Nano manganese dioxide coupling carbon source preloading granular activated carbon biofilter enhancing biofilm formation and pollutant removal.

The formation of stable and mature biofilms affects the efficient and stable removal of ammonium by biological activated carbon (BAC). In this study, the new granular activated carbon (GAC) was preloaded with the carbon source (glucose and sucrose) and nano manganese dioxide (nMnO2) before using. Then tests were performed to determine whether substrate preloading promoted ammonium removal. The ammonium removal treated by nMnO2 coupled with sucrose-loaded BAC reached 49.1 ± 2.5%, which was 1.7 times higher than that by the nonloaded BAC 28.2 ± 1.9%). The biomass on the substrate-loaded BAC reached 5.83 × 106-1.22 × 107 cells/g DW GAC on Day 7, which was 4.6-9.5 times higher than the value of the nonloaded BAC (1.28 × 106 cells/g DW GAC). The amount of extracellular polymer (i.e., protein) on nMnO2 coupled to sucrose-loaded BAC was promoted significantly. Flavobacterium (0.7%-11%), Burkholderiaceae (13%-20%) and Aquabacterium (30%-67%) were the dominant functional bacteria on the substrate-loaded BAC, which were conducive to the nitrification or denitrification process. The results indicated that loading nMnO2 and/or a carbon source accelerated the formation of biofilms on BAC and ammonium removal. Additionally, the ammonium removal treated by nMnO2 coupled with sucrose-loaded BAC was contributed by microbial degradation (56.0 ± 2.5%), biofilm adsorption (38.7 ± 2.1%) and GAC adsorption (5.3 ± 0.3%), suggesting a major role of microbial degradation.

Generation of active Co(III) and peroxodiphosphate by synergistic electrocatalytic system with phosphate and the mediator cobalt(II) and its degradation performance.

The promising synergistic electrocatalytic system of phosphate (PO43-) with the mediator cobalt(II) (for short E-Co(II)-PO43-) was employed to degrade cationic dye methylene blue (MB). The exploration in the electrocatalytic process revealed that the main intermediate active oxidation products were Co(III), accompanied with hydroxyl radicals and peroxodiphosphates (P2O84-). Their synergistic electrocatalytic degradation rate to MB and total organic carbon (TOC) was up to 100 and 60% in 40 min, respectively, which was 5 times and 2.6 times that in a direct electrocatalytic system, correspondingly. The degradation process of the E-Co(II)-PO43- system on MB started with the bond being broken at the N-C junction of the MB molecule and intermediate active oxidation substances being generated, such as phenothiazine, 2-amino-5-(N-methylformamide) benzene sulfonic acid and N1,N1-dimethyl-1,4 diaminobenzene. Then, the intermediates were degraded into aniline, phenol and benzene sulfonic acid, and eventually decomposed into inorganic substances like CO2 and water. The electrocatalytic degradation mechanism of E-Co(II)-PO43- system on MB was the combination of indirect oxidation of the intermediate oxidants like Co(III), P2O84- and the hydroxyl radical with direct electrocatalysis on the platinum titanium electrode, where the electrocatalytic oxidation of Co(III) was dominant.

Systems Analysis of Transcriptomic and Proteomic Profiles Identifies Novel Regulation of Fibrotic Programs by miRNAs in Pulmonary Fibrosis Fibroblasts.

Fibroblasts/myofibroblasts are the key effector cells responsible for excessive extracellular matrix (ECM) deposition and fibrosis progression in both idiopathic pulmonary fibrosis (IPF) and systemic sclerosis (SSc) patient lungs, thus it is critical to understand the transcriptomic and proteomic programs underlying their fibrogenic activity. We conducted the first integrative analysis of the fibrotic programming in these cells at the levels of gene and microRNA (miRNA) expression, as well as deposited ECM protein to gain insights into how fibrotic transcriptional programs culminate in aberrant ECM protein production/deposition. We identified messenger RNA (mRNA), miRNA, and deposited matrisome protein signatures for IPF and SSc fibroblasts obtained from lung transplants using next-generation sequencing and mass spectrometry. SSc and IPF fibroblast transcriptional signatures were remarkably similar, with enrichment of WNT, TGF-ß, and ECM genes. miRNA-seq identified differentially regulated miRNAs, including downregulation of miR-29b-3p, miR-138-5p and miR-146b-5p in disease fibroblasts and transfection of their mimics decreased expression of distinct sets of fibrotic signature genes as assessed using a Nanostring fibrosis panel. Finally, proteomic analyses uncovered a distinct "fibrotic" matrisome profile deposited by IPF and SSc fibroblasts compared to controls that highlights the dysregulated ECM production underlying their fibrogenic activities. Our comprehensive analyses of mRNA, miRNA, and matrisome proteomic profiles in IPF and SSc lung fibroblasts revealed robust fibrotic signatures at both the gene and protein expression levels and identified novel fibrogenesis-associated miRNAs whose aberrant downregulation in disease fibroblasts likely contributes to their fibrotic and ECM gene expression.

Spontaneous genomic alterations in a chimeric model of colorectal cancer enable metastasis and guide effective combinatorial therapy.

Colon cancer is the second most common cause of cancer mortality in the Western world with metastasis commonly present at the time of diagnosis. Screening for propagation and metastatic behavior in a novel chimeric-mouse colon cancer model, driven by mutant p53 and ß-Catenin, led to the identification of a unique, invasive adenocarcinoma. Comparison of the genome of this tumor, CB42, with genomes from non-propagating tumors by array CGH and sequencing revealed an amplicon on chromosome five containing CDK6 and CDK14, and a KRAS mutation, respectively. Single agent small molecule inhibition of either CDK6 or MEK, a kinase downstream of KRAS, led to tumor growth inhibition in vivo whereas combination therapy not only led to regression of the subcutaneous tumors, but also near complete inhibition of lung metastasis; thus, genomic analysis of this tumor led to effective, individualized treatment.

Progranulin is a chemoattractant for microglia and stimulates their endocytic activity.

Mutations resulting in progranulin haploinsufficiency cause disease in patients with a subset of frontotemporal lobar degeneration; however, the biological functions of progranulin in the brain remain unknown. To address this subject, the present study initially assessed changes in gene expression and cytokine secretion in rat primary cortical neurons treated with progranulin. Molecular pathways enriched in the progranulin gene set included cell adhesion and cell motility pathways and pathways involved in growth and development. Secretion of cytokines and several chemokines linked to chemoattraction but not inflammation were also increased from progranulin-treated primary neurons. Therefore, whether progranulin is involved in recruitment of immune cells in the brain was investigated. Localized lentiviral expression of progranulin in C57BL/6 mice resulted in an increase of Iba1-positive microglia around the injection site. Moreover, progranulin alone was sufficient to promote migration of primary mouse microglia in vitro. Primary microglia and C4B8 cells demonstrated more endocytosis of amyloid ß1-42 when treated with progranulin. These data demonstrate that progranulin acts as a chemoattractant in the brain to recruit or activate microglia and can increase endocytosis of extracellular peptides such as amyloid ß.