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Bis(β-ketoiminate) dioxo tungsten(VI) complexes WO 2 L 2 (L = acNac, acNacMe, acNacEt) have been synthesized and characterized. The performance of WO 2 (acNacMe) 2 as an AACVD precursor was evaluated at growth temperatures of 250–550 °C using nitrogen as the carrier gas. The deposited films were analyzed by XPS, XRD and SEM. Bis(β-ketoiminate) dioxo tungsten(VI) complexes WO 2 L 2 (L = acNac, acNacMe, acNacEt) have been synthesized and characterized. The thermal behaviors and possible decomposition mechanisms of these dioxo compounds were studied by TGA, MS and thermolysis. The performance of WO 2 (acNacMe) 2 as an AACVD precursor was evaluated at growth temperatures of 250–550 °C using nitrogen as the carrier gas. The elemental compositions of the as-deposited and sputtered tungsten oxide films were determined by XPS. The morphology and stoichiometry of the as-deposited films were studied by SEM and XRD. [ABSTRACT FROM AUTHOR]

Rationale Chlorine gas (Cl 2 ) is a potent oxidant and trigger of irritant induced asthma. We explored NF-E2–related factor 2 (Nrf2)-dependent mechanisms in the asthmatic response to Cl 2 , using Nrf2 -deficient mice, buthionine sulfoximine (BSO), an inhibitor of glutathione (GSH) synthesis and sulforaphane (SFN), a phytochemical regulator of Nrf2. Methods Airway inflammation and airway hyperresponsiveness (AHR) were assessed 24 and 48 h after a 5-min nose-only exposure to 100 ppm Cl 2 of Nrf2 -deficient and wild type Balb/C mice treated with BSO or SFN. Animals were anesthetized, paralyzed and mechanically ventilated (FlexiVent™) and challenged with aerosolized methacholine. Bronchoalveolar lavage (BAL) was performed and lung tissues were harvested for assessment of gene expression. Results Cl 2 exposure induced a robust AHR and an intense neutrophilic inflammation that, although similar in Nrf2 -deficient mice and wild-type mice at 24 h after Cl 2 exposure, were significantly greater at 48 h post exposure in Nrf2 -deficient mice. Lung GSH and mRNA for Nrf2 -dependent phase II enzymes (NQO-1 and GPX2) were significantly lower in Nrf2 -deficient than wild-type mice after Cl 2 exposure. BSO reduced GSH levels and promoted Cl 2 -induced airway inflammation in wild-type mice, but not in Nrf2 -deficient mice, whereas SFN suppressed Cl 2 -induced airway inflammation in wild-type but not in Nrf2- deficient mice. AHR was not affected by either BSO or SFN at 48 h post Cl 2 exposure. Conclusions Nrf2-dependent phase II enzymes play a role in the resolution of airway inflammation and AHR after Cl 2 exposure. Moderate deficiency of GSH affects the magnitude of acute inflammation but not AHR. [ABSTRACT FROM AUTHOR]

Inhaled oxidative toxicants present in ambient air cause airway epithelial injury, inflammation, and airway hyperresponsiveness. Effective adaptation to such environmental insults is essential for the preservation of pulmonary function, whereas failure or incomplete adaptation to oxidative injury can render the host susceptible to the development of airway disease. We sought to explore the mechanisms of airway adaptation to oxidative injury. For a model to study pulmonary adaptation to oxidative stress–induced lung injury, we exposed mice to repeated nose-only chlorine gas exposures. Outcome measures were evaluated 24 hours after the last chlorine exposure. Lung mechanics and airway responsiveness to methacholine were assessed by using the flexiVent. Inflammation and antioxidant responses were assessed in both bronchoalveolar lavage fluid and lung tissue. Using both loss or gain of function and genomic approaches, we further dissected the cellular and molecular mechanisms involved in pulmonary adaptation. Repeated exposures to oxidative stress resulted in pulmonary adaptation evidenced by abrogation of neutrophilic inflammation and airway hyperresponsiveness. This adaptation was independent of antioxidant mechanisms and regulatory T cells but dependent on residential alveolar macrophages (AMs). Interestingly, 5% of AMs expressed forkhead box P3, and depletion of these cells abolished adaptation. Results from transcriptomic profiling and loss and gain of function suggest that adaptation might be dependent on TGF-β and prostaglandin E 2. Pulmonary adaptation during oxidative stress–induced lung injury is mediated by a novel subset of forkhead box P3–positive AMs that limits inflammation, favoring airway adaptation and host fitness through TGF-β and prostaglandin E 2. [ABSTRACT FROM AUTHOR]