Shimada Municipal Hospital

Shimada, Japan

Shimada Municipal Hospital

Shimada, Japan
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Sumi A.,University of Shizuoka | Yamanaka-Hanada N.,University of Shizuoka | Bai F.,Nagoya City University | Makino T.,Nagoya City University | And 3 more authors.
Biological and Pharmaceutical Bulletin | Year: 2011

The active type of coagulation factor X (factor Xa) activates various cell-types through protease-activated receptor 2 (PAR2). We previously reported that a factor Xa inhibitor could suppress Thy-1 nephritis. Considering that fibrin deposition is observed in diabetic nephropathy as well as in glomerulonephritis, this study examined the roles of the coagulation pathway and factor Xa in the development of diabetic nephropathy using type 2 diabetic model mice. Diabetic (db/db) and normoglycemic (m+/m+) mice were immunohistochemically evaluated for their expression/deposition of PAR2, transforming growth factor (TGF)-β, fibrin, extracellular matrix (ECM) proteins, and CD31 at week 20. Significantly greater numbers of PAR2-positive cells and larger amounts of fibronectin, and collagen IV depositions were observed in the glomeruli of db/db mice than those in m+/m+ mice. Next, expression of PAR2 versus deposition of collagen IV and fibronectin was compared between week 20 and week 30, and the number of PAR2-positive cells in the glomeruli decreased in contrast with the increased accumulation of ECM proteins. In an intervention study, fondaparinux, a factor Xa inhibitor, was subcutaneously administered for ten weeks from week 10 to 20. Fondaparinux treatment significantly suppressed urinary protein, glomerular hypertrophy, fibrin deposition, expression of connective tissue growth factor, and ECM proteins deposition together with CD31-positive capillaries. These results suggest that coagulation pathway and glomerular PAR2 expression are upregulated in the early phase of diabetes, together with the increase of profibrotic cytokines expression, ECM proteins deposition and CD-31-positive vessels. Factor Xa inhibition may ameliorate glomerular neoangiogenesis and ECM accumulation in diabetic nephropathy. © 2011 Pharmaceutical Society of Japan.


PubMed | Red Cross, Kobe City Medical Center General Hospital, Juntendo University, Kishiwada City Hospital and 11 more.
Type: | Journal: Cardiovascular intervention and therapeutics | Year: 2016

One-month duration of dual antiplatelet therapy (DAPT) has widely been adopted after bare-metal stent (BMS) implantation in the real clinical practice. However, it has not been adequately addressed yet whether DAPT for only 1-month could provide sufficient protection from ischemic events beyond 1-month after BMS implantation. We assessed the effects of short DAPT relative to prolonged DAPT on clinical outcomes with the landmark analysis at 2 month after BMS implantation. Among 13,058 consecutive patients enrolled in the CREDO-Kyoto registry cohort-2, this study population consisted of 4905 patients treated with BMS only in whom the information on the status of antiplatelet therapy was available at 2 month after stent implantation [single-antiplatelet therapy (SAPT) group: N=2575 (acute myocardial infarction (AMI): N=1257, and non-AMI: N=1318), and DAPT group: N=2330 (AMI: N=1304, and non-AMI: N=1026)]. Cumulative 3-year incidence of the primary outcome measure (a composite of cardiovascular death, myocardial infarction, stroke, definite stent thrombosis, and GUSTO moderate/severe bleeding) was not significantly different between the SAPT and DAPT groups (9.8 versus 10.6%, P=0.34). After adjusting confounders, the risk of SAPT relative to DAPT for the primary outcome measure remained insignificant in the entire cohort (HR 0.97, 95% CI 0.79-1.19, P=0.77), and in both AMI and non-AMI strata without any significant interaction between clinical presentation (AMI versus non-AMI) and the effect of SAPT relative to DAPT (P interaction=0.56). In conclusion, short DAPT <2 month after BMS implantation was as safe as prolonged DAPT 2-month in both AMI and non-AMI patients.


Saheki T.,Tokushima Bunri University | Inoue K.,Tokushima Bunri University | Tushima A.,Tokushima Bunri University | Mutoh K.,Shimada Municipal Hospital | Kobayashi K.,Kagoshima University
Molecular Genetics and Metabolism | Year: 2010

In this paper, we describe the historical aspects of citrin and citrin deficiency, characteristic food preference and food aversion of citrin-deficient subjects, and carbohydrate toxicity in relation to ureogenesis and issues of the conventional treatment procedures for hyperammonemia in citrin deficiency, leading to current treatment concepts for citrin deficiency. We also emphasize the importance of a citrin deficiency mouse model in elucidating the pathophysiology and developing novel therapeutics based on the pathophysiology, such as sodium pyruvate. © 2010 Elsevier Inc. All rights reserved.


