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Biomedical subjects

Joseph J Cullen

Publications and source records attributed to Joseph J Cullen.

24 records · Page 2Linked to original sources
PubMed2002

Intranasal mupirocin to prevent postoperative Staphylococcus aureus infections.

BACKGROUND: Patients with nasal carriage of Staphylococcus aureus have an increased risk of surgical-site infections caused by that organism. Treatment with mupirocin ointment can reduce the rate of nasal carriage and may prevent postoperative S. aureus infections. METHODS: We conducted a randomized, double-blind, placebo-controlled trial to determine whether intranasal treatment with mupirocin reduces the rate of S. aureus infections at surgical sites and prevents other nosocomial infections. RESULTS: Of 4030 enrolled patients who underwent general, gynecologic, neurologic, or cardiothoracic surgery, 3864 were included in the intention-to-treat analysis. Overall, 2.3 percent of mupirocin recipients and 2.4 percent of placebo recipients had S. aureus infections at surgical sites. Of the 891 patients (23.1 percent of the 3864 who completed the study) who had S. aureus in their anterior nares, 444 received mupirocin and 447 received placebo. Among the patients with nasal carriage of S. aureus, 4.0 percent of those who received mupirocin had nosocomial S. aureus infections, as compared with 7.7 percent of those who received placebo (odds ratio for infection, 0.49; 95 percent confidence interval, 0.25 to 0.92; P=0.02). CONCLUSIONS: Prophylactic intranasal application of mupirocin did not significantly reduce the rate of S. aureus surgical-site infections overall, but it did significantly decrease the rate of all nosocomial S. aureus infections among the patients who were S. aureus carriers.

Administration, Intranasal↗
PubMed2002

Expression of inducible nitric oxide synthase in the lower esophageal sphincter of the endotoxemic opossum.

BACKGROUND: Endotoxin modulates esophageal motor function by increasing nitric oxide (NO) production. The aims of this study were to examine inducible nitric oxide synthase (iNOS) induction in the lower esophageal sphincter (LES) of endotoxemic opossums and to investigate the effects of aminoguanidine (AG), a selective inhibitor of iNOS, on plasma nitrite/nitrate levels and on iNOS protein and mRNA expression after exposure to lipopolysaccharide (LPS). METHODS: Before and 12 h after the intravenous administration of LPS and/or AG, plasma nitrite/nitrate levels were determined. The iNOS protein and mRNA expression were investigated in the tissues taken from the LES by Western blot and reverse-transcriptase polymerase chain reaction (RT-PCR). RESULTS: Plasma nitrite/nitrate levels were significantly increased by LPS. The increase in plasma nitrite/nitrate produced by LPS was significantly decreased by AG. Western blot and RT-PCR demonstrated that iNOS expression was markedly increased by LPS, and attenuated slightly by AG. CONCLUSIONS: These studies support the hypothesis that endotoxin increases NO production by the induction of iNOS protein and mRNA.

Animals↗
PubMed2000

Preventing Staphylococcus Infections in High-Risk Patients.

UP to 30% of those who undergo surgery potentially develop a surgical site infection depending on the procedure performed. Infection increases the risk of further complications, lengthens hospital stays and increases management costs. A significant proportion of surgical site infections are caused by Staphyloccoccus spp. and prior nasal carriage is a risk factor for post surgical infection.

Journal Article↗
PubMedDate not supplied

Mechanisms of impaired gallbladder contractile response in chronic acalculous cholecystitis.

The mechanisms involved in the impaired gallbladder contractile response in chronic acalculous cholecystitis are unknown. To determine the mechanisms that may lead to impaired gallbladder emptying in chronic acalculous cholecystitis, gallbladder specimens removed during hepatic resection (controls) and after cholecystectomy for chronic acalculous cholecystitis were attached to force transducers and placed in tissue baths with oxygenated Krebs solution. Electrical field stimulation (EFS) (1 to 10 Hz, 0.1 msec, 70 V) or the contractile agonists, CCK-8 (10(-9) to 10(-5)) or K(+) (80 mmol/L), were placed separately in the tissue baths and changes in tension were determined. Patients with chronic acalculous cholecystitis had a mean gallbladder ejection fraction of 12% +/- 4%. Pathologic examination of all gallbladders removed for chronic acalculous cholecystitis revealed chronic cholecystitis. Spontaneous contractile activity was present in gallbladder strips in 83% of control specimens but only 29% of gallbladder strips from patients with chronic acalculous cholecystitis (P < 0.05 vs. controls). CCK-8 contractions were decreased by 54% and EFS-stimulated contractions were decreased by 50% in the presence of chronic acalculous cholecystitis (P < 0.05 vs. controls). K(+)-induced contractions were similar between control and chronic acalculous cholecystitis gallbladder strips. The impaired gallbladder emptying in chronic acalculous cholecystitis appears to be due to diminished spontaneous contractile activity and decreased contractile responsiveness to both CCK and EFS.

Adult↗
PubMedDate not supplied

Human pancreatic carcinoma cells activate maspin expression through loss of epigenetic control.

The maspin gene is not expressed in normal human pancreas, but its expression is acquired during human pancreatic carcinogenesis. In other normal human cells and their malignant counterparts, maspin expression is controlled through the epigenetic state of its promoter. In studies presented herein, we used bisulfite genomic sequencing and chromatin immunoprecipitation studies to show that maspin-negative pancreas cells have a methylated maspin promoter, and that the associated H3 and H4 histones are hypoacetylated. In contrast to normal pancreas, four of six human pancreatic carcinoma cell lines investigated displayed activation of maspin expression. This activation of maspin expression in pancreatic carcinoma cells was linked to demethylated promoters and hyperacetylation of the associated H3 and H4 histones. In addition, 5-aza-2'-deoxycytidine treatments activated maspin expression in the two maspin-negative pancreatic carcinoma cell lines, suggesting a causal role for cytosine methylation in the maintenance of a transcriptionally silent maspin gene. Thus, human pancreatic carcinoma cells acquire maspin expression through epigenetic derepression of the maspin locus, and in so doing appear to co-opt a normal cellular mechanism for the regulation of this gene.

Azacitidine↗