Single-molecule magnets (SMMs) that can be trapped in one of the bistable magnetic states separated by an energy barrier are among the most promising candidates for high-density information storage, quantum processing, and spintronics. To date, a considerable series of achievements have been made. However, the presence of fast quantum tunnelling of magnetization (QTM) in most SMMs, especially in single-ion magnets (SIMs), provides a rapid relaxation route and often sets up a limit for the relaxation time. Here, we pursue the pentagonal bipyramidal symmetry to suppress the QTM and present pentagonal bipyramidal Dy(III) SIMs [Dy(Cy3PO)2(H2O)5]Cl3·(Cy3PO)·H2O·EtOH (1) and [Dy(Cy3PO)2(H2O)5]Br3·2(Cy3PO)·2H2O·2EtOH (2), (Cy3PO = tricyclohexyl phosphine oxide). Magnetic characterizations reveal their fascinating SMM properties with high energy barriers as 472(7) K for 1 and 543(2) K for 2, along with a record magnetic hysteresis temperature up to 20 K for 2. These results, combined with the ab initio calculations, offer an illuminating insight into the vast possibility and potential of what the symmetry rules can achieve in molecular magnetism.

Longevity has been a long-standing concern for hybrid perovskite photovoltaics. We demonstrate high-resilience positive-intrinsic-negative perovskite solar cells by incorporating a piperidinium-based ionic compound into the formamidinium-cesium lead-trihalide perovskite absorber. With the bandgap tuned to be well suited for perovskite-on-silicon tandem cells, this piperidinium additive enhances the open-circuit voltage and cell efficiency. This additive also retards compositional segregation into impurity phases and pinhole formation in the perovskite absorber layer during aggressive aging. Under full-spectrum simulated sunlight in ambient atmosphere, our unencapsulated and encapsulated cells retain 80 and 95% of their peak and post-burn-in efficiencies for 1010 and 1200 hours at 60° and 85°C, respectively. Our analysis reveals detailed degradation routes that contribute to the failure of aged cells.

Multiple sclerosis (MS) is an inflammatory disease of the central nervous system (CNS) characterized by localized areas of demyelination. Although the etiology and pathogenesis of MS remain largely unknown, it is generally assumed that immune responses to myelin antigens contribute to the disease process. The exact sequence of events, as well as the molecular mediators that lead to myelin destruction, is yet to be defined. As a potent mediator of inflammation, the cytopathic cytokine, tumor necrosis factor (TNF) has been considered to be a strong candidate in the pathogenesis of MS and its animal model, experimental autoimmune encephalomyelitis (EAE). However, its role in immune-mediated demyelination remains to be elucidated. To determine the contribution of TNF to the pathogenesis of the MS-like disease provoked by the myelin oligodendrocyte glycoprotein (MOG), we have tested mice with an homologous disruption of the gene encoding TNF. Here we report that upon immunization with MOG, mice lacking TNF develop severe neurological impairment with high mortality and extensive inflammation and demyelination. We show further that inactivation of the TNF gene converts MOG-resistant mice to a state of high susceptibility. Furthermore, treatment with TNF dramatically reduces disease severity in both TNF-/- mice and in other TNF+/+ mice highly susceptible to the MOG-induced disease. These findings indicate that TNF is not essential for the induction and expression of inflammatory and demyelinating lesions, and that it may limit the extent and duration of severe CNS pathology.

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Myelin oligodendrocyte glycoprotein (MOG) is postulated to be a target autoantigen in multiple sclerosis (MS). Here we investigated the encephalitogenicity of an immunodominant epitope of MOG, peptide 35-55, in various strains of mice. An MS-like disease was induced in NOD/Lt mice (H-2g7) and C57BL/6 mice (H-2b) by a single injection of MOG35-55 in CFA. The disease followed a relapsing-remitting course in NOD/Lt mice, whereas C57BL/6 mice developed a chronic paralytic disease. Histologically, the disease in both strains was characterized by cellular infiltration and multifocal demyelination in the CNS. Significant DTH type reactions to MOG35-55 were only seen in MOG-susceptible animals, with the NOD/Lt mice showing the strongest responses. Susceptible mice also showed specific antibody responses to MOG35-55 but not to a panel of other MOG peptides. These results provide further evidence for the role of MOG as a highly autoantigenic molecule capable of inducing severe demyelinating disease.

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