吡格列酮对胰岛α细胞胰岛素抵抗的影响

目的 研究高脂饲养大鼠胰岛α细胞的分泌功能和胰岛素信号转导分子基因的表达变化以及吡格列酮干预的影响.方法 雄性SD大鼠分为正常饲养组(NC)、高脂饲养组(HF)、高脂+吡格列酮组(HP).喂养20周后检测空腹血胰岛素(FINS)、胰高血糖素、游离脂肪酸(FFA)水平;正常血糖高胰岛素钳夹试验评价外周胰岛素抵抗程度;胰岛表面灌注检测高糖状态胰高血糖素的动态分泌变化;同时各组大鼠随机人组8只给予大剂量链脲佐菌素去β细胞处理,得到去β细胞正常组(NC-B)、高脂组(HF-B),高脂+吡格列酮干预组(HP-B).实时定量PCR方法比较3组去β细胞大鼠α细胞胰高血糖素、胰岛素受体底物1(IRS-1)、胰岛素受体底物2(IRS-2)、磷脂酰肌醇3激酶(P13K)的mRNA表达.结果 (1)HF组葡萄糖输注率(GIR)明显低于NC组,血FINS、胰高血糖素、FFA均显著高于NC组(P＜0.05或P＜0.01);而HP组以上各项指标较HF组均明显改善.(2)胰岛表面灌注HF组基础胰高血糖素的分泌高于NC组(P＜0.01),16.7 mmol/L葡萄糖灌注后NC组胰岛胰高血糖素的分泌明显下降,HF组胰岛的胰高血糖素分泌灌注后未受高糖抑制,HP组逆转了这种变化.(3)与NC-B组相比,HF-B组α细胞胰高血糖素mRNA的表达增高34.2%,IRS-2及P13K mRNA分别降低28.5%、21.3%(均P＜0.01),而IRS-1仅降低7-1%(P＞0.05).HP-B组较HF-B组胰高血糖素、IRS-2及P13K mRNA分别增加40.6%、57.2%、60.6%.结论 高脂饲料诱导的肥胖大鼠胰岛α细胞胰高血糖素分泌功能亢进并存在胰岛素信号转导分子表达降低,二者均与血FFA水平升高有关,而吡格列酮能逆转这种变化.     

2型糖尿病胃促生长素受体的表达与胃排空关系

目的 探讨2型糖尿病大鼠下丘脑和胃组织中胃促生长素(ghrelin)受体(GHSR)表达变化与胃排空的关系.方法 将大鼠分为糖尿病组、单纯肥胖组和对照组.糖尿病组和单纯肥胖组大鼠给予高糖和高脂饮食,糖尿病组8周后注射小剂量链脲佐菌素(STZ).检测各组大鼠体重、空腹血糖和胰岛素水平,并计算胰岛素抵抗指数.酚红灌胃法检测胃排空,实时定量荧光RT-PCR测定下丘脑和胃组织中GHSR mRNA表达.结果 糖尿病组和单纯肥胖组饲养8周后,体重和胰岛素水平较对照组明显升高(P＜0.01),血糖较对照组增高,但差异无统计学意义(P＞0.05).注射STZ后,糖尿病组胰岛素水平显著下降,血糖水平明显升高(P＜0.05).糖尿病组和单纯肥胖组液体胃排空低于对照组(P＜0.05),下丘脑和胃组织GHSR mRNA表达均明显下降(P＜0.05),并与胃排空下降呈正相关(P＜0.05).结论 2型糖尿病大鼠下丘脑和胃组织中GHSR mRNA的表达下降,降低了胃促生长素的促胃肠动力作用,从而有可能参与了糖尿病胃排空的延迟.可能与糖尿病胃排空障碍有关.     

