Understanding the improvement mechanism of plasma etching treatment on oxygen reduction reaction catalysts.

Plasma etching treatment is an effective strategy to improve the electrocatalytic activity, but the improvement mechanism is still unclear. In this work, a nitrogen-doped carbon nanotube-encased iron nanoparticles (Fe@NCNT) catalyst is synthesized as the model catalyst, followed by plasma etching treatment with different parameters. The electrocatalytic activity improvement mechanism of the plasma etching treatment is revealed by combining the physicochemical characterizations and electrochemical results. As a result, highly active metal-nitrogen species introduced by nitrogen plasma etching treatment are recognized as the main contribution to the improved electrocatalytic activity, and the defects induced by plasma etching treatment also contribute to the improvement of the electrocatalytic activity. In addition, the prepared catalyst also demonstrates superior ORR activity and stability than the commercial Pt/C catalyst.

Novel prognostic nomograms for female patients with breast cancer and bone metastasis at presentation.

BACKGROUND: There is a paucity of literature about prognostic evaluation for patients with breast cancer (BC) and bone metastasis at presentation. To date, little is known about how to accurately predict the prognosis of BC patients with bone metastasis at presentation. Thus, an accurate prediction tool of prognosis in this population is urgently needed. Our goal is to construct novel and prognostic nomograms for BC patients with bone metastasis at presentation. METHODS: We searched Surveillance, Epidemiology, and End Results (SEER) database for BC patients with bone metastasis at presentation between 2010 and 2016. Multivariate analysis was performed to obtain significantly independent variables. Then, novel prognostic nomograms were constructed based on those independent predictors. RESULTS: Tumor grade, histological type, primary tumor size, tumor subtype, surgery, chemotherapy and number of metastatic organs except bone were recognized as significantly independent variables of both overall survival (OS) and cancer-specific survival (CSS). Then those significant variables were integrated to construct nomograms for 3- and 5-year survival. Calibration plots for the 3- and 5-year survival in training and validation sets showed that the prediction curve was close to a 45 degree slash. The C-indices of OS in training and validation cohorts were 0.705 and 0.678, respectively. Similar results were observed for CSS in training and validation cohorts. CONCLUSIONS: Our proposed nomograms can effectively and accurately predict the prognosis of BC patients with bone metastasis at presentation, which provide a basis for individual treatments for metastatic lesions.

Long non-coding RNA TUG1 sponges miR-197 to enhance cisplatin sensitivity in triple negative breast cancer.

Breast cancer is the leading cause of women death worldwide. Several long non-coding RNAs (lncRNAs) have been identified as oncogenes or tumor suppressors during the progression of cancers. However, the role of taurine upregulated gene (TUG1) in mediating the chemotherapy sensitivity of triple negative breast cancer (TNBC) has not been studied yet. In TNBC patients, we observed a significant decrease of TUG1 in tumor tissues compared to the normal tissues. Similarly, TUG1 expression was significantly decreased in TNBC cell lines compared with normal breast epithelial cell line and cell lines of other subtypes of breast cancer. In MDA-MB-231 and BT549, cisplatin induced cell growth arrest was remarkably augmented by overexpression of TUG1 and was significantly reduced by TUG1 silencing. Moreover, very low concentration of cisplatin caused cell proliferation inhibition in TUG1-overexpressed-TNBC cells. In addition, we found that TUG1 negatively regulated miR-197 expression in the tested TNBC cell lines. Sponging of TUG1 to miR-197 was proved by a dual luciferase reporter assay. We further predicted and validated that nemo-like kinase (NLK), which was positively controlled by TUG1, was a target gene of miR-197. Via regulation of miR-197/NLK, TUG1 inactivated WNT signaling pathway and thus increasing chemotherapy sensitivity of TNBC cells. Analysis of TCGA database showed that higher expression of TUG1 was associated with better prognosis in breast cancer patients. Our current study drew a preliminary conclusion that TUG1 was involved in chemotherapy sensitivity in TNBC cells.

[Preparation and characterization of mono PEGylated recombinant human interferon omega].

The amino group PEGylation of rhIFNomega with monomethoxy polyethylene glycol succinimidyl succinate (mPEG-SS, 20 000) was investigated, and the modified mixture was separated and purified by ion exchange chromatography and gel filtration chromatography. Under the optimized purification conditions, the average content ofmono PEG-rhIFNomega in the collect liquid reached 182 microg x mL(-1). The average purified yield of mono PEG-rhIFNomega exceed to 22%, and the purity of mono PEG-rhIFNomega was greater than 98% by SDS-PAGE and RP-HPLC. Relative molecular mass of mono PEG-rhIFNomega was 43 790 detected by MALDI-TOF MS. The apparent molecular mass measured by SDS-PAGE was about 60 810. The purified PEG-rhIFNomega has the characteristics of typical PEGylated protein. Activity reservation rate of mono PEG-rhIFNomega was 15.0%, while the antigenicity decreased by at least 64 folds. In addition, the acid stability, thermal stability and stability in serum and trypsin solution of mono PEG-rhIFNomega were markedly better than those of the rhIFNomega. The pharmacological properties of mono PEG-rhIFNomega were significantly improved. The prepared PEG-rhIFNomega might be developed to a novel safe and long-acting interferon.

cDNA cloning, DNA binding, and evolution of mammalian transcription factor IIIA.

cDNA for rat transcription factor IIIA (TFIIIA) was cloned by degenerate PCR and rapid amplification of cDNA ends. This cDNA coded for a protein with nine Cys(2)His(2) zinc fingers and a non-finger C-terminal tail; 63% amino acid (aa) sequence identity was observed with the Xenopus TFIIIA zinc finger region. Recombinant rat protein containing only the nine fingers afforded DNase I protection of the identical nucleotides protected by Xenopus laevis native TFIIIA on the Xenopus 5S RNA gene internal control region. A putative mouse TFIIIA clone was identified in an expressed sequence tag database by sequence similarity to rat TFIIIA. Recombinant nine-finger protein from this clone afforded DNase I protection of the Xenopus 5S rRNA gene like the native frog protein as did a recombinant nine-finger form of a putative human TFIIIA clone. These DNA binding results demonstrate that these clones code for the respective mammalian TFIIIAs. Rodent and human TFIIIAs share about 87% aa sequence identity in their zinc finger regions and have evolved to about the same extent as X. laevis and Xenopus borealis TFIIIAs. A monoclonal antibody against human p53 tumor suppressor bound to rat and mouse TFIIIA but not to human TFIIIA in Western blots. The N-terminal regions of rodent and human TFIIIA do not contain the oocyte-specific initiating Met and accompanying conserved residues found in fish and amphibian TFIIIAs. In their non-finger C-terminal tails, mammalian and amphibian TFIIIAs share a conserved transcription activation domain as well as conserved nuclear localization and nuclear export signals.