Leveraging Intramolecular π-Stacking to Access an Exceptionally Long-Lived MC Excited State in an Fe(II) Carbene Complex.

The ability to manipulate excited-state decay cascades using molecular structure is essential to the application of abundant-metal photosensitizers and chromophores. Ligand design has yielded some spectacular results elongating charge-transfer excited state lifetimes of Fe(II) coordination complexes, but triplet metal-centered (MC) excited states─recently demonstrated to be critical to the photoactivity of isoelectronic Co(III) polypyridyls─have to date remained elusive, with temporally isolable examples limited to the picosecond regime. With this report, we show how strong-field donors and intramolecular π-stacking can conspire to stabilize a long-lived MC excited state for a remarkable 4.

Perforin-2 is dispensable for host defense against and .

Unlabelled: Myeloid phagocytes are essential for antifungal immunity against pulmonary and systemic infections. However, the molecular mechanisms underlying fungal clearance by phagocytes remain incompletely understood. In this study, we investigated the role of Perforin-2 () in antifungal immunity.

Site-Selective Ligand Functionalization Reverses Hypsochromic Luminescence Shifts in Platinum(II) Complexes of Benzannulated NCN-Coordinating Ligands.

Ligands containing phenanthridine (benzo[c]quinoline) have presented notable exceptions to the conventional logic that increasing ligand benzannulation leads to bathochromic (red) shifts in the absorption and emission of their coordination complexes. The counterintuitive blue shifts have been attributed to the peculiar structure of phenanthridines, whose ground states are dominated by imine-bridged biphenyl resonance contributors. These serve to isolate the C=N unit electronically from the rest of the ligand framework and allow the C=N moiety to act as a 'shock-absorber', buffering against larger molecular distortions in a molecule's excited state, and reducing the observed pseudo-Stokes' shift.

MrgprA3 neurons drive cutaneous immunity against helminths through selective control of myeloid-derived IL-33.

Skin uses interdependent cellular networks for barrier integrity and host immunity, but most underlying mechanisms remain obscure. Herein, we demonstrate that the human parasitic helminth Schistosoma mansoni inhibited pruritus evoked by itch-sensing afferents bearing the Mas-related G-protein-coupled receptor A3 (MrgprA3) in mice. MrgprA3 neurons controlled interleukin (IL)-17 γδ T cell expansion, epidermal hyperplasia and host resistance against S.