Higashi A.Y.,Kyoto University | Nogaki F.,Shimada Municipal Hospital | Kato I.,Shimada Municipal Hospital | Ono T.,University of Shizuoka | Fukatsu A.,Kyoto University
Clinical and Experimental Nephrology | Year: 2012

This report describes a patient presenting with recurrent acute renal failure occurring in the course of POEMS syndrome, a multisystem disease associated with plasma cell dyscrasia. Several combined immunosuppression therapies failed to resolve recurrent acute renal failure; autologous peripheral blood stem cell transplantation was therefore applied. A renal biopsy was performed on each of four occasions when he developed renal dysfunction. The renal biopsy showed typical renal histology of POEMS, membranoproliferative glomerulonephritis-like lesions and narrowing of vessel lumina of various sizes caused by endothelial injury, which progressed to glomerulosclerosis and vessel occlusion. Recurrent acute renal failure might be caused by ischemia due to arterial occlusion. Serum levels of vascular epithelial growth factor (VEGF), which is considered to be a causative factor of endothelial lesions in POEMS syndrome, were not elevated throughout the course of this case. © 2011 Japanese Society of Nephrology.


Tokura Y.,Hamamatsu University School of Medicine | Yagi H.,Shizuoka General Hospital | Yanaguchi H.,Hamamatsu University School of Medicine | Majima Y.,Shizuoka General Hospital | And 4 more authors.
British Journal of Dermatology | Year: 2014

Summary IgG4-related disease (IgG4-RD) is a recently established clinical entity characterized by high levels of circulating IgG4, and tissue infiltration of IgG4+ plasma cells. IgG4-RD exhibits a distinctive fibroinflammatory change involving multiple organs, such as the pancreas and salivary and lacrimal glands. The skin lesions of IgG4-RD have been poorly characterized and may stem not only from direct infiltration of plasma cells but also from IgG4-mediated inflammation. Based on the documented cases together with ours, we categorized the skin lesions into seven subtypes: (1) cutaneous plasmacytosis (multiple papulonodules or indurations on the trunk and proximal part of the limbs), (2) pseudolymphoma and angiolymphoid hyperplasia with eosinophilia (plaques and papulonodules mainly on the periauricular, cheek and mandible regions), (3) Mikulicz disease (palpebral swelling, sicca syndrome and exophthalmos), (4) psoriasis-like eruption (strikingly mimicking psoriasis vulgaris), (5) unspecified maculopapular or erythematous eruptions, (6) hypergammaglobulinaemic purpura (bilateral asymmetrical palpable purpuric lesions on the lower extremities) and urticarial vasculitis (prolonged urticarial lesions occasionally with purpura) and (7) ischaemic digit (Raynaud phenomenon and digital gangrene). It is considered that subtypes 1-3 are induced by direct infiltration of IgG4+ plasma cells, while the other types (4-7) are caused by secondary mechanisms. IgG4-related skin disease is defined as IgG4+ plasma-cell-infiltrating skin lesions that form plaques, nodules or tumours (types 1-3), but may manifest secondary lesions caused by IgG4+ plasma cells and/or IgG4 (types 4-7). What is already known about this topic? IgG4-related disease (IgG4-RD) is a recently established clinical entity characterized by fibroinflammatory lesions, high levels of circulating IgG4 and tissue infiltration of IgG4+ plasma cells. What does this study add? We comprehensively categorized the skin lesions of IgG4-RD into primary lesions with direct infiltration of IgG4+ plasma cells (three subtypes) and secondary nonspecific inflammatory lesions where the role of IgG4 remains to be elucidated (four subtypes). Our study clarifies IgG4-related skin disease and its differential diagnoses.


