An Ir(III) cyclometalate-functionalized molecularly imprinted polymer: photophysics, photochemistry and chemosensory applications.

A luminescent trimethylamine (TMA) sensor, PTMA-Ir, has been designed and synthesized through immobilizing a phosphorescent iridium(III) complex on a TMA-imprinted polymer. Detailed study shows that the quenching of phosphorescence of PTMA-Ir can serve as a reporter for the binding of TMA on the imprinting sites, thus providing a sensitive, selective, and rapid detection of TMA in both aqueous solutions and gaseous states. Loading PTMA-Ir on filter paper produced a deposition T-Ir, the phosphorescence of which is quenched within 5 s upon exposure to TMA vapor with detection limits of 9.0 ± 0.1 ppm under argon and 15.0 ± 0.1 ppm in an air atmosphere. This work provided an effective method for establishing an imprinting polymer-immobilized luminescent amine sensor.

A small molecule M1 promotes optic nerve regeneration to restore target-specific neural activity and visual function.

Axon regeneration is an energy-demanding process that requires active mitochondrial transport. In contrast to the central nervous system (CNS), axonal mitochondrial transport in regenerating axons of the peripheral nervous system (PNS) increases within hours and sustains for weeks after injury. Yet, little is known about targeting mitochondria in nervous system repair. Here, we report the induction of sustained axon regeneration, neural activities in the superior colliculus (SC), and visual function recovery after optic nerve crush (ONC) by M1, a small molecule that promotes mitochondrial fusion and transport. We demonstrated that M1 enhanced mitochondrial dynamics in cultured neurons and accelerated in vivo axon regeneration in the PNS. Ex vivo time-lapse imaging and kymograph analysis showed that M1 greatly increased mitochondrial length, axonal mitochondrial motility, and transport velocity in peripheral axons of the sciatic nerves. Following ONC, M1 increased the number of axons regenerating through the optic chiasm into multiple subcortical areas and promoted the recovery of local field potentials in the SC after optogenetic stimulation of retinal ganglion cells, resulting in complete recovery of the pupillary light reflex, and restoration of the response to looming visual stimuli was detected. M1 increased the gene expression of mitochondrial fusion proteins and major axonal transport machinery in both the PNS and CNS neurons without inducing inflammatory responses. The knockdown of two key mitochondrial genes, Opa1 or Mfn2, abolished the growth-promoting effects of M1 after ONC, suggesting that maintaining a highly dynamic mitochondrial population in axons is required for successful CNS axon regeneration.

Luminescent Rhenium(I) Pyridyldiaminocarbene Complexes: Photophysics, Anion-Binding, and CO2-Capturing Properties.

A series of luminescent isocyanorhenium(I) complexes with chelating acyclic diaminocarbene ligands (N^C) has been synthesized and characterized. Two of these carbene complexes have also been structurally characterized by X-ray crystallography. These complexes show blue-to-red phosphorescence, with the emission maxima not only considerably varied with a change in the number of ancillary isocyanide ligands but also extremely sensitive to the electronic and steric nature of the substituents on the acyclic diaminocarbene ligand. A detailed study with the support of density functional theory calculations revealed that the lowest-energy absorption and phosphorescence of these complexes in a degassed CH2Cl2 solution are derived from the predominantly metal-to-ligand charge-transfer [dπ(Re) → π*(N^C)] excited state. The unprecedented anion-binding and CO2-capturing properties of the acyclic diaminocarbene have also been described.