Logistic regression analysis of risk factors for pediatric burns: a case-control study in underdeveloped minority areas in China.

Background: Pediatric burns are common, especially in underdeveloped countries, and these can physically affect the children involved and have an impact on their mental health. The aim of the present study was to assess the effect of pediatric burns in underdeveloped minority areas of China. Methods: Case information from 192 children was collected from outpatient and inpatient clinics using a survey questionnaire. These included 90 pediatric burn cases and 102 controls who were children without burns. A stepwise logistic regression analysis was used to determine the risk factors for pediatric burns in order to establish a model. The goodness-of-fit for the model was assessed using the Hosmer and Lemeshow test as well as receiver operating characteristic and internal calibration curves. A nomogram was then used to analyze the contribution of each influencing factor to the pediatric burns model. Results: Seven variables, including gender, age, ethnic minority, the household register, mother's employment status, mother's education and number of children, were analyzed for both groups of children. Of these, age, ethnic minority, mother's employment status and number of children in a household were found to be related to the occurrence of pediatric burns using univariate logistic regression analysis (p < 0.05). After a collinearity diagnosis, a multivariate logistic regression analysis of variables with tolerances of >0.2 and variance inflation factor <5 showed that age was a protective factor for pediatric burns [odds ratio (OR) = 0.725; 95% confidence interval (CI): 0.665-0.801]. Compared with single-child parents, those with two children were at greater risk of pediatric burns (OR = 0.389; 95% CI: 0.158-0.959). The ethnic minority of the child and the mother's employment status were also risk factors (OR = 6.793; 95% CI: 2.203-20.946 and OR = 2.266; 95% CI: 1.025-5.012, respectively). Evaluation of the model used was found to be stable. A nomogram showed that the contribution in the children burns model was age > mother's employment status > number of children > ethnic minority. Conclusions: This study showed that there are several risk factors strongly correlated to pediatric burns, including age, ethnic minority, the number of children in a household and mother's employment status. Government officials should direct their preventive approach to tackling the problem of pediatric burns by promoting awareness of these findings.

Healing mechanism of diabetic foot ulcers using single-cell RNA-sequencing.

Background: Diabetic foot ulcer (DFU) is one of the common and severe complications in diabetic patients, mainly caused by the interaction of various factors such as peripheral neuropathy, peripheral vascular disease, and infection. Moreover, vascular damage, disorder of tissue cells, decreased expression level of neurotrophic factor, and decreased growth factor caused by long-term exposure to a high glucose environment can also lead to prolonged or incomplete wound healing. This imposes a tremendous financial burden on the patients' family and society. Although various innovative techniques and drugs have been developed to treat DFU, the therapeutic effect is still unsatisfactory. Methods: We filtered and downloaded the single-cell dataset of diabetic patients from the Gene Expression Omnibus (GEO) website and used the Seurat package in R for creation of single-cell objects, integration, control of quality, clustering, cell type identification, differential gene analysis, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, and intercellular communication analysis. Results: Diabetic healing-related differentially expressed gene (DEG) analysis showed that there were 1,948 differential genes between tissue stem cells in healing and non-healing wounds, of which 1,198 genes were up-regulated and 685 genes were down-regulated. The results of GO functional enrichment analysis in tissue stem cells showed that they were closely related to wound healing. The CCL2-ACKR1 signaling pathway activity in tissue stem cells influenced the biological activity of endothelial cell subpopulation, which ultimately promoted the healing of DFU wounds. Conclusions: The CCL2-ACKR1 axis is closely associated with DFU healing.

The lysosomal membrane protein Sidt2 is a vital regulator of mitochondrial quality control in skeletal muscle.

The role of Sidt2 in the process of glucose and lipid metabolism has been recently reported. However, whether Sidt2 is involved in the metabolic regulation in skeletal muscle remains unknown. In this study, for the first time, using skeletal muscle-selective Sidt2 knockout mice, we found that Sidt2 was vital for the quality control of mitochondria in mouse skeletal muscle. These mice showed significantly reduced muscle tolerance and structurally abnormal mitochondria. Deletion of the Sidt2 gene resulted in decreased expression of mitochondrial fusion protein 2 (Mfn2) and Dynamin-related protein 1 (Drp1), as well as peroxisome proliferator-activated receptor γ coactivator-1 (PGC1-α). In addition, the clearance of damaged mitochondria in skeletal muscle was inhibited upon Sidt2 deletion, which was caused by blockade of autophagy flow. Mechanistically, the fusion of autophagosomes and lysosomes was compromised in Sidt2 knockout skeletal muscle cells. In summary, the deletion of the Sidt2 gene not only interfered with the quality control of mitochondria, but also inhibited the clearance of mitochondria and caused the accumulation of a large number of damaged mitochondria, ultimately leading to the abnormal structure and function of skeletal muscle.

Deletion of ApoM gene induces apoptosis in mouse kidney via mitochondrial and endoplasmic reticulum stress pathways.

Apolipoprotein M (ApoM) is involved in lipid metabolism, and especially is involved in reverse cholesterol transport. However, the relationship between ApoM and apoptosis has been rarely reported. This study aimed to investigate the effect of ApoM on apoptosis using an ApoM gene-deficient mice (ApoM-/-) model and a mouse mesangial cell model with suppressed ApoM gene expression. First, we observed by transmission electron microscopy that mitochondrial damage and endoplasmic reticulum stress were abnormally altered in the kidneys of ApoM-/- mice compared with wild-type mice, showing mitochondrial swelling, vacuolization, myeloid changes, and expansion of the rough endoplasmic reticulum. At the molecular level, the expression of pro-apoptotic related proteins such as AIF, Bax, chop, clever-caspase 3, clever-caspase 7, clever-caspase 9, and clever-caspase 12 increased, and the expression of anti-apoptotic protein Bcl-2 decreased. Secondly, by interfering with the expression of the ApoM gene in mouse mesangial cells, we found that, compared with the control group (NC-si), the cells of the experimental group (siApoM) showed decreased cell viability, nuclear chromatin condensation, nuclear lysis, and an increased proportion of early apoptotic cells. The results in cells at the molecular level were consistent with those at the tissue level. These data indicated that the deletion of the ApoM gene led to upregulation of apoptosis in mouse kidney tissues and mesangial cells through the mitochondrial and endoplasmic reticulum pathways.