GFPT2在胃癌中的表达及作用的研究

目的通过检测胃癌和癌旁正常组织以及5种细胞株中谷氨酰胺果糖-6-磷酸转氨酶2(GFPT2)mRNA和蛋白的表达水平,探讨GFPT2表达与胃癌发生、转移的关系及意义。方法利用实时荧光定量PCR及Western blotting法检测GFPT2在33例患者配对的新鲜胃癌组织和癌旁正常组织(距离肿瘤边缘5 cm)标本、5种细胞株GES、MGC803、MKN45、BGC823及AGS中的表达情况,并利用免疫组织化学技术检测GFPT2在82例患者配对的胃癌及癌旁正常组织石蜡标本中的表达情况。结果 GFPT2 mRNA和蛋白在81.82%(27例)胃癌中呈高表达,且其在伴有肝转移的胃癌组织中的表达水平明显高于不伴有肝转移者。正常胃黏膜上皮细胞株GES中GFPT2 mRNA的表达水平明显低于胃癌细胞株MGC803、MKN45、BGC823和AGS(P0.05);胃黏膜上皮细胞株GES中GFPT2蛋白表达水平低于胃癌细胞株MGC803、MKN45、BGC823(P0.05),但与胃癌细胞株AGS中GFPT2蛋白表达水平差异无统计学意义。高转移潜能细胞株MKN45和BGC823中GFPT2的表达水平明显高于低转移潜能细胞株AGS及MGC803(P0.05)。GFPT2表达水平与胃癌分化程度呈负相关,与远处转移呈正相关(P0.05)。结论 GFPT2在胃癌组织中的表达上调,且与其转移密切相关,推测GFPT2可能具有促进胃癌转移的作用。     

5-氮杂-2’-脱氧胞苷诱导CDX2基因表达对人胃癌细胞株MKN45增殖和凋亡的影响

背景：DNA甲基化导致基因表达沉默是胃癌发生的重要步骤。近年发现肠表型调节因子CDX2在胃癌中具有抑癌基因的作用。目的：探讨5-氮杂-2’-脱氧胞苷（5-aza—CdR）对人胃癌细胞株MKN45中CDX2基因表达的影响及其对细胞增殖和凋亡的作用。方法：以不同浓度5-aza—CdR（2．5、5、10μmo]／L）处理胃癌细胞株MKN45,甲基化特异性PCR（MSP）检测CDX2启动子区甲基化状态;实时荧光定量RT-PCR和蛋白质印迹法分别检测CDX2mRNA和蛋白表达：CCK8法检测MKN45细胞增殖活性,AnnexinV．FITC／PI检测细胞凋亡和Hoechst33258染色观察其凋亡形态：比色法检测caspase-3活性。结果：MKN45细胞中CDX2基因启动子区高甲基化．CDX2mRNA表达极低且蛋白不表达：经3种浓度5-aza-CdR处理72h后．MKN45细胞CDX2基因启动子区高甲基化发生逆转．CDX2mRNA和蛋白表达均上调。与对照组相比,5-aza-CdR呈剂量依赖性地抑制MKN45细胞增殖和促进凋亡（P〈0．05）：Hoechst33258染色示细胞核致密浓染、细胞核碎裂;caspase-3活性随着5．aza．CdR浓度的增加而升高（P〈0．05）。结论：MKN45细胞中CDX2基因表达缺失可能与其启动子区CpG岛高甲基化有关;5-aza—CdR能有效逆转CDX2基因的异常甲基化．诱导其再表达．并抑制MKN45细胞增殖和促进凋亡．该作用可能与caspase-3活性有关．     

YM155对人胃癌细胞株MKN28的作用及其机制研究

背景:研究发现生存素(survivin)在胃癌组织中高表达,YM155是survivin的特异性抑制剂。目的:探讨YM155对人胃癌细胞株MKN28的作用及其机制。方法:以不同浓度YM155作用于人胃癌细胞株MKN28。采用甲基噻唑基四唑(MTT)法检测细胞增殖抑制率;以原位末端标记(TUNEL法)检测细胞凋亡率;以逆转录聚合酶链反应(RTPCR)、蛋白质印迹法分别检测survivin mRNA和survivin、多聚ADP核糖聚合酶(PARP)、caspase-3蛋白表达。结果:YM155作用后,MKN28细胞增殖抑制,凋亡增加。随着YM155浓度升高,survivin mRNA和蛋白表达水平明显降低,并伴随PARP、caspase-3蛋白裂解。结论:YM155可抑制人胃癌细胞株MKN28增殖,并诱导其凋亡,此机制可能与抑制survivin表达,继而激活caspase凋亡信号通路有关。     

