A coumarin-hemicyanine dye was reported for ratiometric fluorescent detection of SO2 derivatives HSO3(-) and SO3(2-) based on a novel addition-rearrangement cascade reaction.

No abstract

A one-pot Au(I)-catalyzed reaction cascade to multi-ring heterocyclic products from alkynoic acids and primary amines is reported. The gold catalyst initially primes the alkynoic acid, via cyclization to an enol lactone, to react with a primary amine tethered to an electron rich heteroaromatic system. Then, via postulated Lewis acid assisted acidity, the Au(I) catalyst activates the amido ketone intermediate to undergo an N-acyl iminium ion cyclization. The reaction sequence is simple to perform, efficient, and broad in its scope to a diverse range of complex heterocyclic products.

A new cluster fullerene, Sc2 O@Td (19151)-C76 , has been isolated and characterized by mass spectrometry, UV/Vis/NIR absorption, (45) Sc NMR spectroscopy, cyclic voltammetry, and single-crystal X-ray diffraction. The crystallographic analysis unambiguously assigned the cage structure as Td (19151)-C76 , which is the first tetrahedral fullerene cage characterized by single-crystal X-ray diffraction. This study also demonstrated that the Sc2 O cluster has a much smaller ScOSc angle than that of Sc2 O@Cs (6)-C82 and the Sc2 O unit is fully ordered inside the Td (19151)-C76 cage. Computational studies further revealed that the cluster motion of the Sc2 O is more restrained in the Td (19151)-C76 cage than that in the Cs (6)-C82 cage. These results suggest that cage size affects not only the shapes but also the cluster motion inside fullerene cages.

Mutations in the Autoimmune regulator (Aire) gene result in a clinical phenomenon known as Autoimmune Polyglandular Syndrome Type I (APS1), which classically manifests as a triad of adrenal insufficiency, hypoparathyroidism, and chronic mucocutaneous infections. In addition to this triad, a number of other autoimmune diseases have been observed in APS1 patients including Sjögren's syndrome, vitiligo, alopecia, uveitis, and others. Aire-deficient mice, the animal model for APS1, have highlighted the role of the thymus in the disease process and demonstrated a failure in central tolerance in aire-deficient mice. However, autoantibodies have been observed against multiple organs in both mice and humans, making it unclear what the specific role of B and T cells are in the pathogenesis of disease. Utilizing the aire-deficient mouse as a preclinical model for APS1, we have investigated the relative contribution of specific lymphocyte populations, with the goal of identifying the cell populations which may be targeted for rational therapeutic design. Here we show that T cells are indispensable to the breakdown of self-tolerance, in contrast to B cells which play a more limited role in autoimmunity. Th1 polarized CD4+ T cells, in particular, are major contributors to the autoimmune response. With this knowledge, we go on to utilize therapies targeted at T cells to investigate their ability to modulate disease in vivo. Depletion of CD4+ T cells using a neutralizing antibody ameliorated the disease process. Thus, therapies targeted specifically at the CD4+ T cell subset may help control autoimmune disease in patients with APS1.