曲匹地尔对兔主动脉球囊损伤后血管壁基质金属蛋白酶-2表达的影响

目的观察曲匹地尔对球囊损伤后血管内膜增生和基质金属蛋白酶-2(MMP-2)mRNA表达的影响,探讨其抑制内膜增生的可能机制。方法在兔腹主动脉球囊损伤的模型上,光镜下观察曲匹地尔对血管内膜增生的影响及应用逆转录聚合酶链反应的方法观察球囊损伤后MMP-2mRNA的动态表达及曲匹地尔对其表达的影响。结果球囊损伤后1,4,7,14,28d,MMP-2mRNA表达均显著高于对照组,且在损伤后第7天达高峰(1·66±0·14vs对照组0·41±0·14,P<0·01)。曲匹地尔可以抑制血管内膜的增生,并能抑制MMP-2mRNA的表达,损伤后7天抑制作用最为显著(1·15±0·18vs对照组1·66±0·14,P<0·01)。结论球囊损伤后MMP-2的表达可能与血管内膜增生有关。曲匹地尔抑制血管内膜增生的作用可能与其抑制MMP-2的表达有关。     

曲匹地尔对兔主动脉球囊损伤后血管壁基质金属蛋白酶-2表达的影响

目的观察曲匹地尔对球囊损伤后血管内膜增生和基质金属蛋白酶-2(MMP-2)mRNA表达的影响,探讨其抑制内膜增生的可能机制.方法在兔腹主动脉球囊损伤的模型上,光镜下观察曲匹地尔对血管内膜增生的影响及应用逆转录聚合酶链反应的方法观察球囊损伤后MMP-2 mRNA的动态表达及曲匹地尔对其表达的影响.结果球囊损伤后1,4,7,14,28 d,MMP-2 mRNA表达均显著高于对照组,且在损伤后第7天达高峰(1.66±0.14 vs对照组0.41±0.14,P＜0.01).曲匹地尔可以抑制血管内膜的增生,并能抑制MMP-2 mRNA的表达,损伤后7天抑制作用最为显著(1.15±0.18 vs对照组1.66±0.14,P＜0.01).结论球囊损伤后MMP-2的表达可能与血管内膜增生有关.曲匹地尔抑制血管内膜增生的作用可能与其抑制MMP-2的表达有关.     

兔髂动脉球囊损伤后血管平滑肌钠氢交换体蛋白变化及阿米洛利对血管狭窄的干预作用

目的通过观察球囊损伤动脉后平滑肌层钠氢交换体(NHE)-1蛋白量的变化及NHE-1抑制剂阿米洛利(AMILORIDE)对血管狭窄的干预作用,探讨NHE-1参与血管再狭窄作用机制。方法32只雄性新西兰白兔随机分为AMILORIDE干预组12只、球囊损伤组10只、假手术组10只。干预组及损伤组制作球囊损伤模型,干预组于手术前3天开始给予AMILORIDE5MG·KG-1·D-1,损伤组以相同剂量生理盐水腹腔注射;假手术组仅分离动脉不行球囊损伤术。术后饲养28天,取髂动脉以WESTERN BLOT方法检测平滑肌NHE-1蛋白量;行HE、Α-肌动蛋白、MASSON三色染色,观察血管管腔、中膜、内膜面积变化、平滑肌细胞增殖、细胞外基质变化情况。结果兔髂动脉球囊损伤后4周出现明显管腔狭窄,新生内膜生长,平滑肌层增生;3组平滑肌NHE-1蛋白量各为0·21±0·02、0·25±0·04、0·11±0·03,P<0·01,损伤组与假手术组比较差异有统计学意义,P<0·01,提示球囊损伤后平滑肌NHE-1蛋白量增高,干预组与损伤组比较P=0·05、与假手术组比较P<0·01,提示经AMILORIDE干预后平滑肌NHE-1蛋白量有所下降,但仍未达正常水平;干预组、损伤组、假手术组髂动脉管腔面积分别为0·91MM2±0·23MM2、0·68MM2±0·19MM2、1·08MM2±0·17MM2,P<0·01,新生内膜面积分别为0·27MM2±0·15MM2、0·67MM2±0·24MM2、0·05MM2±0·03MM2,P<0·01,内膜/中膜面积比分别为1·21±0·24、1·39±0·26、0·15±0·08,P<0·01;经AMILORIDE干预后管腔面积明显增大、内膜面积显著下降、内膜/中膜面积比下降。干预组与损伤组内膜比较,Α-肌动蛋白染色阳性面积减小,4164·15ΜM2±1788·37ΜM2对16328·31ΜM2±6220·27ΜM2,P<0·01;MASSON染色绿色面积下降,8910·62ΜM2±7041·62ΜM2对33358·76ΜM2±7290·17ΜM2,P<0·01,提示干预组内膜平滑肌增生及细胞外基质增生均减轻。结论兔髂动脉球囊损伤后,出现血管平滑肌细胞增殖、向内膜迁移、细胞外基质分泌增多,形成新生内膜,管腔缩小,平滑肌层NHE-1蛋白量增高。NHE-1抑制剂AMILORIDE可抑制球囊损伤兔髂动脉所致血管狭窄,为应用NHE-1抑制剂防止经皮冠状动脉腔内成形术后再狭窄提供依据。     

