高浓度葡萄糖对人胰岛β细胞凋亡影响的分子机制

目的　初步探讨高浓度葡萄糖对人胰岛 β细胞凋亡的影响及其分子机制。　 方法　分离培养人胰岛细胞 ,并分为对照组、高糖组和高糖 氨基胍组 ,3 7℃ ,5 %CO2 培养 72h ,测定培养液上清液中胰岛素、一氧化氮 (NO)、还原性谷胱甘肽 (GSH)水平。原位末端核苷酸标记法 (TUNEL)和胰岛素免疫组化双染色法及ELISA法检测胰岛 β细胞凋亡 ,RT PCR检测胰岛细胞p5 3、Bcl 2和胰岛素基因启动转录因子 1 (PDX 1 )mRNA表达水平。　结果　高糖组胰岛 β细胞凋亡小体富计因子(1 91± 0 6 9)、β细胞凋亡率 (1 4 8% )、NO〔(1 82 3± 1 5 5 ) μmol/L〕和 p5 3mRNA(0 3 0 6± 0 0 3 9)表达水平均显著高于高糖 氨基胍组〔分别为 1 1 9± 0 3 3、6 8%、(1 5 4 2± 1 9 7) μmol/L、0 1 3 9±0 0 6 9,P <0 0 1〕和对照组〔分别为 1 0 6± 0 2 6、4 2 %、(1 1 7 3± 2 1 7) μmol/L、0 1 2 5± 0 0 1 5 ,P <0 0 5〕 ,而胰岛素释放量、GSH、bcl 2mRNA和PDX 1mRNA表达水平则显著低于高糖 氨基胍组(P <0 0 5 )和对照组 (P <0 0 5 )。　结论　高浓度葡萄糖可通过诱导人胰岛 β细胞凋亡及PDX 1表达降低使胰岛素分泌减少 ,其机制与高糖状态下胰岛 β细胞抗氧化能力降低引起NO介导的p5 3高表达和PDX 1低表     

迷迭香酸通过核转录因子-κB信号通路对抗谷氨酸诱导PC12细胞损伤

目的观察迷迭香酸(RA)对抗谷氨酸诱导的PC12细胞损伤发挥神经保护作用,探讨其机制是否与NF-κB信号通路相关。方法将培养细胞分为对照组、损伤组(16 mmol/L谷氨酸)、RA1组(30μmol/L RA+16 mmol/L谷氨酸)、RA2组(60μmol/L RA+16 mmol/L谷氨酸)。采用MTT法检测细胞活力;Hoechst33258荧光染色观察细胞核形态的改变,碘化丙啶染色流式细胞仪检测细胞凋亡;Western blot检测NF-κB信号通路相关蛋白表达水平的变化。结果不同浓度谷氨酸(0、4、8、12、16、20 mmol/L)作用PC12细胞24 h后,细胞存活率呈剂量依赖性下降。与损伤组比较,RA1组和RA2组细胞存活率明显升高(P<0.05)。16 mmol/L谷氨酸作用PC12细胞1 h后,细胞质中IκBα蛋白和NF-κB p65蛋白表达明显减少,p-IκBα蛋白表达明显增加,NF-κB p65蛋白在细胞核中表达明显增加,2 h达到高峰;给予30、60μmol/L RA预处理1 h后,能抑制NF-κB p65蛋白活化进入细胞核。结论 RA通过抑制NF-κB信号通路的活化,对谷氨酸诱导损伤的PC12细胞有保护作用。     

三氧化二砷对类风湿关节炎滑膜细胞凋亡影响的体外研究

目的 探讨类风湿关节炎(RA)患者滑膜细胞的凋亡异常,以及三氧化二砷(As_2O_3)对体外培养RA的滑膜细胞凋亡的诱导作用.方法 用光镜、电镜、流式细胞仪检测As_2O_3对体外培养的RA滑膜细胞凋亡的诱导作用,As_2O_3,作用于RA滑膜后酶联免疫吸附试验(ELISA)检测凋亡过程中细胞色素C的变化,反转录-聚合酶链反应(RT-PCR)检测Caspase-3.Bel-2 mRNA表达,采用单因素方差分析和LSD-t检验、Dunnet-t检验进行统计学处理.结果 流式细胞仪检测发现不同浓度的As_2O_3作用后,滑膜细胞的凋亡较空白对照组(NC)增加[NC(0.95±0.87)%,RA(0.21±0.12)%,P<0.05],呈一定的剂量依赖性,尤其以80 μmol/L药物浓度最为明显.凋亡早期(6 h)细胞色素C水平升高80 μmol/L组升高明显[NC(0.34±0.27),80 μmol/L组(32.04±1.62),P<0.05];不同浓度的As_2O_3作用后细胞中Caspase-3 mRNA表达显著增强[NC(0.144±0.022),RA(0.323±0.047),(0.824±0.109),(1.213±0.196),P<0.05],Bcl-2的mRNA表达显著减弱[NC(1.08±0.23),RA(0.94±0.15),(0.46±0.08),(0.22±0.06),P<0.05].结论 RA患者滑膜细胞凋亡较健康埘照减少,As_2O_3通过升高细胞色素c及Caspase-3,抑制Bcl-2诱导RA滑膜细胞凋亡.     