吡格列酮对高脂血症大鼠缺血/再灌注心肌细胞膜流动性的影响

目的 建立食源性高脂血症大鼠心肌缺血/再灌注模型,观察吡格列酮对高脂血症并发缺血/再灌注大鼠心肌细胞膜流动性的影响.方法 Wistar大鼠随机分为对照组(基础饲料喂养)、高脂组(高脂饲料喂养).4周后,高脂组大鼠再随机分为高脂组和高脂+吡格列酮干预组,8周末实施心肌缺血/再灌注,通过Langendorff灌流装置酶液灌流分离单个心肌细胞,利用荧光标记物DPH插入其细胞膜脂质双层,测定荧光偏振值(p),并计算膜脂微黏度(η).4周和8周(实验期末)末分别采血,检测血清中总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDLC)含量.实验期末测定谷胱甘肽过氧化物酶(GPX)、超氧化物歧化酶(SOD)和丙二醛(MDA)的含量.结果 与对照组比较,高脂组血清中TG、TC、HDLC含量显著升高(P＜0.05);吡格列酮组与高脂组比较可显著降低血清中TG、TC含量(P＜0.01);吡格列酮使血清中MDA含量下降(P＜0.05),GPX和SOD活性上升(P＜0.05);吡格列酮组荧光偏振度p值和膜脂微黏度η值均小于高脂组(P＜0.05).结论 吡格列酮保护心肌细胞膜的正常流动性,可能与其降脂、抗氧化保护细胞膜的结构相关.     

糖尿病大鼠胰岛脂质分解的变化及意义

目的 观察糖尿病大鼠胰岛中甘油三酯(TG)、脂质分解和激素敏感性脂肪酶(HSL)的变化,探讨胰岛细胞内脂质分解在糖脂毒性中的作用.方法 采用雄性Wistar大鼠,通过高脂饮食+小剂量链脲佐菌素建立糖尿病模型(DM组),同时设立正常对照组(NC组)和单纯高脂饮食组(HF组).成模4周后,检测各组大鼠的血糖、血脂、胰岛素分泌、胰岛中TG含量及HSL mRNA和蛋白的表达;测定胰岛细胞游离脂肪酸的释放以代表脂质分解.结果 与NC组相比,HF组大鼠血糖没有明显变化,但是胰岛素和血脂均明显升高(P＜0.05或P＜0.01);DM组大鼠血糖、血脂水平显著高于NC组(P＜0.05或P＜0.01),而胰岛素水平与NC组相似.HF组大鼠胰岛内TG含量较NC组有明显的增加(P＜0.05),DM组胰岛内脂质积聚更严重,约为NC组的2.15倍.与NC 组相比,HF组和DM组大鼠胰岛脂质分解和HSL表达明显增加(P＜0.05或P＜0.01).结论 糖尿病状态下,胰岛细胞内脂解和HSL的表达明显增加,这既是维持细胞内脂质代谢平衡的重要因素,又体现了机体对脂毒性的保护.     

抑制胰岛素过度分泌对大鼠脂肪代谢和胰岛β细胞功能的影响

目的 用二氮嗪干预高脂喂养大鼠,探讨抑制胰岛素过度分泌对大鼠脂肪代谢和胰岛β细胞功能的影响.方法 2007年5月至2008年7月,10周龄雄性SD大鼠30只按随机数字表法分为正常对照组(n=10,给予普通饲料)、高脂喂养组(n=10,给予高脂饲料)及二氮嗪组(n=10,给予高脂饲料+30 mg·kg-1·d-1二氮嗪).干预8周后,行腹腔注射葡萄糖耐量试验,测定血清甘油三酯和游离脂肪酸浓度以及肝脏和肌肉中甘油三酯含量,通过聚合酶链反应观测关键脂代谢基因的表达水平.多组间差异比较采用单因素方差分析及Student-Newman-Kewls检验.结果 腹腔注射匍萄糖耐量试验显示:高脂喂养组胰岛素曲线下总面积低于正常对照组(分别为624±83和919±145),二氮嗪干预后明显增加(2220±383;F=15.73,P<0.01).高脂喂养组血清甘油三酯和游离脂肪酸浓度以及肌肉和肝脏中甘油三酯含量明显增加,肝脏呈中至重度脂肪变,二氮嗪干预可明显逆转这些变化.高脂喂养组肝脏ACC1 mRNA表达增加,二氮嗪干预可明显逆转这一变化(F=3.71,P<0.05).高脂喂养组肝脏和肌肉CPT1 mRNA表达增加,二氮嗪可促进这一变化(分别为F=3.61,P<0.05;F=4.93,P<0.05).结论 二氮嗪可抑制胰岛素过度分泌,保护胰岛β细胞,还可能通过改变肝脏及肌肉脂肪代谢减轻脂肪堆积,降低血清甘油三酯和游离脂肪酸水平.     

