肺炎克雷伯杆菌感染引起大鼠小气道炎症的免疫学特征

本文观察了肺炎克雷伯杆菌气道感染引起大鼠小气道炎症细胞和肺组织中TNF α含量动态变化。结果显示 ,肺炎克雷伯杆菌感染第 1天至第 1周 ,小气道壁中炎症细胞以中性粒细胞增多为主。感染第 2周至第 16周 ,小气道壁T淋巴细胞较对照组明显增多 (P <0 0 1) ,其阳性细胞百分率范围在 39%～ 67%。感染第 8周和第 16周 ,小气道壁CD4/CD8比值下降 ,分别为 0 5 7和 0 41,同时间对照组为 0 75和 0 78。树突状细胞 (S 10 0阳性细胞 )分布在小气道上皮 ,固有膜和粘膜下层。感染第 1周至第 8周 ,肺组织中TNF α含量明显升高 (P <0 0 1)。因此 ,在克雷伯杆菌感染引起的小气道炎症中 ,小气道壁T淋巴细胞 ,尤其CD8T细胞浸润值得重视。同时 ,肺组织中TNF α含量增高可能是T淋巴细胞在肺内积聚和数量增多机制之一。     

细支气管病变的分类及临床病理特点

细支气管特殊的解剖和生理功能特点,导致该部位是呼吸系统病变最常累及的部位之一。细支气管病变也称广义的细支气管炎,指各种致病原因,导致细支气管的损伤,引起反应性炎症细胞浸润和纤维组织增生性改变的一组病变。该文通过对小气道病变的分类介绍并配以图片,以提高病理医师的认识和诊断水平。     

慢性支气管炎吸烟患者外周气道粘膜层内炎性细胞特点

观察吸烟的慢性支气管炎患者外周气道粘膜层内炎性细胞的特点。非吸烟对照组 12例 ,吸烟非慢支组 2 0例 ,吸烟并慢支组 2 8例 ,非吸烟慢支组 12例 ,手术取得的肺标本。应用免疫组化法检测外周气道粘膜层内CD3+ 、CD8+ 、CD6 8+ 、CD2 0 + 细胞 ,并与FEV1 0做相关性分析。吸烟并慢支组外周气道粘膜层内CD3+ 、CD8+ 细胞明显高于非吸烟对照组 (P <0 0 5 ) ,单纯吸烟组CD3+ 细胞数也明显高于非吸烟对照组。吸烟者CD3+ 、CD6 8+ 细胞与FEV1 0呈显著负相关。慢支患者吸烟组与非吸烟组相比无差异。吸烟并慢支患者外周气道以T淋巴细胞 ,尤其是CD8+ 细胞为主的炎症。     

小剂量罗红霉素对小气道疾病患者血清中三种细胞因子的影响

小气道疾病(SAD)是慢性阻塞性肺疾病(COPD)的早期病理过程,有多种细胞因子参与,目前无确切的干预方法,本课题研究SAD细胞因子的变化及小剂量罗红霉素对SAD各种细胞因子的影响。首先研究健康查体确诊的SAD患者及非SAD患者的细胞因子的变化;其次对161例支原体抗体阴性的SAD患者,随机分为罗红霉素治疗组81例、对照组80例进行研究。治疗组口服小剂量罗红霉素0.15/d,3个月,对照组未予任何治疗,治疗开始前、治疗后1、3、6、12个月测定细胞因子TNF-α、TGF-β1、IL-8的变化,同时检查肺功能。结果SAD组患者TNF-α、TGF-β1、IL-8明显高于非SAD组,两组差异显著(P<0.05);治疗组SAD随着时间的延长TNF-α、TGF-β1、IL-8逐渐下降,肺功能逐渐好转,相关性分析,肺功能与细胞因子的变化成明显负相关(P<0.05),1年后统计治疗组SAD治愈率50%,对照组10%,两者差异显著,治疗组SAD发生率低因此,小剂量罗红霉素可有效抑制SAD细胞因子TNF-α、TGF-β1、IL-8的生成,抑制气道的慢性非特异性炎症,减少SADCOPD的发生。     

