Day 1 :
University of Central Florida, USA
Time : 9:00-09.50AM
Kiminobu Sugaya is a Professor of Medicine in Burnett School of Biomedical Science, College of Medicine, University of Central Florida (UCF) since 2004. He is a Director of Multidisciplinary Neuroscience Alliance of UCF, a Chair of Neuroscience Consortium for Central Florida and a Chair of Central Florida Chapter of Society for Neuroscience. He earned BSM and PhD from the Science University of Tokyo. He received a Post-doctoral training from Dr. Ezio Giacobini, who built the base for the current cholinesterase Alzheimer’s disease therapies, at the Southern University of Illinois. He moved to the Department of Psychiatry in the School of Medicine at the University of Illinois at Chicago in 1997 where he became Associate Professor. He has further expanded his research area to the use of stem cell. His publication regarding improvement of memory in the aged animal by stem cell transplantation was reported Washington Post, BBC, NBC, ABC and other media in all over the world.
Advances in stem cell technologies; including the ability to produce pluripotent stem cells from adult stem cells by the over expression of an embryonic stem cell gene and to increase endogenous stem cells by administration of a small molecule may bring a cure for neurodegenerative diseases. However in order for the stem cells to be functional, they have to be differentiated into the proper types of cells and integrated into the proper part of the host brain. Thus we need to consider the pathological condition of the disease, which may. Thus, we have to consider the pathological environment that might alter environmental cues for migrate and differentiate of the stem cells. Here we show the effects of amyloid precursor protein (APP) and reelin on neural stem cell (NSC) differentiation and how to regulate this effect to produce desirable cells under pathological conditions. We found that APP increases glial differentiation via the notch and cytokine-signaling pathway, while reelin induces radial glial differentiation followed by neuronal differentiation via increasing phosphorylation of adapter protein disable-1. Since amyloid and reelin are found in the plaques within Alzheimer's disease (AD), these findings may closely associate with NSC biology under its pathology. By regulating these factors in AD, we may be able to not only guide differentiation of transplanted NSCs but also modify progression of disease by guiding differentiation of endogenous NSCs.
The Williams Research Laboratory, USA
Keynote: Malignant hyperthermia: The genetic disease is characterized by a runaway futile cycle operating at the acetylcholine receptor (sodium channel) level
Time : 15.00-16.00
Charles H Williams completed his PhD in 1968 and then a Post-Doctoral at the Institute for Enzyme Research with David E Green on mitochondrial studies. He also published with Henry A Lardy at the Enzyme Institute. He moved to Missouri as Associate Professor of Biochemistry and Assistant Professor of Medicine. He relocated to TTUHSC-El Paso in 1982 where MH research was his primary area of interest. He has published over 50 papers in refereed journals and has presented posters and lectures at many international events.
Introduction: The malignant hyperthermia gene is inherited as a dominant gene. There are variable degrees of penetrance so a colony of MHS pigs must be established to provide susceptible animals for experimental studies. We have used our MHS pig colony for over 20 years. The MHS pig colony was started in January 1969 at Wisconsin; it was moved to Missouri in 1973 and on to El Paso, TX in 1982. Methods: We completed an experimental study of Sevoflurane in 1984 with MHS pigs. We found Sevoflurane to be an exceptionally smooth anesthetic with no side effects. Sevoflurane usage in clinical practice has reduced the incidence of MH by eleven fold since it was approved for human use. It is an outstandingly good anesthetic with minimal side Results: Non-depolarizing muscle relaxants such as Pancuronium, Vecuronium, Metubine iodide and Orgnon 9416 (Rocuronium) do not trigger an MH episode in experimental MHS pigs. Similar results are observed in human patients. Succinyl choline is a potent trigger of MH in pigs and human patients. Organon 9426 offers protective effects after 100% muscle twitch response has been recovered in MHS pigs. MHS pigs have a 30-35% decrease in acetylcholine receptors at the myoneural junction. These observations suggest either a decrease in the synthesis of acetylcholine receptor proteins or an increased degradation of dysfunctional acetylcholine receptors. Conclusion: The Ryanodine receptor appears to be involved in MH as a secondary or tertiary participant in triggering the MH syndrome.