防风对大鼠结肠平滑肌收缩的抑制作用及其机制

目的: 观察防风(RS)对离体大鼠结肠平滑肌的影响,并探讨其机制.方法: 制备大鼠结肠平滑肌肌条,以9 g/LNaCl溶液为对照,观察防风对肌条自发收缩以及对乙酰胆碱(Ach)引起的肌每收缩的影响.并观察防风对用3种工具药,即纳络酮(NLT)、心得安(XDA)和酚妥拉明(FTLM)充分孵育后的平滑肌肌条的抑制作用.结果: RS各组较NS组均对离体大鼠结肠平滑肌收缩有一定程度的抑制(振幅:F=8.388,P<0.01;面积:F=33.390,P<0.01),在10-40 g/L范围内随浓度的增大而增强.RS可以抑制Ach引起的离体大鼠结肠平滑肌收缩,加入Ach后加入不同浓度的RS平滑肌收缩振幅和面积均可部分抑制(F=6.093,P<0.0l:F=15.383,P<0.01).与对照组(NS RS)比较,FTLM组对平滑肌收缩的振幅(88.92%±9.93%)和面积(91.5%±12.59%)均可抑制(均P<0.01),NIT RS组面积有差异(72.6%±15.26%,P<0.05),而XDA组振幅和面积均无统计学意义.结论: 防风能够抑制离体大鼠结肠平滑肌收缩,其机制与肾上腺素能α-受体、M胆碱受体有关.     

P物质NK1受体对大鼠结肠动力的调节作用

[目的]探讨P物质(substance P,SP)不同受体对大鼠结肠动力的调节作用。[方法]取大鼠近端结肠制备纵行肌(LMS)及环形肌(CMS)肌条,用张力换能器及多通道生理信号采集处理系统观察SP及其受体拮抗剂对SP诱导的LMS和CMS收缩活动的影响。[结果]SP显著促进大鼠结肠LMS和CMS自发性收缩活动[LMS:正常(0.85±0.06)g∶SP(1.02±0.05)g;CMS:正常(0.22±0.03)g∶SP(0.81±0.07)g,P0.01];CMS孵育河豚毒素TTX后加入SP收缩幅度显著增加[正常(1.15±0.11)g∶SP(2.25±0.18)g,P0.05];NK1受体特异性阻断剂L-703孵育肌条后加入SP,平滑肌收缩无显著增强,NK2受体特异性阻断剂GR159孵育后,SP能显著诱导平滑肌收缩增强(P0.05)。[结论]NK1和NK2受体均参与SP对结肠动力的调节,且对CMS的调节过程中,NK1受体发挥更重要的作用,SP对LMS的调节可能主要通过肠神经系统。     

白细胞介素-6介导抑郁模型大鼠结肠变化的机制研究

目的 研究慢性应激抑郁模型大鼠结肠动力变化、血清白细胞介素(IL)-6与抑郁的关系及对离体结肠肌条收缩的影响.方法 健康成年Wistar大鼠30只,其中15只建立慢性应激抑郁模型,其余15只为对照组.以糖水偏爱实验检测两组大鼠的糖水消耗与体质量比、糖水偏爱百分比.以旷场实验检测两组大鼠的行为学变化.以模拟粪便排出实验评价结肠动力.以酶联免疫吸附测定(ELISA)检测血清IL-6水平.逆转录(RT)-PCR检测结肠组织中IL-6 mRNA水平.检测大鼠离体结肠肌条的收缩功能.用不同浓度的IL-6处理对照组结肠肌条,检测IL-6对正常结肠肌条的影响及其对乙酰胆碱(Ach)的反应.结果 模型组大鼠糖水消耗与体质量比为0.12±0.03、糖水偏爱百分比为(16.17±2.61)％、总行程为(741.54±341.10)cm、直立次数为(15.69±8.00)次,均显著低于对照组[0.18±0.02、(25.54±2.32)％、(1336.20±698.80)cm、(24.87±7.90)次,P值分别=0.041、0.044、0.002、0.001].模型组大鼠粪便排出时间为(109.78±48.00)min,较对照组明显延长[(28.00±11.10) min,P=0.002].模型组大鼠血清和结肠组织IL-6水平均较高.模型组离体结肠肌条对Ach反应弱于对照组(P=0.035).对照组离体结肠肌条对200、500、1000 pg/mlIL-6的反应差异均无统计学意义(P值分别=0.935、0.825和0.766),再加入Ach后,500和1000pg/ml IL-6组对Ach的反应(R值分别为1.15±0.10和1.14±0.15)与对照组单加Ach时的R值(1.61±0.45)比较,差异均有统计学意义(P值分别=0.000、0.004).结论 慢性应激抑郁模型大鼠血清及结肠组织IL-6水平上升,并通过降低肠道对Ach的敏感性而导致平滑肌收缩障碍.     

