Mass removal efficiencies in water and consequences after a river diversion into coastal wetlands: second thoughts

Salinity control, nutrient additions, and sediment supply were directly or indirectly the rationale for a $220 million coastal wetland restoration project (Davis Pond River Diversion) that began in 2002. We sampled Mississippi River water going in and out of the receiving basin from 1999 to 2018 to understand why wetland loss increased after it began. There was a reduction in inorganic sediments, nitrogen (N), and phosphorus (P) concentrations within the ponding area of 77%, 39% and 34%, respectively, which is similar to that in other wetlands. But the average sediment accumulation of 0.6 mm year(-1) inadequately balances the present-day 5.6 mm year(-1) sea level rise or the 7.9 +/- 0.13 mm year(-1) accretion rates in these organic soils. Nutrients added likely reduced live belowground biomass and soil strength, and increased decomposition of the organic matter necessary to sustain elevations. The eutrophication of the downstream aquatic system from the diversion, principally by P additions, increased Chl a concentrations to a category of \u27poor\u27 water quality. We conclude that this diversion, if continued, will be a negative influence on wetland area and will eutrophy the estuary. It is a case history example for understanding the potential effects arising from proposed river diversions

Mechanism of Cd-Induced Inhibition of Na-Glucose Cotransporter in Rabbit Proximal Tubule Cells: Roles of Luminal pH and Membrane-Bound Carbonic Anhydrase

Background/Aims: We have previously reported that a complex of cadmium-metallothionein (Cd-MT) directly affects the apical Na-glucose cotransporter on the luminal side in proximal tubules, suggesting that Cd-MT is more toxic than CdCl2 in causing tubulopathy. To find the potential mechanisms, we evaluated the effect of luminal pH alteration and carbonic anhydrase (CA) inhibition on Cd-MT-induced reduction of glucose-dependent transmural voltage in rabbit S2 segments perfused in vitro. Methods: Before and after the addition of Cd-MT (1 µg Cd/ml) to the lumen, the deflections of transmural voltage upon the elimination of glucose from the perfusate (DeltaVtglu) were measured as a parameter of activity of the Na-glucose cotransporter. Results: During perfusion with a control solution of pH 7.4, the DeltaVtglu significantly decreased after addition of Cd-MT for 10 min. A reduction in pH to 6.8 significantly shortened the time needed to reduce the DeltaVtglu to 20 min. Furthermore, simultaneous addition of acetazolamide with control perfusate prevented the reduction. P-Fluorobenzyl-aminobenzolamide (pFB-ABZ), a membrane-impermeable CA inhibitor, added to the lumen also completely prevented the reduction in DeltaVtglu. In rabbits with chronic Cd exposure, acetazolamide prevented the glucosuria. Conclusion: Cd-MT-induced inhibition of Na-glucose cotransporter activity in the S2 segment strongly depends on luminal pH, and that an increase in pH by inhibition of luminal membrane-bound CA is useful to prevent renal Cd toxicity

Dielectric secondary relaxation of water in aqueous binary glass-formers

The dielectric relaxation of water in glassy aqueous binary mixtures exhibits an Arrhenius behaviour with a nearly universal activation energy. We here demonstrate that its characteristic relaxation time follows a remarkably general functional dependence on the weight fraction of water for a wide range of molecular systems

Cycling stability of Poly(Ethylene Glycol) of six molecular weights: influence of thermal conditions for energy applications

Utilizing energy storage technologies is beneficial for bridging the gap between supply and demand of energy, and for increasing the share of renewable energy in the energy system. Phase change materials (PCM) offer higher energy density and compact storage design compared to conventional sensible heat storage materials. Over the past years, polyethylene glycol (PEG) gained attention in the PCM field, and several new composites of PEGs are developed for thermal energy storage purposes. PCMs are investigated at a given heating/cooling rate to evaluate their phase change temperature and enthalpy. In the case of PEG, some molecular weights show a melting behavior that depends on the thermal history, such as the crystallization conditions. This study investigates the relationship between the molecular weight of PEGs (400 to 6000 g/mol), cooling/heating rates, and the behavior during phase transitions. To evaluate the performance of PEGs as a PCM under various thermal conditions. Experiments were performed using differential scanning calorimeter (DSC) and the transient plane source method (TPS). All PEG molecular weights were subjected to the same cooling and heating conditions, cooling and heating rate and number of cycles, to decouple the thermal effects from molecular weight effects. The behavior of phase transition for different thermal conditions was thoroughly analyzed and discussed. It was found that the melting temperature range of PEGs with different molecular weight was between 5.8 \ub0C and 62 \ub0C (at 5 \ub0C/min). Each PEG showed unique responses to the cooling and heating rates. Generally, the behavior of the crystallization is changing most between the thermal cycles, while the melting peak is stable regardless of the molecular weight. Finally, it is recommended that the characterization of PEGs and their composites should be conducted at a heating and cooling rate close to the thermal conditions of the intended thermal energy storage application

