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Correct reprogramming of the DLK1-DIO3 imprinted region is critical for the development of cloned animals. However, in pigs, the imprinting and regulation of the DLK1-DIO3 region has not been systematically analyzed. The objective of this study was to investigate the imprinting status and methylation regulation of the DLK1-DIO3 region in wild-type and cloned neonatal pigs. We mapped the imprinting control region, IG-DMR, by homologous alignment and validated it in sperm, oocytes, fibroblasts, and parthenogenetic embryos. Subsequently, single nucleotide polymorphism-based sequencing and bisulfite sequencing polymerase chain reaction were conducted to analyze imprinting and methylation in different types of fibroblasts, as well as wild-type and cloned neonatal pigs. The results showed that Somatic cell nuclear transfer (SCNT) resulted in hypermethylation of the IG-DMR and aberrant gene expression in the DLK1-DIO3 region. Similar to wild-type pigs, imprinted expression and methylation were observed in the surviving cloned pigs, whereas in dead cloned pigs, the IG-DMR was hypermethylated and the expression of GTL2 was nearly undetectable. Our study reveals that abnormal imprinting of the DLK1-DIO3 region occurs in cloned pigs, which provides a theoretical basis for improving the cloning efficiency by gene editing to correct abnormal imprinting.

In order to accurately evaluate the safety of electromagnetic exposure generated by wireless charging of pacemakers, the modeling constructions and simulation calculations were performed by the finite element simulation software COMSOL. Firstly, the models of human brain tissue, a simple thorax and heart were constructed. The distributions of magnetic induction intensity (B), induced electric field intensity (E), as well as the distribution of SAR values in human head tissue generated in those three parts were obtained. In the calculations, the operating frequency of the wireless charging system was set to 251 kHz. Simulation results showed that maximum B value in human head model was 0.337 µT, accounting for 9.26% of ICNIRP threshold, the maximum E value was 0.393 V/m, accounting for 0.45% of ICNIRP threshold. In human heart model, the maximum B value was 3.118 µT, accounting for 85.01% of ICNIRP threshold, the maximum E value was 0.278 V/m, accounting for 0.32% of ICNIRP threshold. And in human brain tissue, SAR value was 3.009×10-7 W/kg, which was much lower than the recommended value of public electromagnetic exposure established by ICNIRP. This indicates that the wireless charging process of the pacemaker will not pose a health risk to users.

Extreme temperature during summer may lead to heat stress in cattle and compromise their productivity. It also poses detrimental impacts on the developmental capacity of bovine budding oocytes, which halt their fertility. To mitigate the adverse effects of heat stress, it is necessary to investigate the mechanisms through which it affects the developmental capacity of oocytes. The primary goal of this study was to investigate the impact of heat stress on the epigenetic modifications in bovine oocytes and embryos, as well as on oocyte developmental capacity, reactive oxygen species, mitochondrial membrane potential, apoptosis, transzonal projections, and gene expression levels. Our results showed that heat stress significantly reduced the expression levels of the epigenetic modifications from histone H1, histone H2A, histone H2B, histone H4, DNA methylation, and DNA hydroxymethylation at all stages of the oocyte and embryo. Similarly, heat stress significantly reduced cleavage rate, blastocyst rate, oocyte mitochondrial-membrane potential level, adenosine-triphosphate (ATP) level, mitochondrial DNA copy number, and transzonal projection level. It was also found that heat stress affected mitochondrial distribution in oocytes and significantly increased reactive oxygen species, apoptosis levels and mitochondrial autophagy levels. Our findings suggest that heat stress significantly impacts the expression levels of genes related to oocyte developmental ability, the cytoskeleton, mitochondrial function, and epigenetic modification, lowering their competence during the summer season. [ABSTRACT FROM AUTHOR]