支气管扩张合并哮喘的临床特点及其治疗的探讨

目的探讨支气管扩张合并哮喘(支扩合并哮喘)此一特殊类型临床特点和治疗方法。方法①用支气管激发试验和支气管舒张试验对临床诊断为支气管扩张的102例患者进行测试,筛选出支扩合并哮喘的病例。②对单纯性支扩和支扩合并哮喘此两类患者的以往病史详细问卷。③对此两类型患者的临床表现进行观察。④对支扩合并哮喘此一类型的病例进行分组试验性治疗。A组按抗支扩加抗哮喘治疗。B组按常规抗支扩治疗,均治疗2个月。结果①102例临床诊断支扩患者,其中98例进行支气管激发试验,其中18例阳性(PD20FEV1<12.8μmol)4例进行支气管舒张试验,其中2例阳性(FEV1增加幅度>15%)。即102例临床诊断支扩患者,发现20例为支扩合并哮喘。另外82例为单纯性支扩。②支扩合并哮喘以往病史的特点是个人过敏病史和家族过敏史的频率很高,分别为120%和110%。而单纯性支扩的发生频率很低,仅为7.3%和3.6%。③支扩合并哮喘的临床特点是发病呈季节性加重(20例);常有上呼吸道过敏症状;痰液多为黏液脓性;除固定部位湿性音外,全部病例有散在性或弥漫性喘鸣音。④支扩合并哮喘类型的分组试验性治疗,用抗支扩+抗哮喘药物治疗的10例,疗效显著,基本属完全治愈,而单独用抗支扩药物的10例,大部分遗留下症状和体征。结论支扩合并哮喘是一个特殊类型,可通过支气管激发试验和支气管舒张试验和以往病史追询、临床特点观察,而与单纯性支扩相鉴别,其治疗方法也和单纯性支扩不同。对支扩合并哮喘应当应用抗支扩+抗哮喘的治疗方案。在抗哮喘方面应用表面糖皮质激素吸入,疗效确实而且安全。     

妥洛特罗贴剂经皮给药治疗小儿支气管哮喘的疗效

目的监测小儿支气管哮喘患者在综合治疗过程中经皮给予妥洛特罗贴剂后病情的缓解及症状的改善。方法将104例轻中度小儿支气管哮喘患者分为2组:对照组50例,给予综合治疗,抗感染、抗病毒、止咳、化痰等常规治疗;治疗组54例,除综合治疗外,根据年龄的不同,给予妥洛特罗贴剂0.5mg或1mg,观察两组咳嗽时限及痰液排出时间。结果治疗组咳嗽及排痰时限均短于对照组,差异有统计学意义(P<0.05)。结论妥洛特罗经皮给药治疗小儿支气管哮喘,能缩短咳嗽、排痰时限,达到缩短病程的效果。     

支气管动脉栓塞术治疗咯血的临床疗效

目的:探讨应用明胶海绵颗粒和/或聚乙烯醇(polyvinglacohol PVA)颗粒进行支气管动脉栓塞对支气管扩张咯血的临床价值。方法:18例支气管扩张咯血患者,数字减影血管照影(digitalangiography DSA)下行双肢支气管动脉造影并应用明胶海绵颗粒和/或聚乙烯醇(polyvinglacohol PVA)颗粒进行栓塞治疗。结果:12例PSA显示出阳性征象,表现为造影外溢,经栓塞治疗后10例患者立即停止,随访6个月,1例咯血患者在治疗5个月咯血复发后,行第二次栓塞止血,未见严重的并发症。结论:支气管动脉造影及栓塞术对支气管扩张咯血有较高的应用价值,其微创伤,并发症少,迅速,有效,安全的控制出血的特点,宜作为支气管扩张咯血治疗首选方法。     

Effects of long-term low-dose formaldehyde exposure on global genomic hypomethylation in 16HBE cells

Formaldehyde (FA), a volatile organic compound, is a ubiquitous air pollutant that is classified as ‘Carcinogenic to humans (Group 1)’ by IARC (2006). As a well-recognized human carcinogen, its carcinogenic mechanisms are still poorly understood. Previous studies have emphasized on genetic changes. However, little is known about the epigenetic mechanisms of FA exposure. In this study, We not only characterized the epigenomic response to long-term low-dose FA exposure in 16HBE cells, but also examined the expression of DNA methyltransferases (DNMTs) and the methyl-CpG-binding protein DNA-binding domain protein 2 (MBD2). Each week the 16HBE cells were treated with 10 μM FA for 24 h (h). After 24 weeks (W) of exposure to FA, the level of genomic DNA methylation gradually decreased in a time-related manner. Moreover, our results showed that FA exposure down-regulated the expression of DNMT3a and DNMT3b at both mRNA and protein level, and up-regulated the levels of DNMT1 and MBD2 at both mRNA and protein level. Our study indicated that long-term FA exposure could disrupt genomic DNA methylation, which may be one of the possible underlying carcinogenic mechanisms of FA.     

The role of miR-506 in transformed 16HBE cells induced by anti-benzo[a]pyrene-trans-7,8-dihydrodiol-9,10-epoxide

Growing evidence indicates that the alteration of microRNA (miRNA) expression in tumors that is induced by chemical carcinogens plays an important role in tumor development and progression. However, the mechanism underlying miRNA involvement in lung carcinogenesis induced by anti-benzo[a]pyrene-trans-7,8-dihydrodiol-9,10-epoxide (anti-BPDE) remains unclear. In our study, we used the malignant transformation of human bronchial epithelial cells (16HBE-T) induced by anti-BPDE to explore the mechanisms of human lung carcinogenesis. We found that expression of miR-506 was reduced in 16HBE-T transformed malignant human bronchial epithelial cells compared with 16HBE normal human bronchial epithelial cells. Restoration of miR-506 in 16HBE-T cells led to a decrease in cell proliferation, G0/G1 phase cell cycle arrest, as well as significantly suppressed anchorage-dependent growth in vitro and tumor growth inhibition in a nude mouse xenograft model. In addition, we provided novel evidence regarding the role miR-506 potentially plays in negatively regulating the protein and mRNA expression level of N-Ras in cancer cells. Together, these findings revealed that miR-506 acts as an anti-oncogenic miRNA (anti-oncomir) in malignantly transformed cells. The identification of tumor suppressive miRNAs could provide new insight into the molecular mechanisms of chemical carcinogenesis.     

