复方丹参滴丸及其与福辛普利联用对自发性高血压大鼠左室肥厚的影响

目的探讨复方丹参滴丸(DSP)及其与福辛普利联用对自发性高血压大鼠(SHR)左室肥厚的影响.方法将48只8周龄雄性SHR随机分为6组:DSP小剂量组、DSP大剂量组、福辛普利组、DSP小剂量与福辛普利联用组、DSP大剂量与福辛普利联用组、SHRs对照组.6组分别干预8周后测大鼠尾动脉收缩压;局部心肌/血浆血管紧张素Ⅱ、血浆醛固酮浓度;左室肥厚指数.结果DSP可降低血浆AngⅡ、Ald及局部心肌AngⅡ浓度(P＜0.01或P＜0.05),并可进一步增强福辛普利的这一作用;与对照组比较DSP可明显减轻左室肥厚(P＜0.01或P＜0.05),与福辛普利联用时可进一步提高后者的抗左室肥厚效应.结论DSP及其与福辛普利联用具有拮抗SHR左室肥厚作用.     

复方丹参滴丸与福辛普利联用对自发性高血压大鼠左室纤维化的影响

目的　探讨复方丹参滴丸 (DSP)与福辛普利联用对自发性高血压大鼠 (SHR)左室纤维化的影响。方法　将 48只8周龄雄性SHR随机分为 6组 :DSP小剂量组 ;DSP大剂量组 ;福辛普利组 ;DSP小剂量与福辛普利联用组 ;DSP大剂量与福辛普利联用组 ;SHR对照组。 6组分别用灌胃法给药8周 ,测大鼠尾动脉收缩压、左室肥厚指数 ;局部心肌 /血浆血管紧张素Ⅱ、血浆醛固酮浓度 ;通过天狼星红染色进行心肌胶原定性和半定量分析。结果　与对照组比较 ,DSP可明显减轻左室肥厚 (P <0 .0 1) ,改善左室纤维化 (P <0 .0 1或P <0 .0 5 ) ,并与福辛普利联用时可进一步提高后者的抗心肌纤维化效应 ;DSP尤其与福辛普利联用时可降低血浆AngII、Ald及局部心肌AngII浓度 (P <0 .0 1或P <0 .0 5 )。结论　DSP与福辛普利联用可改善SHR心肌纤维化(MF)。     

福辛普利对自发性高血压大鼠心室重塑时左室心肌细胞凋亡和Bcl2及BaX基因表达的影响

目的研究福辛普利对自发性高血压大鼠(SHR)左室心肌细胞凋亡和Bcl2、Bax基因表达的影响.方法①使用左室重量指数作为大鼠左室重构的指标;②使用末端脱氧核苷酸转移酶标记技术和DNA电泳技术,研究心肌细胞凋亡的发生情况;③使用核酸原位杂交技术研究左室心肌细胞Bcl2、Bax基因表达的变化.结果①福辛普利使SHR左室重量指数显著降低,由3.31±0.17下降至2.56±0.25,P＜0.05;②福辛普利能显著减少左室心肌细胞凋亡的发生[(214±28)下降至(54±11)个凋亡细胞/105细胞,P＜0.01];③福辛普利能显著增加细胞Bc12基因的表达,同时减少Bax的基因表达.福辛普利使切片的Bcl2与Bax基因表达阳性面积百分数之比恢复正常(均P＜0.01).结论血管紧张素转换酶抑制剂能有效地抑制心室重塑的发生以及此过程中的心肌细胞凋亡;福辛普利使心肌细胞Bcl2及Bax基因表达阳性面积百分数之比恢复正常是其抗细胞凋亡作用的一个机制.     

