β榄香烯对肝星状细胞分泌ANGⅡ及表达AT_1R mRNA的影响

目的为肝纤维化的治疗提供新思路。方法将肝星状细胞（HSC）-T6细胞株培养24h，分别以质量浓度为10．0、5．0、2．5mg／L的β榄香烯（实验1、2,3组）作用4、12、24h，收集细胞上清及细胞，并设空白对照组。放射免疫法检测培养上清中血管紧张素Ⅱ（ANGⅡ）水平，RT—PCR检测ANGⅡ的Ⅰ型受体（AT1R）mRNA表达。结果作用12、24h时各实验组ANGⅡ水平及均较空白对照组降低（P〈0．05、0．01）；三个时间点各实验组AT1RmRNA表达均显著低于空白对照组（P〈0．01），并呈剂量依赖性。结论β榄香烯可能延缓肝纤维化的发生、发展。     

Ang-Ⅱ对血管内皮细胞线粒体膜电位的影响及阿托伐他汀的保护作用

目的:观察血管紧张素-Ⅱ(Ang-Ⅱ)对血管内皮细胞线粒体膜电位的影响及阿托伐他汀的保护作用.方法:将血管内皮细胞分为:空白对照组(仅给予细胞培养液)、Ang-Ⅱ组(细胞培养液中加入Ang-Ⅱ,使其终浓度为10-7mol/L)、Ang-Ⅱ加小剂量阿托伐他汀组(在单纯Ang-Ⅱ组的基础上加入阿托伐他汀,使阿托伐他汀的终浓度为0.1 μmol/L)、Ang-Ⅱ加大剂量阿托伐他汀组(在单纯Ang-Ⅱ组的基础上加入阿托伐他汀,使阿托伐他汀的终浓度为1 μmol/L).用激光共聚焦显微镜测量各组细胞的线粒体膜电位水平.结果:①Ang-Ⅱ组的线粒体膜电位显著低于空白对照组(P<0.01);②Ang-Ⅱ加阿托伐他汀组的线粒体膜电位显著高于Ang-Ⅱ组(P<0.01).③Ang-Ⅱ加大剂量阿托伐他汀组的线粒体膜电位水平高于Ang-Ⅱ加小剂量阿托伐他汀组(P<0.05).结论:Ang-Ⅱ可引起血管内皮细胞线粒体膜电位的显著降低,而阿托伐他汀可呈剂量依赖性的逆转Ang-Ⅱ的这一作用.     

别嘌呤醇对高糖诱导损伤的人脐静脉血管内皮细胞的保护作用

目的探讨别嘌呤醇对高糖损伤后的人脐静脉血管内皮细胞（HUVEC）的保护作用及其机制。方法以HUVEC为研究对象,体外培养至第三代,分为：①20mmol／L高糖损伤对照组;②别嘌呤醇保护组（浓度分别为0．1mmol／L、0．2mmol／L、0．3mmol／L）;③维生素C阳性对照组（浓度为100mg／L）。不同浓度别嘌呤醇及维生素C先与HUVEC孵育24h,再加入20mmol／L高糖诱导损伤48h,测定各组细胞上清液中一氧化氮（NO）、丙二醛（MDA）、超氧化物歧化酶（SOD）、细胞间黏附分子-1（ICAM-1）含量及细胞凋亡率。结果别嘌呤醇（0．1mmol／L、0．2mmol／L、0．3mmol／L）药物保护组的细胞凋亡率低于20mmol／L高糖组,其中以0．3mmol／L更为明显（P〈0．01）;细胞培养液中SOD、NO的量均较20mmol／L高糖组增高,其中以0．3mmd／L别嘌呤醇组更为明显（P〈0．01）。药物保护组细胞培养液中合成MDA、ICAM-1较波动性高糖组降低,且在一定浓度范围内（0．05-49．30mmol／L）呈浓度依赖性（P〈0．05）。结论①别嘌呤醇对高糖体外诱导的HUVEC损伤有保护作用,呈浓度依赖性。②别嘌呤醇对高糖体外诱导HUVEC损伤保护作用的机制包括抑制氧化应激、炎症反应及细胞凋亡。     

