Expression profiles of seven candidate reference genes from 43 samples using SYBR Green (A) or EvaGreen (B).

<p>The expression data are displayed as Ct values for each reference gene in all samples. The red point is the mean, and the line across the box is the median. The boxes indicate the 25/75 percentiles. The whisker caps indicate the minimum and maximum values.</p

Expression of the candidate reference genes in the transcriptomic sequencing data.

<p>Expression of the candidate reference genes in the transcriptomic sequencing data.</p

Pairwise variation (PV) analysis of seven candidate genes in four sample sets using SYBR Green (A) or EvaGreen (B).

<p>Asterisk indicates the optimal number of reference genes for four sample sets.</p

Expressional stability values (M) of seven candidate reference genes in four sample sets using SYBR Green (A) or EvaGreen (B) generated by the geNorm software.

<p>Average expressional stability values (M) following stepwise exclusion of the least stable gene across all experimental sets. The least stable genes are on the left, and the most stable genes are on the right.</p

Mixed Potential Plays a Key Role in Leaching of Chalcopyrite: Experimental and Theoretical Analysis

The mixed potential plays a key role in leaching of chalcopyrite. Therefore, the impact of Fe²⁺ and Fe³⁺ on chalcopyrite leaching was investigated in this work. Simultaneously, the chalcopyrite passive film was studied by applying cyclic voltammetry (CV), potentiodynamic, potentiostatic, and Tafel polarization. X-ray photoelectron spectroscopy (XPS) was used to analyze the products formed during the electrochemical treatment of chalcopyrite. Furthermore, the band theory was used to analyze the oxidation and reduction of chalcopyrite. High copper extraction percentage was obtained at a low mixed potential or ratio of Fe³⁺/Fe²⁺. The empty states of chalcopyrite overlapped with filled states of Fe²⁺; chalcopyrite captured electrons from Fe²⁺ and was reduced to chalcocite, which was very easily oxidized by Fe³⁺. The Fe dissolves preferentially from the chalcopyrite surface in the potential range from 475 to 700 mV and leave behind a S₂^2– and S_<i>n</i>^2– passive film. The chalcopyrite transpassive dissolution occurs above 700 mV

Additional file 1 of Biocatalytic cascade to polysaccharide amination

Additional file 1: Figure S1. Acetophenone evaporation at 37 °C. Figure S2. The initial activity of CvATA and SpATA. Figure S3. Absorption spectra of red precipitates formed in the Q-NPEA assay. Figure S4. HPLC results confirming pyruvate depletion. Figure S5. Gel formation by acetyl bond formation in oxidized intermediates. Figure S6. Docking of galactomannan oligosaccharide on SpATA surface before and after alanine substitutions. Figure S7. PGBC in SpATA hosting the PLP cofactor. Figure S8. Discoloration of PLP catalyzed by CvATA. Figure S9. Formation of PMP-derived compounds in the discolored PLP solution. Figure S10. Initial rates of the wild-type SpATA and SpATA E407A measured on pyruvate with varying concentrations. Figure S11. The location of E407A mutation near the interfacial loops. Figure S12. Galactose oxidase inhibition by the aminated product measured using the ABTS assay. Table S1. A list of primers used in the site-directed mutagenesis of SpATA

Association between the Epidermal Growth Factor +61G/A Polymorphism and Glioma Risk: A Meta-Analysis

<div><p>Background</p><p>Gliomas account for almost 80% of primary malignant brain tumors. Epidermal growth factor (EGF) is an interesting research candidate in which to look for genetic polymorphisms because of its role in mitogenesis and proliferation. Extensive studies have found that a single nucleotide polymorphism (SNP) +61G/A (rs4444903) in the EGF gene is associated with the susceptibility of glioma, however, the results have been controversial. Furthermore, the association between EGF +61G/A polymorphism with the development and grade progress of glioma has not been established.</p><p>Methods</p><p>We examined the association of EGF +61G/A polymorphism and glioma by performing a meta-analysis. Nine studies testing the associations between EGF +61G/A polymorphism and risk of glioma with 1758 cases and 2823 controls were retrieved. Odds ratios (ORs) and 95% confidence intervals (CIs) were used to assess the strength of the association. The pooled ORs were performed for the allele model, codominant model, dominant model, and recessive model, respectively.</p><p>Results</p><p>Overall, this meta-analysis showed significant associations between the EGF +61G/A polymorphism and glioma susceptibility in all four genetic models. However, in the stratified analysis by the grade of glioma, we only found this association existed in patients with Grade IV glioblastoma, but not in patients with Grade I-III glioma. We further compared EGF +61G/A polymorphism in patients with glioblastoma and Grade I-III glioma accordingly, the stronger association between the EGF +61G/A polymorphism and the malignancy of glioma was found.</p><p>Conclusions</p><p>The results of this meta-analysis suggested that the EGF +61G/A polymorphism is associated with both the susceptibility of glioma and the malignance of glioma.</p></div

