People — adjunct and affiliate faculty

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.

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.

Pat came to the Upper Midwest Environmental Sciences Center in August of 2002. Her current research interests include inventory and monitoring processes and wildlife- habitat relationships modeling.

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.

Michael B. Laskowski

• Professor
• Office: Student Health Center 302
• Phone: +01 (208) 885-6696
• Lab: Student Health Center 307
• Lab Phone: +01 (208) 885-6904
• mlaskow [at] uidaho.edu

Laskowski’s main research interest is the development of the nervous system, specifically the understanding of cues used by developing neurons in selecting their appropriate targets. He examines the specificity of neuron development in two contexts: normal embryonic development in the mammalian neuromuscular junction and reinnervation of muscle after acute nerve injury. The techniques used combine morphology, electrophysiology and tissue culture.

This receptor uses glutamate as a transmitter. The NMDA receptor shows greater declines in binding of glutamate with increased age than any of the other glutamate receptors. We’ve found relationships between NMDA receptor binding and expressions of two NMDA receptor subunits, epsilon2 and epsilon1, during aging. We’ve also shown associations between age-related changes in NMDA binding densities and subunit expressions and declines in both working (short-term) and reference (long-term) memory ability.

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.

1. Characterizing the expression pattern of each C/EBP isoform in human brain tissue and in brain cell cultures.
2. Assessing the functionality of C/EBPs in modulating the expression of cytokine, chemokine, complement, iNOS, and other inflammatory genes.
3. Assessing the role of C/EBPs in glial cell activation and differentiation in response to inflammatory stimuli and amyloid protein.
4. 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.