The aim of this study is to introduce experiences of reconstruction of total degloving injuries of the foot in children.Seven children, five male and two female, were treated for total degloving injury of the foot at our medical institution between January 2002 and December 2008. Patients were between 5 years and 9 years of age with a mean age of 7 years. All injuries involved the total foot. In cases 1-3, the foot was covered by intermediate split-thickness skin graft. In cases 4-7, the dorsal aspect of the foot was covered by full-thickness skin graft obtained from the degloving flap in emergency operation and the planta aspect of the foot was covered by posteriortibial artery flap in the second operation.The mean time to wound healing was 29 days to 50 days in cases 1-3 and 21 days to 28 days in cases 4-7. The posteriortibial artery flaps in cases 4-7 all survived. Both the donor and the recipient site healed successfully. All patients were followed for at least 12 months (range, 12-24 months; mean, 17.9 months). All patients showed insensitivity at the recipient sites. No patient complained of cold intolerance in the foot. Cases 1-3 had pain, deformity, and dysfunction to some extent at follow-up. Cases 4-7 did not exhibit pain, deformity, or dysfunction. All toes were amputated in all cases. Patients 1-3 scored fair or poor on the Maryland Foot Score (two fair, one poor), and patients 4-7 scored either good or fair (three good, one fair).This method, the dorsal aspect of the foot covered by full-thickness skin and the planta aspect of the foot covered by posteriortibial artery flap, is a good choice for treatment of total degloving injury of foot in children. At the same time, the early exercise should be emphasized for the functional recovery.Therapeutic study, level IV.
Abstract Background: To report on the technique and results of parallel endplate osteotomy (PEO) for severe rigid spinal deformity. Methods: Between July 2016 and December 2018, 36 patients with severe rigid spinal deformities who underwent PEO were retrospectively reviewed after a minimum follow-up of 24 months. Results: Following PEO, the kyphosis and scoliosis correction rates reached 77.4 ± 14% and 72.2 ± 18.2%, respectively. The median intraoperative estimated blood loss was 1500 mL and the operative time was 6.8 h. The SF-36 scores of physical function, role-physical, bodily pain, general health, vitality, social function, role-emotional and mental health changed from 62 ± 28, 51 ± 26, 49 ± 29, 35 ± 30, 53 ± 28, 45 ± 30, 32 ± 34 and 54 ± 18 at baseline to 81 ± 16, 66 ± 41, 72 ± 40, 64 ± 44, 75 ± 25, 71 ± 46, 66 ± 34 and 76 ± 28 at one year postoperatively , 82 ± 32, 67 ± 42, 81 ± 30, 71 ± 41, 80 ± 30, 74 ± 36, 68 ± 35 and 85 ± 33 at 18 months postoperatively, and 86 ± 21, 83 ± 33, 88 ± 26, 79 ± 39, 86 ± 36, 86 ± 48, 80 ± 47 and 91 ± 39 at 24 months postoperatively, respectively. Conclusions: PEO is an effective technique for successful correction of spinal deformities. At the two year follow-up visit, all patients achieved better clinical results based on the SF-36 scores.
To report on the technique and results of parallel endplate osteotomy (PEO) for severe rigid spinal deformity.We retrospectively reviewed the clinical data of 36 patients with severe rigid spinal deformities who underwent PEO between July 2016 and December 2018 and who were followed up for at least 24 months.Following PEO, the kyphosis and scoliosis correction rates reached 77.4 ± 14.0% and 72.2 ± 18.2%, respectively. The median intraoperative estimated blood loss was 1500 mL and the median operative time was 6.8 h. The SF-36 scores of physical function, role-physical, bodily pain, general health, vitality, social function, role-emotional and mental health changed from 62 ± 28, 51 ± 26, 49 ± 29, 35 ± 30, 53 ± 28, 45 ± 30, 32 ± 34 and 54 ± 18 at baseline to 81 ± 16, 66 ± 41, 72 ± 40, 64 ± 44, 75 ± 25, 71 ± 46, 66 ± 34 and 76 ± 28 at 12 months postoperatively, 82 ± 32, 67 ± 42, 81 ± 30, 71 ± 41, 80 ± 30, 74 ± 36, 68 ± 35 and 85 ± 33 at 18 months postoperatively, and 86 ± 21, 83 ± 33, 88 ± 26, 79 ± 39, 86 ± 36, 86 ± 48, 80 ± 47 and 91 ± 39 at 24 months postoperatively, respectively.PEO is an effective technique for successful correction of spinal deformities. At the two-year follow-up visit, all patients achieved better clinical results based on the SF-36 scores.