雷帕霉素对球囊损伤后血管平滑肌细胞表型及内膜增生的影响

目的建立大鼠腹主动脉球囊损伤模型,研究雷帕霉素对血管平滑肌细胞表型和内膜增生的影响。方法26只大鼠随机分为假手术组、球囊损伤组、羧甲基纤维素钠组和雷帕霉素组。雷帕霉素组行腹主动脉球囊损伤术前3天开始每天肌肉注射雷帕霉素0.5mgkg,术后连续14天每天肌肉注射雷帕霉素0.25mgkg。球囊损伤14天后进行电镜观察、组织学观察和形态学分析。结果假手术组电镜下血管平滑肌细胞呈收缩表型,球囊损伤后血管平滑肌细胞呈合成表型,雷帕霉素干预后血管平滑肌细胞电镜下表现介于两者之间。术后14天雷帕霉素组新生内膜面积比羧甲基纤维素钠组减少36.4%(0.14±0.03mm2比0.23±0.06mm2,P<0.01),内膜中膜比减少28.9%(17.7%±3.37%比28.86%±10.25%,P<0.01)。结论以上提示雷帕霉素可以抑制血管平滑肌细胞表型的改变,减轻球囊损伤后新生内膜的增生程度。     

黄芪甲苷对大鼠颈动脉球囊损伤后内膜增生的影响

目的:研究黄芪甲苷对球囊损伤后大鼠颈动脉内膜增生的影响。方法:SD雄性大鼠50只,随机分为假手术组、模型组、黄芪甲苷(20mg·kg-1·d-1)、(40mg·kg-1·d-1)及(60mg·kg-1·d-1)组。建立大鼠颈动脉球囊损伤模型,黄芪甲苷组大鼠术前3d开始给药,每天1次,假手术组、模型组同时给予1%羧甲基纤维素钠,共给药17d。术后第15dHE染色观察血管内膜的形态学变化;免疫组织化学法检测新生内膜增殖细胞核抗原(PCNA)的表达;比色法检测大鼠血浆超氧化物歧化酶(SOD)、丙二醛(MDA)含量。结果:黄芪甲苷低、中、高剂量组均能明显减少球囊损伤后新生内膜面积、内膜/中膜比(P0.05),并使PCNA蛋白表达降低(P0.05);升高球囊损伤后大鼠血浆SOD含量(P0.05),降低血浆MDA水平(P0.05)。结论:黄芪甲苷能够抑制大鼠颈动脉球囊损伤后的内膜增生,其主要是通过抑制血管平滑肌的移行、增殖,抗氧化应激反应发挥作用。     

功能性药物洗脱支架对冠状动脉介入治疗后内膜增生及TFPI-2的影响

目的 探讨新型双面复合药物涂层支架体内抑制血管平滑肌细胞增殖及促进内皮修复的作用。方法65只中华小型猪非高脂饮食喂养4周,随机分为假手术组、球囊损伤+双面涂层支架植入组和球囊损伤组,造模后继续喂养4周,抽血检查血浆TFPI-2水平,行冠状动脉OCT检查后处死并取冠状动脉血管组织行分子生物学检测。结果 OCT图像可见球囊损伤组斑块明显扩大,内膜增厚,纤维帽厚度明显增加,假手术组基本正常,支架植入组居中;内膜/中膜面积比球囊损伤组（2.23±0.72）,支架植入组（2.01±0.56）稍高于假手术组（1.89±0.27）;内膜/中膜厚度比分别为球囊损伤组（2.12±0.74）,支架植入组（1.74±0.66）与假手术组（1.52±0.47）。支架植入组较球囊损伤组下降,差异有统计学意义（P<0.05）。假手术组、支架植入组、球囊损伤组三组血浆TIFI-2水平分别为135.2±22.6 μg/L、127.2±23.4 μg/L和52.4±22.6 μg/L前两组基本相仿,但球囊损伤组明显下降,差异有统计学意义（P<0.01）。假手术组、支架植入组、球囊损伤三组TIFI-2与β-actin比值分别为2.45±0.22、2.22±0.26、1.27±0.33、TFPI-2在正常动脉血管组织中较少表达,支架植入组表达水平与假手术组比较差异无显著性（P>0.05）,而球囊损伤组则表达明显下降,差异有统计学意义（P<0.01）。结论 双面药物涂层支架较球囊损伤组比较能降低血管内膜增生;同时促进冠状动脉内膜表达TFPI-2,血浆TFPI-2水平升高,进而可能减少支架内血栓的形成。     

