05). A priori exploratory mediation analysis identified concern about child weight as a significant mediator between weight stigma and parental feeding practices. A discussion of the potential limitations of this study, future directions of research, and implications of these findings are included. BACKGROUND Physical inactivity contributes to muscle wasting and reductions in mitochondrial oxidative phenotype (OXPHEN), reducing physical performance and quality of life during aging and in chronic disease. Previously, it was shown that inactivation of glycogen synthase kinase (GSK)-3β stimulates muscle protein accretion, myogenesis, and mitochondrial biogenesis. Additionally, GSK-3β is inactivated during recovery of disuse-induced muscle atrophy. AIM Therefore, we hypothesize that GSK-3 inhibition is required for reloading-induced recovery of skeletal muscle mass and OXPHEN. METHODS Wild-type (WT) and whole-body constitutively active (C.A.) Ser21/9 GSK-3α/β knock-in mice were subjected to a 14-day hind-limb suspension/14-day reloading protocol. Soleus muscle mass, fiber cross-sectional area (CSA), OXPHEN (abundance of sub-units of oxidative phosphorylation (OXPHOS) complexes and fiber-type composition), as well as expression levels of their main regulators (respectively protein synthesis/degradation, myogenesis and peroxisome proliferator-activated receptor-γ co-activator-1α (PGC-1α) signaling) were monitored. RESULTS Subtle but consistent differences suggesting suppression of protein turnover signaling and decreased expression of several OXPHOS sub-units and PGC-1α signaling constituents were observed at baseline in C.A. https://www.selleckchem.com/products/ABT-263.html GSK-3 versus WT mice. Although soleus mass recovery during reloading occurred more rapidly in C.A. GSK-3 mice, this was not accompanied by a parallel increased CSA. The OXPHEN response to reloading was not distinct between C.A. GSK-3 and WT mice. No consistent or significant differences in reloading-induced changes in the regulatory steps of protein turnover, myogenesis or muscle OXPHEN were observed in C.A. GSK-3 compared to WT muscle. CONCLUSION This study indicates that GSK-3 inactivation is dispensable for reloading-induced recovery of muscle mass and OXPHEN. Malectin is a carbohydrate-binding lectin protein found in the endoplasmic reticulum (ER). It selectivity binds to Glc2-N-glycan and is involved in a glycoprotein quality control mechanism. Even though malectin may play a role in immunity, its role in innate immunity is not fully known. In the present study, we identified and characterized the malectin gene from Hippocampus abdominalis (HaMLEC). We analyzed sequence features, spatial expression levels, temporal expression profiles upon immune responses, bacterial and carbohydrate binding abilities and anti-viral properties to investigate the potential role of HaMLEC in innate immunity. The molecular weight and isoelectric point (pI) were estimated to be 31.99 kDa and 5.17, respectively. The N-terminal signal peptide, malectin superfamily domain and C-terminal transmembrane region were identified from the amino acid sequence of HaMLEC. The close evolutionary relationship of HaMLEC with other teleosts was identified by phylogenetic analysis. According to quantitative PCR (qPCR) results, HaMLEC expression was observed in all the examined tissues and high expression was observed in the ovary and brain, compared to other tested tissues. Temporal expression of HaMLEC in liver and blood tissues were significant modulated upon exposure to immunogens Edwardasiella tarda, Streptococcus iniae, polyinosinicpolycytidylic and lipopolysaccharide. The presence of carbohydrate binding modules (CBMs) of bacterial glycosyl hydrolases were functionally confirmed by a bacterial binding assay. Anti-viral activity significantly reduced viral hemorrhagic septicemia virus (VHSV) replication in cells overexpressing HaMLEC. The observed results suggested that HaMLEC may have a significant role in innate immunity in Hippocampus abdominalis. Virulent pathogenic microorganisms often enhance their infectivity through immune evasion mechanisms. Our research on the integrative and conjugative element (ICE(r2)) of the virulent fish pathogen Yersinia ruckeri SC09 led to the identification of genes related to immune evasion (designated stir-1, stir-2, stir-3 and stir-4), among which stir-1 and stir-2 were determined as the key contributors to bacterial toxicity and immune evasion. Here, we further examined the ability of stir-3 to mediate immune evasion based on detailed bioinformatic analysis of ICE(r2) from Y. ruckeri SC09. Interactions among the translated STIR-1, STIR-2, STIR-3 and STIR-4 proteins in the secretory process were additionally explored. STIR-3 was positively correlated with bacterial toxicity and inhibited host toll-like receptor (TLR) signaling by interacting with MyD88, thereby facilitating bacterial survival in host cells. Importantly, our data showed co-secretion of STIR-1, STIR-2 and STIR-3 as a complex, with secretion failure occurring in the absence of any one of these proteins. While stir-1, stir-2, stir-3 and stir-4 genes werespecific to Y. ruckeri SC09, the ICE(r2) region where these genes were located is a mobile component widely distributed in bacteria. Therefore, the potential transmission risk of these immune evasion genes requires further research attention. This study investigated the function of Troponin T (TnT) in the mud crab, Scylla paramamosain. The 1952 bp cDNA sequence of TnT was cloned from S. paramamosain using rapid amplification of cDNA ends (RACE) PCR. The quantitative real-time PCR analysis showed that TnT was highly expressed in the muscle and heart of S. paramamosain. Challenging with white spot syndrome virus (WSSV) or Vibrio alginolyticus (VA), two common pathogens that infect mud crabs, enhanced the expression of TnT in S. paramamosain. Knockdown of TnT using TnT-dsRNA led to up-regulating the expression of immune-related genes, such as c-type-lectin, toll-like-receptor, crustin antimicrobial peptide and prophenoloxidase. The cumulative mortality of WSSV- and VA-infected crabs was significantly increased following TnT knockdown. After WSSV or VA infection, TnT knockdown caused a significant reduction in phenoloxidase (PO) activity, superoxide dismutase (SOD) activity and total hemocyte count (THC), indicating a regulatory role of TnT in the innate immune response of S.