阿托伐他汀逆转腹主动脉缩窄型高血压大鼠心肌重构的机制

目的 观察阿托伐他汀对腹主动脉缩窄型高血压大鼠血清血管紧张素(1-7)浓度及左心室肥厚心肌组织中p-ERK1/2表达水平的影响,探讨阿托伐他汀逆转心肌重构的可能机制.方法 50只SD雄性大鼠随机分为5组:假手术组、模型组、10 mg/(kg·d)阿托伐他汀组、30 mg/(kg·d)阿托伐他汀组及缬沙坦组,每组10只.术后第1天,将阿托伐他汀研磨成粉,溶于少量蒸馏水中制成悬液,采用灌胃法给药;假手术组和模型组大鼠均用等量生理盐水灌胃.每日上午定时一次,共4周.鼠尾容积法测定药物干预前及干预后2周、4周的血压变化.4周后处死大鼠,测定大鼠体重、左心室重量、左心室重量指数;HE染色检测心肌细胞平均直径;酶联免疫吸附法测定血清血管紧张素(1-7)浓度;免疫印迹法检测心肌p-ERK1/2蛋白表达水平.结果 30 mg/(kg·d)阿托伐他汀组和10 mg/(kg·d)阿托伐他汀组收缩压明显低于模型组(P<0.01),30 mg/(kg·d)阿托伐他汀组收缩压明显低于10mg/(kg·d)阿托伐他汀组(P<0.01),缬沙坦组收缩压明显低于30 mg/(kg·d)阿托伐他汀组和10 ms/(kg·d)阿托伐他汀组(P<0.01);假手术组、30 mg/(kg·d)阿托伐他汀组、10 mg/(kg·d)阿托伐他汀组及缬沙坦组左心室重量指数明显低于模型组(P<0.01),30 mg/(kg·d)阿托伐他汀组左心室重量指数明显低于10 mg/(kg·d)阿托伐他汀组(P<0.05);假手术组、30 mg/(kg·d)阿托伐他汀组及缬沙坦组心肌细胞平均直径明显低于模型组(P<0.01).10 mg(kg·d)阿托伐他汀组与模型组无差异(P>0.05);10 mg/(kg·d)阿托伐他汀组、30 mg/(kg·d)阿托伐他汀组及缬沙坦组血清Ang-(1-7)浓度显著高于模型组(P<0.01),30 mg/(kg·d)阿托伐他汀组及缬沙坦组血清Ang.(1-7)浓度明显高于10 mg/(kg·d)阿托伐他汀组(P<0.05);10 mg/(kg·d)阿托伐他汀组、30mg/(kg·d)阿托伐他汀组及缬沙坦组p-ERK1/2蛋白表达水平显著低于模型组(P<0.01),但高于假手术组.结论 阿托伐他汀对腹主动脉缩窄型高血压大鼠心肌重构具有逆转作用,其机制与降低压力负荷诱导的心肌肥厚组织中p-ERK1/2 蛋白表述水平有关.     

阿托伐他汀防止压力负荷导致心肌肥厚的抗炎机制

背景他汀类药物具有多种临床功效包括调脂、改善内皮功能等,有报道表明他汀类药物可以防治压力负荷增大引起的心肌肥厚,但其确切机制尚不明确.目的 观察阿托伐他汀对压力负荷导致的心肌肥厚的保护作用,并探讨其可能的机制.方法 缩窄腹主动脉的方法 制备大鼠心肌肥厚模型.Wistar大鼠随机分为未治疗组(n=10)、阿托伐他汀组(n=10),假手术组(n=10)、空白对照组(n=10).阿托伐他汀组术后每日灌胃给予阿托伐他汀2 mg/kg,余各组给予生理盐水灌胃.实验结束后处死大鼠,测定其心脏/体质量、左心室/体质量及病理切片左室壁厚度和心肌细胞直径.通过RT-PCR方法 检测心肌组织中心肌营养素1(CT-1)和白细胞介素18(IL-18)的表达.结果 未治疗组[(174±9)mmHg]收缩压明显高于对照组[(112±15)mmHg](P<0.01),虽然阿托伐他汀组[(169±8)mmHg]血压仅有不明显下降(P>0.05),但能减轻心脏质量/体质量[阿托伐他汀:(3.2±0.2)×10-3比未治疗组(4.2±0.29)×10-3,P<0.05]、左心室质量/体质量[阿托伐他汀:(2.2±0.09)×10-3比未治疗组(2.8±0.27)×10-3,P<0.05]、阿托伐他汀还降低心肌中炎症因子,如CT-1[阿托伐他汀:(0.244±0.042)比未治疗组(0.371±0.054),P<0.05]、IL-18 mRNA含量[阿托伐他汀:(0.231±0.071)比未治疗组(0.462±0.038),P<0.05]及心肌细胞直径[阿托伐他汀:(9.74±0.38)μm比未治疗组(10.94±0.65)μm,P<0.05].结论 阿托伐他汀对压力负荷导致的心肌肥厚有明显的保护作用,同时伴有炎症因子水平的降低,说明阿托伐他汀的保护作用可能与其抗炎作用有关.     

