Biography:

David Van Thiel obtained his MD from the University of California at Los Angeles and completed his Internal Medicine residencies at Cornell University Hospitals and Boston University. He completed a Gastrointestinal/Hepatology fellowship at Boston University and the University of Pittsburgh. At the latter institution, he progressed from an Instructor of Medicine to Professor of Medicine and Director of the Gastroenterology & Hepatology Program and served as the medical Director of Liver transplantation. He has published more than 100 peer reviewed papers in a variety of journals and is on the Editorial Board of several journals as well as serves as a reviewer

Abstract:

Hepatitis non-A and non-B hepatitis was recognized as a unique form of viral hepatitis distinct from hepatitis A, hepatitis B, and other unusual types of a chronic hepatitis such as CMV, EBV as well other more uncommon types of viral hepatitis in the late 1970s. His clinical characteristics, biochemical manifestations as well as its chronicity from its initial presentation followed by increasing stages of chronic hepatitis and hepatic fibrosis ultimately resulting in cirrhosis and occasionally progressing to hepatic cancer and required an additional 15-30 years. A host of potentially antiviral agents were utilized initially to treat the disease process with minimal or no success. With the introduction of interferons (alfa 2a or alfa 2b) with or without additional ribavirin, a modicum of success defined as a reduction in transaminase levels was achieved with little or no retrospectively determined viral clearance. With the isolation and characterization of the hepatitis C virus genome and the various polypeptides it codes for, a new era of treatment directed at inhibiting viral replication as opposed to enhancing the immune response against the virus began. The initial direct acting antiviral agents increased viral clearance rates to 40%. Agents more recently developed have increased the rates of viral clearance to 95 to 100%. This initiated reports (a promise) that hepatitis C would be eliminated as a disease process by 2020 with a progressive decline in the rates of cirrhosis and hepatocellular carcinoma thereafter through at least 2030. Unfortunately this does not appear to be the case as multiple obstacles prevent the favourable outcome. The issues and remaining and prohibit the promises full film and include the following: Lack of knowledge of primary care physician's that the disease is a serious hepatic disease that slowly and quietly progresses to cirrhosis and potentially hepatic cancer and is treatable. As a result large numbers estimated to be three quarters of the infected population failed to be identified. Secondly the cost of the drugs is prohibitive to those individuals with no insurance and contributes to the effort by third party pears and cover mental agencies to limit treatment to selected groups with advanced liver disease. As a result only a minor fraction of the infected population is identified for treatment and receives treatment. In addition, individuals with non-hepatic manifestations of hepatitis C are not recognized this having the disease process and are excluded from treatment despite the fact that this population represents the largest group of individuals perpetuating the disease in the community as they do not know they have the disease. In order with a promise of the elimination of hepatitis C and a reduction in long-term consequences of the infection universal defecation of infected patient's to include all forms of hepatic dysfunction as well as non-hepatic manifestations of the disease need to be recognized in treated. To accomplish this, the cost of treatment will have to be dramatically reduced and includes not only the cost of the therapeutic agent but also through numerous tests required to justify
treatment. Some progress is being made by governmental agencies that are looking at the concept of micro-elimination as a potential means of reducing the prevalence of the disease in high prevalence groups such as men having sex with men, individuals enrolled in drug treatment programs, who said receive multiple transfusions as result of clotting disorders and/or hemolytic anemias. This is clearly a started but only if start.

Biography:

Giovanni Gasbarrini was President of the Italian Society of Alcology and Member of the Board of Directors of the Italian Society of Gastroenterology, of the Italian Society of Internal Medicine, from which he was awarded the title of Member of Honor. He is the founder and President of the “Club del Tenue” and of the “FONCRE” (Operative Cancer Rectus-Colon), and currently the corporate framework for digestive diseases (Club del Tenue, FONCRE, Hp Italian Section, Intestinal Motility). He was Vice-President of the International Association of Surgeons & Gastroenterologists. He was President and is now a Member of the European Helicobacter Study Group (of which the Italian section is also the President); he was President of EAGEN (European Associate Gastroenterol, Nutrition) and is currently past-President of EAGEN. He is a member of over 15 Italian and International Scientific Societies (Italian Society of Internal Medicine -Italian Geriatrics Society -Italian Gastroenterology Society - Italian Electronic Microscopy Society -Italian Society of Alcology - European Society Liver Study - French Society of Gastroenterology.

