大黄素对TNBS诱导大鼠肠纤维化的影响

目的:观察大黄素对结肠炎大鼠模型肠纤维化的影响,探讨其抗纤维化作用机制.方法:以三硝基苯磺酸(trinitrobenzene sulphonic acid,TNBS)诱导的结肠炎大鼠为纤维化模型,将34只SD大鼠分成正常对照组、模型组和大黄素组,模型组和大黄素组予以TNBS诱导肠纤维化,大黄素组每日给予大黄素40mg/kg灌胃,其余组则给予等体积盐溶液.实验过程中观察小鼠体质量、大便性状和活动变化,给予DAI评分,实验结束后收集结肠组织标本,给予大体和组织学评分,并采用HE染色及Masson胶原三色染色观察大鼠结肠组织损伤和纤维化程度,采用荧光定量PCR法检测结肠黏膜中TGF-1、胶原Ⅰ、胶原Ⅲ、Smad3、-SMA和E-cad mRNA表达.结果:与模型组相比,大黄素组一般情况、结肠组织大体和组织学评分及纤维化程度均出现明显改善.大黄素组TGF-β1、胶原Ⅰ、胶原Ⅲ、Smad3和-SMA mRNA表达较模型组明显降低(1.27±0.78vs4.56±3.14;0.60±0.59vs2.15±1.22;0.92±1.38vs3.34±1.47;3.11±2.81vs8.77±6.40;0.87±0.62vs2.40±1.15,均P<0.05),而E-cad mRNA表达明显升高(1.01±0.34vs0.30±0.23,P<0.05).结论:大黄素对TNBS诱导的大鼠肠纤维化模型具有一定的抗纤维化作用,该作用可能与其下调TGF-1/Smad信号通路抑制EMT发生有关.     

牛磺酸对三硝基苯磺酸诱导的结肠炎大鼠肠纤维化的抑制作用

目的 探讨牛磺酸对三硝基苯磺酸(TNBS)诱导的结肠炎大鼠肠纤维化的影响.方法 32只SD大鼠均分为对照组、模型组、低剂量和高剂量牛磺酸组.对照组以0.9%氯化钠溶液灌肠,其余3组以TNBS灌肠诱导建立结肠炎模型.低剂量和高剂量牛磺酸组于造模前1周每日分别给予牛磺酸400和800 mg/kg干预,直至造模结束.观察大鼠临床表现及疾病活动指数(DAI),行结肠大体评分和组织学评分,检测大鼠结肠长度、结肠重量.测定结肠组织中羟脯氨酸(Hyp)、Ⅰ型胶原蛋白、转化生长因子-β1(TGF-β1)蛋白和mRNA、Smad3蛋白和mRNA水平.结果 与对照组相比,模型组大鼠体重减轻、DAI评分升高、结肠狭窄伴近端扩张、结肠长度缩短、结肠重量增加、大体评分也显著升高(P<0.01).牛磺酸干预后,大鼠体重、DAI评分、结肠长度等指标均有所改善.模型组纤维化评分为1.88±0.35.较对照组明显增加(0.25±0.46,P<0.01);低剂量和高剂量牛磺酸组纤维化评分分别为1.25±0.71和0.75±0.47,较模型组下降(P<0.05).模型组大鼠结肠Hyp、TGF-β1、Ⅰ型胶原蛋白、Smad3蛋白和mRNA含量均较低剂量和高剂量牛磺酸组明显上升(P值均<0.05).结论 牛磺酸能有效抑制TNBS诱导的结肠炎大鼠肠纤维化,其抗纤维化机制可能与下调TGF-β1、抑制TGF-β/Smad3通路有关,为解决克罗恩病肠纤维化和肠狭窄提供一定的实验依据.     

