Effect of medium voltage electrical stimulation and prior ageing on beef shear force during superchilled storage.

The effect of medium voltage electrical stimulation (ES), prior ageing (0-4 °C, 7 days), and their combination on the decrease of shear force in beef during superchilled storage (-4 °C) for 24 weeks was evaluated, in the context of a high shear force obtained under this storage condition. Both ES and prior ageing significantly reduced the initial Warner-Bratzler shear force, and the combination of ES and prior ageing shortened the storage time needed to reach an acceptable shear force of superchilled beef, which is mainly due to increased myofibrillar degradation as indicated by changes in desmin (P < 0.01, r = 0.35). Additionally, ES and prior ageing did not negatively affect lipid oxidation, total volatile basic nitrogen or water loss of superchilled beef. Consequently, ES combined with ageing for 7 days offered an effective approach for decreasing shear force and ensuring good quality superchilled beef.

Interleukin-37 Attenuates Lipopolysaccharide (LPS)-Induced Neonatal Acute Respiratory Distress Syndrome in Young Mice via Inhibition of Inflammation and Cell Apoptosis.

BACKGROUND Neonatal acute respiratory distress syndrome (ARDS) is a common clinical syndrome caused by lung immaturity and the abnormal synthesis of pulmonary surfactant in preterm newborns, and it has high morbidity and mortality rates. The present study investigated the roles of interleukin-37 (IL-37) in the pathogenesis of neonatal ARDS and the underlying biochemical mechanism. MATERIAL AND METHODS We used 6-day-old neonatal C57BL/6 mice to establish the ARDS model. Inflammatory cytokines levels were measured with enzyme-linked immunosorbent assay (ELISA) Kits. The pathological morphology of lung tissues was observed by hematoxylin-eosin (HE) staining. The expression levels of proteins were assessed by Western blotting and apoptotic cells were detected via TUNEL assay. Further, the expression of nucleotide-bound oligomerization domain (Nod)-like receptor P3 (NLRP3) was detected with immunohistochemistry and Western blotting. RESULTS IL-37 attenuated lipopolysaccharide (LPS)-induced cell apoptosis and excessive inflammatory cytokines levels, including IL-1ß, IL-8, TNF-alpha, and MCP-1, and ameliorated lung pathological manifestations in an LPS-induced neonatal ARDS model. Moreover, IL-37 suppressed the abnormal expression of proteins related to the CXCR4/SDF-1 chemokine axis and NLRP3 inflammasome pathway. CONCLUSIONS The present results suggest that IL-37 protect against LPS-induced lung injury through inhibition of inflammation and apoptosis in lung tissue in an LPS-induced neonatal ARDS model. Hence, IL-37 may be considered as a potential therapeutic agent for neonatal ARDS.