一氧化氮对急性肺损伤发病过程中核因子-κB活化的调节作用

目的:探讨一氧化氮(NO)在急性重症胰腺炎急性肺损伤大鼠发病中的作用及肺泡巨噬细胞核因子-κB(NF-κB)活化的关系．方法:健康雄性SD大鼠随机分为:假手术组、模型组、硝普钠(SNP)组、左旋精氨酸组、氨基胍组,每组6只．经胰管逆行注入去氧胆酸钠复制大鼠急性重症胰腺炎急性肺损伤模型．采用凝胶电泳迁移率方法检测肺泡巨噬细胞中NF-κB活性,RT-PCR分析iNOS mRNA 的表达,同时亦检测NO、TNF-α、iNOS的水平和肺组织病理学的改变．结果:模型组中NF-κB活性、iNOS mRNA表达及TNF-α、NO、iNOS的含量均显著高于假手术组(P=0．02)．肺组织病理学显示严重损害．NO的供体硝普钠及iNOS选择性抑制剂氨基胍可降低NF-κB活性(213．47±12．34, 222．98±17．69 vs 327．13±13．46,P<0．05),下调iNOS mRNA表达(SNP:2．35±0．34 vs 3．1 ±0．38,P<0．05)以及TNF-α(0．38±0．034, 0．45±0．043 μg/L vs 0．76±0．045 μg/L)、 NO(168．2±0．78,146．4±0．59 mmol/L vs 229．3 ±0．98 mmol/L)的水平,减轻肺组织病理学损伤．而左旋精氨酸组则无明显调节作用．离体实验结果与体内试验一致．结论:外源性NO可抑制NF-κB活化,降低 iNOS mRNA的表达,进而减少NO、TNF-α的释放．同样,经iNOS选择性抑制剂抑制内源性 NO的产生,也可控制机体的过度炎症反应．     

环氧合酶-2对人肝癌细胞增殖和凋亡的调节作用

目的:观察环氧合酶-2(cyclooxygenase-2, COX-2)在肝癌细胞中表达,探讨COX-2抑制剂celecoxib对肝癌细胞增殖和凋亡的作用．方法:免疫细胞化学、逆转录聚合酶链反应(RT-PCR)方法研究COX-2在肝癌细胞株中表达;MTT法观察COX-2抑制剂对肝癌细胞增殖的影响;透射电镜及流式细胞仪观察 celecoxib诱导肝癌细胞凋亡的作用、对细胞周期的影响及MDR1／P-gp表达的变化;用RTPCR 方法检测Survivin mRNA药物处理后表达的变化．结果:celecoxib对肝癌细胞抑制增殖、诱导凋亡呈时间和剂量依赖性．celecoxib作用HepG2 48 h抑制率为70．98％±0．67％(200 μmol／L)、 47．93％±1．08％(100 μmol／L);Bel-7402为 57．29％±0．67％(200 μmol／L)、43．84％± 0．86％(100 μmol／L);同样浓度但作用20 h, HepG2为45．51％±1．35％(200 μmol／L), 14.35％±1．55％(100 μmol／L);Bel-7402则为34．35％±0．63％(200 μmol／L),15．35％± 0．88％(100 μmol／L),不同浓度以及不同作用时间相比均有显著差异(P<0．01);100 μmol／L celecoxib作用24,48,72,96 h的肝癌细胞凋亡率分别为12．2％±2．44％,4．0％±1．67％,20．4％±4．38％,57．9％±5．74％(HepG2)和3．0％± 1．05％,18．5％±3．51％,29.3％±3．25％,48．4％±4．77％(Bel-7402),与对照组相比有显著差异(P<0．01);细胞周期分布改变,G0／G1期细胞比例增加,24,48,72 h分别为:44．17％±1．01％,59．60％±0．61％,62．7％±1．22％ (HepG2)和47．80％±0．41％,58．60％±0．46％, 78．40％±1．95％(Bel-7402),与对照组比较有显著差异(P<0．01);对照组PCNA蛋白表达呈强阳性( ),经药物处理后表达减弱,并随时间延长而显著;HepG2中COX-2蛋白表达明显弱于Bel-7402,药物处理后表达也不同．Survivin在肝癌细胞株中呈高表达状态, celecoxib作用48 h mRNA表达降至零,而72 h 后表达水平又有上升;两株肝癌细胞中经 celecoxib处理后,MDR1／P-gp表达有降低的趋势(Bel-7402),或是基本上不受影响(HepG2)．结论:COX-2抑制剂celecoxib体外对肝癌细胞有较强的细胞毒作用且以剂量、时间依赖方式抑制细胞增殖,并诱导凋亡,使细胞周期阻滞于G1／S期．COX-2与P-gp,Survivin表达密切相关．     

