Day 1 :
National Chiayi University, Taiwan
Keynote: Retinoic Acid Protects Zebra fish Retinal Photoreceptor Cells from the toxicity of Paclobutrazol
Time : 10:30-11:30
Wen‐Der Wang has his expertise in biological toxicology and molecular pathology, and he applies h s expertise to investigate the toxic effects and the molecular mechanisms of environmental pollutant s (especially environmental hormones and pesticides). He also applied his research results to environmental education to correct people’s environmental attitude and behaviors.
Paclobutrazol (P BZ), a fungicide and plant growth retardant, shows toxicity to aquatic embryos, probably through rain‐wash. Here, we show the toxic effect of PBZ on eye development in zebra fish, as well as the role of the vitamin A metabolite, retinoic acid (RA), controls proliferation an d differentiation of retinal photoreceptor cells, in PBZ toxicity. Embryos were expose d to PBZ with or without RA from 2 to 72 h post‐fertilization (hpf), and PBZ‐treat d embryos (2‐72 hpf) were exposed to RA for additional hours until 120 hpf. Eye size and histology were examined. Examination of the expression levels of gnat1 (rod photoreceptor marker), gnat2 (cone photo receptor marker), aldehyde dehydrogenases (encoding key enzymes for RA synthesis), and phospho‐histone H3 (an M‐phase marker) in the eyes of control and treated embryos were examined and the results indicated that PBZ exposure dramatically reduces photo receptor proliferation, thus resulting in a thinning of the photoreceptor cell layer and leading to a small eye. Co‐treatment of PBZ with RA, or post‐treatment of PBZ‐treated embryos with RA, partially rescues photoreceptor cells, revealed by expression levels of marker proteins and by retinal cell proliferation. PBZ has strong embryonic toxicity to retinal photoreceptors, probably via suppressing the production of RA, with effects including impaired retinal cell division.
North Eastern Indira Gandhi Regional Institute of Medical Sciences, India
Keynote: Clinical profile of patients presenting to a tertiary hospital with mushroom poisoning in North east India –A retrospective study
Time : 12:00-13:00
Iadarilang Tiewsoh is a Physician Intensivist, did her intensive care medicine from Christian Medical College, Vellore, Tamil Nadu, India. She has continued her field of medicine as Assistant Professor in PGIMER, Chandigarh for a while and joined the Central Medical Institute, North Eastern Indira Gandhi Regional Institute of Medical Sciences, Shillong, Meghalaya, from April, 2017. She has great passion in the field of critical care medicine which toxicology is a part of it. Having joined the present institute she has started to encounter the fatal cases of mushroom poisoning and has a goal of studying more about to poisoning to help create awareness to the affected areas.
Statement of the Problem: Mushroom poisoning has been encountered frequently in the Indian sub-continent and worldwide. It is known to be one of the cause of fulminant hepatitis for which the definitive treatment being liver transplant. In the case reports reported till date the patients of mushroom poisoning are being diagnosis by clinical presentations and history of mushroom intake, because the availability of the mycologist and toxicologists required for mushroom identification and diagnosis were not available in many places. Mushroom forms part of the diet in the ethnic tribes of our country and most of the case reports of mushroom poisoning till date are from north India and south India among the tribes of the areas with the intake of wild mushrooms unintentional. The type of syndrome presentation in patients with mushroom poisoning and awareness is being provided about the non-edible mushroom in this region. The purpose of this study is to describe the clinical presentation of all the patients presenting to the hospital in the last 4 years with mushroom poisoning where a fair idea of the existing poisonous mushroom species can be made from the specified syndrome.
Methodology: The hospital records of all the patients with a diagnosis of mushroom poisoning were reviewed from January 2014 to May 2018 and all relevant information were recorded in a structured performa. A descriptive analysis of all collected variables was carried out.
Findings: Over 28 cases of mushroom poisoning presented to our hospital in the last 4 years, mainly in the raining season (March-May) and autumn season (August-October). All cases were from the tribal areas of the four neighboring 4 districts of the state. The wild mushrooms were self-picked from the forest. 15 patients had developed early symptoms (less than 6 hours) and were less fatal, however 13 patients developed the symptoms after 6 hours of consumption and were more seriously ill out of which 4 cases expired due to acute hepatic failure. The clinical syndrome presentation were acute gastroenteritis with liver failure in 8 cases (suspected Aminata poisonin), 13 cases of acute gastroenteritis (suspected mushroom species Chlorophyllum molybdites, Clitocybe nebularis, Omphalates illudens), one case of Acute renal failure (suspected Cortinarius violaceus species), one case showing Disulfiram like reaction (suspected Coprinus atramentarius, Clitocybe clavipes species), 5 cases of Cholinergic mushroom poisoning (suspected Citocybe dealbata, C. illudens, Inocybe fastigiata species). The mortality from mushroom poisoning resulted mainly due to fulminant hepatitis in 4 cases.
Conclusion: The mushroom poisoning in this part of the country is mainly due to consumption of wild poisonous mushrooms, with amanita species type being responsible for most of the fatalities. From the clinical syndrome presentation and on visiting the affected areas, the Aminata species seems to be common, a variety of the other poisonous mushroom are also present as evident from the clinical presentation. The Aminata biosporigera and Cortinarius violaceus species has been identified at the affected villages.