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Limb muscle is responsible for physical activities and myogenic cell migration during embryogenesis is indispensable for limb muscle formation. Maternal obesity (MO) impairs prenatal skeletal muscle development, but the effects of MO on myogenic cell migration remain to be examined. C57BL/6 mice embryos were collected at E13.5. The GeoMx DSP platform was used to customize five regions along myogenic cell migration routes (myotome, dorsal/ventral limb, limb stroma, limb tip), and data were analyzed by GeomxTools 3.6.0. A total of 2224 genes were down-regulated in the MO group. The GO enrichment analysis showed that MO inhibited migration-related biological processes. The signaling pathways guiding myogenic migration such as hepatocyte growth factor signaling, fibroblast growth factor signaling, Wnt signaling and GTPase signaling were down-regulated in the MO E13.5 limb tip. Correspondingly, the expression levels of genes involved in myogenic cell migration, such as Pax3, Gab1, Pxn, Tln2 and Arpc, were decreased in the MO group, especially in the dorsal and ventral sides of the limb. Additionally, myogenic differentiation-related genes were down-regulated in the MO limb. MO impedes myogenic cell migration and differentiation in the embryonic limb, providing an explanation for the impairment of fetal muscle development and offspring muscle function due to MO. [ABSTRACT FROM AUTHOR]

The persistence of Listeria monocytogenes biofilms on equipment surfaces poses a significant risk of cross-contamination, necessitating effective surface decontamination strategies. This study assessed the effectiveness of hurdle treatments combining peroxyacetic acid (PAA) and saturated steam against 7-day-old L. innocua (a non-pathogenic surrogate for L. monocytogenes) biofilms on stainless steel (SS), polyester (PET), and rubber surfaces. Results demonstrated >6 log10 CFU/coupon L. innocua reductions on SS and PET surfaces after PAA (40 ppm, 1 min) followed by steam treatment (100 °C, 6 s). On rubber surfaces, PAA (80 ppm, 1 min) followed by steam treatment (100 °C, 6 s) resulted in ~5 log10 CFU/coupon L. innocua reduction. The presence of apple juice soil reduced the efficacy of hurdle treatments, with PAA (40 ppm, 1 min) and steam exposure (6 s) resulting in 5.6, 5.8, and 4.2 log10 CFU/coupon reductions of L. innocua on SS, PET, and rubber, respectively. The efficacy of this antimicrobial combination was further reduced by surface defects, especially in the presence of organic matter. Nevertheless, the treatment still achieved >5 log10 CFU/coupon reductions of L. innocua on worn SS and PET soiled with apple juice and ~4.5 log10 CFU/coupon reduction on worn, soiled rubber surfaces. These findings highlight that PAA treatments followed by a brief steam exposure are effective strategies for controlling Listeria on food-contact surfaces. [ABSTRACT FROM AUTHOR]

The incidence of colorectal cancer (CRC) is closely linked to metabolic diseases. Accumulating evidence suggests the regulatory role of AMP-activated protein kinase (AMPK) in cancer metabolic reprogramming. In this study, wild-type and AMPK knockout mice were subjected to azoxymethane-induced and dextran sulfate sodium (AOM/DSS)-promoted colitis-associated CRC induction. A stable AMPK-deficient Caco-2 cell line was also established for the mechanistic studies. The data showed that AMPK deficiency accelerated CRC development, characterized by increased tumor number, tumor size, and hyperplasia in AOM/DSS-treated mice. The aggravated colorectal tumorigenesis resulting from AMPK ablation was associated with reduced α-ketoglutarate production and ten-eleven translocation hydroxylase 2 (TET2) transcription, correlated with the reduced mismatch repair protein mutL homolog 1 (MLH1) protein. Furthermore, in AMPK-deficient Caco-2 cells, the mRNA expression of mismatch repair and tumor suppressor genes, intracellular α-ketoglutarate, and the protein level of TET2 were also downregulated. AMPK deficiency also increased hypermethylation in the CpG islands of Mlh1 in both colonic tissues and Caco-2 cells. In conclusion, AMPK deficiency leads to reduced α-ketoglutarate concentration and elevates the suppressive epigenetic modifications of tumor suppressor genes in gut epithelial cells, thereby increasing the risk of colorectal tumorigenesis. Given the modifiable nature of AMPK activity, it holds promise as a prospective molecular target for the prevention and treatment of CRC. [ABSTRACT FROM AUTHOR]