青黛颗粒对溃疡性结肠炎大鼠结肠黏膜MUC2和iNOS基因表达的影响

目的:观察青黛颗粒对TNBS诱导的溃疡性结肠炎(UC)大鼠结肠黏膜黏蛋白(MUC2)及诱导型一氧化氮合成酶(iNOS)基因表达的影响,探讨其治疗UC的可能作用机制.方法:将54只SD实验大鼠随机分为正常对照组、模型对照组、阳性药物治疗组(SASP,500 mg/kg)、青黛颗粒600、900、1 200 mg/kg治疗组.造模后第3天开始灌胃给药,共给药10d.实验第14天,处死大鼠,剖取其病变结肠组织,比较各组大鼠的DAI积分和CMDI评分,用逆转录聚合酶链反应(RT-PCR)法检测MUC2及iNOS基因的表达.结果:较模型组青黛颗粒900、1200 mg/kg治疗组能显著降低实验大鼠DAI积分和CMDI评分,上调结肠组织中MUC2的基因表达(2.06±0.70 vs 1.24±0.47;2.34±0.86 vs 1.24±0.47.均P<0.01),且青黛颗粒1 200 mg/kg治疗组能下调iNOS的基因表达(0.35±0.12vs 0.62±0.31.P<0.05).结论:青黛颗粒可能通过上调结肠黏膜MUC2的基因表达并下调iNOS的基因表达而起到抗TNBS诱导的大鼠溃疡性结肠炎的作用.     

甘草酸二铵对溃疡性结肠炎大鼠M30表达的影响

目的:观察甘草酸二铵(diammonium glycyrrhi-zinate,DG)对2,4,6-三硝基苯磺酸(2,4,6-trin-itrobenzene sulfonic acid,TNBS)诱导的大鼠溃疡性结肠炎(ulcerative colitis,UC)的疗效及其对大鼠结肠组织M30及Fas/FasL蛋白表达的影响,继而从细胞凋亡方面探讨DG治疗大鼠UC可能的作用机制.方法:♀Wistar大鼠30只,随机分为正常对照组、模型组和DG组,每组10只.用TNBS/乙醇灌肠法复制大鼠UC模型,10d后收集结肠标本,观察大鼠疾病活动指数(disease activity index,DAI)、结肠大体形态损伤评分和组织学改变,用免疫组织化学法观察大鼠结肠黏膜中M30及Fas/FasL蛋白的表达.结果:与正常对照组相比,DG组、模型组DAI评分、结肠大体形态损伤评分和组织学损伤评分均显著增高(7.06±0.80vs0.32±0.14;6.03±0.61vs0.19±0.16;5.84±0.53vs0.22±0.11,P<0.01);而与模型组相比,DG治疗组能显著改善UC症状(3.33±0.27vs7.06±0.80;3.29±0.36vs6.03±0.61;2.98±0.24vs5.84±0.53,P<0.05).模型组大鼠M30及Fas/FasL蛋白表达水平明显高于正常组(5.76±0.66vs0.42±0.18;26.62±4.20vs10.81±2.20;17.11±3.12vs6.02±1.02,P<0.01);与模型组相比,DG治疗组M30及Fas/FasL蛋白表达显著降低(2.24±0.48vs5.76±0.66;17.23±3.20vs26.62±4.20;11.02±2.12vs17.11±3.12,P<0.05).结论:DG对TNBS诱导的大鼠UC有较好的疗效,DG通过下调Fas/FasL的表达抑制结肠上皮细胞的凋亡,这可能是其减轻结肠黏膜损伤的机制之一.     

红花注射液对溃疡性结肠炎大鼠VEGF和bFGF表达的影响

目的:观察红花注射液(safflower solution,SS)对2,4,6-三硝基苯磺酸(2,4,6-trinitrobenzene sulfonic acid,TNBS)诱导的大鼠溃疡性结肠炎(ulcerative colitis,UC)的疗效及其对大鼠结肠组织血管内皮生长因子(vascular endothelial growth factor,VEGF)和碱性成纤维细胞生长因子(basal fibroblast growth factor,bFGF)表达的影响.方法:将30只Wistar大鼠随机分为正常对照组、模型组、红花组,每组10只.用TNBS灌肠法复制大鼠UC模型,红花组同时给予腹腔注射SS2mL/(kg·d)干预治疗,模型组与对照组给予等量生理盐水.造模10d后,收集标本.对大鼠行疾病活动指数(disease activity index,DAI)、结肠大体形态评分及组织学损伤评分,分别用免疫组织化学法及实时荧光定量PCR(real time-polymerase chain reaction,RT-PCR)技术检测大鼠结肠黏膜中VEGF、bFGF的表达.结果:与正常对照组相比,红花组、模型组DAI评分,结肠大体形态损伤评分和组织学损伤评分均显著增高(P<0.01);而与模型组相比,红花组能显著改善UC症状(P<0.05).模型组大鼠VEGF、bFGF表达水平明显高于正常组(P<0.01);与模型组相比,红花组VEGF表达显著降低(P<0.05).结论:SS能够显著改善UC大鼠结肠损伤及炎症反应,这可能与其有效下调VEGF的表达,抑制病理性血管生成有关.     

