Chronic stress refers to the non-specific systemic reaction that occurs when the body is stimulated by various internal and external negative factors over a long time. The physiological response to chronic stress exposure has long been recognized as a potent modulator in the occurrence of atherosclerosis. Furthermore, research has confirmed the correlation between atherosclerosis and cardiovascular events. Chronic stress is pervasive during negative life events and may lead to the formation of plaque. Several epidemiological studies have shown that chronic stress is an independent risk factor for the development of vascular disease and for increased morbidity and mortality in patients with pre-existing coronary artery disease. One possible mechanism for this process is that chronic stress causes endothelial injury, directly activating macrophages, promoting foam cell formation and generating the formation of atherosclerotic plaque. This mechanism involves numerous variables, including inflammation, signal pathways, lipid metabolism and endothelial function. The mechanism of chronic stress in atherosclerosis should be further investigated to provide a theoretical basis for efforts to eliminate the effect of chronic stress on the cardiocerebral vascular system.

Background Atherosclerotic cardiovascular disease (ASCVD) refers to a series of diseases caused by atherosclerosis (AS). It is one of the most important causes of death worldwide. According to the inflammatory response theory, macrophages play a critical role in AS. However, the potential targets associated with macrophages in the development of AS are still obscure. This study aimed to use bioinformatics tools for screening and identifying molecular targets in AS macrophages. Methods Two expression profiling datasets (GSE7074 and GSE9874) were obtained from the Gene Expression Omnibus dataset, and differentially expressed genes (DEGs) between non-AS macrophages and AS macrophages were identified. Functional annotation of the DEGs was performed by analyzing the Gene Ontology and Kyoto Encyclopedia of Genes and Genomes databases. STRING and Cytoscape were employed for constructing a protein–protein interaction network and analyzing hub genes. Results A total of 98 DEGs were distinguished between non-AS macrophages and AS macrophages. The functional variations in DEGs were mainly enriched in response to hypoxia, respiratory gaseous exchange, protein binding, and intracellular, ciliary tip, early endosome membrane, and Lys63-specific deubiquitinase activities. Three genes were identified as hub genes, including KDELR3 , CD55 , and DYNC2H1 . Conclusion Hub genes and DEGs identified by using microarray techniques can be used as diagnostic and therapeutic biomarkers for AS.

Gut microbes are known as the body’s second gene pool. Symbiotic intestinal bacteria play a major role in maintaining balance in humans. Bad eating habits, antibiotic abuse, diseases, and a poor living environment have a negative effect on intestinal flora. Abnormal intestinal microbes are prone to cause a variety of diseases, affecting life expectancy and long-term quality of life, especially in older people. Several recent studies have found a close association between intestinal microorganisms and osteoporosis. The potential mechanism of intestinal flora affecting bone formation or destruction by mediating nitric oxide, the immune and endocrine systems, and other factors is briefly described in this review. All of these factors may be responsible for the intestinal flora that causes osteoporosis. Studying the relationship between intestinal flora and bone health not only provides new ideas for studying the role of intestinal microorganism in osteoporosis, but also provides a new therapeutic direction for clinically refractory osteoporosis. Study of the relationship between intestinal microbiota and osteoporosis is important for maintaining bone health and minimizing osteoporosis.

Multiple vaginal delivery (MVD) is an important factor for pelvic floor muscle (PFM) function decline and pelvic floor dysfunction (PFD). PFD is common in middle-aged and elderly women, but its pathogenesis is not clear. In this study, we found that the expression of CACNA1H was lower in the PFM of old mice after MVD compared with old or adult mice. In in-vitro studies, we found that treatment with the T-type Ca 2+ channel (T-channel) inhibitor NNC-55 or downregulation of the CACNA1H gene by siRNA intervention promoted myotube atrophy and apoptosis. Mechanistically, we revealed that NNC-55 increased the expression of GRP78 and DDIT3 in myotubes, indicating endoplasmic reticulum stress (ERS) activation, and that the IRE1 and PERK pathways might be involved in this effect. NNC-55 induced the formation of autophagosomes but inhibited autophagy flux. Moreover, rapamycin, an autophagy activator, did not rescue myotube atrophy or apoptosis induced by NNC-55, and the autophagy inhibitors 3-MA and HCQ accelerated this damage. Further studies showed that the ERS inhibitors 4-PBA and TUDAC relieved NNC-55-induced damage and autophagy flux blockade. Finally, we found multisite muscle atrophy and decreased muscle function in Cacna1h −/− (TH-null) mice, as well as increased autophagy inhibition and apoptotic signals in the PFM of old WT mice after MVD and TH-null mice. Taken together, our results suggest that MVD-associated PFD is partially attributed to CACNA1H downregulation-induced PFM atrophy and that ERS is a potential therapeutic target for this disease.

