International conference on Liver and Hepatitis April 24-25, 2019 Novotel Budapest City, Budapest, Hungary

Biography:

William J Rowe FBIS (Fellow British Interplanetary Society), FACN (Fellow American College of Nutrition, Retired Fellow Royal Society of Medicine), is a Board Certified Specialist in Internal Medicine. He has received his MD degree from the University of Cincinnati and was in private practice in Toledo, Ohio for 34 years. During that time, he supervised over 5000 symptom - limited maximum hospital-based treadmill stress tests. He has studied three world class extraordinary endurance athletes and published their exercise-related magnesium deficiencies. This triggered a 20 year pursuit of the cardiovascular complications of space flight. All his publications are posted on his website

Abstract:

Of 12 moon walkers, James Irwin on day after return from Apollo 15 mission, showed extraordinary bicycle (B) stress test (ST) hypertension (275/125) after three minutes exercise; supervising >5000 maximum treadmill  ST, author never witnessed ST-blood pressure approaching this level. Symptom-limited maximum B stress test showed “cyanotic fingernails”; possibly venous blood trapped peripherally, supporting author’s “Apollo 15 Space Syndrome,” postulating that severe fingertip pain during space walks, triggered by plasma fluid, trapped distally; mechanism could be related to endothelial dysfunction, providing “silent ischemia” warning. Neil Armstrong returned to Earth with severe diastolic hypertension (160/135), consistent with ischemic left ventricular dysfunction; 50 mm increase in comparison with resting  BP 110/85. With inhalation of lunar dust, brought into habitat on space suit, with high lunar iron (I) this dust inhalation, along with reduced (R) space flight- transferrin, R antioxidant, calcium  (Ca) blocker - magnesium, conducive to severe oxidative stress, Ca overload with potential endothelial injuries. Using moon walker studies as example, show that I dust, released from brakes, with over 90% of brakes made of I, is a major hypertension factor and may  also contribute to myocardial infarctions.

Biography:

Dimitar Tonev was trained as an Internal Disease Specialist in Sofia Medical Academy with two subsequent specializations in Gastroenterology/Hepatology and Pharmaceutical Medicine. He is trilingual with 11 years of experience in Clinical Practice and 20 years of Clinical Development and Medical Affairs. During this time, he served as a Medical Monitor for a variety of clinical trials in motility and acid related disorders; HCV-PACIFIC, STEPS in G3, PRINCIPAL; HBV ENTEBE trial as well as studies in pandemic influenza and HIV co-infection. In the last four years he has created ICPT Medical Organization across EU, Canada and Australasia and contributed to pivotal trials in NASH, PBC, PSC and biliary acid diarrhea. He has been an invited Speaker at national (BASL, BVHG) and international level (Global NASH Conference). He joined IQVIA as Medical Strategy Lead for liver diseases and is responsible for building our internal capabilities related to NASH in Europe

Abstract:

Nonalcoholic fatty liver disease (NAFLD) is becoming the leading cause of liver disease worldwide, and the prevalence is still increasing, potentially becoming a leading cause of liver transplantation in the developed world. NAFLD is defined in the presence of increased hepatic fat content not explained by at risk alcohol intake, and is epidemiologically associated with obesity, insulin resistance and metabolic disorders. It covers a broad histological spectrum ranging from simple uncomplicated steatosis, to nonalcoholic steatohepatitis (NASH), which is characterized by hepatocellular damage and inflammation and may progress to advanced liver disease and hepatocellular carcinoma. The pathogenesis of NASH is multifactorial and badly understood and stratified, but an important role is likely played by inflammation triggered by predisposing genetic factors, oxidative stress, and bacterial products derived from the gut. Recent data seem to suggest that hepatic lipid accumulation itself may also be involved in NASH by inducing lipotoxicity and driving secondary inflammation, leading to activation of fibrogenesis. Although lifestyle modification, weight loss and increased physical activity are effective in improving liver histology in patients with NASH, these goals are only achieved in a minority of patients. Unfortunately, pharmacological treatments for this condition are not yet registered and we have seen multiple, largely a negative results from the initial wave of predominantly academic research cohorts. Pharmaceutical companies’ efforts in this field have been reinvigorated after the publication of the successful NIDDK study FLINT. Multiple drug classes under development either tackle hepatic fat accumulation or act downstream by modulating inflammation and fibrogenesis. Among drugs that influence hepatic lipid metabolism, particularly promising results have been reported for agonists of Farnesoid X receptor (FXR), ASK inhibitors and PPAR agonists, which are the agents currently in phase three trials in patients with NASH and was associated with a higher rate of amelioration of hepatic steatosis or fibrosis as compared to placebo. This presentation will address complicated topic of current patient’s pathways, non-invasive biomarkers and recruitment hurdles associated with big scale clinical trials with multiple liver biopsies. As a parallel analysis this presentation will cover intriguing similarities with historical developments in HCV field and some potentially helpful recruitment enrichment strategies that’s has been utilized in the preceding wave of clinical trials in viral hepatitis domain.