复方黄柏液对大鼠TNBS结肠炎的治疗机制探讨

背景：临床上采用复方黄柏液保留灌肠辅助治疗溃疡性结肠炎（UC）疗效满意,但其作用机制尚不清楚。目的：探讨复方黄柏液对三硝基苯磺酸（TNBS）诱发的大鼠结肠炎模型炎症损伤的治疗作用及其可能机制。方法：40只成年雌性Sprague-Dawley大鼠随机分成四组,正常对照组不予处理,其余三组以TNBS／乙醇溶液灌肠制作结肠炎模型后．分别予0．9％NaCl溶液1ml、5-氨基水杨酸（5-ASA）200mg／kg和复方黄柏液1ml灌肠,连续14d。治疗后评估大鼠疾病活动指数（DAI）以及结肠大体、组织学损伤情况;检测结肠组织髓过氧化物酶（MPO）活性和白三烯B4（LTB4）含量;心脏采血,流式细胞术检测中性粒细胞凋亡率。结果：与正常对照组相比,TNBS模型组DAI、结肠大体和组织学评分、结肠组织MPO活性和LTB。含量均显著升高,血中性粒细胞凋亡率显著降低（P〈0．01）;5-ASA治疗组和复方黄柏液治疗组上述指标均较TNBS模型组显著改善（P〈0．01）,两组间差异则无统计学意义。结论：复方黄柏液灌肠对大鼠TNBS结肠炎具有明显治疗作用,促进中性粒细胞凋亡、清除结肠局部损伤因子（MPO、LTB。）可能为其作用机制之一。     

吉法酯对三硝基苯磺酸诱导大鼠实验性结肠炎的作用

目的 观察吉法酯对三硝基苯磺酸(TNBS)诱导的大鼠实验性结肠炎髓过氧化物酶(MPO)、环氧合酶(COX)-1及COX-2表达的影响,探讨吉法酯对溃疡性结肠炎的治疗作用.方法 选用雌性健康SD大鼠40只,均分为A、B、C、D组.A、B、C三组大鼠采用TNBS/乙醇灌肠制作大鼠结肠炎模型.造模后第2天,A组每天给予0.9%氯化钠溶液1 ml灌肠;B组每天给予5-氨基水杨酸(5-ASA)1 ml灌肠(100 mg/kg);C组每天给予吉法酯1 ml灌胃.D组为正常对照组.分别于造模后第7天及第14天每组处死5只大鼠,按疾病活动指数(DAI)的评分标准进行大体损伤评分,HE染色进行组织损伤评分.同时取结肠病变部位组织,生化法检测MPO活性,免疫组化法检测COX-1与COX-2的组织表达.结果 与A组比较,B组和C组的DAI评分、大体损伤形态和组织学损伤评分及MPO活性均降低(P<0.05).与A组相比,B、C、D组第7天和第14天COX-1表达水平升高(P<0.05),分别为0.87±0.18和0.93±0.15比1.86±0.51和1.96±0.41,1.73±0.68和1.79±0.6以及1.91±0.34和1.99±0.45;COX-2水平降低(P<0.05),分别为3.50±0.23和3.06±0.27比1.53±0.19和0.73±0.15,1.73±0.94和0.86±0.29,0.24±0.18和0.18±0.16.D组COX-2表达极弱,与B、C两组间差异有统计学意义(P<0.05).结论 吉法酯对TNBS诱导的大鼠结肠炎有较好的治疗作用,其疗效与5-ASA相似,其作用机制可能是降低肠组织中MPO的活性和调节COX-1/COX-2表达.     

