G蛋白β3亚单位C825T等位基因多态性与原发性高血压的关系

目的 探讨温州地区汉族人群G蛋白β3亚单位(GNB3)C825T等位基因多态性与原发性高血压的相关性.方法 原发性高血压患者109例,正常对照组378例,聚合酶链反应(PCR)/酶解-琼脂糖凝胶电泳检测基因型.结果 (1)温州地区汉族人群GNB3 825T等位基因频率为43.5%,与其他人种的该基因频率显著不同.(2)原发性高血压组的TT基因型携带率明显升高(P＜0.01),TT基因型携带者与CT型携带者比较,其致高血压的比数比(OR值)为2.5(P＜0.01);TT型与CC型比,其OR值为2.4(P＜0.01);等位基因T与C比较,致高血压的OR值为1.5(P＜0.05).(3)GNB3不同基因型间的血压水平比较,收缩压CT和TT携带者与CC携带者比较均增高(P＜0.05和P＜0.01),TT携带者与CT携带者比较亦有升高(P＜0.01),舒张压TT携带者比CC携带者增高(P＜0.05),而CT携带者与CC携带者比较差异无显著性(P＞0.05),TT携带者与CT携带者比较,收缩压和舒张压均增高(P＜0.01和P＜0.05).结论 GNB3 825T基因型可作为早期预测原发性高血压的遗传学指标之一.     

MTHFR基因多态性与河南中部地区汉族人群急性冠脉综合征发生的关联性研究

目的探讨5,10-亚甲基四氢叶酸还原酶(MTHFR)基因多态性与河南中部地区汉族人群急性冠脉综合征(ACS)发生的关联性。方法招募河南中部地区汉族ACS患者280例作为观察组,选取同期行健康体检的河南中部地区汉族健康受试者286名作为对照组。采用荧光染色原位杂交技术检测两组MTHFR基因C677T、A1298C位点基因型,比较两组受试者各基因型及等位基因分布的差异,采用二元Logistic回归分析MTHFR基因多态性与ACS发生的关联性。结果两组各基因型分布频率均符合Hardy-Weinberg平衡(P0.05)。对照组MTHFR C677T位点CC、CT、TT型分布频率分别为31.82%、47.90%、20.28%,MTHFR A1298C位点AA、AC、CC型分布频率分别为73.78%、21.68%、4.54%;观察组MTHFR C677T位点CC、CT、TT型分布频率分别为16.43%、40.71%、42.86%,MTHFR A1298C位点AA、AC、CC型分布频率分别为69.29%、27.14%、3.57%。两组受试者MTHFR C677T各基因型分布频率及等位基因频率比较差异有统计学意义(P0.05),而MTHFR A1298C各基因型分布频率及等位基因频率比较差异无统计学意义(P0.05)。二元Logistic回归分析显示,MTHFR C677T基因型是ACS发生的影响因素(P0.05),以TT型为参照,CC型发生ACS的可能性是TT型的24.4%,CT型发生ACS的可能性是TT型的40.2%。结论 MTHFR基因多态性与河南中部地区汉族人群ACS发生有关,其中C677T位点突变可能是ACS发生的影响因素,而A1298C位点基因多态性与ACS发生的关联性较低。     