Nishino K.,Toyohashi University of Technology | Fujiyama T.,Hamamatsu University School of Medicine | Hashizume H.,Shimada Municipal Hospital | Nakauchi S.,Toyohashi University of Technology
Skin Research and Technology | Year: 2013

Background/purpose: This study aimed to develop a method for the assessment of allergic dermatitis by using the long-wavelength near-infrared spectrum (more than 1000 nm) to detect intracutaneous allergic type-specific elements. Such a method was realized by establishing a spectral classifier for the spectra of type I and type IV allergic dermatitis reactions. Methods: Near-infrared spectral images of histamine-induced cutaneous reaction (type I) and contact hypersensitivity erythema elicited by squaric acid dibutylester (SADBE; type IV) were obtained, and the absorption spectra of normal and inflamed skin were extracted from these spectral images. A spectral classifier was established from these training datasets, and it was then applied to two test cases, red flare by methyl nicotinate (normal) and metal allergy (type IV). Results: The spectral classifier established by canonical discriminant analysis (CDA) achieved very accurate detection (normal: 87.67%, type I: 87.00%, type IV: 98.5%). Furthermore, the test cases were also correctly classified: the red flare induced by methyl nicotinate was categorized as normal skin and the metal allergy was categorized as a type IV allergic reaction. Conclusions: These results suggest a possible application of near-infrared spectral imaging to the assessment of allergic dermatitis. © 2012 John Wiley & Sons A/S.


Fujiyama T.,Hamamatsu University School of Medicine | Ito T.,Hamamatsu University School of Medicine | Ogawa N.,Hamamatsu University School of Medicine | Suda T.,Hamamatsu University School of Medicine | And 2 more authors.
Clinical and Experimental Immunology | Year: 2014

Dermatomyositis (DM) and polymyositis (PM) are collectively termed autoimmune myopathy. To investigate the difference between muscle- and skin-infiltrating T cells and to address their role for myopathy, we characterized T cells that were directly expanded from the tissues. Enrolled into this study were 25 patients with DM and three patients with PM. Muscle and skin biopsied specimens were immersed in cRPMI medium supplemented with interleukin (IL)-2 and anti-CD3/CD28 antibody-conjugated microbeads. The expanded cells were subjected to flow cytometry to examine their phenotypes. We analysed the cytokine concentration in the culture supernatants from the expanded T cells and the frequencies of cytokine-bearing cells by intracellular staining. There was non-biased in-vitro expansion of tissue-infiltrating CD4+ and CD8+ T cells from the muscle and skin specimens. The majority of expanded T cells were chemokine receptor (CCR) type 7-CD45RO+ effecter memory cells with various T cell receptor (TCR) Vβs. The skin-derived but not muscle-derived T cells expressed cutaneous lymphocyte antigen (CLA) and CCR10 and secreted large amounts of IL-17A, suggesting that T helper type 17 (Th17) cells may have a crucial role in the development of skin lesions. Notably, the frequency of IL-4-producing chemokine (C-X-C motif) receptor (CXCR)4+ Th2 cells was significantly higher in the muscle-derived cells and correlated inversely with the serum creatine phosphokinase (CPK) and lactate dehydrogenase (LDH) levels. stromal-derived factor (SDF)-1/CXCL12, a ligand for CXCR4, was expressed at a high level in the vascular endothelial cells between muscular fasciculi. Our study suggests that T cell populations in the muscle and skin are different, and the Th2 cell infiltrate in the muscle is associated with the low severity of myositis in DM. © 2014 British Society for Immunology.


Inoue Y.,Shimada Municipal Hospital
Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society | Year: 2010

A 73-year-old man was admitted with high fever and right chest pain. Chest X-ray showed a rapidly growing mass shadow in the right lower lung field. The patient had been in remission for malignant lymphoma and had developed interstitial pneumonia and diabetes mellitus following 1 year of corticosteroid therapy. His illness was diagnosed as invasive aspergillosis because of a high level of beta-D-glucan and cultured Aspergillus fumigatus in the sputum. He was treated with a combination of micafungin and itraconazole. However, because these agents did not improve his clinical condition, transbronchial lung biopsy was performed. Histologically, Mucor hyphae were detected in these specimens. Micafungin and itraconazole were stopped and infusion of liposomal amphotericin B was initiated. Because his condition worsened, a right lower lobectomy was performed. Rhizopus Oryzae was detected in the lung tissue. We report a case of pulmonary mucormycosis in which mixed infection with A. fumigatus was suspected. Pulmonary mucormycosis is a life-threatening infection in which it is rare that an antemortem diagnosis is established and organisms are isolated. We believe diagnostic tests should be performed aggressively, even when pulmonary aspergillosis is suspected.