Abstract:

Few data exist on differences in gut microbiota composition among principal gastrointestinal diseases.  We evaluated the differences in gut microbiota composition among uncomplicated diverticular disease (DD), IBS and IBD patients.  DD, IBS and IBD patients along with healthy controls (CT) were enrolled in our Italian GI outpatient clinic.  Stool samples were collected.  Microbiota composition was evaluated through a metagenomic gene-targeted approach.  GI pathology represented a continuous spectrum of diseases where IBD displayed one extreme while healthy controls displayed the other.  Among Phyla, Biplot PC2/PC3 and dendogram plot showed major differences in samples from IBS and IBD.  DD resembled species CT composition, but not for Bacteroides fragilis.  In IBS, Dialister spp and then Faecalibacterium prausnitzii were the most representative species.  UC showed a reduced concentration of Clostridium difficile and an increase of Bacteroides fragilis.  In CD, Parabacteroides distasonis was the most represented, while Faecalibacterium prausnitzii and Bacteroides fragilis were significantly reduced.  Each disorder has its definite overall microbial signature, which produces a clear differentiation from the others.  On the other side, shared alterations constitute the “core dysbiosis” of GI diseases.  The assessment of these microbial markers represents a parameter that may complete the diagnostic assessment.

Biography:

Fong Fong Chu has her expertise in gastrointestinal diseases especially in inflammatory bowel disease (IBD). Her team has established a mouse model of IBD which is very-early onset. These mice are deficient in two isoenzymes which reduce hydrogen peroxide named GPx1/2-double knockout (DKO). This model is a better model than chemical-induced colitis models because it is not injury based and mimic closely to human IBD. She has built this model through 20 years of research and has identified new targets for IBD therapy. She joined Beckman Research Institute of the City of Hope, Duarte CA USA (1987). She is currently associated with the Department of Gastroenterology & Hepatology and the First Affiliated Hospital and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, Henan, P R China since 2016.

Abstract:

Statement of the Problem: Gut microbes play an essential role in pathogenesis of inflammatory bowel disease (IBD). Host cells respond to microbe colonization by releasing cytokines and chemokines. Some inflammatory cytokines such as IL-4 and IL-13 induce NADPH oxidase-1 (NOX1) and dual oxidase-2 (DUOX2) gene expression in the epithelial cells. Elevated NOX1 or DUOX2 can produce reactive oxygen species (ROS) to regulate various cellular functions including cell proliferation, migration and apoptosis. NOX1 and DUOX2 have been linked to very-early-onset IBD, beginning before 6 years old. But the exact role of NOX1 and DUOX2 in IBD is not known.

Methodology: Mice deficient in antioxidant enzymes, glutathione peroxidase (GPx)-1 and -2, so called GPx1/2-DKO mice, develop ileocolitis around weaning. The hall-mark of pathology includes high crypt apoptosis, Paneth cell depletion, exfoliation and crypt abscess. Germ-free DKO mice are disease-free. To explore the role of Nox1 and Duox2 in gut inflammation, we studied the pathology and phenotype of Nox1-GPx1/2-triple KO (TKO) and Duox GPx1/2-TKO mice at 35 days of age (comparable to human very-earlyonset IBD).

Findings: Nox1-Gpx1/2-TKO mice virtually do not have pathology. Duox-GPx1/2-TKO mice have intermediate pathology except crypt apoptosis remain as high as the DKO mice.

Conclusions & Significance: Both Nox1 and Duox2 contribute to inflammation, while Nox1 has a stronger impact than Duox2 probably because it is expressed in the crypt of the gland. Drugs that have been effective in treating IBD, such as dexamethasone and antibiotics, are likely mediated through suppression of NOX1 and DUOX2 gene expression.