沉默结缔组织生长因子对大鼠肝纤维化及细胞外基质积聚的影响

目的 研究结缔组织生长因子(CTGF)小干扰RNA(siRNA)在CCl4诱导的大鼠肝纤维化模型中的抗肝纤维化作用及其对细胞外基质积聚的影响.方法 雄性SD大鼠30只,随机分成5组.模型组:皮下注射CCl4及经门静脉注射等渗盐水,3 d 1次,连续6周;预防组:皮下注射CCl4及经门静脉注射CTGF siRNA,连续6周;治疗组:皮下注射CCl4 2周,随后给予CTGF siRNA及CCl4 4周;对照siRNA干预组:皮下注射CCl4及经门静脉注射对照siRNA,连续6周;空白对照组:经门静脉注射等渗盐水6周.用HE和Sirius red染色评估大鼠肝组织学变化,RTPCR或(和)Western blot检测肝组织CTGF、Ⅰ与Ⅲ型胶原及层黏连蛋白的表达,放射免疫法检测外周血Ⅲ型前胶原及透明质酸含量.结果 模型组及对照siRNA组大鼠肝组织CTGF、Ⅰ与Ⅲ型胶原及层黏连蛋白基因表达显著上调;与模型组相比,预防组及治疗组由CCl4诱导的CTGF mRNA和蛋白表达及Ⅰ与Ⅲ型胶原、层黏连蛋白mRNA表达分别下调76%±8%、95%±2%、74%±8%、78%±8%、31%±7%和80%±3%、93%±3%、57%±6%、59%±10%、43%±9%(F值分别为68.630,21.234,24.219,16.315和9.716,P值均＜0.01),肝纤维化程度明显减轻,大鼠外周血Ⅲ型前胶原和透明质酸含量也显著降低.结论 经门静脉注射CTGF siRNA能显著抑制实验大鼠肝CTGF基因表达,由此通过阻止细胞外基质积聚而缓解肝纤维化.     

白头翁醇提物对大鼠结肠炎肠黏膜上皮细胞紧密连接蛋白的保护作用

目的:探讨白头翁醇提物对三硝基苯磺酸诱导大鼠结肠炎肠黏膜上皮细胞紧密连接蛋白的调控,进一步阐明白头翁醇提物对大鼠实验性结肠炎的肠黏膜屏障的保护作用.方法:建立TNBS诱导大鼠结肠炎模型.实验分为正常组、模型组、白头翁醇提物治疗组和双歧杆菌嗜酸乳杆茵肠球菌三联活菌(金双歧)组.进行疾病活动指数(DAI)和组织学损伤评分,用ELISA法测定结肠组织TNF-α、IL-10和血清内毒素,采用免疫组织学染色检测紧密连接(tight iunction,TJ)相关蛋白occludin的分布.结果:TNBS诱导大鼠结肠炎后,DAI和组织学损伤评分增高,结肠组织TNF-α水平升高、IL-10水平降低和血清内毒素水平升高,而经白头翁醇提物和双歧杆菌嗜酸乳杆菌肠球菌三联活菌处理后,DAI和组织学损伤评分有明显下降(6.50±1.27,5.90±1.67 vs 9.20±1.75:5.00±1.05,4.80±1.25 vs 7.10±0.99,均P<0.05),结肠组织TNF-α水平降低(521.24±109.37 ng/L,503.98±126.63 ng/L vs 657.54±149.60 ng/L,均P＜0.05)、血清内毒素水平降低(0.148±0.093EU/mL,0.153±0.106 EU/mL vs 0.213±0.023EU/mL,均P＜0.05)和IL-10水平升高(92.19±30.09 ng/L,95.57±27.71 ng/L vs 42.92±23.74ng/L,均P＜0.05);TNBS诱导大鼠结肠炎后,TJ结构遭到破坏,TJ相关蛋白的表达减少,而白头翁醇提物和双歧杆菌嗜酸乳杆菌肠球菌三联活茵(金双歧)处理后可使TNBS引起的TJ结构受损减轻,相关蛋白的表达增多.结论:白头翁醇提物可以对TNBS诱导大鼠结肠炎肠黏膜屏障具有明显的保护作用,其机制可能是通过调节肠道微生态、上调肠上皮细胞紧密连接蛋白ocluudin的表达、降低结肠组织TNF-α含量、提高IL-10水平,从而抑制内毒素通过紧密连接进入体循环.     