姜黄素对肝星状细胞增殖与凋亡的影响

目的　观察姜黄素对体外培养肝星状细胞 (HSC)增殖与凋亡的影响。方法　不同浓度姜黄素处理HSC株HSC T6 ,MTT法检测细胞增殖 ,流式细胞仪、透射电镜和琼脂糖凝胶电泳法检测细胞凋亡。结果　在 2 0～ 10 0 μmol/L浓度范围内 ,姜黄素可剂量依赖性地抑制HSC增殖 (P <0 .0 1)。 2 0、4 0、6 0 μmol/L姜黄素处理HSC 2 4h后 ,细胞周期分析发现S期细胞减少 ,G2 /M期细胞显著增加 (P <0 .0 1) ;流式细胞术检测到明显的亚G1峰 ,各组的凋亡指数 (% )分别是 15 .3± 1.9,2 6 .7± 2 .8,37.6± 4 .4 ,与对照组 (1.9± 0 .6 )相比 ,差异有显著性 (P <0 .0 1) ;4 0 μmol/L姜黄素作用 12、2 4、36、4 8h ,凋亡指数 (% )分别是 12 .0± 2 .4、2 6 .7± 3.5、33.8± 1.8和 4 9.3± 1.6 ,与对照组相比 ,差异有显著性 (P <0 .0 1) ;透射电镜观察到细胞皱缩、核染色质浓缩沿核膜排列和凋亡小体形成等 ;琼脂糖凝胶电泳可见到明显的DNA梯带形成。结论　姜黄素可显著抑制HSC增殖 ,使细胞周期停滞于G2 /M期 ,并诱导其凋亡 ,其作用具有时间和剂量依赖性     

钾通道对人支气管平滑肌细胞增殖与凋亡及其相关基因表达的影响

目的　探讨电压依赖性延迟整流钾通道 (KV)、钙激活钾通道 (KCa)和ATP敏感性钾通道 (KATP)对人支气管平滑肌细胞 (HBSMCs)增殖与凋亡及其相关基因表达的影响。方法　支气管组织取材于 5例肺癌切除术患者癌旁正常的肺组织 ,将培养的HBSMCs分为 4组 :(1)对照组 (用不含药物的无血清培养基处理 ) ;(2 ) 4 氨基吡啶 (4 AP)组 (含 4mmol/L的 4 AP) ;(3)四乙铵 (TEA)组 (含 1mmol/L的TEA) ;(4)格列本脲 (Glib)组 (含 0 1mmol/L的Glib)。采用流式细胞术观察细胞的周期 ;应用荧光光度法检测细胞内钙 ;四甲基偶氮唑盐 (MTT)微量比色分析法检测细胞的增殖 ;原位末端标记法 (TUNEL)检测细胞的凋亡 ;免疫细胞化学技术检测增殖细胞核抗原 (PCNA)及凋亡相关基因Fas和FasL的表达 ,以观察 3种钾通道阻断剂对培养的HBSMCs增殖及凋亡的影响。结果 (1)对照组HBSMCs吸光度 (A)值为 0 30± 0 0 8,4 AP组为 0 6 7± 0 14 ,两组比较差异有统计学意义 (P <0 0 1) ;对照组PCNA的阳性率为 (2 3± 5 ) % ,4 AP组为 (89± 7) % ,两组比较差异有统计学意义 (P <0 0 1) ;对照组细胞内Ca2 浓度为 (98± 7)nmol/L ,4 AP组为 (2 5 5± 17)nmol/L ,两组比较差异有统计学意义 (P <0 0 1) ;对照组S G2 M期细胞数为 (12 6±     