阿托伐他汀防止压力负荷导致心肌肥厚的抗炎机制

背景他汀类药物具有多种临床功效包括调脂、改善内皮功能等,有报道表明他汀类药物可以防治压力负荷增大引起的心肌肥厚,但其确切机制尚不明确。目的观察阿托伐他汀对压力负荷导致的心肌肥厚的保护作用,并探讨其可能的机制。方法缩窄腹主动脉的方法制备大鼠心肌肥厚模型。Wistar 大鼠随机分为未治疗组(n=10)、阿托伐他汀组(n=10)、假手术组(n=10)、空白对照组(n=10)。阿托伐他汀组术后每日灌胃给予阿托伐他汀2 mg/kg,余各组给予生理盐水灌胃。实验结束后处死大鼠,测定其心脏/体质量、左心室/体质量及病理切片左室壁厚度和心肌细胞直径。通过 RT-PCR 方法检测心肌组织中心肌营养素1(CT-1)和白细胞介素18(IL-18)的表达。结果未治疗组[(174±9)mmHg]收缩压明显高于对照组[(112±15)mmHg](P<0.01),虽然阿托伐他汀组[(169±8)mmHg]血压仅有不明显下降(P>0.05),但能减轻心脏质量/体质量[阿托伐他汀:(3.2±0.2)×10~(-3)比末治疗组(4.2±0.29)×10~(-3),P<0.05]、左心室质量/体质量[阿托伐他汀:(2.2±0.09)×10~(-3...     

阿托伐他汀改善自发性高血压大鼠心室重构的机制

目的 研究阿托伐他汀(Ato)对自发性高血压大鼠(SHR)心室重构的作用,并探讨其作用机制.方法 16周龄雄性SHR 40只,随机分为4组,即SHR组、阿托伐他汀10 mg组(Ato-1组)、25 mg组(Ato-2组)和50 mg组(Ato-3组).Wistar-Kyoto(WKY)大鼠10只作为正常对照组(WKY组).Ato-1组、Ato-2组和Ato-3组每日分别用阿托伐他汀10、25、50 mg/kg灌胃.实验8周后,测定血液动力学指标,左室质量指数(LVMI),RT-PCR检测心肌转化生长因子β1(TGFβ1)mRNA、Smad3 mRNA和Smad7 mRNA.结果 SHR组心室功能障碍,LVMI明显增高[(3.20±0.21)mg/g比WKY:(2.10±0.14)mg/g](P＜0.01),心肌TGFβ1 mRNA(125.4±3.2比WKY:73.6±2.1,P＜0.01)、Smad3 mRNA(6.40±0.43比WKY:3.10±0.75,P＜0.01)增加,心肌Smad7 mRNA(2.30±0.86比WKY:4.10±1.23,P＜0.01)降低.Ato呈剂量依赖性改善左室功能,降低SHRLVMI,降低心肌TGFβ1 mRNA、Smad3 mRNA,增加心肌Smad7 mRNA.结论 阿托伐他汀可能通过下调心肌TGFβ1 mRNA、Smad3 mRNA和上调心肌Smad7 mRNA,改善SHR心室重构.     