福辛普利拉预处理对心肌细胞缺氧/复氧损伤的预防作用

目的:探讨福辛普利拉对培养乳鼠心肌细胞缺氧/复氧(A/R)损伤的预防作用。方法:取SD新生大鼠(1~3 d),培养成心肌细胞,在培养的第4天随机分为5组:①正常对照组,②A/R组,③0.2 mmol/L福辛普利拉预处理组(F1组),④0.6 mmol/L福辛普利拉预处理组(F2组),⑤1.8 mmol/L福辛普利拉预处理组(F3组)。分别观察各组心肌细胞搏动频率、细胞存活率、培养液中乳酸脱氢酶(LDH)活性、心肌细胞肌浆网钙泵(SERCA)mRNA的表达水平和心肌细胞内游离[Ca2 ]浓度。结果:①细胞搏动频率:A/R组比正常对照组明显减低(P<0.01);福辛普利拉各剂量组比A/R组显著加快(P<0.01),比正常对照组稍慢(P>0.05)。②细胞存活率:A/R组比正常对照组明显降低(P<0.01);福辛普利拉各剂量组比A/R组明显增高(P<0.01),而与正常对照组相比差异无统计学意义(P>0.05)。③LDH活性:A/R组比正常对照组明显升高(P<0.01);福辛普利拉各剂量组比A/R组明显降低(P<0.01),与正常对照组相比虽有升高但差异无统计学意义(P>0.05)。④SER-CA mRNA的表达水平:A/R组比正常对照组mRNA表达下调,为正常对照组的(0.78±0.30)倍(P<0.01);福辛普利拉各剂量组比A/R组显著上调(P<0.01)。⑤心肌细胞内游离[Ca2 ]浓度:A/R组比正常对照组明显升高(P<0.01);福辛普利拉各剂量组比A/R组明显降低(P<0.01),而与正常对照组相比差异无统计学意义(P>0.05)。结论:福辛普利拉预处理后对A/R心肌细胞损伤具有预防作用,其机制可能与SERCA表达上调、减轻细胞内Ca2 超载有关。     

福辛普利对自发性高血压大鼠心室重塑时左室心肌细胞凋亡和Bcl_2及Bax基因表达的影响

目的 :研究福辛普利对自发性高血压大鼠 ( SHR)左室心肌细胞凋亡和 Bcl2 、Bax基因表达的影响。方法 :1使用左室重量指数作为大鼠左室重构的指标 ;2使用末端脱氧核苷酸转移酶标记技术和 DNA电泳技术 ,研究心肌细胞凋亡的发生情况 ;3使用核酸原位杂交技术研究左室心肌细胞 Bcl2 、Bax基因表达的变化。结果 :1福辛普利使 SHR左室重量指数显著降低 ,由 3 .3 1± 0 .17下降至 2 .5 6± 0 .2 5 ,P <0 .0 5 ;2福辛普利能显著减少左室心肌细胞凋亡的发生〔( 2 14± 2 8)下降至 ( 5 4± 11)个凋亡细胞 / 10 5细胞 ,P<0 .0 1〕;3福辛普利能显著增加细胞 Bcl2 基因的表达 ,同时减少 Bax的基因表达。福辛普利使切片的 Bcl2 与 Bax基因表达阳性面积百分数之比恢复正常 (均 P <0 .0 1)。结论 :血管紧张素转换酶抑制剂能有效地抑制心室重塑的发生以及此过程中的心肌细胞凋亡 ;福辛普利使心肌细胞 Bcl2 及 Bax基因表达阳性面积百分数之比恢复正常是其抗细胞凋亡作用的一个机制。     

