Adjunct & Affiliate Faculty
Consumption of beverage alcohol (ethanol) by humans can disrupt many normal metabolic processes. The cells of liver and other tissues must divert processing enzymes from normal functions to process ethanol, thus reducing the production of important compounds such as the vitamin A (retinol) derivative, retinoic acid.
It has been hypothesized that the disruption in synthesis of retinoic acid by ethanol is an underlying cause of fetal alcohol syndrome. The main enzyme responsible for retinoic acid synthesis is alcohol dehydrogenase IV (ADH-IV), most abundant in the stomach and intestines in adults, and essential for proper fetal development.
Research interests: Evolutionary theory
University of Idaho
Sara J. Heggland
Professor of Biology
Albertson College of Idaho
Our research explores the cellular mechanisms involved in heavy metal toxicity and focuses on the heavy metal cadmium. There are a variety of sources of cadmium, however, increasing discard into landfills of electronic products (e-waste) that contain heavy metals makes cadmium exposure a growing public health concern. Cadmium is an environmental pollutant that is toxic to many tissues. Human exposure to cadmium is linked to many diseases including kidney, skeletal and liver disease, and several types of cancer. A key to understanding cadmium’s toxic action is to decipher the mechanisms within cells that cause and protect against cadmium toxicity.
Patrick J. Hrdlicka
I am a nucleic acid chemist with interests at the interface of chemistry, molecular biology and materials science. My research team specifically aims to i) develop and characterize oligonucleotides that enable sequence-unrestricted targeting of double-stranded DNA, and ii) utilize these molecular tools to detect and regulate genes in different biological models.
Projects may accordingly incorporate elements from synthetic organic chemistry, molecular biology, bioanalytical chemistry and biophysical chemistry.
My laboratory’s research interests are directed towards elucidation of the molecular mechanisms that promote tumor progression. We have been working on the effects of the cytokine Oncostatin M (OSM) on breast tumor progression and metastasis. Oncostatin M (OSM), an IL-6 family cytokine, is produced by breast cancer cells and tumor-associated cells of the immune system, including macrophages and neutrophils. OSM has been shown to inhibit the proliferation of breast cancer cells, and this effect initially focused much attention on OSM as a potential breast cancer therapy. Data from our lab, however, suggests that OSM could actually contribute to tumor progression and the development of a metastatic state. We have shown that OSM induces vascular endothelial cell growth factor (VEGF), cyclooxygenase-2 (COX-2), cell detachment, and invasive capacity in vitro. In vivo studies involving the role of OSM in breast, prostate, and colon cancer progression are underway.
I am interested in how ecological, evolutionary and ecosystem processes interact to determine how populations function over time. Much of the work in our lab is currently focused on the community ecology and population dynamics of salmon in river ecosystems. Projects include studying the evolution of life history strategies for fish and understanding how changing flow dynamics of river systems alter food web dynamics and fish bioenergetics.
Distinguished Research Professor, Northern Illinois University, Emeritus
I recently retired to Moscow from 35 years of teaching at Northern Illinois University (DeKalb, IL); courses I taught there as well as at the University of Idaho in 1975-1976 included mammalogy, ornithology, biogeography, and ecology. I continue to be involved in a long-term ecological study of small mammals, vertebrate predators, plants, and other organisms in a semiarid community near La Serena, north-central Chile. Now in its 27th year, we are conducting experimental manipulations of predators, competitors, and herbivores, and monitoring long-term responses of the biota to on-going climatic change supported by grants from the National Science Foundation, FONDECYT Chile, and the Institute of Ecology and Biodiversity (Santiago).
Lab: Gibb Hall 235
Office: (208) 885-6057
My background is in endocrine regulation of growth in fishes, focusing on the roles of growth hormone and the insulin-like growth factors. A general goal of my research is to develop bioindicators based on fish physiology and endocrinology, and to apply these in the conservation and management of fish populations. In my current position, I am developing methods to capture, evaluate, and recondition post-spawning anadromous steelhead kelts. I am employed by the Columbia River Inter-Tribal Fish Commission (CRITFC), and stationed in the Department of Biological Sciences at the University of Idaho.
Research Interests: I am broadly interested in mathematical biology, developing and applying mathematical techniques to answer important biological questions. Much of my research uses mathematical methods to analyze how animals process nutrients and toxins with applications in medicine and ecology. I have applied mathematical methods to issues as diverse as acetaminophen (paracetamol, Tylenol) overdose, incorporation of stable isotopes into animal tissues, and microbial detoxification of ingested toxins in mammals. The mathematics are diverse, including dynamical systems, bifurcation theory, probability, inverse methods, statistics, numerical analysis, and simulations.
Erica Bree Rosenblum
The Rosenblum lab studies the processes that generate and impact biological diversity. We are particularly interested in both sides of the evolutionary speciation/extinction “coin” and in determining the mechanisms of rapid adaptation of animals to changing environments. We work across levels of biological organization (from genes to phenotypes to behaviors to community assemblages) and use a variety of methodologies (from genomics to field ecology). Topically, many of our projects focus on reptile and amphibians in the western US. Currently, we are studying disease-related declines in amphibians and ecological speciation in lizards, but we are open to other collaborations in evolutionary ecology, ecological genomics, and global change biology.
R. Frank Rosenzweig
The overall goal of my research is to elucidate the mechanisms that produce and maintain diversity in microbial populations. This research is grounded in the belief that to understand the adaptive role of genetic variation we must understand the physiological consequences of differences in gene expression. My lab group is engaged in several projects related to this theme. In collaboration with researchers at Stanford University we are investigating how yeast and bacterial genomes respond to chronic resource limitation over evolutionary time. Replicate populations of Saccharomyces cerevisae and Escherichia coli originating from a common ancestor are propagated clonally for hundreds of generations under nutrient-limiting conditions. The tempo of evolutionary change is inferred from changes in the frequency of neutral markers in these populations, and a living record of the evolutionary trajectories is preserved by periodically archiving samples as -80°C glycerol stocks. Evolved strains and their ancestor can then be compared physiologically and genetically in order to understand the basis for differences in Darwinian fitness. The complete sequencing of these genomes makes it possible to construct DNA microarrays that hybridize specifically to all open reading frames and most intergenic regions. Using arrays we can now globally assess how changes in genome architecture and transcript levels underlie, or attend, evolutionary adaptation to limiting resources.
Irvin R. Schultz
Pacific Northwest National Laboratory
Research Areas: Ecotoxicology and Biotechnology, Marine and Coastal Resources, Marine and Environmental Chemistry, Water Resources Modeling
School of Health & Science
Department of Biology
Northwest Nazarene University
Chronic Inflammation in the Alzheimer's Disease Brain
Dr. Strohmeyer’s research currently encompasses the following four detailed objectives:
- Characterizing the expression pattern of each C/EBP isoform in human brain tissue and in brain cell cultures.
- Assessing the functionality of C/EBPs in modulating the expression of cytokine, chemokine, complement, iNOS, and other inflammatory genes.
- Assessing the role of C/EBPs in glial cell activation and differentiation in response to inflammatory stimuli and amyloid protein.
- Determining whether C/EBPs may be modulated by anti-inflammatory drugs such as non-steroidal anti-inflammatory drugs (NSAIDs) (i.e. ibuprofen), cholesterol-lowering drugs collectively known as statins, and natural compounds such as plant-derived polyphenols.