In Situ Probing the Structure Change and Interaction of Interfacial Water and Hydroxyl Intermediates on Ni(OH)2 Surface over Water Splitting.

There is growing acknowledgment that the properties of the electrochemical interfaces play an increasingly pivotal role in improving the performance of the hydrogen evolution reaction (HER). Here, we present, for the first time, direct dynamic spectral evidence illustrating the impact of the interaction between interfacial water molecules and adsorbed hydroxyl species (OHad) on the HER properties of Ni(OH)2 using Au/core-Ni(OH)2/shell nanoparticle-enhanced Raman spectroscopy. Notably, our findings highlight that the interaction between OHad and interfacial water molecules promotes the formation of weakly hydrogen-bonded water, fostering an environment conducive to improving the HER performance. Furthermore, the participation of OHad in the reaction is substantiated by the observed deprotonation step of Au@2 nm Ni(OH)2 during the HER process. This phenomenon is corroborated by the phase transition of Ni(OH)2 to NiO, as verified through Raman and X-ray photoelectron spectroscopy. The significant redshift in the OH-stretching frequency of water molecules during the phase transition confirms that surface OHad disrupts the hydrogen-bond network of interfacial water molecules. Through manipulation of the shell thickness of Au@Ni(OH)2, we additionally validate the interaction between OHad and interfacial water molecules. In summary, our insights emphasize the potential of electrochemical interfacial engineering as a potent approach to enhance electrocatalytic performance.

Label-free SERS strategy for rapid detection of capsaicin for identification of waste oils.

Identification of waste oils is challenging in the field of food safety due to the lack of common markers and straightforward analytical methods. Herein, we developed a novel label-free surface-enhanced Raman spectroscopy (SERS) strategy to identify waste oils using Ag nanoparticles solution (Ag NPs sol.) as a SERS substrate to significantly enhance the Raman signal of capsaicin marker molecule usually contained in the waste oils. The enhanced signal was directly detected by a portable Raman spectrometer with the limit of detection (LOD) of 2.9 µg L-1 within 10 min. Concentration-dependent SERS investigation showed the linear relationship between the SERS signal intensity of the characteristic peaks and the concentrations of capsaicin in the range of 10-2500 µg L-1 and the correlation coefficient was 0.9895. Our findings show the sensitivity, accessibility, and reliability of this method for the rapid identification of waste oils and furthermore for the practical applications in the field of food safety.

Direct and Simultaneous Identification of Multiple Mitochondrial Reactive Oxygen Species in Living Cells Using a SERS Borrowing Strategy.

Identification of different mitochondrial reactive oxygen species (ROS) simultaneously in living cells is vital for understanding the critical roles of different ROS in biological processes. To date, it remains a great challenge to develop ROS probes for direct and simultaneous identification of multiple ROS with high specificity. Herein, we report a SERS-borrowing-strategy-based nanoprobe (Au@Pt core-shell nanoparticles) for simultaneous and direct identification of different ROS by their distinct Raman fingerprints. Isotope substitution experiments and DFT calculations confirmed the ability of Au@Pt nanoprobe to capture and identify different mitochondrial ROS (i.e. ⋅OOH, H2 O2 , and ⋅OH). When functionalized with triphenylphosphine (TPP), the Au@Pt-TPP nanoprobe located to mitochondria and detected multiple ROS simultaneously in living cells under oxidative stimulation. Our method offers a new tool for the study of the functions of various ROS in biological processes.

Bisphenol A Initiates Excessive Premature Activation of Primordial Follicles in Mouse Ovaries via the PTEN Signaling Pathway.

The essence of primary ovarian insufficiency (POI) is the premature exhaustion of primordial follicles in the follicle pool, which is caused by the excessive premature activation of primordial follicles after birth. Bisphenol A (BPA) exposure promotes the transition of primordial follicles to primary follicles, thus the number of primordial follicles in the primordial follicle pool decreases significantly. However, the molecular mechanisms underlying abnormal follicle activation are poorly understood. Phosphatase and tensin homologue (PTEN) signal system is a negative regulator of follicle activation, which is called the brake of follicle activation. Besides, BPA induces Michigan Cancer Foundation-7 breast cancer cells proliferation by dysregulating PTEN/serine/threonine kinase/p53 axis. Whether BPA initiates the excessive premature activation of primordial follicles in the mouse ovaries via PTEN signaling pathway is unclear. In this study, we treated 6-week-old female CD-1 mice with different concentrations of BPA to study the effect of BPA on follicular activation and development in vivo, as well as the role of PTEN signaling in this process. We observed that BPA in concentrations from 1 µg/kg to 10 mg/kg groups downregulated PTEN expression and initiated excessive premature activation of primordial follicles in the mouse ovaries, and this effect was partly reversible by PTEN overexpression. Our results improve the understanding of both the effect of BPA in occurrence of POI and molecular mechanisms underlying initiation of primordial follicle pool activation, thus providing insight for POI treatment and theoretical basis for reducing the risk of POI.