凋亡基因在心肌梗死的表达及血管紧张素转化酶抑制剂的干预作用

目的探讨凋亡基因对大鼠心肌梗死的表达及血管紧张素转化酶抑制剂(ACEI)的干预作用。方法将大鼠随机分为假手术组、梗死模型组、梗死模型 福辛普利小剂量组、梗死模型 福辛普利大剂量组,用逆转录-聚合酶链反应(RT-PCR)方法检测大鼠心肌梗死24h和4周时心肌细胞内凋亡抑制基因Bcl-2与凋亡基因Bax、P53、Fas的mRNA表达量,并探讨它们之间的相互关系。结果急性心肌梗死24hBcl-2表达下降,福辛普利促进其高表达,Bax、P53、Fas增高,福辛普利抑制其表达;急性心肌梗死4周,Bcl-2表达下降,福辛普利促进其表达,Bax、P53表达变化不大,福辛普利对其表达无影响,Fas高表达,福辛普利抑制其表达。结论大鼠急性心肌梗死后心肌细胞存在凋亡现象,Bcl-2表达下降,Bax、P53、Fas表达上调介导心肌梗死后心肌细胞凋亡的发生。ACEI可通过干预上述基因抑制急性心肌梗死后的心肌细胞凋亡。     

福辛普利对慢性心力衰竭大鼠心肌细胞凋亡及半胱氨酸天冬氨酸蛋白酶-3的影响

目的探讨福辛普利对慢性心力衰竭(CHF)大鼠心肌细胞凋亡及半胱氨酸天冬氨酸蛋白酶(Caspase)-3表达水平的影响。方法雄性Wistar大鼠50只随机抽取10只为假手术组,其余大鼠采用肾上腹主动脉缩窄法建立大鼠CHF模型,6 w后将成模大鼠随机分为CHF组、Fos10组、FOS20组(福辛普利10、20 mg·kg~(-1)·d~(-1))。治疗8 w后,观察各组大鼠血流动力学指标和左心室重量指数(LVMI);透射电镜观察左室心肌组织形态的改变;TUNEL法检测大鼠左心室心肌细胞的凋亡指数;SP免疫组织化学染色法检测左心室心肌组织Caspase-3蛋白的表达。结果 CHF组与假手术组相比,大鼠左心室舒张末压(LVEDP)、LVMI、心肌细胞凋亡指数、Caspase-3蛋白的表达均明显升高(P<0.01),左心室内压最大上升和下降速率(±dp/dtmax)显著下降(P<0.01);与CHF组比较,Fos10组和Fos20组大鼠LVEDP、LVMI、心肌细胞凋亡指数、Caspase-3蛋白的表达均明显降低(P<0.01),左心室内压最大上升和下降速率(±dp/dtmax)显著升高(P<0.01),且Fos20组效果明显。电镜下观察:Fos10组和Fos20组心肌损伤程度较CHF组明显减轻。结论福辛普利可通过下调Caspase-3的表达抑制心肌细胞凋亡,改善CHF大鼠心室功能及心肌超微结构。     

福辛普利对实验性心力衰竭大鼠心肌细胞凋亡和Fas、Fas配体基因表达的影响

目的:探讨实验性心力衰竭大鼠心肌细胞凋亡和心肌组织Fas、Fas配体(FasL)蛋白及其信使核糖核酸(mRNA)表达的变化及血管紧张素转换酶抑制剂(ACEI)干预的影响及意义.方法:将30只健康Wistar大鼠,随机分为假手术组(n=10)、慢性心力衰竭组(n=10)和福辛普利组(n=10).通过缩窄Wistar大鼠腹主动脉建立慢性心力衰竭模型,以福辛普利进行干预,对照观察血流动力学、心肌细胞凋亡、心肌组织Fas、FasL蛋白及其mRNA表达的变化.结果:与假手术组相比,慢性心力衰竭组左心室舒张末压、心率显著升高(P＜0.01);收缩压、舒张压、平均压、左心室收缩压、左心室内压最大收缩率、左心室内压最大舒张率显著降低(P＜0.01).福辛普利组舒张压、左心室收缩压、左心室舒张末压、心率显著低于慢性心力衰竭组(P＜0.01),左心室内压最大收缩率、左心室内压最大舒张率显著高于慢性心力衰竭组(P＜0.01).慢性心力衰竭组心肌细胞凋亡指数、心肌组织Fas、FasL蛋白及其mRNA表达水平显著高于假手术组(P＜0.05),福辛普利组心肌细胞凋亡指数、心肌组织Fas、FasL蛋白及其mRNA表达水平显著低于慢性心力衰竭组(P＜0.05).结论:慢性心力衰竭的发生、发展过程中有心肌细胞凋亡的变化及Fas/FasL系统的参与;心力衰竭大鼠心肌细胞凋亡指数、心肌组织Fas、FasL蛋白及其mRNA表达水平增高,福辛普利长期干预慢性心力衰竭,能够降低细胞凋亡及Fas、FasL基因的表达,可能与其减少Fas/FasL系统介导的细胞凋亡的发生、改善心肌功能有关.     

