心房扑动1∶1传导酷似心室扑动1例

患者男,72岁。临床诊断:冠心病、原发性高血压。有心房扑动、颤动史10余年。彩色多普勒超声心动描记术示:左心室增大,左心室舒张功能下降。24h动态心电图监测示:心房扑动呈2∶1至9∶1传导,F波频率214次/min(附图上)。于晨间锻炼时出现一系列宽大畸形的正弦样曲线波(附图下),心室率214次/min,较规则,持续4min6s后自行恢复2∶1—3∶1传导的心房扑动。当时患者感心悸、头晕。动态心电图诊断:心房扑动伴二度房室传导阻滞,阵发性室性心动过速,短阵心室扑动?患者因     

甲型H1N1流感1例报告

1病例报告 患者,男,69岁,因发热15h于2009年5月22日入院。患者于当地时间2009年5月15日乘机从加拿大蒙特利尔离开,经多伦多转机,2009年5月16日下午16时到达北京。5月21日10时许自觉头痛不适,测体温37．9℃,无其他不适,白服板兰根2袋,12时自测体温37．5℃,遂到我院发热门诊就诊。     

危重甲型H1N1流感1例报道

甲型H1N1流感作为一种传染性强、危重病例可能致死的全新的呼吸道传染病,人类对其缺乏了解。总结此类患者临床特点具有十分紧迫的现实意义。为此,特将近期我科收住的一例重症甲型H1N1流感病例汇报如下。     

心房扑动1∶1房室传导酷似心室扑动1例

患者男性,61岁。患者5年前因活动时突然心悸、气促、头晕、乏力、咽部堵塞感伴晕厥来我院住院,多次心电图检查示心房扑动2∶1～6∶1下传。临床诊断为冠心病(缺血性心肌病型),慢性支气管炎、阻塞性肺气肿。近半年来每遇情绪激动、上楼梯、双上肢伸展活动时即出现类似症状,下蹲数s至数m in后可自行缓解,无意识障碍,再次来我院就诊。体检:BP110/70m m H g。心界不大,心率82次/m in,心律不齐,未闻及病理性杂音。彩色超声心动描记术检查示:右心房增大,三尖瓣反流。X线胸片示:慢性支气管炎,阻塞性肺气肿。实验室检查:电解质、肝功能、肾功能、心…     

1例重症甲型H_1N_1流行性感冒救治体会

病例:患者,女,55岁,因"咳嗽、发热1周,加重伴气促3 d"于2009年9月入院。患者入院前8 d下午无明显诱因下出现干咳,次日开始发热,体温最高39.5℃,畏寒,咳黄脓痰。入院前4 d出现痰中带血,后咳粉红色痰,至外院就诊,胸片检查提示双下肺肺炎(见图1),住院治疗,予阿奇霉素、     

心房扑动1:1房室传导酷似心室扑动1例

患者男性，61岁。患者5年前因活动时突然心悸、气促、头晕、乏力、咽部堵塞感伴晕厥来我院住院，多次心电图检查示心房扑动2：1～6：1下传。临床诊断为冠心病(缺血性心肌病型)，慢性支气管炎、阻塞性肺气肿。近半年来每遇情绪激动、上楼梯、双上肢伸展活动时即出现类似症状，下蹲数s至数min后可自行缓解，无意识障碍，再次来我院就诊。     

心律平致心房扑动1：1传导1例

心律平致心房扑动１：１传导１例河北省张家口市下花园区医院（０７５３００）郭玉龙心律平（ｐｒｏｐａｆｅｎｏｎｅ）又名丙胺苯丙酮．具有Ｉｃ类抗心律失常药物的电生理效应，为一广谱抗心律失常药物。我们在用其纠正房补时，出现房扑１：１传导，报告并讨论如下。患者...     

