The Short History of Gastroenterology
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Structural Characterization of Helicobacter Pylori Proteins Contributing to Stomach Colonization
Università degli Studi di Padova Dipartimento di Biologia Scuola di Dottorato di Ricerca in Bioscienze e Biotecnologie Indirizzo: Biotecnologie Ciclo XXVIII STRUCTURAL CHARACTERIZATION OF HELICOBACTER PYLORI PROTEINS CONTRIBUTING TO STOMACH COLONIZATION Direttore della Scuola: Ch.mo Prof. Paolo Bernardi Coordinatore di Indirizzo: Ch.ma Prof.ssa Fiorella Lo Schiavo Supervisore: Ch.mo Prof. Giuseppe Zanotti Dottorando: Maria Elena Compostella 31 Gennaio 2016 Università degli Studi di Padova Department of Biology School of Biosciences and Biotechnology Curriculum: Biotechnology XXVIII Cycle STRUCTURAL CHARACTERIZATION OF HELICOBACTER PYLORI PROTEINS CONTRIBUTING TO STOMACH COLONIZATION Director of the Ph.D. School: Ch.mo Prof. Paolo Bernardi Coordinator of the Curriculum: Ch.ma Prof.ssa Fiorella Lo Schiavo Supervisor: Ch.mo Prof. Giuseppe Zanotti Ph.D. Candidate: Maria Elena Compostella 31 January 2016 Contents ABBREVIATIONS AND SYMBOLS IV SUMMARY 9 SOMMARIO 15 1. INTRODUCTION 21 1.1 HELICOBACTER PYLORI 23 1.2 GENETIC VARIABILITY 26 1.2.1 GENOME COMPARISON 26 1.2.1.1 HELICOBACTER PYLORI 26695 26 1.2.1.2 HELICOBACTER PYLORI J99 28 1.2.2 CORE GENOME 30 1.2.3 MECHANISMS GENERATING GENETIC VARIABILITY 31 1.2.3.1 MUTAGENESIS 32 1.2.3.2 RECOMBINATION 35 1.2.4 HELICOBACTER PYLORI AS A “QUASI SPECIES” 37 1.2.5 CLASSIFICATION OF HELICOBACTER PYLORI STRAINS 38 1.3 EPIDEMIOLOGY 40 1.3.1 INCIDENCE AND PREVALENCE OF HELICOBACTER PYLORI INFECTION 40 1.3.2 SOURCE AND TRANSMISSION 42 1.4 ADAPTATION AND GASTRIC COLONIZATION 47 1.4.1 ACID ADAPTATION 49 1.4.2 MOTILITY AND CHEMIOTAXIS 60 1.4.3 ADHESION 65 1.5 PATHOGENESIS AND VIRULENCE FACTORS 72 1.5.1 VACUOLATING CYTOTOXIN A 78 1.5.2 CAG PATHOGENICITY ISLAND AND CYTOTOXIN-ASSOCIATED GENE A 83 1.5.3 NEUTROPHIL-ACTIVATING PROTEIN 90 1.6 HELICOBACTER PYLORI AND GASTRODUODENAL DISEASES 92 1.7 ERADICATION AND POTENTIAL BENEFITS 97 2. -
Evaluation of Abnormal Liver Chemistries
ACG Clinical Guideline: Evaluation of Abnormal Liver Chemistries Paul Y. Kwo, MD, FACG, FAASLD1, Stanley M. Cohen, MD, FACG, FAASLD2, and Joseph K. Lim, MD, FACG, FAASLD3 1Division of Gastroenterology/Hepatology, Department of Medicine, Stanford University School of Medicine, Palo Alto, California, USA; 2Digestive Health Institute, University Hospitals Cleveland Medical Center and Division of Gastroenterology and Liver Disease, Department of Medicine, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA; 3Yale Viral Hepatitis Program, Yale University School of Medicine, New Haven, Connecticut, USA. Am J Gastroenterol 2017; 112:18–35; doi:10.1038/ajg.2016.517; published online 20 December 2016 Abstract Clinicians are required to assess abnormal liver chemistries on a daily basis. The most common liver chemistries ordered are serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase and bilirubin. These tests should be termed liver chemistries or liver tests. Hepatocellular injury is defined as disproportionate elevation of AST and ALT levels compared with alkaline phosphatase levels. Cholestatic injury is defined as disproportionate elevation of alkaline phosphatase level as compared with AST and ALT levels. The majority of bilirubin circulates as unconjugated bilirubin and an elevated conjugated bilirubin implies hepatocellular disease or cholestasis. Multiple studies have demonstrated that the presence of an elevated ALT has been associated with increased liver-related mortality. A true healthy normal ALT level ranges from 29 to 33 IU/l for males, 19 to 25 IU/l for females and levels above this should be assessed. The degree of elevation of ALT and or AST in the clinical setting helps guide the evaluation. -
Inside the Minds: the Art and Science of Gastroenterology