甘草酸二铵对溃疡性结肠炎大鼠结肠炎症及MCP-1表达的影响

目的探讨甘草酸二铵（DG）治疗溃疡性结肠炎（UC）的效果及机制。方法将30只雌性SD大鼠随机分为观察组、模型组和对照组各10只,观察组、模型组大鼠用2,4,6-三硝基苯磺酸（TNBS）灌肠制备UC模型,观察组同时腹腔注射DG40mg/（kg·d）行干预治疗,10d后观察三组疾病活动指数（DAI）、组织学损伤评分,并以RT-PCR方法检测结肠组织单核细胞趋化蛋白-1（MCP-1）表达。结果观察组和模型组DAI、组织学损伤评分及MCP-1相对表达量均显著高于对照组,尤其以模型组为著（P均〈0.05）。结论 DG能减轻UC大鼠结肠炎症程度,可能机制为下调低MCP-1表达。     

Role of pentoxifylline in non-alcoholic fatty liver disease in high-fat diet-induced obesity in mice

AIM:To study pentoxifylline effects in liver and adipose tissue inflammation in obese mice induced by high-fat diet(HFD).METHODS: Male swiss mice(6-wk old) were fed a highfat diet(HFD; 60% kcal from fat) or AIN-93(control diet; 15% kcal from fat) for 12 wk and received pentoxifylline intraperitoneally(100 mg/kg per day) for the last 14 d. Glucose homeostasis was evaluated by measurements of basal glucose blood levels and insulin tolerance test two days before the end of the protocol. Final body weight was assessed. Epididymal adipose tissue was collected and weighted for adiposity evaluation. Liver and adipose tissue biopsies were homogenized in solubilization buffer and cytokines were measured in supernatant by enzyme immunoassay or multiplex kit, respectively. Hepatic histopathologic analyses were performed in sections of paraformaldehyde-fixed, paraffin-embedded liver specimens stained with hematoxylin-eosin by an independent pathologist. Steatosis(macrovesicular and microvesicular), ballooning degeneration and inflammation were histopathologically determined. Triglycerides measurements were performed after lipid extraction in liver tissue. RESULTS: Pentoxifylline treatment reduced microsteatosis and tumor necrosis factor(TNF)-α in liver(156.3 ± 17.2 and 62.6 ± 7.6 pg/mL of TNF-α for non-treated and treated obese mice, respectively; P 0.05). Serum aspartate aminotransferase levels were also reduced(23.2 ± 6.9 and 12.1 ± 1.6 U/L for nontreated and treated obese mice, respectively; P 0.05) but had no effect on glucose homeostasis. In obese adipose tissue, pentoxifylline reduced TNF-α(106.1 ± 17.6 and 51.1 ± 9.6 pg/mL for non-treated and treated obese mice, respectively; P 0.05) and interleukin-6(340.8 ± 51.3 and 166.6 ± 22.5 pg/mL for non-treated and treated obese mice, respectively; P 0.05) levels; however, leptin(8.1 ± 0.7 and 23.1 ± 2.9 ng/mL for non-treated and treated lean mice, respectively; P 0.05) and plasminogen activator inhibitor-1(600.2 ± 32.3 and 1508.6 ± 210.4 pg/mL for non-treated and treated lean mice, respectively; P 0.05) levels increased in lean adipose tissue. TNF-α level in the liver of lean mice also increased(29.6 ± 6.6 and 75.4 ± 12.6 pg/mL for non-treated and treated lean mice, respectively; P 0.05) while triglycerides presented a tendency to reduction.CONCLUSION: Pentoxifylline was beneficial in obese mice improving liver and adipose tissue inflammation. Unexpectedly, pentoxifylline increased pro-inflammatory markers in the liver and adipose tissue of lean mice.     

