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Abstract Milk fat is the most important and energy-rich substance in milk, and its content and composition are important reference elements in the evaluation of milk quality. However, the current identification of valuable candidate genes affecting milk fat is limited. IlluminaPE150 was used to sequence bovine mammary epithelial cells (BMECs) with high and low milk fat rates (MFP), the weighted gene co-expression network (WGCNA) was used to analyze mRNA expression profile data in this study. As a result, a total of 10,310 genes were used to construct WGCNA, and the genes were classified into 18 modules. Among them, violet (r = 0.74), yellow (r = 0.75) and darkolivegreen (r = − 0.79) modules were significantly associated with MFP, and 39, 181, 75 hub genes were identified, respectively. Combining enrichment analysis and differential genes (DEs), we screened five key candidate DEs related to lipid metabolism, namely PI4K2A, SLC16A1, ATP8A2, VEGFD and ID1, respectively. Relative to the small intestine, liver, kidney, heart, ovary and uterus, the gene expression of PI4K2A is the highest in mammary gland, and is significantly enriched in GO terms and pathways related to milk fat metabolism, such as monocarboxylic acid transport, phospholipid transport, phosphatidylinositol signaling system, inositol phosphate metabolism and MAPK signaling pathway. This study uses WGCNA to form an overall view of MFP, providing a theoretical basis for identifying potential pathways and hub genes that may be involved in milk fat synthesis.

Abstract Although opioids are necessary for the treatment of acute pain, cancer pain, and palliative care, opioid abuse is a serious threat to society. Heroin (Diacetylmorphine) is the most commonly abused opioid, and it can have a variety of effects on the body's tissues and organs, including the well-known gastrointestinal depression and respiratory depression; however, there is little known about the effects of diacetylmorphine on cardiac damage. Here, we demonstrate that diacetylmorphine induces abnormal electrocardiographic changes in rats and causes damage to cardiomyocytes in vitro by an underlying mechanism of increased autophosphorylation of CaMKII and concomitant regulation of myocardial contractile protein TPM1 and MYOM2 protein expression. The CaMKII inhibitor KN-93 was first tested to rescue the toxic effects of heroin on cardiomyocytes in vitro and the abnormal ECG changes caused by heroin in SD rats, followed by the TMT relative quantitative protein technique to analyze the proteome changes. Diacetylmorphine causes increased phosphorylation at the CaMKII Thr287 site in myocardium, resulting in increased autophosphorylation of CaMKII and subsequent alterations in myocardial contractile proteins, leading to myocardial rhythm abnormalities. These findings provide a theoretical basis for the treatment and prevention of patients with arrhythmias caused by diacetylmorphine inhalation and injection.