Gifu University of Medical Science

About: Gifu University of Medical Science is a education organization based out in Gifu City, Japan. It is known for research contribution in the topics: Imaging phantom & Motion sickness. The organization has 89 authors who have published 202 publications receiving 1350 citations.

Anchoring and length regulation of Porphyromonas gingivalis Mfa1 fimbriae by the downstream gene product Mfa2.

Abstract: Porphyromonas gingivalis, a causative agent of periodontitis, has at least two types of thin, single-stranded fimbriae, termed FimA and Mfa1 (according to the names of major subunits), which can be discriminated by filament length and by the size of their major fimbrilin subunits. FimA fimbriae are long filaments that are easily detached from cells, whereas Mfa1 fimbriae are short filaments that are tightly bound to cells. However, a P. gingivalis ATCC 33277-derived mutant deficient in mfa2, a gene downstream of mfa1, produced long filaments (10 times longer than those of the parent), easily detached from the cell surface, similar to FimA fimbriae. Longer Mfa1 fimbriae contributed to stronger autoaggregation of bacterial cells. Complementation of the mutant with the wild-type mfa2 allele in trans restored the parental phenotype. Mfa2 is present in the outer membrane of P. gingivalis, but does not co-purify with the Mfa1 fimbriae. However, co-immunoprecipitation demonstrated that Mfa2 and Mfa1 are associated with each other in whole P. gingivalis cells. Furthermore, immunogold microscopy, including double labelling, confirmed that Mfa2 was located on the cell surface and likely associated with Mfa1 fimbriae. Mfa2 may therefore play a role as an anchor for the Mfa1 fimbriae and also as a regulator of Mfa1 filament length. Two additional downstream genes (pgn0289 and pgn0290) are co-transcribed with mfa1 (pgn0287) and mfa2 (pgn0288), and proteins derived from pgn0289, pgn0290 and pgn0291 appear to be accessory fimbrial components.

Assessment of Spatial Uncertainties in the Radiotherapy Process With the Novalis System

Abstract: Purpose: The purpose of this study was to evaluate the accuracy of a new version of the ExacTrac X-ray (ETX) systemwithstatisticalanalysisretrospectivelyinordertodeterminethetoleranceofsystematiccomponentsofspatial uncertainties with the Novalis system. Methods and Materials: Three factors of geometrical accuracy related to the ETX system were evaluated by phantom studies. First, location dependency of the detection ability of the infrared system was evaluated. Second, accuracy of the automated calculation by the image fusion algorithm in the patient registration software was evaluated. Third, deviation of the coordinate scale between the ETX isocenter and the mechanical isocenter was evaluated. From the values of these examinations and clinical experiences, the total spatial uncertainty with the Novalis system was evaluated. Results: As to the location dependency of the detection ability of the infrared system, the detection errors between the actual position and the detected position were 1% in translation shift and 0.1 � in rotational angle, respectively. As to the accuracyof patient verification software, the repeatability and the coincidence of the calculationvalue by image fusion were good when the contrast of the X-ray image was high. The deviation of coordinates between the ETX isocenter and the mechanical isocenter was 0.313 ± 0.024 mm, in a suitable procedure. Conclusions: The spatial uncertainty will be less than 2 mm when suitable treatment planning, optimal patient setup, and daily quality assurance for the Novalis system are achieved in the routine workload. 2009 Elsevier Inc. Spatial uncertainty, Image-guided radiotherapy, Geometrical accuracy, Patient setup, Stereotactic radiotherapy.

Myogenin promoter‐associated lncRNA Myoparr is essential for myogenic differentiation

Abstract: Promoter-associated long non-coding RNAs (lncRNAs) regulate the expression of adjacent genes; however, precise roles of these lncRNAs in skeletal muscle remain largely unknown. Here, we characterize a promoter-associated lncRNA, Myoparr, in myogenic differentiation and muscle disorders. Myoparr is expressed from the promoter region of the mouse and human myogenin gene, one of the key myogenic transcription factors. We show that Myoparr is essential both for the specification of myoblasts by activating neighboring myogenin expression and for myoblast cell cycle withdrawal by activating myogenic microRNA expression. Mechanistically, Myoparr interacts with Ddx17, a transcriptional coactivator of MyoD, and regulates the association between Ddx17 and the histone acetyltransferase PCAF Myoparr also promotes skeletal muscle atrophy caused by denervation, and knockdown of Myoparr rescues muscle wasting in mice. Our findings demonstrate that Myoparr is a novel key regulator of muscle development and suggest that Myoparr is a potential therapeutic target for neurogenic atrophy in humans.

Depressive symptoms as a side effect of Interferon-α therapy induced by induction of indoleamine 2,3-dioxygenase 1

Abstract: Depression is known to occur frequently in chronic hepatitis C viral (HCV) patients receiving interferon (IFN)-α therapy. In this study, we investigated whether indoleamine 2,3-dioxygenase1 (IDO1)-mediated tryptophan (TRP) metabolism plays a critical role in depression occurring as a side effect of IFN-α therapy. Increases in serum kynurenine (KYN) and 3-hydroxykynurenine (3-HK) concentrations and in the ratios of KYN/TRP and 3-HK/kynurenic acid (KA) were much larger in depressive HCV patients than in non-depressed patients following therapy. Furthermore, transfection of a plasmid continuously expressing murine IFN-γ into normal mice significantly increased depression-like behavior. IFN-γ gene transfer also resulted in a decrease in serum TRP levels in the mice while KYN and 3-HK levels were significantly increased in both serum and frontal cortex. Genetic deletion of IDO1 in mice abrogated both the increase in depression-like behavior and the elevation in TRP metabolites' levels, and the turnover of serotonin in the frontal cortex after IFN-γ gene transfer. These results indicate that the KYN pathway of IDO1-mediated TRP metabolism plays a critical role in depressive symptoms associated with IFN-α therapy.

Local immune response to respiratory syncytial virus infection is diminished in senescence-accelerated mice.

Abstract: The effect of ageing on the local defence system against respiratory syncytial virus (RSV) infection was investigated using an aged mouse model of the senescence-accelerated mouse (SAM) strain P1. Following intranasal infection with RSV, SAM-P1 mice showed a marked loss in weight, with elevated virus growth in the lungs and prolonged virus shedding. The increased susceptibility to RSV infection was associated mainly with diminished cellular immunity by local virus-specific cytotoxic T lymphocytes and natural killer cells. The deficiency in cellular immune responses was due to a lack of clonal expansion of CD4+ and CD8+ T lymphocytes, together with an imbalance of T-helper type 1 (Th1)/Th2 cytokine production in the respiratory tract, including the lungs. Furthermore, the production of virus-specific local IgA antibody was restrained. Prolonged virus loading in the lungs of SAM-P1 mice caused a massive infiltration of CD16+/32+ inflammatory cells, which was one factor responsible for severe pneumonia. The adoptive transfer of immune-competent spleen cells achieved an appreciable protection for SAM-P1 mice against RSV challenge infection. These results suggested that age-related immune dysfunction, especially defects in cellular immune responses, accounts for the increased morbidity and mortality in RSV infection of the elderly.