Gastroenterology_ptr.qxd 8/24/07 11:29 AM Page 1 Inside the Minds ™ Inside the Minds ™ The Secrets to Success in The Art and Science of Gastroenterology Gastroenterology The Art and Science of Gastroenterology is an authoritative, insider’s perspective on the var- ious challenges in this field of medicine and the key qualities necessary to become a successful Top Doctors on Diagnosing practitioner. Featuring some of the nation’s leading gastroenterologists, this book provides a Gastroenterological Conditions, Educating candid look at the field of gastroenterology—academic, surgical, and clinical—and a glimpse Patients, and Conducting Clinical Research into the future of a dynamic practice that requires a deep understanding of pathophysiology and a desire for lifelong learning. As they reveal the secrets to educating and advocating for their patients when diagnosing their conditions, these authorities offer practical and adaptable strategies for excellence. From the importance of soliciting a thorough medical history to the need for empathy towards patients whose medical problems are not outwardly visible, these doctors articulate the finer points of a profession focused on treating disorders that dis- rupt a patient’s lifestyle. The different niches represented and the breadth of perspectives presented enable readers to get inside some of the great innovative minds of today, as experts offer up their thoughts around the keys to mastering this fine craft—in which both sensitiv- ity and strong scientific knowledge are required. ABOUT INSIDETHE MINDS: Inside the Minds provides readers with proven business intelligence from C-Level executives (Chairman, CEO, CFO, CMO, Partner) from the world’s most respected companies nationwide, rather than third-party accounts from unknown authors and analysts. -
Nutrition Considerations in the Cirrhotic Patient
NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #204 NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #204 Carol Rees Parrish, MS, RDN, Series Editor Nutrition Considerations in the Cirrhotic Patient Eric B. Martin Matthew J. Stotts Malnutrition is commonly seen in individuals with advanced liver disease, often resulting from a combination of factors including poor oral intake, altered absorption, and reduced hepatic glycogen reserves predisposing to a catabolic state. The consequences of malnutrition can be far reaching, leading to a loss of skeletal muscle mass and strength, a variety of micronutrient deficiencies, and poor clinical outcomes. This review seeks to succinctly describe malnutrition in the cirrhosis population and provide clarity and evidence-based solutions to aid the bedside clinician. Emphasis is placed on screening and identification of malnutrition, recognizing and treating barriers to adequate food intake, and defining macronutrient targets. INTRODUCTION The Problem ndividuals with cirrhosis are at high risk of patients to a variety of macro- and micronutrient malnutrition for a multitude of reasons. Cirrhotic deficiencies as a consequence of poor intake and Ilivers lack adequate glycogen reserves, therefore altered absorption. these individuals rely on muscle breakdown as an As liver disease progresses, its complications energy source during overnight periods of fasting.1 further increase the risk for malnutrition. Large Well-meaning providers often recommend a variety volume ascites can lead to early satiety and decreased of dietary restrictions—including limitations on oral intake. Encephalopathy also contributes to fluid, salt, and total calories—that are often layered decreased oral intake and may lead to inappropriate onto pre-existing dietary restrictions for those recommendations for protein restriction. -
Infantile Cirrhosis of the Liver
INFANTILE CIRRHOSIS OF THE LIVER P. KRISHNA RAO, B.SC., M.B.B.S., D.T.M. • H. (Eng.) (Pathologist, Victoria, Vani Vilas and Minta Hospitals, and Lecturer in Pathology and Bacteriology, University Medical School, Bangalore) Received July 16, 1941 CONTENTS PAGE INTRODUCTION .... 310 CLINICAL FEATURES .... 313 LABORATORY FINDINGS .. 314 MORBID ANATOMY AND HISTOLOGY 318 DISCUSSION .... 321 iEtiology .... 321 Type of Cirrhosis .... 326 Formation of Cirrhosis .. 332 SUMMARY .... 335 ACKNOWLEDGMENT .... 336 BIBLIOGRAPHY .... 337 Introduction PHYSICIANS and Pathologists in India have interested themselves in the study of the "Infantile Cirrhosis of the Liver" in view of the appalling mortality of the children claimed by this disease; yet our knowledge of the a~tiology and pathology of the disease is singularly defective. A case report by Sen in 1887 at the Calcutta Medical Association is, so far as I am aware, the first contribution to the literature on the subject, and he has described the disease as " a peculiar enlargement of the liver in young children only, both male and female, without any enlarge- ment of the spleen and associated with low fever, gradual emaciation, loss of appetite, sallow complexion and very slight jaundice, but not in all" In the discussion that followed the case report, Ghose, Coomer, Rakhaldas Ghose, Devendranath Dey, Bannerjee, Ahmed, Gibbons, Mcleod and Birch participated and the conclusions arrived at were as follows :-- (i) Infantile Cirrhosis of the liver was undoubtedly a peculiar disease found only amongst Indian children of the rich and the poor families alike. 310 Infantile Cirrhosis of tke Liver 311 (ii) The probable causative factors were the over-feeding of the children and bad hygenic conditions in which they were brought up. -