三种降压药单用及联用对肾性高血压大鼠左心室肥厚及离子泵活性的影响

目的探讨依那普利、厄贝沙坦和氨氯地平单用及联用改善肾性高血压大鼠(RHR)左心室肥厚(LVH)的疗效及对左心室肌离子泵活性的影响。方法 42只大鼠用两肾一夹制造RHR模型,随机分为模型组、依那普利组[10 mg/(kg·d)]、厄贝沙坦组[50 mg/(kg·d)]、氨氯地平组[5 mg/(kg·d)]和联合用药3组(依厄组、依氨组、厄氨组),每组6只;另6只为假手术组。测大鼠术前、术后血压,用药6周后,测大鼠左心室重量指数(LVMI),HE染色观察左心室病理变化,用生物酶学方法测左心室肌钠泵、钙泵活性。结果与假手术组比较,模型组收缩压和LVMI显著增高,左心室离子泵活性降低(P<0.01);与模型组比较,各用药组收缩压和LVMI明显降低(P<0.01),氨氯地平组收缩压和LVMI明显高于其他用药组(P<0.05)。结论 RHR单用依那普利、厄贝沙坦的降压及逆转LVH作用优于单用氨氯地平;3种降压药均能增加左心室肌离子泵活性,联合用药无明显协同作用。     

丹参酮Ⅱ A对左心室肥厚的逆转作用及其机制

目的研究丹参酮ⅡA对大鼠腹主动脉缩窄术后左室肥厚心肌的作用及一氧化氮的影响。方法SD大鼠行腹主动脉缩窄术建立高血压左室心肌肥厚模型,术后4周将手术大鼠随机分为假手术组、未治疗左室肥厚(LVH)组、丹参酮低剂量组[10mg/(kg.d),腹腔注射]、丹参酮高剂量组[20mg/(kg.d),腹腔注射]及缬沙坦组[10mg/(kg.d),灌胃],每组各8只。用药8周后通过超声心动图测定左室后壁、室间隔的厚度;取左心室组织检测左心室质量指数(LVMI)、病理切片HE染色测量心肌纤维直径(MFD);硝酸还原法测定心肌组织NO的含量、免疫印迹法(Western blot)检测蛋白激酶C(PKC)蛋白的表达。结果腹主动脉缩窄术后,SD大鼠血压明显升高,出现左心室肥厚。缬沙坦可降低大鼠的血压[(136±15)mm Hg]并减轻左心室肥厚。低剂量、高剂量丹参酮组与LVH组相比虽不能降低血压[(188±11)、(187±14)mm Hg vs(186±13)mm Hg,P>0.05],但能明显减低左室后壁、室间隔厚度、LVMI、MFD值(P<0.01),同时可使心肌的NO明显增加[(12.8±1.7)、(12.0±1.4)vs(5.8±1.1)μmol/g,P<0.01],心肌PKC蛋白的表达明显下调[(0.605±0.051)、(0.519±0.062)vs(1.291±0.117),P<0.01]。结论丹参酮ⅡA对心肌肥厚的逆转作用是非血压依从性的,丹参酮Ⅱ A可能通过促进心肌局部NO的产生、抑制PKC蛋白的表达起到阻止、逆转高血压心肌肥厚的发展。     

丹参酮Ⅱ A对左心室肥厚的逆转作用及其机制

目的 研究丹参酮Ⅱ A对大鼠腹主动脉缩窄术后左室肥厚心肌的作用及一氧化氮的影响.方法 SD大鼠行腹主动脉缩窄术建立高血压左室心肌肥厚模型,术后4周将手术大鼠随机分为假手术组、未治疗左室肥厚(LVH)组、丹参酮低剂量组[10 mg/(kg·d),腹腔注射]、丹参酮高剂量组[20 mg/(kg·d),腹腔注射]及缬沙坦组[10 mg/(kg·d),灌胃],每组各8只.用药8周后通过超声心动图测定左室后壁、室间隔的厚度;取左心室组织检测左心室质量指数(LVMI)、病理切片HE染色测量心肌纤维直径(MFD);硝酸还原法测定心肌组织NO的含量、免疫印迹法(Western blot)检测蛋白激酶C(PKC)蛋白的表达.结果 腹主动脉缩窄术后,SD大鼠血压明显升高,出现左心室肥厚.缬沙坦可降低大鼠的血压[(136±15)mm Hg]并减轻左心室肥厚.低剂量、高剂量丹参酮组与LVH组相比虽不能降低血压[(188±11)、(187±14)mm Hg vs(186±13)mm Hg,P＞0.05],但能明显减低左室后壁、室间隔厚度、LVMI、MFD值(P＜0.01),同时可使心肌的NO明显增加[(12.8±1.7)、(12.0±1.4)vs(5.8±1.1)μmol/g,P＜0.01],心肌PKC蛋白的表达明显下调[(0.605±0.051)、(0.519±0.062)vs(1.291±0.117),P＜0.01].结论 丹参酮对心肌肥厚的逆转作用是非血压依从性的,丹参酮Ⅱ A可能通过促进心肌局部NO的产生、抑制PKC蛋白的表达起到阻止、逆转高血压心肌肥厚的发展.     

