Effect of hydrocolloid dressings on preventing air leakage when applying negative pressure wound therapy to the perineum, buttocks, and sacrococcygeal region.

Maintaining a vacuum when applying negative pressure wound therapy (NPWT) is the key to its function, which is a challenge in the perineum, buttocks, and sacrococcygeal region. A retrospective cohort study was conducted to assess the effect of hydrocolloid dressings on preventing air leakage when applying NPWT in these regions. There were 61 patients in Group A (without the aid of hydrocolloid dressings) and 65 patients in Group B (with the aid of hydrocolloid dressings). The hydrocolloid dressing-assisted NPWT significantly reduced the incidence of air leakage compared with conventional NPWT placement (24.6% vs. 7.7%; risk ratio, 3.20; 95% confidence interval, 1.24-8.27; p = 0.009), while decreasing the number of open NPWT applications (2.2 vs. 1.7; difference, 0.43; 95% confidence interval, 0.19-0.66; p < 0.001), shortening hospital stays (20.1 vs. 16.1; difference, 4.07; 95% confidence interval, 1.68-6.46; p = 0.01), and reducing the incidence of adverse skin events (18.0% vs. 4.6%; risk ratio, 3.91; 95% confidence interval, 1.14-13.34; p = 0.017). These findings support the routine use of hydrocolloid dressing-assisted NPWT placement in the perineum, buttocks, and sacrococcygeal region.

Identification of inflammation-related biomarkers in keloids.

Background: The relationship between inflammation-related genes (IRGs) and keloid disease (KD) is currently unclear. The aim of this study was to identify a new set of inflammation-related biomarkers in KD. Methods: GSE145725 and GSE7890 datasets were used in this study. A list of 3026 IRGs was obtained from the Molecular Signatures Database. Differentially expressed inflammation-related genes (DEGs) were obtained by taking the intersection of DEGs between KD and control samples and the list of IRGs. Candidate genes were selected using least absolute shrinkage and selection operator (LASSO) regression analysis. Candidate genes with consistent expression differences between KD and control in both GSE145725 and GSE7890 datasets were screened as biomarkers. An alignment diagram was constructed and validated, and in silico immune infiltration analysis and drug prediction were performed. Finally, RT-qPCR was performed on KD samples to analyze the expression of the identified biomarkers. Results: A total of 889 DEGs were identified from the GSE145725 dataset, 169 of which were IRGs. Three candidate genes (TRIM32, LPAR1 and FOXF1) were identified by the LASSO regression analysis, and expression validation analysis suggested that FOXF1 and LPAR1 were down-regulated in KD samples and TRIM32 was up-regulated. All three candidate genes had consistent changes in expression in both the GSE145725 and GSE7890 datasets. An alignment diagram was constructed to predict KD. Effector memory CD4 T cells, T follicular helper cell, Myeloid derived suppressor cell, activated dendritic cell, Immature dendritic cell and Monocyte were differentially expressed between the KD and control group. Sixty-seven compounds that may act on FOXF1, 108 compounds that may act on LPAR1 and 56 compounds that may act on TRIM32 were predicted. Finally, RT-qPCR showed that the expression of LPAR1 was significantly lower in KD samples compared to normal samples whereas TRIM32 was significantly higher, while there was no difference in the expression of FOXF1. Conclusion: This study provides a new perspective to study the relationship between IRGs and KD.

The regulatory role of the apelin/APJ axis in scarring: Identification of upstream and downstream mechanisms.

Scarring, a prevalent issue in clinical settings, is characterized by the excessive generation of extracellular matrix within the skin tissue. Among the numerous regulatory factors implicated in fibrosis across various organs, the apelin/APJ axis has emerged as a potential regulator of fibrosis. Given the shared attribute of heightened extracellular matrix production between organ fibrosis and scarring, we hypothesize that the apelin/APJ axis also plays a regulatory role in scar development. In this study, we examined the expression of apelin and APJ in scar tissue, normal skin, and fibroblasts derived from these tissues. We investigated the impact of the hypoxic microenvironment in scars on apelin/APJ expression to identify the transcription factors influencing apelin/APJ expression. Through overexpressing or knocking down apelin/APJ expression, we observed their effects on fibroblast secretion of extracellular matrix proteins. We further validated these effects in animal experiments while exploring the underlying mechanisms. Our findings demonstrated that the apelin/APJ axis is expressed in fibroblasts from keloid, hypertrophic scar, and normal skin. The regulation of apelin/APJ expression by the hypoxic environment in scars plays a significant role in hypertrophic scar and keloid development. This regulation promotes extracellular matrix secretion through upregulation of TGF-ß1 expression via the PI3K/Akt/CREB1 pathway.