Biography:

Magdy El-Salhy is a Professor of Gastroenterology and Hepatology at Bergen University, and consultant Gastroenterologist at Stord Hospital, Norway. He is a Member of the Editorial Boards of nine international journals. Furthermore, he is on the referee list of a large number of international journals. He has evaluated grant applications for national and international research foundations. He has also attended and contributed to several national and international meetings as invited Speaker, or Chairman. He has authored 242 publications, which include original articles, invited reviews, book chapters, and books. His work has been cited in 6074 scientific articles. His research field for the last 40 years has been the neuroendocrine system of the gut, from basic science to clinical applications.

 

Abstract:

Gastrointestinal (GI) symptoms are common in patients with diabetes, and these symptoms are referred to as diabetes gastroenteropathy. These symptoms include nausea and vomiting, heartburn, abdominal pain diarrhea, constipation and fecal incontinence. Diabetes gastroenteropathy not only reduces considerably the quality of life of diabetic patients, but also impairs metabolic control with increased risk of hyper-/hypoglycemia. The poorly controlled blood glucose level increases in turn the risk of the secondary diabetes complications such as retinopathy, nephropathy, neuropathy and cardiovascular affection. Diabetes gastroenteropathy may also cause malnutrition, which together with the disturbed immune defense in these patients may cause intercurrent infections. Diabetes gastroenteropathy is attributed to GI dysmotility, which is believed to be caused by autonomic neuropathy and/or hyperglycemia. The neuroendocrine system (NES) of the gut comprises the GI endocrine cells and the enteric nervous system (ENS). The NES of the gut secretes peptide/amines that regulate the GI motility through endocrine, paracrine and/or synaptic neurotransmission. The two components of the NES of the gut, namely the GI endocrine cells and the ENS have been found to be abnormal in patients with diabetes and in animal models of human diabetes. The abnormalities in the NES system of the gut can explain the GI dysmotility seen in patients with diabetes. The etiology of diabetes gastroenteropathy seems to be multifactorial and autonomic neuropathy, hyperglycemia and abnormal gut NES appear to be important factors.

 

Biography:

Amr Amin has completed his PhD at University of Illinois at Chicago, and received a Post-doctoral training in the field of Molecular Genetics at University of Pennsylvania School of Medicine. He started his academic career at UAE University, where he serves now as a Full Professor of Cell and Molecular Biology. His research focuses on ways to control cancer, particularly liver cancer. He has published many research articles, reviews, and serves as Ad Hoc reviewer and as an Editorial Member of many specialized peer-reviewed journals. He is also a Member of many specialized societies and the sole recipient of multiple national and international scientific awards.

Abstract:

The multikinase inhibitor, sorafenib, remains for a decade now the first and only systemic therapy for the treatment of hepatocellular carcinoma (HCC). Thus, a novel approach against HCC is essential for a better therapeutic outcome. The aim of this study is to assess the chemopreventive action of Saffron’s main biomolecules against chemically-induced liver cancer in rats, and to explore the mechanisms by which Saffron’s biomolecules employ their anti-tumor effects. We provide a network analysis of differentially expressed genes in tissues of animals pre-treated with Saffron’s biomolecules in comparison to induced-HCC animals’ tissue. To further support our results, we assessed the in vitro effects of those natural products on cells viability and cell cycle distribution. Network analysis was also conducted and identified NF-_kB as a potential regulatory hub, and therefore, a candidate therapeutic drug target.