Day 2 :
University of Toronto, Canada
Time : 09:05-09:40
Prof. H Michael Dosch received all his schooling & training in, then, West Germany, graduating with the German MD, PhD degree in 1970 from Phillips University in Marburg/rnLahn. In 1974 he began postdoctoral training at Toronto University, Canada, joined the Faculty 1977 and was promoted to full Professor of Pediatrics and Immunology. Hisrncore interest molecular & cellular elements of (mostly) Type-1 Diabetes documented in over 500 often high profile articles.
Our Diabetes Research Program focused on neuronal elements in T1D pathogenesis. We found that in T1D mouse models as wellrnas patients, 1.) a major subset of autoimmune targets have neuronal derivation; 2.) TRPV1 (transient receptor potential, vanilloid-rn1, a Ca++channel) mutations are a core disease-prerequisite, which consequent deficiency of TRPV1-dependent neuropeptidesrnsuch as substance P (sP). Hypofunctional/hyposecretory mutations in T1D-prone NOD mice have analogs in T1D patients: humanrnTRPV1 (chromosome 17) is polymorphic with possibly thousands of varied alleles, but we found the exclusive presence of the same,rn4 alleles in over 50 patients. Th e sole exception was one T1D patient, carrying non-polymorphic, African TRPV1. Single nucleotidernpolymorphisms (SNP) Analysis of 1000-Genomes data showed 59 severe SNP mutations TRPV1(2.3%). Remarkably, there were 159rnTRPV1 SNPs in our fi rst 21 T1D patients, clustered mainly in 6 of 28 genomic PCR fragments sequenced, and this trend is sustainedrnin 28 additional patients. Collectively, these data emphasize similarities between NOD mice and patients, with TRPV1 clearly arnprominent if not the major element. T1D is reversed in NOD mice for months following a single pancreatic sP injection via the celiacrnartery, a routine medical access route in Interventional Image-Guided therapies (IGT). Recently, substantial reserves of pre-betacellsrnwith re-diff erentiation of functionality were discovered well aft er T1D onset. Here we describe our approved translational trial,redesigned to determine if and at what doses can reverse human T1D.
Icahn School of Medicine at Mount Sinai, USA
Time : 09:40-10:15
Alejandro Berenstein has graduated from the UNAM and is currently a Professor of Neurosurgery, Radiology and Pediatrics. He is the Director of the Hyman-NewmanrnInstitute for Neurology and Neurosurgery at Mount Sinai Health System in NYC. He has authored over 150 publications in peer-reviewed journals, more than 25 chaptersrnin the fi eld and 9 books including the fi ve volumes ground-breaking textbook, “Surgical Neuro-angiography”. He has been a Visiting Professor, Lecturer and Faculty in overrn600 occasions. He became the fi rst President of the World Federation of Interventional and Therapeutic Neuro-radiology and third President of the American Society ofrnInterventional and Therapeutic Neuro-radiology and has been the President of SILAN the Latin-American Society of Neuro-radiology for 2012-2013.
Vascular malformations are most frequent located in the maxillofacial area. It is important that a proper diagnosis is made, asrnthe treatment is diff erent for the diff erent types of vascular lesions. Arteriovenous Malformations and A-V fistulae, are high fl owrnlesions, with a reddish discoloration, the temperature over the area is increased, with prominent pulsations, a thrill and a bruit mayrnbe present. Th ere will be mass effect, compression of vital structures, pain and hemorrhage. It is the most difficult type to treat, and itrnis the most aggressive in presentation. Venous Malformations are slow flow lesions, and the most frequent type of vascular birthmark.rnFrequently multifocal. Symptoms depend on the location, mass effect, cosmetic and functional manifestations, discomfort and pain. The skin over the area is of normal temperature with bluish discoloration, there easily compressible, none pulsatile and they willrnexpand with Valsalva maneuvers. Lymphatic Malformations are very low fl ow collections of lymphatic fluid. They present as noncompressiblernmass lesions with contour deformities, compression of vital structures may occur. The skin is of normal temperature, rnnonpulsatile. Th ey may be macrocystic or microcystic, or mixed. Hemangiomas are proliferative tumors of infancy they appearsrnshortly aft er birth and will go through a rapid growth cycle the proliferative phase, reach her maximum within months or severalrnyears and then spontaneously involute. We will present the various endovascular techniques, including transarterial embolization,rnpercutaneous embolization, sclerotherapy, combination treatments.