呼吸道合胞病毒感染巨噬细胞诱导炎性基因表达的部分机制研究

目的探讨呼吸道合胞病毒(RSV)感染巨噬细胞时前炎介质肿瘤坏死因子-α(TNF-α)和诱导型一氧化氮合酶(iNOS)的基因表达变化及其调控的相关机制,为研究RSV的致病机制及有效预防和治疗RSV疾病提供新的思路。方法以RSV感染RAW264.7巨噬细胞,并设立不同的感染时间点(1h、4h、8h、16h和24h),同时给予PDTC(核转录因子NF-κB的特异性抑制剂)处理。以紫外线灭活RSV(UV-RSV)来分析有传染性的病毒的感染变化。收集各组细胞,用Western blot法检测细胞核内活性NF-κBp65蛋白的表达,半定量RT-PCR法检测TNF-α和iNOS mRNA表达量。结果RSV感染4h后,细胞核内活性NF-κBp65蛋白、TNF-α和iNOS mRNA表达均明显升高,各指标的变化与正常对照相比,差异均有显著性,并且与RSV感染存在时间依赖关系。当加入PDTC抑制NF-κB的入核活化后,则可显著下调相应时间点的RSV感染升高的TNF-α和iNOS mRNA表达量,使其降低至基线水平。而UV-RSV感染后并不引起NF-κB蛋白、TNF-α和iNOS mRNA的表达量增加(P>0.05)。结论RSV感染巨噬细胞可诱导前炎基因TNF-α和iNOS的大量表达,其表达可能主要依赖NF-κB活化,并且与病毒复制有关。提示在RSV感染的巨噬细胞中,NF-κB活化对TNF-α和iNOS基因表达具有重要的正调控作用。     

塞来昔布对人肝癌细胞株HepG2细胞核转录因子-KB活性及蛋白表达的抑制

目的: 探讨环氧合酶-2选择性抑制剂塞来昔布(celecoxib)对人肝癌细胞株HepG2细胞核转因子-κB(nuclear factor-kappa B, NF-κB)活性和蛋白表达的影响.方法:不同浓度的塞来昔布作用于HepG2细胞后,应用凝胶电泳迁移率改变分析技术检测H印G2细胞中NF-κB DNA结合活性;用Western blotting法检测H印G2细胞NF-κB p65蛋白表达.结果:25、50μmol/L塞来昔布作用于HepG2细胞后,药物处理组HepG2细胞NF-κd DNA结合活性明显降低,与空白对照组相比有显著性差异(t=12.58,P=0.000;t=17.97,P=0.000);塞来昔布可明显抑制HepG2细胞NF-κB p65蛋白表达水平,与空白对照组相比,差异均有统计学意义(t=4.24,P=0.013;t=6.38,P=0.003).结论:塞来昔布能有效抑制HepG2细胞NF-κB活性及NF-κB p65蛋白表达.     

约氏疟原虫环子孢子蛋白对TNF-α刺激人肝癌细胞株核转录因子活化的抑制作用

目的 观察约氏疟原虫环子孢子蛋白（CSP）对肿瘤坏死因子α（TNF-α）刺激人肝癌细胞株HepG2核转录因子-κB （NF-κB）活化的影响。 方法 以约氏疟原虫BY265株子孢子总RNA为模板,用RT-PCR扩增CSP基因的编码区序列并克隆至pFLAG-CMV8载体,构建重组质粒pFLAG-CMV8-CSP。以兔抗CSP多克隆抗体间接免疫荧光法观察pFLAG-CMV8-CSP能否在HepG2细胞中正确表达,及其在细胞中的分布。实验分为3组,A组（阴性对照组）为转染质粒pFLAG-CMV8的HepG2细胞,B组以100 ng/ml TNF-α刺激转染质粒pFLAG-CMV8的HepG2细胞,C组以100 ng/ml TNF-α刺激转染质粒pFLAG-CMV8-CSP的HepG2细胞。采用双荧光素酶试验和凝胶迁移试验（EMSA）检测NF-κB 的核转位及其活化,观察pFLAG-CMV8?鄄CSP对于TNF-α刺激HepG2细胞活化NF-κB是否具有抑制作用。 结果 　质粒pFLAG-CMV8-CSP主要在HepG2细胞胞浆中表达。 检测HepG2细胞浆中NF-κB活性,C组萤火虫荧光素酶活性与海肾荧光素酶活性比值为0.228±0.029,明显低于B组（0.571±0.030）和A组（0.438±0.085）（P＜0.05）。EMSA结果显示,C组的条带明显弱于B组。　结论 位于细胞浆中的疟原虫CSP蛋白通过抑制NF-κB核转位, 从而抑制TNF-α刺激HepG2细胞活化NF-κB。     

