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; and The Z-score Project 2nd Stage Study Group IMPORTANCE Few studies with sufficient statistical power have shown the association of the z score of the coronary arterial internal diameter with coronary events (CE) in patients with Kawasaki disease (KD) with coronary artery aneurysms (CAA). OBJECTIVE To clarify the association of the z score with time-dependent CE occurrence in patients with KD with CAA. DESIGN, SETTING, AND PARTICIPANTS This multicenter, collaborative retrospective cohort study of 44 participating institutions included 1006 patients with KD younger than 19 years who received a coronary angiography between 1992 and 2011. MAIN OUTCOMES AND MEASURES The time-dependent occurrence of CE, including thrombosis, stenosis, obstruction, acute ischemic events, and coronary interventions, was analyzed for small (z score, <5), medium (z score, Ն5 to <10; actual internal diameter, <8 mm), and large (z score, Ն10 or Ն8 mm) CAA by the Kaplan-Meier method. The Cox proportional hazard regression model was used to identify risk factors for CE after adjusting for age, sex, size, morphology, number of CAA, resistance to initial intravenous immunoglobulin (IVIG) therapy, and antithrombotic medications. RESULTS Of 1006 patients, 714 (71%) were male, 341 (34%) received a diagnosis before age 1 year, 501 (50%) received a diagnosis between age 1 and 5 years, and 157 (16%) received a diagnosis at age 5 years or older. The 10-year event-free survival rate for CE was 100%, 94%, and 52% in men (P < .001) and 100%, 100%, and 75% in women (P < .001) for small, medium, and large CAA, respectively. The CE-free rate was 100%, 96%, and 79% in patients who were not resistant to IVIG therapy (P < .001) and 100%, 96%, and 51% in patients who were resistant to IVIG therapy (P < .001), respectively. Cox regression analysis revealed that large CAA (hazard ratio, 8.9; 95% CI, 5.1-15.4), male sex (hazard ratio, 2.8; 95% CI, 1.7-4.8), and resistance to IVIG therapy (hazard ratio, 2.2; 95% CI, 1.4-3.6) were significantly associated with CE. CONCLUSIONS AND RELEVANCE Classification using the internal diameter z score is useful for assessing the severity of CAA in relation to the time-dependent occurrence of CE and associated factors in patients with KD. Careful management of CE is necessary for all patients with KD with CAA, especially men and IVIG-resistant patients with a large CAA.

The use of thermophilic microorganisms as biocatalysts for electromethanogenesis was investigated. Single-chamber reactors inoculated with thermophiles and operated at 55 °C showed high CH4 production rates (max. 1103 mmol m(–2) day(–1) at an applied voltage of 0.8 V) with current-capture efficiencies >90%, indicating that thermophiles have high potential as biocatalysts. To improve the electromethanogenic activity, the developed biocathode was transferred to a two-chamber reactor and operated at a poised potential of −0.5 V vs SHE. The CH4 production rates of the biocathode were enhanced approximately 6-fold in 160 h of poised-potential incubation, indicating that the acclimation of the biocathode resulted in performance improvement. Compositional alteration of the cathodic microbiota suggested that a Methanothermobacter-related methanogen and synergistetes- and thermotogae-related bacteria were selected during the acclimation. Cyclic voltammetry of the “acclimated” biocathode showed an augmented cathodic catalytic wave with a midpoint potential at ca. −0.35 V vs SHE. Moreover, the biocathode was able to catalyze electromethanogenesis at −0.35 V vs SHE. These results suggested that the ability of the biocathode to catalyze electromethanogenesis via direct electron transfer was enhanced by the acclimation. This study provides new technological and fundamental information on electromethanogenic bioelectrochemical systems (BESs) that may be extended to other BESs.

There is increasing evidence for the role of basophils in the pathogenesis of bronchial asthma. To examine the presence of basophils in the airways of patients with fatal asthma by immunohistochemistry, we stained lung tissues from four post-mortem cases who had died from severe asthmatic attacks and four controls with a monoclonal antibody raised against tryptase (AA-1) and anti-IgE. Mast cells and basophils were identified in the bronchioles as AA-1- and anti-IgE-positive cells, and anti-IgE-positive cells, respectively. Airway mast cells were found beneath the basement membrane, near blood vessels in the submucosa, and adjacent to the submucosal glands, and scattered throughout the muscle bundles. There was a significant increase of mast cells in the asthma group compared with the control group (203.5+/-84.6/mm2, mean+/-s.d. vs 37.7+/-8.7/mm2, P<0.05, n=4). In contrast, basophils were observed in the airway lumen, in the bronchial epithelium and in the submucosa. The number of basophils in the bronchioles was 81.8+/-55.5/mm2 (n = 4); however, basophils were not found at all in the airways of the control group. Although eosinophils, B lymphocytes and macrophages bear low affinity IgE receptors and could react with anti-IgE, the location of these cells in the close sections did not correspond closely with basophils. The presence of basophils in lung tissues obtained from fatal asthma patients supports the view that basophils play a role in the pathogenesis of bronchial asthma.