脉冲振荡技术阻力流速依赖对气道病变诊断价值的初步探讨

目的　探讨脉冲振荡技术 (IOS)阻力和流速依赖 (dR/dV′)对气道病变的诊断价值。方法　采用德国IOS肺功能仪对正常、吸烟和慢性阻塞性肺病 (COPD)共 72例进行阻力 /流速依赖 (dR/dV′)和FVC曲线有关指标检测、比较 ,并做回归分析。结果　dR/dV′正常组分别与吸烟组和COPD组之间均有显著差异 (P <0 0 1) ,但COPD组与吸烟组无差异 (P >0 0 5 ) ;dR/dV′与FEV1、V50 和V2 5分别呈显著负相关 (P <0 0 0 1) ;采用“正常组的均值+1 6 5标准差”作为异常判别标准对正常组的误检率为 4 17% ,对吸烟组和COPD组共 4 8例阳性率为 4 1 6 7%。结论　dR/dV′可以作为判断有无气道阻塞比较特异的指标 ,但可能无法反映病情的严重程度。     

小切口治疗胆囊病变238例体会

目的评估小切口治疗胆囊病变的效果,探讨小切口治疗胆囊病变在基层医院的应用。方法采用回顾性资料,统计1995年1月至2006年12月利用小切口治疗的238例胆囊病变患者,观察手术时间、出血量、并发症发生率、术后下床活动、保留胃管及肛门排气时间和出院后随访情况。结果本组238例胆囊病变患者采用小切口切除胆囊,全部痊愈出院。手术时间、出血量、并发症发生率、术后下床活动、保留胃管及肛门排气时间均优于传统手术方法。结论小切口治疗胆囊病变操作简单,与常规手术比较,有创伤较小、手术时间较短、出血较少、患者术后恢复较快等特点。术后早期即可下床活动,胃肠减压时间及排气时间较常规手术短。     

肺气虚证大鼠气道病变和免疫复合物相关性的研究

目的:探讨肺气虚证大鼠IC和气道病变发生发展的相关性.方法:将铜绿假单胞菌以滴鼻法感染大鼠辅以寒冷疲劳刺激,诱导肺气虚证的发生,观察气道病理改变.直接法免疫组化染色检测肺支气管小血管壁的IC,PEG 沉淀法检测CIC.并设一组补肺益气治疗组予以反证.结果:模型组大鼠支气管慢性炎症明显并伴有急性炎症,组织IC和血清中CIC与正常对照组比较平均光密度及浊度均值显著升高,P＜0.01.补肺益气治疗组支气管慢性炎症不明显,组织IC和血清中CIC接近正常对照组P＞0.05.结论:用呼吸道生物被膜菌铜绿假单胞菌复制的肺气虚大鼠,在呼吸道慢性感染中可以刺激机体产生IC,气道的炎性改变和免疫复合物的形成相关.补肺益气治疗可以消除组织IC、血清CIC,促进支气管慢性炎症消退.     

糖尿病视网膜病变患者瘦素水平的变化

目的 :探讨糖尿病视网膜病变患者血清瘦素水平变化规律。方法 :受试对象 12 0例 ,分为对照组 30例 (男 18,女 12 )、糖尿病无视网膜病变组 30例 (男 18,女 12 ) ,非增殖性视网膜病变组 30例 (男 18,女 12 )及增殖性视网膜病变组 30例 (男 18,女 12 ) ,检测血清瘦素、胰岛素、Ⅳ型胶原及血糖浓度 ,分析瘦素水平与其它指标的相关性。结果 :对照组、无视网膜病变组、NPDR组及PDR组血清瘦素浓度分别为 6 91± 1 87μg/L ,7 83± 2 11μg/L ,9 5 6± 2 4 3μg/L和 11 6 9± 2 5 7μg/L ,经协方差分析排除体重指数的影响 ,PDR组血清瘦素浓度高于NPDR组 (t=2 15 ,p<0 0 5 )、无视网膜病变组 (t=2 71,p <0 0 1)及对照组 (t =3 5 0 ,p <0 0 0 1) ;NPDR组高于无视网膜病变组 (t=2 2 3,p <0 0 5 )及对照组 (t=2 75 ,p<0 0 1)。血清瘦素浓度与体重指数、胰岛素呈正相关 (r=0 2 2 ,p <0 0 5 ;r=0 2 8,p<0 0 1)。结论 :糖尿病视网膜病变患者血清瘦素浓度升高 ,且增高的幅度与病情的严重程度正相关     

EICU危重患者人工气道的护理体会

本文主要探讨了EICU建立人工气道的危重患者的护理体会,由此可见,良好的人工气道护理不仅能有效预防呼吸道并发症,促进患者排痰,防止痰痂形成,促进患者康复,还能最大限度的降低危重患者死亡率,提高护理质量.     

