The skin is one of the most vital organs in the human body, and skin wounds caused by various factors can severely impact patients’ physical and mental health. Among the therapeutic strategies for skin wound repair, mesenchymal stem cell-derived exosomes (MSC-Exos) have emerged as a promising biological therapy, attracting significant attention in related research. As critical mediators of stem cell biological effects, MSC-Exos fuse with target cells and transfer bioactive proteins and nucleic acids from stem cells into recipient cells. These exosomes modulate inflammatory responses, promote cell proliferation, migration, and angiogenesis, and regulate extracellular matrix remodeling, thereby accelerating wound healing. In recent years, studies on the mechanisms by which exosomes promote skin wound repair have advanced and refined continuously. This article summarized the key signaling pathways through which MSC-Exos participate in skin wound repair, aiming to enhance the understanding of their roles in facilitating wound healing.

The skin is one of the most vital organs in the human body, and skin wounds caused by various factors can severely impact patients’ physical and mental health. Among the therapeutic strategies for skin wound repair, mesenchymal stem cell-derived exosomes (MSC-Exos) have emerged as a promising biological therapy, attracting significant attention in related research. As critical mediators of stem cell biological effects, MSC-Exos fuse with target cells and transfer bioactive proteins and nucleic acids from stem cells into recipient cells. These exosomes modulate inflammatory responses, promote cell proliferation, migration, and angiogenesis, and regulate extracellular matrix remodeling, thereby accelerating wound healing. In recent years, studies on the mechanisms by which exosomes promote skin wound repair have advanced and refined continuously. This article summarized the key signaling pathways through which MSC-Exos participate in skin wound repair, aiming to enhance the understanding of their roles in facilitating wound healing.

The clinical data of a case of adrenal alveolar echinococcosis treated and misdiagnosed in our hospital were reported retrospectively. The pre-operative CT examination of this patient showed that the liver S7 segment-the right adrenal gland area showed irregular masses of mixed density lesions, the boundary was unclear, consider the possibility of liver hydatid. During the operation, hydatid was found to only invade the liver capsule, and the primary lesion was the adrenal gland. The right adrenal gland and lesion were resected by urological surgeons. The pathological diagnosis was adrenal alveolar echinococcosis. When the imaging examination considers hepatic alveolar echinococcosis, and the lesion is mainly in the right adrenal gland area, it should be considered that the primary lesion could be in the adrenal gland.

Objective To analyze the age difference of gram negative isolates(GNB)from blood culture and antibiotic resistance profile between children and adults. Methods Age difference of pathogen distribution of GNB isolated from blood culture during 2015-2017 were retrospectively analyzed. WHONET 5.6 and Graphpad Prism 6 were used to perform Chi-square test on the pathogen proportion and antibiotic resistance rate. Results A total of 20 145 bacterial strains were isolated in Chongqing from 2015 to 2017. The top three strains of GNB were E. coli(56.7％, 6 688/11 799), K. pneumoniae(19.6％, 2 308/11 799), and P. aeruginosa(4.4％, 522/11 799). The resistant rate of E. coli to carbapenems was less than 1％. The resistant rate of K. pneumoniae to carbapenems was about 5％, while the resistant rate of S. marcescens was approximately 9％, similar to E. cloacae. The overall resistance rates of E. coli from adult patients to most antiobiotic agents were significantly higher than those of children, but the overall resistance rate of K. pneumoniae from children was higher than those of adults. The drug resistance rate of A. baumannii was higher than P. aeruginosa. A. baumannii isolates from adult patients were highly resistant to all drugs tested and more resistant than those from pediatric patients. Conclusions Majority of GNB strains isolated from blood culture were E. coli and K. pneumoniae, for which carbapenems are still active. More attention should be paid to carbapenem-resistant K. pneumoniae from children and A. baumannii from adults. National surveillance of nosocomial bloodstream infection should be highly evaluated.

