BackgroundThis study aimed to evaluate the combined effect of vacuum sealing drainage (VSD) and antibiotic-loaded bone cement on soft tissue defects and infection.Material/MethodsThis prospective non-blinded study recruited 46 patients with soft tissue defects and infection from January 2010 to May 2014 and randomly divided them into experimental and control groups (n=23). Patients in the experimental group were treated with VSD and antibiotic-loaded bone cement, while the patients in the control group were treated with VSD only.ResultsIn the experimental group, the wound was healed in 23 cases at 4 weeks postoperatively, of which direct suture was performed in 12 cases, and additional free flap transplantation or skin grafting was performed in 6 cases and 5 cases, respectively. No infection reoccurred in 1-year follow-up. In the control group, the wound was healed in 15 cases at 6 weeks postoperatively, of which direct suture was performed in 8 cases, and additional free flap transplantation or skin grafting was performed in 3 cases and 4 cases, respectively. In the other 8 cases the wound was healed at 8 weeks postoperatively. Infection reoccurred in 3 cases during the follow-up. The experimental group had significantly fewer VSD dressing renewals, shorter time needed until the wound was ready for surgery, shorter duration of antibiotic administration, faster wound healing, and shorter hospital stay than the control group (p<0.01).ConclusionsThe combination of VSD and antibiotic bone cement might be a better method for treatment of soft tissue defects and infection.

Articular cartilage injury and defect caused by trauma and chronic osteoarthritis vascularity are very common, while the repair of injured cartilage remains a great challenge due to its limited healing capacity. Stem cell-based tissue engineering provides a promising treatment option for injured articular cartilage because of the cells potential for multiple differentiations. However, its application has been largely limited by stem cell type, number, source, proliferation, and differentiation. We hypothesized that (1) adipose-derived stem cells are ideal seed cells for articular cartilage repair because of their accessibility and abundance and (2) the microenvironment of articular cartilage could induce adipose-derived stem cells (ADSCs) to differentiate into chondrocytes. In order to test our hypotheses, we isolated stem cells from rabbit adipose tissues and cocultured these ADSCs with rabbit articular cartilage chondrocytes. We found that when ADSCs were cocultured with chondrocytes, the proliferation of articular cartilage chondrocytes was promoted, the apoptosis of chondrocytes was inhibited, and the osteogenic and chondrogenic differentiation of ADSCs was enhanced. The study on the mechanism of this coculture system indicated that the role of this coculture system is similar to the function of TGF-β1 in the promotion of chondrocytes.

Melanoma, which is usually induced by ultraviolet light exposure and the following DNA damage, is the most dangerous skin cancer. The purpose of the present study was to screen key molecules involved in melanoma.Microarray data of E-MTAB-1862 were downloaded from the ArrayExpress database, which included 21 primary melanoma samples and 11 benign nevus samples. In addition, the RNASeq version 2 and microRNA (miRNA) sequencing data of cutaneous melanoma were downloaded from The Cancer Genome Atlas database. After identifying the differentially expressed genes (DEGs) using Limma package, enrichment analysis and protein-protein interaction (PPI) network analysis were performed separately for them using DAVID software and Cytoscape software. In addition, survival analysis and regulatory network analysis were further performed by log-rank test and Cytoscape software, respectively. Moreover, real-time reverse transcription polymerase chain reaction (RT-PCR) was performed to further verify the expression patterns of several selected DEGs.A total of 382 DEGs were identified in primary melanoma samples, including 206 upregulated genes and 176 downregulated genes. Functional enrichment analysis showed that COL17A1 was enriched in epidermis development. In the PPI network, CXCL8 (degree = 29) and STAT1 (degree = 28) had higher degrees and could interact with each other. Survival analysis showed that 21 DEGs, 55 long noncoding RNAs (lncRNAs) and 32 miRNAs were found to be associated with prognosis. Furthermore, several regulatory relationships were found in the lncRNA-gene regulatory network (such as RP11-361L15.4 targeting COL17A1) and the miRNA-gene regulatory network (such as hsa-miR-375 targeting CCL27 and hsa-miR-375 targeting insulin-like growth factor 1 receptor [IGF1R]). Real-time RT-PCR results showed that the overall direction of differential expression was consistent except COL17A1.CXCL8 interacted with STAT1, CCL27, and IGF1R targeted by hsa-miR-375, and COL17A1 targeted by RP11-361L15.4 might function in the development and progression of melanoma, which should be verified by more detailed experiments.