// Zi-Feng Zhang 1, * , Yong-Jian Wang 1, * , Shao-Hua Fan 1 , Shi-Xin Du 2 , Xue-Dong Li 2 , Dong-Mei Wu 1 , Jun Lu 1 and Yuan-Lin Zheng 1 1 Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, P.R. China 2 Department of Orthopedics, The Third Affiliated Hospital, Shenzhen University, Shenzhen 518002, P.R. China * Co-first authors Correspondence to: Dong-Mei Wu, email: wdm8610@jsnu.edu.cn Jun Lu, email: lu-jun75@163.com Yuan-Lin Zheng, email: ylzheng@jsnu.edu.cn Keywords: microRNA-182, homeobox A9, wingless-type/β-catenin signaling pathway, osteosarcoma Received: April 14, 2017 Accepted: September 04, 2017 Published: September 22, 2017 ABSTRACT We investigated the mechanisms by which microRNA (miR)-182 promotes apoptosis and inhibits proliferation in human osteosarcoma (OS) cells. Levels of miR-182 and Homeobox A9 (HOXA9) expression were compared between human OS and normal cells. Subjects were divided into OS and normal groups. We analyzed the target relationship of miR-182 and Homeobox A9 (HOXA9). Cells were then assigned into blank, negative control, miR-182 mimics, miR-182 inhibitors, siRNA-HOXA9, or and miR-182 inhibitors + siRNA-HOXA9 groups. Cell function was assayed by CCK-8, flow cytometry and wound healing assay. Additionally, we analyzed OS tumor growth in a xenograft mouse model. Dual-luciferase reporter assays indicated miR-182 directly targets HOXA9. Reverse transcription quantitative PCR and western blotting revealed elevated expression of miR-182, WIF-1, BIM, and Bax, and reduced expression of HOXA9, Wnt, β-catenin, Survivin, Cyclin D1, c-Myc, Mcl-1, Bcl-xL, and Snail in osteosarcoma cells treated with miR-182 mimic or siRNA-HOXA9 as compared to controls. Osteosarcoma cells also exhibited decreased cell proliferation, migration, and tumor growth, and increased apoptosis when treated with miR-182 mimic or siRNA-HOXA9. Correspondingly, in a xenograft mouse model, osteosarcoma tumor volume and growth were increased when cells were treated with miR-182 inhibitor and decreased by miR-182 mimic or siRNA-HOXA9. These results indicate that miR-182 downregulates Wnt/β-catenin signaling, inhibits cell proliferation, and promotes apoptosis in osteosarcoma cells by suppressing HOXA9 expression.
Osteosarcoma is the most common primary malignant bone tumor in children and adolescents. Many patients with osteosarcoma readily develop resistance to chemotherapy and have an extremely dismal prognosis. Dioscin, a saponin, is known to exhibit potent anticancer activities and induce cellular death of a variety of cancer types. However, the inhibitory effect of dioscin on osteosarcoma cells and its underlying mechanisms have not been fully elucidated. We investigated the responses of human U2-OS and MG63 osteosarcoma cells to dioscin with regard to proliferation, apoptosis, migration, and invasion, and studied the effect of dioscin on MAPK-related proteins by western blot analysis assays. Dioscin inhibited osteosarcoma cell proliferation, migration, and invasion. Moreover, it induced osteosarcoma cell apoptosis via reactive oxygen species (ROS)-dependent apoptotic signaling. N-acetylcysteine, a reactive oxygen species inhibitor, suppressed dioscin-induced apoptosis, indicating that ROS play an essential role in dioscin-induced apoptosis. Western blot analysis assays showed that p38 MAPK was upregulated after dioscin treatment, and that dioscin induced apoptosis by upregulating ROS-mediated p38 MAPK signaling. Our study suggests that dioscin possesses antitumor activities against human osteosarcoma cells, inhibits osteosarcoma cell proliferation, migration and invasion, and induces osteosarcoma cell apoptosis through upregulating ROS-mediated p38 MAPK signaling. This study may provide a new therapeutic strategy and potential clinical applications for the treatment of osteosarcoma.