AIM:To investigate the role of caveolin-1 on epithelial-mesenchymal transition (EMT) in human bronchial epithelial (HBE) cells induced by transforming growth factor beta 1 (TGF-β1).METHODS:Immunofluorescence, real-time PCR and Western blot were applied to detect the mRNA and the protein expression of caveolin-1 in the 16HBE cells during EMT.The influence of siRNA-mediated silencing of caveolin-1 on EMT in the 16HBE cells was detected by Western blot.RESULTS:Caveolin-1 was widely present on the cell membrane of the 16HBE cells.The expression of caveolin-1 at mRNA and protein levels was significantly decreased in a time-dependent manner in the 16HBE cells compared with control group (P<0.05) after stimulation with TGF-β1.The morphologic changes of the 16HBE cells induced by TGF-β1 were promoted by caveolin-1 silencing compared with TGF-β1 group.The protein expression of E-cadherin and α-SMA induced by TGF-β1 was promoted by caveolin-1 silencing compared with TGF-β1 group (P<0.05).The phosphorylation levels of AKT and Smad3 were the highest at 30 min and increased significantly compared with control group (P<0.05) after stimulated with TGF-β1.Treatment of the 16HBE cells with TGF-β1 for 30 min after silencing caveolin-1 gene for 24 h significantly increased the phosphorylation levels of AKT and Smad3 compared with TGF-β1 group (P<0.05).CONCLUSION:TGF-β1 down-regulates the expression of caveolin-1 in the 16HBE cells.Caveolin-1 may participate in TGF-β1/Smad pathway and PI3K-AKT pathway, which are the signal transduction pathways for TGF-β1 inducing EMT.

Objective To determine whether field triage would reduce median contact-to-device ( C2D ) time in patients with ST-segment elevation acute myocardial infarction ( STEMI ) . Methods Consecutive patients with STEMI underwent primary percutaneous coronary intervention( PCI) from March 2010 to February 2014 in Shanghai Pudong Gongli Hospital were analyzed. Patients were divided into two groups. A total of 121 patients were admitted by field triage and 101 patients by non-field triage. The primary study point was C2D time and the study points secondary included ( door-to-balloor, D2B) time, peak Troponin I ( TnI) levels, hospital mortality and 30 days follow-up mortality. Results Baseline and procedural characteristics between the two groups were comparable. Comparing to non-field triage group, the C2D time was reduced [(92. 0 ± 56. 0)min vs. (131. 0 ± 61. 0)min,P﹤0. 01]. The D2B time was lower in the field triage group vs. the non-field triage group [(55. 0 ±26. 0)min vs. (96. 0 ±31. 0)min,P﹤0. 01]. The percentage of patients with C2D time less than 90 minutes increased significantly from 85. 1% to 98. 3%( P﹤0. 01 ) in the field triage group. Peak TnI level was significantly reduced in the field triage group [(23. 5 ±22. 0) μg/L vs. (43. 5 ± 39. 0) μg/L,P﹤0. 01]. In-hospital mortality and 30 days follow-up mortality did not significantly differ between the 2 groups (3. 3% and 3. 0%, P=0. 885;3. 3% and 5. 0%, P=0. 544, respectively). Conclusions In STEMI patients, field triage was associated with significantly reduced C2D and D2B times.

AIM:To investigate the role of canonical transient receptor potential channel 1 ( TRPC1 ) in the migration of human bronchial epithelial cells (16HBE) induced by transforming growth factor-β1 ( TGF-β1).METH-ODS:Silencing of TRPC1 gene expression was performed by siRNA.The cell activity and apoptosis were measured by CCK-8 assay and flow cytometry, respectively.The migration and invasion abilities of the 16HBE cells were detected by wound-healing assay and Transwell assay.The protein expression of E-cadherin and vimentin was determined by Western blot.RESULTS:TGF-β1 treatment significantly enhanced the cell migration distance compared with control groups ( P<0.01 ) .The results of CCK-8 assay and flow cytometry indicated that there were no significant difference in proliferation and apoptosis among TRPC1 siRNA group, TGF-β1 group and control group (P>0.05).The results of wound-healing and Tr-answell assays showed that migration and invasion abilities in TRPC1 siRNA +TGF-β1 group were markedly suppressed compared with TGF-β1 group (P<0.01).The protein expression of E-cadherin and vimentin induced by TGF-β1 was in-hibited by TRPC1 silencing compared with TGF-β1 group (P<0.05).CONCLUSION:TRPC1 is involved in the migra-tion of human bronchial epithelial cells induced by TGF-β1 through regulating the protein expression of E-cadherin and vim-entin.

