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Paul Standley, PhDProfessor, Department of Basic Medical Sciences - The University of Arizona College of Medicine—Phoenix in partnership with Arizona State University Adjunct Professor - Arizona State University
UA Office Phone: (602) 827-2107 |
Education:Post-Doc, Vascular Endocrinology and Hypertension; Wayne State University Department of Internal Medicine; 1992-1994 PhD; Wayne State University School of Medicine Department of Physiology; 1992
Background:Dr. Standley trained as a vascular physiologist at Wayne State University School of Medicine in Detroit, Michigan. His first faculty appointments were in the Departments of Physiology and Internal Medicine where he continued his work investigating the vascular effects of insulin and its actions as a calcium channel blocking agent. Upon his move to Arizona in 1996 to help found the Arizona College of Osteopathic Medicine at Midwestern University, his research gained new focus in the field of biophysical regulation of gene expression in vascular smooth muscle. During his tenure at MWU, he also developed a new innovative medical physiology curriculum there and has taught medical students in all subdisciplines of medical physiology for 12 years. Dr. Standley moved to the University of Arizona College of Medicine - Phoenix in 2006 to help found its new medical school track. Here, he serves as the block director for the cardiovascular/pulmonary/renal section of the year I medical curriculum. In addition, he continues his NIH-funded research program, continuing to investigate how biophysical stimuli regulate cytokine and growth gene expression in vascular smooth muscle and fascial fibroblasts. His academic passions include student-centric instruction / curriculum development, his ongoing vascular research and taking modern medical information into the community using a variety of outreach strategies. Research Interests:Virtually all adult human cells in vivo exist in a biophysically dynamic environment. Our laboratory is interested in how such biophysical stimuli impact cell physiology in a number of important ways. For example, one line of our research is focused on how biophysical strain impacts vascular smooth muscle cell (VSMC) proliferation. Such cell proliferation is a hallmark of vascular neointimal formation observed, for example, post angioplasty as well as post vein grafting. The clinical consequences of untreated reocclusion are dire and an understanding of the mechanisms responsible for it is crucial. To this end, our laboratory models tissue-specific strain profiles and investigates, using a variety of techniques, changes in VSMC growth, proliferation and apoptosis. Further, we assess gene expression and secretory profiles of suspect growth factors and inflammatory cytokines by protein arrays and subsequently inhibit their expression and actions utilizing a variety of methodologies. Our work in this area has shown that strain-induced autocrine insulin-like growth factor 1 (IGF-1), nitric oxide, and vascular endothelial growth factor (VEGF) appear to reciprocally mediate VSMC hyperplasia, and perhaps clinical neointimal formation, in environments of increased cyclic mechanical strain. Also in response to mechanical strain is the observation that VSMC align in a manner perpendicular to the dominant strain vector presumably to establish an ideal energy efficient conformation. We have investigated various signaling pathways potentially responsible for this occurrence, and it appears that these are separate and distinct from those regulating the hyperproliferative response. Our work has expanded to include investigation of the putative mechanotransducer responsible for such signaling. Stretch activated calcium channels (SACCs) appear to play an important proximal step in strain-mediated gene expression by coding for intracellular calcium pulses that result in gene activation and vesicle release. Our cardiovascular lines of investigation have recently brought our laboratory in a new and timely direction: that being development of an in vitro strain model used to investigate cellular and molecular events that may form an evidence base for manual therapies such as osteopathic manipulative medicine, chiropracty, physical therapy, and others. Utilizing human fibroblast cultures, we have developed clinically relevant injurious and manual medicine therapy strain profiles to investigate production of pro-and anti-inflammatory interleukin expression in these cells. We have reported that modeled therapies decrease inflammatory and increase anti-inflammatory cytokine secretion, thereby lending a potential mechanism responsible for reduced pain and swelling and increased range of motion in injured joints and tissues following manual therapies. Our goals include developing a cellular evidence base to support positive clinical outcome documented post-treatment, a situation that may lead to expanded use and reimbursement rates for these alternative medicine modalities. PubMed Link:Search PubMed for a complete listing of Dr. Standley's publications Selected Publications:
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