BACKGROUND: Studies have demonstrated that dexamethasone can reduce type Ⅱ collagen and increase type I collagen in articular cartilage surface matrix, but the action mechanism of glucocorticoid to articular chondrocyte proliferation remains unclear. OBJECTIVE: To investigate the effects of dexamethasone sodium phosphate on rabbit articular chondrocytes cultured in vitro. DESIGN: Comparative observation.MATERIALS: New Zealand rabbits, 1 month old, were used for chondrocyte isolation and culture.METHODS: Rabbit articular chondrocytes cultured in vitro were randomly divided into control and experimental groups. Cells of the control group were cultured in DMEM media without dexamethasone sodium phosphate. Cells of experimental groups were cultured in DMEM media with different concentrations of dexamethasone sodium phosphate (0.02, 0.1, 0.5 g/L), respectively. MAIN OUTCOME MEASURES: Primary and passage chondrocytes were observed. Flow cytometry and immunocytochemistry were used to observe the effect of dexamethasone sodium phosphate on cell proliferation and type Ⅱ collagen synthesis. The ultrastructural changes of cultured chondrocytes were observed by transmission electron microscopy. RESULTS: The attachment and proliferation of experimental group chondrocytes was slower than control group. There average gray scale values of the experimental groups were significantly greater than the control group (P < 0.05). The cellular proportions of S phase and G_2+M phase of the experimental groups decreased but the cellular proportions of G0/G1 period increased. Under transmission electron microscope the amount of rough endoplasmic reticulum and mitochondria of the experimental groups decreased. CONCLUSION: Dexamethasone sodium phosphate inhibited articular chondrocyte proliferation, possibly due to the decrease of type Ⅱcollagen and protein synthesis ability of chondrocyte.

The present study retrospectively analyzed 13 patients with fibrous dysplasia of the adult proximal femur who received treatment at the Department of Orthopedics,Shenzhen Hospital,Peking University between March 2000 and June 2006.These patients comprised 6 males and 7 females,with an age of 21-35 years.Among 11 patients suffering from mild hip pain,6 presented with mild limping due to worsened pains,and 2 exhibited obvious manifestations of bone fracture.All patients underwent X-ray,CT examinations,and 3 were subjected to MRI examinations,prior to bone grafting and internal fixation.Monostotic lesion was observed in 10 patients and polystotic lesion in 3 patients,but endocrine disturbance was not observed in any patient.Nine patients suffered from lesions in the femoral neck and 4 from lesions in the femoral rotator.Curettage,autogenous and allogeneic bone grafting,and internal fixation with dynamic hip screws and proximal femoral nails were successfully performed in each patient.Internal fixation time averaged 165 minutes (range 120-210 minutes).During the early stage after surgery,weight-bearing activities were not permitted.Bone fracture healed after an average of 3 months.Eighteen to forty-eight months of follow-up demonstrated that clinical symptoms were relieved,with good hip joint function and basically normal gait.X-ray plains showed thickened cortical bone,as well as compacted ossification shadow in bone grafting region.In addition,partial bone absorption,but not recurrent clinically,was observed in 4 patients.These findings imply that thorough curettage,autogenous and allogeneic bone grafting,and internal fixation with dynamic hip screws and proximal femoral nails is a reliable method to treat fibrous dysplasia of the adult proximal femur and it can acquire satisfactory curative effects.

Objective To discuss the surgical treatment of the ankle and the foot soft tissue defects. Methods 41 cases of the ankle and the foot soft tissue defects were treated with different types of pedicle flaps transfer 9 types of flaps were used in all patients. Results 36 flaps of 41 cases were completely survived, 2 ease with superficial necrosis and 3 cases with distal edge partially necrosis and these 5 cases all healed by dressing change. All the easeswere followed up 3 to 36 months(averaged 12 months). The flaps completely survived. Conclusion The study showed that the soft tissue defects in ankle and foot can be constructed satisfactory by selecting a reasonable pedicle flap, especially the sural neurocutaneons island flaps.

