Reliability and validity of the Japanese version of the Peritraumatic Distress Inventory.

OBJECTIVE: To assess the reliability and validity of the Japanese version of the Peritraumatic Distress Inventory (PDI). METHOD: One hundred thirty-five participants with physical injury resulting from motor vehicle accidents were consecutively recruited in this cross-sectional study, from Aug. 18, 2005, to Jan. 8, 2008. A subsample (n=71) were retested on the PDI an average of 96.4 days after initial measure completion. RESULTS: Correlational analyses revealed an overall Cronbach's alpha coefficient of 0.83. The item-total correlations for the 13 items ranged from 0.29 to 0.75. The test-retest correlation coefficient was 0.61. The PDI was significantly correlated with the external validators such as peritraumatic dissociation as measured by the Peritraumatic Dissociative Experiences Questionnaire (PDEQ); the intrusion, avoidance and hyperarousal scores of the Impact of Events Scale-Revised (IES-R); and the depression and anxiety subscales of the Hospital Anxiety Depression Scale (HADS) (P<.01). CONCLUSION: The present study indicated that the Japanese version of the PDI has a high degree of internal consistency, acceptable reliability and a high degree of concurrent validity with measures of peritraumatic dissociation and posttraumatic symptoms. The Japanese version of the PDI can be used as a validated instrument in future research.

Speciation of antimony in PET bottles produced in Japan and China by X-ray absorption fine structure spectroscopy.

The oxidation state and coordination environment of antimony (Sb) incorporated into polyethylene terephthalate (PET) bottles were estimated based on X-ray absorption fine structure (XAFS) at Sb K-edge. Prior to XAFS analyses, Sb concentrations in 177 PET bottles collected in Japan and China were determined, showing that 30.5% and 100% of Japanese and Chinese PET bottles, respectively, contained more than 10 mg/kg of Sb. Most of the bottles used for aseptic cold filling and carbonated drinks contained a larger amount of Sb. Extended X-ray absorption fine structure (EXAFS) showed that the first neighboring atom of Sb in PET was estimated to be oxygen with a coordination number of about three. In addition, the contribution of Sb to Sb shell was discounted in the EXAFS, showing that Sb was not present as Sb2O3 in PET, although Sb was initially added as Sb2O3 in the production of PET. This information is consistent with the coordination environment estimated from the polycondensation reaction catalyzed by Sb, where Sb can be present as either Sb glycolate or Sb glycolate binding to the end group of the PET polymer. X-ray absorption near-edge structure (XANES) showed that Sb(III) initially added as Sb2O3 into PET was partially oxidized and the Sb(V) fractions reached approximately 50% in some samples. However, the oxidation state and coordination environment of Sb in PET had no relationship with the concentrations of Sb that leached into water from PET. Based on the present XAFS results and previous studies on the effects of temperature and others, it was concluded that the leaching behavior of Sb into water is primarily due to the degradation of PET itself, but is not related to the Sb species in the PET bottles.

Evaluation of glutathione deficiency in rat livers by microarray analysis.

Hepatic glutathione content was measured and gene expression data were obtained using an Affymetrix RG U34 array after treatment with tap water containing 20mM l-buthionine (S, R)-sulfoximine (BSO) to male F344 rats for four consecutive days. Both Spearman's and Pearson's correlation coefficients were calculated between the glutathione content and the mRNA content level obtained from the microarray analysis individually. Sixty-nine gene probes, which were statistically significant (Spearman's correlation, P < 0.05) and showed a Pearson's correlation coefficients (Pearson's r) less than -0.8 between mRNA content and hepatic glutathione content, were identified as glutathione deficiency-correlated probes. By comparing the hepatic gene expression profiles between BSO- and butylated hydroxyanisole (BHA)-treated rats, 14 probes of genes that showed an increase in the corresponding gene mRNA levels only after the BSO treatment were thought to be good indicators of glutathione deficiency. A principal component analysis successfully illustrated the time-course of hepatic gene expression after the treatment with acetaminophen, phenobarbital and clofibrate, and the expression profiles were thought to reflect the changes in hepatic glutathione levels. The identified gene probes in the present study would be useful as markers for assessing hepatocellular glutathione deficiency, or oxidative stress level, based on microarray data.

Molecular mechanism investigation of phenobarbital-induced serum cholesterol elevation in rat livers by microarray analysis.