Hashizume H.,Shimada Municipal Hospital | Fujiyama T.,Shimada Municipal Hospital | Kanebayashi J.,Shimada Municipal Hospital | Kito Y.,Shimada Municipal Hospital | And 2 more authors.
Allergy: European Journal of Allergy and Clinical Immunology | Year: 2013

Background In drug-induced hypersensitivity syndrome (DIHS), latent human herpesvirus (HHV)-6 is frequently reactivated in association with flaring of symptoms such as fever and hepatitis. We recently demonstrated an emergence of monomyeloid precursors expressing HHV-6 antigen in the circulation during this clinical course. Methods To clarify the mechanism of HHV-6 reactivation, we immunologically investigated peripheral blood mononuclear cells (PBMCs), skin-infiltrating cells, and lymphocytes expanded from skin lesions of patients with DIHS. Results The circulating monomyeloid precursors in the patients with DIHS were mostly CD11b+CD13+CD14-CD16 high and showed substantial expression of skin-associated molecules, such as CCR4. CD13+CD14- cells were also found in the DIHS skin lesions, suggesting skin recruitment of this cell population. We detected high levels of high-mobility group box (HMGB)-1 in blood and skin lesions in the active phase of patients with DIHS and showed that recombinant HMGB-1 had functional chemoattractant activity for monocytes/monomyeloid precursors in vitro. HHV-6 infection of the skin-resident CD4+ T cells was confirmed by the presence of its genome and antigen. This infection was likely to be mediated by monomyeloid precursors recruited to the skin, because normal CD4+ T cells gained HHV-6 antigen after in vitro coculture with highly virus-loaded monomyeloid precursors from the patients. Conclusions Our results suggest that monomyeloid precursors harboring HHV-6 are navigated by HMGB-1 released from damaged skin and probably cause HHV-6 transmission to skin-infiltrating CD4+ T cells, which is an indispensable event for HHV-6 replication. These findings implicate the skin as a cryptic and primary site for initiating HHV-6 reactivation. © 2013 John Wiley & Sons A/S. Published by Blackwell Publishing Ltd.


Ito T.,Hamamatsu University School of Medicine | Hashizume H.,Shimada Municipal Hospital | Shimauchi T.,Hamamatsu University School of Medicine | Funakoshi A.,Hamamatsu University School of Medicine | And 4 more authors.
Journal of Dermatological Science | Year: 2013

Background: Alopecia areata (AA) is an organ-specific and cell-mediated autoimmune disease. T lymphocytes densely surround lesional hair bulbs, which is histologically referred to as " swarm of bees" However, pathomechanisms of " swarm of bees" are still uncertain. Objective: We investigated the pathological mechanisms of " swarm of bees" , focusing on T-cell chemotaxis so that inhibition of chemotaxis may be strong candidate of novel treatments for AA. Methods: We investigate the expression of chemokine receptors on T cells obtained from peripheral blood mononuclear cells (PBMCs) and skin infiltrating cells in AA patients. In addition, real-time chemotaxis assay was also demonstrated. Results: In PBMCs, the frequency of CXCR3+CD4+ T cells (Th1) was significantly higher in acute-phase AA than in chronic-phase AA or healthy control, while CXCR3+CD8+ T cells (Tc1) were significantly increased in chronic-phase AA. In the skin lesions of acute-phase AA, CXCR3+CD4+ and CXCR3+CD8+ T cells infiltrated in the juxta-follicular area. In chronic-phase AA, CXCR3+CD8+ T cells dominated the infiltrate around hair bulbs, possibly contributing to the prolonged state of hair loss. Lymphocytes obtained from a lesional skin of acute-phase AA contained CXCR3+CD4+ and CXCR3+CD8+ T cells at higher percentages than those of PBMCs, suggesting preferential emigration from the blood. Immunohistochemical and real-time RT-PCR studies demonstrated that hair follicles of acute-phase AA expressed a high level of Th1-associated chemokine CXCL10. By chemotaxis assay, freshly isolated PBMCs from acute-phase AA patients had a strong velocity of chemotaxis toward CXCL10 with increased expression of F-actin. Conclusions: These results suggest that the increased production of CXCL10 from hair follicles induces preferential infiltrates of highly chemoattracted Th1 and Tc1 cells in the acute phase of AA, and Tc1 infiltration remains prolonged in the chronic phase. © 2012 Japanese Society for Investigative Dermatology.

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