CCAR-1 is a negative regulator of the heat-shock response in Caenorhabditis elegans.

Defects in protein quality control during aging are central to many human diseases, and strategies are needed to better understand mechanisms of controlling the quality of the proteome. The heat-shock response (HSR) is a conserved survival mechanism mediated by the transcription factor HSF1 which functions to maintain proteostasis. In mammalian cells, HSF1 is regulated by a variety of factors including the prolongevity factor SIRT1.

Fluorodeoxyuridine enhances the heat shock response and decreases polyglutamine aggregation in an HSF-1-dependent manner in Caenorhabditis elegans.

The heat shock response (HSR) protects cells from protein-denaturing stress through the induction of chaperones. The HSR is conserved in all organisms and is mediated by the transcription factor HSF-1. We show here that a compound commonly used to prevent larval development in Caenorhabditis elegans, 5-fluoro-2'-deoxyuridine (FUdR), can enhance heat shock induction of hsp mRNA in an HSF-1-dependent manner.

Microbial growth on the anesthesia machine.

The purpose of this study was to determine the amount of microbial growth that develops on the anesthesia machine after a full day's use in the operating room. This descriptive bacteriology study is relevant to anesthesia practice because of the proximity of the oropharynx and multiple body fluids to anesthesia equipment and the potential for cross-contamination to patients and staff. The Wilcoxon signed rank test was used to evaluate the change in colony-forming units (CFUs) before and after use of equipment.