Diltiazem Does Not Prevent Postoperative Atrial Fibrillation After Thoracoscopic Lobectomy.

OBJECTIVE: Thoracoscopic lobectomy is associated with lower rates of adverse events compared to thoracotomy. Despite this, postoperative atrial fibrillation (POAF) occurs in at least 10% of patients. Our objective is to determine if prophylaxis with diltiazem significantly reduced POAF events. METHODS: Patients without prior history of atrial fibrillation who underwent thoracoscopic lobectomy from 2007 to 2016 at one institution were analyzed in a retrospective cohort study utilizing a prospective database. Patients treated from 2007 to 2012 received no prophylaxis. Patients treated after 2012 received diltiazem postoperatively. All patients were monitored with continuous telemetry postoperatively. Multivariate direct logistic regression was performed to determine independent predictors of POAF. We report adjusted odds ratios and accompanying 95% confidence intervals, with P < 0.05 denoting statistical significance. RESULTS: The final regression model included 416 patients (52 with POAF, 364 without). In univariate analysis, the variables of body mass index and history of congestive heart failure, diabetes, or hypertension, and prophylaxis status did not meet inclusion criteria. Age, gender, history of stroke or transient ischemic attack, and vascular disease were included. Only ages 65 to 74 (P = 0.03) and ≥75 (P = 0.02), compared to <65, were statistically significant predictors of POAF. Adjusted odds ratios of ages 65 to 74 and ≥75 were 2.88 and 2.62, respectively. CONCLUSIONS: Diltiazem prophylaxis did not significantly reduce POAF incidence following thoracoscopic lobectomy. Further study is warranted since POAF remains an unwanted source of morbidity and cost for lobectomy patients.

Heterogeneous Reactions of Limonene on Mineral Dust: Impacts of Adsorbed Water and Nitric Acid.

Biogenic volatile organic compounds (BVOCs), including the monoterpene limonene, are a major source of secondary organic aerosol (SOA). While gas-phase oxidation initiates the dominant pathway for BVOC conversion to SOA, recent studies have demonstrated that biogenic hydrocarbons can also directly react with acidic droplets. To investigate whether mineral dust may facilitate similar reactive uptake of biogenic hydrocarbons, we studied the heterogeneous reaction of limonene with mineral substrates using condensed-phase infrared spectroscopy and identified the formation of irreversibly adsorbed organic products. For kaolinite, Arizona Test Dust, and silica at 30% relative humidity, GC-MS identified limonene-1,2-diol as the dominant product with total organic surface concentrations on the order of (3-5) × 1018 molecules m-2. Experiments with 18O-labeled water support a mechanism initiated by oxidation of limonene by surface redox sites forming limonene oxide followed by water addition to the epoxide to form limonenediol. Limonene uptake on α-alumina, γ-alumina, and montmorillonite formed additional products in high yield, including carveol, carvone, limonene oxide, and α-terpineol. To model tropospheric processing of mineral aerosol, we also exposed each mineral substrate to gaseous nitric acid prior to limonene uptake and identified similar surface adsorbed products that were formed at rates 2 to 5 times faster than without nitrate coatings. The initial rate of reaction was linearly dependent on gaseous limonene concentration between 5 × 1012 and 5 × 1014 molecules cm-3 (0.22-20.5 ppm) consistent with an Eley-Rideal-type mechanism in which gaseous limonene reacts directly with reactive surface sites. Increasing relative humidity decreased the amount of surface adsorbed products indicating competitive adsorption of surface adsorbed water. Using a laminar flow tube reactor we measured the uptake coefficient for limonene on kaolinite at 25% RH to range from γ = 5.1 × 10-6 to 9.7 × 10-7. After adjusting for reactive surface areas, we estimate uptake coefficients for limonene on HNO3-processed mineral aerosol on the order of (1-6) × 10-6. Although this heterogeneous reaction will not impact the atmospheric lifetime of gaseous limonene, it does provide a new pathway for mineral aerosol to acquire secondary organic matter from biogenic hydrocarbons, which in turn will alter the physical properties of mineral dust.

Radiation exposure induces inflammasome pathway activation in immune cells.

Radiation exposure induces cell and tissue damage, causing local and systemic inflammatory responses. Because the inflammasome pathway is triggered by cell death and danger-associated molecular patterns, we hypothesized that the inflammasome may signal acute and chronic immune responses to radiation. Using a mouse radiation model, we show that radiation induces a dose-dependent increase in inflammasome activation in macrophages, dendritic cells, NK cells, T cells, and B cells as judged by cleaved caspase-1 detection in cells. Time course analysis showed the appearance of cleaved caspase-1 in cells by day 1 and sustained expression until day 7 after radiation. Also, cells showing inflammasome activation coexpressed the cell surface apoptosis marker annexin V. The role of caspase-1 as a trigger for hematopoietic cell losses after radiation was studied in caspase-1(-/-) mice. We found less radiation-induced cell apoptosis and immune cell loss in caspase-1(-/-) mice than in control mice. Next, we tested whether uric acid might mediate inflammasome activation in cells by treating mice with allopurinol and discovered that allopurinol treatment completely blocked caspase-1 activation in cells. Finally, we demonstrate that radiation-induced caspase-1 activation occurs by a Nod-like receptor family protein 3-independent mechanism because radiation-exposed Nlrp3(-/-) mice showed caspase-1 activation profiles that were indistinguishable from those of wild-type mice. In summary, our data demonstrate that inflammasome activation occurs in many immune cell types following radiation exposure and that allopurinol prevented radiation-induced inflammasome activation. These results suggest that targeting the inflammasome may help control radiation-induced inflammation.