Arsenic (As) and cadmium (Cd) concentrations in rice grains are a human health concern. We conducted field experiments to investigate optimal conditions of Eh and pH in soil for simultaneously decreasing As and Cd accumulation in rice. Water managements in the experiments, which included continuous flooding and intermittent irrigation with different intervals after midseason drainage, exerted striking effects on the dissolved As and Cd concentrations in soil through changes in Eh, pH, and dissolved Fe(II) concentrations in the soil. Intermittent irrigation with three-day flooding and five-day drainage was found to be effective for simultaneously decreasing the accumulation of As and Cd in grain. The grain As and Cd concentrations were, respectively, linearly related to the average dissolved As and Cd concentrations during the 3 weeks after heading. We propose a new indicator for expressing the degree to which a decrease in the dissolved As or Cd concentration is compromised by the increase in the other. For minimizing the trade-off relationship between As and Cd in rice grains in the field investigated, water management strategies should target the realization of optimal soil Eh of -73 mV and pH of 6.2 during the 3 weeks after heading.

Aims/hypothesis T helper type (Th) 17 cells have been shown to play important roles in mouse models of several autoimmune diseases that have been classified as Th1 diseases. In the NOD mouse, the relevance of Th1 and Th17 is controversial, because single-cytokinedeficient NOD mice develop diabetes similarly to wildtype NOD mice. Methods We studied the impact of IL-17/IFN-γ receptor double deficiency in NOD mice on the development of insulitis/diabetes compared with IL-17 single-deficient mice and wild-type mice by monitoring diabetes-related phenotypes. The lymphocyte phenotypes were determined by flow cytometric analysis. Results IL-17 single-deficient NOD mice showed delayed onset of diabetes and reduced severity of insulitis, but the cumulative incidence of longstanding diabetes in the IL-17-deficient mice was similar to that in wild-type mice. The IL-17/IFN-γ receptor double-deficient NOD mice showed an apparent decline in longstanding diabetes onset, but not in insulitis compared with that in the IL-17 single-deficient mice. We also found that double-deficient NOD mice had a severe lymphopenic phenotype and preferential increase in regulatory T cells among CD4 + T cells compared with the IL-17 single-deficient mice and wildtype NOD mice. An adoptive transfer study with CD4 + CD25 − T cells from young non-diabetic IL-17 single-deficient NOD mice, but not those from older mice, showed significantly delayed disease onset in immune-deficient hosts compared with the corresponding wild-type mice. Conclusions/interpretation These results indicate that IL-17/Th17 participates in the development of insulitis and that both IL-17 and IFN-γ signalling may synergistically contribute to the development of diabetes in NOD mice.

The aim of this study was to evaluate the humoral autoreactivity to zinc transporter 8 (ZnT8) depending on the clinical phenotype of type 1 diabetes (T1D). ZnT8 autoantibodies (ZnT8A) were determined by radioimmunoassay using carboxy-terminal ZnT8 constructs in 57 childhood-onset (CO), 97 adult-onset (AO), and 85 fulminant T1D. The ZnT8A frequency was higher in CO patients and decreased with increasing age of onset from 70% to 24% (P trend <0.005). None of patients with fulminant T1D were positive for ZnT8A. There were at least two distinct ZnT8A epitope patterns associated with the aa325-restriction, CO patients have aa325-nonrestricted response more frequently compared to the AO group (P<0.05). The level of ZnT8A was inversely associated with the copy number of HLA-DR4 allele (P<0.05). These results suggest differences in the humoral autoreactivity to ZnT8 depending on the clinical phenotype, which should provide strategy for autoantibody measurement in subjects to allow early diagnosis of autoimmune T1D.

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OBJECTIVEInterferon therapy can trigger induction of several autoimmune diseases, including type 1 diabetes. To assess the clinical, immunologic, and genetic characteristics of type 1 diabetes induced by interferon therapy, we conducted a nationwide cross-sectional survey.RESEARCH DESIGN AND METHODSClinical characteristics, anti-islet autoantibodies, and HLA-DR typing were examined in 91 patients for whom type 1 diabetes developed during or shortly after interferon therapy.RESULTSMedian age at the onset of type 1 diabetes was 56 (interquartile range 48–63) years and mean ± SD BMI was 20.8 ± 2.7 kg/m2. The time period from the initiation of interferon therapy to type 1 diabetes onset in patients receiving pegylated interferon and ribavirin was significantly shorter than that in patients with nonpegylated interferon single therapy (P < 0.05). Anti-islet autoantibodies were detected in 94.5% of patients at diabetes onset. Type 1 diabetes susceptibility HLA-DRs in the Japanese population, DR4 and DR9, were also associated with interferon treatment–related type 1 diabetes. Furthermore, the prevalence of HLA-DR13 was significantly higher in interferon treatment–related type 1 diabetes than in healthy control subjects (odds ratio 3.80 [95% CI 2.20–7.55]; P < 0.0001) and classical type 1 diabetes (2.15 [1.17–3.93]; P < 0.05).CONCLUSIONSAnti-islet autoantibodies should be investigated before and during interferon therapy to identify subjects at high risk of type 1 diabetes. Stronger antiviral treatment may induce earlier development of type 1 diabetes. Furthermore, patients who develop interferon-induced type 1 diabetes are genetically susceptible.