RESUMO
The low specific capacity and low voltage plateau are significant challenges in the advancement of practical magnesium ion batteries (MIBs). Here, a superior aqueous electrolyte combining with a copper foam interlayer between anode and separator is proposed to address these drawbacks. Notably, with the dynamic redox of copper ions, the weakened solvation of Mg2+ cations in the electrolyte and the enhanced electronic conductivity of anode, which may offer effective capacity-compensation to the 3,4,9,10-perylenetetracarboxylic diimide (PTCDI)-Mg conversion reactions during the long-term cycles. As a result, the unique MIBs using expanded graphite cathode coupled with PTCDI anode demonstrate exceptional performance with an ultra-high capacity (205 mAh g-1 , 243 Wh kg-1 at 5 A g-1 ) as well as excellent cycling stability after 600 cycles and rate capability (138 mAh g-1 , 81 Wh kg-1 at 10 A g-1 ).
RESUMO
The aim of this study was to verify whether anti-miR-101 participates in the treatment of hepatocellular carcinoma (HCC) as a small-molecule antitumor agent, and to explore the effect on phosphatase and tensin homolog deleted on chromosome 10 (PTEN). Patients who received consecutive hepatectomies were followed-up, and miR-101 expressions in their tumor and paracancerous tissues were detected. Correlation between miR-101 expression and clinical pathological factors and prognosis was studied. Highthroughput sequencing was used to detect the genetic and microRNA (miRNA) levels of tumor tissues. Expression of anti-miR-101 in different HCC cell lines was determined, and those of desired genes and proteins were detected by qRT-PCR and western blotting to obtain the target gene. miR-101 was significantly upregulated in HCC patients compared with that in paracancerous tissues. High miR-101 expression, vascular invasion, tumor size ≥7 cm and late pathological stage were the risk factors of recurrence-free survival rate. High miR-101 expression was the independent prognostic factor of total and recurrence-free survival rates. CXCL12, IL6R, FOXO3 and PTEN were screened as desired genes, and only PTEN was expressed significantly differently in three cell lines. miR-101 could bind 3'-UTR of WT-PTEN with reduced fluorescent intensity, suggesting that PTEN was the target gene. SMMC-7721, HepG2 and Huh7 were eligible cell lines for miR-101 studies. miR-101 was an applicable molecular marker of HCC. Anti-miR-101 regulated the transcription of PTEN and may promote cell proliferation, differentiation and apoptosis by regulating downstream genes with PTEN. The regulatory effects of anti-miR-101 on PTEN provide valuable evidence for finding novel miRNA drugs.
Assuntos
Carcinoma Hepatocelular/genética , Neoplasias Hepáticas/genética , MicroRNAs/genética , PTEN Fosfo-Hidrolase/biossíntese , Idoso , Idoso de 80 Anos ou mais , Antagomirs , Apoptose/genética , Carcinogênese/genética , Carcinoma Hepatocelular/patologia , Proliferação de Células/genética , Quimiocina CXCL12/biossíntese , Intervalo Livre de Doença , Feminino , Proteína Forkhead Box O3/biossíntese , Regulação Neoplásica da Expressão Gênica , Células Hep G2 , Humanos , Neoplasias Hepáticas/patologia , Masculino , MicroRNAs/antagonistas & inibidores , Pessoa de Meia-Idade , Oligodesoxirribonucleotídeos Antissenso , PTEN Fosfo-Hidrolase/genética , Prognóstico , Receptores de Interleucina-6/biossínteseRESUMO
Parkinson's disease (PD) is the second most common age-related neurodegenerative disease. MicroRNA-7 (miR-7) displays neuroprotective properties against PD. However, the biological roles of miR-7 and its underlying molecular mechanisms in PD remain unclear. We demonstrated herein that 1-methyl-4-phenylpyridinium ion (MPP(+)) confers toxic effects on dopaminergic neuron in a dose-dependent manner in a cellular PD model, although this phenomenon is attenuated by miR-7 treatment. Introduction of miR-7 inhibits MPP(+)-induced neuronal apoptosis as reflected by the reduced terminal transferase-mediated dUTP nick end labeling-positive rate, mitochondrial permeability potential, caspase 3 activity, and nucleosomal enrichment factor. Bax and sirtuin 2 (Sirt2) are the direct targets of miR-7. Moreover, the effects of miR-7 were counteracted by Bax and Sirt2 overexpression, respectively. The altered molecular expressions downstream of Bax and Sirt2 are also involved in miR-7 regulation of the MPP(+)-triggered neuronal apoptosis. These findings have implications on the potential application of miR-7 in PD treatment.
