12 research outputs found

    Shade, light, and stream temperature responses to riparian thinning in second-growth redwood forests of northern California.

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    Resource managers in the Pacific Northwest (USA) actively thin second-growth forests to accelerate the development of late-successional conditions and seek to expand these restoration thinning treatments into riparian zones. Riparian forest thinning, however, may impact stream temperatures-a key water quality parameter often regulated to protect stream habitat and aquatic organisms. To better understand the effects of riparian thinning on shade, light, and stream temperature, we employed a manipulative field experiment following a replicated Before-After-Control-Impact (BACI) design in three watersheds in the redwood forests of northern California, USA. Thinning treatments were intended to reduce canopy closure or basal area within the riparian zone by up to 50% on both sides of the stream channel along a 100-200 m stream reach. We found that responses to thinning ranged widely depending on the intensity of thinning treatments. In the watersheds with more intensive treatments, thinning reduced shade, increased light, and altered stream thermal regimes in thinned and downstream reaches. Thinning shifted thermal regimes by increasing maximum temperatures, thermal variability, and the frequency and duration of elevated temperatures. These thermal responses occurred primarily during summer but also extended into spring and fall. Longitudinal profiles indicated that increases in temperature associated with thinning frequently persisted downstream, but downstream effects depended on the magnitude of upstream temperature increases. Model selection analyses indicated that local changes in shade as well as upstream thermal conditions and proximity to upstream treatments explained variation in stream temperature responses to thinning. In contrast, in the study watershed with less intensive thinning, smaller changes in shade and light resulted in minimal stream temperature responses. Collectively, our data shed new light on the stream thermal responses to riparian thinning. These results provide relevant information for managers considering thinning as a viable restoration strategy for second-growth riparian forests

    Same admission cardiac catheterization and cardiac surgery: is there an increased incidence of acute kidney injury?

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    BACKGROUND: Acute kidney injury (AKI) is predictive of increased long-term mortality after cardiac surgery. Patients often undergo surgery after cardiac catheterization during the same admission for reasons of instability and threatening anatomy as well as nonurgent reasons such as patient convenience. We hypothesized that patients undergoing cardiac catheterization and cardiac surgery during the same admission are more likely to develop AKI after cardiac surgery than patients for whom surgery is performed on a later admission. METHODS: We prospectively enrolled 668 nonemergent adult cardiac surgical cases. Patients having heart catheterization were divided into two groups: cardiac catheterization followed by cardiac surgery during the same hospital admission (same admission) or catheterization followed by surgery during a later admission (later admission). The AKI was defined by an increase in serum creatinine from baseline by 50% or greater or 0.3 (mg/dL) or greater. Univariable and multivariable logistic regression and propensity-matched analyses were conducted. RESULTS: The incidence of AKI was significantly higher in the patients who had same admission cardiac catheterization and surgery (50.2%) compared with patients who had surgery on a later admission (33.7%, p = 0.009). The adjusted odds ratio for surgery on a later admission was 1.54 (95% confidence interval: 1.11 to 2.13) suggesting a 54% increased risk of AKI. Propensity-matched results were similar with 1.58 (95% confidence interval: 1.13 to 2.22). CONCLUSIONS: When cardiac catheterization and cardiac surgery occur during the same hospitalization, there is an increased risk for postoperative AKI. After cardiac catheterization, discharge and readmission for nonurgent surgery should be considered as such an approach might reduce the risk of AKI

    Microemboli from cardiopulmonary bypass are associated with a serum marker of brain injury.

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    An increasing number of reports surrounding neurologic injury in the setting of cardiac surgery has focused on utilizing biomarkers as intermediate outcomes. Previous research has associated cerebral microemboli and neurobehavioral deficits with biomarkers. A leading source of cerebral microemboli is the cardiopulmonary bypass (CPB) circuit. This present study seeks to identify a relationship between microemboli leaving the CPB circuit and a biomarker of neurologic injury. We enrolled 71 patients undergoing coronary artery bypass grafting at a single institution from October 14, 2004 through December 5, 2007. Microemboli were monitored using Power-M-Mode Doppler in the inflow and outflow of the CPB circuit. Blood was sampled before and within 48 hours after surgery. Neurologic injury was measured using S100beta (microg/L). Significant differences in post-operative S100beta relative to microemboli leaving the circuit were tested with analysis of variance and Kruskal-Wallis. Most patients had increased serum levels of S100beta (mean .25 microg/L, median .15 microg/L) following surgery. Terciles of microemboli measured in the outflow (indexed to the duration of time spent on CPB) were associated with elevated levels of S100beta (p = .03). Microemboli leaving the CPB circuit were associated with increases in postoperative S100beta levels. Efforts aimed at reducing microembolic load leaving the CPB circuit should be adopted to reduce brain injury
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