Publications by authors named "Yoshitomo Hamano"

Article Synopsis
  • - Lupus nephritis (LN) is a type of kidney inflammation linked to systemic lupus erythematosus (SLE) and is associated with immune complex issues, while antineutrophil cytoplasmic autoantibody (ANCA)-associated vasculitis (AAV) leads to serious conditions like lung hemorrhage and kidney failure.
  • - Research has identified specific genetic factors related to AAV using a mouse model (SCG/Kj) that mimics human AAV, by creating congenic mice to study the roles of these genetic traits.
  • - The study found that B6/lpr mice, a kind of congenic model, displayed symptoms of glomerulonephritis and vasculitis
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Vancomycin hydrochloride (VCM) is a glycopeptide antibiotic that is commonly used against methicillin-resistant, Gram-positive cocci despite the nephrotoxic side effects. VCM-induced nephrotoxicity has been reported in 5-28% of recipient patients. Therefore, renal failure induced by VCM has become an important clinical problem.

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A 76-year-old man was admitted with general fatigue, weight loss, fever, headache, renal failure, and a high serum level of myeloperoxidase-antineutrophil cytoplasmic antibody. Biopsy revealed citrullinated histone H3 (citH3)-positive neutrophils adherent to the temporal artery endothelium. Three days after completing pulse steroid therapy, he suffered from a sudden disturbance of consciousness and died.

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Objective: There are differences between Europe and Japan in the incidence and antineutrophil cytoplasmic antibody (ANCA) serotype of patients with microscopic polyangiitis (MPA). However, differences in phenotype or outcome have not been explored. We aimed to identify differences in phenotype and outcome of MPA between Europe and Japan.

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Background: Antineutrophil cytoplasmic autoantibody (ANCA) directed against myeloperoxidase (MPO), a diagnostic criterion in MPO-ANCA-associated vasculitis (MPO-AAV), does not always correlate with disease activity. Here, we detected autoantibodies against moesin, which was located on the surface of stimulated endothelial cells, in the serum of patients.

Methods: The anti-moesin autoantibody titer was evaluated by ELISA.

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Article Synopsis
  • * Despite negative tests for HIV and hepatitis B and C, the patient's immune response was found to involve anti-PR3-ANCA antibodies and hypocomplementemia.
  • * Treatment with rituximab improved her kidney function and nephrotic syndrome symptoms, but did not help with her periodic fever; genetic testing suggested a rare mutation linked to adult-onset hereditary periodic fever.
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Background: It has been well-recognized that cancer patients occasionally develop renal disorders independently of direct tumor invasion. However, the clinical entity of paraneoplastic glomerulopathy remains poorly understood, in part due to the lack of an animal model for basic research. In the present study, we investigated whether cancer-bearing rats develop features of glomerulopathy.

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In ordinary settings, human immunodeficiency virus (HIV)-associated nephropathy should be considered when HIV infection is associated with heavy proteinuria. On the other hand, hepatitis B virus (HBV) may also play a role in the development of glomerular injury among patients with HIV infection, since HIV and HBV infections commonly occur together due to shared modes of transmission. We present here a case of nephrotic syndrome in an HIV-positive patient complicated with HBV infection.

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  • A 61-year-old woman with multiple myeloma presented severe renal failure and anemia, with evidence of urinary Bence Jones protein leading to her hospital referral.
  • A bone marrow biopsy showed high plasma cell levels, confirming her multiple myeloma diagnosis, while a kidney biopsy identified neoplastic plasma cell infiltration and other kidney damages.
  • Despite treatment that improved her bone marrow condition, her renal function continued to decline, necessitating hemodialysis, indicating a need for more research on renal outcomes in multiple myeloma patients.
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Genetic crossing experiments were performed between tuberous sclerosis-2 (Tsc2) KO and expressed in renal carcinoma (Erc) KO mice to analyze the function of the Erc/mesothelin gene in renal carcinogenesis. We found the number and size of renal tumors were significantly less in Tsc2+/-;Erc-/- mice than in Tsc2+/-;Erc+/+ and Tsc2+/-;Erc+/- mice. Tumors from Tsc2+/-;Erc-/- mice exhibited reduced cell proliferation and increased apoptosis, as determined by proliferating cell nuclear antigen (Ki67) and TUNEL analysis, respectively.

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  • The SCG/Kj mouse model mimics human crescentic glomerulonephritis and vasculitis, characterized by the production of MPO-ANCA autoantibodies, primarily influenced by the lpr mutation of the Fas gene and additional non-Fas genetic factors.
  • Genome-wide QTL mapping on intercross mice identified 14 non-Fas QTLs linked to various disease characteristics, such as glomerulonephritis, vasculitis, splenomegaly, and hypergammaglobulinemia, located on multiple chromosomes.
  • The study highlights specific QTLs labeled Scg and Sxb, focusing on the distinct role of Man-1 in regulating MPO-ANCA
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  • A rat monoclonal antibody (mAb) called RE2 can rapidly kill activated murine lymphocytes through a unique cell death mechanism, differing from typical forms like apoptosis or necrosis.
  • This cell death process doesn't rely on common pathways involving Fas, caspase, or phosphoinositide-3 kinase, and is linked to specific interactions within MHC class I proteins.
  • In mouse models of severe liver damage, mAb RE2 significantly reduced injuries, suggesting it could be a potential treatment for immunological diseases related to activated lymphocytes.
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Systemic lupus erythematosus (SLE), a complex multigenic disease, is characterized by hypergammaglobulinemia, autoantibody production and immune complex-type lupus nephritis. In addition to these signs and symptoms in SLE, there can be symptoms of neurological disorders, including anxiety. To clarify mechanisms governing the anxiety seen in lupus, we carried out genome-wide scans, and found that the region including interferon-alpha (IFN-alpha) on NZB chromosome 4 is significantly linked to the anxiety-like behavior seen in SLE-prone New Zealand Black (NZB) x New Zealand White (NZW) F(1) (B/W F(1)) mice.

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Systemic lupus erythematosus, a complex multigenic disease, is characterized by a wide variety of clinical manifestations, as a result of the contribution of different genes or different combinations of genes. Recent advances in molecular genetics has led to a better understanding of the genes predisposing to systemic lupus erythematosus in both humans and laboratory animal models. Identification of susceptibility genes provides key insights into the pathogenesis of systemic lupus erythematosus, making new prophylactic and therapeutic approaches feasible.

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  • FcgammaRIIB1 molecules play a critical role in regulating B cell activation, and any impairment in their function could lead to abnormal B cell responses.
  • The study discovered a deletion polymorphism in the Fcgr2b promoter among certain autoimmune-prone mouse strains that affects FcgammaRIIB1 expression and IgG antibody levels.
  • Results from luciferase assays and other analyses suggest that this polymorphism reduces transcriptional activity by preventing the binding of the transcription factor AP-4, which may contribute to autoimmune susceptibility.
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Much of the pathology of systemic lupus erythematosus (SLE) is caused by deposition of immune complexes (ICs) into various tissues, including renal glomeruli. Because clearance of ICs depends largely on early complement component C1q, homozygous C1q deficiency is a strong genetic risk factor in SLE, although it is rare in SLE patients overall. In this work we addressed the issue of whether genetic polymorphisms affecting C1q levels may predispose to SLE, using the (NZB x NZW)F(1) model.

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