多潘立酮在增强结肠运动中的作用

目的 观察多潘立酮对结肠的促动力作用,并与莫沙必利及西沙必利比较.方法 ①在体实验:将40只大鼠分为对照组、多潘立酮组、莫沙必利组和西沙必利组,每组10只.在各组大鼠近端结肠和远端结肠埋植应力传感器,记录清醒大鼠结肠运动.②离体实验:在恒温灌流肌槽中,采用张力传感器测定多巴胺和多巴胺+多潘立酮对大鼠离体结肠肌条的收缩活动.结果 在体实验:①清醒大鼠在消化间期的静息状态下,结肠呈现节律性相位收缩活动.②多潘立酮可明显增加结肠的收缩活动,使近端结肠和远端结肠平均振幅分别比对照组增加84.61%±7.26%和76.37%±8.47%,呈剂量-效应关系.同等剂量的莫沙必利对近端结肠和远端结肠平均振幅分别比对照组增加50.32%±8.16%和45.13%±7.16%.莫沙必利对结肠的促动力作用明显低于多潘立酮.而同等剂量的西沙必利对近端结肠和远端结肠平均振幅分别比对照组增加92.55%±8.37%和81.27%±9.95%,其促动力作用与多潘立酮相同.离体实验:①灌流多巴胺(40 mg/ml)可明显抑制离体结肠肌条收缩活动,较Krebs-Ringer液对照组减少91.56%±10.24%.②多潘立酮可阻断多巴胺对离体结肠肌条的舒张作用.结论 多潘立酮可明显增强结肠动力,其作用明显优于莫沙必利,并与西沙必利作用相同.多潘立酮增强结肠动力作用是通过抗多巴胺作用实现.     

羟基红花黄色素A对大鼠避水应激所致结肠高动力的抑制作用及其机制

目的通过体内和体外研究探讨羟基红花黄色素(hydroxy safflower yellow A,HSYA)在大鼠应激性结肠高动力中的作用及其可能的作用机制。方法将15只雄性Wistar大鼠分为3组,分别为:SWAS(假性避水应激)组、WAS(避水应激)组、WAS+HSYA组,每组5只。WAS组和SWAS组大鼠连续10 d每天分别暴露于避水应激和假性避水应激中1 h,建立大鼠模型;WAS+HSYA组大鼠于每天进行避水应激前半小时,以60 mg/kg的HSYA灌胃,而WAS组以相同的生理盐水灌胃,SWAS组则不做处理。整个实验期间,分别记录各组大鼠的每天粪球排出量。于实验第11天,大鼠处死后取近端结肠制备肌条,以张力换能器测定结肠平滑肌肌张力变化。另取正常大鼠离体近端结肠制备肌条,以张力换能器测定结肠平滑肌肌张力变化,当出现一段规律收缩信号后,分别进行其他的相关处理:(1)加入浓度梯度的HSYA溶液(终浓度分别为0.6、1.2、1.8 mol/L),观察并记录其自发性收缩活性变化;(2)用1μmol/L TTX孵育肌条10 min,再以浓度梯度的HSYA溶液处理肌条,观察并记录其自发性收缩活性变化;(3)用30μmol/L Tak-242孵育肌条15 min,再以浓度梯度的HSYA溶液处理肌条,观察并记录其自发性收缩活性的变化。采用SPSS 26.0统计软件、Graphpad 8.0软件对实验所得数据进行分析。结果避水应激诱发大鼠结肠动力亢进。HSYA明显抑制结肠肌条收缩活性,这种作用未被TTX阻断,而TLR4受体拮抗剂Tak-242能显著阻断HSYA对结肠肌条收缩活性的抑制作用。结论 HSYA能逆转应激性结肠动力亢进,这种效应可能与TLR4受体通路有关。     

内吗啡肽对"泻剂结肠"大鼠离体肠肌条收缩反应的影响

目的研究内吗啡肽（EM）对“泻剂结肠”大鼠结肠动力的影响,以探讨慢传输性便秘（STC）的发病机制.方法以“泻剂结肠”大鼠为模型,用电刺激离体肌条收缩反应试验方法观察EM对离体肌条的影响.结果与对照组相比,EM-1和EM-2明显抑制电刺激“泻剂结肠”大鼠离体肌条收缩反应,收缩波振幅降低,对远端结肠抑制尤其明显;EM-1的抑制作用强于EM-2,这种抑制作用与浓度相关,不同浓度的Naloxone（u阿片受体拮抗剂）明显加强EM作用后电刺激“泻剂结肠”大鼠离体肌条的收缩反应,收缩波振幅增加.结论EM-1和EM-2参与“泻剂结肠”动力的调控,可能是STC发病的一个重要因素.     

