Identification of serum miR-378 and miR-575 as diagnostic indicators and predicting surgical prognosis in human epilepsy.

Background: Epilepsy (EP) is a common neurological disorder which is characterized by excessive abnormal synchronization of neuronal discharges in the brain due to chronic recurrent seizures of multiple etiologies. Variety of microRNAs have been associated with the occurrence and development of EP. This study aimed to determine the aberrant expression of miR-378 and miR-575 in EP patients to validate their potential to distinguish EP from healthy patients. Methods: RT-qPCR was used to determine the expressions of miR-378 and miR-575 from serum specimens of 106 EP and 103 control individuals. Clinical indicators between EP patients and controls were assessed. Based on surgical outcome, EP patients were further divided into Engel I-IV EP. The potentials of miR-378 and miR-575 in discriminating EP from healthy participants and predicting surgical prognosis were calculated by receiver operating characteristic (ROC) analysis. Results: We found the miR-378 and miR-575 were significantly declined (P<0.001) in Engel I-II and III-IV EP patients with no difference in clinical parameters compared. Moreover, miR-378 and miR-575 displayed high sensitivity, specificity, and accuracy in distinguishing EP patients and predicting surgical outcomes. Moreover, after surgical treatment, miR-378 and miR-575 levels were increased compared with those at admission, suggesting their potentials in treatment response. Conclusions: miR-378 and miR-575 could be utilized as novel and non-invasive serum biomarkers in discriminating EP from healthy controls and predicting surgical outcome, shedding new insights on epileptogenesis and EP treatment.

Microbial induced solidification and stabilization of municipal solid waste incineration fly ash with high alkalinity and heavy metal toxicity.

This paper presents an experimental study on the applicability of microbial induced carbonate precipitation (MICP) to treat municipal solid waste incineration (MSWI) fly ash with high alkalinity and heavy metal toxicity. The experiments were carried out on fly ashes A and B produced from incineration processes of mechanical grate furnace and circulating fluidized bed, respectively. The results showed that both types of fly ashes contained high CaO content, which could supply sufficient endogenous Ca for MICP treatment. Moreover, S. pasteurii can survive from high alkalinity and heavy metal toxicity of fly ash solution. Further, the unconfined compressive strength (UCS) of MICP treated fly ashes A and B reached 0.385MPa and 0.709 MPa, respectively. The MICP treatment also resulted in a reduction in the leaching toxicity of heavy metals, especially for Cu, Pb and Hg. MICP had a higher solidification and stabilization effect on fly ash B, which has finer particle size and higher Ca content. These findings shone a light on the possibility of using MICP technique as a suitable and efficient tool to treat the MSWI fly ash.

Sirt1 AS lncRNA interacts with its mRNA to inhibit muscle formation by attenuating function of miR-34a.

Recent studies demonstrate the functions of long non-coding RNAs (lncRNAs) in mediating gene expression at the transcriptional or translational level. Our previous study identified a Sirt1 antisense (AS) lncRNA transcribed from the Sirt1 AS strand. However, its role and regulatory mechanism is still unknown in myogenesis. Here, functional analyses showed that Sirt1 AS lncRNA overexpression promoted myoblast proliferation, but inhibited differentiation. Mechanistically, Sirt1 AS lncRNA was found to activate its sense gene, Sirt1. The luciferase assay provided evidences that Sirt1 AS lncRNA interacted with Sirt1 3' UTR and rescued Sirt1 transcriptional suppression by competing with miR-34a. In addition, RNA stability assay showed that Sirt1 AS lncRNA prolonged Sirt1 mRNA half-life from 2 to 10 h. Ribonuclease protection assay further indicated that it fully bound to Sirt1 mRNA in the myoblast cytoplasm. Moreover, Sirt1 AS overexpression led to less mouse weight than the control because of less lean mass and greater levels of Sirt1, whereas the fat mass and levels of miR-34a were not altered. Based on the findings, a novel regulatory mechanism was found that Sirt1 AS lncRNA preferably interacted with Sirt1 mRNA forming RNA duplex to promote Sirt1 translation by competing with miR-34a, inhibiting muscle formation.