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OBJECTIVE: Osteosarcoma is the third most frequently diagnosed cancer among adolescents. Immunotherapy is an effective curative treatment for metastatic osteosarcoma patients. This study aimed to further reveal the significance of metabolism in tumor progression, and to categorize molecular subtypes for guiding personalized therapy. MATERIALS AND METHODS: Univariate Cox regression analysis was performed to screen metabolism-related genes associated with osteosarcoma prognosis. A molecular subtyping system was developed by unsupervised consensus clustering. Survival analysis and functional analysis were used to evaluate the performance of subtyping and characterize the TME of subtypes. Stepwise Akaike information criterion (stepAIC) was employed to optimize the prognostic model. RESULTS: C1 and C2 subtypes showed distinct prognosis, with more favorable survival in C2 subtype. C2 subtype presented a higher immune infiltration and active anti-tumor response. Notably, C2 subtype was predicted to have better immune response to immune checkpoint blockade. In addition, a 5-gene prognostic signature with robust ability to classify patients into high-risk and low-risk groups was developed. CONCLUSIONS: The study revealed the critical role of metabolism in tumorigenesis by comparing the features between the two subtypes. Oncogenic pathways including epithelial mesenchymal transition (EMT), glycolysis and hypoxia may be closely involved in the correlation with metabolism. Importantly, we developed a novel subtyping system and a 5-gene signature with high potential to be applied in clinical practice. [ABSTRACT FROM AUTHOR]

Addresses problems associated with thermal annealing and doping in copper indium sulphide[sub2]. Description of the electrical properties of chemical vapor transport in copper indium sulphide; Vacuum annealing of copper indium sulphide; Details of phosphorous implantation with thermal annealing.

OBJECTIVE: The use of adipose-derived stem cells (ADSCs) to cure the optic nerve injury was never shown previously. Here, we implanted purified ADSCs into optic nerve injury of rats. MATERIALS AND METHODS: Male Sprague Dawley (SD) rats were used in this study. The vision degeneration was detected by Flash-visual evoked potential (F-VEP) assay. The expression of Macrophage-1 (Mac-1), myeloid differentiation factor 88 (MyD88), and nuclear transcription factor-κB (NF-κB) were studied by Western blot. The expression of interleukin (IL)-6 and tumor necrosis factor (TNF)-α in the optical nerve lysates were assessed by enzyme-linked immunosorbent assay (ELISA). RESULTS: We f ound o ut t hat A DSC i mplantation inhibits the amplitude decrease and latency increase of the P1 wave caused by the optic nerve injury. The expression of the inflammation associated proteins of the toll-like receptor 4 (TLR4) signaling pathway, including Mac-1, MyD88, NF-κB, IL-6, and TNF-α, were inhibited in the ADSC therapy group compared to the control group. CONCLUSIONS: Our results indicated that ADSC implantation can inhibit the inflammation after the optic nerve injury and improve the functional vision impairment. These findings suggested ADSC implantation as a translational therapy method for optic nerve injury in clinics. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The purpose of this study was to investigate the effects of int-2 transfection on the invasiveness and metastasis of oral cancer BcaCD885 cells, and to determine the relevant mechanisms of action. MATERIALS AND METHODS: High-purity int- 2 eukaryotic expression plasmids were prepared and transfected using a modified cationic liposome- mediated transfection protocol. Nucleoside diphosphate kinase A (NDPKA) expression before and after transfection was examined, as well as changes in cell invasiveness and metastasis capabilities. RESULTS: Int-2 was confirmed to be stably expressed post-transfection into oral cancer cells. Expression of int-2 in BcaCD885 cells was significantly different before and after transfection. The proportion of invasive cells were 70.3%±8.2% and 46.5%±5.7%, and the proportion of chemotaxis cells were 78.5%±7.9% and 49.6%±7.5%, in the in the control and experimental groups respectively. The adhesion capability of cells in the experimental group was also significantly reduced. CONCLUSIONS: Upregulation of int-2 expression can significantly inhibit the invasion and metastasis of BcaCD885 cells. [ABSTRACT FROM AUTHOR]