急性心肌梗塞患者心率变异性与心室晚电位和左室射血分数以及室性心律失常关系的探讨

采用动态心电图统计２４小时全部窦性ＲＲ间期，以测定３０例急性心肌梗塞（ＡＭＩ）后１７±４ｄ的心率变异性（ＨＲＶ）ＲＲ间期均值的标准差（ＳＤ）指标，并同时测定心室晚电位（ＶＬＰ）、左室射血分数（ＬＶＥＦ）和用Ｈｏｌｔｅｒ记录室性心律失常，分析它们之间的关系。ＶＬＰ阳性与阴性组的ＨＲＶ无显著性差异（Ｐ＞０．０５）；ＨＲＶ与ＬＶＥＦ呈显著正相关（Ｐ＜０．００５）；Ｈｏｌｔｅｒ记录到短阵室性心动过速、成对室性早搏（简称室早）和每小时室早数＞１００次的ＳＤ值显著低于未记录到室早和每小时室早数＜１０次者（Ｐ＜０．００１）。提示ＡＭＩ后ＨＲＶ降低与ＶＬＰ阳性与否无关；低ＬＶＥＦ者ＨＲＶ亦降低；ＨＲＶ降低者其室性心律失常发生率显著增加。联合应用上述方法和指标，可望提高对ＡＭＩ后高危患者预测的准确率。     

心率变异性能谱分析法对评价急性心肌梗死预后的临床意义

本文运用心率能谱分析法（ＨＲＰＳ）研究急性心肌梗死不同病程患者的心率变异性（ＨＲＶ），发现两周内急性心肌梗死患者存在明显植物神经调节失衡，表现交感神经功能亢进，迷走神经张力受损。在１年追踪观察中，发现其心率能谱图的低频峰逐渐降低，高频峰逐渐升高，提示这种植物神经调节逐渐恢复平衡；而急性期合并休克、心力衰竭或室性心动过速患者，心率能谱图各频峰均降低，且无明显恢复。这说明植物神经调节失衡同各种疾病发展过程关系密切，且提示ＨＲＰＳ分析法是一种敏感的、非侵入性检测植物神经活性定量方法。     

心律平治疗室性早搏的评价

为评价心律平治疗室性早搏（室早）的地位，本文对３９例室早患者随机分组给予心律平或慢心律治疗。治疗前后的动态心电图结果显示：以室早数减少＞７５％作为有效，则两药的有效率相似，分别为６１％和６４％（Ｐ＞０．０５），心律平还使１０例非持续性室性心动过速（ＮＳＶＴ）中的８例消失。认为：心律平治疗效果佳，安全度高，可作为治疗室早的一线药物。     

心率变异评价Ⅱ型糖尿病患者自主神经功能

目的 研究Ⅱ型糖尿病患者心率变异（ＨＲＶ）与自主神经病及心、肾脏器受损的关系。方法 ５７例Ⅱ型糖尿病患者,分３组：单纯糖尿病组２９例,糖尿病合并冠心病组（糖冠组）１７例,糖尿病肾病组（糖肾组）１１例,正常对照组１５例,全部进行心血管反射试验及ＨＲＶ分析。结果 糖尿病患者合并自主神经病变为４５．６％,各组在ＨＲＶ时域指标及非线性定量分析指标上均较对照组降低,以糖肾组最为显著。比较Ｒ－Ｒ间期散点图,对     

伴有心功能不全的肺心病患者的心率变异分析

对４８例伴有心功能不全的肺源性心脏病（肺心病）患者连续２４小时动态心电图记录和心率变异分析，并与３０例正常人对照，结果表明，心率变异指数（ＨＲＶＩ）包括面积法（ＨＲＶ（Ｉ－ｓ））和直测法（ＨＲＶ（Ｉ－Ｄ））缩小的阳性率在肺心病组高于正常组，而ＨＲＶＩ的均值明显小于正常组，两组间相差均非常显著（Ｐ＜０．０１～０．００１）。以心功能≥Ⅲ级，右室肥厚及室性心律失常（参考Ｌｏｗｎ分级）≥Ⅳ级为标准，将４８例肺心病患者分为高危、低危两组，高危组ＨＲＶＩ均值小于低危组，ＨＲＶＩ缩小的阳性率高于低危组，高危、低危两组间有显著的统计学意义（Ｐ＜０．０１～０．００１）。说明肺心病患者合并心功能不全、右室肥厚、室性心律失常对心率变异有一定的影响。     

