Switchable aptamer-fueled colorimetric sensing toward agricultural fipronil exposure sensitized with affiliative metal-organic framework.

Persistent usage of pesticides in agriculture has posed serious damage to overall ecosystem and human health, and thereby it is imperative to develop sensitive and efficient tools to evaluate residual pesticides in food and environmental setting. Herein, we reported a switchable colorimetric probe toward fipronil residue sensitized with aptamer-fueled catalytic activity of affiliative ZIF-8. Innovatively, it was found that the attached aptamer preferred to adsorb 3,3',5,5'-tetramethylbenzidine (TMB) rather than 2,2-azinobis (3-ethylbenzothiazo-line-6-sulfonic acid) (ABTS), greatly promoting catalytic oxidation of ZIF-8 toward TMB for further improving sensitivity.

Development and validation of the UPLC-MS method for simultaneous determination of six new psychoactive substances.

The combined abuse of benzodiazepines and antipsychotics has become a global problem, and to develop a highly sensitive and selective method for monitoring of benzodiazepine hypnotics and antipsychotics is urgently necessary. In this work, we established a rapid method for the simultaneous determination of benzodiazepines (diazepam, alprazolam, triazolam, and estazolam) and antipsychotic drugs (clozapine, and chlorpromazine) based on ultra performance liquid chromatography-mass spectrometry (UPLC-MS). The accuracy, precision, limit of detection (LOD), limit of quantification (LOQ), specificity, matrix effect and carry-over effect were verified in detail.

Thioredoxin-1 blocks methamphetamine-induced injury in brain through inhibiting endoplasmic reticulum and mitochondria-mediated apoptosis in mice.

Methamphetamine (METH) has been reported to induce endoplasmic reticulum (ER) stress and neuronal apoptosis in the central nervous system (CNS) during the development of addiction. Thioredoxin-1 (Trx-1) is a redox regulating protein and plays an important role in inhibiting apoptosis and protects neurons from cytotoxicity through ER and mitochondria-mediated pathways. Our previous study has been reported that Trx-1 protects mice from METH-induced rewarding effect.