动力相关蛋白-1参与糖皮质激素诱导的胰岛β细胞凋亡

目的探讨动力相关蛋白-1（DRP-1）对糖皮质激素诱导的胰岛13细胞凋亡的影响。方法采用地塞米松（Dex）处理大鼠胰岛13细胞系INS-1细胞，通过亚G1（Sub-G1）法检测细胞凋亡，Westernblotting检测DRP-1的表达。利用四环素诱导表达系统在INS-1细胞构建可诱导表达野生型DRP-1（DRP-1wt）基因和突变型DRP-1（DRP-1 k38A）基因的稳转细胞系，并用细胞免疫荧光和Westernblotting验证强力霉素（Dox）对转染基因的可诱导性。采用TUNEL法分析在Dex处理情况下，DRP-1wt基因或DRP．1k38A基因表达对Dex诱导的胰岛B细胞凋亡的影响，并同时测定相应细胞凋亡蛋白酶Caspase-3活性及细胞内活性氧（ROS）的变化情况。多组间均数比较采用单因素方差分析，组间两两比较采用t检验。结果不同浓度Dex处理组细胞凋亡率[（15．7±4．2）％、（30．4±3．3）％、（61．6±5．4）％]明显高于未处理组[（3．3±1．3）％，t=6．44、14．07、30．26，均P〈0．05]；200nmol／LDex处理24、48及96h后细胞凋亡率[（10．6±1．2）％、（15．1±4．6）％、（42．6±9．8）％]明显高于处理0h组[（2．4±1．3）％，t=2．99、4．63、14．66，均P〈0．05]。Westernblotting显示Dex可诱导胰岛β细胞DRP-1基因的表达。DRP-1wt基因表达能够显著促进Dex诱导的β细胞凋亡[（53．8±7．2）％比（16．2±3．2）％，t=10．02，P〈0．05]，而DRP-1k38A基因表达反而抑制Dex诱导的B细胞凋亡[（6．2±1．1）％比（14．5±1．8）％，t=10．63，P〈0．05]。DRP-1wt基因表达能够促进Dex诱导的caspase-3活化[（1979±132）比（921±182），t=11．13，P〈0．05]及ROS产生[（772±62）比（290±56），t=13．66，P〈0．05]，而DRP-1k38A基因表达反而抑制了Dex诱导的caspase-3活化[（506±47）比（681±44），t=5．25，P〈0．05]及ROS产生[（235±14）比（309±44），t=3．86，P〈0．05]。结论DRP-1参与了糖皮质激素诱导的胰岛β细胞凋亡。     

β-淀粉样肽(25-35)对PC12细胞Cyclin D1、CDK4、pRb、E2F1基因表达的影响

目的 观察β-淀粉样肽(25-35)[β-amyloid peptide (25-35),Aβ25-35]对体外血清饥饿培养PC12细胞的Cyclin D1、CDK4、pRb、E2F1基因表达的影响.方法 用终浓度为25 μmol/L Aβ25-35处理PC12细胞,流式细胞仪检测分析细胞周期的改变,通过RT-PCR检测Cyclin D1、CDK4、E2F1基因mRNA表达变化,Western印迹检测Cyclin D1、CDK4、pRb蛋白表达的变化.结果 流式细胞仪分析表明血清饥饿培养24 h可使约90%PC12细胞停滞于G0/G1期,25 μmol/L Aβ25-35诱导组8、16、24 h与对照组比较,S期百分率明显增加(P＜0.01),16 h后细胞凋亡率明显增加(P＜0.01),可见明显的亚二倍体峰(Ap峰);Aβ25-35浓度诱导血清饥饿培养的PC12细胞0～20 h,Cyclin D1、CDK4、pRb 、E2F1 mRNA和蛋白表达增高.结论 Aβ25-35诱导同步化于G0/G1的PC12细胞重新进入细胞周期,并阻滞于S期,同时出现凋亡,可能与增加Cyclin D1、CDK4、pRb 、E2F1 mRNA和蛋白的表达有关.     

