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1.
ChemSusChem ; 12(23): 5063-5069, 2019 Dec 06.
Artigo em Inglês | MEDLINE | ID: mdl-31642194

RESUMO

For renewable and sustainable energy, developing cut-price and high-efficiency electrocatalysts for the hydrogen evolution reaction (HER) by alkaline water electrolysis is of paramount importance. In this study, a compound electrocatalyst composed of nickel-vanadium sesquioxide nanoparticles supported on porous nickel foam (Ni-V2 O3 /NF) is found to exhibit electrocatalytic performance towards HER that is superior to that of the commercial Pt/C catalyst, with nearly zero onset overpotential, an extremely low overpotential of 25 mV to obtain a current density of -10 mA cm-2 , a Tafel slope of 58 mV dec-1 , and a good durability for 24 h in 1.0 m KOH. Theoretical calculations reveal that the presence of V2 O3 optimizes the electronic structure of active Ni components and continuously accelerates the dissociation of water molecules, which in turn improves the HER kinetics. The present work will advance the development of highly efficient nanocomposite electrocatalysts for alkaline water electrocatalysis.

2.
Gene ; 714: 143996, 2019 Sep 25.
Artigo em Inglês | MEDLINE | ID: mdl-31348980

RESUMO

The uniquely human α7-nAChR gene (CHRFAM7A) is evolved from the fusion of two partially duplicated genes, FAM7 and α7-nAChR gene (CHRNA7), and is inserted on same chromosome 15, 5' end of the CHRNA7 gene. Transcription of CHRFAM7A gene produces a 1256-bp open reading frame encoding dup-α7-nAChR, where a 27-aminoacid residues from FAM7 replaced the 146-aminoacid residues of the N-terminal extracellular ligand binding domain of α7-nAChR. In vitro, dup-α7-nAChR has been shown to form hetero-pentamer with α7-nAChR and dominant-negatively regulates the channel functions of α7-nAChR. However, the contribution of CHRFAM7A gene to the biology of α7-nAChR in the brain in vivo remains largely a matter of conjecture. CHRFAM7A transgenic mouse was created and differentially expressed proteins were profiled from the whole brain using iTRAQ-2D-LC-MS/MS proteomic technology. Proteins with a fold change of ≥1.2 or ≤0.83 and p < 0.05 were considered to be significant. Bioinformatics analysis showed that over-expression of the CHRFAM7A gene significantly modulated the proteins commonly involved in the signaling pathways of α7-nAChR-mediated neuropsychiatric disorders including Parkinson's disease, Alzheimer's disease, Huntington's disease, and alcoholism, suggesting that the CHRFAM7A gene contributes to the pathogenesis of neuropsychiatric disorders mostly likely through fine-tuning the functions of α7-nAChR in the brain.


Assuntos
Camundongos Transgênicos/genética , Receptor Nicotínico de Acetilcolina alfa7/genética , Animais , Encéfalo/metabolismo , Cromatografia Líquida/métodos , Cromossomos Humanos Par 15/genética , Perfilação da Expressão Gênica/métodos , Genes Duplicados/genética , Humanos , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Proteômica/métodos , Transdução de Sinais/genética , Espectrometria de Massas em Tandem/métodos
3.
J Cell Mol Med ; 23(9): 6085-6097, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31270949

RESUMO

The surged systemic vascular inflammation after acute myocardial infarction (AMI) aggravates the atherosclerotic endothelial injury. To explore roles of miR-499 released from cardiomyocytes during AMI in endothelial injury. Using qPCR and ELISA, we discovered that patients with AMI had significantly increased plasma miR-499, which was directly correlated with serum thrombomodulin, a marker for endothelial injury. Plasma of AMI patients, when incubated with human umbilical vein endothelial cells (HUVECs), significantly increased the expression of endothelial injury markers, which could be abrogated by antagomiR-499. In vitro, neonatal rat cardiomyocytes subjected to hypoxia/reoxygenation (HX/R) released miR-499 that could be internalized into rat pulmonary microvascular endothelial cells (RPMECs), worsening the high glucose-induced injury. In silico analysis demonstrated that CHRNA7 encoding α7-nAchR is a target of miR-499, which was validated in cell lines expressing endogenous α7-nAchR. In high glucose-induced RPMECs injury model, miR-499 aggravated, whereas forced CHRNA7 expression ameliorated the injury. Moreover, the perfusate from Langendorff perfused rat heart subjected to HX/R contained higher level of miR-499 that significantly impaired the Bradykinin-mediated endothelium-dependent relaxation in both conduit and resistance arteries, which could be partially abrogated by antagomiR-499. Finally, the correlation between plasma miR-499 and endothelial injury was further confirmed in another cohort of AMI patients. We conclude that miR-499 released from injured cardiomyocytes contributes to the endothelial injury by targeting α7-nAchR. This study implies that miR-499 may serve as a potential target for the treatment of the surged vascular inflammation post-AMI.

