Research Day Book 2013 - College of Medicine - Florida Atlantic ...

CONCLUSIONS: The Ca 2+ desensitizing molecule, (‐)‐epigallocatechin gallate (EGCg), can reverse the
impaired relaxation and delayed Ca 2+ decay in RCM cardiac myocytes by restoring the myofilament Ca 2+
sensitivity. EGCg improves diastolic function in RCM mice without damaging the systolic function. The
restored diastolic function was manifested by the correction of the prolonged IVRT in the RCM animals and
the increased of the left ventricular end diastolic dimension in RCM mice following the treatment. The Ca 2+
desensitizing properties of the green tea extract, EGCg, are beneficial for RCM and provide a therapeutic
alternative for diastolic dysfunction due to increased myofilament Ca 2+ sensitivity.
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Robertson IM, MX Li, BD Sykes. J Biol Chem 284:23012‐23023, 2009.
Tadano N, et al. Bri J Pharmacology 161:1034‐1043, 2010.
Li Y, et al. J Mol Cell Cardiol 49:402‐411, 2010.
Jean‐Charles P, Y Li, C Nan, XP Huang. J Geriatr Cardiol 8:168‐183, 2011.
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ABSTRACT TITLE: Annotation of neurodevelopmental regulators in dopaminergic and GABAergic
neurons for links to ischemia‐hypoxia response
AUTHORS: Kim McKain, Maryanne Joseph, Rainald Schmidt‐Kastner
DEPARTMENT: Integrated Medical Science
BACKGROUND: A leading concept for the pathogenesis of schizophrenia (SCZ) is based on gene –
environment interactions during neurodevelopment. In previous in silico work, genes associated with the
risk of SCZ were examined for links to ischemia‐hypoxia responses and vascular factors, and a significant
overlap was demonstrated (1, 2). Our analysis has stimulated clinical studies of gene x environment
interactions in SCZ (3). In preparation for translational research, we are now developing strategies to create
gene databases related to a) known pathophysiological mechanisms for SCZ, b) regulation of
neurodevelopment, and c) ischemia‐hypoxia responses in the brain. Dysfunction of the dopaminergic (DA)
system in SCZ has been confirmed by recent PET studies of dopamine receptors, and abnormalities of
GABAergic cortical interneurons have been described in post‐mortem tissue.
OBJECTIVES: The aim of this study is to define possible interactions between neurodevelopmental
mechanisms for DA and GABAergic neurons and ischemia‐hypoxia responses. Using literature‐mining, we
generated databases for genes/proteins broadly related to the development of the DA midbrain neurons or
GABAergic telencephalic interneurons, and then looked for an overlap with our own databases for
ischemia‐hypoxia responses.
METHODS: Lists of genes related to regulation of DA and GABAergic neurogenesis were generated via
literature mining (PubMed, Web of Knowledge) and by compilation of gene expression profiling studies.
Genes expressed during development of DA and GABAergic were annotated using the ischemia‐hypoxia