PGE2对胃癌MKN28细胞VEGF表达的影响

目的:观察前列腺素E2(PGE2)对胃癌MKN28细胞血管内皮生长因子(VEGF)mRNA转录、蛋白表达水平的影响．方法:对胃癌MKN28细胞分别给予0．1,1,5, 10μmol／L浓度的PGE2处理3 h,分别以实时PCR,Western blot检测VEGF mRNA转录水平及VEGF蛋白表达水平的变化．结果:胃癌MKN28细胞经用不同浓度的PGE2作用3 h,VEGF mRNA表达呈剂量依赖性增加,其表达在PGE2浓度为0．1,1,5,10μmol／L时与对照组之间的差异均有统计学意义(0．67±0．093,0．74±0．13,0．87±0．07,1．49±0．15 vs 0．42±0．10．P<0．05或P<0．01)．VEGF蛋白表达量与PGE2浓度存在正相关,其表达在PGE2浓度为1,5,10μmol／L组与对照组之间的差异均有统计学意义(51．02±2．16,66．69±9．85,136．49±6．89 vs 26．87±3．98,P<0．05或P<0．01)．结论:外源性PGE2可显著增加胃癌MKN28细胞VEGF的表达．     

胃癌细胞对细小病毒H-1敏感性差异的实验研究

目的 探讨不同胃癌细胞株对细小病毒细胞毒作用的敏感性差异及可能的机制。方法共选用HGC27(未分化)、BGC823(未分化)、MKN45(低分化)、AGS(低分化)、SGC7901(中分化)和MKN28(高分化)等6株不同分化状态的胃癌细胞株，用流式细胞仪分析其各自的细胞周期，H-1病毒感染后采用MTT方法检测不同胃癌细胞株对其细胞毒作用的敏感性差异，用RT-PCR来检测H-1病毒中的非结构蛋白基因(NS-1)在6株不同胃癌细胞中的表达。结果 HGC27、BGC823、MKN45、AGS、SGC7901和MKN28等不同分化状态细胞株中，S期细胞的比率分别为24．72％，30．15％，27．10％，29．03％，31．82％和33．73％。其中HGC27细胞对H-1病毒的细胞毒作用敏感；SGC7901细胞其次；MKN45、AGS细胞对H-1病毒的细胞毒作用中等敏感；MKN28细胞对H-1病毒的细胞毒作用不敏感；而BGC823则对H-1病毒的细胞毒作用抵抗。病毒NS-1的mRNA在HGC27、BGC823、MKN45和SGC7901等细胞中的表达水平较高，而在AGS和MKN28中的表达水平却较低。结论 H-1病毒的细胞毒作用在不同的胃癌细胞株中的差异显著。总体上，与高分化细胞株MKN28细胞相比，分化差的细胞对细小病毒H-1的细胞毒作用敏感性增加。其机制至少部分与分化差细胞中病毒NS-1蛋白的产生和积聚能力增高相关。未分化的BGC823细胞对H-1病毒的细胞毒作用抵抗，进一步证实并非所有的肿瘤细胞都对细小病毒的溶胞性作用敏感。     

siRNA靶向沉默PcG蛋白EZH2对人胃癌细胞株MKN45增殖和侵袭力的影响

背景：PcG蛋白是一组转录抑制因子,其核心成分EZH2在胃癌组织中表达增高,并与胃癌的进展相关。目的：应用RNA干扰（RNAi）技术研究EZH2对人胃癌细胞株MKN45增殖和侵袭力的影响,从细胞水平探讨EZH2参与胃癌发生的机制。方法：使用EZH2小干扰RNA（siRNA）转染MKN45细胞,以实时逆转录聚合酶链反应（RT-PCR）和蛋白质印迹法检测EZH2mRNA和蛋白表达,CCK-8（Cell Counting Kit-8）实验检测细胞增殖情况,流式细胞仪分析细胞周期．MatrigelTM侵袭实验检测细胞侵袭力。结果：EZH2siRNA能有效抑制MKN45细胞的EZH2mRNA和蛋白表达。与阴性对照siRNA组相比,EZH2siRNA组MKN45细胞增殖抑制率为14．7％（P＜0．05）,侵袭能力显著降低[穿过Transwell小室膜细胞数：（38．5±3．4）个／HPF对（92．7±9．7）个／HPF,P＜0．05）,细胞周期阻滞于G0／G1和G2／M期。结论：EZH2siRNA可抑制人胃癌细胞的增殖和侵袭力,证实EZH2通过促进细胞增殖和侵袭在胃癌发生中发挥作用。     

老年大鼠Clara细胞的分泌蛋白CC16 mRNA及CC16蛋白表达

目的探讨老年大鼠Clara细胞的分泌蛋白CC16 mRNA及CC16蛋白的表达。方法观察老年组大鼠(26月龄)及青年组大鼠(3月龄)光镜下肺组织结构、肺组织CC16 mRNA表达及细支气管CC16蛋白的表达。结果老年组大鼠细支气管上皮细胞排列欠规则,肺组织呈轻度肺气肿表现。老年组大鼠肺组织CC16 mRNA表达为3．08±1．71,较青年组的10．02±4．66下降,两组比较差异有统计学意义(P<0．05)。老年组大鼠终末细支气管CC16阳性的上皮细胞百分比[(35．00±7．58)％]较青年组[(55．20±6．10)％]降低(P<0．05),呼吸性细支气管CC16阳性的上皮细胞百分比[(47．20±8．01)％]较青年组[(63．00±7．11)％]也降低(P<0．05)。结论老年大鼠CC16 mRNA及蛋白表达下降,可能参与了肺老化过程。     