Points to Remember
Points To Remember Digestion : The process in alimentary canal by which the complex food is converted mechanically and biochemically into simple substances suitable for absorption and assimilation. Food : A substance which on taken and digested in the body provides material for growth, repair, energy, reproduction, resistance from disease or regulation of body processes. Thecodont : The teeth embedded in the sockets of the jaw bone, e.g., in mammals. Diphyodont : The teeth formed twice in life time e.g., in mammals. Heterodont : An adult human has 32 permanent teeth which are of four different types. Different Types of Teeth (a) Canine—for tearing (b) Incisors —for cutting (c) Premolars for grinding (d) Molars for churning and grinding Digestion and Absorption 143 Dental formula of man : Permanent Teeth) 1 C PM M 32 = 2 × 2 1 2 3 Upper Jaw 2 1 2 3 Lower Jaw Dental formula of man : (Milk Teeth) 1 C PM 20 = 2 × 2 1 2 Upper Jaw 2 1 2 Lower Jaw Peristalsis : The involuntary moveent of the gut by which the food bolus is pushed forward. Deglutition : The process of swallowing of food bolus. It is partly voluntary and partly involuntary. Ruminants : The herbivours animals ( e.g., cow, buffalo etc.) which have symbiotic bacteria in the rumen ! of their stomach which synthesize enzymes to hydrolyse cellulose into monosaccharides. Diarrhoea : The abnormal frequent discharge of semisolid or fluid faecal matter from the bowel. Vomitting : The ejection of stomach contents through the mouth, caused by antiperistalsis. Dysentery : Frequent watery stools often with blood and mucus and with pain, fever and causes dehydration. -
Classification of Helicobacter Pylori According to National Strains Using Bayesian Learning
Mathematical and Computational Applications , Vol. 14, No. 3, pp. 241-251, 2009. © Association for Scientific Research CLASSIFICATION OF HELICOBACTER PYLORI ACCORDING TO NATIONAL STRAINS USING BAYESIAN LEARNING Bekir Karlık, Alpaslan Avcı, A. Talha Yabanıgül Fatih University, Department of Computer Engineering, Istanbul, Turkey [email protected], [email protected], [email protected] Abstract- There is many studies about Helicobacter pylori genome and many instances of national strains are sequenced completely. To make a successful classification, the same functional portions have to be used a classifier like Bayesian Learning. Thus suitable genes will be used for classification since genes are portions that work functionally same. The cagA and vacA genes are selected for classification. cagA gene stands for ‘cytotoxin-associated protein A’ gene and vacA gene stands for ‘vacuolating cytotoxin precursor’ gene and these genes have a role of coding of these proteins. The reasons for selecting these genes are that these genes are the genes which affect the bacteria being a pathogen, Nucleotide numbers of these genes are higher than the most of other genes of bacteria, and these genes are the most popular genes of Helicobacter pylori. There are some instances of these genes which are classified with respect to national strains. The national strains are based on the nation of the host human. The cause of the difference on national strains is the difference of the cultural activities. If the national strain of a random Helicobacter pylori bacterium is known, the host human's nation can also be known approximately. The aim of this study is to classify Helicobacter pylori according to National strain using a well-know classification technique named Bayesian Learning. -
Period Prevalence Rate of Helicobacter Pylori Infection in Egyptian Children with Type 1 Diabetes
