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The research in my lab is primarily concerned with understanding the effects of dietary genistein and other nutriceuticals (and exercise) on intestinal function. Genistein is an isoflavonic phytoestrogen found naturally in soy, and a known activator of the CFTR chloride channel. Cystic fibrosis (CF) is an inherited disease in which epithelia are adversely affected by loss of proper CFTR function (i.e. sweat duct, pancreas, vas deferens, airway and intestine). \We have shown that consuming dietary genistein increases basal and cAMP-mediated chloride secretion in female wild-type (Wt) murine jejuna and in the well established DeltaF508-CF mouse dietary genistein eliminates the dependence of CF mice for laxatives. Current work is aimed to evaluate how genistein mediates benficial effect on survival and weight gain in CF mice. We have shown that diabetic/obese ob/ob mice have significantly reduced jejunal basal chloride secretion, and furthermore, we demonstrate that consuming genistein-diet will rescue this deficit in basal secretion via influences on intestinal ion transporters. Recent work in my lab is aimed to evaluate the influence of genistein and exercise in mice fed a high-fat/high-sugar (HFHS) diet, a model of diet-induced diabetic obesity, known to lead to Alzheimer's like pathology. In this model we are examining the gut brain axis. Current studies in the lab are aimed at determining the mechanism(s) of action of genistein on intestinal function in Wt, CF, ob/ob and HFHS-fed mice, and importantly understanding the sex-dependent differences observed.
As faculty in the Department of Physiology at MWU, we have the dual mission of providing physiology education and conducting high quality scientific research.
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regarding the pathogenesis of this disease ( Traka et al., J Neurosci. 2008 ); the Wdr81nur5 mouse model for cerebellar ataxia, mental retardation and quadrupedal locomotion syndrome (CAMRQ2; Traka et al., J Neurosci. 2013 ); the diphtheria-toxin A chain (DTA) mouse model that allows for the tamoxifen-induced ablation of oligodendrocytes throughout the CNS. Our studies on the DTA mouse have revealed that the CNS has a robust innate capacity to repair myelin damage and restore neuronal function upon inducing oligodendrocyte cell loss ( Traka et al., Brain 2010 ). Moreover, we recently
rats ( Briyal, Ranjan et al, Nature Scientific Reports 2019 ). At present, I am leading these projects independently and have recently demonstrated a new role of sovateltide in promoting neuronal progenitor cells (NPCs) mediated regeneration and preventing mitochondrial dysfunction ( Ranjan et al., Nature Scientific Reports, July, 2020 ), without disturbing the equilibrium of the pluripotent and multipotent stem cell pool in ischemic stroked adult rat brains ( Ranjan et al., Canadian J of Physiology and Pharmacology, June, 2020 ). These findings uncovered a unique regenerative
Dr. Joshua Baker, originally from Blossvale, New York, came to Midwestern University after serving as the Chief of Optometry Service at the U.S. Army Health Clinic in Stuttgart. An Army Major, he spent time deployed in Al Asad, Iraq from August 2007 to November 2008 and received the Bronze Star. Dr. Baker served as Chief of Optometry Services at Bassett Army Community Hospital, Ft Wainwright, Alaska prior to his deployment in support of Operation Iraqi Freedom. Dr. Baker received his bachelor’s degree from Ithaca College in 1999, earned a Master of Science in Secondary Science Education
Check out this page to read about highlights of relevant published scholarly research work by our Nanomedicine COE-TCR members
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