Osteosarcoma (OS) is the most common primary bone malignancy. It predominantly occurs in adolescents, but can develop at any age. The age at diagnosis is a prognostic factor of OS, but the molecular basis of this remains unknown. The current study aimed to identify age‑induced differentially expressed genes (DEGs) and potential molecular mechanisms that contribute to the different outcomes of patients with OS. Microarray data (GSE39058 and GSE39040) obtained from the Gene Expression Omnibus database and used to analyze age‑induced DEGs to reveal molecular mechanism of OS among different age groups (<20 and >20 years old). Differentially expressed mRNAs (DEMs) were divided into up and downregulated DEMs (according to the expression fold change), then Gene Ontology function enrichment and Kyoto Encyclopedia of Genes and Genomes pathway analysis were performed. Furthermore, the interactions among proteins encoded by DEMs were integrated with prediction for microRNA‑mRNA interactions to construct a regulatory network. The key subnetwork was extracted and Kaplan‑Meier survival analysis for a key microRNA was performed. DEMs within the subnetwork were predominantly involved in 'ubiquitin protein ligase binding', 'response to growth factor', 'regulation of type I interferon production', 'response to decreased oxygen levels', 'voltage‑gated potassium channel complex', 'synapse part', 'regulation of stem cell proliferation'. In summary, integrated bioinformatics was applied to analyze the potential molecular mechanisms leading to different outcomes of patients with OS among different age groups. The hub genes within the key subnetwork may have crucial roles in the different outcomes associated with age and require further analysis.
Aims: The Chinese medicinal herb, Panax notoginseng, has long been used to treat bone fractures and Panax notoginseng saponins (PNS) could promote bone formation. We investigated the effects of PNS on gap junction intercellular communication (GJIC) and osteogenesis-associated genes in rat bone marrow stromal cells (BMSCs). Methods and Results:Our MTT assays demonstrated that PNS enhanced BMSC proliferation under basal medium culture in vitro. Alkaline phosphatase (ALP) assays and alizarin Red staining showed that PNS stimulated ALP activity and calcium deposition by BMSCs. Measurement of the traversing of Lucifer yellow through intercellular junctions revealed that PNS significantly stimulated GJIC activities. RT-PCR assays further showed that PNS augmented the increase in the mRNA levels of ALP, core-binding factor a1, and bone sialoprotein while decreasing the mRNA level of PPARΓ2. PNS also reduced RANKL levels and increased osteoprotegerin levels. Gap junction inhibitor, 18a-glycyrrhetinic acid, could partially reverse the actions of PNS on BMSCs. Conclusions: Our findings indicate that PNS could promote osteogenesis of BMSCs by targeting osteogenesis-associated genes, which could be mediated by their actions on GJIC.
The Limb Morphogenetic Differentiation Scoring system introduced by Neubert and Barrach in 1977 has been used in drug testing as a measure of the degree of cartilage growth inhibition especially for forelimb in vitro. There is no scoring system to quantify the degree of hindlimb bud cartilage differentiation in vivo. A total of 60 female Sprague-Dawley rats weighing 220-250 g were assigned at random to six control groups and six experimental groups on day 0 of pregnancy. The experimental groups were treated with all-trans-retinoic acid (ATRA). A new limb morphogenetic differentiation scoring system was developed and used to quantify the degree of development of the hindlimb buds from the fetuses at embryonic days E13 to E18. The differentiation of cartilages assessed by the new scoring system showed a statistically significant difference between the experimental group and the control group from E13 to E18 (T-test, p < 0.05). Cartilage growth (the proximodistal length) in the control group increased gradually from E14, reaching its peak at E17, but in the experimental group the growth at E13, E16, E17, and E18 was significantly shorter (p < 0.05). In conclusion, the new limb morphogenetic differentiation scoring system described here can be used to quantify the degree of inhibition of the hindlimb bud development by teratogenic drugs or materials, and morphogenetic differentiation in vivo.
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