甲型H1N1与季节性H1N1流感病毒血凝素基因比较分析

目的分析泰安市2008～2009年度季节性流感与2009年度甲型H1N1流感病原学检测结果 ,比较季节性H1N1与甲型H1N1血凝素基因变异情况。方法选择国家级流感监测哨点医院以及暴发疫情的疫点,采集流感样病例的鼻咽拭子标本,通过RealtimePCR进行病毒检测,用MDCK细胞进行病毒分离,通过RT-PCR扩增血凝素HA1片段的基因并测序,利用生物信息学进行序列分析。结果 2008～2009年共检测鼻咽拭子标本283份,分离出流感病毒33株,分离阳性率为11.67%,其中季节性H1N1亚型31株。2009年5月1日～12月31日,检测鼻咽拭子标本996份,流感核酸检测阳性417份,阳性率为41.86%,其中甲型H1N1337份,季节性H1N1亚型1份。6株季节性H1N1病毒均在多个氨基酸位点上发生变异,与疫苗株A/Brisbane/59/2007(H1N1)比较,有11个位点发生了突变,其中5个位点位于抗原决定簇上;测序成功的6株甲型H1N1病毒在多个氨基酸位点发生变异,与疫苗株A/California/07/2009(H1N1)比较,有6个位点发生突变,其中1个位点位于抗原决定簇的B区。结论 2008～2009年度季节性H1N1为优势株,甲流暴发后,甲型H1N1成为绝对优势毒株。季节性H1N1分离株有多处氨基酸替换,抗原决定簇B区变异频繁;甲型H1N1病毒分离株的基因有变异,但关键位点第222位仍为D(天冬氨酸),与疫苗株相比抗原决定簇的关键位点变化不大。     

Expression of Transforming Growth Factor β1 in Bronchial Biopsies in Asthma and COPD

The role of transforming growth factor β₁ (TGF β₁) in airway remodeling in asthma and chronic obstructive pulmonary disease (COPD) has not been fully described. To evaluate the possible pathogenetic role of TGF β₁ in asthma and COPD, immunohistochemical expression of TGF β₁ was described in bronchial biopsies from patients with asthma and COPD compared with healthy individuals. Twelve subjects with asthma, 13 subjects with COPD, and 10 healthy individuals enrolled in the study. Bronchial biopsies were stained with hematoxylin and eosin and anti-TGF β₁ antibody. As a result, immunoreactive TGF β₁ was mainly localized in association with connective tissue in all groups. The staining intensity was not statistically different among the groups in bronchial epithelium, whereas it was significantly higher in the group of asthma in the submucosa. Because there is evidence showing a significant increase of staining intensity in the submucosa from asthmatics but not from subjects with COPD, we may conclude that TGF β₁ may play a significant role in pathogenesis of asthma but not in COPD.     

双氢青蒿素干预实验大鼠肺纤维化机制的研究

目的研究双氢青蒿素干预肺纤维化的作用机制。方法构建博来霉素诱导的大鼠肺纤维化模型[1],造模后行灌胃治疗。用HE染色、Masson染色法观察大鼠肺组织病理变化,碱水解法检测羟脯氨酸含量,Ellisa法检测血清中TGFβ1(转化生长因子β1)含量,荧光定量PCR法检测TGFβ1、SMAD2、SMAD3基因表达,免疫组化法检测大鼠肺组织中TGFβ1、SMAD2/3、p SMAD2/3蛋白表达。结果双氢青蒿素可减轻肺纤维化模型大鼠肺组织炎症和纤维化程度,抑制TGFβ1、SMAD2、SMAD3基因表达和TGFβ1、SMAD2/3、p SMAD2/3蛋白表达。结论双氢青蒿素可能通过抑制TGFβ1-SMAD2/3通路干预肺纤维化。     

Airway smooth muscle cells from ovalbumin-sensitized mice show increased proliferative response to TGFβ1 due to upregulation of Smad3 and TGFβRII

