Forecasting carbon price using empirical mode decomposition and evolutionary least squares support vector regression

Conventional methods are less robust in terms of accurately forecasting non-stationary and nonlineary carbon prices. In this study, we propose an empirical mode decomposition-based evolutionary least squares support vector regression multiscale ensemble forecasting model for carbon price forecasting. Firstly, each carbon price is disassembled into several simple modes with high stability and high regularity via empirical mode decomposition. Secondly, particle swarm optimization-based evolutionary least squares support vector regression is used to forecast each mode. Thirdly, the forecasted values of all the modes are composed into the ones of the original carbon price. Finally, using four different-matured carbon futures prices under the European Union Emissions Trading Scheme as samples, the empirical results show that the proposed model is more robust than the other popular forecasting methods in terms of statistical measures and trading performances

Forecasting carbon price using empirical mode decomposition and evolutionary least squares support vector regression

Conventional methods are less robust in terms of accurately forecasting non-stationary and nonlineary carbon prices. In this study, we propose an empirical mode decomposition-based evolutionary least squares support vector regression multiscale ensemble forecasting model for carbon price forecasting. Firstly, each carbon price is disassembled into several simple modes with high stability and high regularity via empirical mode decomposition. Secondly, particle swarm optimization-based evolutionary least squares support vector regression is used to forecast each mode. Thirdly, the forecasted values of all the modes are composed into the ones of the original carbon price. Finally, using four different-matured carbon futures prices under the European Union Emissions Trading Scheme as samples, the empirical results show that the proposed model is more robust than the other popular forecasting methods in terms of statistical measures and trading performances

The expression of FOXQ1 was higher in NPC cell lines and tissues.

<p>(A) qRT-PCR analysis was used to detect the expression of FOXQ1 in all NPC cell lines (5–8 F, 6-10B, CNE1 and CNE2) and one nasopharyngeal epithelial cell line NP69. (B) qRT-PCR analysis was used to detect the expression of FOXQ1 in NPC tissues and normal nasopharyngeal epithelial specimens. The expression of FOXQ1 was normalized to GAPDH.</p

The tumor suppressor role of miR-506 was mediated by downregulating FOXQ1.

<p>(A) Western blot analysis showed that pcDNA-FOXQ1 can restore FOXQ1 expression. The expression of FOXQ1 was normalized to GAPDH. (B) The inhibitory role of miR-506 in proliferation was rescued under the condition of overexpression of FOXQ1. (C) The inhibitory role of miR-506 in invasion was rescued under the condition of overexpression of FOXQ1. *p<0.05, ** p<0.01, ***p<0.001</p

Overexpression of miR-506 inhibited NPC cell proliferation and colony formation.

<p>(A) The highly up-regulated expression of miR-506 was confirmed by qPCR in both 5–8 F and 6-10B cell lines (B) Overexpression of miR-506 repressed the 5–8 F cell line proliferation when compared with those of scramble infected cells using CCK-8 proliferation assay. (C) Overexpression of miR-506 repressed the 6-10B cell line proliferation when compared with those of scramble infected cells using CCK-8 proliferation assay. (D) Colony formation assay also showed that overexpression of miR-506 inhibited both the 5–8 F and 6-10B cell colony formation. ** p<0.01, and ***p<0.001.</p

MiR-506 directly targeted FOXQ1.

<p>(A) Predicted miR-506 target sequence in the 3’UTR of FOXQ1 (FOXQ1-3’-UTR-WT) and mutant containing 7 altered nucleotides in the 3’UTR of FOXQ1 (FOXQ1-3’-UTR-MUT). (B) The analysis of the relative luciferase activities of FOXQ1-WT, FOXQ1-MUT in the 5–8 F cells and 6-10B cells. (C) Western blot analysis of FOXQ1 expression in the 5–8 F and 6-10B cells transfected with miR-506 mimics or scramble. GAPDH was detected as a loading control. (D) qRT-PCR analysis of FOXQ1 mRNA expression in the 5–8 F and 6-10B cells after treatment with miRNA mimics or scramble. The expression of FOXQ1 was normalized to GAPDH. ***p<0.001.</p

Overexpression of miR-506 repressed invasion of NPC cells.

<p>Invasion analysis has shown that the percentage of invasive cells was significantly lower in cells transfected with miR-506 mimic compared with those infected with scramble. ***p<0.001.</p

MiR-506 Suppresses Tumor Proliferation and Invasion by Targeting FOXQ1 in Nasopharyngeal Carcinoma

<div><p>MiRNAs are small noncoding RNAs that play important roles in various biological processes including tumorigenesis. However, little is known about the expression and function of miR-506 in nasopharyngeal carcinoma (NPC). In this study, we showed that miR-506 was downregulated in nasopharyngeal carcinoma (NPC) cell lines and tissues. Ectopic expression of miR-506 dramatically suppressed cell proliferation, colony formation and invasion. Moreover, we identified the Forkhead box Q1 (FOXQ1) gene as a novel direct target of miR-506. MiR-506 exerts its tumor suppressor function through inhibition of the FOXQ1, which was involved in tumor metastasis and proliferation in various cancers. Furthermore, the expression of FOXQ1 is up-regulated in NPC cell lines and tissues. Taken together, our results indicate that miR-506 functions as a tumor suppressor miRNA in NPC and that its suppressive effects are mediated chiefly by repressing FOXQ1 expression.</p></div

Data_Sheet_2_Antitumor Activity of Extract From the Sporoderm-Breaking Spore of Ganoderma lucidum: Restoration on Exhausted Cytotoxic T Cell With Gut Microbiota Remodeling.XLSX

<p>As breast cancer is the leading cause of cancer-related deaths in women population worldwide, ongoing endeavor has been made for alternative regimens with improved efficacy but fewer adverse effects. Recently, active components from the spores of Ganoderma lucidum have attracted much attention for their versatile biological activities owing to the advance in sporoderm-breaking technology. Here, anticancer potential of an extract derived from the sporoderm-breaking spores of G. lucidum (ESG) was explored in a 4T1-breast cancer xenograft mice model. Results showed that ESG was able to suppress 4T1 tumor growth in vivo rather than in vitro. Flowcytometry analysis revealed that ESG could significantly increase both cytotoxic T cell (Tc) population and the ratio of Tc to helper T cell (Th) in peripheral blood of the tumor-bearing mouse; similar promotion on Tc was also found in tumor-infiltrating lymphocyte. Moreover, ESG evidently downregulated the two immune checkpoints, programmed cell death protein-1 (PD-1, in the spleen) and cytotoxic T lymphocyte antigen-4 (CTLA-4, in the tumor), suggesting that ESG could effectively restore the T cell paradigm by recovering the exhaustion status via suppressing the co-inhibitory checkpoints. By 16S rRNA gene sequence analysis on the fecal microbiota, it was found that ESG would remodeling the overall structure of the samples from tumor-bearing mice toward that of the normal counterparts, including 18 genera in 5 phyla, together with regulations on several genes that are responsible for signaling pathways involved in metabolism, cellular processes, and environmental information processing. Collectively, this study demonstrated that ESG would serve as a natural anticancer adjuvant via a restoration on the exhausted Tc, highlighting important clinical implications for the treatment of breast cancer.</p