哮喘等慢性气道疾病中气道缩窄的生物力学模型研究最新进展

虽然对于探索哮喘等气道疾病的潜在治疗方法和揭示气道系统中有趣的生物物理现象等意义重大,气道缩窄的生物力学模型研究一直是既吸引人又充满挑战的研究领域。近年来,这方面的研究呈现方兴未艾的形势,新的现象和新的研究思路不断出现。本文简要介绍这方面部分最新的研究进展,重点介绍针对哮喘气道缩窄行为,致力于解释在体气道行为的生物力学模型,尤其是不仅探讨孤立气道力学行为,而且也探讨气道间相互耦合和与周围环境耦合的气道力学模型。这些相互作用涉及气道和缠绕其上的气道平滑肌层,也涉及气道动态相互作用导致的气道—肺实质通气的空间分布形态等新颖的行为和现象。     

Inflammatory cytokines in small intestinal mucosa of patients with potential coeliac disease

T helper cell type 1 (Th1) response to gluten has been implicated in the pathogenesis of coeliac disease (CD). To characterize immunological activation and mild inflammations leading to overt CD in potential coeliac patients, jejunal biopsies were obtained from family members of patients with CD or dermatitis herpetiformis (DH). Nine family members and one latent CD, eight CD patients and eight normal controls furnished jejunal biopsy specimens. Immunohistochemical staining of sections for interleukin-1alpha (IL-1alpha), IL-2, IL-4, interferon-gamma (IFN-gamma), tumour necrosis factor alpha (TNF-alpha), CD3, gammadelta-T cell receptor (gammadelta-TCR), and alphabeta-TCR was carried out with monoclonal antibodies. Further, expression of IL-4 and IFN-gamma messenger RNA was detected by radioactive in situ hybridization in these same samples. In lamina propria, CD patients and potential CD patients had higher densities of IL-2 (P = 0.028, P = 0.043), IL-4 (P = 0.021, P = 0.034) and IFN-gamma positive cells (P = 0.000, P = 0.009) than did controls. Moreover, CD patients showed a higher density of TNF-alpha positive cells (P = 0.012, P = 0.001) than the other two groups, and expression of IFN-gamma mRNA (P = 0.035) was higher in them than in the other two study groups. Additionally, higher densities of TNF-alpha and IFN-gamma positive cells occurred in potential CD patients with high gammadelta-TCR+ intraepithelial lymphocytes (IELs). Our findings support the hypothesis that lamina propria T cells and macrophages, through their secretion of cytokines, play a central role in the pathogenesis of coeliac disease. The inflammatory cytokines found in potential CD specimens strongly suggest that these inflammatory markers can be identified long before visible villous changes have occurred.     

趋化因子及其受体与气道疾病关系的研究进展

气道慢性炎症是哮喘和慢性阻塞性肺疾病的本质特点。炎症细胞浸润组织是炎症和宿主免疫应答的基础，这一过程受到趋化因子的控制。本文将阐述趋休因子及其受体家族的特点，特别是在慢性气道炎症病理生理过程中的作用以及作为气道慢性炎症靶向性治疗的可能性。     

Inhaled corticosteroids decrease vascularity of the bronchial mucosa in patients with asthma