成对室性早搏、易颤指数与短阵室性心动过速关系探讨

３１０例２４小时动态心电图资料中有室性早搏（室早）１７１例，其中成对室早３０例，短阵室性心动过速（短阵室速）９例。计算易颤指数（ＶＩ＝ＲＲ·ＱＴ／ＣＩ），结果室早ＶＩ＝０．５６±０．１５，成对室早ＶＩ＝０．５９±０．１２，与短阵室速有关的成对室早ＶＩ＝０．５８±０．１８，与室速无关的成对室早ＶＩ＝０．６０±０．１４，短阵室速ＶＩ＝０．６１±０．１１。将室早ＶＩ与短阵室速ＶＩ和成对室早的ＶＩ比较，室速有关的成对室早与室速无关的成对室早的ＶＩ比较，结果均无显著性意义（Ｐ＞０．０５）。提示用易颤指数判断室性早搏与短阵室速的关系意义不大。成对室性早搏中２７％（８／３０）发生短阵室速，９例短阵室速中８例与成对室早有关，其中７７％（７／９）与单形成对室早有关，单形成对室早中８３％（１０／１２）由室内异位起搏点自律性增高引起，同时提示单形性短阵室速机制是室内异位起搏点自律性增高。频发成对室早的病例，短阵室速的次数也多，而短阵室速是否发生与成对室早的频发程度无明显关系。     

冠心病患者心率变异性检测的临床意义

通过频域分析法，分析６５例冠心病患者的心率变异性（ＨＲＶ），发现其昼夜规律消失；心梗塞组的ＨＲＶ较心绞痛组降低。提示：ＨＲＶ分析可定量检测心脏自主神经系统活性，可以在一定程度上反映心功能受损程度，对临床治疗有一定的参考价值。     

心率变异分析对急性心肌梗塞预后的预测价值

近年来，心率变异分析（ＨＲＶ）作为植物神经功能状态的无创伤性测定方法愈来愈受到人们的重视。我们对７４例急性心肌梗塞（ＡＭＩ）患者进行了ＨＲＶ指标检测，现报告如下。１资料与方法１．１临床资料本组均为１９９２年３月至１９９４年５月在山东省立医院心内科住院...     

充血性心力衰竭伴室性心动过速患者心率变异与预后的关系

为探讨充血性心力衰竭（ＣＨＦ）患者自主神经张力变化与室性心律失常的关系，我们对ＣＨＦ患者有或与持续性室性心动过速（ＮＳＶＴ），ＣＨＦ患者与正常组各项心率变异（ＨＲＶ）时域指标进行比较。结果：ＣＨＦ组的ＨＲＶ降低，其ＨＲＶ各项指标与患者的ＬＶＥＦ不存在直线相关，死亡者的ＳＤＲＲ、ＳＤＡＮＮ明显低于存活者（Ｐ＜０．００１）；ＣＨＦ有ＮＳＶＴ者与无ＶＴ者ＨＲＶ差异无显著性（Ｐ＞０．０５）。作者认为ＨＲＶ低表示自主神经张力失衡，容易导致猝死。在预测ＣＨＦ患者预后时，ＨＲＶ优于ＬＶＥＦ和ＮＳＶＴ；ＨＲＶ时域指标ＳＤＲＲ、ＳＤＡＮＮ敏感性优于ＰＮＮ５０。     

老年人心脏病检测心率变异性的临床意义

用Ｈｏｌｔｅｒ检测了１５３例不同年龄的健康人及１００例老年心脏病患者的心率变异性（ＨＲＶ），进行对比分析。发现：（１）健康老年人的ＨＲＶ明显低于老年前期及青中年人；（２）老年心衰患者的ＨＲＶ明显低于无心衰的心脏病患者，其减低程度与心衰程度相一致，分节段的ＨＲＶ比２４小时总的ＨＲＶ有更高的诊断价值；（３）老年人心脏病的ＨＲＶ明显减低者可伴有病死率的增高。     

