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Dr. Thomas McCarthy
Chair of Biology

(315) 792-2510
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Fall 2013 Seminars
September 23, 2013
Amanda Butler
Graduate Student, Mayo Clinic Jacksonville – Department of Cancer Research
Title: Therapeutically targeting the atypical Protein Kinase C isozymes in Pancreatic Cancer
 
Abstract: Pancreatic cancer (PC) is a very aggressive disease with few therapeutic options. PKCiota is required for the transformed growth of pancreatic, ovarian, lung, and intestinal cancers; however, the role of the other atypical PKC, PKCzeta (PKCz), in cancer is controversial. In this study, we investigate the role of PKCz and the therapeutic potential of the aPKCs in PC. We find that PKCz expression is either maintained or elevated in primary human pancreatic tumors. Genetic inhibition of PKCz reduced the transformed phenotype of human PC cells in vitro, and orthotopic tumor size and metastasis in vivo. STAT3 plays an important role in PC cell survival and metastasis. Inhibition of PKCz significantly reduced constitutive STAT3 activation in PC cells in vitro and in vivo, and expression of a constitutively active STAT3 construct rescued the transformed phenotype in PKCz-deficient cells. These data suggest that STAT3 is an important downstream mediator of the pro-carcinogenic effects of PKCz in PC cells. Furthermore, a high throughput screen identified the gold-containing drugs, aurothiomalate (ATM) and auranofin (AFN), as potent inhibitors of aPKC signaling. Pharmacologic inhibition of the aPKCs using ATM or AFN mimicked the phenotype of genetic inhibition of the aPKCs in PC. Treatment with ATM or AFN reduced activation of downstream targets of aPKCs, and PC cell transformed growth and invasion in vitro and tumorigenesis and metastasis in vivo. These data suggest a tumor promotive role for PKCζ in PC and indicate that therapeutically targeting the aPKCs may be an effective treatment option for PC patients.
 
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October 7, 2013
Greta A. Van Slyke, M.S.
Research Scientist, New York State Department of Health, Wadsworth Center, Division of Infectious Disease, Arthropod-borne virus laboratory
Title: West Nile virus: Looking Beyond the Consensus
 
Abstract:In 1999 West Nile virus (WNV) was first detected in North America in the New York City area and within a decade had spread throughout North America and the Caribbean, causing annual seasonal outbreaks after introduction; this is in stark contrast to other Flaviviruses and arthropod-borne viruses which exist largely in endemic regions and exhibit sporadic outbreaks. Extensive examination of genomic diversity at the consensus level has reviled that WNV has remained highly homogeneous throughout its geographical spread over time. However, in 2002 there emerged a new consensus WNV genotype (WNV02) which displaced the introduced strain; thus far the phenotypic advantages of the WNV02 consensus genotype have been elusive. In vivo, RNA virus polymerases (RdRps) are highly processive but lack the ability to proofread, high error rate results in genetically diverse intrahost infections referred to as mutant swarms; this combination of characteristics increases the RNA viruses capacity for rapid adaptation and evolution in disparate host environments. Non-consensus genotypes play a significant role in host range, viral fitness, adaptability, immune evasion, replicative fitness, viral pathogenesis, and vector competence, there is also correlation between mutant swarm breadth and both phenotypic plasticity and viral fitness in vivo. Breadth of a mutant swarm depends not just on error rate, but selection; our studies focus on the contribution of the WNV mutant swarm to overall viral fitness, specifically in the mosquito vector, and the complex genomic and adaptive mechanisms that render WNV a unique RNA virus possessing a superior ability to infect and replicate in almost any host it encounters regardless of environmental factors.
 
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October 21, 2013
Kristen Brubaker, Ph.D.
Assistant Professor of Environmental Studies, Hobart and William Smith Colleges
Title: Estimating canopy height and site productivity of deciduous forests at a regional scale with leaf off, low density LiDAR
 
Abstract: LiDAR (Light Detection and Ranging) is increasingly being used to improve our understanding of forested ecosystems on a broad spatial scale. Using freely available low density, leaf off LiDAR and software, we established methodology to create an accurate state-wide tree height model for State Forests in Pennsylvania and validated it using a ground truthed inventory dataset with over 3000 sample points. Our canopy height model was accurate to about 10% of the tree height, with a RMSE of approximately 2 m. Using these tree height data, ecologists and foresters will be able to model important ecosystem metrics including productivity, total biomass, total carbon storage, and site index, which are difficult and time-intensive to measure in the field. With LiDAR-derived height data, in addition to the accurate bare earth model, we should be able to understand relationships between soil, topography, and terrain and their relationship to forest communities. Many states and counties, including many counties in New York, are currently flying low density, leaf off LiDAR with the purpose of generating high resolution bare earth models for FEMA flood plain mapping, which could make this technique much more widespread.     
 
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November 4th 2013
 
Christopher R. Collins, Ph. D.
Assistant Professor
St. John Fisher College
 
"The short, dangerous lives of mammals: a study of causes of mortality in the wild"

Abstract: The proportion of different causes of death (cause specific mortality) is an important indicator of local ecology and local selective forces shaping behavioral and morphological adaptations, and can be easily compared between species. These mortality causes are best measured by remotely monitoring individuals with radio transmitter tags to detect their eventual demise and conducting post-mortem examinations to determine the exact cause of death. In an attempt to understand broad patterns in mammal mortality I compiled data from over 80 studies, and analyzed it to determine what factors influence the likelihood of dying from different causes, ranging from disease to roadkill. I found that humans are the largest cause of mortality for North American mammals, especially in larger mammal species. I also found that there was little or no data on small mammal mortality, so I radio collared white footed mice, and studied their behavior and survival. Our data showed that parasites and weather influenced behavior and activity, and that predators were the primary cause of death in this common rodent species.

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November 18, 2013
Matthew Betzenhauser, Ph.D.
Research Scientist, Masonic Medical Research Laboratory
Title: Regulation of intracellular Ca2+ release channels in physiology and disease
 
Abstract: A regulated rise in intracellular Ca2+ represents a ubiquitous signaling paradigm utilized by cells to control a wide range of physiological processes. Cytosolic Ca2+ can be increased by promoting Ca2+ entry across the plasma membrane or by mobilizing Ca2+ release from intracellular stores. The endoplasmic/sarcoplasmic reticulum (ER/SR) is the major intracellular Ca2+ storage organelle in mammalian cells. Specialized ER/SR resident Ca2+ permeable channels named the inositol (1,4,5)-trisphosphate receptors (IP3R) and the ryanodine receptors (RyR) allow for rapid, highly controlled release of this stored Ca2+ in response to cell stimulation. Given the central importance of these channels to physiological systems, it is not surprising that they are subject to multiple modes of regulation. Furthermore, alterations in IP3R and RyR are thought to underlie numerous pathologies, especially in cardiovascular systems. The goal of my research is to understand the molecular bases and physiological consequences of IP3R and RyR regulation and to probe how these channels are disrupted in cardiovascular diseases and aging.