Objective: This study aimed to elucidate the role of Transforming growth factor (TGF)-β1 signaling in the proliferation of airway smooth muscle cells (ASMCs). Background: TGF-β1 is an important cytokine in airway remodeling in asthma. However, results of studies focusing on the effect of TGFβ1 on proliferation of ASMCs are controversial. Methods: An allergic model that mimics airway remodeling in chronic asthma was established and primary ASMCs were cultured. Cell proliferation was detected by viable cell counting and Cell Counting Kit (CCK)-8 analysis. Expression and phosphorylation of Smad3, type 1 TGFβ receptor (TGFβRI), type 2 TGFβ receptor (TGFβRII), extracellular signal-regulated kinase (ERK)-1/2, p38 mitogen-activated protein kinase (MAPK), C-Jun N-terminal kinase (JNK) and AKT were detected by western blot. siRNAs were used to knock down Smad3 and TGFβRII. Results: Smad3 and TGFβRII were up-regulated in primary ASMCs isolated from ovalbumin (OVA)-sensitized mice as compared with ASMCs isolated from unsensitized control mice, which persisted for at least four passages. TGFβ1 stimulated proliferation of ASMCs isolated from OVA-sensitized mice, which was inhibited by specific siRNA targeting Smad3 or TGFβRII. However ASMCs from control mice showed no proliferative response to TGFβ1. TGFβ1-induced proliferation of ASMCs from OVA-sensitized mice was markedly attenuated by PD-98059, a specific ERK1/2 inhibitor. TGFβ1 induced ERK1/2 phosphorylation within 15 minute, which was partially blocked by specific inhibitor of Smad3 (SIS3). Conclusions: ASMCs isolated from OVA-sensitized mice showed hyper-proliferation upon TGFβ1 stimulation. This might have been associated with up-regulated Smad3 and TGFβRII and mediated by ERK1/2 downstream to Smad3.     

柔肝消癥饮对肝硬化大鼠血清及肝脏转化生长因子β1的影响

目的：观察柔肝消癥饮对肝硬化大鼠血清转化生长因子β1（TGFβ1）水平以及肝脏TGFβ1 mRNA表达的影响。方法：采用复合因素造模法复制肝硬化大鼠模型,实验分组为正常组、模型组、阳性药（复方鳖甲软肝片）对照组和柔肝消癥饮高、低剂量组。观察柔肝消癥饮对肝硬化大鼠肝组织病理形态学、血清TGFβ1水平以及肝脏TGFβ1 mRNA表达的影响。结果：模型组大鼠出现肝小叶损害,纤维组织增生,假小叶形成;血清TGFβ1水平显著升高、肝脏TGFβ1 mRNA表达明显增强。各治疗组大鼠肝脏病理损害较轻、血清TGFβ1水平明显降低、肝脏TGFβ1 mRNA表达明显减少。结论：柔肝消癥饮通过显著抑制肝硬化大鼠血清TGFβ1水平升高和肝脏TGFβ1 mRNA的表达,以达到抗肝硬化的作用。     

胃癌组织中TGFβ1,Smad3,Smad7与ki-67 mRNA表达及其相关性

目的探讨转化生长因子(TGF)β1、Smad3、Smad7与ki-67 mRNA在胃癌中的表达及其相关性。方法选择经病理证实为胃癌组织的标本60例,正常胃组织标本20例,采用RT-PCR技术检测TGFβ1 mRNA、Smad3 mRNA、Smad7 mRNA与ki-67 mRNA的表达水平。结果在胃癌组织中,TGFβ1、Smad7与ki-67 mRNA水平明显高于正常胃组织(P0.05),Smad3 mRNA水平明显低于正常胃组织(P0.05)。低分化胃癌组织中TGFβ1、Smad7与ki-67 mRNA水平明显高于高中分化胃癌组织(P0.05),Smad3 mRNA水平明显低于高中分化胃癌组织(P0.05)。TGFβ1、Smad7与ki-67 mRNA三者在胃癌中的表达呈正相关,Smad3 mRNA与TGFβ1、Smad7、ki-67 mRNA呈负相关。结论正常胃组织和胃癌组织中TGFβ1、Smad3、Smad7与ki-67 mRNA的表达有差异,其与胃癌的发生、发展及分化程度密切相关。     

