阻断局部肾素-血管紧张素-醛固酮系统不同环节对大鼠肺间质纤维化肿瘤坏死因子α表达的影响

目的:观察阻断肾素-血管紧张素-醛固酮系统不同环节对实验性肺纤维化大鼠肺组织肿瘤坏死因子α的影响。方法:实验于2005-08/2006-08在南华大学附属第一医院临床研究所及南华大学医学院组胚、生理实验室完成。取6周龄SD大鼠50只,随机分为正常对照组、模型组、卡托普利组、螺内酯组和氯沙坦组,每组10只。正常对照组气管内注入生理盐水,其他40只SD大鼠气管内注入博莱霉素5mg/kg复制肺纤维化模型。次日胃管内灌注血管紧张素转换酶抑制剂卡托普利60mg/kg(卡托普利组)、血管紧张素Ⅱ的Ⅰ型受体阻断剂氯沙坦10mg/kg(氯沙坦组)、醛固酮受体拮抗剂螺内酯100mg/kg(螺内酯组)、等量生理盐水(模型组和正常对照组),1次/d。各组动物均于给药后第28天处死,通过苏木精-伊红染色和Mallory染色观察肺组织病理变化,用免疫组织化学法和图像分析系统定量检测肺组织肿瘤坏死因子α的表达。结果:41只大鼠进入结果分析。①肿瘤坏死因子α蛋白表达:模型组高于正常对照组(166.82±4.14,61.44±1.94,P<0.01),卡托普利组、氯沙坦组、螺内酯组低于模型组(107.50±4.60,113.64±8.47,118.00±7.14,P<0.01),各用药组间无差异。②模型组肺泡炎程度、肺纤维化程度显著高于正常对照组(P<0.01,0.05),卡托普利组、氯沙坦组、螺内酯组较模型组好转(P<0.01),各用药组间无差异。结论:肺局部肾素-血管紧张素-醛固酮不同环节可能通过刺激肺部肿瘤坏死因子α表达而发挥致纤维化作用,阻断其不同环节可阻止肿瘤坏死因子α水平升高,抑制肺纤维化形成。     

明胶改性壳聚糖纤维表征及其体内降解特点

目的：采用明胶处理壳聚糖纤维,考察其表征及在大鼠肌袋内的生物相容性.方法：实验于2006-09/2007-01在解放军第八十九医院全军创伤骨科研究所实验室完成.①实验分组：分别以磷酸盐缓冲液、50,100 g/L明胶处理壳聚糖纤维.②实验评估：测定壳聚糖纤维膨胀率、拉伸强度;扫描电镜、红外光谱观察壳聚糖纤维的形态及结构;分离大鼠脊柱两侧椎旁肌肉形成3个肌袋,分别植入经γ射线灭菌的3种纤维20 mg.术后1周,1,3个月将纤维连同包膜完整取出,计算体内降解率.另取标本连同周围肌肉行苏木精-伊红染色. 结果：①壳聚糖纤维的膨胀率及拉伸强度：磷酸盐缓冲液组纤维膨胀率最高,拉伸强度最小;100 g/L明胶组膨胀率最低,拉伸强度最大.100 g/L明胶组拉伸强度与磷酸盐缓冲液组和50 g/L明胶组间差异有显著性意义（P＜0.05）,3组壳聚糖纤维膨胀率差异无显著性意义.②壳聚糖纤维的形态和结构：扫描电镜下磷酸盐缓冲液组纤维束交织,结构略显松散,50、100 g/L明胶改性后纤维结构更为致密.红外光谱分析显示明胶和壳聚糖间有相互作用.③体内降解率：磷酸盐缓冲液组体内平均降解率65%,50,100 g/L明胶组平均降解率分别为78%和81%,3组间差异无显著性意义.④壳聚糖纤维植入肌袋后的组织相容性：改性后壳聚糖纤维植入后与大鼠周围肌肉连接紧密,表面包膜薄,细胞主要为淋巴细胞,植入12周后3组纤维大部分吸收. 结论：明胶改性可进一步提高壳聚糖纤维的强度和生物相容性.     