The present study aimed to investigate the genetic effects of hydrocortisone (HC) treatment on keloids and screen medicines to be used in a combination therapy of keloids with HC. The dataset GSE7890 was downloaded from Gene Expression Omnibus. It contained data regarding 4 fibroblast samples from normal scar tissue and 5 samples from keloid tissue with HC treatment, as well as 5 samples from normal scar and 5 samples from keloids without HC treatment. Following the identification of differentially expressed genes (DEGs), the functions of these DEGs were analyzed by Gene Ontology (GO) and pathway enrichment analyses. Furthermore, adverse effects of HC were identified using WebGestalt. Additionally, candidate small molecule drugs associated with keloids were selected from a connectivity map database. A total of 166 and 41 DEGs, with and without HC treatment respectively, were only present in dermal fibroblasts from keloids (termed genesets A and B, respectively). A set of 26 DEGs was present following both treatments (geneset C). A number of DEGs in geneset B (COL18A1 and JAG1) were associated with endothelial cell differentiation. However, in genesets A and C, certain genes (CCNB1 and CCNB2) were involved in the cell cycle and p53 signaling pathways, and a number of genes (IL1R1 and COL1A1) were associated with bone loss. Additionally, numerous small molecule drugs (including acemetacin) were associated with keloids. Thus, it has been determined that HC may treat keloids by targeting genes associated to endothelial cell differentiation (COL18A1 and JAG1). However, HC has a number of adverse effects, including bone loss. Acemetacin may be applied in a combination therapy, along with HC, to treat keloids.

The present study aimed to investigate the molecular mechanisms underlying non-syndromic cleft lip, with or without cleft palate (NSCL/P), and the association between this disease and cancer. The GSE42589 data set was downloaded from the Gene Expression Omnibus database, and contained seven dental pulp stem cell samples from children with NSCL/P in the exfoliation period, and six controls. Differentially expressed genes (DEGs) were screened using the RankProd method, and their potential functions were revealed by pathway enrichment analysis and construction of a pathway interaction network. Subsequently, cancer genes were obtained from six cancer databases, and the cancer-associated protein-protein interaction network for the DEGs was visualized using Cytoscape. In total, 452 upregulated and 1,288 downregulated DEGs were screened. The upregulated DEGs were significantly enriched in the arachidonic acid metabolism pathway, including PTGDS, CYP4F2 and PLA2G16; and transforming growth factor (TGF)-β signaling pathway, including SMAD3 and TGFB2. The downregulated DEGs were distinctly involved in the pathways of DNA replication, including MCM2 and POLA1; cell cycle, including CDK1 and STAG1; and viral carcinogenesis, including PIK3CA and HIST1H2BF. Furthermore, the pathways of cell cycle and viral carcinogenesis, with higher degrees of interaction were found to interact with other pathways, including DNA replication, transcriptional misregulation in cancer, and the TGF-β signaling pathway. Additionally, TP53, CDK1, SMAD3, PIK3R1 and CASP3, with higher degrees, interacted with the cancer genes. In conclusion, the DEGs for NSCL/P were implicated predominantly in the TGF-β signaling pathway, the cell cycle and in viral carcinogenesis. The TP53, CDK1, SMAD3, PIK3R1 and CASP3 genes were found to be associated, not only with NSCL/P, but also with cancer. These results may contribute to a better understanding of the molecular mechanisms of NSCL/P.