Objective:To investigate the efficacy of vacuum sealing drainage (VSD) in the treatment of severe maxillofacial and neck space infection.Methods:9 patients (6 males,3 females) with severe maxillofacial and neck space infection were treated with VSD.After incision of abscess,the incision was covered by VSD material and 40-60 KPa continuous negative pressure drainage was given.Results:Swelling and pain of the patients reduced rapidly.The period of VSD treatment was 4 to 10 days (mean 5.8 days).9 patients were all cured without mediastinitis.Conclusion:VSD ehhance the dranage efficiency and prevent infection spreading.

Objective:Heart failure(HF),a worldwide health condition,is the result of many cardiovascular diseases.The traditional Chinese medicine(TCM)Xiaoyu Jiangzhi capsule(XYC)has long been in use in China to treat hyperlipidemia and inhibit platelet aggregation.This study explores the effects of XYC on heart failure(HF)and its detailed mechanisms.Methods:Isoproterenol(ISO,30 mg/kg)was injected intraperitoneally for 7 days to copy a HF model of 10-12 weeks old,20-30 g male mice.We then compared the CON(control)group,ISO(HF model)group,MET(metoprolol)group,and XYC group.Cardiac systolic function and left wall thickness were evaluated by echocardiograph.Using western blot analysis,we detected the proteins of calmodulin dependent protein kinase Ⅱ(CaMKII)and sarco/endoplasmic reticulum Ca2+-ATPase(Serca).Further-more,tsA201 cells were cultured and the human CaV1.2 calcium channel current(hCaV1.2)were detected by patch clamp experiments.Results:XYC reduced HF,inhibiting the protein expression of CaMKII,but Serca did not change signifi-cantly.Moreover,XYC inhibited the peak amplitude of the hCaV1.2 current,depolarizing shifted the activation curve 27.6 mV,and shifted the inactivation curve toward a positive potential 17.6 mV.The fraction recovered from inaction was reduced in XYC group compared with that in CON group.Conclusion:XYC could inhibit ISO-induced HF by reducing the Ca2+/CaMKII signaling pathway in mice.

Carcinoma-associated fibroblasts (CAFs) are the main cellular components of the tumor microenvironment and promote cancer progression by modifying the extracellular matrix (ECM). The tumor-associated ECM is characterized by collagen crosslinking catalyzed by lysyl oxidase (LOX). Small extracellular vesicles (sEVs) mediate cell-cell communication. However, the interactions between sEVs and the ECM remain unclear. Here, we demonstrated that sEVs released from oral squamous cell carcinoma (OSCC)-derived CAFs induce collagen crosslinking, thereby promoting epithelial-mesenchymal transition (EMT). CAF sEVs preferably bound to the ECM rather than being taken up by fibroblasts and induced collagen crosslinking, and a LOX inhibitor or blocking antibody suppressed this effect. Active LOX (αLOX), but not the LOX precursor, was enriched in CAF sEVs and interacted with periostin, fibronectin, and bone morphogenetic protein-1 on the surface of sEVs. CAF sEV-associated integrin α2β1 mediated the binding of CAF sEVs to collagen I, and blocking integrin α2β1 inhibited collagen crosslinking by interfering with CAF sEV binding to collagen I. CAF sEV-induced collagen crosslinking promoted the EMT of OSCC through FAK/paxillin/YAP pathway. Taken together, these findings reveal a novel role of CAF sEVs in tumor ECM remodeling, suggesting a critical mechanism for CAF-induced EMT of cancer cells.
Humans ; Paxillin/metabolism* ; Protein-Lysine 6-Oxidase/metabolism* ; Carcinoma, Squamous Cell/pathology* ; Epithelial-Mesenchymal Transition ; Integrin alpha2beta1/metabolism* ; Mouth Neoplasms/pathology* ; Collagen/metabolism* ; Fibroblasts ; Extracellular Vesicles/metabolism* ; Cell Line, Tumor ; Tumor Microenvironment