阿托伐他汀对大鼠心肌梗死后心肌纤维化的干预作用

目的通过研究阿托伐他汀对大鼠急性心肌梗死(AMI)后periostin蛋白及转化生长因子β1(TGF-β1)mRNA的表达水平的影响,探讨阿托伐他汀对于AMI后心肌纤维化的干预作用机制。方法将60只SD雄性大鼠随机分为正常组(Sham)、单纯心肌梗死组(MI)和心肌梗死联合阿托伐他汀组(Ato);注射异丙肾上腺素造心肌梗死模型,Ato组于心肌梗死造模成功后给予阿托伐他汀5 mg/(kg·d)灌胃,MI组及Sham组以同等剂量生理盐水灌胃;各组分别于术后8周取材,病理技术:Masson染色观察并计算心肌纤维化中胶原纤维的容积分数(CVF);利用RT-PCR技术检测心肌periostin蛋白及TGF-β1 mRNA的表达水平。结果 Masson染色提示MI组及Ato组CVF均显著高于Sham组(P0.01);而Ato组CVF明显低于MI组(P0.05);RT-PCR结果MI组和Ato组较Sham组的TGF-β1 mRNA及periostin蛋白表达量均显著增加(P0.01);Ato组比MI组TGF-β1 mRNA及periostin蛋白的表达量显著下降(P0.05)。结论阿托伐他汀能够抑制periostin蛋白和TGF-β1 mRNA的表达,其机制可能为抑制TGF-β1/periostin信号传导通路,进而抑制心肌纤维化,并保护心脏功能。     

阿托伐他汀对兔舒张性心力衰竭模型心室重构的影响

目的:研究阿托伐他汀改善舒张性心力衰竭(心衰)心室重构的作用.方法:30只新西兰白兔随机分为3组,舒张性心衰组(n=10,腹主动脉缩窄术),阿托伐他汀组[n=10,腹主动脉缩窄术后给予阿托伐他汀5mg/(kg·d)],假手术组(n=10,进行假手术操作);通过心脏超声和血流动力学检查比较3组心功能的差异,通过心肌胶原含量测定(羟脯氨酸法)和天狼猩红染色(PRS)测定胶原面积(CA)、容积分数(CVF)及Ⅰ和Ⅲ型胶原的面积比值比较3组间质重构的差异.结果:心脏超声检查显示,术后12周与假手术绢比较,舒张性心衰组室间隔厚度、左心室后壁厚度明显增厚,二尖瓣舒张早期血流峰值/舒张晚期血流峰值下降,等容舒张期时间延长;左心室舒张末压升高,等容舒张期松弛时间常数延长,左心室重量/体重增高,肺脏重量/体重增高;胶原含量增高,胶原面积增大,胶原容积分数升高及Ⅰ型和Ⅲ型胶原面积比例升高,差异均有统计学意义(P<0.05或P<0.01).阿托伐他汀组上述指标(除左心室重量/体重)与舒张性心衰组比较差异均有统计学意义(P<0.05或P<0.01).结论:阿托伐他汀可以明显改善心室重构,延缓整个舒张性心衰的病程.     

