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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]

What is known and objective Warfarin is a widely used anticoagulant with a narrow therapeutic index. Polymorphisms in the VKORC1, CYP2C9 and CYP4F2 genes have been verified to correlate with warfarin stable dosage ( WSD). Whether any other genes or variants affect the dosage is unknown. The aim of our study was to investigate the relationship between GGCX, miR-133 variants and the WSD in Han Chinese patients with mechanical heart valve replacement ( MHVR). Methods A total of 231 patients were enrolled in the study. Blood samples were collected for genotyping. The average WSD among subjects with different GGCX or miR-133 genotypes was compared. Regression analyses were performed to test for any association of genetic polymorphisms with WSD. Results and discussion The warfarin dosage in patients with the GGCX rs699664 TT and rs12714145 TT genotypes was 3.77±0.93 (95% CI: 3.35-4.19) mg/d and 3.70±1.00 (95% CI: 3.32-4.09) mg/d, respectively. The GGCX rs699664 and rs12714145 genotypes were significantly associated with WSD ( P<.05). But they were ruled out in the multivariate regression analysis. There were no significant differences in the average warfarin stable dosage between subjects with MIR133B rs142410335 wild-type and variant genotypes ( P>.05). What is new and conclusion The genotypes of GGCX rs699644 and rs12714145 were significantly associated with WSD ( P<.05), but their contributions were not significant after accounting for other factors. MIR133B rs142410335 makes no significant contributions to warfarin stable dosage in Han Chinese patients with MHVR neither in univariate regression nor in multivariate regression analyses. [ABSTRACT FROM AUTHOR]