|Damon Jacobs Ph.D., Postdoctoral Fellow
Mentor: Pamela Tran
Research interest: Obesity is a growing epidemic in industrialized nations of the world and is the primary cause of several life-threatening metabolic disorders, such as hypertension, liver disease, and diabetes. Primary cilia are antennae-like extensions present on most cells of the body, they contain receptors (such as Hedgehog, Wnt, PDGFa, ...etc.) that are important for communicating signals from the extracellular environment into the cell. ‘Ciliopathies' arise due to defects in proteins that localize to primary cilia and can cause developmental and postnatal defects such as polydactyly, cystic kidney disease and obesity. Thm1 is a critical ciliary protein that is important in maintaining proper cell signaling programs, and I am working with a THM1-/- mouse model to characterize the postnatal obesity phenotype and examine the physiological and neurological causes of obesity onset. We are working toward identifying potential therapeutic targets for controlling the onset of obesity.
|Yomna Badawi Ph.D., Postdoctoral Fellow
Mentor: Hiroshi Nishimune
Amyotrophic lateral sclerosis (ALS) patients and animal models show denervation of neuromuscular junctions (NMJs), which is a dying-back neuropathy. However, the etiology of ALS and this neuropathy is not known, and interventions are lacking. My research focuses on the evaluation of exercise and stem cells for the amelioration of NMJ denervation in ALS models.
|Angela N. Pierce, D.C., Ph.D., Postdoctoral Fellow
Mentor: Julie Christianson
Patients with chronic visceral pain syndromes commonly report stress-related symptom onset and may suffer from depression, anxiety, and/or panic disorder. Comorbidity between chronic pelvic pain syndromes and mood disorder is associated with altered functioning of the hypothalamic-pituitary-adrenal (HPA) axis. Exposure to early life stress is a significant risk factor for developing HPA axis abnormalities and accompanying pain syndromes, and voluntary exercise has been shown to attenuate changes associated with a dysfunctional HPA axis. My research investigates how voluntary exercise normalizes output of the HPA axis and attenuates visceral hypersensitivity, dysfunction, and inflammation in adult female mice that underwent early life stress.