阿托伐他汀对高血压大鼠心脏血管紧张素转换酶2表达的影响

目的 观察阿托伐他汀对两肾一夹高血压大鼠心脏血管紧张素转换酶2及心肌重构表达的影响,探讨阿托伐他汀改善心肌重构可能的新作用机制.方法 40只雄性Wistar大鼠随机分为5组,每组8只:假手术组、血管紧张素转换酶2高血压组、缬沙坦组、阿托伐他汀10 mg/(kg·d)组和阿托伐他汀30 mg/(kg·d)组.测定药物干预后血压变化及全心重量、左心室重量、左心室重量指数;免疫组织化学法检测心脏血管紧张素转换酶2蛋白表达;放射免疫法测定心肌组织血管紧张素Ⅱ水平;逆转录聚合酶链反应法检测心脏血管紧张素转换酶2 mRNA表达.结果 (1)高剂量阿托伐他汀组较高血压组血压降低显著(P<0.01).(2)药物干预后高剂量阿托伐他汀组全心重量、左心室重量、左心室重量指数低于高血压组(P<0.05).(3)高剂量阿托伐他汀组较高血压组降低心肌组织血管紧张素Ⅱ浓度显著(P<0.01).(4)缬沙坦组、阿托伐他汀组心脏血管紧张素转换酶2蛋白表达较高血压组增强.(5)逆转录聚合酶链反应显示各组大鼠心脏组织中均有血管紧张素转换酶2 mRNA的表达,缬沙坦组,低剂量、高剂量阿托伐他汀组较高血压组不同程度增高(P<0.05).结论 阿托伐他汀在降低血压的同时,具有改善心肌重构作用,其可能是通过降低心肌组织血管紧张素Ⅱ浓度,增加心脏组织血管紧张素转换酶2蛋白表达,增加心脏组织血管紧张素转换酶2 mRNA表达来实现的.     

胰岛素瘤的解剖分布特点分析

目的胰岛素瘤是最常见的胰腺神经内分泌肿瘤，因其临床表现多样，导致诊断困难。影像学诊断尤其是超声内镜(EUS)在胰岛素瘤的诊断中起着重要作用，拥有较高的敏感性和特异性。本研究拟通过明确胰岛素瘤的解剖分布特点，以期有助于提高影像学的诊断准确率和降低漏诊率，尤其是在教育和培训实践中对于EUS的学习者更具有指导价值。 方法回顾性分析解放军总医院第一医学中心病案资料数据库1993年1月至2019年11月经外科手术、病理确诊为胰岛素瘤的患者的临床资料，检索方法采取搜索术后病理诊断为"胰岛素瘤"的病例，通过查阅病例的方法，提取出胰岛素瘤的大小和解剖分布等数据，进一步分析其特点。 结果共检索到确诊为胰岛素瘤的患者116例，其中，男45例、女71例，年龄13～76岁，平均年龄(44.4±14.85)岁。胰岛素瘤单发110例(94.8%)、多发6例(5.2%)。位置分布：头颈部46例(39.7%)，单发45例、多发1例；体尾部68例(58.6%)，单发65例、多发3例；全胰腺多发2例(1.7%)。病变大小特点：最大径0.4～3.4 cm，平均大小(1.53±0.58)cm。≤1 cm 29例、>1 cm而≤1.5 cm41例、>1.5 cm而≤2.0 cm28例，≤3 cm 15例，>3 cm 3例。年龄与肿瘤的大小相关，≤44岁患者肿瘤平均大小为(1.36±0.51)cm、>44岁患者肿瘤平均大小为(1.70±0.60)cm，P<0.05。头颈部的肿瘤大于体尾部的肿瘤，头颈部肿瘤平均大小(1.66±0.63)cm，体尾部(1.42±0.52)cm，P<0.05。 结论胰岛素瘤在胰腺体尾部较头颈部更好发；绝大多数单发，但可以全胰腺多发；多数小于1.5 cm，肿瘤的大小与患者年龄和肿瘤的解剖分布相关。     

Pathogenesis of carcinoma of the papilla of Vater

Most adenomas and carcinomas of the small intestine and extrahepatic bile ducts arise in the region of the papilla of Vater. In familial adenomatous polyposis (FAP) it is the main location for carcinomas after proctocolectomy. In many cases symptoms due to stenosis lead to diagnosis at an early tumor stage. In about 80%, curative intended resection is possible. Operability is the most relevant prognostic factor. Most ampullary carcinomas resp. carcinomas of the papilla of Vater develop from adenomatous or flat dysplastic precursor lesions. They can be sited in the ampulloduodenal part of the papilla of Vater, which is lined by intestinal mucosa. They also can develop in deeper parts of the ampulla, which are lined by pancreaticobiliary duct mucosa. Intestinal-type adenocarcinoma and pancreaticobiliary-type adenocarcinoma represent the main histological types of ampullary carcinoma. Furthermore, there exist unusual types and undifferentiated carcinomas. Many carcinomas of intestinal type express the immunohistochemical marker profile of intestinal mucosa (keratin 7?, keratin 20+, MUC2+). Carcinomas of pancreaticobiliary type usually show the immunohistochemical profile of pancreaticobiliary duct mucosa (keratin 7+, keratin 20?, MUC2?). Even poorly differentiated carcinomas, as well as unusual histological types, may conserve the marker profile of the mucosa they developed from. These findings underline the concept of histogenetically different carcinomas of the papilla of Vater which develop either from intestinal- or from pancreaticobiliary-type mucosa of the papilla of Vater. Molecular alterations in ampullary carcinomas are similar to those of colorectal as well as pancreatic carcinomas, although they appear at different frequencies. In future studies, molecular alterations in ampullary carcinomas should be correlated closely with the different histologic tumor types. Consequently, the histologic classification should reflect the histogenesis of ampullary tumors from the two different types of papillary mucosa.     

