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Technologies for increasing carbon storage in soils are gathering attention as a means for mitigating atmospheric CO2 emissions. Carbon sequestration can be achieved by controlling the organic carbon stock in soil and by accelerating mineral carbonation. In this study, carbon sequestration capacity was measured in soil columns treated with flue gas desulfurization gypsum (FGDG), a by-product of electric power generation. The feasibility of using FGDG as an environmentally benign alternative to gypsum or anhydrite was examined using a toxicity characteristic leaching procedure and Microtox bioassay. While no toxic leachate was generated from the FGDG treatment, some toxic elements in the soil were removed through absorption reactions. Test results for carbon sequestration based on unsaturated soil column experiments suggest that the application of FGDG for soil treatment holds promise of less microbial CO2 emission from soil. The net benefits of carbon sequestration from the FGDG treatment were calculated as 87 and 621 g C/m2/m of infiltrated water, for the 1 % calcite-added column and 3 % calcite-added columns, respectively. The presented test results show that the FGDG treatment for soil carbon sequestration holds a promise when it is applied to slightly alkaline soils.

Aging is associated with cardiac contractile abnormalities, but the etiology of these contractile deficits is unclear. We hypothesized that cardiac contractile and regulatory protein expression is altered during aging. To investigate this possibility, left ventricular (LV) lysates were prepared from young (6 months) and old (24 months) Fischer344 rats. There are no age‐related changes in SERCA2 expression or phospholamban phosphorylation. Additionally, neither titin isoform expression nor phosphorylation differed. However, there is a significant increase in β‐isoform of the myosin heavy chain (MyHC) expression and phosphorylation of TnI and MyBP‐C during aging. In permeabilized strips of papillary muscle, force and Ca2+ sensitivity are reduced during aging, consistent with the increase in β‐MyHC expression and TnI phosphorylation. However, the increase in MyBP‐C phosphorylation during aging may represent a mechanism to compensate for age‐related contractile deficits. In isolated cardiomyocytes loaded with Fura‐2, the peak of the Ca2+ transient is reduced, but the kinetics of the Ca2+ transient are not altered. Furthermore, the extent of shortening and the rates of both sarcomere shortening and re‐lengthening are reduced. These results demonstrate that aging is associated with changes in contractile and regulatory protein expression and phosphorylation, which affect the mechanical properties of cardiac muscle. [ABSTRACT FROM AUTHOR]

Abstract Airway diseases such as asthma are triggered by inflammation and mediated by proinflammatory cytokines such as tumor necrosis factor alpha (TNFα). Our goal was to systematically examine the potential mechanisms underlying the effect of TNFα on airway smooth muscle (ASM) contractility. Porcine ASM strips were incubated for 24 h with and without TNFα. Exposure to TNFα increased maximum ASM force in response to acetylcholine (Ach), with an increase in ACh sensitivity (hyperreactivity), as reflected by a leftward shift in the dose–response curve (EC50). At the EC50, the [Ca2+]cyt response to ACh was similar between TNFα and control ASM, while force increased; thus, Ca2+ sensitivity appeared to increase. Exposure to TNFα increased the basal level of regulatory myosin light chain (rMLC) phosphorylation in ASM; however, the ACh‐dependent increase in rMLC phosphorylation was blunted by TNFα with no difference in the extent of rMLC phosphorylation at the EC50 ACh concentration. In TNFα‐treated ASM, total actin and myosin heavy chain concentrations increased. TNFα exposure also enhanced the ACh‐dependent polymerization of G‐ to F‐actin. The results of this study confirm TNFα‐induced hyperreactivity to ACh in porcine ASM. We conclude that the TNFα‐induced increase in ASM force, cannot be attributed to an enhanced [Ca2+]cyt response or to an increase in rMLC phosphorylation. Instead, TNFα increases Ca2+ sensitivity of ASM force generation due to increased contractile protein content (greater number of contractile units) and enhanced cytoskeletal remodeling (actin polymerization) resulting in increased tethering of contractile elements to the cortical cytoskeleton and force translation to the extracellular matrix.

Ni‐rich layered oxides are envisioned as the most promising cathode materials for next‐generation lithium‐ion batteries; however, their practical adoption is plagued by fast capacity decay originating from chemo‐mechanical degradation. The intrinsic chemical–mechanical instability, inherited from atomic‐ and nanoscale defects generated during synthesis, is not yet resolved. Here, atomic‐ and nanoscale structural evolution during solid‐state synthesis of Ni‐rich layered cathode, Li[Ni0.92Co0.03Mn0.05]O2, is investigated using combined X‐ray/neutron scattering and electron/X‐ray microscopy. The multiscale analyses demonstrate the intertwined correlation between phase transition and microstructural evolution, with atomic‐scale defects derived from the decomposition of precursors leading to the creation of intra/inter‐granular pores. The nucleation and coalescence mechanism of pore defects during the synthesis of Ni‐rich layered cathodes are quantitatively revealed. Furthermore, a modified synthetic route is proposed to effectively circumvent the formation of nanoscale defects in Ni‐rich layered cathodes by facilitating uniform synthetic reactions, resulting in superior electrochemical and microstructural stability. [ABSTRACT FROM AUTHOR]