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Theories about crime control in Japan have largely been based around two opposing traditions. On the one hand, cultural explanations have emphasized the exceptional attributes of Japanese social relations that contribute towards shaming and re-integrative processes. On the other hand, more recent explanations assert that Japanese crime control is converging with other countries, particularly towards penal populism. Both approaches tend to reduce explanations to a monolithic characterization that disguises variegation within Japan. Through considering the governance of illegal drug use and the Kamagasaki area of Osaka, a 'geo-historical' perspective is advocated to better capture the complexity and contradictions of globalizing processes and social culture and their resulting manifestations in crime control within contemporary Japan. [ABSTRACT FROM AUTHOR]

Study Question: What is the impact of cancer in females aged ≤39 years on subsequent chance of pregnancy?Summary Answer: Cancer survivors achieved fewer pregnancies across all cancer types, and the chance of achieving a first pregnancy was also lower.What Is Known Already: The diagnosis and treatment of cancer in young females may be associated with reduced fertility but the true pregnancy deficit in a population is unknown.Study Design, Size, Duration: We performed a retrospective cohort study relating first incident cancer diagnosed between 1981 and 2012 to subsequent pregnancy in all female patients in Scotland aged 39 years or less at cancer diagnosis (n = 23 201). Pregnancies were included up to end of 2014. Females from the exposed group not pregnant before cancer diagnosis (n = 10 271) were compared with general population controls matched for age, deprivation quintile and year of diagnosis.Participants/materials, Setting, Methods: Scottish Cancer Registry records were linked to hospital discharge records to calculate standardized incidence ratios (SIR) for pregnancy, standardized for age and year of diagnosis. Linkage to death records was also performed. We also selected women from the exposed group who had not been pregnant prior to their cancer diagnosis who were compared with a matched control group from the general population. Additional analyses were performed for breast cancer, Hodgkin lymphoma, leukaemia, cervical cancer and brain/CNS cancers.Main Results and the Role Of Chance: Cancer survivors achieved fewer pregnancies: SIR 0.62 (95% CI: 0.60, 0.63). Reduced SIR was observed for all cancer types. The chance of achieving a first pregnancy was also lower, adjusted hazard ratio = 0.57 (95% CI: 0.53, 0.61) for women >5 years after diagnosis, with marked reductions in women with breast, cervical and brain/CNS tumours, and leukaemia. The effect was reduced with more recent treatment period overall and in cervical cancer, breast cancer and Hodgkin lymphoma, but was unchanged for leukaemia or brain/CNS cancers. The proportion of pregnancies that ended in termination was lower after a cancer diagnosis, and the proportion ending in live birth was higher (78.7 vs 75.6%, CI of difference: 1.1, 5.0).Limitations, Reasons For Caution: Details of treatments received were not available, so the impact of specific treatment regimens on fertility could not be assessed. Limited duration of follow-up was available for women diagnosed in the most recent time period.Wider Implications Of the Findings: This analysis provides population-based quantification by cancer type of the effect of cancer and its treatment on subsequent pregnancy across the reproductive age range, and how this has changed in recent decades. The demonstration of a reduced chance of pregnancy across all cancer types and the changing impact in some but not other common cancers highlights the need for appropriate fertility counselling of all females of reproductive age at diagnosis.Study Funding/competing Interest(s): This study was funded by NHS Lothian Cancer and Leukaemia Endowments Fund. Part of this work was undertaken in the MRC Centre for Reproductive Health which is funded by the MRC Centre grant MR/N022556/1. RAA has participated in Advisory Boards and/or received speaker's fees from Beckman Coulter, IBSA, Merck and Roche Diagnostics. He has received research support from Roche Diagnostics, Ansh labs and Ferring. The other authors have no conflicts to declare. [ABSTRACT FROM AUTHOR]

Poor environmental conditions and poor child health in remote Australian Aboriginal communities are a symptom of a disjuncture in the cultures of a disadvantaged (and only relatively recently enfranchised) minority population and a proportionally large, wealthy dominant immigrant population, problematic social policies and the legacy of colonialism. Developing effective health promotion interventions in this environment is a challenge. Taking an ecological approach, the objective of this study was to identify the key social, economic, cultural and environmental factors that contribute to poor hygiene in remote Aboriginal communities, and to determine approaches that will improve hygiene and reduce the burden of infection among children. The methods included a mix of quantitative and qualitative community-based studies and literature reviews. Study findings showed that a combination of crowding, non-functioning health hardware and poor standards of personal and domestic hygiene underlie the high burden of infection experienced by children. Also, models of health promotion drawn from developed and developing countries can be adapted for use in remote Australian Aboriginal community contexts. High levels of disadvantage in relation to social determinants of health underlie the problem of poor environmental conditions and poor child health in remote Australian Aboriginal communities. Measures need to be taken to address the immediate problems that impact on children's health—for example, by ensuring the availability of functional and adequate water and sanitation facilities—but these interventions are unlikely to have a major effect unless the underlying issues are also addressed. [ABSTRACT FROM PUBLISHER]

A correction is presented to the article "Crime control in Japan: exceptional,convergent or what else" attributing to Johnson, E. instead of Johnson, D.

