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Litter decomposition is a fundamental process underpinning multiple ecosystem services. Despite a long history of research on decomposition, direct and indirect effects of multiple interactive land management on wetland decomposition yet remain less well understood. Here, we used a long-term whole-ecosystem wetland experiment in south-central Florida to investigate interactive effects of land-use intensification, cattle grazing and prescribed fire on in situ wetland plant litter decomposition. We further examined the direct and indirect pathways of land management effects on litter decomposition through changes in associated litter traits, soil properties, and soil microbial attributes using structural equation models. We used the litterbag technique that quantifies decomposition rates (k-values) and recalcitrant fractions (A-values). Our results showed that land-use intensification increased k-values in ungrazed wetlands and decreased k-values in grazed wetlands, but consistently reduced A-values regardless of other treatments. Prescribed fire individually suppressed litter decomposition by reducing k and increasing A. Further, these effects occurred through altering litter, soil, and microbial properties. Our results revealed that litter traits and soil properties were the first two strongest factors in determining wetland decomposition processes. Particularly, litter P and Mg contents and soil P and K contents were the best predictors for k, while litter Ca and lignin contents and soil pH, N and water content best predicted A. Moreover, microbial traits exhibited interactive effects with litter and soil properties to affect wetland litter decomposition. Our research suggests that cattle grazing could buffer against stimulating effect of land-use intensification on decomposition rates and thus avoid nutrient releases pulses. Our study further indicates that land-use intensification and fire suppression in subtropical wetlands could promote organic matter depletion and thus nutrient loss, highlighting the need to reduce anthropogenic disturbances to natural wetlands to maintain their capacity for providing associated regulating and supporting services., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Diabetics have an increased risk of developing renal insufficiency, as well as congestive heart failure independent of coronary atherosclerotic or hypertensive heart disease. Aluminum toxicity is being recognized with increased frequency in patients with reduced renal function and aluminum accumulates to a greater degree in tissues of patients with diabetes. Studies in patients with end stage renal disease have implicated aluminum overload as a potential cause of reduced cardiac function. Since both diabetes and aluminum decrease the activity of (Ca + Mg)-ATPase, a key enzyme involved in myocardial calcium transport, the interaction of experimental diabetes mellitus and aluminum toxicity on myocardial sarcoplasmic reticulum calcium transport was investigated in rats. Aluminum alone had no effect on (Ca + Mg)-ATPase activity, while activities in both the diabetic ([DM]) and diabetic plus aluminum loaded ([DM + Al]) groups were significantly lower than controls ([C]). Oxalate-dependent calcium uptake in the [DM] rats was slightly, but not significantly lower than controls, however, uptake was markedly reduced in rats which were both diabetic and aluminum loaded. The calcium regulatory protein calmodulin was measured by a functional assay in the soluble fraction of myocardial tissue prepared from each of the four groups. Compared to [C], calmodulin activity was significantly reduced in both the [DM] and [DM + Al] groups but not affected by aluminum alone. These data indicate that diabetes mellitus is associated with decreased myocardial calmodulin activity that may contribute to reduced sarcoplasmic reticulum (Ca + Mg)-ATPase and calcium transport activities and that aluminium toxicity potentiates the adverse effects of diabetes on decreasing sarcoplasmic reticulum calcium uptake.