Demonstration of the mechanism of action of biguanides

Summary Palmitic acid oxidation in rat diaphragm homogenate is depressed by biguanide concentrations that are still incapable of inhibiting oxidative phosphorylation. Glucose oxidation is not directly effected by the same biguanide concentrations: however, the inhibitory effect of palmitic acid on glucose oxidation is partly removed by biguanides. Inhibition of fatty acid oxidation, which accounts for most of the metabolic effects caused by these drugs, can be regarded as the fundamental mechanism of action of biguanides. There is some evidence suggesting that these drugs might interact with carnitine, thus preventing long-chain fatty acids from being transported across the mitochondrial membrane to the site of oxidation. Traduzione a cura degli AA.     

Lack of correlation of degree of villous atrophy with severity of clinical presentation of coeliac disease

BACKGROUND AND AIM: Both the clinical presentation and the degree of mucosal damage in coeliac disease vary greatly. In view of conflicting information as to whether the mode of presentation correlates with the degree of villous atrophy, we reviewed a large cohort of patients with coeliac disease. PATIENTS AND METHODS: We correlated mode of presentation (classical, diarrhoea predominant or atypical/silent) with histology of duodenal biopsies and examined their trends over time. RESULTS: The cohort consisted of 499 adults, mean age 44.1 years, 68% females. The majority had silent coeliac disease (56%) and total villous atrophy (65%). There was no correlation of mode of presentation with the degree of villous atrophy (p=0.25). Sixty-eight percent of females and 58% of males had a severe villous atrophy (p=0.052). There was a significant trend over time for a greater proportion of patients presenting as atypical/silent coeliac disease and having partial villous atrophy, though the majority still had total villous atrophy. CONCLUSIONS: Among our patients the degree of villous atrophy in duodenal biopsies did not correlate with the mode of presentation, indicating that factors other than the degree of villous atrophy must account for diarrhoea in coeliac disease.     

血吸虫童虫生长发育及其机制的研究进展

血吸虫童虫是宿主免疫系统攻击的重要靶标,包括皮肤型、肺型和肝门型童虫。宿主分子对童虫生长发育具有重要作用。童虫生长发育机制包括免疫调节、信号转导、性别发育及凋亡等。肌动蛋白、组织蛋白酶、烯醇化酶和葡萄糖基转移酶等分子为血吸虫童虫生长发育的重要分子。本文对血吸虫童虫生长发育及其机制的研究进展做一综述。     

氯硝柳胺悬浮剂的毒性评价

目的评价氯硝柳胺悬浮剂的毒性，为现场大规模应用灭螺提供依据。方法按照中华人民共和国国家标准GB 15670-1995《农药登记毒理学试验方法》和鱼类毒性试验方法进行。结果经口、经皮肤的LDso雌、雄性大鼠均>5 000 mg/kg，经呼吸道的LCso雌、雄性大鼠均>5 000mg/m3，该药经口、经皮肤、经呼吸道毒性均属微毒类药物；兔眼用药后，观察期内无不良反应，对眼无刺激性；皮肤用药后对皮肤无刺激性。与氯硝柳胺原药、氯硝柳胺乙醇胺盐原药和氯硝柳胺乙醇胺盐可湿性粉剂相比，氯硝柳胺悬浮剂对鱼急性毒性最低。结论氯硝柳胺悬浮剂属微毒类药物，对鱼的毒性低于其乙醇胺盐可湿性粉剂，适合于现场应用。     

