DataSheet1_Variability and controls of stable carbon isotopic fractionation during aerobic methane oxidation in temperate lakes.docx

The aerobic oxidation of methane (CH4) by methanotrophic bacteria (MOB) is the major sink of this highly potent greenhouse gas in freshwater environments. Yet, CH4 oxidation is one of the largest uncertain components in predicting the current and future CH4 emissions from these systems. While stable carbon isotopic mass balance is a powerful approach to estimate the extent of CH4 oxidation in situ, its applicability is constrained by the need of a reliable isotopic fractionation factor (αox), which depicts the slower reaction of the heavier stable isotope (13C) during CH4 oxidation. Here we explored the natural variability and the controls of αox across the water column of six temperate lakes using experimental incubation of unamended water samples at different temperatures. We found a large variability of αox (1.004–1.038) with a systematic increase from the surface to the deep layers of lake water columns. Moreover, αox was strongly positively coupled to the abundance of MOB in the γ-proteobacteria class (γ-MOB), which in turn correlated to the concentrations of oxygen and CH4, and to the rates of CH4 oxidation. To enable the applicability in future isotopic mass balance studies, we further developed a general model to predict αox using routinely measured limnological variables. By applying this model to δ13C-CH4 profiles obtained from the study lakes, we show that using a constant αox value in isotopic mass balances can largely misrepresent and undermine patterns of the extent of CH4 oxidation in lakes. Our αox model thus contributes towards more reliable estimations of stable carbon isotope-based quantification of CH4 oxidation and may help to elucidate large scale patterns and drivers of the oxidation-driven mitigation of CH4 emission from lakes.</p

Risk of cardiac events in patients with asthma and long-QT syndrome treated with beta(2) agonists.

The clinical course and risk factors associated with beta(2)-agonist therapy for asthma have not been investigated previously in patients with the long-QT syndrome (LQTS). The risk of a first LQTS-related cardiac event due to beta(2)-agonist therapy was examined in 3,287 patients enrolled in the International LQTS Registry with QTc > or = 450 ms. The Cox proportional hazards model was used to assess the independent contribution of clinical factors for first cardiac events (syncope, aborted cardiac arrest, or sudden death) from birth through age 40. Time-dependent beta(2)-agonist therapy for asthma was associated with an increased risk for cardiac events (hazard ratio [HR] = 2.00, 95% confidence interval 1.26 to 3.15, p = 0.003) after adjustment for relevant covariates including time-dependent beta-blocker use, gender, QTc, and history of asthma. This risk was augmented within the first year after the initiation of beta(2)-agonist therapy (HR = 3.53, p = 0.006). The combined use of beta(2)-agonist therapy and anti-inflammatory steroids was associated with an elevated risk for cardiac events (HR = 3.66, p <0.01); beta-blocker therapy was associated with a reduction in cardiac events in those using beta(2) agonists (HR = 0.14, p = 0.05). In conclusion, beta(2)-agonist therapy was associated with an increased risk for cardiac events in patients with asthma with LQTS, and this risk was diminished in patients receiving beta blockers