RESUMO
Petroleum cokes prepared from naphthenic crude oil differ significantly in terms of the oxygen content and hydrogen/carbon (H/C) ratio, which mainly depend on the different coking temperatures. Thermogravimetric-differential scanning calorimetry was applied to study the heat release and combustion weight loss of petroleum cokes prepared at 350 and 500 °C, respectively. The effect of different coke formation temperatures on the combustion properties of the coke formed during air injection in situ combustion (ISC) was also investigated. The results showed that the petroleum coke formed under oxygen exhibited an H/C ratio of 0.895 and an O/C ratio of 0.109 at 350 °C and an H/C ratio of 0.395 and an O/C ratio of 0.054 at 500 °C. As the temperature rises, the hydrogen atoms on the petroleum coke molecules intensify to separate and form water molecules and thus giving off heat. It can be further inferred that under the combustion temperature of air injection ISC, the coke at 350 °C can release more heat in the lower combustion temperature range, and the combustion weight loss is faster; however, the formation temperature continues to rise due to combustion at 500 °C, coke begins to release massive heat, and the combustion weight loss is as high as 97.95%. The combustion residuals of both temperature cokes and the residual solid content of the formation after combustion in porous media are both little, which can be used as fire flooding fuels at different formation temperatures to provide heat energy for oil displacement.
RESUMO
BACKGROUND: The human antimicrobial peptide defensin beta 1 (DEFB1) has been found to play antimicrobial and anti-inflammatory roles in oral diseases; however, its tumor-regulating role in oral squamous cell carcinoma (OSCC) has not yet been researched by using an integrative bioinformatics approach. OBJECTIVE: To investigate the regulating mechanisms of the DEFB1 gene in OSCC in terms of its expression patterns, prognostic values, biological functions, and implication for tumor immunity. METHODS: The DEFB1 gene expression pattern and regulatory involvement in OSCC were investigated using publically accessible data from TCGA database. R software tools and public web servers were utilized to conduct statistical analysis of data from cancer and noncancerous samples. RESULTS: DEFB1 was found to be significantly downregulated in OSCC tumor samples compared with healthy control oral samples. The DEFB1 gene was found associated with the prognostic outcomes of OSCC, and its upregulation represented better survival outcome. Gene set enrichment analysis (GSEA) results showed that DEFB1-significantly correlated genes were mainly enriched in four signaling pathways mediating the antitumor role of DEFB1 in OSCC, including extracellular matrix-related pathway, RTK/PI3K/AKT/mTOR pathway, keratinization, and cytokine-related pathway. The gene-gene interaction network showed that DEFB1 was closely correlated with several genes, for example, CCR6 (C-C motif chemokine receptor 6), CXCL1 (C-X-C motif chemokine ligand 1), MAP4K2 (mitogen-activated protein kinase kinase kinase kinase 2), PTGER3 (prostaglandin E receptor 3), and MMP7 (matrix metallopeptidase 7). Moreover, DEFB1 was found to be involved in the tumor immunity of OSCC by regulating the function of tumor macrophage cells, mast cells, T cells, and NK cells. CONCLUSIONS: Given the dysregulation, prognostic value, and tumor progression-related biological pathway alteration, indicating the tumor immune-modulatory role of DEFB1 in OSCC, the DEFB1 gene should be regarded as a potential therapeutic target for treating oral cancer.