曲匹地尔及阿司匹林对球囊血管成形术后兔血管增生的作用及机制的研究

目的 :研究曲匹地尔及阿司匹林对兔球囊血管成形术后血管增生的作用及机制。方法 :对髂动脉粥样硬化模型兔 2 0只行球囊血管成形术 ,同时给予曲匹地尔 ( 8只 )或阿司匹林 ( 8只 ) 2 5mg/ (只· d) ,至术后 2 8d。采用病理学方法观察两药对病变血管段增生的影响 ,并采用核酸探针杂交技术观测两药对血管血小板源生长因子 ( PDGF)及受体表达的影响 ,并与未用药组 ( 4只 )进行比较。结果 :两药对血管中膜增生均有抑制作用 ,曲匹地尔抑制 PDGF及受体的表达 ,而阿司匹林仅抑制其受体的表达。结论 :两药对血管增生反应的抑制与特异性抑制生长因子或受体有关。     

粒细胞-巨噬细胞集落刺激因子对损伤血管内膜增生及凝血纤溶功能的影响

目的:建立兔髂动脉球囊损伤模型,观察粒细胞-巨噬细胞集落刺激因子(granulocyte-macrophagecolony-stimulatingfactor,GM-CSF)对血管损伤后内膜增生及机体凝血纤溶功能的影响。方法:健康新西兰雄性大白兔24只,随机分为GM-CSF组和对照组。GM-CSF组皮下注射GM-CSF10μg·kg-1·d-1,对照组皮下注射同等量生理盐水。7d后球囊扩张损伤一侧髂动脉。术后4周处死动物,采集标本,观察内膜增生情况;分别于术前、术后1周,2周,4周耳缘静脉采血检测一氧化氮(NO)浓度、组织型纤溶酶原激活剂(tissue-typeplasminogenactivator,t-PA)活性和纤溶酶原激活物抑制剂-1(plasminogenactivatorinhibitor-1,PAI-1)活性。结果:术后4周病理组织学见GM-CSF组内膜增生程度较对照组明显减轻,新生内膜中血管平滑肌细胞和纤维组织较对照组明显减少,内皮较完整、光滑,管腔狭窄程度较轻。GM-CSF组术后2周,4周NO浓度明显高于对照组[(91·9±11·6)μmol/Lvs(81·7±12·2)μmol/L];[(97·7±10·1)μmol/Lvs(83·2±12·6)μmol/L];术后1周,2周,4周t-PA活性2组均高于术前,但2组间差异无统计学意义;2组术前、术后PAI-1活性差异无显著性,2组间亦差异无显著性。结论:GM-CSF能促进损伤内膜修复,恢复正常内皮功能,且并未诱导球囊损伤动物机体的高凝状态。     

葛根素抑制家兔髂动脉球囊损伤后再狭窄

观察家兔髂动脉球囊损伤后葛根素抑制损伤部位平滑肌细胞增殖的药效。复制球囊损伤家兔髂动脉造成血管狭窄模型 ,实验分为 5 0mg (kg·d)葛根素治疗组、10 0mg (kg·d)葛根素治疗组和手术对照组 ,通过体外超声定期检测血管腔直径 ,病理切片观察血管内膜和中膜面积。结果发现 ,球囊损伤术后第 5周 5 0mg (kg·d)葛根素治疗组的血管直径 (1.6 6± 0 .4 1mm)和 10 0mg (kg·d)葛根素治疗组的血管直径 (1.5 9± 0 .17mm)显著高于对照组(1.13± 0 .4 3mm)。病理切片结果发现 10 0mg (kg·d)葛根素治疗组内膜 /中膜面积比 (36 %± 18% )显著低于对照组(12 4 %± 6 4 % )。结果提示 ,葛根素对球囊损伤术后血管平滑肌细胞增殖有一定抑制作用。     

重组腺病毒介导的人一氧化氮合酶基因转染对大鼠颈总动脉球囊损伤后新生内膜的影响

目的 :研究重组腺病毒介导的人内皮型一氧化氮合酶基因 (eNOS)表达生成的一氧化氮合酶 (NOS)对球囊损伤后大鼠颈总动脉新生内膜的抑制作用。方法 :在 2 93细胞内扩增、纯化Ad LacZ和Ad eNOS ,鉴定其是否携带有LacZ和eNOS基因。建立大鼠颈总动脉球囊损伤模型后 ,将磷酸缓冲液 (PBS)、Ad LacZ和Ad eNOS在体内分别转染到损伤血管段 ,以X gal染色、苏木精 伊红染色 ,免疫组化及计算机图像分析处理等方法观察转染动脉节段外源性eNOS蛋白表达及其对新生内膜的影响。结果 :重组腺病毒携带有eNOS基因 ,并且在损伤血管段得到有效表达。转染后PBS组、Ad LacZ组和Ad eNOS组的新生内膜面积分别为 (0 .187± 0 .0 18)、(0 .134± 0 .0 6 1)和 (0 .0 6 3± 0 .0 2 6 )mm 2 ,新生内膜与中膜面积比值 (I/M)分别为 1.5 76± 0 .2 73、1.342± 0 .35 7和 0 .5 6 0± 0 .16 1。与PBS组、Ad LacZ组相比Ad eNOS组无论新内膜面积 ,还是管腔狭窄程度都明显减小。结论 :腺病毒介导的eNOS基因转染能有效抑制球囊损伤后血管内膜的增生 ,可防治血管成形术后再狭窄     

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.