Summary mi RNA s contribute to plant resistance against pathogens. Previously, we found that the function of miR398b in immunity in rice differs from that in Arabidopsis. However, the underlying mechanisms are unclear. In this study, we characterized the mutants of miR398b target genes and demonstrated that multiple superoxide dismutase genes contribute to miR398b‐regulated rice immunity against the blast fungus Magnaporthe oryzae . Out of the four target genes of miR398b, mutations in Cu/Zn‐Superoxidase Dismutase1 ( CSD 1 ), CSD 2 and Os11g09780 ( Superoxide DismutaseX , SODX ) led to enhanced resistance to M. oryzae and increased hydrogen peroxide (H 2 O 2 ) accumulation. By contrast, mutations in Copper Chaperone for Superoxide Dismutase ( CCSD ) resulted in enhanced susceptibility. Biochemical studies revealed that csd1 , csd2 and sodx displayed altered expression of CSD s and other superoxide dismutase ( SOD ) family members, leading to increased total SOD enzyme activity that positively contributed to higher H 2 O 2 production. By contrast, the ccsd mutant showed CSD protein deletion, resulting in decreased CSD and total SOD enzyme activity. Our results demonstrate the roles of different SOD s in miR398b‐regulated resistance to rice blast disease, and uncover an integrative regulatory network in which miR398b boosts total SOD activity to upregulate H 2 O 2 concentration and thereby improve disease resistance.

Background To determine if global brain hypoperfusion and oxygen hypometabolism occur in patients with amnestic mild cognitive impairment (aMCI). Methods Thirty-two aMCI and 21 normal subjects participated. Total cerebral blood flow (TCBF), cerebral metabolic rate of oxygen (CMRO2) and brain tissue volume were measured using color-coded duplex ultrasonography (CDUS), near-infrared spectroscopy (NIRS), and MRI. TCBF was normalized by total brain tissue volume (TBV) for group comparisons (nTCBF). Cerebrovascular resistance (CVR) was calculated as mean arterial pressure divided by TCBF. Results Reductions in nTCBF by 9%, CMRO2 by 11%, and increase in CVR by 13% were observed in aMCI relative to normal subjects. No group differences in TBV were observed. nTCBF was correlated with CMRO2 in normal controls, but not in aMCI. Conclusions Global brain hypoperfusion, oxygen hypometabolism and neurovascular decoupling observed in aMCI suggest that changes in cerebral hemodynamics occur early at prodromal stage of Alzheimer’s disease, which can be assessed using low cost and bed-side available CDUS and NIRS technology.