Relationship between changes in the public health nurses' workforce and the empirical Bayes estimates of standardized mortality ratio: a longitudinal ecological study of municipalities in Japan.

BACKGROUND: The role of public health nurses (PHNs) in the community is expected to become increasingly important, along with the promotion of a comprehensive community care system. However, a comprehensive study of all municipalities is yet to be undertaken, and the relationship between the workforce of PHNs and health indicators is yet to be clarified. This study examined the effect of workforce change among PHNs, one of the structural indicators of PHNs' activities regarding changes in the empirical Bayes estimate of standardized mortality ratios (EBSMRs). METHODS: An ecological study was conducted using municipality-level aggregate data. The data used were publicly available Japanese government statistics. The first-difference model of panel data analysis was used to examine the relationship between changes in EBSMR and changes in the number of PHNs per 100,000 population from 2010 to 2015, adjusting for the effects of population and other healthcare resources, including the number of physicians, medical clinics, general hospitals, and welfare facilities. The variation by the 47 prefectures was added to the linear model as a random effect. We also performed a sensitivity analysis using the full Bayesian inference using the Besag-York-Mollie model. RESULTS: For males, EBSMRs for all causes and malignant neoplasms significantly decreased with an increase in the number of PHNs per population (coefficients: -1.00 and -0.89, p values: 0.008 and 0.043, respectively). For females, although all EBSMRs except malignant neoplasms showed decreased tendencies due to the increase in the number of PHNs per population, none of them were significant. The full Bayesian inference confirmed these associations. CONCLUSIONS: An increase in the number of PHNs per population was significantly associated with a greater reduction in deaths from all causes and malignant neoplasms in males. The results of the full Bayesian inference also suggest that the workforce of PHNs may be related to changes in standardized mortality ratios for deaths from all causes in females.

The association between high birth weight and the risks of childhood CNS tumors and leukemia: an analysis of a US case-control study in an epidemiological database.

BACKGROUND: High birth weight (BW), 4000 g or larger, is an established risk factor for childhood leukemia. However, its association with central nervous system (CNS) tumor risk is yet unclear. The present study examined it, analyzing data obtained from a case-control study conducted among three states from the US. The association with childhood leukemia risk was also further examined. METHODS: In this study, a data set provided by the Comprehensive Epidemiologic Data Resource was analyzed with an official permission. The original case-control study was conducted to examine the association between paternal preconception exposure to ionizing radiation and childhood cancer risk. Cases with childhood cancer were mainly ascertained from local hospitals, and controls were selected, matched with birth year (1-year category), county of residence, sex, ethnicity and maternal age (+/-2 years). Since the ID numbers were unavailable, conventional logistic analyses were conducted adjusting for those matching variables except for the county of residence. In addition to those variables, gestational age, age at diagnosis and study sites as covariables were included in the logistic models. RESULTS: Analyzed subjects were 72 CNS tumor cases, 124 leukemia cases and 822 controls born from 1945 to 1989. The odds ratios (ORs) of CNS tumor risk for children with low BWs (<2500 g) and high BWs (>4000 g) were 2.0 (95% confidence interval [CI]) = 0.7, 5.9) and 2.5 (95%CI = 1.2, 5.2)], respectively. When high-BW children were restricted to those who were large for gestational age (LGA), the OR for high-BW children remained similar (OR = 2.7; 95%CI = 1.1, 6.2). On the other hand, the ORs of leukemia risk for children with low and high BWs were 0.8 (95%CI = 0.2, 3.0) and 1.4 (95%CI = 0.7, 2.6), respectively. In the normal range of BW (2500-4000 g), higher BW was positively associated with CNS tumor risk (beta = 0.0011, p for trend = 0.012). However, the association with leukemia risk was not significant (beta = -0.0002, p for trend = 0.475). CONCLUSION: High-BW and LGA children had an elevated childhood CNS tumor risk. In the normal BW range, the BW itself was positively related to CNS tumor risk. No significant association between BW and childhood leukemia risk was observed in this study.

Radiation-induced Epstein-Barr virus reactivation in gastric cancer cells with latent EBV infection.

Epstein-Barr virus, a ubiquitous human herpes virus with oncogenic activity, can be found in 6%-16% of gastric carcinomas worldwide. In Epstein-Barr virus-associated gastric carcinoma, only a few latent genes of the virus are expressed. Ionizing irradiation was shown to induce lytic Epstein-Barr virus infection in lymphoblastoid cell lines with latent Epstein-Barr virus infection. In this study, we examined the effect of ionizing radiation on the Epstein-Barr virus reactivation in a gastric epithelial cancer cell line (SNU-719, an Epstein-Barr virus-associated gastric carcinoma cell line). Irradiation with X-ray (dose = 5 and 10 Gy; dose rate = 0.5398 Gy/min) killed approximately 25% and 50% of cultured SNU-719 cells, respectively, in 48 h. Ionizing radiation increased the messenger RNA expression of immediate early Epstein-Barr virus lytic genes (BZLF1 and BRLF1), determined by real-time reverse transcription polymerase chain reaction, in a dose-dependent manner at 48 h and, to a slightly lesser extent, at 72 h after irradiation. Similar findings were observed for other Epstein-Barr virus lytic genes (BMRF1, BLLF1, and BcLF1). After radiation, the expression of transforming growth factor beta 1 messenger RNA increased and reached a peak in 12-24 h, and the high-level expression of the Epstein-Barr virus immediate early genes can convert latent Epstein-Barr virus infection into the lytic form and result in the release of infectious Epstein-Barr virus. To conclude, Ionizing radiation activates lytic Epstein-Barr virus gene expression in the SNU-719 cell line mainly through nuclear factor kappaB activation. We made a brief review of literature to explore underlying mechanism involved in transforming growth factor beta-induced Epstein-Barr virus reactivation. A possible involvement of nuclear factor kappaB was hypothesized.