A multifactorial action plan improves hand hygiene adherence and significantly reduces central line-associated bloodstream infections.

BACKGROUND: Although hand hygiene (HH) is key to reducing health care-associated infections, it is well documented that health care worker (HCW) adherence to appropriate HH protocols is relatively low. METHODS: This was a collaborative quality improvement project with multiple interventions conducted in a 570-bed academic hospital in Columbia, MO between April 2006 and September 2012. A multimodal action plan to improve HH adherence among all HCWs was developed, addressing 4 key areas: staff education, staff accountability, hand sanitizer product selection and accessibility, and organizational culture. HH adherence and central line-associated bloodstream infection (CLABSI) rates were monitored as outcome measures. RESULTS: The overall HH adherence rate increased from 58% in April 2006 to 98% in September 2012. The adherence rates increased among all hospital units and among all HCW categories; in September 2012, HH adherence was 96% for physicians, 99% for nursing staff, and 99% for food services staff. CLABSI rates decreased over the same period, from 4.08 per 1000 device-days to 0.42 per 1000 device-days. CONCLUSIONS: This multifactorial quality improvement project resulted in an institution-wide increase in HH adherence and a significant decrease in CLABSIs.

Platelet activating factor-induced apoptosis is inhibited by ectopic expression of the platelet activating factor G-protein coupled receptor.

The pro-inflammatory lipid mediator platelet activating factor (PAF: 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine) accumulates in ischemia, epilepsy, and human immunodeficiency virus-1-associated dementia and is implicated in neuronal loss. The present study was undertaken to establish a role for its G-protein coupled receptor in regulating neurotoxicity. PC12 cells do not express PAF receptor mRNA as demonstrated by northern analysis and RT-PCR. In the absence of the G-protein coupled receptor, PAF (0.1-1 micro m) triggered chromatin condensation, DNA strand breaks, oligonucleosomal fragmentation, and nuclear disintegration characteristic of apoptosis. Lyso-PAF (0.001-1 micro m), the immediate metabolite of PAF, did not elicit apoptotic death. Concentrations of PAF or lyso-PAF that exceeded critical micelle concentration had physicochemical effects on plasma membrane resulting in necrosis. Apoptosis but not necrosis was inhibited by the PAF antagonist BN52021 (1-100 micro m) but not CV3988 (0.2-20 micro m). Ectopic PAF receptor expression protected PC12 transfectants from ligand-induced apoptosis. PAF receptor-mediated protection was inhibited by CV3988 (1 micro m). These data provide empirical evidence that: (i) PAF can initiate apoptosis independently of its G-protein coupled receptor; (ii) PAF signaling initiated by its G-protein coupled receptor is cytoprotective to PC12 cells; (iii) the pro- and anti-apoptotic effects of PAF on PC12 cells can be pharmacologically distinguished using two different PAF antagonists.