Atrial fibrillation (AF) increases the risk of ischemic stroke and systemic arterial embolism. However, the risk factors or predictors of stroke in AF patients have not been clarified. Therefore, it is necessary to find effective diagnostic and therapeutic targets. Two datasets were downloaded from the Gene Expression Omnibus (GEO) database. Differently expressed genes (DEGs) were identified between samples of atrial fibrillation without stroke and atrial fibrillation with stroke. Enrichment analysis of Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) by Gene Set Enrichment Analysis (GSEA), construction and analysis of protein-protein interaction (PPI) network and significant module, and the receiver operator characteristic (ROC) curve analysis were performed. A total of 524 DEGs were common to both datasets. Analysis of KEGG pathways indicated that the top canonical pathways associated with DEGs were ubiquitin-mediated proteolysis, endocytosis, spliceosome, and so on. Ten hub genes (SMURF2, CDC42, UBE3A, RBBP6, CDC5L, NEDD4L, UBE2D2, UBE2B, UBE2I, and MAPK1) were identified from the PPI network and were significantly associated with a diagnosis of atrial fibrillation and stroke (AFST). In summary, a total of 524 DEGs and 10 hub genes were identified between samples of atrial fibrillation without stroke and atrial fibrillation with stroke. These genes may serve as the target of early diagnosis or treatment of AF complicated by stroke.

Objective Obesity has been linked to cardiovascular disease, diabetes, and osteoarthritis. Obesity and overweight pose a serious threat to human health, with an estimated 190 million overweight and obese people worldwide. Thus, we investigated the influence of certain eating habits on weight among Chinese college students. Methods We conducted a cross-sectional survey of 536 college students in Shijiazhuang, China. The survey included questions about eating habits. We analyzed the relationship between participants’ responses and obesity. Results Sex, residence, speed of eating, number of meals eaten per day, and a diet high in sugar were found to be correlated with obesity. Our results suggest that increasing the number of meals per day, slowing down the pace of eating, and reducing the intake of high-sugar foods have potential benefits for reducing obesity among college students. Conclusions In the present study, we found that some dietary habits are related to the occurrence of obesity among college-aged individuals.

Atrial fibrillation (AF) is a rapid supraventricular arrhythmia. However, the pathogenesis of atrial fibrillation remains controversial. We obtained transcriptome expression profiles GSE41177, GSE115574 and GSE79768 from GEO database. WGCNA was performed, DEGs were screened, PPI network was constructed using STRING database. CTD database was used to identify the reference score of hub genes associated with cardiovascular diseases. Prediction of miRNAs of hub genes was performed by TargetScan. DIANA‐miRPath v3.0 was applied to make functional annotation of miRNA. The animal model of atrial fibrillation was constructed, RT‐PCR was used to verify the expression of hub genes. Immunofluorescence assay for THBS2 and VCAN was made to identify molecular. Design of BP neural network was made to explore the prediction relationship of CXCR4 and TYROBP on AF. The merged datasets contained 104 up‐regulated and 34 down‐regulated genes. GO and KEGG enrichment analysis results of DEGs showed they were mainly enriched in ‘regulation of release of sequestered calcium ion into cytosol’, ‘actin cytoskeleton organization’ and ‘focal adhesion’. The hub genes were CXCR4, SNAI2, S100A4, IGFBP3, CSNK2A1, CHGB, VCAN, APOE, C1QC and TYROBP, which were up‐regulated expression in the AF compared with control tissues. There was strong correlation among the CXCR4, TYROBP and AF based on the BP neural network. Through training, best training performance is 9.6474e‐05 at epoch 14, and the relativity was 0.99998. CXCR4 and TYROBP might be involved in the development of atrial fibrillation by affecting inflammation‐related signalling pathways and may serve as targets for early diagnosis and preventive treatment.

Loss of T‐type calcium channel (TCC) function has been reported to result in decreased cell viability and impaired muscle regeneration. In this study, we report a novel mechanism whereby TCC blockade promotes ERS and contributes to Ca 2+ homeostasis disorder of endoplasmic reticulum, thereby resulting in mitochondrial‐related apoptotic cell death in C2C12 myotubes and skeletal muscle.