Eigensystem and Full Character Formula of the W_{1+infinity} Algebra with c=1

By using the free field realizations, we analyze the representation theory of the W_{1+infinity} algebra with c=1. The eigenvectors for the Cartan subalgebra of W_{1+infinity} are parametrized by the Young diagrams, and explicitly written down by W_{1+infinity} generators. Moreover, their eigenvalues and full character formula are also obtained.Comment: 12 pages, YITP/K-1049, SULDP-1993-1, RIMS-959, Plain TEX, ( New references

Cryptococcus gattii Genotype VGIIa Infection in Man, Japan, 2007

We report a patient in Japan infected with Cryptococcus gattii genotype VGIIa who had no recent history of travel to disease-endemic areas. This strain was identical to the Vancouver Island outbreak strain R265. Our results suggest that this virulent strain has spread to regions outside North America

An In Vitro Model for Lewy Body-Like Hyaline Inclusion/Astrocytic Hyaline Inclusion: Induction by ER Stress with an ALS-Linked SOD1 Mutation

Neuronal Lewy body-like hyaline inclusions (LBHI) and astrocytic hyaline inclusions (Ast-HI) containing mutant Cu/Zn superoxide dismutase 1 (SOD1) are morphological hallmarks of familial amyotrophic lateral sclerosis (FALS) associated with mutant SOD1. However, the mechanisms by which mutant SOD1 contributes to formation of LBHI/Ast-HI in FALS remain poorly defined. Here, we report induction of LBHI/Ast-HI-like hyaline inclusions (LHIs) in vitro by ER stress in neuroblastoma cells. These LHI closely resemble LBHI/Ast-HI in patients with SOD1-linked FALS. LHI and LBHI/Ast-HI share the following features: 1) eosinophilic staining with a pale core, 2) SOD1, ubiquitin and ER resident protein (KDEL) positivity and 3) the presence of approximately 15–25 nm granule-coated fibrils, which are morphological hallmark of mutant SOD1-linked FALS. Moreover, in spinal cord neurons of L84V SOD1 transgenic mice at presymptomatic stage, we observed aberrant aggregation of ER and numerous free ribosomes associated with abnormal inclusion-like structures, presumably early stage neuronal LBHI. We conclude that the LBHI/Ast-HI seen in human patients with mutant SOD1-linked FALS may arise from ER dysfunction

Mff functions with Pex11pβ and DLP1 in peroxisomal fission

Summary Peroxisomal division comprises three steps: elongation, constriction, and fission. Translocation of dynamin-like protein 1 (DLP1), a member of the large GTPase family, from the cytosol to peroxisomes is a prerequisite for membrane fission; however, the molecular machinery for peroxisomal targeting of DLP1 remains unclear. This study investigated whether mitochondrial fission factor (Mff), which targets DLP1 to mitochondria, may also recruit DLP1 to peroxisomes. Results show that endogenous Mff is localized to peroxisomes, especially at the membrane-constricted regions of elongated peroxisomes, in addition to mitochondria. Knockdown of MFF abrogates the fission stage of peroxisomal division and is associated with failure to recruit DLP1 to peroxisomes, while ectopic expression of MFF increases the peroxisomal targeting of DLP1. Co-expression of MFF and PEX11β, the latter being a key player in peroxisomal elongation, increases peroxisome abundance. Overexpression of MFF also increases the interaction between DLP1 and Pex11pβ, which knockdown of MFF, but not Fis1, abolishes. Moreover, results show that Pex11pβ interacts with Mff in a DLP1-dependent manner. In conclusion, Mff contributes to the peroxisomal targeting of DLP1 and plays a key role in the fission of the peroxisomal membrane by acting in concert with Pex11pβ and DLP1

Familial Spread of a Virulent Clone of Klebsiella pneumoniae Causing Primary Liver Abscess▿

Capsule-forming Klebsiella pneumoniae K1 caused primary liver abscess in two household members of a family. The causative isolates had identical pulsed-field gel electrophoresis patterns and were determined to be sequence type 23. An additional member of the family was found to carry the same strain without clinical manifestation

Quasifinite Highest Weight Modules over Super W1+∞W_{1+\infty} Algebra

We study quasifinite highest weight modules over the supersymmetric extension of the $W_{1+\infty}$ algebra on the basis of the analysis by Kac and Radul. We find that the quasifiniteness of the modules is again characterized by polynomials, and obtain the differential equations for highest weights. The spectral flow, free field realization over the $(B,C)$--system, and the embedding into \Glinf are also presented.Comment: 38 pages, Plain Tex, YITP/K-1055, UT-670, SULDP-1994-