急性冠状动脉综合征患者基质金属蛋白酶9基因多态性

目的 探讨基质金属蛋白酶9基因C1562T多态性与中国南方汉族人群冠心病的关系.方法 对经冠状动脉造影证实的急性冠状动脉综合征患者150例(急性冠状动脉综合征组)、稳定型心绞痛患者110例(稳定型心绞痛组)和同期冠状动脉造影阴性、排除冠心病诊断的患者70例(对照组)进行研究,采用酶联免疫吸附试验测定血浆基质金属蛋白酶9水平,采用聚合酶链反应-限制片长多态性技术分析基质金属蛋白酶9基因中C1562T基因多态性,比较各组的基因型和等位基因频率.结果 急性冠状动脉综合征组血浆基质金属蛋白酶9水平明显高于稳定型心绞痛组(P＜0.05)和对照组(P＜0.01),而稳定型心绞痛组与对照组比较,差异无统计学意义(P＞0.05).急性冠状动脉综合征组基质金属蛋白酶9基因CT、CT TT基因型频率以及T等位基因频率均高于对照组和稳定型心绞痛组(P＜0.05或0.01),稳定型心绞痛组与对照组各基因型和等位基因频率分布差异无统计学意义(P＞0.05).C1562T位点CT/TT基因型患者血浆基质金属蛋白酶9水平显著高于CC基因型患者(P＜0.01).结论 基质金属蛋白酶9基因C1562T多态性可能与中国南方汉族人群急性冠状动脉综合征有关,1562T等位基因是动脉粥样硬化斑块不稳定性的易感基因.     

内皮脂肪酶584C/T多态性与急性冠脉综合征相关性研究

目的:探讨内皮脂肪酶(endothelial lipase,EL)基因 584C/T多态性与急性冠脉综合征(acute coronary syndrome,ACS)及血脂的相关性。方法: 采用聚合酶链反应-限制性片段长度多态性方法检测324例ACS患者和299例健康体检者内皮脂肪酶基因584C/T基因型。结果: ACS组血清HDL、ApoA-I水平及ApoA-I/ApoB明显低于对照组,而LP(α)却明显高于对照组。中国常州地区汉族人群存在EL 584C/T基因多态性,基因型及等位基因频率分布符合Hard-Weinberg平衡。ACS组CC、CT、TT基因型频率分别为60.2%、35.8%、4.0%;对照组CC、CT、TT基因型频率分别为56.2%、40.8%、3.0%;两组间基因型频率分布无统计学意义（P=0.389）。ACS组C等位基因频率为78.1%;对照组C等位基因频率为76.6%,两组间等位基因频率差异也无统计学意义（P=0.528)。经校正性别、年龄、糖尿病、高血压、吸烟、高脂血症等冠心病危险因素后,结果仍然表明该多态性与ACS无明显相关性。T等位基因携带者（CT+TT）血脂水平及其比值与CC基因型者比较差异无统计学意义。结论: 中国常州地区汉族人群EL 584C/T基因多态性与ACS无明显相关性,与血脂及其比值也无明显相关性,EL 584C/T多态性可能不是中国常州地区汉族人群ACS发病的易感因素。     

血管内皮生长因子基因多态性与糖尿病视网膜病变的相关性

目的探讨血管内皮生长因子（VEGF）-460C/T基因多态性与糖尿病视网膜病变（DR）的相关性。方法病史超过10年的2型糖尿病（T2DM）患者204例,分为非增殖型视网膜病变组（NP-DR,65例）、增殖型视网膜病变组（PDR,64例）及单纯2型糖尿病组（DM,75例）。用PCR-RFLP方法检测各组基因型,比较各组基因型和等位基因的频率。结果DR组VEGF-460位点TT基因型频率显著低于DM组（P〈0.01）,C等位基因频率显著高于DM组（P〈0.01）;NPDR组与PDR组基因型和等位基因频率差异无统计学意义（P〉0.05）。DM中CC、CT、TT基因型的DR发生率分别为69.8%、68.9%和42.2%,CC和CT基因型的DR发生率显著高于TT基因型（P〈0.01）。结论VEGF-460C/T多态性与DR的发生发展有关,C等位基因可能是DR的易感基因。     