5-脂氧合酶抑制TNF-α诱导的胰腺癌细胞凋亡

目的:检测胰腺癌细胞中5-脂氧合酶(5-lipoxygenase,5-LOX)及其代谢产物的表达情况,分析高表达5-LOX及LTB4对胰腺癌细胞生长凋亡的影响.方法:体外培养人胰腺癌细胞株ASPC-1,PANC-1和SW1990,并构建5-LOX基因稳定转染细胞株.用RT-PCR和Western blot检测细胞5-LOX mRNA和蛋白的表达,ELISA检测细胞培养上清中LTB4的含量,采用流式细胞仪、Annexin V/PI双染法检测TNF-α诱导细胞的细胞凋亡.结果:三种胰腺癌细胞株均表达5-LOX mRNA和蛋白,细胞上清中也都检测到一定量LTB4分泌.5-LOX基因稳定转染细胞株表达5-LOX和LTB4的水平上升.TNF-α(20μg/L)处理野生型SW1990细胞,12和24 h后凋亡率分别为25.4%±3.65%和43.5%±5.23%,但该效应在高表达5-LOX的细胞株中明显减弱,分别为13.2%±2.01%和21.7%±3.65%.在野生型SW1990细胞培养中加入外源性LTB4(10 nmol/L)能抑制TNF-α诱导的细胞凋亡,野生型与处理组细胞24 h后凋亡率有显著性差异(47.6%±5.32%vs 18.5%±5.69%,P<0.01).用LTB4受体阻断剂处理5-LOX高表达细胞株,能恢复其对凋亡诱导的敏感性.结论:胰腺癌细胞均能表达5-LOX并产生LTB4,高表达5-LOX能抑制TNF-α诱导的胰腺癌细胞凋亡.     

胺碘酮对外源性羟自由基诱导心肌细胞凋亡的影响

目的　观察胺碘酮对外源性羟自由基诱导心肌细胞凋亡的影响。方法　采用培养的第 2代心肌细胞 ,随机分成 4组 :1正常对照组 :仅用 DMEM培养 ;2羟自由基组 :OH-终浓度为 0 .1 mmol/ L;3胺碘酮组 :胺碘酮终浓度为 1 0μmol/ L;4胺碘酮 +羟自由基组 :胺碘酮 1 0μmol/ L+OH- 0 .1 mmol/ L。观察心肌细胞存活率和形态学 ,流式细胞仪双标法检测细胞凋亡率。结果　 1羟自由基组心肌细胞存活率降低 ,与对照组比较有显著性差异 (P<0 .0 5) ;胺碘酮 +羟自由基组细胞存活率较羟自由基组高 (P<0 .0 5)。 2 Annexin V+ / PI-细胞即凋亡细胞在羟自由基组有较高的发生率 ,明显高于其他各组 (P<0 .0 5) ;胺碘酮 +羟自由基组的细胞凋亡率显著低于羟自由基组 (P<0 .0 5)。 3羟自由基组凋亡心肌细胞呈特征性超微结构及 Annexin V+ / PI-荧光染色。结论　胺碘酮能减轻外源性羟自由基诱导的心肌细胞凋亡。     

高糖环境下美罗华对B淋巴细胞株Ramos增殖的抑制作用

目的探讨在高糖状态下美罗华对B淋巴细胞周期、增殖和凋亡的影响。方法体外培养人B淋巴细胞株Ramos,将细胞分别以单纯5．5、10．0、15．0、25．0mmol/L葡萄糖培养或另外分别加入10mg／L美罗华培养,即分为葡萄糖组和美罗华组。以上两组培养3—7d,检测细胞增殖、凋亡及其周期情况。细胞增殖和活性以台盼蓝染色法测定。细胞凋亡和周期采用流式细胞技术检测。两组间数据比较采用配对t检验。结果5．5、10．0、15．0、25．0mmol/L葡萄糖组B淋巴细胞数量分别为（1．96±0．41）×10^6、（3．49±0．51）×10^6、（3．44±0．67）×10^6、（3．04±0．52）×10^6,凋亡率分别为5．0％±0．9％、4．0％±0．8％、6．2％±1．8％、7．6％±1．3％,S期比例分别为32％±6％、41％±8％、40％±7％、36％±6％;美罗华组细胞数量分别为（1．23±0．23）×10^6、（1．52±0．29）×10^6、（1．38±0．23）××10^6、（1．06±0．23）×10^6,细胞凋亡率则分别23．1％±3．2％、21．2％±4．2％、24．4％±4．8％、26．9％±6．0％,S期细胞比例则分别22％±4％、28％±5％、26％±4％、20％±5％。与葡萄糖组比较,美罗华组B细胞增殖在不同糖浓度亚组均显著减少（t=9．19、5．52、9．75、14．22,均P〈0．01）,细胞凋亡率显著增加（t：16．62、12．51、11．53、9．12,均P〈0．01）,S期细胞比率显著减少（t=5．87、5．19、9．91、7．73,均P〈0．01）。两组细胞增殖数量和S期比率均在10．0mmol/L葡萄糖时最高;两组细胞凋亡率均在25．0mmol/L葡萄糖时最多。结论美罗华通过抑制细胞周期以及促进细胞凋亡实现对B淋巴细胞增殖的抑制作用,其抑制作用在高糖状态下更为明显。     

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.     

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.     

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.     

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。     

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     

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。     

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.