Phenobarbital (PB) increases serum total cholesterol levels in rodents and humans. To investigate the underlying molecular mechanisms, we performed a microarray analysis on liver of rats treated repeatedly with 100 mg/kg PB, and examined the serum blood chemistry. The serum concentration of non-esterified fatty acids was decreased from day 1 to day 14 except for day 7, and that of cholesterol was increased from day 4 to day 14. The serum concentration of total ketone bodies was increased on day 7, and that of triglycerides was decreased on day 14. Transcript content of glycolytic genes was decreased by PB treatments, while that of lipoprotein lipase was continuously increased, suggesting a notion that repetitive PB treatments impaired glycolysis and stimulated lipolysis in the liver. The hypothesis was examined by using a previously reported flux-balance model. The increase in mRNA content of malic enzyme after the PB treatment agreed well with the flux-balance model result, suggesting the validity of our hypothesis. The findings also suggested that there was an abundance of acetyl-CoA and shortage of glycolytic products after the repeated PB treatments. Although ketogenesis would normally occur under such cellular conditions, it was only weakly observed after the repeated PB treatments, presumably owing to a decrease in HMG-CoA synthase mRNA content. On the other hand, the mRNA content of several cholesterogenic genes was slightly induced by PB treatments. Thus, serum chemistry and microarray results suggested that repeated PB treatments induced cholesterogenesis in rat livers, which may have contributed to the elevation of the serum total cholesterol concentration.

Effect of serum cholesterol on the mRNA content of amyloid precursor protein in rat livers.

Genes that showed mRNA content profiles, which correlated with serum concentrations of total cholesterol (T.CHO), were screened from the microarray data of phenobarbital (PB)- or clofibrate (CLO)-treated rat livers, and the correlation was evaluated based on Spearman's correlation coefficient. Many genes involved in the cholesterol or bile acid metabolism were highly correlated such as UDP-glucuronosyltransferase-21, apolipoprotein A-I and cMOAT. The mRNA content of the amyloid precursor protein (APP) showed the 5th highest correlation among the 8799 probes in the Affymetrix Rat Genome U34 Array. In the livers of rats fed a high-cholesterol (1%) diet for 33 days, serum T.CHO levels increased by 4.6-fold, and the hepatic APP mRNA content also increased by 1.9-fold compared to the control group. These data suggest that the hepatic APP mRNA content was affected by serum T.CHO, and that hepatic APP was involved in cholesterol metabolism in rat livers.

Gene expression profiles in pregnant rats treated with T-2 toxin.

Pregnant rats on day 13 of gestation were treated orally with T-2 toxin at a single dose of 2 mg/kg and sacrificed at 24 hours after treatment. Histopathologically, apoptosis was increased in the liver, placenta and fetal liver. Microarray analysis was performed to examine the gene expression in the liver, placenta, and fetal liver. The results of microarray analysis showed that the changes in the expression of apoptosis genes, metabolic enzymes and oxidative stress-related genes were detected in these tissues. Suppression of phase I and II enzymes-related genes expression in the liver, and suppression of phase II enzymes-related genes expression in the placenta and fetal liver were observed. Semiquantitive RT-PCR analysis also showed the same results as those of microarray analysis. From the results of microarray analysis and histopathological examination, T-2 toxin seems to induce oxidative stress in these tissues, following the changes in metabolism-related genes expression. These changes may alter the intracellular environments resulting in the induction of apoptosis. Further studies on the gene expression profiles at the earlier time point are necessary to clarify the detailed mechanisms of T-2 toxin-induced toxicity in pregnant rats.

Phylogenetic tree facilitates the understanding of gene expression data on drug metabolizing enzymes obtained by microarray analysis.

The gene expression data of drug metabolizing enzymes (DMEs) in male F344 rat livers were examined after treatments with phenobarbital (PB), clofibrate (CPIB), 3-methylcholanthrene (3-MC) or butylated hydroxyanisole (BHA) using an Affymetrix GeneChip system. Nucleotide sequence-based phylogenetic trees combined with a heat map, that presents both quantitative and qualitative data, were created. Most DME gene probes were successfully classified into the corresponding gene families, although a few were not due to the presence of non-coding or promoter region sequences in the target gene. There were also some data discrepancies among probes of the same gene family, indicating the inappropriate design of these probes. With this method, microarray probes with confusing nomenclature and quality differences can be identified. In addition, a good correlation between the gene expression data and protein data was confirmed, indicating the usefulness of this method for the comprehensive monitoring of DME activity in rat livers treated with xenobiotics.