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The analysis of breath VOC biomarkers is an efficient method for the early diagnosis of lung cancer. In this work, the zirconium UiO-66 was post-synthetically modified by using methylamine (MA), ethylenediamine (ED) and N,N′ -dimethylethylenediamine (MMEN), respectively. The modified UiO-66 materials were thoroughly characterized, including PXRD, FTIR, TGA, physical adsorption at 77 ​K by nitrogen and photoluminescence analysis. The sensing properties of the modified UiO-66 materials toward the selected five potential breath VOC biomarkers were investigated. Results showed that after modification, the BET surface area and total pore volume all decreased, and followed the order: UiO-66 ​> ​UiO-66-MA ​> ​UiO-66-MMEN ​> ​UiO-66-ED. Furthermore, the N–H group was successfully grafted into the modified UiO-66 samples. In comparison with UiO-66, the fluorescence intensities of UiO-66-MA, UiO-66-ED and UiO-66-MMEN toward hexanal, styrene and isoprene all obviously increased, while the fluorescence intensities of the modified UiO-66 materials toward 1-propanol and ethylbenzene all decreased a lot, accompanied by the frequency shift. In addition, the LOD of hexanal on UiO-66-MA was calculated to be as low as 12 ​ppm, which was obviously lower than that of UiO-66 (31 ​ppm). The fluorescence quenching of hexanal was mainly due to the FRET mechanism. The results of this study would provide information for the development of early breath diagnosis of lung cancer. [Display omitted] • The UiO-66 was postsynthetically modified by introducing N–H groups. • The modified UiO-66 presented turn-off effects toward hexanal. • The LOD of hexanal on UiO-66-MA was estimated to be as low as 12 ​ppm. • The modified UiO-66 exhibited good anti-interferent ability and recyclability. • The fluorescence quenching of hexanal was mainly due to the FRET mechanism. [ABSTRACT FROM AUTHOR]

Epilepsy is considered to result from an imbalance between excitation and inhibition of the central nervous system. Pathogenic mutations in the methyl-CpG binding domain protein 5 gene (MBD5) are known to cause epilepsy. However, the function and mechanism of MBD5 in epilepsy remain elusive. Here, we found that MBD5 was mainly localized in the pyramidal cells and granular cells of mouse hippocampus, and its expression was increased in the brain tissues of mouse models of epilepsy. Exogenous overexpression of MBD5 inhibited the transcription of the signal transducer and activator of transcription 1 gene (Stat1), resulting in increased expression of N -methyl- d -aspartate receptor (NMDAR) subunit 1 (GluN1), 2A (GluN2A) and 2B (GluN2B), leading to aggravation of the epileptic behaviour phenotype in mice. The epileptic behavioural phenotype was alleviated by overexpression of STAT1 which reduced the expression of NMDARs, and by the NMDAR antagonist memantine. These results indicate that MBD5 accumulation affects seizures through STAT1-mediated inhibition of NMDAR expression in mice. Collectively, our findings suggest that the MBD5-STAT1-NMDAR pathway may be a new pathway that regulates the epileptic behavioural phenotype and may represent a new treatment target. • MBD5 was mainly localized in the cytoplasm and nucleus of neurons. • Expression of MBD5 was increased in brain tissues of epileptic mouse models. • Increased MBD5 inhibited the transcription of Stat1 , resulting in increased expression of NMDAR subunits and aggravation of epileptic behavioural phenotype in mice. • Upregulation of STAT1 expression or the use of the NMDAR antagonism alleviated this phenotype. • MBD5-STAT1-NMDAR pathway may be a new pathway that regulates the epileptic behavioural phenotype and may represent a new treatment target. [ABSTRACT FROM AUTHOR]