硝普钠对人血管平滑肌细胞合成胶原的抑制作用

目的 探讨内皮素（ET-1）对人血管平滑肌细胞（HVSMC）合成胶原的影响，并观察硝普钠（SNP）对HVSMC合成胶原的影响。方法 将ET-l10^-8mol／L和不同浓度SNP加人体外培养HVSMC。培养24h后测培养液中NO含量，测细胞内cGMP含量及^3H-脯氨酸掺人量即总胶原含量。结果 加入梯度浓度SNP，NO水平呈剂量依赖性增加（均P〈0．01）；ET-1使胶原合成量增加80％（P〈0．01），加入梯度浓度SNP较ET-1组胶原合成量分别减少了38％、42％、57％（均P〈0．01），呈剂量依赖性；ET-1＋SNP低、中、高浓度组较ET-1组细胞内cGMP含量明显增加（均P〈0．01），且cGMP含量随SNP增加而增加；细胞内cGMP含量与胶原合成量呈良好负相关关系（r=-0．93）。结论 ET-1可引起HVSMC合成胶原增多；SNP可剂量依赖地抑制HVSMC合成胶原；SNP对胶原合成的抑制作用可能是通过cGMP途径起作用。     

尾加压素Ⅱ对体外高糖培养大鼠肾小球系膜细胞细胞外基质分泌的影响

目的观察尾加压素Ⅱ（UⅡ）对体外高糖培养大鼠肾小球系膜细胞（MC）细胞外基质（ECM）纤连蛋白（FN）、Ⅳ型胶原（ColⅣ）及转化生长因子（TGF）β分泌的影响。方法体外高糖培养大鼠MC,加入不同浓度UⅡ（终浓度10-7、10-8、10-9、10-10mol/L）,并设立UⅡ抑制组,37℃孵育24h,留取上清,应用ELISA法测定上清中FN、ColⅣ及TGFβ含量。结果10-8mol/LUⅡ作用下的大鼠MC培养上清中,FN、ColⅣ及TGFβ含量同对照组相比有显著升高（P〈0.05）;UⅡ10-8mol/L＋Ca2＋阻断剂尼卡地平组、UⅡ10-8mol/L＋Ca2＋螯合剂EDTA组及UⅡ10-8mol/L＋抗UⅡ抗体组同UⅡ10-8mol/L组相比较,细胞培养上清中FN、ColⅣ及TGFβ含量显著减少（P〈0.05）。结论一定浓度尾加压素Ⅱ能促进体外高糖培养的大鼠MC分泌ECMFN、ColⅣ及TGFβ。     

不同的脂肪酸对人血管内皮细胞增殖和凋亡的影响

目的 了解游离脂肪酸（FFAs）对体外培养的人脐静脉内皮细胞（human umbilical veinen dothelialcells，HUVEC）凋亡及生长周期的影响。方法 用不同种类，不同浓度的FFAs培养人血管内皮细胞（VEC），然后应用流式细胞术（FCM）对培养的人VEC生长周期及细胞凋亡进行分析。结果 饱和脂肪酸（SFA）（C16：0，C18：0，C24：0），使培养的人VEC生长受到抑制，随浓度升高细胞凋亡率升高；不饱和脂肪酸（USFA）（C18：1，C18：2），当低浓度时，VEC凋亡率较低（P〉0．05，P〉0．01），而当达400或600μmol／L时凋亡率升高（P〈0．05，P〈0．01）。结论 SFA对培养的人VEC具有抑制增殖及诱导凋亡的作用。低浓度USFA对VEC凋亡及生长周期的影响不大，但高浓度时，其诱导凋亡的作用增强。     

冠心病血清NO、NOS、ET水平变化的临床研究

目的 探讨内皮细胞功能障碍与冠心痛（CAD）的关系。方法 利用生化比色法测定155倒CAD患者（A组）血浆NO、NOS班度．用放射免疫涪洲定ET浓度,并以50例健康人做时腻（B组）。A组中45倒行冠脒造影（CAG）。其中稳定型心娥痛（A1组）．不稳定型心垃痛（A2组）。急性肌梗死（A3组）各15例。结果 A组NO、NoS、NO／ET较B组明显降低（P〈0．01）,ET则较B组明显升高（P〈0．01）而A2、A3组的NO、N0／ET较A1组降低（P〈0．01）,ET较A1组升南（P〈0．01）,A2、A3组之间无显著性差异。CAG结果表明。A1组的冠脒病变比A2、A3组更广泛更严重。结论 内皮功能障碍在冠心病的不同缺血形式之中具有重要作用。     

刺五加皂甙对PC12细胞缺氧诱导因子-1α表达的影响

目的 观察刺五加皂甙（ASS）对PC12细胞缺氧诱导因子-1α（HIF-1α）表达的影响,探讨其抗缺血缺氧脑损伤作用的机制。方法将PC12细胞分为三组,对照组在无血清的DMEM培养基中培养;模型组加入终浓度为125μmol／L的CoCl2共同作用4h;ASS组先用终质量浓度为50μg／ml的ASS预处理24h,再加入终浓度为125μmol／L的CoCl2共同作用4h。采用MTT比色分析法测定各组PC12细胞活性,Western Blot法检测HIF-1α表达的变化。结果对照组、模型组、ASS组细胞活性OD值分别为0．538±0．027、0．320±0．045、0．615±0．039;HIF-1α表达灰度比值分别为0．085±0．033、0．782±0．050、0．976±0．070。各组间相比,P均〈0．01。结论ASS对缺血缺氧性脑损伤有保护作用,其机制与诱导HIF-1α表达有关。     

