Objective:To demonstrate the feasibility of the osteosarcoma devitalization method by vacuum dehydration at room tem-perature. Methods:For the in vivo study, the VX2 tumor mass was treated by vacuum dehydration, rehydrated in ice water, and im-planted in the rabbit to determine the safety time to deactivate the tumor. For the in vitro study, the osteosarcoma mass was devital-ized by vacuum dehydration, and the dehydration rate and ATPase activity were determined. Histopathological changes in the tumor were also observed. The change in the biomechanical strength of rabbit bone and tendon after vacuum devitalization treatment was detected. Results:At room temperature, the safety time to deactivate the VX2 tumor was 60 min, and the dehydration rate was 93.8%at this time point. After vacuum dehydration, the tumor mass evidently shrunk, presenting a porous structure. The osteosarcoma cell became small, and cell structure damage was observed under light microscope. Disrupted cell membrane and organelles were seen un-der transmission electron microscope as well as broken down chromosomes. The activity of ATPase was evidently lower than in the control group. The strength of bone and tendon did not decrease significantly after vacuum dehydration. Conclusion:Treatment by vacuum dehydration at room temperature for 60 min does not result in differences of the bone and tendon strength. However, it can inactivate both soft tissue and bone tumor mass completely.

Objective To investigate the association between the osteogenic differentiation in the soft tissue lump and the clinicopathological characteristics of osteosarcoma patients. Methods We retrospectively reviewed the clinical data of conventional osteosarcoma patients with soft tissue lumps, including Enneking stages, chemotherapy sensitivity, overall survival and post-metastatic survival time. The ossification level in soft tissue lumps was assessed by imaging and the proportion of osteoid matrix was assessed by pathological examination. Results A total of 189 cases were included in this study. In patients with Enneking IIIB, non-osteoblastic, partially osteoblastic and osteoblastic types accounted for 30.2%, 9.6% and 6.3%, respectively. Non-osteoblastic osteosarcoma patients had a higher rate of initial metastasis (P < 0.05); Chemotherapy efficiency of non-osteoblastic, partially osteoblastic and osteoblastic types were 60.5%, 59.6% and 31.3%, respectively. The osteoblastic osteosarcoma held the worst rate of chemotherapy sensitivity (P < 0.05). The overall survival of non-osteoblastic osteosarcoma was shorter than those of partially osteoblastic and osteoblastic types (P < 0.05). Post-metastatic survival time of osteoblastic osteosarcoma was longer than that of non-osteoblastic osteosarcoma (P=0.078). Conclusion For conventional osteosarcoma, the osteogenesis level in soft tissue lumps is related to the surgical stage, chemotherapy sensitivity and prognosis of tumors, which may provide guidance for the individual decision regarding chemotherapy and surgery timing on patients.

BACKGROUND:The sclerotic zone in the femoral head is an important imaging feature in the progression of steroid-induced femoral head necrosis,which is associated with disease prognosis.Peroxisome proliferator-activated receptor γ coactivator 1α(PGC-1α)has been shown to possess biological activities such as osteogenesis,angiogenesis and anti-mitochondrial apoptosis,which may be closely related to bone repair of steroid-induced femoral head necrosis. OBJECTIVE:To screen for the differential proteins in the sclerotic zone of steroid-induced osteonecrosis of the femoral head versus the normal zone,to screen for hub proteins in the sclerotic zone,and to verify the differential expression of hub proteins in the femoral head specimens following steroid-induced femoral head necrosis,and to to explore the repair pattern of the sclerotic zone following steroid-induced femoral head necrosis. METHODS:Femoral head samples were collected from patients with steroid-induced osteonecrosis of the femoral head receiving total hip arthroplasty.The differentially expressed genes in the sclerotic zone and the normal zone were screened by Tandem Mass Tags and analyzed by GO and KEGG signaling pathways to construct a protein-protein interaction network and screen hub genes.In addition,the expression of hub genes in the sclerotic zone was verified by immunohistochemistry and western blot. RESULTS AND CONCLUSION:Quantitative protein profiling by Tandem Mass Tags revealed that 609 proteins were significantly differentially expressed(Log2FC＞1.20,Log2FC＜0.84 and P＜0.05)in the sclerotic zone of the femoral head compared with the normal zone,of which 290 proteins were upregulated and 319 proteins were downregulated.The GO and KEGG pathway enrichment analyses revealed that among the top 10 enriched pathways,Wnt signaling pathway and life-cycle regulatory pathway were closely related to bone repair;in the life-cycle regulatory pathway,PGC-1α was one of the important proteins.In addition,western blot results verified the low expression of PGC-1α and NRF1 in the sclerotic zone and high expression of Cleaved Caspase-3 in the sclerotic zone compared with the normal zone of steroid-induced femoral head necrosis specimens.Light microscopic immunohistochemical results showed the distribution of PGC-1α,NRF1 and Cleaved Caspase-3 positive expression in the sclerotic and normal zones in the femoral head tissue specimens,indicating the presence of their expression in bone trabeculae,osteoblasts and bone marrow.In contrast,the brown area of the sclerotic zone of femoral head necrosis stained darker and showed more obvious expression of Cleaved Caspase-3.To conclude,in the sclerotic zone of steroid-induced femoral head necrosis,biological behaviors including activation of osteogenesis-related pathways such as Wnt and oxidative apoptosis characterized by low expression of PGC-1 are observed.Low expression of PGC-1α in the sclerotic zone of steroid-induced femoral head necrosis may be associated with the activation of oxidative apoptosis.

Objective: To explore the association of TBX5 polymorphisms and environmental exposure index with susceptibility to oral cancer. Methods: A case-control study was conducted to collect 300 oral cancer patients hospitalized in the Department of Oral and Maxillofacial Surgery, the First Affiliated Hospital of Fujian Medical University from September 2010 to December 2016. A total of 445 non-tumor patients were selected as the control group. Questionnaires were used to collect the information of all subjects and 5 ml peripheral blood was collected to detect single nucleotide polymorphisms (SNPs) of the rs10492336 locus of TBX5 gene. According to the environmental exposure index score, subjects were divided into two groups, low risk group (0-2.31) and high risk group (2.32-11.76). To analyze the association of TBX5 gene rs10492336 SNPs, environmental exposure index and oral cancer and its interactions. Results: The age of all subjects in the case group and control group were (56.19±13.10) years and (54.56±12.48) years old. Compared with CC genotype, the OR (95%CI) values of the co-dominant genetic model AC genotype and the dominant genetic model AC+AA genotype were 0.69 (0.49-0.98) and 0.70 (0.51-0.97), respectively. Compared with the low risk group, the OR (95%CI) risk of oral cancer in the high risk group was 3.72 (2.55-5.43). The results of gene-environment interaction analysis showed that compared with the group with CC genotype and high risk of environmental exposure index, the OR (95%CI) value of oral cancer in the group with AC+AA genotype and low risk of environmental exposure index was 0.18(0.10-0.31). Furthermore there was a multiplicative interaction between rs10492336 SNPs and environmental exposure index (β=-0.405, P<0.001). Conclusion This study suggests that the TBX5 gene rs10492336 SNPs and environmental exposure index were associated with oral cancer. And there was a multiplication interaction between rs10492336 SNPs and environmental exposure index.