PERIOD PREVALENCE RATE OF HELICOBACTER PYLORI INFECTION IN EGYPTIAN CHILDREN WITH TYPE 1 DIABETES Thesis in PediatricsSubmitted for partial fulfillment of M.Sc. degree in pediatrics. Investigator Physician: MarwaMamdouh Salem Elgamal M.B & B.ch. Cairo University Supervisors Prof. Dr. Mona Ahmed Abu Zekry Professor of Pediatrics Head of gastroenterology Department Faculty of Medicine Cairo University Pro.Dr. Lubna Mohamed AnasFawaz Professor of Pediatrics Faculty of Medicine Cairo University Prof. Dr. MagdyMoradMansy Professor of Pathology Faculty of Medicine Cairo University CAIRO UNIVERSITY 2012 Acknowledgement First and Foremost, Thanks to GOD for his grace which is all what we need. I owe special thanks to Prof. Dr.Mona abu zekry . Professor of Paediatrics. Faculty of Medicine, Cairo University. For her outstanding support, generous advice, and valuable guidance. But for her support, this work wouldn’t come to light. I want to express my heart appreciation and deep gratitude to Prof. Dr.lubna fawaz, Professor of Pediatric, Cairo University for her outmost help, constructive advice. I am deeply indebted to Prof. Dr.Magdy morad, Professor of pathology, Faculty of medicine, Cairo University for the most valuable help and advice. I owe special thanks to Prof. Dr.Ayman Enail . Professor of Pediatrics. Faculty of Medicine, Cairo University. Dedication With all my love, To my mother, father, husband And my beloved son And all my Colleagues. List of contents 1- List of tables…………………………………………. I 2- List of figures……………………………………… II 3- List of abbreviations ……………………………… III-IV 4- Introduction …………………………….…………... 1 5- Aim of the work ………………………….………… 3 6- Review of literature …………………….………….. 4 ▪Helicobacter pylori ………………... ……. 4 I-Historical background II-Morphology III-Epidemiology of infection IV-Pathogenesis V- Clinical manifestation VI- Diagnosis VII- Treatment ▪ Diabetes mellitus ………………………..…… 53 7- Patients and methods …………………………….. -
Helicobacter Pylori
Helicobacter pylori From Wikipedia, the free encyclopedia Helicobacter pylori Scientific classification Kingdom: Bacteria Phylum: Proteobacteria Class: Epsilonproteobacteria Order: Campylobacterales Family: Helicobacteraceae Genus: Helicobacter Species: H. pylori Binomial name Helicobacter pylori (Marshall et al. 1985) Goodwin et al., 1989 Contents • 1 Signs and symptoms • 2 Microbiology o 2.1 Genome • 3 Pathophysiology • 4 Diagnosis • 5 Prevention o 5.1 Vaccines • 6 Treatment • 7 Prognosis • 8 Epidemiology • 9 History • 10 See also • 11 References • 12 External links Helicobacter pylori (English pronunciation: /ˌhɛlɨkɵˈbæktər pɪˈlɔraɪ/) is a Gram-negative, microaerophilic bacterium that can inhabit various areas of the stomach, particularly the antrum. It causes a chronic low-level inflammation of the stomach lining and is strongly linked to the development of duodenal and gastric ulcers, stomach cancer. Over 80 percent of individuals infected with the bacterium are asymptomatic.[1] The bacterium was initially named Campylobacter pyloridis, then renamed C. pylori (pylori being the genitive of pylorus) to correct a Latin grammar error. When 16S ribosomal RNA gene sequencing and other research showed in 1989 that the bacterium did not belong in the genus Campylobacter, it was placed in its own genus, Helicobacter. The genus derived from the ancient Greek hělix/έλιξ "spiral" or "coil".[2] The specific epithet pylōri means "of the pylorus" or pyloric valve (the circular opening leading from the stomach into the duodenum), from the Ancient Greek word πυλωρός, which means gatekeeper.[2] More than 50% of the world's population harbor H. pylori in their upper gastrointestinal tract. Infection is more prevalent in developing countries, and incidence is decreasing in Western countries. -
Diarrhea Gastroenterology
Diarrhea Referral Guide: Gastroenterology Page 1 of 2 Diagnosis/Definition: The rectal passage of an increased number of stools per day which are watery, bloody or loosely formed. By history and stool sample. Initial Diagnosis and Management: Most patients don’t need to be worked up for their diarrhea. Most cases of diarrhea are self-limiting, caused by a gastroenteritis viral agent. Patients need to be advised to drink plenty of fluids, take some NSAIDSs or Tylenol for fevers and flu-related myalgias. If the patient comes to you with a history of bloody diarrhea, fever, severe abdominal pain, and diarrhea longer than 2 weeks or associated with electrolyte abnormalities or is elderly or immunocompromised, they need to be seen by GI. Work-up in these patients should consist of a thorough history (be sure to get travel history, medications including herbal remedies and possible infectious contacts) and physical examination. Labs should include a chem. 7, CBC with differential and stool WBCs, cultures, qualitative fecal fat. If there is the possibility that this could be antibiotic related C. difficile then order a C. diff toxin on the stool. Only order an O and P on the stool\l if the patient gives you a recent history of international travel, wildern4ess camping/hiking or may be immunocompromised. Make sure to ask about mil product ingestion as it relates to the diarrhea. Fifty percent of adult Caucasians and up to 90% of African Americans, Hispanics, and Asians have some degree of milk intolerance. If from your history and laboratory studies indicate a specific etiology the following chart may help with initial therapy. -