Heart Failure in South America

Continued assessment of temporal trends in mortality and epidemiology of specific heart failure in South America is needed to provide a scientific basis for rational allocation of the limited health care resources, and strategies to reduce risk and predict the future burden of heart failure. The epidemiology of heart failure in South America was reviewed. Heart failure is the main cause of hospitalization based on available data from approximately 50% of the South American population. The main etiologies of heart failure are ischemic, idiopathic dilated cardiomyopathy, valvular, hypertensive and chagasic etiologies. In endemic areas, Chagas heart disease may be responsible by 41% of the HF cases. Also, heart failure presents high mortality especially in patients with Chagas etiology. Heart failure and etiologies associated with heart failure may be responsible for 6.3% of causes of deaths. Rheumatic fever is the leading cause of valvular heart disease. However, a tendency to reduction of HF mortality due to Chagas heart disease from 1985 to 2006, and reduction in mortality due to HF from 1999 to 2005 were observed in selected states in Brazil. The findings have important public health implications because the allocation of health care resources, and strategies to reduce risk of heart failure should also consider the control of neglected Chagas disease and rheumatic fever in South American countries.     

岳阳市城区小学生血吸虫病防治健康教育现状调查

目的 调查湖南省岳阳市城区小学生血吸虫病防治知识、行为现状及健康教育需求情况,为制定科学有效的小学生血吸虫病健康教育方案提供参考依据。方法 采用分层整群抽样方法,抽取岳阳市城区洞庭湖湖畔学校和中心城区学校各2所,每所再从五、六年级分别抽取2个班的学生,通过调查问卷了解小学生血吸虫病相关知识、预防行为及健康教育需求,并进行统计分析。结果 共调查湖畔小学353人、中心城区小学363人,两组学校小学生年龄、性别、年级构成差异无统计学意义(t=-0.494,χ_性别²=1.615,χ_年级²=2.152;P均>0.05)。学生血吸虫病防治知识总知晓率为42.60%(305/716),其中,湖畔学校小学生血防知识知晓率(52.97%)高于中心城区(32.51%),差异有统计学意义(χ²=30.661,P<0.05);学生行为正确率为76.68%(549/716),血防知识知晓组行为正确率(81.31%)高于不知晓组(71.24%),差异有统计学意义(χ²=6...     

Antioxidant therapies in COPD

Oxidative stress is an important feature in the pathogenesis of COPD. Targeting oxidative stress with antioxidants or boosting the endogenous levels of antioxidants is likely to be beneficial in the treatment of COPD. Antioxidant agents such as thiol molecules (glutathione and mucolytic drugs, such as N-acetyl-L-cysteine and N-acystelyn), dietary polyphenols (curcumin, resveratrol, green tea, catechins/quercetin), erdosteine, and carbocysteine lysine salt, all have been reported to control nuclear factor-kappaB (NF-κ B) activation, regulation of glutathione biosynthesis genes, chromatin remodeling, and hence inflammatory gene expression. Specific spin traps such as α-phenyl-N-tert-butyl nitrone, a catalytic antioxidant (ECSOD mimetic), porphyrins (AEOL 10150 and AEOL 10113), and a superoxide dismutase mimetic M40419 have also been reported to inhibit cigarette smoke-induced inflammatory responses in vivo. Since a variety of oxidants, free radicals, and aldehydes are implicated in the pathogenesis of COPD, it is possible that therapeutic administration of multiple antioxidants will be effective in the treatment of COPD. Various approaches to enhance lung antioxidant capacity and clinical trials of antioxidant compounds in COPD are discussed.     

Rising incidence of oesophageal adenocarcinoma in men in Australia

Adenocarcinomas of the oesophagus and of the gastric cardia have been reported to be increasing in incidence in many countries, while the incidence of squamous cell carcinoma of the oesophagus is stable and non-cardia gastric cancers are decreasing in incidence. Age-standardized incidence rates for the years 1982–93 for oesophageal adenocarcinoma and non-adenocarcinoma, and gastric cardia and non-cardia cancers were calculated based on state cancer registry incidence data. Time trends in the age-standardized rates were assessed using linear regression. A consistent increasing trend in the incidence of oesophageal adenocarcinoma in men was seen in all states of Australia and was statistically significant in all states except South Australia. There were no consistent nationwide trends in the incidence of oesophageal adenocarcinoma in women, although a trend towards an increase in the incidence of this cancer reached statistical significance ( P < 0.05) in three states (New South Wales, Victoria, Queensland). There were no important trends in the incidence of oesophageal non-adenocarcinoma in either men or women. There were no consistent nationwide changes in the incidence of gastric cardia cancer in either men or women, although this cancer was significantly increasing in Tasmania in both men and women. The incidence of cancer of the stomach not arising at the gastric cardia was significantly decreasing in men in all states and was also decreasing in women in all states, although in women this decrease was statistically significant only in New South Wales, Victoria and Western Australia. There has been a dramatic increase in the incidence of oesophageal adenocarcinoma in men in Australia. The incidence of this cancer in men is now approximately equal with that of non-adenocarcinoma of the oesophagus. The incidence of non-cardia stomach cancer continues to fall.     

