Clear experimental evidence from X-ray photoelectron spectroscopy and (31)P NMR spectroscopy has been obtained for the first time to confirm that the combination of Ag(+) cation with [L-Au](+) results in the formation of different complexes in solution. Re-evaluation of literature-reported gold-catalyzed reactions revealed a significant difference in the reactivities with and without silver. In extreme cases (more than "rare"), the conventional [L-Au](+) catalysts could not promote the reaction without the presence of silver. This investigation has therefore revealed a long-overlooked "silver effect" in gold catalysis and should lead to revision of the actual mechanism.

Intravenously infused synthetic 500 nm nanoparticles composed of poly(lactide-co-glycolide) are taken up by blood-borne inflammatory monocytes via a macrophage scavenger receptor (macrophage receptor with collagenous structure), and the monocytes no longer traffic to sites of inflammation. Intravenous administration of the nanoparticles after experimental spinal cord injury in mice safely and selectively limited infiltration of hematogenous monocytes into the injury site. The nanoparticles did not bind to resident microglia, and did not change the number of microglia in the injured spinal cord. Nanoparticle administration reduced M1 macrophage polarization and microglia activation, reduced levels of inflammatory cytokines, and markedly reduced fibrotic scar formation without altering glial scarring. These findings thus implicate early-infiltrating hematogenous monocytes as highly selective contributors to fibrosis that do not play an indispensable role in gliosis after SCI. Further, the nanoparticle treatment reduced accumulation of chondroitin sulfate proteoglycans, increased axon density inside and caudal to the lesion site, and significantly improved functional recovery after both moderate and severe injuries to the spinal cord. These data provide further evidence that hematogenous monocytes contribute to inflammatory damage and fibrotic scar formation after spinal cord injury in mice. Further, since the nanoparticles are simple to administer intravenously, immunologically inert, stable at room temperature, composed of an FDA-approved material, and have no known toxicity, these findings suggest that the nanoparticles potentially offer a practical treatment for human spinal cord injury.

Fluorescent active triazapentalene zwitterions (TAPZs) were prepared through Au(I) catalyzed triazole-alkyne 5-endo-dig cyclization. While an effective gold catalyst turnover (0.5% loading, up to 96% yield) was achieved, the stability of these new 10-π-electron bicyclic structures was also significantly improved, which warranted future applications of these fluorescent dyes.

Objective There are currently no definitive disease‐modifying therapies for traumatic brain injury (TBI). In this study, we present a strong therapeutic candidate for TBI, immunomodulatory nanoparticles (IMPs), which ablate a specific subset of hematogenous monocytes (hMos). We hypothesized that prevention of infiltration of these cells into brain acutely after TBI would attenuate secondary damage and preserve anatomic and neurologic function. Methods IMPs, composed of US Food and Drug Administration–approved 500nm carboxylated‐poly(lactic‐co‐glycolic) acid, were infused intravenously into wild‐type C57BL/6 mice following 2 different models of experimental TBI, controlled cortical impact (CCI), and closed head injury (CHI). Results IMP administration resulted in remarkable preservation of both tissue and neurological function in both CCI and CHI TBI models in mice. After acute treatment, there was a reduction in the number of immune cells infiltrating into the brain, mitigation of the inflammatory status of the infiltrating cells, improved electrophysiologic visual function, improved long‐term motor behavior, reduced edema formation as assessed by magnetic resonance imaging, and reduced lesion volumes on anatomic examination. Interpretation Our findings suggest that IMPs are a clinically translatable acute intervention for TBI with a well‐defined mechanism of action and beneficial anatomic and physiologic preservation and recovery. Ann Neurol 2020;87:442–455