In order to explain the mechanism of high meat quality in Laiwu pigs and investigate the relation between myosin heavy chains (MyHC) composition and meat quality, meat quality analysis was conducted and mRNA expression of MyHC I, IIa, IIx, IIb was quantified by real-time fluorescence PCR in longissimus muscle (LM) and semimembranous muscle of Laiwu pigs and Duroc. The result indicated that, compared with Duroc, mRNA expression of MyHC IIa, IIx in LM and semimembranous muscle of Laiwu pigs was significantly increased, mRNA expression of MyHC IIb was dramatically decreased. However, the expression of MyHC I was not significantly affected by breeds. The correlation between mRNA expression of MyHC I, IIa, IIx in LM and meat color, pH value, marbling, intramuscular fat content was positive, but shear value of LM was negative. The relation between MyHC IIb mRNA expression and marbling, intramuscular fat content was dramatically negative, whereas shear value was strikingly positive, as well as fiber diameter, but without reaching statistical significance. Therefore, the composition of MyHC I, IIa, IIx, IIb affected meat quality, furthermore, expression of MyHC I, IIa, IIx, IIb mRNA prominently influenced meat characteristics, especially edible quality of muscle, suggesting that mRNA expression level of MyHC I, IIa, IIx, IIb can exactly and impersonally estimate meat quality.
Particulate organic matter (POM) is a fraction of organic matter with dissimilar properties in different soils. POM isolated from soils and sediments (wetland, oil waste field, farmlands and aquaculture pond sediment) was used to study its sorption behavior on the antibiotic oxytetracycline (OTC). Impacts of solution pH, ionic strength and temperature on the OTC sorption were studied. The sorption rates of OTC in POM from wetland (POM-w) and farmland (POM-f1, POM-f2) were rapid during the first 3 h and gradually decreased with reaction time until reaching the equilibrium. Linear sorption occurred from 3 to 12 h in POM from oil waste field land (POM-o) and aquaculture pond sediment (POM-a). The organic carbon normalized partition coefficient (k oc ) varied from 215.0 to 4493.6 L kg −1 , and it was nearly 10× higher for the POM-w, POM-f1 and POM-f2 than in the POM-o and POM-a. Sorption of OTC by POM exhibited strong pH dependence. Ionic factors affected OTC sorption in POM-f1, POM-f2 and POM-a. The sorption capacity declined N50% in a solution with Ca 2+ compared to other ions with similar ionic strength. Sorption thermodynamics showed an entropy increasing and endothermic progress during the OTC sorption in POM, implying a spontaneous sorption process. Several mechanisms were involved in OTC sorption in POM, including hydrogen bonding, cation exchange, hydrophobic partitioning and surface complexation.
This study aimed to explore the molecular regulatory network among microRNA-125b (miR-125b), forkhead box Q1 (FOXQ1), prostaglandin-endoperoxide synthase 2 (PTGS2), and cyclin-dependent kinase 5 (CDK5), as well as their effects on cell apoptosis, neurite outgrowth, and inflammation in Alzheimer disease (AD). Rat embryo cerebral cortex neurons and nerve growth factor–stimulated PC12 cells were insulted by Aβ1−42 to construct two AD cellular models. Negative control (NC) inhibitor, miR-125b inhibitor, NC siRNA, FOXQ1 siRNA, PTGS2 siRNA, and CDK5 siRNA were transferred into the two AD cellular models alone or combined. Then, cell apoptosis, neurite outgrowth, proinflammatory cytokines, miR-125b, FOXQ1, PTGS2, and CDK5 expressions were detected. MiR-125b inhibition facilitated neurite outgrowth but suppressed cell apoptosis and proinflammatory cytokines (tumor necrosis factor-α, interleukin 1β, and interleukin 6); meanwhile, it upregulated FOXQ1 but downregulated PTGS2 and CDK5. Furthermore, FOXQ1 inhibition promoted cell apoptosis and proinflammatory cytokines but repressed neurite outgrowth; PTGS2 inhibition achieved the opposite effects; CDK5 inhibition attenuated cell apoptosis, whereas it less affected neurite outgrowth and inflammation. Notably, FOXQ1 inhibition attenuated, whereas PTGS2 inhibition elevated the effect of miR-125b inhibition on regulating neurite outgrowth, cell apoptosis, and proinflammatory cytokines. As for CDK5 inhibition, it enhanced the effect of miR-125b inhibition on regulating cell apoptosis, but less impacted the neurite outgrowth and proinflammatory cytokines. Additionally, PTGS2 inhibition and CDK5 inhibition both reversed the effect of FOXQ1 inhibition on regulating cell apoptosis, neurite outgrowth, and proinflammatory cytokines. In conclusion, targeting miR-125b alleviates AD progression via blocking PTGS2 and CDK5 in a FOXQ1-dependent way.
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