Current Research

• Verification and monitoring of biodegradation of dihaloethane contamination in New Mexico aquifers. 2000-2001
• Instrumentation and Laboratory Improvement.

Dr. Tom Kieft

• Biological hazard detection system for pathogen detection and surveillance, Phase I Proposal. Office of Naval Research.
• Collaborative Research: South African Ultradeep Mines - Long-Term Sites for Interdisciplinary Studies (LSLIS) into the Extreme Environment of the Deep Subsurface. National Science Foundation (Subcontract to Princeton University) and NASA.
• Biomarkers in Extreme Environments: Analogs for Astromaterials. Astrobiology Institute, National Aeronautics and Space Administration. 06/01/99 -- 05/31/04.

Dr. Snezna Rogelj

• Regulation of adhesive interactions between cells.
• Biochemical mechanism of leukocyte L-selectin shedding.
• Modulation of the human immune response by certain pesticides and pollutants.
• High sensitivity detection of pathogenic organisms in our environment.
• Biomimetic approaches to CO2 sequestration.

Dr. Kevin Kirk

• Biology of aging. Evolution of aging. Mechanisms for increased lifespan during dietary restriction.
• Population and community ecology. Factors affecting species diversity.

Dr. Scott Shors

• In my laboratory we are investigating how viruses overcome the innate immune response. The innate immune response to viral infection contributes to both the duration of the infection and it’s resulting morbidity and mortality.  In response to viral infection the host attempts to limit virus production by inhibiting protein synthesis. At least two kinases can respond to limit viral infection; PKR and Perk. Both of these kinases inhibit protein synthesis by phosphorylating the translation initiation factor eIF2.  eIF2 is a rate liming factor in the initiation of all protein synthesis.  When phosphorylated, eIF2 cannot participate in the initiation of protein synthesis.  This inhibition of protein synthesis can be localized within subcellular ‘factories’ or it can global in which case it culminates in apoptosis.

  Dr. Jay Naik 

• Jay Naik is a vascular physiologist who studies how disease states affect vascular function. The long-term goal of his laboratory is to define the physiological mechanisms linking blood flow to the metabolic state of the tissue, and how these mechanisms are altered under pathophysiological conditions. For example, obesity is associated with hypertension, dyslipidemia, and type II diabetes, a collection of conditions often referred to as metabolic syndrome affecting ~45 million US residents. Dysfunction of the inner lining of blood vessels (i.e.
  endothelium) is a major component of metabolic syndrome. Experiments in Jay’s laboratory investigate the mechanisms responsible for the dysfunction of the endothelium.
  It is reasonable well established that fetal under-nutrition can ‘program’ an individual to develop cardiovascular disease in adulthood.
  Jay is also interested in investigating by what mechanisms maternal metabolic derangements (obesity or diabetes) during fetal development can affect the cardiovascular health of adult children.
  These experiments are performed in rodent models of obesity/diabetes.
  Jay’s laboratory addresses these questions using molecular, isolated artery, and whole animal techniques.