124例耐多药结核分枝杆菌基因突变特征分析

目的对临床分离的耐多药结核分枝杆菌相关基因的突变特征进行分析。方法对124例耐多药结核分枝杆菌以及50株敏感株的耐药相关基因(包括异烟肼inh A、kat G、oxyR-ahp C间隔区以及利福平rpo B)进行序列测定,分析其基因突变情况。结果异烟肼耐药inh A基因突变率为14.5%;kat G基因突变率为70.2%(87/124),主要位于315位;oxyR-ahp C间隔区突变率为15.3%;inh A、kat G两种基因同时突变率75.0%,三种基因同时突变率为89.5%。利福平rpo B基因突变的检出率高达95.2%,突变主要发生在531、526、516位点。结论我省耐多药菌异烟肼耐药相关基因最常见突变为kat G 315、inh A C-T(-15)、axyR-ahp C间隔区(-10)C-T,利福平为rpo B531、526、516。结合MDR-TB耐药相关基因的特征分析,可以建立一种快速、准确、特异的适合于我省的检测结核菌耐多药性的新方法。     

Assessment of quality of life of parents of children with juvenile chronic arthritis

The aim of the study was to assess the quality of life (QOL) and the psychological status of parents of children with juvenile chronic arthritis (JCA). The QOL, anxiety and depression of the parents of 28 children with JCA were evaluated and compared to those of the parents of 28 healthy children. Mothers of JCA children and mothers of healthy children reported similar QOL. The reported anxiety and depression levels were similar for mothers and fathers in both groups. The parents of children with pauciarticular-type JCA reported lower QOL and higher levels of anxiety and depression than the parents of children with other types, namely polyarticular and systemic JCA. These findings may be explained by the fact that the pauciarticular patients had shorter disease duration and were less frequently seen in the outpatient clinic. The QOL of mothers of children with JCA was found to be slightly impaired in the group of children with pauciarticular JCA. Future larger studies are needed to confirm these results, as the number of subjects in the three groups was rather low. Received: 26 September 2001 / Accepted: 8 February 2002     

Numerical Simulation of the Effect of Rate of Change of Glucose on Measurement Error of Continuous Glucose Monitors

Background

A 5-day in-patient study designed to assess the accuracy of the FreeStyle Navigator® Continuous Glucose Monitoring System revealed that the level of accuracy of the continuous sensor measurements was dependent on the rate of glucose change. When the absolute rate of change was less than 1 mg•dl⁻¹•min⁻¹ (75% of the time), the median absolute relative difference (ARD) was 8.5%, with 85% of all points falling within the A zone of the Clarke error grid. When the absolute rate of change was greater than 2 mg•dl⁻¹•min⁻¹ (8% of the time), the median ARD was 17.5%, with 59% of all points falling within the Clarke A zone.

Method

Numerical simulations were performed to investigate effects of the rate of change of glucose on sensor measurement error. This approach enabled physiologically relevant distributions of glucose values to be reordered to explore the effect of different glucose rate-of-change distributions on apparent sensor accuracy.

Results

The physiological lag between blood and interstitial fluid glucose levels is sufficient to account for the observed difference in sensor accuracy between periods of stable glucose and periods of rapidly changing glucose.

Conclusions

The role of physiological lag on the apparent decrease in sensor accuracy at high glucose rates of change has implications for clinical study design, regulatory review of continuous glucose sensors, and development of performance standards for this new technology. This work demonstrates the difficulty in comparing accuracy measures between different clinical studies and highlights the need for studies to include both relevant glucose distributions and relevant glucose rate-of-change distributions.     

Study of constancy of hydrogen-consuming flora of human colon

The constancy of the hydrogen consuming flora of the human colon was studied in 15 healthy subjects via two measurements obtained 18 to 36 months apart. Hydrogen disappearance rate and the major products of H₂-consuming bacteria, methane and sulfide, were measured during incubation of fecal homogenates with excess hydrogen and sulfate. In 11/15, the hydrogen consumption rate and the predominant hydrogen-consuming pathway (methanogenesis, sulfate reduction, or neither) remained constant. However, major shifts in these pathways were observed in four subjects, with two losing and two gaining the ability to produce methane. Methanogenesis was associated with the highest hydrogen consumption rate. This study demonstrates that clinically unrecognizable, major alterations of the colonic flora occur in healthy subjects. Understanding of the factors responsible for these alterations might allow for therapeutic manipulation of the colonic flora.Supported in part by the Department of Veterans Affairs and NIDDKD RO1 DK 13309-25.