Orbital magnetization provides a sensitive probe of topology and interactions, with particularly rich phenomenology in Chern insulators in which the topological edge states carry large equilibrium currents. Here we use a nanoscale superconducting sensor1,2 to map the magnetic fringe fields in twisted bilayers of MoTe2, in which transport3,4 and optical sensing5,6 experiments have revealed the formation of fractional Chern insulator (FCI) states at zero magnetic field. We observe oscillations in the local magnetic field associated with fillings ν = −1, −2/3, −3/5, −4/7 and −5/9 of the first moiré hole band, consistent with the formation of FCIs at these fillings. We determine the local thermodynamic gaps of the most robust FCI state at ν = −2/3, finding −2/3Δ as large as 7 meV. We also characterize sample spatial disorder, which is dominated by both inhomogeneity in the effective unit cell area7 as well as inhomogeneity in the band edge offset and bound dipole moment. Our results highlight both the challenges posed by structural disorder in the study of twisted homobilayer moiré systems and the opportunities afforded by the robust nature of the underlying correlated topological states.
Organic halides are highly useful compounds in chemical synthesis, where the halide serves as a versatile functional group for elimination, substitution, and cross-coupling reactions with transition metals or photocatalysis1-3. However, the activation of carbon-fluorine bonds, the most commercially abundant organohalide and found in PFAS, or “forever chemicals”, are much rarer. Current approaches based on photoredox chemistry for activation of small molecule carbon-fluorine (C–F) bonds are limited by the substrates and transition-metal catalysts needed4. A general method for the direct activation of organofluorines would have significant value in organic and environmental chemistry. Here, we report an organic photoredox catalyst system that can efficiently reduce C–F bonds to generate carbon-centered radicals, which can then be intercepted for hydrodefluorination (swapping F for H) and cross-coupling reactions. This system enables the general use of organofluorines as synthons under mild reaction conditions. We extend this method to the defluorination of polyfluoroalkyl substances (PFAS) and fluorinated polymers, a critical challenge in the breakdown of persistent and environmentally damaging forever chemicals.
Herpes simplex virus 1 (HSV-1) encephalitis (HSE) is the most common sporadic viral encephalitis in humans. It is life-threatening and has a first peak of incidence in childhood, during primary infection. Children with HSE are not particularly prone to other infections, including HSV-1 infections of tissues other than the brain. About 8–10% of childhood cases are due to monogenic inborn errors of 19 genes, two-thirds of which are recessive, and most of which display incomplete clinical penetrance. Childhood HSE can therefore be sporadic but genetic, enabling new diagnostic and therapeutic approaches. In this Review, we examine essential cellular and molecular mechanisms of cell-intrinsic antiviral immunity in the brain that are disrupted in individuals with HSE. These mechanisms include both known (such as mutations in the TLR3 pathway) and previously unknown (such as the TMEFF1 restriction factor) antiviral pathways, which may be dependent (for example, IFNAR1) or independent (for example, through RIPK3) of type I interferons. They operate in cortical or brainstem neurons, and underlie forebrain and brainstem infections, respectively. Conversely, the most severe inborn errors of leukocytes, including a complete lack of myeloid and/or lymphoid blood cells, do not underlie HSE. Thus congenital defects in intrinsic immunity in brain-resident neurons that underlie HSE broaden natural host defences against HSV-1 from the leukocytes of the immune system to other cells in the organism.
replying to: M. O. Cuthbert et al. Nature https://doi.org/10.1038/s41586-024-08082-9 (2024).