BACKGROUND: Increased vascularity in airway mucosa is a distinctive feature of airway remodelling in asthma. While corticosteroids have proved most effective in modifying airway inflammation, the effect of inhaled corticosteroids on increased airway mucosal vascularity in asthmatics has been little studied. OBJECTIVE: We examined the effect of inhaled corticosteroid on airway vascularity in bronchial biopsy specimens taken from asthmatic patients. SUBJECTS AND METHODS: We studied bronchial biopsies from 28 asthmatic patients before and after treatment with inhaled beclomethasone dipropionate (BDP) 800 microg/daily, or placebo, for 6 months in a double-blind manner. Biopsy specimens were evaluated for number of vessels and percentage of area occupied by vessels, using computerized image analysis after staining for type IV collagen in vessel walls. Specimens were also examined for extent of collagen III in the subepithelial basement membrane. In addition, we compared asthmatic specimens with biopsy specimens taken from non-asthmatic control subjects. RESULTS: There was a significant increase in number of vessels (P < 0.01) and percent vascularity (P < 0.001) in the submucosa of asthmatic patients compared with control subjects. After 6 months of treatment, we observed significant improvements in forced expiratory volume in 1 s (FEV1), FEV1% and airway responsiveness (P < 0.05, each) in the BDP treatment group compared with the placebo group. This was accompanied by significant decreases in both vessel number and percent vascularity in the airways of BDP-treated patients (P < 0.05, each). We also observed a significant correlation between change in percent vascularity and change in collagen III thickness in the BDP-treated patients (rs = 0.90, P < 0.001). Furthermore, the change in percent vascularity was inversely correlated with both FEV1 (rs = -0.49, P < 0.05) and airway responsiveness (rs = -0.36, P < 0.05). CONCLUSION: These findings suggest that inhaled corticosteroid treatment of asthma reduced airway wall vascularity during airway remodelling.     

Gluten affects epithelial differentiation-associated genes in small intestinal mucosa of coeliac patients

In coeliac disease gluten induces an immunological reaction in genetically susceptible patients, and influences on epithelial cell proliferation and differentiation in the small-bowel mucosa. Our aim was to find novel genes which operate similarly in epithelial proliferation and differentiation in an epithelial cell differentiation model and in coeliac disease patient small-bowel mucosal biopsy samples. The combination of cDNA microarray data originating from a three-dimensional T84 epithelial cell differentiation model and small-bowel mucosal biopsy samples from untreated and treated coeliac disease patients and healthy controls resulted in 30 genes whose mRNA expression was similarly affected. Nine of 30 were located directly or indirectly in the receptor tyrosine kinase pathway starting from the epithelial growth factor receptor. Removal of gluten from the diet resulted in a reversion in the expression of 29 of the 30 genes in the small-bowel mucosal biopsy samples. Further characterization by blotting and labelling revealed increased epidermal growth factor receptor and beta-catenin protein expression in the small-bowel mucosal epithelium in untreated coeliac disease patients compared to healthy controls and treated coeliac patients. We found 30 genes whose mRNA expression was affected similarly in the epithelial cell differentiation model and in the coeliac disease patient small-bowel mucosal biopsy samples. In particular, those genes involved in the epithelial growth factor-mediated signalling pathways may be involved in epithelial cell differentiation and coeliac disease pathogenesis. The epithelial cell differentiation model is a useful tool for studying gene expression changes in the crypt-villus axis.     

强直性脊柱炎患者气道管理分析

目的分析强直性脊柱炎患者的气道管理。方法对2004年1月至2014年12月在北京协和医院因强直性脊柱炎行骨科手术的171名患者的气道管理资料进行回顾性分析。结果 96.5%患者选择全麻手术。Macintosh喉镜和Glidescope喉镜声门暴露Cromack分级Ⅲ-Ⅳ级分别占9.6%和6.6%。90.9%的患者首次插管成功。9例患者需要更换插管工具,并有2例出现困难通气。5例患者选择椎管内麻醉,其中1例因效果不佳而改为全身麻醉。结论强直性脊柱炎患者由于脊柱和关节受累,属于困难气道高危,术前应充分评估和准备,选择最佳麻醉方案,减少并发症的发生。     

Transforming growth factor‐beta 1 pathways in inflammatory airway diseases

Transforming growth factor‐beta 1 (TGF‐β1) has been reported being involved in the remodeling and immunosuppression processes of inflammatory airway diseases; understanding the regulation of TGF‐β1 is therefore a key to unravel the pathomechanisms of these diseases. This review briefly summarizes the current knowledge on the influencing factors for driving TGF‐β1 and its regulatory pathways in inflammatory airway diseases and discusses possible therapeutic approaches to TGF‐β1 control. The factors include smoking and oxidative stress, prostaglandins (PGs), leukotrienes (LTs), bradykinin (BK), and microRNAs (miRs). Based on the summary, new innovative treatment strategies may be developed for inflammatory airway diseases with an impaired expression of TGF‐β1.