Image_1_APOBEC3B is overexpressed in cervical cancer and promotes the proliferation of cervical cancer cells through apoptosis, cell cycle, and p53 pathway.jpeg

ObjectiveAPOBEC3B (A3B), a member of the APOBEC family of cytidine deaminases, has been gradually regarded as a key cancerous regulator. However, its expression and mechanism in cervical cancer (CC) have not been fully elucidated. This study was to investigate its expression pattern and potential mechanism on the cell cycle, as well as HPV oncogenes in CC.MethodsData from The Cancer Genome Atlas (TCGA) and Gene Expression (GEO) were used to indicate the mRNA expression pattern of A3B in cervical cancer. Western blot assay was used to detect A3B levels in SiHa and Hela cell lines. Immunohistochemistry (IHC) was used to explore A3B protein abundance and sublocation in cervical cancer as well as normal cervical tissues. Based on the Protein atlas (www.proteinatlas.org), A3B expression in the SiHa cell line is lower than in the HeLa cell line. Therefore, the SiHa cell line was used for A3B gene overexpression experiments while the HeLa cell line was used for knockdown experiments. Flow cytometry analysis was used to detect cell apoptosis. Biological function and cancer-related pathways of A3B were conducted using bioinformatics analysis.ResultsA3B mRNA was significantly overexpressed in cervical cancer in TCGA-cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC), GSE67522, and GSE7803. A3B was more highly expressed in cervical cancers than in high-grade squamous intraepithelial lesions and normal controls. A3B expression was found to be progressively activated during cervical cancer development. IHC results showed that A3B was significantly higher in cervical cancer tissues than in normal cervical tissues. A3B plasmid-mediated overexpression experiments and A3B siRNA-mediated knockdown experiments showed that A3B significantly promotes cell proliferation, migration, cell cycle, and chemoresistance in cervical cancer cells by the p53 pathway. GO and KEGG analyses showed that A3B expression was strikingly associated with cell proliferation, apoptosis, and immune-associated pathways.ConclusionsTaken together, our study implies that A3B promotes cell proliferation, migration, and cell cycle and inhibits cancer cell apoptosis through the p53-mediated signaling pathway. Moreover, A3B could also contribute to chemoresistance in cervical cancer cells. It may be a potential diagnostic biomarker and therapeutic target for chemoresistant cervical cancers.</p

Flow chart of the study selection process.

<p>Flow chart of the study selection process.</p

Table_1_APOBEC3B is overexpressed in cervical cancer and promotes the proliferation of cervical cancer cells through apoptosis, cell cycle, and p53 pathway.docx

ObjectiveAPOBEC3B (A3B), a member of the APOBEC family of cytidine deaminases, has been gradually regarded as a key cancerous regulator. However, its expression and mechanism in cervical cancer (CC) have not been fully elucidated. This study was to investigate its expression pattern and potential mechanism on the cell cycle, as well as HPV oncogenes in CC.MethodsData from The Cancer Genome Atlas (TCGA) and Gene Expression (GEO) were used to indicate the mRNA expression pattern of A3B in cervical cancer. Western blot assay was used to detect A3B levels in SiHa and Hela cell lines. Immunohistochemistry (IHC) was used to explore A3B protein abundance and sublocation in cervical cancer as well as normal cervical tissues. Based on the Protein atlas (www.proteinatlas.org), A3B expression in the SiHa cell line is lower than in the HeLa cell line. Therefore, the SiHa cell line was used for A3B gene overexpression experiments while the HeLa cell line was used for knockdown experiments. Flow cytometry analysis was used to detect cell apoptosis. Biological function and cancer-related pathways of A3B were conducted using bioinformatics analysis.ResultsA3B mRNA was significantly overexpressed in cervical cancer in TCGA-cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC), GSE67522, and GSE7803. A3B was more highly expressed in cervical cancers than in high-grade squamous intraepithelial lesions and normal controls. A3B expression was found to be progressively activated during cervical cancer development. IHC results showed that A3B was significantly higher in cervical cancer tissues than in normal cervical tissues. A3B plasmid-mediated overexpression experiments and A3B siRNA-mediated knockdown experiments showed that A3B significantly promotes cell proliferation, migration, cell cycle, and chemoresistance in cervical cancer cells by the p53 pathway. GO and KEGG analyses showed that A3B expression was strikingly associated with cell proliferation, apoptosis, and immune-associated pathways.ConclusionsTaken together, our study implies that A3B promotes cell proliferation, migration, and cell cycle and inhibits cancer cell apoptosis through the p53-mediated signaling pathway. Moreover, A3B could also contribute to chemoresistance in cervical cancer cells. It may be a potential diagnostic biomarker and therapeutic target for chemoresistant cervical cancers.</p