Investigation of the Effect of a Mixed-Ligand on the Accommodation of a Templating Molecule into the Structure of High-Nucleus Silver Clusters.

Advancement of the synthesis and control of the self-assembly process of new high-nucleus silver clusters with desired structures is important for both the material sciences and the many applications. Herein, three new silver clusters, 20-, 22-, and 8-nucleus, based on alkynyl ligands were constructed and their structures were confirmed by single-crystal X-ray diffraction, powder X-ray diffraction, elemental analyses, and Fourier-transform infrared spectroscopy (FT-IR). For the first time, the trivalent tetrahedron anion of AsO43-, as a template, and the surface ligand of Ph2PO2H, with new coordination modes, were employed in preparation of the silver clusters. The role of surface ligands and template anions in the size and structure of the clusters was investigated. The presence of the template in the structure of the clusters led to the formation of the high-nucleus clusters. Also, in this report, it was shown that the participation of the template in the assembly of a cluster can be controlled by the surface ligands. UV-vis absorption and luminescent properties of the clusters and the thermal stability of the 8-nucleus cluster were also studied.

Trivalent Tetrahedral Anion Template: A 26-Nucleus Silver Alkynyl Cluster Encapsulating Vanadate.

In order to study the charge effect on the formation of an anion-templated silver cluster, a trivalent tetrahedral anion was incorporated into the silver assembly. A 26-nuclear silver cluster was prepared, and its structure was confirmed by single-crystal X-ray diffraction. Also, the resulting structure was characterized by powder X-ray diffraction data. Its light absorption and photoluminescent properties were studied by solid-state UV diffuse-reflectance and fluorescence spectroscopy. Compared with the other reported silver clusters with tetrahedral anion templates, the more negative VO43- anion led to the formation of a bigger silver cluster. Also, the supramolecular motif O-H(CH3OH)···O(trifluoroacetate) was confirmed on the cluster surface for the first time.

Photochromism, photoluminescence modulation and selective recognition of small molecules of two highly stable dynamic metal-organic frameworks.

Two highly stable dynamic metal-organic frameworks exhibit photochromism, tunable photoluminescence, and selective detection of oxygen, which can be recognised by the naked eye through color changes. Furthermore, they also display selective recognition of benzyl alcohol and halogenated solvents, respectively.

Two bilayer metal-organic frameworks with rare trinuclear heterometal clusters and tunable photoluminescence.

Two bilayer metal-organic frameworks (MOFs) respectively containing trinuclear Pb/K and Cd/Na clusters have been solvothermally synthesized. Photoluminescence studies showed that they exhibit tunable purple-to-red-to-green and purple-to-green luminescence behaviours by variation of excitation light, respectively.

Inhibition on the S-nitrosylation of MKK4 can protect hippocampal CA1 neurons in rat cerebral ischemia/reperfusion.

S-nitrosylation, the nitric oxide-derived post-translational modification of proteins, plays critical roles in various physiological and pathological functions. In this present study, a rat model of cerebral ischemia and reperfusion by four-vessel occlusion was generated to assess MKK4 S-nitrosylation. Immunoprecipitation and immunoblotting were performed to evaluate MKK4 S-nitrosylation and phosphorylation. Neuronal loss was observed using histological detection. These results indicated that endogenous NO promoted the S-nitrosylation of MKK4. However, application of the exogenous NO donor S-nitrosoglutathione (GNSO), an inhibitor of the neuronal nitric oxide synthase 7-nitroindazole (7-NI), and the N-methyl-d-aspartate receptor (NMDAR) antagonist MK801 diminished I/R-induced S-nitrosylation and phosphorylation. These compounds also markedly decreased cerebral I/R-induced degeneration and death of neurons in hippocampal CA1 region in rats. Taken together, we demonstrated for the first time, that cerebral ischemia/reperfusion can induce S-nitrosylation of MKK4. We also found that inhibiting S-nitrosylation and activation of MKK4 resulted in marked decreases in neuronal degeneration and apoptosis, potentially via NMDAR-mediated mechanisms. These findings may lead to a new field of inquiry to investigate the underlying pathogenesis of stoke and the development of novel treatment strategies.

Neuroprotection of co-activation of GABA receptors by preventing caspase-3 denitrosylation in KA-induced seizures.

Previous studies have demonstrated that kainic acid (KA)-induced seizures can cause the enhancement of excitation and lead to neuronal death in rat hippocampus. Co-activation of the inhibitory GABA receptors can attenuate the excitatory JNK3 apoptotic signaling pathway via inhibiting the increased assembly of the GluR6-PSD-95-MLK3 signaling module induced by KA in epileptic rat hippocampal CA1 and CA3 regions. Caspase-3 is a cysteine protease located in both the cytoplasm and mitochondrial intermembrane space that is a central effector of many apoptotic pathways. We designed experiments to elucidate the underlying molecular mechanisms of procaspase-3 activation and neuroprotection of co-activation of GABA receptors against neuronal death induced by KA. In this study, we show that co-activation of GABA receptors can attenuate the Fas/FasL apoptotic signaling pathway and inhibit the increased of thioredoxin reductase activity induced by KA, subsequently inhibit the activation of procaspase-3 by diminishing the denitrosylation of its active-site thiol and decreasing the cleavage of the caspase-3 zymogen to its active subunits. These results indicate that co-activation of GABA receptors results in neuroprotection by preventing caspase-3 denitrosylation in KA-induced seizure of rats.