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The new center will coordinate with the ASU Center for Evolutionary Medicine and Bioinformatics in the Biodesign Institute, directed by Regents' Professor Sudhir Kumar, by augmenting existing strengths in phylogenetics with new faculty whose research uses basic evolutionary principles to understand problems such as antibiotic resistance, cancer, autoimmune disease, aging and behavioral disorders.
Schedule of events (open to the public)
*Speaker abstracts below
"Galen, hagfish and the bench-to-bedside gap in endothelial biomedicine: a noisy affair"
2-3:15 p.m. Jan. 17, LSE 104 (refreshments served beforehand)
Willaim Aird, professor of medicine, Harvard Medical School and director, Center for Vascular Biology Research, Beth Israel Deaconess Medical Center
Symposium on Evolution, Medicine & Public Health: The Great Opportunity
1-6:30 p.m., Jan. 21, Memorial Union 241
• 1 p.m., "Hormones in the wild: Physiological adaptations for human social relationships," Mark Flinn, professor and chair of anthropology, University of Missouri
• 2:30 p.m., "The evolution of drug resistance and the curious orthodoxy of aggressive chemotherapy," Andrew Read, alumni professor in the biological sciences, professor of entomology and director of the Center for Infectious Disease Dynamics
• 4 p.m. "Making evolutionary biology a basic science for medicine worldwide: What can ASU do?" Panel discussion with the four visitors and ASU faculty, led by Randolph Nesse
• 5:30 p.m. Open reception for all who share an interest in evolution and medicine
"Where Darwin meets Freud: Evolutionary biology and the genetics of autism, psychosis, and the social brain"
noon-1 p.m., Jan. 22, ISTB-1 401
Bernard Crespi, professor of biology, Simon Fraser University
To join the listserv for CEMPH events, send a note to CEMPH@asu.edu. To view the speakers' bios and papers, click here.
"Galen, hagfish and the bench-to-bedside gap in endothelial biomedicine: a noisy affair," William Aird
The vascular endothelium, which forms the inner lining of the blood vascular system, is an under-appreciated organ system that has enormous, though largely untapped diagnostic and therapeutic potential. There exists a wide bench-to-bedside gap in endothelial biomedicine. Future advances in vascular medicine are contingent upon narrowing the gap and translating knowledge to improve patient care. A first step is to recognize the origins of the existing chasm. One reason relates to medicine’s present-day preoccupation with large arteries, at the expense of the vast expanses of microscopic small blood vessels or capillaries. While large arteries are vulnerable to developing atherosclerosis, microvessels hold important clues about the mechanisms of virtually every other disease in humans. I will discuss how our focus on large vessels is rooted in Ancient Greek medicine, and was further sharpened by William Harvey’s discovery of the circulation. In the 1900s, the compartmentalization of medicine into organ-specific disciplines further hampered our ability to approach the vasculature as an integrated organ. Another reason for the lack of progress in knowledge translation is our focus on cell culture. I will discuss how traditional in vitro studies have shaped our view of the endothelial cell as a homogeneous entity and precluded analysis of its emergent properties. I will emphasize the remarkable adaptability of the intact endothelium, review proximate mechanisms of endothelial cell heterogeneity and introduce the novel role of multistability and biological noise in mediating phenotypic differences between endothelial cells. Finally, I will address evolutionary mechanisms of endothelial heterogeneity. I will present data from our studies in hagfish, the oldest extant vertebrate, showing that phenotypic heterogeneity evolved as a core feature of the endothelium. In conclusion, I will argue that future breakthroughs in endothelial biomedicine will require an understanding of the dynamical regulatory network of the endothelium at multiple scales.
"Hormones in the wild: Physiological adaptations for human social relationships," Mark Flinn
We humans are highly sensitive to our social environments. Our brains have special abilities such as empathy and social foresight that allow us to understand each other’s feelings and communicate in ways that are unique among all living organisms. Our bodies use internal chemical messengers – hormones and neurotransmitters – to help guide responses to our social worlds. Understanding this chemical language is important for many research questions in anthropology. For the past 25 years I have conducted a field study of child stress and family environment in a rural community in Dominica. The primary objective is to document hormonal responses of children to everyday interactions with their parents and other care providers, concomitant with longitudinal assessment of developmental and health outcomes. Results indicate that difficult family environments and traumatic social events are associated with temporal elevations of cortisol and morbidity risk. The long-term effects of traumatic early experiences on cortisol profiles are complex and indicate domain-specific effects, with normal recovery from physical stressors, but some heightened response to negative-affect social challenges.
"The evolution of drug resistance and the curious orthodoxy of aggressive chemotherapy," Andrew Read
Drug-resistance is a major public health problem. Conventional wisdom on resistance management is to use aggressive chemotherapy to kill pathogens as rapidly as possible so as to prevent them from acquiring resistance. This is the reason why physicians frequently exhort patients to finish drug courses even after they no longer feel sick. I will argue that that aggressive chemotherapy will not be the best way to retard resistance evolution in some – perhaps many – circumstances.
"Where Darwin meets Freud: Evolutionary Biology and genetics of autism, psychosis, and the social brain," Bernard Crespi
Mental disorders are usually conceptualized in terms of pathology and disease. I describe a new perspective, based in evolutionary biology and genetics, that the forms and risks of human psychiatric conditions have evolved. Under this rubric, such conditions represent hypo-development, or hyper-development, of human evolved adaptations and tradeoffs. I present evidence from genetics, endocrinology, neuroscience, psychology and psychiatry that autism spectrum and psychotic-affective conditions (mainly schizophrenia, bipolar disorder and depression) represent diametric (opposite) conditions with regard to human social and non-social cognition. This evolutionary perspective has direct implications for the study, understanding and treatment of psychiatric conditions.