The dynamic formation characteristics of droplets in a cross-junction can be captured via a high-speed image setup. The experimental results show four flow regimes: slug, dripping, jetting (threading and tubing), and viscous displacement. When Ca_d and Ca_c are small, the slug regime occurs. The dripping regime occurs when Ca_c is relatively high. The jetting regime appears when Ca_d increases to a considerable value. When Ca_c is much smaller than Ca_d, the viscous displacement regime occurs. In the slug and dripping regimes, the dispersed phase will experience growing, squeezing, and pinching off stages in the formation of droplets. These four flow regimes are strongly affected by Ca_c and Ca_d. In addition, the flow rates of the two phases can be changed to adjust the sizes of the generated droplet in the cross-junction under the slug regime and dripping regime. The dimensionless droplet length l* can be predicted via l* = (0.248 + 0.55Q)Ca_c^−0.203.

Purpose: Atopic dermatitis (AD) is a common inflammatory skin condition characterized by erythema and pruritus. Its precise pathogenesis remains unclear, though factors such as genetic predisposition, autoantigen response, allergen exposure, infections, and skin barrier dysfunction are involved. Research suggests a correlation between AD and mitochondrial dysfunction, as well as oxidative stress in skin tissues. Methods: Skin sample datasets related to AD (GSE36842, GSE120721, GSE16161, and GSE121212) were retrieved from the GEO database. Differential gene analysis identified differentially expressed genes (DEGs) in AD. Three potential biomarkers—COX17, ACOX2, and ADH1B—were identified using LASSO and Support Vector Machine (SVM) algorithms. These biomarkers were validated through ROC curve analysis, nomogram modeling, calibration curves, and real-time PCR. Immune infiltration analysis assessed correlations of the biomarkers. Additionally, single-cell analysis of the GSE153760 dataset identified nine cell clusters and confirmed expression patterns of the three hub genes. Results: Differential analysis identified 150 upregulated and 367 downregulated genes. Enrichment analysis revealed significant pathways related to mitochondrial function, oxidative stress, and energy metabolism in skin samples from AD patients. Area under the curve (AUC) values for biomarkers COX17, ACOX2, and ADH1B were 1.000, 0.928, and 0.895, respectively, indicating strong predictive capacity. qPCR results showed COX17 was highly expressed in AD lesions, while ACOX2 and ADH1B were higher in normal skin, consistent with previous findings. Correlation analysis indicated ACOX2 and ADH1B were positively correlated with resting mast cells but negatively with activated T cells and NK cells, while COX17 showed a positive correlation with activated T cells and a negative correlation with resting mast cells. Conclusion: This study suggests that the hub genes COX17, ACOX2, and ADH1B may serve as potential biomarkers in the pathogenesis of AD. These findings could provide insights for the treatment and prognosis of AD and related inflammatory skin conditions.

Systemic lupus erythematosus (SLE) is characterized by autoimmune dysregulation, elevated autoantibody production, and persistent inflammation, predisposing patients to atherosclerosis (AS). Atherogenesis is dependent on lipid homeostasis and inflammatory processes, with the formation of lipid-laden, macrophage-derived foam cells (MDFC) essential for atherosclerotic lesion progression. Elevated cholesterol levels within lipid rafts trigger heightened pro-inflammatory responses in macrophages via Toll-like receptor 9 (TLR9). Artesunate (ART), an artemisinin derivative sourced from Artemisia annua, exhibits therapeutic potential in modulating inflammation and autoimmune conditions. Nonetheless, its impact and mechanisms in SLE-associated AS (SLE-AS) remain largely unexplored. Our investigation demonstrated that ART could effectively ameliorate lupus-like symptoms and atherosclerotic plaque development in SLE-AS mice. Moreover, ART enhanced cholesterol efflux from MDFC by upregulating ABCA1, ABCG1, and SR-B1 both in vivo and in vitro. Moreover, ART reduced cholesterol accumulation in bone marrow-derived macrophages (BMDMs), thereby diminishing TLR9 recruitment to lipid rafts. ART also suppressed TLR9 expression and its downstream effectors in the kidney and aorta of SLE-AS mice, attenuating the TLR9-mediated inflammatory cascade in CPG2395 (ODN2395)-stimulated macrophages. Through bioinformatics analysis and experimental validation, PPARγ was identified as a pivotal downstream mediator of ART in macrophages. Depleting PPARγ levels reduced the expression of ABCA1, ABCG1, and SR-B1 in macrophages, consequently impeding cholesterol efflux. In conclusion, these findings suggest that ART ameliorates SLE-AS by restoring cholesterol homeostasis through the PPARγ-ABCA1/ABCG1/SR-B1 pathway and suppressing lipid raft-driven TLR9/MyD88 inflammation.