Safety and efficacy of controlled-release mesalamine for maintenance of remission in ulcerative colitis

This 12-month, double-blind, placebo-controlled study randomized 205 ulcerative colitis patients in remission to placebo or controlled-release mesalamine at 4 g/day for 12 months. Patients were stratified to either pancolitis or left-sided disease, based on previous diagnosis. Maintenance of remission was defined as a sigmoidoscopic index of <5, less=" than=" five=" stools=" per=" day,=" and=" the=" absence=" of=" rectal=" bleeding.=" a=" significantly=" greater=" number=" of=" patients=" maintained=" remission=" on=" mesalamine=" 4=" g/day=" than=" on=" placebo=" at=" each=" of=" five=" study=" visits,=" following=" the=" first=" one-month=" visit=">P<0.05). the=" estimated=" 12-month=" remission=" rates=" for=" the=" mesalamine=" group=" were=" 64%=" (38%=" for=">P=0.0004). Baseline subgroups (disease location, time since last flare of active disease, and previous response to oral/rectal steroids or sulfasalazine) did not influence remission rates. Treatment-related adverse events were rare. Controlled-release mesalamine is a safe and efficacious single agent for maintaining remission of ulcerative colitis.The members of the Pentasa Study Group are as follows: Austin Diagnostic Clinic, Austin, Texas: Rambie L. Briggs, MD (Chief Investigator), V. Lawlis, MD, C. Felger, MD, G. Kitzmiller, MD, T. Liebermann, MD, Robert Frachtman, MD, Cindy Fischer, RN; San Francisco General Hospital, San Francisco, California: John P. Cello, MD (Chief Investigator), James Grendell, MD, Julie Satow, RN; University of Chicago School of Medicine, Chicago, Illinois: Stephen B. Hanauer, MD (Chief Investigator), Ira Hanan, MD, Pat Schultz, RN, Debbie James, RN; Nalle Clinic, Charlotte, North Carolina: James Mertesdorf, MD (Chief Investigator), Fitzgerald Hiestand, Jr., MD, Paul Tucker, Jr., MD, Thomas Roberts, MD, Pepper Brundage, CMA, Theresa Griffin, Medical Assistant, Janet E. Beck, CMA; Gastrointestinal Association, PA, Shawnee Mission, Kansas: Gregory Rick, Jr., MD (Chief Investigator), William Hartong, MD, William Buser, MD, Stanley Brand, MD, Peggy Bryant, RN, Michelle Kliewer, RN; HCA Presbyterian Hospital, Oklahoma City, Oklahoma: Malcolm Robinson, MD (Chief Investigator), Mark Mellow, MD, Robert McFadden, MD, David Neumann, MD, Karen Helin, Connie J. Privett-Cointepas, Rosemary R. Meek; Forsyth Medical Specialists, Winston-Salem, North Carolina: Walter Roufail, MD (Chief Investigator), Robert Brice, MD, Thomas P. Hughes, MD, Michael Fina, MD, Daniel Murphy, MD, Lacole Clinard, RN, Debbie Allman, Brenda Bowen; Northwest Gastroenterologists, Arlington Heights, Illinois: Jerrold L. Schwartz, MD (Chief Investigator), Igor Jurcik, MD, Loren B. White, MD, Michael Cohen, MD, David Sales, MD, PhD, Sandra Gochnour, RN, Nora M. York, RN; Digestive Healthcare, Minneapolis, Minnesota: David Weinberg, MD (Chief Investigator), Richard A. Dubow, MD, James Pries, MD, Joseph Tombers, MD, Stephen Gilberstadt, MD, Philip Hanna, MD, Mary Jane Watson, PharmD, Michele Mattison, LPN; Greater Cincinnati Gastroenterology Associates, Cincinnati, Ohio: Michael Safdi, MD (Chief Investigator), Alan Safdi, MD, Ronald Schneider, MD, George Waissbluth, MD, Michael D. Kraines, MD, Linda Magaw, CRC, Nancy Emrath, CRC; New England Medical Center, Boston, Massachusetts: Sanjeev Arora, MD, Marshall Kaplan, MD, Augusta McKusick, RN; Gastroenterology of Lake City, Waukegan, Illinois: Fred Rosenberg, MD (Chief Investigator), E.P. Kirch, MD, Hugh A. Allen, MD, Beth Weber, RN, Valley Health Care Medical Group, Binghamton, New York: Marcelo A. Barriero, MD (Chief Investigator), Leslie Bank, MD, Linda Gitchell, RN; Scripps Clinic Medicine Group, Inc, La Jolla, California: Williamson B. Strum, MD (Chief Investigator), Leona Goodman; University of Kansas Medical Center, Kansas City, Kansas: Philip Miner, MD (Chief Investigator), Steven Matter, MD, Dace Miller, MD, Clark Antonson, MD, Roland Christian, MD, Wendy Biddle, RN, Susan Clark, RN, Dorinda S. Sutton, RN; Oregon Health Sciences University, Portland, Oregon: Ronald M. Katon, MD (Chief Investigator), Fred Smith, MD, Kent Benner, MD, Emmet Keeffe, MD, David Lieberman, MD, Clifford Melnyk, MD, Flordeliz Lindenburg, Sue Webster; Medical College of Virginia, Richmond, Virginia: Alvin Zfass, MD, Donald Kirby, MD, Alfred Lee, MD, Yuen San Yee, MD, Paula Goshgarian-Patrick; Wake Research Associates, Raleigh, North Carolina: Charles Barish, MD, Philip Ashburn, MD, Diedrich C. Waterman, MD, Patricia M. Patterson, RN; Birmingham Gastroenterology Associates, Birmingham, Alabama: W. Roger Carlisle, MD (Chief Investigator), Leonard OuTim, MD, Raymond Tobias, MBChB, J. Lynn Cochran, MD, Walter J. Bristow, III, MD, Peter D. Miller, MD, Sarah Ingle, RN; Bowman-Gray School of Medicine, Wake Forest University, Winston-Salem, North Carolina: Robert M. Kerr, MD, Donald Castell, MD, Wallace C. Wu, MD, Joel E. Richter, MD, John H. Gilliam, III, MD, Greg Stark, PA; Marion Merrell Dow Inc., Kansas City, Missouri: Ruthanna Law, BSN, MA, Neil Malone, MA, Larry Roi, PhD, Michael Coen, MA, Doug Moore, BA, Mike McPherson, PharmD, MBA.     