阿司匹林抑制肿瘤坏死因子α诱导的人脐静脉内皮细胞分形趋化因子表达

背景 分形趋化因子通过介导炎症细胞的趋化与血管内皮损伤相关,阿司匹林具有抗炎作用,抑制多种细胞因子表达,其对分形趋化因子的影响尚无报道.目的 探讨阿司匹林对肿瘤坏死因子α(TNF-α)刺激的人脐静脉内皮细胞(HUVEC)分形趋化因子表达的影响和作用机制.方法 将HUVEC随机分为:空白组(无TNF-α刺激和药物干预),TNF-α刺激组,TNF-α PDTC干预组(PDTC系核因子κB的特异性活性抑制剂),TNF-α NS398干预组(NS398是COX-2的特异性活性抑制剂).TNF-α 阿司匹林0 02 mol/L干预组,TNF-α 阿司匹林0 2 mol/L干预组,TNF-α 阿司匹林1 mol/L干预组,TNF-α 阿司匹林5 mol/L干预组,共8组,每组3例.分别用RT-PCR法和Western blot法检测各组细胞分形趋化因子(分形素)和核因子κB p65(NF-κB p65)的mRNA水平和蛋白表达.结果 1)4 μg/L TNF-α使HUVEC的分形趋化因子mRNA水平和蛋白表达明显增加(P<0 01).2)阿司匹林浓度依赖性抑制TNF-α诱导的HUVEC分形趋化因子mRNA水平和蛋白表达(P<0 01);阿司匹林浓度依赖性地抑制HUVEC的NF-κB p65 mRNA水平和蛋白表达(P<0 01).3)PDTC抑制TNF-α诱导的HUVEC分形趋化因子mRNA水平和蛋白表达(均P<0 01).结论 阿司匹林通过NF-κB p65途径抑制TNF-α诱导的HUVEC 分形趋化因子mRNA水平和蛋白表达,并可能借此发挥抗动脉粥样硬化作用.     

Toll样受体4和核因子-κB信号通路在溶血磷脂酸致动脉粥样硬化中的作用

目的探讨Toll样受体4(TLR4)/NF-κB信号通路在溶血磷脂酸(LPA)致动脉粥样硬化中的作用。方法以不同浓度LPA(0¹0μmol/L)刺激人单核细胞株THP-1细胞4h,以及LPA 1μmol/L处理THP-1细胞不同时间(010μmol/L)刺激人单核细胞株THP-1细胞4h,以及LPA 1μmol/L处理THP-1细胞不同时间(0⁸h),荧光定量RT-PCR法测定TLR4mRNA表达,Western blot检测TLR4蛋白、细胞核NF-κB p65表达变化,ELISA法测定细胞因子TNF-α,随后在LPA 1μmol/L条件下,TLR4单抗干预THP-1细胞,观察其对LPA诱导的细胞核NF-κB p65表达及TNF-α分泌水平的影响。结果当LPA 1μmol/L时,TLR4mRNA和蛋白及细胞核NF-κB p65表达较0μmol/L、0.1μmol/L、0.5μmol/L、5μmol/L、10μmol/L LPA明显增高,差异有统计学意义(P<0.01)。LPA 1μmol/L处理THP-1细胞4h时,THP-1细胞TLR4mRNA和蛋白及细胞核NF-κB p65表达水平明显高于0、1、2、8h(P<0.01)。与TLR4单抗干预前比较,TLR4干预后LPA诱导的THP-1细胞NF-κB p65表达及TNF-α分泌水平明显升高,差异有统计学意义(P<0.01)。结论 LPA可显著上调THP-1细胞TLR4表达及促进NF-κB的活化,LPA致动脉粥样硬化作用可能部分是由TLR4/NF-κB信号途径介导的。     