结缔组织生长因子rs9399005单核苷酸多态性与冠心病的关系

目的探讨结缔组织生长因子(CTGF)rs9399005基因多态性与血清CTGF水平及冠心病的相关性。方法纳入冠心病组214例和正常对照组64例,酶联免疫吸附法检测其血清CTGF水平。采用Sanger法分析CTGF基因rs9399005单核苷酸多态性(SNP)。比较两组基线临床资料、血清CTGF和基因型分布频率。非条件Logistic回归分析CTGF rs9399005 SNP与冠心病的遗传易感性,比较不同基因型CTGF水平。分析CTGF水平与冠状动脉病变支数、冠心病严重程度的关系。结果两组年龄、吸烟、高血压、体质指数、高密度脂蛋白胆固醇、载脂蛋白A1、CTGF差异有统计学意义(P0.05)。rs9399005基因型CC、CT、TT及等位基因C和T在两组间的分布有统计学差异(χ2值分别为12.935和17.148,均P0.01)。携带CT发生冠心病的危险性是CC的1.134倍,TT是CC的1.406倍,T等位基因是C等位基因的1.327倍。血清CTGF水平在各基因型间差异有统计学意义(F=3.284,P=0.034)。各基因型间冠心病所累及的冠状动脉主要分支的差异有统计学意义(χ2=13.872,P=0.022)。结论CTGF rs9399005 SNP与冠心病的遗传易感性相关;等位基因T与冠心病严重程度、冠状动脉病变支数及血清CTGF水平相关。     

血管内皮生长因子基因3'-非翻译区936C/T多态性与2型糖尿病外周神经病变相关

目的 探讨血管内皮生长因子(VEGF)基因3'-非翻译区936C/T多态性与山东地区汉族人2型糖尿病合并周围神经病变(DPN)之间的关系.方法 194例糖尿病患者分为单纯糖尿病组(n=92)和糖尿病神经病变组(n=102),另120名健康个体设为健康对照组.采用PCR-限制性片段长度多态性(RFLP)方法确定全部个体的基因型;对不同基因型间及病例组间的临床与生化参数、血清VEGF浓度以及VEGF基因936C/T多态性进行了统计分析.结果 糖尿病神经病变组C等位基因及CC基因型频率显著高于对照组(x2为9.406和9.677,P＜0.05)和糖尿病组(x2为5.578和5.614,P＜0.05),而携带T等位基因的基因型(CT+TT)频率及T等位基因频率显著低于对照组(x2为9.406和9.677,P＜0.05)和糖尿病组(x2为5.578和5.614,P＜0.05).Logistic多元回归分析显示血清低密度脂蛋白胆固醇(LDL-C)、总胆固醇、HbA1c水平以及VEGF浓度与DPN发生呈正相关,而VEGF基因936C/T多态性与糖尿病周围神经病变发病危险呈负相关(β=-1.046,OR=0.457,P=0.006,95%CI:0.166～0.741).结论 中国山东地区汉族人群中存在VEGF基因936C/T多态性,C等位基因及CC基因型患者可能是糖尿病易于发生神经病变危险性的遗传标志,而T等位基因和携带T等位基因的基因型(936TF基因型和936CT基因型)可能是降低糖尿病发生神经病变风险的遗传标志.

Abstract：

Objective To elucidate the relationship between a 936C/T mutation at 3'-untranslated region of human vascular endothelial growth factor(VEGF) gene and diabetic peripheral neuropathy ( DPN ). Methods All subjects recruited in this study were assigned into DM (n = 92, diabetes without neuropathy, retinopathy or nephropathy), DPN (n = 102, diabetes with peripheral neuropathy only ), and healthy control (n = 120 ) groups,respectively. The gene polymorphism was determined by PCR-RFLP, as well as the other clinical parameters including serum VEGF by ELISA. Results The frequencies of both genotype CC and allele C were significantly higher in DPN group than those in either DM group(x2 = 5.578 and 5.614, P＜0. 05 ) or control group (x2 = 9. 406 and 9. 677, P＜0. 05 ). However, the frequencies of genotype(CT+TT) and allele T were significantly lower in DPN group than that in either DM group(x2 =5.578 and 5.614, P＜0. 05) and control group (x2=9.406 and 9.677, P＜0.05). The multivariate logistic regression analysis showed that the levels of HbA1c, total cholesterol, low-density lipoproteincholesterol( LDL-C ), and serum VEGF positively correlated with DPN, while the 936C/T polymorphism of VEGF gene negatively correlated with DPN(β= -1. 046, OR=0. 457, P=0. 006, 95% CI: 0. 166-0. 741 ). Conclusions Allele 936C of VEGF gene may serve as a genetic marker susceptible to DPN, while allele 936T may be a protective genetic marker of DPN.     