Secretion of the intestinotropic hormone glucagon-like peptide 2 is differentially regulated by nutrients in humans

Background & Aims: Glucagon-like peptide 21, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33 (GLP-21, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33), an intestinally derived hormone, stimulates growth in rodent small and large bowel. To explore the physiology of GLP-21, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33 secretion, we measured plasma GLP-2 levels in 6 healthy male volunteers, before and after test meals. Methods: Blood samples were collected over 24 hours with the subjects consuming a normal, solid mixed diet (2500 kcal) and for 4 hours after liquid test meals (400 kcal/300 mL) composed of carbohydrate, fat, or protein. All studies commenced at 9 AM. Plasma was extracted and analyzed in radioimmunoassays for N-terminal immunoreactive GLP-2 (N-IR-GLP-2; measures bioactive GLP-21, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33) as well as total IR-GLP-2 (T-IR-GLP-2), which includes GLP-21, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, GLP-23, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33 (an inactive degradation product of GLP-21, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33), and the pancreatic major proglucagon fragment (an inactive precursor that contains GLP-2). Basal and nutrient-stimulated plasma samples were also analyzed by high-performance liquid chromatography to determine the levels of GLP-21, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33 and GLP-23, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33. Results: N-IR-GLP-2 levels were increased 2.0 ± 0.2– to 2.8 ± 0.5–fold 40 minutes after each mixed meal (P < 0.05–0.01) and returned to basal overnight, whereas T-IR-GLP-2 levels were increased 1.3 ± 0.1–fold 40 minutes after breakfast only (P < 0.05). After ingestion of carbohydrate or fat alone, plasma N-IR-GLP-2 concentrations increased by 5.6 ± 2.0– and 2.7 ± 0.6–fold within 1 hour (P < 0.05). High-performance liquid chromatography analysis showed a relative increase in the levels of GLP-21, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33 compared with GLP-23, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33 (P < 0.05). Ingestion of the protein meal did not alter N-IR-GLP-2 levels, whereas T-IR-GLP-2 was increased by fat and protein (by 1.7 ± 0.2–fold for each, P < 0.01) but not by carbohydrate. Conclusions: These results show that secretion of GLP-21, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33 from the intestine is regulated in a nutrient-dependent manner in normal humans.GASTROENTEROLOGY 1999;117:99-105     