Histamine antagonists in the treatment of shock hyperglycemia in the rat

The present study was undertaken to determine the effect of exogenous histamine and histamine blockers on blood glucose and hepatic glycogen in the rat. Forty-one nonfasted male Sprague-Dawley rats that had been anesthetized with intraperitoneal injections of urethane were injected intravenously (femoral) with histamine (10 mg/kg) five minutes after pretreatment with Ringer's solution (control), diphenhydramine (1 mg/kg) (H-1 blocker); metiamide (1 mg/kg) (H-2 blocker); or a combination of these blockers. Mean arterial pressure (carotid), blood glucose, and hepatic glycogen were measured. Within 30 minutes, histamine evoked a significant increase in blood glucose, and a decrease in hepatic glycogen, and a reduction in blood pressure. However, rats treated with the H-2 blocker metiamide or with a combination of H-1 and H-2 blockers did not show as significant a hypotensive response as rats treated with the H-1 blocker diphenhydramine alone. The hyperglycemic-glycogenolytic response to histamine was modified by diphenhydramine as well as by a combination of blockers, but not by metiamide alone. These results suggest that a) the hypotension did not initiate the hyperglycemic and glycogenolytic response; b) the H-2 blocker metiamide has little effect on the hyperglycemic response to exogenous histamine; and c) the H-1 blocker diphenhydramine may have antihyperglycemic properties.     

Ethnic variation in the annual rates of adult inflammatory bowel disease in hospitalized patients in Vancouver, British Columbia

BACKGROUND:

There is currently little available information regarding the impact of ethnicity on the clinical features of inflammatory bowel disease (IBD). Migrating populations and changing demographics in Vancouver, British Columbia (BC) provide a unique opportunity to examine the role of ethnicity in the prevalence, expression and complications of IBD.

OBJECTIVES:

To determine the demographics of IBD and its subtypes leading to hospitalization in the adult population of BC.

METHODS:

A one-year retrospective study was performed for all patients who presented acutely with IBD to Vancouver General Hospital from January 1, 2006 to December 31, 2006. Data regarding sex, age, ethnicity, IBD type and extent of disease, complications and management strategies were collected. Clinical data were confirmed by pathology and radiology reports.

RESULTS:

There were 186 cases of IBD comprising Crohn’s disease (CD) 56%, ulcerative colitis (UC) 43% and indeterminate colitis (1%) 1%. The annual rate of IBD cases warranting hospitalization in Caucasians was 12.9 per 100,000 persons (7.9 per 100,000 persons for CD and 5.0 per 100,000 persons for UC). This was in contrast to the annual rate of IBD in South Asians at 7.7 per 100,000 persons (1.0 per 100,000 persons for CD and 6.8 per 100,000 persons for UC) and in Pacific Asians at 2.1 per 100,000 persons (1.3 per 100,000 persons for CD, 0.8 per 100,000 persons for UC). The male to female ratio was higher in South Asians and Pacific Asians than in Caucasians. The extent of disease was significantly different across racial groups, as was the rate of complications.

CONCLUSIONS:

These early results suggest that there are ethnic disparities in the annual rates of IBD warranting hospitalization in the adult population of BC. There was a significantly higher rate of CD in the Caucasian population than in South Asian and Pacific Asian populations. The South Asian population had a higher rate of UC, with an increased rate of complications and male predominance. Interestingly, the rate of CD and UC was lowest in the Pacific Asian population. These racial differences – which were statistically significant – suggest a role for ethnodiversity and environmental changes in the prevalence of IBD in Vancouver.