Background Survivors of childhood leukemia and lymphoma experience high risks of second malignant neoplasms. We quantified such risk using a large dataset from 13 population-based cancer registries. Methods The registries provided individual data on cases of leukemia, Hodgkin lymphoma, and non-Hodgkin lymphoma occurring in children aged 0–14 years and on subsequent second malignant neoplasms for different time periods from 1943 to 2000. Risks of second malignant neoplasms were assessed through standardized incidence ratios (SIRs) and corresponding 95% confidence intervals (CIs), using the incidence rates in the general populations covered by the registries as a reference. Cumulative absolute risks were also calculated. Results A total of 133 second malignant neoplasms were observed in 16540 patients (12731 leukemias, 1246 Hodgkin lymphomas, and 2563 non-Hodgkin lymphomas) after an average follow-up of 6.5 years. The most frequent second malignancies after leukemia were brain cancer (19 cases, SIR = 8.52, 95% CI = 5.13 to 13.3), non-Hodgkin lymphoma (nine cases, SIR = 9.41, 95% CI = 4.30 to 17.9), and thyroid cancer (nine cases, SIR = 18.8, 95% CI = 8.60 to 35.7); the most frequent after Hodgkin lymphoma were thyroid cancer (nine cases, SIR = 52.5, 95% CI = 24.0 to 99.6), breast cancer (six cases, SIR = 20.9, 95% CI = 7.66 to 45.4), and neoplasms of skin (non-melanoma) (six cases, SIR = 34.0, 95% CI = 12.5 to 74.0); and the most frequent after non-Hodgkin lymphoma were thyroid cancer (six cases, SIR = 40.4, 95% CI = 14.8 to 88.0) and brain cancer (four cases, SIR = 6.97, 95% CI = 1.90 to 17.9). Cumulative incidence of any second malignant neoplasm was 2.43% (95% CI = 1.09 to 3.78), 12.7% (95% CI = 8.29 to 17.2), and 2.50% (95% CI = 1.04 to 3.96) within 30 years from diagnosis of leukemia, Hodgkin lymphoma, and non-Hodgkin lymphoma, respectively. Conclusions This population-based study provides, to our knowledge, the most precise and up-to-date estimates for relative and absolute risks of second malignant neoplasms after childhood leukemia and lymphoma. [ABSTRACT FROM AUTHOR]

Studies of pancreatic cancer in the setting of second primary malignant neoplasms can provide etiologic clues. An international multicenter study was carried out using data from 13 cancer registries with a registration period up to year 2000. Cancer patients were followed up from the initial cancer diagnosis, and the occurrence of second primary malignant neoplasms was compared with expected values derived from local rates, adjusting for age, sex, and period of diagnosis. Results from individual registries were pooled by use of a fixed-effects model. People were at higher risk of developing pancreatic cancer within 10 years of a diagnosis of cancers of the pharynx, stomach, gallbladder, larynx, lung, cervix, corpus uteri, bladder, and eye and 10 years or later following a diagnosis of cancers of the stomach, colon, gallbladder, breast, cervix, placenta, corpus uteri, ovary, testis, bladder, kidney, and eye, as well as Hodgkin's and non-Hodgkin's lymphomas. Pancreatic cancer was connected with smoking-related cancers, confirming the etiologic role of tobacco. The associations with uterine and ovarian cancers suggest that reproductive factors might be implicated in pancreatic carcinogenesis. The elevated pancreatic cancer risk in young patients observed among several types of cancer implies a role of genetic factors. Radiotherapy is also suggested as a risk factor. [ABSTRACT FROM AUTHOR]

Regional and national databases of routinely collected data contain large quantities of health information, usually covering whole populations and often spanning prolonged time periods. Using routine data involves identifying useful sources, assessing the quality of the data and deciding whether what is available is ‘fit for purpose’. As long as adequate care is taken, these data may be used in a number of different ways beyond their traditional uses for population health assessments and health service planning. [ABSTRACT FROM PUBLISHER]

Chronic administration of alachlor in the diet at a level of 126 mg/kg/day has previously been shown to cause an increase in benign thyroid follicular cell tumors in male Long—Evans rats. Studies were conducted to elucidate the mechanism of the alachlor-induced thyroid tumors in the male rat by evaluating changes in parameters that are collectively associated with a hormonally mediated mode of action for thyroid neoplasia. Male Long—Evans rats were administered 126 mg alachlor/kg body wt/day via the diet for up to 120 days. One group of animals was removed from alachlor-treated diet after 60 days and received untreated diet for an additional 60 days. Liver and thyroid weights and serum levels of triiodothyronine (T3), thyroxine (T4) and thyroid-stimulating hormone (TSH), as well as hepatic uridine diphosphate glucuronosyl transferase (UDPGT) activity, were determined at 7, 14, 28, 60, and 120 days of treatment. Liver and thyroid weights, hepatic UDPGT activity, and circulating levels of TSH were significantly increased in animals administered alachlor. These increases were seen as early as 7 days after alachlor administration. Circulating levels of T4 in alachlor-treated animals were significantly decreased compared with controls at 7 days, but had returned to control levels by 60 days. T3 levels were elevated at all time points except at 28 days. The changes in TSH and T3 levels, hepatic UDPGT activity, and liver weights were all reversible on elimination of alachlor from the diet. Thyroid weights did not completely return to control levels after removal of alachlor from the diet, although some recovery was evident. The results of this study clearly suggest that alachlor-induced thyroid neoplasia, observed in previous chronic bioassays with alachlor, was associated with increases in circulating TSH levels. Increased metabolism of T4 via hepatic enzymatic conjugation (i.e., T4-UDPGT) appeared to be responsible for the increased TSH levels. These effects were shown to be reversible on cessation of exposure to alachior. In summary, evidence is presented for a hormonally mediated process for the development of thyroid follicular cell tumors. [ABSTRACT FROM AUTHOR]