福辛普利对慢性心力衰竭大鼠心肌细胞凋亡及相关基因表达的影响

目的:探讨福辛普利对慢性心力衰竭大鼠心肌细胞凋亡及相关基因表达的影响。方法:采用肾上腹主动脉缩窄法建立大鼠慢性心力衰竭模型,随机分为假手术组、慢性心力衰竭组、福辛普利组,每组10只大鼠。术后假手术组和慢性心力衰竭组给予生理盐水灌胃,福辛普利组给予福辛普利10 mg/(kg·d)灌胃。8周后,观察各组大鼠左心室舒张末压(LVEDP)、左心室内压最大上升及下降速率(±dp/dtmax)和左心室质量指数(LVMI);脱氧核糖核苷酸末端转移酶介导的缺口末端标记法(TUNEL)检测大鼠左心室心肌细胞的凋亡指数(AI);SP免疫组织化学染色法检测左心室心肌组织B细胞白血病/淋巴瘤相关抗原2(Bcl-2)、B细胞白血病/淋巴瘤相关抗原相关X(Bax)蛋白的表达;蛋白免疫印记法(Western blotting)检测半胱氨酸天冬氨酸蛋白酶3(Caspase-3)蛋白的表达。结果:慢性心力衰竭组与假手术组相比,大鼠LVEDP、LVMI、心肌细胞凋亡指数、Bax蛋白、Caspase-3蛋白的表达均明显升高(P0.01),±dp/dtmax、Bcl-2蛋白的表达、Bcl-2/Bax比值显著下降(P0.01);与慢性心力衰竭组比较,福辛普利组大鼠LVEDP、LVMI、心肌细胞凋亡指数、Bax蛋白、Caspase-3蛋白的表达均明显降低(P0.01),±dp/dtmax、Bcl-2蛋白的表达、Bcl-2/Bax比值显著升高(P0.01),差异均有统计学意义。结论:慢性心力衰竭过程中发生了心肌细胞凋亡,福辛普利可通过上调Bcl-2的表达及下调Bax及Caspase-3的表达抑制心肌细胞凋亡,改善慢性心力衰竭大鼠心室功能及心肌肥厚。     

胶体~(32)P对原代培养大鼠前列腺细胞的内辐射研究

目的 观察不同浓度胶体~(32)P对原代培养大鼠前列腺细胞凋亡的影响.方法 原代培养大鼠前列腺细胞,分为大剂量辐射组、小剂量辐射组和对照组,采用流式细胞术、TUNEL染色和细胞活力测定检测大鼠前列腺细胞在不同辐射剂量下的细胞凋亡变化.结果 小剂量辐射组细胞凋亡率虽然很低,但是高于对照组(P＜0.01),大剂量辐射组细胞凋亡率明显高于小剂量辐射组和对照组(P＜0.01),并可见亚二倍体峰.与对照组比较,小剂量辐射组细胞活力下降(P＜0.05),大剂量辐射组细胞活力则明显下降(P＜0.01).结论 小剂量辐射对大鼠前列腺细胞的致死性损伤作用不大,仅能引起少量细胞凋亡,大剂量辐射可致大量细胞凋亡.     

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.     

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.