BACKGROUND:Placenta is a valuable source of mesenchymal stem cels for stem cel therapy and future application in the field of regenerative medicine. However, conventional methods cannot acquire a large amount of purified human placenta-derived mesenchymal stem cels. Here, we present a new method for isolating human placenta-derived mesenchymal stem cels suitable for banking strategies and for future clinical applications. OBJECTIVE:To analyze the biological characteristics of human placenta-derived mesenchymal stem cels cultured by tissue dissociating and colagenase digestion. METHODS: Human placenta-derived mesenchymal stem cels were obtained from human placenta by tissue dissociating and colagenase digestion method. Immunophenotype was analyzed by flow cytometry. Growth curve was determined by MTT assay, and differentiation ability was evaluated byin vitro adipogenic, osteogenic and chondrogenic induction as wel. RESULTS AND CONCLUSION:Human placenta-derived mesenchymal stem cels could be passaged stablyin vitro. Furthermore, the cels expressed CD73, CD90, CD105, but were negative for the markers of CD11b, CD19, CD34, CD45, and HLA-DR. Human placenta-derived mesenchymal stem cels proliferated actively and began to grow logarithmicaly at days 3-5 folowed by a plateau period at day 6. In addition, the isolated cels could be induced into adipocytes, osteocytes, chondrocytesin vitro. In a word, the results of this study demonstrated that the tissue dissociating and colagenase digestion method is an efficient method for obtaining a large amount of human placenta-derived mesenchymal stem cels that can be stably cultured in vitro and have strong proliferative ability.

[ ABSTRACT] AIM:To investigate the role of canonical transient receptor potential channel 1 ( TRPC1 ) in the epithelial-mesenchymal transition ( EMT) of human bronchial epithelial ( HBE) cells induced by transforming growth fac-tor-β1 (TGF-β1).METHODS:EMT of 16HBE cells induced by TGF-β1 were identified by microscopy, immunofluores-cence and Western blotting.Immunofluorescence, real-time PCR and Western blotting were applied to detect the mRNA and the protein expression of TRPC1 in the 16HBE cells.The influence of SKF96365 (a TRPC1 blocker) and siRNA-me-diated silencing of TRPC1 on the EMT of the 16HBE cells were detected by microscopy and Western blotting.RESULTS:Treatment with TGF-β1 induced significant morphological changes of the 16HBE cells.Exposure to TGF-β1 decreased the expression of E-cadherin protein (P<0.01) and increased the expression of α-SMA protein (P<0.05) in the 16HBE cells.Immunofluorescence observation indicated that TRPC1 expression in the 16HBE cells was positive.The expression of TRPC1 at mRNA and protein levels was significantly increased in the 16HBE cells after stimulation with TGF-β1 ( P<0.05).The morphological changes of the 16HBE cells induced by TGF-β1 were inhibited by SKF96365 and TRPC1 silen-cing compared with TGF-β1 group.The protein expression of E-cadherin andα-SMA induced by TGF-β1 were inhibited by SKF96365 and TRPC1 silencing compared with TGF-β1 group (P<0.05).CONCLUSION:TGF-β1 induces EMT with the mechanism of up-regulating TRPC1 in human bronchial epithelial cells.

Objective To establish an aging model of mesenchymal stem cells (MSCs) and to investigate aging related biological mechanism for the purpose of studying the senesence of MSCs .Methods MSCs were separated and purified from human placenta, and the cells of the third passage(P3-MSCs) were cultured in the medium for 2 hours, then 100,200 and 300 μmol/L hydrogen peroxide ( H2 O2 ) was added to the cells for 2 hours to establish the MSCs aging model in vitro. Biological characteristics of aging MSCs were evaluated by cell cycle assay and senescence associated β-galactosidase staining.The expression of p16,p21 and p53 genes was further measured using quantitative real-time PCR (RT-PCR).Re-sults Compared with the control , the number of MSCs treated with 200μmol/L H2 O2 for 2 hours was significantly decreased and the cells displayed less adipogenic ,osteogenic and chondrogenic differentiation .Moreover ,after exposure to 200 μmol/L H2 O2 , the majority of the cells were in the G 0/G1 phase as showed by cell cycle analysis .The percentage of senescence-associated β-galactosidase-positive cells was increased , and the expression of p 16 , p21 and p53 mRNA and protein was significantly increased.Conclusion The results of this study has demonstrated that the H 2 O2 (200 μmol/L) can be used to establish the aging model of MSCs in vitro, and the cellular phenotypic alteration may attribute to the cell cycle associated gene expression (p16, p21, and p53).