二甲双胍对胰岛素抵抗大鼠内脏脂肪组织chemerin表达的影响

将雄性4周龄SD大鼠分为正常饲料组和高脂饲料组,喂养10周后分别以二甲双胍治疗(200mg/kg)6周.以正常血糖-高胰岛素钳夹试验评估胰岛素敏感性,留取肾周脂肪组织,采用实时定量PCR及Western印迹法检测脂肪组织中chemerin mRNA和蛋白的表达水平.结果显示,高脂饲料诱导的胰岛素抵抗、大鼠肾周脂肪组织chemerin mRNA和蛋白水平高于正常饲料喂养大鼠(均P＜0.05),二甲双胍治疗6周后明显降低(均P＜0.01).脂肪组织中chemerin mRNA、蛋白表达水平均与附睾脂肪质量指数显著相关(均P＜0.05).     

强化胰岛素治疗对2型糖尿病大鼠胰岛β细胞凋亡的影响

目的 观察强化胰岛素治疗对2型糖尿病大鼠胰岛β细胞凋亡的影响.方法 将36只Wistar大鼠随机分为正常对照组和高脂组,正常对照组给予基础饲料喂养,高脂组给予脂肪乳灌胃+基础饲料喂养10 d,然后给高脂组大鼠腹腔注射链脲佐菌素,3 d后再将高脂组大鼠随机分为2个亚组,即糖尿病对照组和糖尿病胰岛素治疗组,治疗4 w.脂肪乳灌胃第10天、注射STZ第3天和治疗4 w末测大鼠各项指标;实验结束时采用TUNEL技术和流式细胞术检测胰岛β细胞的凋亡.结果 大鼠在强化胰岛素治疗4 w末,分别采用TUNEL和流式细胞术检测凋亡,与糖尿病对照组比较,糖尿病胰岛素治疗组胰岛β细胞凋亡率明显下降,分别为(0.73±0.02)% vs (0.19±0.04)%和(13.50±0.12)% vs (3.56±0.71)%,差异均有统计学意义(P＜0.05).结论 强化胰岛素治疗可减轻2型糖尿病大鼠胰岛β细胞凋亡.     

吡格列酮对L6肌细胞脂联素和葡萄糖转运蛋白4表达的影响及其机制研究

建立棕榈酸诱导的大鼠L6肌细胞胰岛素抵抗模型后,以吡格列酮、c-Jun氨基末端激酶(JNK)抑制剂SP600125、p38丝裂原活化蛋白激酶(p38MAPK)抑制剂SB203580进行干预.应用Western 印迹法检测脂联素、葡萄糖转运蛋白4(GLUT4)蛋白表达和JNK、p38MAPK磷酸化水平.结果显示,吡格列酮可显著增加胰岛素抵抗状态下L6细胞p38MAPK磷酸化、脂联素和GLUT4蛋白表达(P＜0.05或P＜0.01),降低JNK磷酸化水平(P＜0.01).阻断p38MAPK信号通路后,吡格列酮上调L6细胞GULT4蛋白表达的效应显著降低(P＜0.01),而阻断JNK信号通路却无显著影响(P＞0.05).     