血栓抽吸治疗急性ST段抬高型心肌梗死前后神经内分泌因子水平的变化

目的探讨应用血栓抽吸装置GuardWire Plus^TM行血栓抽吸治疗急性sT段抬高型心肌梗死（STEMI）对神经内分泌因子水平、外周血肌钙蛋白（cTnI）、TIMI血流变化的影响及其临床价值。方法将2004年9月至2006年9月在我院行急诊PCI的72例STEMI患者分为两组，抽吸组（TA组，38例）血栓抽吸后支架置入；非抽吸组（NTA组，34例）单纯PCI。于手术当天、术后第1、2、3、5天分别测定外周血中内皮素（ET）、血浆肾素活性（PRA）、醛固酮（ALD）、血管紧张素Ⅱ（AngⅡ）、去甲肾上腺素（NE）、肾上腺素（E）的水平。于术前、术后4h、8h、12h、16h、24h、2d、3d、5d分别测定外周血中cTnI的水平。支架置入后常规行冠状动脉造影，观察心肌血流灌注情况，测定支架置入后两组患者的TIMI血流。比较术后2h心电图ST段回落。术后1周及3个月应用彩色超声心动图测定左室射血分数（LVEF），评价心功能。结果两组病例均成功置入支架，术前两组患者的神经内分泌因子水平均显著升高，两组间差异无统计学意义。浓度-时间曲线显示术后神经内分泌因子水平均迅速下降，TA组较NTA组ET、PRA、AngⅡ、ALD、NE、E等神经内分泌因子水平于术后第1天或第2天下降明显[ET：术前152．37ng／L比153．63ng／L（P：0．858），术后第1天128．11ng／L比147．07ng／L（P=0．037），术后第2天122．22ng／L比139．64ng／L（P=0．040）；PRA：术前2．87μL／（L·h）比2．87μL／（L·h）（P=0．998），术后第1天1．74μL／（L·h）比2．54μL／（L·h）（P=0．036），术后第2天1．70μL／（L·h）比2．29μL／（L·h）（P=0．032）；ALD：术前200．14pmol／L比181．19pmol／L（P=0．508），术第1天156．06pmol／L比172．19pmol／L（P=0．001）；AngⅡ：术前199．11ng／L比。212．32ng／L（P=0．539），术后第1天149．26ng／L比188．37ng／L（P=0．040），术后第2天135．57     

血管紧张素Ⅱ及转化生长因子在糖尿病心肌病发病机制中的作用

摘要：目的探讨血清血管紧张素Ⅱ（angiotensin1I,Ang-Ⅱ）及转化生长因子α（transfomunggrowthfactorot,TGF-α）浓度在糖尿病（diabetesmellitus,DM）心肌病（diabeticcardiomyopathy．DCM）发病机制中的作用．．方法检测118例DCM患者、40例单纯2型DM患者及50名健康体检者（正常对照组）的血清Ang-Ⅱ及TGF-α浓度,并进行对比分析。DCM患者按心功能分级（纽约心脏学会标准）分为3个亚组：35例心功能正常者设为DCMI组,42例心功能Ⅱ级者设为DCM2组,41例心功能Ⅲ-IV级者设为DCM3组。DCM组及DM组血清Ang-Ⅱ及TGF-仪浓度进行直线相关分析。结果血清Ang-Ⅱ及TGF-α的浓度在DCM各亚组[Ang-Ⅱ：（99．6_＋20．3）、（116．9±26．5）、（137．5±33．7）pg／mL;TGF-α：（62．6±9．8）、（75．3±11．2）、（89．3±13．6）pg／mL]及DM组[Ang-1I：（83．9±17．1）pg／mL;TGF-α：（48．5±8．4）pg／mL]均显著高于正常对照组[Ang-U：（56．2±14．4）pg／mL;TGF-α：（26．8±5．1）pg／mL],差异有统计学意义（P均〈0．05）。DCM各亚组血清Ang-Ⅱ及TGF-α的浓度均屁著高于DM组．差异有统计学意义（P均〈0．05）。DCM组及DM组血清Ang-11与TGF-仪浓度呈正相关（r=0．93,P〈0．05;r=0．90．P〈0．05）。结论血清Ang-Ⅱ及TGF-仅浓度的升高,激活肾素血管紧张素系统,导致心肌纤维化可能是DCM的发病机制之一。     

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.