Azo-Cyanamide Bridged Dinuclear Iron Complexes Exhibiting no Electronic Coupling but Moderate Magnetic Coupling between the two Iron Centers.

To investigate the effect of long-distance organic ligand on electronic coupling between metallic atoms, the mononuclear and dinuclear complexes [Cp(dppe)Fe(apc)] (1), [{Cp(dppe)Fe}(μ-adpc)] (2), [{CpMe(dppe)Fe}(μ-adpc) (3) and their oxidized complexes [Cp(dppe)Fe(apc)][PF] (1[PF]), [{Cp(dppe)Fe}(μ-adpc)][PF] (2[PF]), [{CpMe(dppe)Fe}(μ-adpc)][PF] (3[PF]) (Cp=1,3-cyclopentadiene, CpMe=1,2,3,4,5-pentamethylcyclopentadiene, dppe=1,2-bis(diphenylphosphino)ethane), apc=4-azo(phenylcyanamido)benzene and adpc=4,4'-azodi(phenylcyanamido)) were synthesized and characterized by cyclic voltammetry, UV-vis, single-crystal X-ray diffraction and Mössbauer spectra. Electrochemical measurements showed no electronic coupling between the two terminal Fe units, However, the investigation results of the magnetic properties of the two-electron oxidized complexes indicate the presence of moderate antiferromagnetic coupling across 18 Å distance.

Resolvin D1, an endogenous lipid mediator for inactivation of inflammation-related signaling pathways in microglial cells, prevents lipopolysaccharide-induced inflammatory responses.

Backgrounds And Aim: Microglial cells as an important part of central nervous system (CNS) have generally believed to play significant role in the process leading to a number of neurodegenerative disorders including Parkinson's disease, Alzheimer's disease, prion diseases, multiple sclerosis, HIV-dementia, and stroke. Although different diseases have quite different pathogenesis, the activation of microglia was shared with all of them. Recently, the resolvin D1 (RvD1) as an endogenous antiinflammatory lipid mediator has been confirmed to be involved in the treatment of inflammation-related neuronal injury in neurodegenerative diseases.