The Freundlich equation provides a good fit (r 2 > 0.99) for the adsorption data on thiram in all the soils. The Freundlich constant (K) value for thiram in Farm Yard Manure (FYM) treated soils were more than in corresponding untreated soils. Thiram showed 'L' type isotherm curve (1/n < 1) indicated non-linear relationship between the thiram concentration and adsorption. The negative magnitude of Gibbs free energy (∆G) indicate that the adsorption was exothermic and spontaneity process. The persistence of thiram indicated a close correspondence to the (r 2 > 0.92) first order exponential degradation kinetics in the soils and mainly influenced by soil organic matter. The half-life (T1/2) value of thiram was highest for alluvial soil followed by sandy loam and black soils.
Diabetes patients
have an increased risk of heart failure (HF). Diabetes is highly prevalent in HF with preserved ejection fraction
(HFpEF), which is on the rise worldwide. The role of diabetes in HF is less
established and available treatments of HF are not effective in HFpEF patients.
Tissue factor (TF), a transmembrane receptor, plays an important role in immune-cell
inflammation and atherothrombosis in diabetes. However, its role in diabetes-induced
cardiac inflammation, hypertrophy, and HF has not been studied. Here, we have
utilized Wildtype (WT), heterozygous, and Low-TF (with 1% human TF) mice to
determine TF’s role in <i>Type1 diabetes</i>-induced
HF. We found significant upregulation of cardiac TF mRNA and protein levels in
diabetic WT hearts compared to non-diabetic controls. WT diabetic hearts also
exhibited increased inflammation and cardiac hypertrophy versus controls. However,
these changes in cardiac inflammation and hypertrophy were not found in
diabetic Low-TF mice compared to their non-diabetic controls. TF deficiency
was also associated with improved
cardiac function parameters suggestive of HFpEF, which was evident in diabetic
WT mice. The TF regulation of inflammation and cardiac remodeling was further
dependent on downstream ERK1/2 and STAT3 pathways. In summary, our study
demonstrated an important role of TF in regulating diabetes-induced
inflammation, hypertrophy, and remodeling of the heart leading to HF with
preserved ejection fraction.
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