreatitis,ANP)大鼠肠道毛细血管内皮屏障功能障碍的影响.方法 160只雄性Sprague-Dawley 大鼠随机分为对照组、ANP组、生理盐水组、地塞米松组及乙酰唑胺组,制模后3、6、12、18h各时间点分别处死8只.记录腹水量,测定血清淀粉酶;HE染色观察肠壁组织病理改变;电镜观察肠壁组织超微结构;伊文思兰染料血管外渗法检测肠壁组织毛细血管通透性;荧光定量PCR检测肠壁组织AQP1 mRNA的表达;Western blot法检测肠壁组织AQP1蛋白表达.结果 (1)ANP组血清淀粉酶水平显著高于对照组,地塞米松组低于ANP组,乙酰唑胺组高于ANP组(P<0.05);(2)ANP组肠壁组织伊文思兰含量明显高于对照组,地塞米松组低于ANP组,乙酰唑胺组高于ANP组(P<0.05);(3)ANP组肠壁组织AQP1 mRNA表达显著低于对照组,地塞米松组表达显著高于ANP组,乙酰唑胺组显著低于ANP组(P<0.05);(4)ANP组肠壁组织AQP1蛋白含量明显低于对照组,地塞米松组高于ANP组,乙酰唑胺组低于ANP组(P<0.05).结论 AQP1在ANP大鼠肠壁组织毛细血管渗漏的发生中起重要作用,调控AQP1的表达对保护血管内皮屏障功能有重要意义.  相似文献   
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