Nosocomial outbreak of multidrug-resistant Pseudomonas aeruginosa caused by damaged transesophageal echocardiogram probe used in cardiovascular surgical operations.

Multidrug-resistant Pseudomonas aeruginosa (MDRP) is a major problem among hospital-acquired infections. We had a one-month outbreak of this strain at a university hospital in Osaka, Japan, from May to June 2004. To determine the cause of the outbreak, we collected and analyzed epidemiological information about the patients from whom MDRP was isolated, and performed microbiological investigations. MDRP was detected in respiratory specimens from eight patients in the intensive care unit. One of these patients developed severe lethal pneumonia accompanied by septicemia, and two contracted less severe non-lethal pneumonia. All the MDRP patients had been monitored with a contaminated transesophageal echocardiography (TOE) probe during their cardiac surgery. The TOE probe proved to have a defect 5 mm in diameter at the surface near the transducer, and the MDRP strain was traced to this defect. Pulsed-field gel electrophoresis showed that the strain isolated from the patients and from the TOE probe were genetically indistinguishable. After use of the damaged TOE probe was terminated, MDRP was not isolated from any patients who underwent cardiac surgery in the subsequent 8 years. In conclusion, TOE is routinely used during cardiac surgery and has been shown to have a significant clinical effect. Prevention of similar post-operative pneumonia outbreaks will require thorough infection control of TOE probes used for monitoring during cardiovascular surgery.

The coantioxidative effects of carboxyethyl-6-hydroxychromans and alpha-Tocopherol.

alpha-Tocopherol (alpha-Toc) is abundant in LDL and thought to prevent the oxidation of LDL together with various water-soluble antioxidants. Recently, it was reported that alpha-Toc and gamma-Toc metabolites, alpha-carboxyethyl-6-hydroxychromans (CEHC) and gamma-CEHC, are water-soluble antioxidants. In this study, we investigated the interaction between alpha-Toc and CEHC against 1,1-diphenyl-2-picryl-hydrazyl (DPPH) radicals and LDL oxidation. We administered 600 mg of alpha-Toc to healthy male volunteers to obtain LDL including high levels of alpha-Toc before antioxidant administration. The alpha-Toc content of their LDL was increased after consumption at 24 h (18.3 microg/mL) above the level before consumption (6.6 microg/mL). The lag time of LDL at 24 h after alpha-Toc consumption (alpha-Toc rich LDL) with alpha-CEHC (98.5+/-8.2 min) or gamma-CEHC (101.3+/-9.0 min) was longer than that of only alpha-Toc-rich LDL (78.1+/-9.0 min). Furthermore, we examined the interaction of LDL with CEHC and alpha-Toc in vitro (5-20 microg/mL). The lag times of 5 and 10 microg/mL alpha-Toc were 65.5+/-18.9 min and 69.5+/-15.5 min, and that of 20 microg/mL alpha-Toc (83.5+/-20.2 min) was longer than the control value (55.7+/-14.1 min). The lag time of 20 microg/mL alpha-Toc with alpha-CEHC (98.7+/-25.7 min) or gamma-CEHC (100.6+/-25.3 min) was longer than that of only alpha-Toc (83.5+/-20.2 min). These results suggest that CEHC has the potential to delay the oxidation of LDL, while enhancing the antioxidative activity of alpha-Toc both in vitro and ex vivo.

gamma-Tocopherol Accelerated Sodium Excretion in a Dose-Dependent Manner in Rats with a High Sodium Intake.

We have previously reported that gamma-tocopherol (gamma-Toc) displays a natriuretic potency in rats fed a NaCl diet and administered 20 mg gamma-Toc. In this study, we investigated whether gamma-Toc has natriuretic potency at a dose lower or higher than 20 mg in rats given a NaCl diet. Male rats were fed a control diet or a NaCl diet and administered either placebo or 10, 20 or 40 mg of gamma-Toc. The rat urine was collected for 24 hours (divided into 6 hour periods) and the 2,7,8-trimethyl-2-(2'-carboxyethyl)-6-hydroxychroman (gamma-CEHC) level, the sodium excretion content, and the urine volume were determined. The 24-hour gamma-CEHC and sodium levels in the urine of the NaCl groups given 20 mg or 40 mg gamma-Toc were significantly higher than those in the placebo group. The peak levels of urine sodium and gamma-CEHC in the NaCl group given 40 mg gamma-Toc appeared at 0-6 h, which was a more rapid increase than that seen in the group given 20 mg gamma-Toc. The 24-hour urine volumes of the NaCl groups given 10 and 20 mg gamma-Toc were significantly higher than the urine volume of the placebo group. Our findings suggested that gamma-Toc increased sodium excretion in a dose-dependent manner in rats fed a NaCl diet. Moreover, a high dose of gamma-Toc may accelerate its metabolism and cause an increase in the rate of sodium excretion.

Global gene expression analysis of gastric cancer by oligonucleotide microarrays.

To gain molecular understanding of carcinogenesis, progression, and diversity of gastric cancer, 22 primary human advanced gastric cancer tissues and 8 noncancerous gastric tissues were analyzed by high-density oligonucleotide microarray in this study. Based on expression analysis of approximately 6800 genes, a two-way clustering algorithm successfully distinguished cancer tissues from noncancerous tissues. Subsequently, genes that were differentially expressed in cancer and noncancerous tissues were identified; 162 and 129 genes were highly expressed (P < 0.05) >2.5-fold in cancer tissues and noncancerous tissues, respectively. In cancer tissues, genes related to cell cycle, growth factor, cell motility, cell adhesion, and matrix remodeling were highly expressed. In noncancerous tissues, genes related to gastrointestinal-specific function and immune response were highly expressed. Furthermore, we identified several genes associated with lymph node metastasis including Oct-2 or histological types including Liver-Intestine Cadherin. These results provide not only a new molecular basis for understanding biological properties of gastric cancer, but also useful resources for future development of therapeutic targets and diagnostic markers for gastric cancer.