MSCT支气管动脉三维成像对中心型肺癌的血供研究及其临床意义(英文)

目的探讨多层螺旋 CT(MSCT)三维支气管动脉成像在中心型肺癌中的影像学表现及应用价值,为中心型肺癌的血供来源和介入治疗提供理论依据。方法对18例中心型肺癌的病人行 MSCT 造影增强检查,采用实时螺旋薄层 CT 扫描,在独立工作站行支气管动脉三维重建,使用不同的旋转轴观察支气管动脉的空间解剖细节。结果其中6例(33.33%)中心型肺癌的支气管动脉三维图像能够清晰显示出去支气管动脉的起源、走行的路径(肺内段和纵隔段)和血管直径等情况。有肺动脉明显狭窄截断的病例支气管动脉显示率最高,且明显增粗,表明此类肺癌的血供来源主要以支气管动脉为主。三维成像中以容积显示技术(SVR 像)显示最佳。结论 MSCT 三维支气管动脉成像能够准确、直观地显示支气管动脉的空间解剖特点,为中心型肺癌的血供研究与介入治疗提供理论基础。     

气管镜针吸术与气管镜毛刷在肺部肿块鉴别诊断中的应用

目的:评价经气管镜针吸术(TBNA)涂片与毛刷涂片(BB)对肺部肿块的诊断价值。方法:对156例肺部肿块患者行支气管镜检查,同时做针吸涂片和BB细胞学检查,结合形态和细胞免疫化学染色做出诊断,与术后病理组织学检查结果或临床诊断进行比较。结果:156例肺部肿块最终确诊为恶性肿瘤132例,非肿瘤性疾病13例,未确诊11例。132例恶性肿瘤中,TBNA诊断准确率为97.7%,而BB只有71.2%,两者差异有统计学意义,P<0.01。TBNA对中心型肺癌、周围型肺癌和纵隔肿瘤诊断准确率分别为98.4%、98.2%和92.3%,毛刷涂片相应数据为91.9%、64.9%和0,后两者差异有统计学意义。24例非肿瘤患者中有11例通过TBNA明确诊断,占最终明确诊断患者的84.6%(11/13),而BB仅确诊2例肺结核。结论:TBNA涂片细胞学检查在肺部肿块的鉴别诊断方面优于BB细胞学检查。     

支气管袖状成形肺切除术治疗支气管肺癌81例报告

目的 回顾分析我院1984－1999年间81例支气管袖状成形术,重点讨论各种袖状成形术的术式,总结经验。方法 术式包括左和右肺上叶支气管袖状切除术33例,右肺中叶袖状切除术6例,左和右肺下叶袖状切除术3例,右肺中叶及基底段支气管袖状切除术5例,右肺上叶、部分中叶及基底段支气管袖状切除术2例,左上叶及部分基底段支气管袖状切除术4例,左肺下叶及舌段袖状切除术5例,下叶背段袖状切除术8例,左肺舌段袖状切除术2例,主支气管袖状切除术4例,主支气管及上叶和中间支气管或下叶支气管袖状切除术3例,右中间和中叶支气管及下叶支气管袖状切除术3例,双袖状切除术3例。结果 本组81例无手术死亡,亦未出现严重的手术并发症。最常见的术后并发症为肺不张（共4例）,主要发生在段支气管袖状肺切除术（占3例）。经协助咳痰、纤支镜吸痰、抗炎治疗而治愈。结论 支气管解剖复杂,同时亦具有较大的可塑性。应根据具体病变的性质、位置、范围和解剖特点选择合理的术式,争取最佳的治疗效果。     

人支气管上皮细胞恶性转化相关基因的克隆

[目的]根据克隆的大鼠气管上皮细胞恶性转化EST片段（GenBane Accession Number AF011363)克隆相应的人全长基因并探索其功能。[方法]根据大鼠EST序列进行生物素探针标记,cDNA文库筛选,cDNA快速终扩增延伸目的基因直到获得全长序列。[结果]HRNT－1全长cDNA 4256bp,开放阅读框架2760bp,位于254bp-3016bp之间,编码区内含有9个TRP序列;位于人类染色体Xq13;cDNA序列收录于GenBank中（Accession Number AF223393).HRNT-1在人支气管上皮恶性转化细胞以及肺癌细胞中具有较高表达。[结论]HRNT－10为一功能基因,其高表达与上支气管上皮细胞恶性转化有关。     

Sphingosine-1-phosphate augments agonist-mediated contraction in the bronchial smooth muscles of mice

The effects of sphingosine-1-phosphate (S1P) on bronchial smooth muscle (BSM) contractility were investigated in naive mice. S1P had no effect on the basal tone of the isolated BSM tissues. However, in the presence of S1P (10(-6) M), the BSM contractions induced by acetylcholine (ACh) and endothelin-1 (ET-1) were significantly augmented: both the ACh and ET-1 concentration-response curves were significantly shifted to the left. In contrast, the pretreatment with S1P had no effect on the contractions induced by high K(+) depolarization. It is thus possible that S1P augments BSM contraction induced by the activation of G protein-coupled receptors.