血脂康胶囊对高脂喂养大鼠内脏脂肪及代谢指标的影响

目的探讨血脂康胶囊对高脂喂养大鼠内脏脂肪及代谢指标的影响。方法选择6周龄健康雄性Wistar大鼠36只,随机分为对照组(n=12)组和高脂组(n=24),分别饲以基础饲料和高脂饲料,高脂组大鼠再随机分成两组:高脂模型组(n=12)和血脂康组(n=12),分别给予等剂量0.5%纤维素钠安慰剂和血脂康300 mg/(kg·d)灌胃,共观察12周后,检测各组大鼠附睾、肾周脂肪等内脏脂肪重量,计算体脂比,同时检测各组大鼠空腹血糖、胰岛素、总胆固醇、三酰甘油,计算胰岛素抵抗指数(HOMA-IR)。结果高脂喂养组大鼠12周后的体重和附睾、肾周脂肪重量及体脂比均显著高于正常对照组(P0.01),血脂康组虽较正常对照组大鼠也有增加(P0.05),但仍显著低于高脂喂养组大鼠(P0.01);高脂喂养组大鼠空腹血糖、空腹胰岛素、总胆固醇、三酰甘油及HOMA IR均显著高于正常对照组大鼠(P0.01)。血脂康组空腹血糖高于正常对照组(P0.01),空腹胰岛素和HOMA IR与正常对照组比较差异无统计学意义,而较高脂喂养组显著降低(P0.05);总胆固醇、三酰甘油虽较正常对照组有明显增加(P0.05或P0.01),但也显著低于高脂喂养组(P0.05或P0.01)。结论血脂康胶囊干预可以有效减少高脂喂养大鼠内脏脂肪聚集,从而显著改善糖脂代谢异常和胰岛素抵抗。     

吡格列酮预防非肥胖糖尿病鼠胰岛β细胞凋亡的机制研究

目的 探讨吡格列酮预防非肥胖糖尿病小鼠胰岛β细胞凋亡的机制.方法 (1)将4周龄NOD雌鼠分为吡格列酮(21只)及对照(21只)组,分别摄食含0.02％吡格列酮的混合饲料和普通营养饲料.观察52周龄的累积糖尿病发病率.(2)各组取12周龄未发病NOD鼠(n=15)胰腺,HE染色观察胰岛炎;TUNEL+SABC法检测胰岛β细胞凋亡.(3)ELISA法测定血清、脾细胞培养上清IFN-γ和IL-4水平及培养脾细胞核因子PPARγ、NF-κB活性.结果 (1)30、52周龄时,吡格列酮及对照组发病率分别为57.1％和76.2％ 、76.2％和90.5％(均P＞0.05);15周龄时,吡格列酮及对照组发病率分别为4.8％和33.3％(P=0.045).(2) 12周龄时,吡格列酮组正常胰岛和胰岛周围炎比例(14.73％,26.02％)高于对照组(5.69％,15.72％;均P＜0.01),胰岛内炎比例(59.25％)则低于对照组(78.59％,P＜0.01);吡格列酮组胰岛β细胞凋亡率(6.17％±3.62％)低于对照组( 10.62％±4.43％,P=0.008).(3)12周龄NOD鼠吡格列酮组血清IFN-γ水平[(561.05 ±78.61) pg/ml]显著低于对照组[(666.43±28.42) pg/ml,P=0.045];在培养的脾细胞上清中,吡格列酮组IFN-γ水平[(605.84±65.60) pg/ml]显著低于对照组[(692.20±44.98)pg/ml,P=0.041].(4)在培养的脾细胞中,吡格列酮组PPARγ活性(0.06±0.01)高于对照组(0.03±0.01,P=0.013),NF-κB活性(0.03±0.01)较对照显著降低(0.08±0.01,P=0.001).结论 吡格列酮活化PPARγ,抑制NF-κB活性,血清和脾细胞上清IFN-γ下降,Th细胞向Th1方向分化减少,NOD鼠胰岛炎减轻、胰岛β细胞凋亡减少.     

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.     

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.