Spin Hall Effect of Excitons

Spin Hall effect for excitons in alkali halides and in Cu_2O is investigated theoretically. In both systems, the spin Hall effect results from the Berry curvature in k space, which becomes nonzero due to lifting of degeneracies of the exciton states by exchange coupling. The trajectory of the excitons can be directly seen as spatial dependence of the circularly polarized light emitted from the excitons. It enables us to observe the spin Hall effect directly in the real-space time.Comment: 5 pages, 2 figure

Castleman's Disease of the Chest Wall

AbstractPrimary Castleman's disease of the chest wall is unusual. Furthermore, such tumors arising from a surgical wound are extremely rare. We report a 33-year-old female with a history of a thoracic surgery at 5 years of age. A round, homogenous 4 × 3.5-cm mass protruded into the thoracic cavity on the posterior portion of the previous posterolateral incision. The tumor was completely removed, with combined rib resection. The resected specimen showed Angiofollicular Lymph Node Hyperplasia (Castleman's disease), hyaline-vascular type. No recurrence has been found for 10 years. This is the first report of primary chest wall Castleman's disease arising from the surgical wound

The Role of Attractin in Neurodegeneration Caused by Oxidative Stress

Oxidative stress is linked to dopaminergic (DA) neurodegeneration in Parkinson’s disease. Our laboratory reported slowly progressive DA neurodegeneration in the zitter (zi) rat, which is Attractin (Atrn) deficient. However, little is known about the function of Atrn in the central nervous system (CNS). Thus, we investigated whether DA neurodegeneration in the zi rat was induced by oxidative stress, and how Atrn affects oxidative stress. First, we summarize our previous in vivo data, which revealed suppression of DA neurodegeneration using antioxidants (vitamin E and melatonin) in zi rats. Second, our current ex vivo and in vitro studies are introduced. Using primary neuronal cultures of zi mesencephalon as a model of Atrn-deficient neurons or Atrn-GFP-overexpressing HEK293 cells, accumulation of reactive oxygen species (ROS) in mitochondria and cell viability was examined under oxidative stress. Atrn-deficient neurons accumulated excess ROS in mitochondria, resulting in neurodegeneration, whereas Atrn-overexpressing cells showed suppression of ROS accumulation under oxidative stress. These results showed that Atrn plays a suppressive role against ROS and that the loss of Atrn function induced excess ROS accumulation and led to DA neurodegeneration. This is the first report to show that Atrn directly modulates mitochondrial ROS accumulation in the CNS

Overexpression of a Brix Domain-Containing Ribosome Biogenesis Factor ARPF2 and its Interactor ARRS1 Causes Morphological Changes and Lifespan Extension in Arabidopsis thaliana

The Brix domain is a conserved domain in several proteins involved in ribosome biogenesis in yeast and animals. In the Arabidopsis genome, six Brix domain-containing proteins are encoded; however, their molecular functions have not been fully characterized, as yet. Here we report the functional analysis of a Brix domain-containing protein, ARPF2, which is homologous to yeast Rpf2 that plays an essential role in ribosome biogenesis as a component of the 5S ribonucleoprotein particle. By phenotypic characterization of arpf2 mutants, histochemical GUS staining, and analysis using green fluorescence protein, we show that ARPF2 is an essential and ubiquitously expressed gene encoding a nucleolar protein. Co-immunoprecipitation and split-GFP-based bimolecular fluorescence complementation assays revealed that ARPF2 interacts with a protein named ARRS1, which is homologous to yeast Rrs1 that forms a complex with Rpf2 in yeast. Furthermore, the result of RNA immunoprecipitation assay indicated that ARPF2 interacts with 5S ribosomal RNA (rRNA) or the precursor of 5S rRNA, as well as with the internal transcribed spacer 2 in the precursors of 25S rRNA. Most intriguingly, we found that the overexpression of ARPF2 and ARRS1 leads to characteristic phenotypes, including short stem, abnormal leaf morphology, and long lifespan, in Arabidopsis. These results suggest that the function of Brix domain-containing ARPF2 protein in ribosome biogenesis is intimately associated with the growth and development in plants

Evaluation of the Relationship Between Cognitive Impairment, Glycometabolism, and Nicotinic Acetylcholine Receptor Deficits in a Mouse Model of Alzheimer's Disease

PURPOSE: In patients with Alzheimer's disease (AD), the loss of cerebral nicotinic acetylcholine receptors (nAChRs) that are implicated in higher brain functions has been reported. However, it is unclear if nAChR deficits occur in association with cognitive impairments. The purpose of this study was to assess the relationship between nAChR deficits and cognitive impairments in a mouse model of AD (APP/PS2 mice). PROCEDURES: The cognitive abilities of APP/PS2 and wild-type mice (aged 2-16 months) were evaluated using the novel object recognition test. Double-tracer autoradiography analyses with 5-[125I]iodo-A-85380 ([125I]5IA: α4β2 nAChR imaging probe) and 2-deoxy-2-[18F]fluoro-D-glucose were performed in both mice of different ages. [123I]5IA-single-photon emission tomography (SPECT) imaging was also performed in both mice at 12 months of age. Furthermore, each age cohort was investigated for changes in cognitive ability and expression levels of α7 nAChRs and N-methyl-D-aspartate receptors (NMDARs). RESULTS: No significant difference was found between the APP/PS2 and wild-type mice at 2-6 months of age in terms of novel object recognition memory; subsequently, however, APP/PS2 mice showed a clear cognitive deficit at 12 months of age. [125I]5IA accumulation decreased in the brains of 12-month-old APP/PS2 mice, i.e., at the age at which cognitive impairments were first observed; this result was supported by a reduction in the protein levels of α4 nAChRs using Western blotting. nAChR deficits could be noninvasively detected by [123I]5IA-SPECT in vivo. In contrast, no significant changes in glycometabolism, expression levels of α7 nAChRs, or NMDARs were associated with cognitive impairments in APP/PS2 mice. CONCLUSION: A decrease in cerebral α4β2 nAChR density could act as a biomarker reflecting cognitive impairments associated with AD pathology