异鼠李素对高糖高脂诱导胰岛β细胞损伤保护作用的研究

目的探讨异鼠李素(ISO)对高糖高脂诱导小鼠胰岛β细胞株MIN6细胞损伤的保护作用及机制。方法不同浓度ISO预处理MIN6细胞后高糖高脂培养48 h,CCK8法筛选ISO最佳干预浓度。细胞分为正常对照(Con)组(11. 1 mmol/L葡萄糖)、高糖高脂损伤模型(M)组(33. 3 mmol/L葡萄糖+0. 25 mmol/L棕榈酸)及ISO预处理(ISO+M)组(10μmol/L ISO+33. 3 mmol/L葡萄糖+0. 25 mmol/L棕榈酸)。流式细胞术测定各组细胞凋亡率;硝酸还原酶法检测一氧化氮(NO)含量;RT-PCR测定IL-1β、IL-6、肿瘤坏死因子α(TNF-α)mRNA表达;Western blot法检测磷酸化核因子κB(NF-κB)抑制蛋白(IκB)激酶β(p-IKKβ)、磷酸化NF-κB抑制蛋白α(p-IκBα)、诱导型一氧化氮合酶(iNOS)及NF-κB p65蛋白的表达。结果细胞凋亡及NO含量M组高于Con组,ISO+M组低于M组(P0. 01)。IL-1β、IL-6、TNF-αmRNA,p-IKKβ、p-IκB、iNOS蛋白与NF-κB p65蛋白表达M组高于Con组,ISO+M组低于M组(P0. 05)。结论 ISO可减轻高糖高脂诱导的胰岛β细胞损伤,可能与抑制IκB激酶(IKK)/IκB/NF-κB/iNOS通路活性有关。     

NF-κB信号传导通路相关基因不同表型肝癌患者尿8-OHdG水平观察

目的观察NF-κB信号传导通路相关基因不同表型的肝癌患者尿8-羟基脱氧鸟苷（8-OHdG）水平。方法 PCR-RFLP法检测155例肝癌患者（肝癌组）NF-κB信号传导通路中TNF-α、NF-κB、iNOS、COX-2的基因表型。采用ELISA法检测肝癌组及151例健康体检者（对照组）的尿8-OHdG。结果肝癌组尿8-OHdG水平为（9.29±8.04）ng/mg Cr,对照组为（7.27±5.06）ng/mg Cr,两组相比,P〈0.05。肝癌组NF-κB信号传导通路相关基因TNF-α、NF-κB、iNOS、COX-2基因不同表型组尿8-OHdG水平相比,P均〉0.05。结论肝癌患者尿8-OHdG水平高于正常,可能与肝癌发病有关。NF-κB信号传导通路相关基因多态性与肝癌患者尿8-OHdG水平无明显关系。     

肝癌耐药细胞中MDR1 mRNA、P-糖蛋白的表达变化及意义

目的观察肝癌耐药细胞中MDR1 mRNA及P-糖蛋白的表达变化,并探讨其临床意义。方法采用药物浓度递增法,诱导产生对盐酸阿霉素（Adr）具有稳定耐药性的肝癌HepG2细胞（HepG2Adr）;采用RT—PCR及免疫组化SP法,分别检测HepG2、HepG2Adr细胞中的MDR1 mRNA、P-糖蛋。结果经0．01、0．10、1．00、10．00μmol／LAdr诱导产生的HepG2Adr细胞中MDR1 mRNA的表达量分别为0．26±0．11、0．56±0．17、10．78±0．2、1．21±0．17,P-糖蛋白阳性表达率分别为15．44％±4．55％、26．76％±5．23％、64．21％±14．22％、90．23％±7．68％;HepG2细胞中MDR1 mRNA、P-糖蛋白分别为0．18±0．08、5．73％±0．52％。肝癌HepG2Adr细胞与HepG2细胞中MDR1 mRNA、P-糖蛋白表达量比较,P均〈0．05;且随着肝癌HepG2Adr细胞耐药性增高,MDR1 mRNA、P-糖蛋白表达量逐渐增高（P均〈0．05）。结论肝癌耐药细胞中MDR1 mRNA及P-糖蛋白高表达,二者可能与肝癌多药耐药的产生有关。     

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。     

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。     

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。     

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.     

Angiographic diagnosis of the degree of serosal invasion of carcinoma of the colon

Angiography using Prostaglandin El^® was performed on 38 patients with carcinoma of the colon in order to diagnose the degree of serosal cancer invasion. The findings at angiography were classified into four groups:1) AG-S3, abnormal change (irregularity and/or encasement) up to marginal vessels; 2) AG-S2, abnormality up to vasa recta; 3) AG-S1, abnormality of penetrating branches of vasa recta within the wall of the colon; and 4) AG-S0, no distinct findings of abovementioned vessels. These angiographic findings were compared with both macroscopic and microscopic serosal cancer invasion. Angiographic diagnosis is in accord with the macroscopic findings in 84.2 percent of cases. Angiographic diagnosis is in accord with the microscopic findings in 32.4 percent of cases. Macroscopic findings confirm the angiographic diagnosis precisely but the conflict with microscopic findings should not be overlooked. This may be the result of inflammatory change, adhesion, and fibrosis around carcinoma of the colon.