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.
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.
This study aimed to identify target genes regulated by KSHV miRNAs in KSHV-infected lymphoma cells. Original Ago HITS-CLIP data of BC-3 and BCBL-1 cell lines were downloaded from SRA database in NCBI, including mRNA and miRNA samples. The raw mRNA reads were mapped into human reference genome hg19 via TopHat for read alignment. PCR duplicates were removed via the SAM tool and the peaks of reads were analyzed via Cufflinks. For miRNA data, the raw data were mapped to the mature miRNA sequences based on miRBase via Bowtie. Peak intersection was computed by using intersectBed in BEDtools. Then, the mature miRNA seeds were identified and then were aligned with 3' UTR merged peaks. The regulationships of miRNAs and their corresponding genes were analyzed based on the signal of RNA-induced silencing complex. Totally, 7 KSHV-related genes regulated by KSHV miRNAs were identified, including IPO5, EDA, NT5C3, WSB1, KCNS1, PRAM1 and MTRNR2L6. Among them, EDA, MTRNR2L6 and IPO5 were regulated by multiple KSHV miRNAs, such as kshv-miR-K12-1-5p, kshv-miR-K12-4-3p and kshv-miR-K12-3-5p, respectively. Furthermore, expression of kshv-miR-K12-1-5p and kshv-miR-K12-3-5p in BCBL-1 cell line were lower than that in BC-3 cell line, conversely, expression of kshv-miR-K12-4-3p in BCBL-1 cell line were higher than that in BC-3 cell line. In conclusion, potential target genes regulated by KSHV miRNAs in KSHV-infected lymphoma cells might play key roles in the nosogenesis of this disease. These findings might provide the basis for deep understanding of KSHV-infected tumors and further molecular experiments.
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