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Background This study was conducted to identify clinical factors associated with development of infection caused by methicillin-resistant Staphylococcus aureus (MRSA) among hospitalized patients with nasal MRSA colonization. Methods We conducted a prospective cohort with nested case-control study at a 672-bed, public, academic hospital in Dallas, Texas. The study duration was from January 1, 2008, to July 28, 2009. From the cohort of patients who had presence of nasal colonization with MRSA at admission, we identified patients who developed subsequent infection with MRSA during a 3-month period. We compared these patients (cases) with colonized patients who remained uninfected (controls; 2 controls per case). We collected demographic and clinical data and performed statistical analyses. Results During the 19-month study period, 426 patients were found to have nasal colonization with MRSA. Of these, 36 (8.5%) developed a subsequent infection with MRSA within 3 months. When these 36 cases were compared with 72 controls, the factors independently associated with the development of subsequent infection were development of pressure ulcer during hospital stay (adjusted odds ratio, 5.82; 95% confidence interval: 2.21–15.31; P value = .000) and preadmission steroid therapy (adjusted odds ratio, 13.2; 95% confidence interval: 2.44–70.97; P value = .003). Conclusion History of steroid therapy prior to admission and development of pressure ulcer are associated with increased risk of subsequent MRSA infection in patients nasally colonized with MRSA.

To determine if factors present in the aqueous humor (AH) protect the corneal endothelium from apoptosis.Mouse and human corneal endothelial cells were cultured in vitro, and apoptosis was induced by nutrient deprivation. AH and supernatant from iris/ciliary body (I/CB) cell cultures were tested for their effect on corneal endothelial cell apoptosis. The effect of I/CB supernatant on Fas, Bax, and Bcl-2 gene transcription was evaluated by Northern blotting. I/CB supernatant was subjected to proteinase analysis to identify the apoptosis inhibitory factor(s).Rabbit AH and supernatant from mouse I/CB cell cultures inhibited the apoptosis of mouse and human immortalized corneal endothelial cell lines. The inhibition of apoptosis was associated with an upregulation of Bcl-2 gene transcription and Bcl-2 protein expression. Bax gene expression was not significantly affected by I/CB cell supernatant. Induction of apoptosis by stimulation of the Fas receptor was unaffected by I/CB cell supernatant. Protease analyses indicated that the apoptosis inhibitory factor was a protein.The inability of corneal endothelial cells to undergo mitosis renders the corneal endothelium vulnerable to loss of physiological function through cellular attrition. However, a protein(s) produced by I/CB cells and present in the AH, upregulates Bcl-2 gene transcription and protects the corneal endothelial cells from apoptosis.