连接蛋白37基因C1019T多态性与缺血性卒中及其转归的相关性

目的 探讨连接蛋白37(connexin37,Cx37)基因C1019T多态性与缺血性卒中及其转归的关系.方法 采用限制性片段长度多态性分析技术检测缺血性卒中组和对照组Cx37基因C1019T多态性的分布,采用改良Rankin量表(modified Rankin Scale,mRS)评价发病后3个月时神经功能转归.结果 纳入急性缺血性卒中患者232例,其中转归良好(mRS评分＜3分)210例,转归不良(mRS评分≥3分)22例;对照组235例.缺血性卒中组TT基因型(12.93％对6.39％;x2=10.087,P=0.006)和T等位基因(31.25％对21.49％;x2 =11.466,P=0.001)频率显著高于对照组.多变量logistic回归分析显示,TT基因型[优势比(odds ratio,OR)5.794,95％可信区间(confidence interval,CI)1.405～23.894;P=0.015]和T等位基因(OR 131.016,95％ CI 6.943～2472.477;P =0.001)可显著增高缺血性卒中的发病风险.单因素分析显示,TT基因型(OR 0.650,95％ CI 0.144～2.934;P=0.575)、CT基因型(OR 0.622,95％ CI 0.234～1.655;P=0.342)、CC基因型(OR 0.654,95％ CI0.268～1.595;P=0.350)与缺血性卒中转归均无显著相关性.结论 Cx37 1019TT基因型和T等位基因可增高缺血性卒中风险,T等位基因是缺血性卒中的遗传易感因素之一,但其基因多态性与缺血性卒中发病3个月时的转归无关.     

急性冠脉综合征斑块超声显像特征与同型半胱氨酸及亚甲基四氢叶酸还原酶C677T基因多态性的相关性

目的 探讨急性冠脉综合征不稳定斑块与血浆同型半胱氨酸(Hey)及亚甲基四氢叶酸还原酶(MTHFR) C677基因多态性的相关性.方法 采用连续病例对照研究,荧光生化法检测血浆Hey水平,血管内超声对病变部位进行定性定量研究,应用Taqman探针技术进行MTHFRC677T基因多态性分析.结果 稳定型心绞痛(SPA)组患者冠脉病变处以硬斑块为主,急性冠脉综合征(ACS)组患者冠脉病变处以软斑块为主(P＜0.001);ACS组患者斑块破裂及血栓形成发生率较SPA组高(P＜0.05);ACS组病变处斑块负荷重(P＜0.05),ACS组病变处以偏心斑块为主(P＜0.05),以正性重构多见(P＜0.001).ACS组与SPA组,高Hcy比率差异显著(P＜0.001).ACS与SPA之间MTHFR C677T基因型构成比差异显著;携带T基因明显增加斑块不稳定的风险.结论 高Hcy和MTHFR C677T基因多态性是ACS斑块不稳定的危险因素,可以作为预测斑块不稳定的指标.     

血管内皮生长因子基因多态性与糖尿病视网膜病变相关性

目的 探讨血管内皮生长因子(VEGF)+450基因的多态性与糖尿病视网膜病变(DR)的关系.方法 运用PCR-RFLP技术检查2型糖尿病(T2DM)患者249例,单纯T2DM患者120例,DR患者129例,及体检的98例对照者的基因型,比较各组的基因型和等位基因的频率.结果 DR组CC基因型及C等位基因频率显著高于T2DM组和健康对照组(P＜0.01,P＜0.05);CC基因糖尿病(DM)患者VEGF产量高.结论 VEGF+450C/G基因多态性可能与DR的发生发展有关,C等位基因可能是DR的易感基因.     

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.     

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.