Nociceptin/Orphanin FQ in PAG modulates the release of amino acids, serotonin and norepinephrine in the rostral ventromedial medulla and spinal cord in rats.

High density Nociceptin/Orphanin FQ (N/OFQ) and its receptor (NOPr) have been found in the ventrolateral periaqueductal gray (vlPAG), a main output pathway involved in the descending pain-control system. Our previous study demonstrated that the microinjection of N/OFQ into the vlPAG markedly facilitated nociceptive responses of spinal dorsal horn neurons. The aim of the present work was to further provide evidence for the supraspinal mechanisms of action for N/OFQ-mediated nociceptive facilitation by examining the effect of N/OFQ in the vlPAG on neurotransmitter release in the descending pain-control system, including the nucleus raphe magnus (NRM), nucleus reticularis gigantocellularis (NGC) and dorsal horn of the spinal cord. The results showed that the microinjection of N/OFQ into the vlPAG produced robust decreases in 5-hydroxytryptamine (5-HT, serotonin), norepinephrine (NE), and gamma-aminobutyric acid (GABA), and increase in glutamate (Glu) release in the spinal dorsal horn. Spinal application of 5-HT, 2-Me-5-HT (5-HT(3) receptor agonist), muscimol (GABA(A) receptor agonist), and baclofen (GABA(B) receptor agonist) significantly blocked intra-vlPAG-induced facilitation on nociceptive responses. However, the extracellular concentrations of these neurotransmitters in the NRM and NGC exhibited diversity following intra-vlPAG of N/OFQ. In the NRM, intra-vlPAG injection of N/OFQ significantly decreased 5-HT, NE, and Glu, but increased GABA release. Differently, in the NGC, both NE and GABA releases were attenuated by intra-vlPAG of N/OFQ, whereas the concentration of 5-HT and Glu exhibited a trend to increase. These findings provide direct support for the hypothesis that intra-PAG of N/OFQ-induced facilitation of nociceptive responses is associated with the release of 5-HT, NE, and amino acids.

The rostral ventromedial medulla mediates the facilitatory effect of microinjected orphanin FQ in the periaqueductal gray on spinal nociceptive transmission in rats.

Single unit extracellular recordings from spinal dorsal horn neurons were obtained with glass micropipettes in pentobarbital-anesthetized rats. A total of 50 wide dynamic range (WDR) neurons were studied in 25 rats. Microinjection of orphanin FQ (OFQ, 0.1 microg/0.1 microl) (a potent endogenous ligand of the opioid receptor-like receptor (ORL-1)) into the ipsilateral ventrolateral parts of periaqueductal gray (vlPAG) significantly increased C-response and post-discharge activity in most of the WDR neurons. Pre-microinjection of lidocaine (4%) into the nucleus raphe magnus (NRM) (0.5 microl), ipsilateral nucleus reticularis gigantocellularis (NGC) (0.6 microl), or nucleus gigantocellularis pars alpha (NGCalpha) and nucleus reticularis paragigantocellularis lateralis (NPGL) (0.5 microl) markedly reduced intra-vlPAG microinjection of OFQ-induced facilitatory effects on nociceptive responses of WDR neurons. Furthermore, if the NRM and ipsilateral NGC were simultaneously pre-microinjected with lidocaine, the intra-vlPAG microinjection of OFQ-induced facilitation on nociceptive responses of WDR neurons was eliminated. Also, a similar effect was observed when all the NRM, ipsilateral NGC, NGCalpha and NPGL were blocked with lidocaine. No significant effect on nociceptive responses of WDR neurons per se was found after blocking the NRM, ipsilateral NGC, NGCalpha/NPGL, or all the NRM, ipsilateral NGC, and NGCalpha/NPGL with lidocaine. These results indicate that (1) the facilitatory effect evoked by microinjection of OFQ into the vlPAG on nociceptive responses of WDR neurons in the spinal dorsal horn is primarily mediated by the NRM and ipsilateral NGC; (2) the NRM, ipsilateral NGC, and NGCalpha/NPGL do not mediate tonic descending inhibition of the spinal dorsal horn neurons.