Children's Gastroenterology, Hepatology, and Nutrition
GI_InsertCard 4/24/09 2:03 PM Page 1 CHILDREN’S GASTROENTEROLOGY, HEPATOLOGY, AND NUTRITION CONSULT AND REFERRAL GUIDELINES FOR COMMON GI PROBLEMS DIAGNOSIS/SYMPTOM SUGGESTIONS FOR POSSIBLE PRE-REFERRAL CONSIDER INITIAL WORK-UP THERAPY REFERRAL WHEN CHRONIC ABDOMINAL PAIN ICD-9 code – 789.0 • Weight and height percentiles • Treatment of constipation, If symptoms persist after Age: toddler to adolescence • Urinanalysis if present improvement of stooling • CBC with dif ESR or CRP • Acid suppression - H2 receptor pattern, trial of a lactose-free • Stool Studies: • Antagonist or proton pump diet and lack of response – guaiac • Inhibitor to acid suppression, referral – consider EIA antigen for giardia • Trial off lactose should be made. The child • Careful evaluation of stooling pattern may require endoscopy • Diary to look for possible triggers such as foods, (EGD) and/or colonoscopy. activities or stressors CHRONIC, NON-BLOODY DIARRHEA ICD-9 code – 787.91 • Weight and height percentiles • Treat any dietary abnormality If Symptoms persist, referral Age: preschool to adolescence • Stool studies: (e.g. high fructose and/or low fat) should be made. The child – guaiac • Try increased fiber in diet may require EGD and/or – consider leukocytes • Diary of dairy and other food colonoscopy. – culture intake in relation to symptoms – EIA antigen for giardia – C. difficile toxin titer – Reducing substances, pH, – Sudan stain (spot test for fecal fat) • CBC with differential, ESR or CRP • Albumin • Quantitative IgA and anti-tTG Antibody (screen for celiac) • Consider sweat test • Consider upper GI with small bowel follow through • Consider laxative abuse, especially in adolescent females BLOODY DIARRHEA (COLITIS) ICD-9 code – 556 • Stool studies: If evaluation is negative, food If symptoms persist, referral Age: infancy – guaiac protein allergy is likely. -
Liver Dysfunction in the Intensive Care Unit ANNALS of GASTROENTEROLOGY 2005, 18(1):35-4535
Liver dysfunction in the intensive care unit ANNALS OF GASTROENTEROLOGY 2005, 18(1):35-4535 Review Liver dysfunction in the intensive care unit Aspasia Soultati, S.P. Dourakis SUMMARY crosis factor-alpha, is pivotal for the development of liver injury at that stage. Liver dysfunction plays a significant role in the Intensive Care Unit (ICU) patients morbidity and mortality. Although determinations of aminotransferases, coagulation Metabolic, hemodynamic and inflammatory factors studies, glucose, lactate and bilirubin can detect hepatic contribute in liver damage. Hemorrhagic shock, septic shock, injury, they only partially reflect the underlying pathophys- multiple organ dysfunction, acute respiratory dysfunction, iological mechanisms. Both the presence and degree of jaun- metabolic disorders, myocardial dysfunction, infection from dice are associated with increased mortality in a number of hepatitis virus, and therapeutic measures such as blood non hepatic ICU diseases. transfusion, parenteral nutrition, immunosuppresion, and Therapeutic approaches to shock liver focus on the drugs are all recognised as potential clinical situations on prevention of precipitating causes. Prompt resuscitation, the grounds of which liver dysfunction develops. definitive treatment of sepsis, meticulous supportive care, The liver suffers the consequences of shock- or sepsis-in- controlling of circulation parameters and metabolism, in ducing circumstances, which alter hepatic circulation pa- addition to the cautious monitoring of therapeutic measures rameters, oxygen supply and inflammatory responses at the such as intravenous nutrition, mechanical ventilation and cellular level. Moreover, the liver is an orchestrator of met- catecholamine administration reduce the incidence and abolic arrangements which promote the clearance and pro- severity of liver dysfunction. Only precocious measures can duction of inflammatory mediators, the scavenging of bac- be taken to prevent hepatitis in ICU.