高齢者における発酵L 型乳酸カルシウム（CV カルシューム）摂取の効果についての研究

This study added fermentation calcium L-lactate（ CV calcium） in an everyday meal for resident of nursing home for the elderly in the long term and evaluated calcaneus by osteo-sono assessment index and we examined the effectiveness of the ingestion fermentation calcium L-lactate（ CV calcium）. We were not able to obtain a result indicating the effectiveness of the ingestion of fermentation calcium L-lactate（ CV calcium）, because a change was not seen in a result of the bone density measurement. However, it may be suggested that fermentation calcium L-lactate（ CV calcium） is effective to easily take in calcium. The because it is easy to cook to have high water solubility and the taste of the meal does not change

A Case of Fisher Syndrome Complicated by Maxillary Sinus Cysts

Fisher syndrome (FS) is an autoimmune peripheral neuropathy that occurs in 1 person per 2 million population. The present report is of a patient with FS who presented with diplopia and discomfort of the right cheek and in whom differentiation from maxillary sinus cysts was necessary. The patient was a 43-year-old man with a history of radical surgery of the right maxillary sinus, so we suspected that his symptoms were due to postoperative maxillary sinus cysts. Although computed tomography demonstrated right maxillary sinus cysts, these cysts were not likely to be the cause of the patient\u27s diplopia. Close neurological examination revealed external ophthalmoplegia, cerebellar ataxia, and the absence of a deep tendon reflex; on this basis, a diagnosis of FS was made. Diplopia is caused by various disorders and FS should be taken into consideration when making a differential diagnosis

Electronic structure investigation of CeB6 by means of soft X-ray scattering

The electronic structure of the heavy fermion compound CeB6 is probed by resonant inelastic soft X-ray scattering using photon energies across the Ce 3d and 4d absorption edges. The hybridization between the localized 4f orbitals and the delocalized valence-band states is studied by identifying the different spectral contributions from inelastic Raman scattering and normal fluorescence. Pronounced energy-loss structures are observed below the elastic peak at both the 3d and 4d thresholds. The origin and character of the inelastic scattering structures are discussed in terms of charge-transfer excitations in connection to the dipole allowed transitions with 4f character. Calculations within the single impurity Anderson model with full multiplet effects are found to yield consistent spectral functions to the experimental data.Comment: 9 pages, 4 figures, 1 table, http://link.aps.org/doi/10.1103/PhysRevB.63.07510

Pexophagy suppresses ROS-induced damage in leaf cells under high-intensity light

Although light is essential for photosynthesis, it has the potential to elevate intracellular levels of reactive oxygen species (ROS). Since high ROS levels are cytotoxic, plants must alleviate such damage. However, the cellular mechanism underlying ROS-induced leaf damage alleviation in peroxisomes was not fully explored. Here, we show that autophagy plays a pivotal role in the selective removal of ROS-generating peroxisomes, which protects plants from oxidative damage during photosynthesis. We present evidence that autophagy-deficient mutants show light intensity-dependent leaf damage and excess aggregation of ROS-accumulating peroxisomes. The peroxisome aggregates are specifically engulfed by pre-autophagosomal structures and vacuolar membranes in both leaf cells and isolated vacuoles, but they are not degraded in mutants. ATG18a-GFP and GFP-2×FYVE, which bind to phosphatidylinositol 3-phosphate, preferentially target the peroxisomal membranes and pre-autophagosomal structures near peroxisomes in ROS-accumulating cells under high-intensity light. Our findings provide deeper insights into the plant stress response caused by light irradiation

エンドトキシン誘発播種性血管内凝固に対する糖尿病の影響

This paper is a study concerning diabetes that have a tendency for blood coagulation whether it was a risk of sudden death. We made a diabetes model mouse by intraperitoneal injection of streptozotocin (STZ), and we caused disseminated intravascular coagulation (DIC) by doing an intra-tailvenous injection of endotoxin (ET) to the mouse. After injection of STZ, a weight loss, decrease of intra-abdominal fat, polyphagy, polyposia are induced and they are the main symptoms of diabetes. Furthermore, with an ET injection to the mouse, it showed increase of weight such as the lung and the liver and extension of PT time with the blood clot formation, and that it was it in a blood coagulation tendency was confirmed by these symptoms. Then, the mouse showed a decrease of plasminogen activator activity in the lung. Therefore, fibrinolysis system was enhanced in the mouse, and it was suggested that a symptom of DIC turned worse under a state of diabetes

A phospho-switch controls RNF43-mediated degradation of Wnt receptors to suppress tumorigenesis.

Funder: Japan Foundation for Applied Enzymology; doi: https://doi.org/10.13039/100008695Funder: Pancreas Research Foundation of Japan Collaborative Research Project Program of the Medical Institute of Bioregulation, Kyushu University, Japan Joint Research Program of the Institute for Molecular and Cellular Regulation, Gunma University, Japan Grant for Joint Research Project of the Research Institute for Microbial Diseases Osaka UniversityFunder: European Research Council (ERC (639050) and the Interpark Bio-Convergence Center Grant Program.Frequent mutation of the tumour suppressor RNF43 is observed in many cancers, particularly colon malignancies. RNF43, an E3 ubiquitin ligase, negatively regulates Wnt signalling by inducing degradation of the Wnt receptor Frizzled. In this study, we discover that RNF43 activity requires phosphorylation at a triplet of conserved serines. This phospho-regulation of RNF43 is required for zebrafish development and growth of mouse intestinal organoids. Cancer-associated mutations that abrogate RNF43 phosphorylation cooperate with active Ras to promote tumorigenesis by abolishing the inhibitory function of RNF43 in Wnt signalling while maintaining its inhibitory function in p53 signalling. Our data suggest that RNF43 mutations cooperate with KRAS mutations to promote multi-step tumorigenesis via the Wnt-Ras-p53 axis in human colon cancers. Lastly, phosphomimetic substitutions of the serine trio restored the tumour suppressive activity of extracellular oncogenic mutants. Therefore, harnessing phospho-regulation of RNF43 might be a potential therapeutic strategy for tumours with RNF43 mutations