Anatomy

David Galbraith obtained undergraduate and graduate degrees in Biochemistry from the University of Cambridge, and postdoctoral training as a NATO Fellow at Stanford University. His first academic appointment was at the University of Nebraska Lincoln, and he became Professor of Plant Sciences at the University of Arizona in 1989. His research has focused on the development of instrumentation and methods for the analysis of biological cells, organs, and systems. He is internationally recognized as a pioneer in the development and use of flow cytometry and sorting in plants, developing widely-used methods for the analysis of genome size and cell cycle status, and for the production of somatic hybrids. He also was among the first to develop methods for the analysis of gene expression within specific cell types, using markers based on Fluorescent Protein expression for flow sorting these cells, and microarray platforms for analysis of their transcriptional activities and protein complements. Current interests include applications of highly parallel platforms for transcript and protein profiling of minimal sample sizes, and for analysis of genetic and epigenetic mechanisms that regulate gene expression during normal development and in diseased states, specifically pancreatic cancer. He is also funded to study factors involved in the regulation of bud dormancy in Vitis vinifera, and has interests in biodiversity and improvement of third-world agriculture. He has published more than 180 scholarly research articles, holds several patents, was elected a Fellow of the American Association for Advancement of Science in 2002, and serves on the editorial board of Cytometry Part A. He is widely sought as a speaker, having presented over 360 seminars in academic, industrial and conference settings. He was elected Secretary of the International Society for Advancement of Cytometry in 2016. Keywords: Plant and Animal Cellular Engineering; Biological Instrumentation; Flow Cytometry and Sorting

The Doyle lab investigates the role of the immune system in causing dementia after stroke. Up to 30% of stroke patients develop dementia in the months and years after their stroke and we are testing the hypothesis that in some patients this is due to a chronic inflammatory response that persists at the site of the stroke infarct. We suspect that in the weeks, months and possibly years after stroke, neurotoxic inflammatory mediators, including T cells, cytokines and antibodies, leak out of the stroke infarct and cause bystander damage to the surrounding tissue, which then both impairs recovery, and in some instances leads to cognitive decline. In support of this hypothesis we have data that demonstrates that inflammation persists for months at the site of the infarct after stroke, and that a single stroke can directly lead to the development of immune-mediated delayed cognitive deficits. We are currently in the process of targeting different components of the prolonged inflammatory response to stroke to determine if post stroke dementia can be treated by selectively ablating individual immune mediators such as B lymphocytes, T lymphocytes, and CCR2. Keywords: Neuroinflammation, stroke, dementia, Alzheimer's disease

Thomas Davis, PhD, and his lab continue its long-term CNS biodistribution research program, funded by NIH since 1981, by studying the mechanisms involved in delivering drugs across the blood-brain barrier to the C.N.S. during pathological disease states. Recently, Dr. Davis and his lab discovered specifica drug transporters which can be targeted to enhance delivery. They are also interested in studying the effect of hypoxia/aglycemia/inflammatory pain on endothelial cell permeability and structure at the blood-brain barrier. Dr. Davis has recently shown that short-term hypoxia/aglycemia leads to significant alterations in permeability which can be reversed by specific calcium channel antagonists. This work has significant consequences to the study of stroke. Additionally, he has discovered that peripheral pain has significant effects on BBB tight junction protein cytoarchitecture leading to variations in the delivery of analgesics to the CNS.

Nearly 50 million couples experience some form of infertility worldwide. Several factors increase a woman’s risk for infertility including aging, stress, and exposure to chemicals. A group of chemicals collectively known as phthalates have been classified as endocrine disruptors based on their ability to interact with the reproductive system. Phthalates have been detected in human urine, animal tissues, and feed. Despite these observations, how phthalates interact with the female reproductive system and what this means for overall fertility is currently unknown. Dr. Craig's work focuses on understanding how phthalates affect the function of the ovary, the major reproductive organ in females. Thus, work in her laboratory is focused on using animal models to help us understand the mechanisms by which phthalates exert their effects on the ovary, determine whether phthalates cause female infertility, and examine whether the effects of phthalates on female reproduction can be prevented or reversed. Using this knowledge she hopes to inspire and guide future work aimed at reducing, preventing, and/or reversing chemical-related infertility in humans and animals. Keywords: Infertility, Toxicology, Endocrine Disruptors, Phthalates, Reproduction

Yin Chen, PhD. is an Assistant Professor in Pharmacology and Toxicology in the College of Pharmacy at UA. Dr. Chen’s research focus is on epithelial biology. He was a research faculty in University of California, Davis and an Assistant Investigator in Chemical Industry Institute of Toxicology (former CIIT and later Hamner Institute). His long-term research objective is to understand the dysfunction of airway epithelial mucosa in the pathogenesis of a variety of acute and chronic airway diseases. His current research programs are: a) understanding the molecular mechanisms underlying airway mucous cell development and mucous cell metaplasia in chronic diseases including cancer, COPD and asthma; (b) understanding the function and regulation of novel COPD associated genes and developing novel compounds to treat COPD; (c) understanding the impact of fungal exposure on airway innate immunity and its contribution to the development and exacerbation of asthma. Dr. Chen has more than 30 publications including peer-reviewed research articles, reviews and book chapters. He has served as the PI on one R01, two R21, one Flight Attendant Medical Institute (FAMRI) Innovative Clinical Award and one Arizona Biomedical Research Commission Award. He has also served as co-PI on two R01 and one P01 grants. He has built a long productive track record in studying airway mucus production and respiratory viral infection using primary airway epithelial cell model. He routinely cultivate and use primary epithelial cells from eye, salivary gland, airway surface and submucosal gland in different species (e.g. human, monkey, pig, rat and mouse) as our in vitro model to study mucin genes. The differentiated primary culture model demonstrates pseudostratified morphology, is composed of ciliated, non-ciliated, and goblet cells, and has a transepithelial barrier with high electro-resistance. He has also established in vivo exposure system to study the pulmonary effect of the exposure to particulates, pathogens and gases. Using this system, he has developed various airway disease models including CS-induced COPD model, ovalbumin-induced asthma model, fungal-induced asthma model and several infection models such as H1N1, rhinovirus, Aspergillus, and Alternaria.

Dr. Brooks is a renal physiologist and has developed microarray technology to address in vivo signaling pathways involved in the hormonal regulation of renal function. Current areas of research in the Brooks Laboratory are focused on importance of sex differences in the onset of postmenopausal hypertension and diabetic kidney disease and identifying new therapies for polycystic kidney disease and lithium-induced nephropathy.

My work investigates the molecular mechanisms of axon degeneration, a molecular program triggered by toxic, metabolic, or traumatic stress to the axonal compartment of neurons. I use both fruit fly and mouse tools to ask questions about genes involved in axon degeneration and to place these genes in the context of pathways required for axon and synapse maintenance in the face of insults. I have discovered a number of axon degeneration mediators, including MORN4 and TMEM184b as well as others, and am currently following up on their roles within neurons during normal neuronal functioning and in the context of neurodegenerative disorders such as ALS and Alzheimer’s Disease. Keywords: Neurodegeneration, Neurogenetics, Behavior