Metabolism of Glyphosate in Sprague-Dawley Rats: Tissue Distribution, Identification, and Quantitation of Glyphosate-Derived Materials following a Single Oral Dose. BREWSTER, D. W., WARREN, J., AND HOPKJNS, W. E., 11(1991). . . . 17,43–51. Five groups of male Sprague-Dawley rats were orally administered a mixture of [C]- and [C]-glyphosate (-phosphonomethylglycine) at a dose level of 10 mg/kg body weight. The majority of radioactivity 2 hr after administration was associated with the gastrointestinal contents and small intestinal tissue. Approximately 35–40% of the administered dose was absorbed from the gastrointestinal tract, and urine and feces were equally important routes of elimination. The total body burden 7 days after administration was approximately 1% of the administered dose and was primarily associated with the bone. Total recovery for this study ranged from 95 to 102% of the administered dose. Metabolic profiles of tissues containing greater than 1% of the administered dose at various times after administration indicated that nearly 100% of the body burden of radioactivity was present as unmetabolized parent glyphosate. A minor component constituting ≪0.1% of the administered dose (≪0.4 ppm) was observed in colon tissue from animals 2 hr after the administration of glyphosate and was also present in the GI contents of one animal 28 hr after administration of the radiolabel. The retention time for this metabolite was similar, but not identical, to the retention time for AMPA (aminomethylphosphonic acid), the major bacterial metabolite of glyphosate found in soil. Tissue extraction efficiency was always greater than 90% and stability assays indicated no significant effect of storage on either parent glyphosate or AMPA. The results from this study indicate that virtually no toxic metabolites of glyphosate were produced since there was little evidence of metabolism and essentially 100% of the body burden was parent compound with no significant persistence of material [ABSTRACT FROM PUBLISHER]

The Acute Toxicity of 2,3,4,7,8-Pentachlorodibenzofuran (4PeCDF) in the Male Fischer Rat. Brewster, D. W., Uraih, L. C, and Birnbaum, L. S. . 11, 236-249 Polychlorinated dibenzofurans are ubiquitous environmental pollutants which have great potential for human exposure. To characterize the toxicity of 2,3,4,7,8-pentachlorodibenzofuran (4PeCDF), male F344 rats were administered a single oral dose of 0, 100, 250, 500, 1000, or 2000 μg 4PeCDF/kg. A progressive and dose-dependent loss of body weight was evident by 3 days after treatment. Signs of toxicity included piloerection, hair loss, hypoactivity, morbidity, and death. Death occurred as soon as 14 days after treatment and continued throughout the 35-day observation period. The LD5O/35 was estimated to be 916 μgAg with a 95% confidence interval of 565–1484 μgAg. Dose-dependent increases were observed in serum cholesterol, tri-glyceride, and bile acid concentrations and in sorbitol dehydrogenase and aspartate aminotrans-ferase activities. The hematocrit, hemoglobin, mean corpuscular volume, and mean corpuscular hemoglobin concentrations were depressed in a dose-dependent fashion. Hepatic ethoxyresoru-fin-O-deethylase (EROD) activity was increased in all treatment groups approximately 25 times above that of control animals. Lymphoid depletion in the thymus and spleen was observed in the three highest doses and thymic atrophy was present at all dose levels. Absolute liver weight and the livenbody weight ratio were significantly increased above controls. Hepatotoxicity was dose-dependent and was characterized by lipid accumulation resulting in hepatocytomegaly. Epithelial hyperplasia and focal ulcerations of the forestomach was observed in animals administered 500 μg 4PeCDF/kg. Spontaneous cardiomyopathy was exacerbated by treatment with 2000 μgKg. Since 4PeCDFand 2,3,7,8-tetrachlorodibenzo--dioxin (TCDD) produce a similiar spectrum of toxic effects, the biochemical mechanism(s) of toxicity for these chemicals may be Similar. [ABSTRACT FROM PUBLISHER]

The article focuses on the suggestion of Carinci and colleagues on the need to emphasize the harmonization of data protection between all European Member States to update the European Union Data protection directive. It says that the public health research especially in the Nordic countries will worsen due to the proposal. It adds that an epidemiological studies will not be conducted in unbiased, reliable, and efficient manner at a low cost if their proposal will be carried out.