ObjectiveTo establish a rat model of diabetic wound by feeding on a high-fat and high-sugar diet combined with intraperitoneal injection of streptozotocin （STZ） and surgical preparation of full-thickness skin defects， observe the effect of cinnamaldehyde on the wound healing of diabetes rats， and explore the therapeutic mechanism of cinnamaldehyde in improving wound healing of diabetes rats based on the PTEN-induced putative kinase （PINK1）/Parkin pathway-mediated mitochondrial autophagy. MethodForty-eight male SD rats were randomly divided into blank group （n=12） and diabetes group （n=36）. The diabetes group was further randomly divided into model group， cinnamaldehyde group， and Beifuxin group， with 12 rats in each group. The blank group and the model group received routine disinfection with physiological saline after creating the wounds， while the cinnamaldehyde group received topical application of polyethylene glycol 400 （PEG 400） gel containing 4 μmol·L^-1 cinnamaldehyde， and the Beifuxin group received topical application of Beifuxin gel. Dressings were changed once daily. The wound healing rate of each group was observed. On the 7th and 14th days after intervention， the wound tissues of the rats were collected. Hematoxylin and eosin （HE） staining was performed to observe the pathological changes in the local tissues. Immunohistochemistry （IHC） was used to detect the expression of interleukin-6 （IL-6）， tumor necrosis factor-α （TNF-α）， vascular endothelial growth factor （VEGF）， and collagen fibers. Immunofluorescence （IF） and Real-time polymerase chain reaction （Real-time PCR） were used to detect the protein， and mRNA expression of PINK1， Parkin， microtubule-associated protein 1 light chain 3 Ⅱ （LC3 Ⅱ）. ResultAfter intraperitoneal injection of STZ， compared with the blank group， the random blood glucose values of rats in the diabetic group increased significantly （P<0.01）， all higher than 16.7 mmol·L^-1， and persistently hyperglycemic for some time after modeling. Compared with the blank group， the model group showed poor growth and healing of granulation tissue in the wounds， and the wound healing rate decreased （P<0.01）. On the 7^th day after intervention， the blank group had squamous epithelial coverage on the wounds. Compared with the blank group， the model group only had a small amount of scab at the wound edges， with a large number of infiltrating inflammatory cells in the wounds. The protein expression levels of IL-6 and TNF-α in the tissues increased （P<0.01）， and the protein and mRNA levels of PINK1， Parkin， and LC3Ⅱ decreased （P<0.01）. On the 14^th day after the intervention， the granulation tissue in the wounds of the blank group was mature and well-healed. Compared with the blank group， the model group still had infiltrating inflammatory cells and red blood cell exudation. The protein expression levels of VEGF and collagen fibers in the tissues decreased （P<0.01）， and the protein and mRNA expression levels of PINK1， Parkin， and LC3Ⅱ increased （P<0.01）. Compared with the model group， the cinnamaldehyde group and the Beifuxin group showed better wound healing， with increased wound healing rates （P<0.01）. On the 7th day after intervention， the protein expression levels of IL-6 and TNF-α in the tissues decreased （P<0.01）， and the protein and mRNA expression levels of PINK1， Parkin， and LC3Ⅱ increased （P<0.01）. On the 14th day after intervention， the protein expression levels of VEGF and collagen fibers in the tissues increased （P<0.01）， and the protein and mRNA expression levels of PINK1， Parkin， and LC3Ⅱ decreased （P<0.01）. ConclusionCinnamaldehyde can promote the wound healing of diabetes rats by increasing the wound healing rate， reducing the levels of inflammatory factors IL-6 and TNF-α， and increasing the levels of VEGF and collagen fibers. Its mechanism may be related to the regulation of the PINK1/Parkin signaling pathway， activation of mitochondrial autophagy， inhibition of inflammatory responses， and promotion of angiogenesis and collagen synthesis， thereby promoting the wound healing of diabetes rats.

Objective : To explore the mechanism of Wenyang Shengji Ointment (温阳生肌膏, WYSJO) in the treatment of diabetic wounds from the perspective of network pharmacology, and to verify it by animal experiments. Methods: The Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP) and related literature were used to screen active compounds in WYSJO and their corresponding targets. GeneCards, Online Mendelian Inheritance in Man (OMIM), DrugBank, PharmGkb, and Therapeutic Target Database (TTD) databases were employed to identify the targets associated with diabetic wounds. Cytoscape 3.9.0 was used to map the active ingredients in WYSJO, which was the diabetic wound target network. Search Tool for the Retrieval of Interaction Gene/Proteins (STRING) platform was utilized to construct protein-protein interaction (PPI) network. Kyoto Encyclopedia of Genes and Genomes (KEGG) andGene Ontology (GO) enrichment analyses were performed to identify signaling pathways between WYSJO and diabetic wounds. AutoDock 1.5.6 was used for molecular docking of core components in WYSJO to their targets. Eighteen rats were randomly divided into control, model, and WYSJO groups (n = 6). The model and WYSJO groups were used to prepare the model of refractory wounds in diabetes rats. The wound healing was observed on day 0, 5, 9, and 14 after treatment, and the wound tissue morphology was observed by hematoxylin-eosin(HE) staining. The expression levels of core genes were detected by quantitative real-timepolymerase chain reaction (qPCR). Result: A total of 76 active compounds in WYSJO, 206 WYSJO drug targets, 3 797 diabetic wound targets, and 167 diabetic wound associated WYSJO targets were screened out through network pharmacology. With the use of WYSJO-diabetic wound target network, core targets of seven active compounds encompassing quercetin, daidzein, kaempferol, rhamnetin, rhamnocitrin, strictosamide, and diisobutyl phthalate (DIBP) in WYSJO were found. GO enrichment analysis showed that the treatment of diabetes wounds with WYSJO may involve lipopolysaccharide, bacteria-derived molecules, metal ions, foreign stimuli, chemical stress, nutrient level, hypoxia, and oxidative stress in the biological processes. KEGG enrichment analysis showed that the treatment of diabetes wounds with WYSJO may involve advanced glycation end products (AGE-RAGE), p53, interleukin (IL)-17, tumor necrosis factor (TNF),hypoxia inducible factor-1 (HIF-1), apoptosis, lipid, atherosclerosis, etc. The results of animal experiments showed that WYSJO could significantly accelerate the healing process of diabetic wounds (P < 0.05), alleviate inflammatory response, promote the growth of granulation tissues, and down-regulate the expression levels of eight core genes [histone crotonyltransferase p300 (EP300), protoc gene-oncogene c-Jun (JUN), myelocytomatosis (MYC), hypoxia inducible factor 1A (HIF1A), mitogen-activated protein kinase 14 (MAPK14), specificity protein 1 (SP1), tumor protein p53 (TP53), and estrogen receptor 1 (ESR1)] predicted by the network pharmacology (P < 0.05). Conclusion The mechanism of WYSJO in treating diabetes wounds may be closely related to AGE-RAGE, p53, HIF-1, and other pathways. This study can provide new ideas for the pharmacological research of WYSJO, and provide a basis for its further transformation and application.