Feature identification in circadian rhythms of mice strains using in vivo information.

The objective of this work was to identify strain-specific characteristics from real-time measurements of circadian rhythms of two inbred mouse strains. In particular, heart rate, temperature, and activity data collected from A/J and C57BL/6J (B6) mice using telemetry are analyzed. The influence of activity on heart rate and temperature is minimized by correlation analysis followed by regression analysis.

Probabilistic modeling of DNA mismatch repair effects on cell cycle dynamics and iododeoxyuridine-DNA incorporation.

Previous studies in our laboratory have described increased and preferential radiosensitization of mismatch repair-deficient (MMR(-)) HCT116 colon cancer cells with 5-iododeoxyuridine (IUdR). Indeed, our studies showed that MMR is involved in the repair (removal) of IUdR-DNA, principally the G:IU mispair. Consequently, we have shown that MMR(-) cells incorporate 25% to 42% more IUdR than MMR(+) cells, and that IUdR and ionizing radiation (IR) interact to produce up to 3-fold greater cytotoxicity in MMR(-) cells.

Antibiotic-induced enterococcal expansion in the mouse intestine occurs throughout the small bowel and correlates poorly with suppression of competing flora.

To test the hypothesis that establishing gastrointestinal colonization with multiresistant Enterococcus faecium (VRE) C68 results from expansion of the enterococcal population in the upper small bowel, we compared VRE quantities recovered from the proximal, middle, and distal segments of the small bowel from mice treated with different antimicrobial agents. Antibiotics associated with high-level VRE fecal colonization (cefotetan, ceftriaxone, clindamycin, and ticarcillin-clavulanic acid) increased VRE quantities in all small-bowel segments, whereas cefepime and piperacillin-tazobactam did not. Enterococcal expansion did not correlate with reductions in numbers of native gram-negative or anaerobic flora.