Maryam Raeeszadeh-Sarmazdeh

Maryam Raeeszadeh-Sarmazdeh joined the University of Nevada, Reno in July 2019 as an assistant professor. Dr. Sarmazdeh was a senior research fellow in the Department of Cancer Biology at Mayo Clinic, Florida from 2017 to 2019 at Dr. Radisky’s lab, during which her work was focused on engineering novel protein-based therapeutics based on natural enzyme inhibitors. Prior to her appointment at Mayo Clinic, she was a postdoctoral scholar at the Chemical and Biomolecular Engineering Department at the University of Delaware at Prof. Wilfred Chen’s lab for 2.5 years. Dr. Sarmazdeh earned her Ph.D. in Chemical and Biomolecular Engineering from the University of Tennessee at Knoxville under Prof. Eric Boder’s supervision. There, her research was focused on generating site-specific protein immobilization on the surface and protein engineering using yeast surface display and directed evolution.

Allen Gibbs

My lab uses experimental evolution in the laboratory to study how physiological systems evolve. We subject populations of fruitflies (Drosophila) to stressful conditions and investigate how they evolve in response to stress over many generations. Our current major projects involve flies that have been selected for resistance to desiccation and starvation stress for >100 generations. To understand the relevance of this laboratory research to nature, we have also studied several other types of insects and their relatives, including grasshoppers, ants, desert fruitflies, scorpions, etc.

Iain Buxton

The Buxton lab is exploring contraction-relaxation coupling in the uterine myometrium in order to better understand and develop treatments for the problem of preterm labor. Preterm delivery of an underdeveloped fetus is a global problem. Babies delivered prior to full development at term have multiple medical problems that plague these individuals throughout their lifetime. Prematurity explains 75% of all fetal morbidity and mortality. Thus, beyond the tragic and costly fact of their prematurity, is the major impact on individuals and societies long-term. There are no effective (or FDA-approved) medications that prevent contractions of the uterus in patients who enter labor preterm (PTL). What is used is ineffective at allowing the fetus to remain in the womb until term. Drugs employed to prevent PTL (tocolytics) are only evaluated for an ability to prevent labor for 48 hours, a time during which treatments can ready the fetus to breath air. PTL leads to preterm delivery (PTD) in over 50% of cases. Spontaneous PTL (sPTL, no explanation such as infection) accounts for the majority of PTL.

The approach to sPTL we are pursuing is based on the non-canonical pathway by which NO relaxes myometrium. Our approach hypothesizes specific S-nitrosation differences in the protein fingerprint of sPTL compared with laboring myometrium. What is needed to investigate sPTL is to know the specific proteins that are post-translationally S-nitrosated and their abundance and/or unique presence and the impact of their S-nitrosation in pregnancy, labor and sPTL.

We have discovered particular unique proteins that are deferentially S-nitrosated and are pursuing their role in mediating relaxation on pregnancy and labor. One such protein is a channel called TREK-1. This channel is stretch-activated. We discovered genetic variants of the channel associated with PTL in women. Electrophysiological measurement of these gene variant channels suggests that their expression in women may constitute a mechanism to explain PTL in these patients. Drug discovery is in process to generate therapeutics to treat this form of PTL.

In a second thrust, the Buxton lab is looking for therapeutic targets in breast cancer. Tumor cells migrate to distant sites in the body before they are capable of forming aggressive metastases and thus remain dormant. We do not know the cellular behavior of disease we label latent but attracting a blood supply may be an early property that precedes and is required for those lesions that become malignant in women. Breast cancer specific mortality is almost exclusively a function of metastasis. Growth of tumor cells as metastases dictates that tumor cells must first develop a capillary blood supply or risk necrosis. Metastatic tumor cells have already attracted a blood supply, a hallmark of cancer. What activates dormant cells at metastatic sites to move from a quiescent to aggressive phenotype is not known. It is critical to determine the effect of a kinase we discovered to be released from cancer cells because every indication is that it produces a blood supply for cells that can later become malignant, an event that cannot take place unless a blood supply is available. Our current experiments are focused on the actions of the kinase that permit intravasation and extravasation of tumor cells that permit their passage to distant sites in the body where they can lodge and remain undetected for years. We have developed an inhibitor of the kinase and hope to demonstrate its potential a breast cancer prophylactic.