4.
Cancer Gene Ther ; 25(9-10): 248-259, 2018 10.
Artigo em Inglês | MEDLINE | ID: mdl-29983418

RESUMO

Esophageal cancer related gene-4 (Ecrg4) has been shown to be a tumor suppressor in many organs. Exosomes are naturally secreted nanosized particles that carry signal molecules including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and messenger RNAs (mRNAs) among others. Upon internalization, exosomes unload their cargos that in turn modulate the biology of the recipient cells. Mounting evidence has shown that exosomal miRNAs are functional. However, reports that exosomes carry functional mRNAs remain scarce. We found that serum exosomes contain ECRG4 open reading frame. To simulate serum exosomal ECRG4, stable cell line expressing ECRG4 was created, from which exosomes were isolated and characterized, and the internalization and the resulting biological effects of exosomal ECRG4 were evaluated. Results showed that serum exosomes contain higher levels of ECRG4 mRNA in healthy individuals than their cancer counterparts. Exosomal ECRG4 can be internalized and unload the encapsulated ECRG4 into recipient cells, which subsequently suppressed cell proliferation in vitro, and inhibited tumor growth in a xenograft mouse model. Mechanistically, ECRG4-containing exosomes, when internalized, suppressed the expression of genes commonly implicated in inflammation, cell proliferation, and angiogenesis. Given that exosome is an ideal vehicle for therapeutics delivery and that ECRG4 is a tumor suppressor gene, the exosomal ECRG4 can be exploited as a formulation for cancer gene therapy.


Assuntos
Proliferação de Células , Exossomos/metabolismo , Genes Supressores de Tumor , Proteínas de Neoplasias/sangue , Neoplasias , Neovascularização Patológica/sangue , RNA Mensageiro/sangue , RNA Neoplásico/sangue , Células A549 , Animais , Exossomos/patologia , Feminino , Células HEK293 , Humanos , Inflamação/sangue , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Nus , Neoplasias/sangue , Neoplasias/irrigação sanguínea , Neoplasias/patologia , Neovascularização Patológica/patologia , Proteínas Supressoras de Tumor
5.
J Colloid Interface Sci ; 495: 19-26, 2017 06 01.
Artigo em Inglês | MEDLINE | ID: mdl-28182956

RESUMO

Single-layered g-C3N4 nanosheets have been fabricated by delaminating directly its bulk counterpart in an alkaline solution. According to the theoretical modeling, the interaction of OH- with terminal NH2 or bridged NH group of the triazine units within bulk g-C3N4 crystal structure could result in decreased bonding energy between layers and promote the total delamination. The resulting g-C3N4 nanosheets colloid has a relatively high concentration (12g/L) compared with the traditional ultrasonic assistant exfoliation method. The delaminated nanosheets are revealed by atomic force microscopy to show a lateral size of a hundred nanometers and a thickness of about 0.4nm, which provides a direct evidence for the total exfoliation of g-C3N4 crystals into their single sheets. More importantly, the X-ray diffraction measurement confirms that the g-C3N4 nanosheets could be re-assembled with well-preserved original crystal structure. The exfoliation mechanism was also confirmed by the DFT calculation.

6.
Adv Mater ; 27(24): 3687-95, 2015 Jun 24.
Artigo em Inglês | MEDLINE | ID: mdl-25989160

RESUMO

A novel strategy for the controlled synthesis of 2D MoS2/C hybrid nanosheets consisting of the alternative layer-by-layer interoverlapped single-layer MoS2 and mesoporous carbon (m-C) is demonstrated. Such special hybrid nanosheets with a maximized MoS2 /m-C interface contact show very good performance for lithium-ion batteries in terms of high reversible capacity, excellent rate capability, and outstanding cycling stability.

7.
Zhongguo Shi Yan Xue Ye Xue Za Zhi ; 18(5): 1138-42, 2010 Oct.
Artigo em Chinês | MEDLINE | ID: mdl-21129247

RESUMO

This study was aimed to investigate the clinical feasibility of using multiplex PT-PCR assay for screening rare/cryptic chromosome translocations in patients with de novo acute myeloid leukemia. For 126 patients with de novo AML-M4/M5 without common chromosome translocations including t(15;17), t(8;21) and t(16;16), 3 parallel multiplex RT-PCR assays were set up to detect 6 mll-related gene rearrangements (mll/af10, mll/af17, mll/ell, mll/af9, mll/af6 and mll/enl) with low detection rate and 4 rare fusion genes (dek/can, tls/erg, aml1/mds (evi1) and npm/mlf1). The results showed that 11 patients with positive result from 126 patients were detected which involved in 5 molecular abnormalities. Among them, 10 cases were AML-M5 (16.67%), 1 cases AML-M4 (1.51%). The marker chromosomes were observed in 2 cases out of 11 cases through conventional karyotyping analysis, the karyotyping analysis in 1 case was not performed because this case had 1 mitotic figure only, no any cytogenetic aberrations were found in other 8 cases through R-band karyotyping analysis. It is concluded that multiplex RT-PCR designed in this study can quickly, effectively and accurately identify the rare/cryptic chromosome translocations and can be used in clinical detection.


Assuntos
Rearranjo Gênico , Leucemia Mieloide Aguda/genética , Reação em Cadeia da Polimerase Via Transcriptase Reversa/métodos , Translocação Genética , Bandeamento Cromossômico , Testes Genéticos , Humanos
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