Thymosinβ4 alleviates cholestatic liver fibrosis in mice through downregulating PDGF/PDGFR and TGFβ/Smad pathways

Liver fibrosis is an important health problem without adequate and effective therapeutics. In this study, effects of thymosinβ4 (Tβ4) on hepatic fibrogenesis and the underlying molecular mechanisms were explored in bile duct ligation (BDL)-induced mice cholestatic liver fibrosis model. Results showed exogenous Tβ4 significantly reduced the mortality and liver/body weight ratio in BDL mice. Histological examinations and biochemical analyses demonstrated that BDL induced evident portal fibrosis and a significant increase in hepatic collagen contents. However, these changes were significantly attenuated by exogenous Tβ4. Quantitative real-time PCR assays showed that Tβ4 suppressed BDL-induced increases in many fibrotic genes expression including α-smooth muscle actin (α-SMA), collagen I, III and fibronectin, TGFβ1, TGFβR II, Smad2, Smad3, and PDGFRβ. Results from immunohistochemistry and Western blots also showed that Tβ4 reduced TGFβ1 and PDGFRβ protein levels in the liver tissues of BDL mice. In vitro studies using LX-2 cells demonstrated that Tβ4 could decrease PDGFRβ and TGFβR II levels in hepatic stellate cells. Taken together, findings in our present studies suggested that exogenous Tβ4 alleviated BDL-induced cholestatic liver fibrosis through downregulating PDGF/PDGFR and TGFβ/Smad pathways.     

TWEAK对新生大鼠心肌细胞增殖力和TGF-β1水平的影响

目的 肿瘤坏死因子样凋亡弱诱导因子（TWEAK）作为一种多功能的细胞因子,在细胞生长、分化、迁移、修复中起重要作用。然而,TWEAK对新生大鼠心肌细胞增殖的影响,及其与转化生长因子-β1（TGF-β1）的关系尚不明确。方法 通过培养新生SD大鼠的原代心肌细胞,应用TWEAK（20ng/ml）干预后培养24-48小时,应用CCK-8法检测心肌细胞增殖情况,以ELISA法检测细胞上清液的TGF-β1水平,同时分析二者相关性。结果 心肌细胞培养24小时,TWEAK干预组的心肌细胞CCK-8法检测OD值显著高于对照组（0.71±0.08vs.0.42±0.08,P=0.012）;培养48小时,TWEAK组的心肌细胞增殖力仍高于对照组（1.18±0.04 vs.0.92±0.03,P〈0.01）;同时,我们发现,TWEAK干预组,细胞上清液的TGF-β1水平显著高于对照组（24小时：133.1±4.3 vs.64.8±10.5 pg/ml,P〈0.01;48小时：187.3±7.9vs.66.8±8.4,P〈0.01）。通过Pearson相关性分析,我们还发现,CCK-8检测的细胞OD值与TGF-β1水平存在正相关,提示后者可能是TWEAK促进心肌细胞增殖的因素。结论 TWEAK可以促进新生大鼠心肌细胞的增殖,该机制可能与TGF-β1表达增高有关。     

溶血磷脂酸协同TGFβ1促进结肠癌细胞上皮间质转化的研究

目的探讨溶血磷脂酸(LPA)协同转化生长因子1(TGFβ1)的促上皮间质转化(EMT)作用。 方法观察TGFβ1及LPA诱导SW480细胞后细胞形态变化,Western blotting方法检测E-Cadherin、Vimentin的表达变化以及细胞增殖活性变化。 结果TGFβ1及LPA均能使SW480细胞形态发生EMT改变;两者联合诱导细胞EMT改变更为明显。空白对照组、LPA组、TGFβ1组、LPA组＋TGFβ1组,E-Cadherin表达依次下降;Vimentin表达未见明显差异。 结论LPA可能协同TGF-β1产生EMT作用,下调LPA的表达或可抑制肿瘤侵袭转移。