原发性高血压与脂肪肝及血脂相关性调查

目的 探讨原发性高血压与血脂代谢水平及脂肪肝发生率的关系.方法 收集海南医学院附属医院原发性高血压患者351例,以及血压正常者100例,抽血检测甘油三酯（TG）、总胆固醇（TC）、低密度脂蛋白胆固醇（LDL-C）、高密度脂蛋白胆固醇（HDL-C）、丙氨酸转氨酶（ALT）、天冬氨酸转氨酶（AST）、血糖、血尿酸、尿素氮和肌酐水平,B超检测脂肪肝比率,同时测量体重及体重指数.结果 高血压患者的TG、TC、AST、血糖、血尿酸、肌酐水平及脂肪肝患病率、体重和体重指数明显高于血压正常者,HDL-C低于血压正常者,差异均有统计学意义,LDL-C、ALT、尿素氮则差异无统计学意义.结论 高血压患者的脂肪肝患病率、体重及体重指数、TG、TC、AST、血糖、血尿酸、尿素氮和肌酐水平明显高于血压正常者,其与高血压呈正相关.     

Survey of molecular profiling during human colon cancer development and progression by immunohistochemical staining on tissue microarray

AIM： To explore the molecular events taking place during human colon cancer development and progression through high-throughput tissue microarray analysis. METHODS： We constructed two separate tissue microarrays containing 1.0 mm or 1.5 mm cylindrical samples acquired from 112 formalin-fixed and paraffinembedded blocks, including carcinomas （n = 85）, adenomatous polyps （n = 18）, as well as normal paracancerous colon tissues （n = 9）. Immunohistochemical staining was applied to the analysis of the consecutive tissue microarray sections with antibodies for 11 different proteins, including p53, p21, bcl-2, bax, cyclin D1, PTEN, p-Aktl, β-catenin, c-myc, nm23-h1 and Cox-2. RESULTS： The protein expressions of p53, bcl-2, bax, cyclin D1, β-catenin, c-myc, Cox-2 and nm23-h1 varied significantly among tissues from cancer, adenomatous polyps and normal colon mucosa （P = 0.003, P = 0.001, P = 0.000, P = 0.000, P = 0.034, P = 0.003, P = 0.002, and P = 0.007, respectively）. Chi-square analysis showed that the statistically significant variables were p53, p21, bax, β-catenin, c-myc, PTEN, p-Aktl, Cox-2 and nm23-h1 for histological grade （P = 0.005, P = 0.013, P = 0.044, P = 0.000, P = 0.000, P = 0.029, P = 0.000, P = 0.008, and P = 0.000, respectively）, β-catenin, comyc and p-Akt1 for lymph node metastasis （P = 0.011, P =0.005, and P = 0.032, respectively）, β-catenin, c-myc, Cox-2 and nm23-h1 for distance metastasis （P = 0.020, P = 0.000, P = 0.026, and P = 0.008, respectively）, and cyclin D1, β-catenin, c-myc, Cox-2 and nm23h1 for clinical stages （P = 0.038, P = 0.008, P = 0.000, P = 0.016, and P = 0.014, respectively）. CONCLUSION： Tissue microarray immunohistochemical staining enables high-throughput analysis of genetic alterations contributing to human colon cancer development and progression. Our results implicate the potential roles of p53, cyclin D1, bcl-2, bax, Cox-2, β-catenin and c-myc in development of human colon cancer and that of bcl-2, nm23-h1, PTEN and p-Akt1 in pro     