外源性一氧化氮对创伤愈合过程中一氧化氮合酶表达及瘢痕形成的影响

目的:应用组织化学、免疫组织化学及计算机辅助图像分析方法,观察外源性一氧化氮在创伤愈合过程不同时间,对一氧化氮合酶表达和胶原形成的影响,探讨其在促进创伤愈合和抑制病理性瘢痕形成中的机制。方法:实验于2004-09/2006-03在河北省人民医院整形烧伤外科及河北省人民医院临床医学研究中心完成。以硝普钠为一氧化氮供体,将60只大鼠随机分为对照组及硝普钠0.5,1,2,4mmol/L组,每组12只,通过建立大鼠创伤模型,并分别在创面局部应用50g/L葡萄糖溶液、0.5,1,2,4mmol/L硝普钠,观察及测量创伤后3,7,10,14d的肉芽组织生长情况、一氧化氮合酶的表达情况和肉芽组织中羟脯氨酸含量。结果:60只大鼠全部进入结果分析。①形态学观察:对照组于创伤后14d可完全愈合;硝普钠0.5mmoL/L组及1mmoL/L组肉芽组织生长良好,且愈合时间较对照组提前三四天;硝普钠2mmoL/L组及4mmoL/L组愈合情况不良,完全愈合时间延迟,皮肤张力较低,炎症反应明显。②一氧化氮合酶蛋白表达:大鼠皮肤创伤后角质形成细胞、汗腺、毛囊和骨骼肌细胞以及创伤后肉芽组织的炎症细胞、成纤维细胞、血管内皮细胞均不同程度的表达一氧化氮合酶蛋白。对照组在第3天和第14天分别呈现一氧化氮合酶阳性颗粒表达高峰,而硝普钠各组仅在第7～10天出现表达一氧化氮合酶阳性高峰,呈先增加后减少的趋势。③羟脯氨酸含量:对照组从创伤后第3,7,10,14天羟脯氨酸含量进行性增加[依次为(1.637±0.127),(2.250±0.169),(2.420±0.201),(2.908±0.241)mg/g];硝普钠0.5mmol/L组在创伤后第3,7天羟脯氨酸含量低于对照组[(1.435±0.147),(1.766±0.211)mg/g,P<0.05或P<0.01],而在第10天和第14天羟脯氨酸含量均高于对照组[(3.128±0.240),(3.437±0.239)mg/g,P<0.01];硝普钠1mmol/L组和2mmol/L组在第10天和第14天的羟脯氨酸含量明显高于对照组[(1mmol/L组:(3.244±0.245)(3.582±0.282)mg/g,P<0.01;硝普钠2mmol/L组:(3.666±0.263),(4.301±0.268)mg/g,P<0.01);硝普钠4mmol/L组仅在创伤后第3天表现比对照组多[(1.912±0.139)mg/g,P<0.01),其余均与对照组水平相近。结论:局部应用外源性一氧化氮具有显著的促修复作用,主要体现在伤后第7～10天,小剂量的一氧化氮促进创面愈合的作用远远大于大剂量一氧化氮。     

Diarrhoeal outbreak of Vibrio cholerae 0139 from North India

Epidemics of cholera caused by Vibrio cholerae 01 occur regularly in India. Until recently, Vibrio cholerae non-01 have been the the causative agents of sporadic cases of gastroenteritis and septicaemia, especially in immunocompromised children. We describe a large outbreak of cholera-like illness from North India caused by Vibrio cholerae non-01, later serotyped as Vibrio cholerae 0139. Forty-one of a total of 391 patients with acute diarrhoea during a 2-month period (May–July 1993) were identified as having Vibrio cholerae in faecal samples. All patients were aged 1.5–12 years. Vibrio cholerae 0139 was isolated in 30 patients (73%–group I) and Vibrio cholerae 01 biotype eltor in 11 patients (27%–group II). The clinical presentation and severity of the cholera-like illness were similar to typical cholera. This strain is toxigenic with an epidemic potential and should be monitored carefully □     

Salivary IgA to cariogenic bacteria in HIV‐positive children and its correlation with caries prevalence and levels of cariogenic microorganisms

The interrelationship of HIV infection, dental caries and mucosal immune responses remains controversial. In our study population of 40 HIV‐infected and 40 healthy control children (ages 2–5 years) there was a significantly higher prevalence of dental caries in HIV‐infected children (P<0.05). The extent of caries correlated with the severity of HIV disease. To determine whether the immunosuppression that ensues after HIV infection could contribute to the increased caries prevalence, the concentrations of total IgA and IgA specific to cariogenic bacteria (Streptococcus mutans, Streptococcus sobrinus and Lactobacillus acidophilus) were determined in whole saliva by enzyme‐linked immunosorbent assay . Levels of the same bacteria were also quantified in saliva using checkerboard DNA–DNA hybridization. A significantly increased level of total salivary IgA was found in the HIV‐positive population (P < 0.05), but there were comparable titers of specific IgA to cariogenic bacteria in HIV‐positive and healthy controls. The microbiological assessment also demonstrated similar levels of cariogenic microorganisms in both groups. We conclude that HIV‐positive children appear to maintain the capacity to mount a mucosal immune response to cariogenic microorganisms, at least until late stages of disease.