马来酸曲美布汀对束缚应激大鼠离体结肠平滑肌张力的调节作用机制

目的 研究曲美布汀对离体结肠平滑肌收缩及舒张运动的作用机制。方法 建立束缚应激诱发排便异常大鼠动物模型，制备离体结肠平滑肌环行肌及纵行肌肌条，应用张力换能器测定其肌张力。结果 束缚应激大鼠平滑肌肌条在基础状态时，曲美布汀可增加环行肌肌条张力，且随着浓度的递增平滑肌肌条张力有增加倾向。低于10^-7g／ml曲美布汀可增加纵行肌肌条张力，但高于10^-6g／ml时则降低肌条张力。曲美布汀可降低K^ 及乙酰胆碱作用下的束缚应激大鼠环行肌及纵行肌肌条张力，随着浓度的递增曲美布汀舒张平滑肌的作用有增加倾向。在Ca^2 作用下，10^-8g／ml曲美布汀增加束缚应激大鼠纵行肌及环行肌肌条张力，但高于10^-7g／ml时降低肌条的张力。结论 曲美布汀具有抑制和兴奋平滑肌双重作用，作用特点是调节平滑肌收缩与舒张运动，纠正肠管平滑肌运动异常。     

莪术对大鼠结肠平滑肌收缩的促进作用及机制

目的:观察莪术对离体大鼠结肠平滑肌收缩运动的影响,并初步探讨其作用机制.方法:制备大鼠结肠平滑肌肌条,以9 g/LNaCl溶液(NS)为对照组,观察不同浓度莪术对结肠平滑肌的收缩效应;以莪术为对照组.分别观察酚妥拉明、维拉帕米和阿托品3种阻断剂孵育肌条后,莪术对肌条的收缩效应.结果:莪术高浓度组对离体大鼠结肠平滑肌的促进作用明显,与NS对照组比较,莪术1g/L、10 g/L组引起的肌条最大收缩振幅和曲线下面积均有统计学意义(63.92±2.06,76.27±2.28vs100%;44.09±11.10,55.66±10.29vs100%,P<0.05或<0.01);与单独莪术组比较,阻断剂维拉帕米和阿托品对莪术引起的肌条收缩有抑制作用,其最大收缩振幅和曲线下面积均有统计学意义(87.35%±50.49%,73.80%±9.37%vs 100%,33.97%±15.18%,27.55%±11.56% vs 100%,P<0.05或<0.01).结论:莪术对大鼠结肠平滑肌的收缩活动有兴奋作用,且与剂量呈正相关,其引起的收缩效应可被阿托品和维拉帕米阻断,而未能被酚妥拉明阻断.     

钙离子在大鼠结肠平滑肌运动中作用机制的研究

目的 应用束缚应激大鼠实验模型,研究离体结肠平滑肌的收缩运动及其影响因素,探讨鸟苷素在结肠运动中的作用。方法 建立束缚应激大鼠动物模型,制备离体结肠平滑肌环行肌及纵行肌肌条,应用张力换能器,测定其肌张力。应用放射配基法测定结肠组织及血浆中鸟苷素含量。结果 束缚应激刺激可诱发大鼠排便增加,该动物模型是较好的模拟人ＩＢＳ的实验动物模型。束缚应激大鼠离体结肠平滑肌的张力升高,对Ｋ＾＋、Ｃａ＾２＋、乙酰胆     

Nesfatin-1对肥胖大鼠胃排空及胃平滑肌条收缩性的影响

目的:观察Nesfatin-1对正常及单纯性肥胖大鼠胃排空及离体胃平滑肌条收缩活性的影响.方法:高脂饲料喂养♂大鼠6wk,制作单纯性肥胖大鼠模型;正常及肥胖大鼠实验组中枢注入不同浓度Nesfatin-1(0.5μmol/L、5μmol/L、50μmol/L)后测胃排空率;生理记录仪记录大鼠胃底、胃体平滑肌条自发收缩及不同浓度Nesfatin-1(0.026μmol/L、0.26μmol/L、2.6μmol/L)作用下对乙酰胆碱(Ach)诱导的肌条收缩的影响.结果:Nesfatin-1可抑制正常及肥胖大鼠胃平滑肌条收缩,低、中、高浓度组与生理盐水对照组相比差异均有统计学意义(q=3.93-15.72,P<0.05-0.01).随Nesfatin-1浓度的增高,其抑制作用呈明显剂量依赖关系(q=3.45-5.69,P<0.05-0.01).低浓度Nesfatin-1抑制正常大鼠、肥胖大鼠胃底平滑肌条收缩作用无显著性差异(P>0.05),中、高浓度对正常大鼠胃底平滑肌条抑制作用强于肥胖大鼠(t=2.14,P<0.05;t=2.63,P<0.05).低、中浓度Nesfatin-1抑制正常大鼠、肥胖大鼠离体胃体平滑肌条收缩作用无显著性差异(P>0.05),但高浓度抑制正常大鼠离体胃体平滑肌条收缩作用显著强于肥胖大鼠(t=2.53,P<0.05).结论:Nesfatin-1可抑制正常及肥胖大鼠胃排空,胃排空率随Nesfatin-1浓度增加而降低.Nesfatin-1可抑制乙酰胆碱诱导的单纯性肥胖大鼠离体胃平滑肌条的收缩活动,其抑制作用随Nesfatin-1浓度增高而增强;相同Nesfatin-1浓度抑制正常大鼠离体平滑肌条收缩作用强于肥胖大鼠.     

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.