Book Reviews

Book reviewed in this article: Bigby, Christine, books reviewed by, 100‐1 Blaikie, Andrew, Ageing and popular culture, reviewed, 201‐2 Butler, Robert N., Life in an older America, reviewed, 152‐3 Caldwell, John C., books reviewed by, 99 Creedy, John, Pensions and population ageing: an economic analysis, reviewed, 99–100 Dandekar, Kurnudini, The elderly in India, reviewed, 99 Gibson, Diane, books reviewed by, 202‐3 Howe, Anna, books reviewed by, 152‐3 Howe, Brian, books reviewed by, 47 Hudson, Robert B., books reviewed by, 45‐6 Jamieson, Anne, Critical approaches to ageing and later life, reviewed, 101‐2 Lanspery, Susan, Staying put: adapting the places instead of the people, reviewed, 47 Lavin, C., Older adults with developmental disabilities, reviewed, 100‐1 McCalman, Janet, books reviewed by, 201 McDermott, Justin, books reviewed by, 101‐2 Means, Robin, From poor law to community care, reviewed, 202‐3 Mears, Jane, books reviewed by, 153‐4 Neysmith, Shiela M., Critical issues for future social work practice with ageing persons, reviewed, 153‐4 Pastalan, Leon A, Shelter and service issues for ageing populations: international perspectives, reviewed, 47 Piggott, John, books reviewed by, 99–100 Policy implications of the ageing of Australia's population: conference proceedings, reviewed, 45‐6 Rajan, S. Irudaya, India's elderly: burden or challenge?. reviewed, 99 Russell, Cherry, books reviewed by, 201‐2 Thane, Pat, Old age in English history: past experiences, present issues, reviewed, 201     

First‐Step Use of Fixed‐Dose Combination Treatment in Stage 2 Hypertensive Patients: Has the Time Come?

A panel discussion was convened on February 14, 2007, to discuss the use of fixed-dose combination therapy for stage 2 hypertensive patients. The panel was moderated by Michael A. Weber, MD, Professor of Medicine, SUNY Downstate College of Medicine, New York, NY. Participants included Luis Ruilope, MD, Chief, Hypertension Unit, Hospital 12 de Octubre, Madrid, Spain, Thomas D. Giles, MD, Professor of Medicine, Tulane University School of Medicine, Metairie, LA, and Joseph L. Izzo, Jr, MD, Professor of Medicine, Department of Medicine, State University of New York at Buffalo, Buffalo, NY.     

The gray rat (Rattus norvegicus) as a carrier of infectious causative agents in Siberia and the Far East

Literary data and antiplague institutions' reports demonstrate that Norway rats carry over 24 nosological forms and groups of infectious diseases: plague, tularemia, pseudotuberculosis, intestinal yersiniosis, salmonellosis, erysipeloid, listeriosis, leptospirosis, pasteurellosis, brucellosis, dysentery, paratuberculosis, hemorrhagic nephroso-nephritis, Omsk hemorrhagic fever and Q fever, tick-borne and Japanese encephalitis, lymphocytic choriomeningitis, tick-borne rickettsiosis and rickettsial pox, murine typhus, tsutsugamushi disease and toxoplasmosis.     

Myocardial infarction Changes in the concentrations of high-energy compounds and free amino acids in erythrocytes

Quantitative determination of the nucleotides AMP, ADP, ATP, GTP, NAD, NADP, 2,3-DPG and the free amino acids Lys, His, Gly, Ala, Val, Met, Phe, Tyr, Pro, Thr, Ser, Glu, Asp in erythrocytes was carried out in early and late stages of myocardial infarction. It was found that in erythrocytes, in the early stage of myocardial infarction, the concentrations of AMP, NADP and 2,3-DPG increased, whereas those of ADP, ATP, GTP and NAD decreased. In the third week of the disease the concentrations of AMP, ADP, NADP, and especially 2,3-DPG remained high, while those of ATP and GTP shifted towards the control. The concentrations of His, Gly, Ala, Val, Met, Phe, Thr and Glu increased, while those of Tyr, Ser and Asp decreased in the first stage of myocardial infarction. At the later stage of the illness (21 days) the concentrations of free amino acids returned to normal.     

