Human dermal fibroblasts (HDFs) are critical for maintaining skin integrity and facilitating tissue repair, but are highly susceptible to apoptosis and impaired migration under inflammatory stress. Adipose-derived stem cells (ADSCs) exert regenerative effects primarily through paracrine signals, including exosomes enriched with trophic factors. In this study, we investigated the dual role of ADSC-derived exosomal hepatocyte growth factor (HGF) in regulating fibroblast apoptosis and migration under T cell-mediated inflammatory conditions. Co-culture of HDFs with activated Jurkat cells significantly increased apoptosis and inflammatory cytokine production, while treatment with ADSC-derived exosomes reduced apoptosis and enhanced fibroblast migration in a dose-dependent manner. Exosomal markers (CD9, CD63, TSG-101) were confirmed by Western blot, and enzyme-linked immunosorbent assay revealed time-dependent increases in HGF, insulin-like growth factor-1, fibroblast growth factor-2, and transforming growth factor-beta secretion following exosome treatment. Knockdown of HGF using siRNA abolished both the anti-apoptotic and pro-migratory effects of exosomes. Mechanistically, exosomal HGF selectively activated AKT phosphorylation in apoptotic regulation and induced FAK (Tyr397) phosphorylation and MMP-2 expression in migration. These findings suggest that exosomal HGF from ADSCs serves as a central mediator in promoting fibroblast survival and motility via the AKT-FAK axis, and may be a promising candidate for cell-free regenerative therapies targeting immune-mediated skin damage.

Myxomatous mitral valve disease (MMVD) is the most prevalent cardiac disease in dogs worldwide. Left atrial enlargement is a prominent feature associated with an increased risk of congestive heart failure in dogs with MMVD. Left atrial anteroposterior diameter (LAD) has been suggested as a supplementary parameter for evaluating LA size in various species. The purpose of our study was to establish a correlation between the left atrial anteroposterior diameter normalized to body weight (LADn) and N-terminal pro-brain natriuretic peptide (NT-proBNP) in dogs with MMVD and to assess the diagnostic potential of LADn for MMVD. We conducted this study on 35 dogs and categorized them into the control and MMVD groups. The control group consisted of 10 dogs, whereas the MMVD group included 25 dogs classified into stages B1, B2, and C according to the American College of Veterinary Internal Medicine (ACVIM) guidelines. LADn was measured using echocardiography, and NT-proBNP levels were assessed using a fluorescent immunoassay. In conclusion, LADn shows promise as a valuable diagnostic marker of MMVD in dogs. The strong positive correlation between LADn and NT-proBNP levels demonstrates the usefulness of LADn as a clinical index for evaluating cardiac function and disease progression in dogs with MMVD.

Esophageal perforation can be caused by Boerhaave syndrome, foreign body ingestion, trauma, operative injury, or tumors. The condition can be fatal and requires emergency treatment. In this case report, we describe an esophageal perforation following gastric calibration tube insertion during laparoscopic sleeve gastrectomy. The female patient developed an esophageal perforation after gastric calibration tube insertion during laparoscopic sleeve gastrectomy, even though there were no complications during the tube insertion. She had mucosal inflammation of the distal esophagus stemming from gastroesophageal reflux disease. Therefore, the perforation has occurred because the repeated adjustments of the calibration tube may have further damaged the mucosal area that was already weakened by gastroesophageal reflux disease. It is estimated that even slight mucosal inflammation can heighten the risk of esophageal perforation. We hope this report will help elucidate the causes and probability of encountering esophageal perforation due to mucosal inflammation.