Carbonic Anhydrase Inhibitors Suppress Platelet Procoagulant Responses and In Vivo Thrombosis

Carbonic anhydrase (CA) inhibitors have a long history of safe clinical use as mild diuretics, in the treatment of glaucoma and for altitude sickness prevention. In this study, we aimed to determine if CA inhibition may be an alternative approach to control thrombosis. We utilized a high-resolution dynamic imaging approach to provide mechanistic evidence that CA inhibitors may be potent anti-procoagulant agents in vitro and effective anti-thrombotics in vivo. Acetazolamide and methazolamide, while sparing platelet secretion, attenuated intracellular chloride ion entry and suppressed the procoagulant response of activated platelets in vitro and thrombosis in vivo. The chemically similar N-methyl acetazolamide, which lacks CA inhibitory activity, did not affect platelet procoagulant response in vitro. Outputs from rotational thromboelastometry did not reflect changes in procoagulant activity and reveal the need for a suitable clinical test for procoagulant activity. Drugs specifically targeting procoagulant remodeling of activated platelets, by blockade of carbonic anhydrases, may provide a new way to control platelet-driven thrombosis without blocking essential platelet secretion responses

Myocardial and mitochondrial effects of the anhydrase carbonic inhibitor ethoxzolamide in ischemia-reperfusion

We have previously demonstrated that inhibition of extracellularly oriented carbonic anhydrase (CA) isoforms protects the myocardium against ischemia-reperfusion injury. In this study, our aim was to assess the possible further contribution of CA intracellular isoforms examining the actions of the highly diffusible cell membrane permeant inhibitor of CA, ethoxzolamide (ETZ). Isolated rat hearts, after 20 min of stabilization, were assigned to the following groups: (1) Nonischemic control: 90 min of perfusion; (2) Ischemic control: 30 min of global ischemia and 60 min of reperfusion (R); and (3) ETZ: ETZ at a concentration of 100 μM was administered for 10 min before the onset of ischemia and then during the first 10 min of reperfusion. In additional groups, ETZ was administered in the presence of SB202190 (SB, a p38MAPK inhibitor) or chelerythrine (Chel, a protein kinase C [PKC] inhibitor). Infarct size, myocardial function, and the expression of phosphorylated forms of p38MAPK, PKCε, HSP27, and Drp1, and calcineurin Aβ content were assessed. In isolated mitochondria, the Ca2+ response, Ca2+ retention capacity, and membrane potential were measured. ETZ decreased infarct size by 60%, improved postischemic recovery of myocardial contractile and diastolic relaxation increased P-p38MAPK, P-PKCε, P-HSP27, and P-Drp1 expression, decreased calcineurin content, and normalized calcium and membrane potential parameters measured in isolated mitochondria. These effects were significantly attenuated when ETZ was administered in the presence of SB or Chel. These data show that ETZ protects the myocardium and mitochondria against ischemia-reperfusion injury through p38MAPK- and PKCε-dependent pathways and reinforces the role of CA as a possible target in the management of acute cardiac ischemic diseases.Fil: Ciocci Pardo, Alejandro. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; ArgentinaFil: González Arbeláez, Luisa Fernanda. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; ArgentinaFil: Fantinelli, Juliana Catalina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; ArgentinaFil: Álvarez, Bernardo V.. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; ArgentinaFil: Mosca, Susana Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; ArgentinaFil: Swenson, Erik R.. Washington University in St. Louis; Estados Unido