15-LOX-1基因表达对胃癌细胞增殖的抑制作用

目的研究15-LOX-1基因对人胃癌细胞增殖的影响。方法通过脂质体介导瞬时转染15-LOX-1基因于培养的胃癌细胞株（AGS）中，以转染空载体pcDNA3．1（＋）的细胞及未转染质粒的细胞作为对照；用RT—PCR和Westernblot检测人胃癌细胞的15-LOX-1mRNA及蛋白表达；倒置显微镜观察转染前后AGS形态变化；用MTT法比较转染前后AGS的增殖水平，流式细胞术检测转染后AGS细胞周期的变化。结果胃癌细胞系巾未检测到15-LOX—1mRNA和蛋白的表达，转染后的AGS表达有15-LOX—1的mRNA及蛋白。转染重组质粒绀细胞增殖显著低于未转染组及空质粒转染组（P〈0．05），转染后AGS细胞G0／G1期细胞明显增加，S期细胞明显减少，与未转染组及空质粒转染组相比均有显著性差异（P〈0．05）。结论15-LOX-1基因能抑制胃癌细胞的增殖，为进一步探讨胃痛的发病机制及治疗提供实验依据。     

siRNA沉默CXCR4基因对胃癌生物学行为的影响

背景:CXCR4在肿瘤细胞中广泛表达,参与肿瘤侵袭和转移。RNA干扰技术可有效降低或关闭基因的表达,从不同水平阻断肿瘤侵袭和转移。目的:研究胃癌组织中CXCR4 mRNA和蛋白表达及其与临床病理特征的关系,并探讨siRNA沉默CXCR4表达对胃癌生物学行为的影响。方法:选取86例胃癌及其癌旁正常黏膜组织,应用RTPCR和蛋白质印迹法分别检测CXCR4 mRNA和蛋白表达,并分析其与临床病理特征的关系。构建CXCR4干扰RNA质粒载体,并转染胃癌MKN45细胞。应用MTT法、Transwell法、流式细胞术分别评估胃癌细胞增殖、迁移和侵袭、凋亡能力。结果:胃癌组织中CXCR4 mRNA和蛋白表达明显高于癌旁正常组织(P 0. 05),且其表达与TNM分期、肿瘤分化、淋巴结转移相关(P 0. 05)。与阴性对照组相比,siRNA转染组转染24、48、72 h后MKN45细胞增殖力均显著降低(P 0. 05),迁移率和侵袭率均显著降低(P 0. 05),细胞凋亡率显著升高(P 0. 05)。结论:CXCR4在胃癌发展过程中具有重要作用;以siRNA沉默CXCR4基因后,可显著抑制MKN45细胞增殖,抑制体外细胞迁移和侵袭,促进细胞凋亡,从而为胃癌的治疗提供新策略。     

EGCG对人胃癌细胞株MKN 45中Bcl-2家族相关基因表达的影响

目的:探讨EGCG干预人胃癌细胞株MKN45后Bcl-2家族相关基因表达的变化情况．方法:运用半定量RT-PCR法和蛋白免疫印迹法分别检测EGCG干预人胃癌细胞株MKN 45后不同时间点上(0,12,24,36 h)抗凋亡相关基因Bcl-xl和Bcl-2及促凋亡相关基因Bax、Bid和Bad的mRNA和蛋白表达水平,并比较不同时间点的Bcl-2与Bax的比值．结果:促凋亡相关基因Bax、Bid和Bad的mRNA与蛋白表达水平随着EGCG作用于人胃癌细胞株MKN45的时间延长(0,12, 24,36 h)逐渐升高(Bax蛋白:0．6292±0．08, 0．6454±0．04,0．8069±0．09,0．8992±0．07, P<0．05;Bid蛋白:1．1214±0．08,1．3697±0．07, 1．610±0．09,2．0623±0．12,P<0．05;Bad蛋白: 0．4327±0．02,0．7531±0．01,1．2827±0．02, 1．6388±0．09,P<0．05),而抗凋亡相关基因Bcl- xl及Bcl-2的mRNA和蛋白表达水平却逐渐降低(Bcl-xl蛋白:0．6444±0．01,0．6060±0．02, 0．5647±0．04,0．5487±0．11,P<0．05;Bcl-2蛋白:0．8112±0．04,0．6716±0．08,0．4664±0．03, 0．3146±0．01,P<0．05)．Bcl-2／Bax比值也随着EGCG作用时间的延长逐渐变小(P<0．05)．结论:EGCG可改变Bcl-2家族不同成员的mRNA与蛋白表达水平,尤其是Bcl-2／Bax比值,这可能与EGCG来调控胃癌细胞凋亡有关．     

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.     

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.