David Alvarez-Ponce

Assistant Professor, University of Nevada, Reno, 2014 – present

Juan de la Cierva Postdoctoral fellow, Consejo Superior de Investigaciones Cientificas, Spain, 2012-2014

Postdoctoral fellow, Trinity College Dublin, 2012

Postdoctoral researcher, National University of Ireland Maynooth, 2010-2012

See our lab webpage for research description: https://genomeevol.wordpress.com

Rochelle Hines

Rochelle Hines’ research is aimed at understanding neurodevelopmental processes under normal and pathological conditions, which include autism spectrum disorders, schizophrenia, and developmental epilepsies. In particular, Rochelle’s studies focus on understanding the formation and stabilization of specific synapse types during development, with an emphasis on inhibitory synapses. Rochelle employs molecular genetics, biochemistry, confocal and electron microscopy, behavioral assessments and electroencephalography in mouse models to gain understanding of how inhibitory synapse function and dysfunction during development impacts brain signaling, circuitry and behavior. The ultimate goal of Rochelle’s research is to improve our understanding of neurodevelopmental disorders and to promote novel therapeutic strategies.

Rochelle earned her PhD in Neuroscience at the University of British Columbia in Vancouver, Canada (2009), followed by a postdoctoral fellowship at Tufts University School of Medicine in Boston, MA (2015).

Dustin Hines

The brain operates as a complex orchestration that involves many different cellular players. Dr. Dustin Hines’ research is aimed at understanding the role that glial cells play under normal and pathological conditions, which include neuropsychiatric disorders (depression), traumatic brain injury, stroke and Alzheimer disease. In particular, Dr. Hines researches how astrocytes and microglia cells both talk and listen to neurons. Dr. Hines employs molecular genetics, biochemistry, confocal and two photon microscopy, electrophysiology and behavioral assessments in mouse models to gain understanding of how glia cells impact brain signaling, circuitry and behavior. Dr. Hines’ research ultimately is directed towards understanding how all of the cells of the brain are orchestrated into the precise symphony that we call behavior.

Ruben Dagda

Ruben K. Dagda, Ph.D., received his doctoral training at the University of Iowa and his postdoctoral training at the University of Pittsburgh School of Medicine. He is currently investigating the molecular mechanisms that lead to mitochondrial dysfunction and oxidative stress in cell culture, tissue and animal models of Parkinson’s disease.

Yong Zhang

Ph.D., Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 2008
B.S., Biochemistry and Molecular Biology, College of Life Sciences, Shandong Normal University, China

Angela Smilanich

My research focuses on the ecology and evolution of diet breadth via physiological studies of multitrophic interactions between plants, herbivores, and natural enemies. Specific avenues of study include: (1) evolutionary ecology of insect immunity (2) investigation of plant secondary chemistry as insect immunosuppressant, and (3) behavioral adaptations of herbivores to host plants.

David Aucoin

The primary focus of the AuCoin laboratory is to develop diagnostics and therapeutics for infectious diseases. Current funding includes three research grants through the National Institutes of Health. Two additional grants were recently secured through the Department of Homeland Security (DHS) and the Naval Research Laboratory (DoD). All these projects rely on the identification of secreted or circulating microbial antigens that can be targeted for diagnosis of disease. The AuCoin laboratory has developed a novel platform technology termed “In vivo Microbial Antigen Discovery” or InMAD to identify such secreted antigens. InMAD is currently being utilized to identify candidate diagnostic antigens secreted during infection with Burkholderia pseudomallei (melioidosis), Aspergillus fumigatus (invasive aspergillosis) and Francisella tularensis (tularemia).