Diagnostic Accuracy of APRI,AAR, FIB-4, FI,King, Lok,Forns, and FibroIndex Scores in Predicting the Presence of Esophageal Varices in Liver Cirrhosis: A Systematic Review and Meta-Analysis

Aspartate aminotransferase-to-platelet ratio (APRI), aspartate aminotransferase-to-alanine aminotransferase ratio (AAR), FIB-4, FI, King, Lok, Forns, and FibroIndex scores may be simple and convenient noninvasive diagnostic tests, because they are based on the regular laboratory tests and demographic data. This study aimed to systematically evaluate their diagnostic accuracy for the prediction of varices in liver cirrhosis.All relevant papers were searched via PubMed, EMBASE, CNKI, and Wanfang databases. The area under the summary receiver operating characteristic curve (AUSROC), sensitivity, specificity, positive and negative likelihood ratio (PLR and NLR), and diagnostic odds ratio (DOR) were calculated.Overall, 12, 4, 5, 0, 0, 4, 3, and 1 paper was identified to explore the diagnostic accuracy of APRI, AAR, FIB-4, FI, King, Lok, Forns, and FibroIndex scores, respectively. The AUSROCs of APRI, AAR, FIB-4, Lok, and Forns scores for the prediction of varices were 0.6774, 0.7275, 0.7755, 0.7885, and 0.7517, respectively; and those for the prediction of large varices were 0.7278, 0.7448, 0.7095, 0.7264, and 0.6530, respectively. The diagnostic threshold effects of FIB-4 and Forns scores for the prediction of varices were statistically significant. The sensitivities/specificities/PLRs/NLRs/DORs of APRI, AAR, and Lok scores for the prediction of varices were 0.60/0.67/1.77/0.58/3.13, 0.64/0.63/1.97/0.54/4.18, and 0.74/0.68/2.34/0.40/5.76, respectively. The sensitivities/specificities/PLRs/NLRs/DORs of APRI, AAR, FIB-4, Lok, and Forns scores for the prediction of large varices were 0.65/0.66/2.15/0.47/4.97, 0.68/0.58/2.07/0.54/3.93, 0.62/0.64/2.02/0.56/3.57, 0.78/0.63/2.09/0.37/5.55, and 0.65/0.61/1.62/0.59/2.75, respectively.APRI, AAR, FIB-4, Lok, and Forns scores had low to moderate diagnostic accuracy in predicting the presence of varices in liver cirrhosis.     

How Is the Liver Primed or Sensitized for Alcoholic Liver Disease?

This article represents the proceedings of a symposium at the 2000 ISBRA Meeting in Yokohama, Japan. The chairs were Hidekazu Tsukamoto and Yoshiyuki Takei. The presentations were (1) Tribute to Professor Rajendar K. Chawla, by Craig J. McClain; (2) Dysregulated TNF signaling in alcoholic liver disease, by Craig J. McClain, S. Joshi-Barve, D. Hill, J Schmidt, I. Deaciuc, and S. Barve; (3) The role of mitochondria in ethanol-mediated sensitization of the liver, by Anna Colell, Carmen Garcia-Ruiz, Neil Kaplowitz, and Jose C. Fernandez-Checa; (4) A peroxisome proliferator (bezafibrate) can prevent superoxide anion release into hepatic sinusoid after acute ethanol administration, by Hirokazu Yokoyama, Yukishige Okamura, Yuji Nakamura, and Hiromasa Ishii; (5) S-adenosylmethionine affects tumor necrosis factor-α gene expression in macrophages, by Rajendar K. Chawla, S. Barve, S. Joshi-Barve, W. Watson, W. Nelson, and C. McClain; (6) Iron, retinoic acid and hepatic macrophage TNFα gene expression in ALD, by Hidekazu Tsukamoto, Min Lin, Mitsuru Ohata, and Kenta Motomura; and (7) Role of Kupffer cells and gut-derived endotoxin in alcoholic liver injury, by N. Enomoto, K. Ikejima, T. Kitamura, H. Oide, Y. Takei, M. Hirose, B. U. Bradford, C. A. Rivera, H. Kono, S. Peter, S. Yamashina, A. Konno, M. Ishikawa, H. Shimizu, N. Sato, and R. Thurman.