90 research outputs found

    Ultrasonication-induced Amyloid Fibril Formation of β2-Microglobulin

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    This research was originally published in the Journal of Biological Chemistry. Yumiko Ohhashi, Miho Kihara, Hironobu Naiki and Yuji Goto. Ultrasonication-induced Amyloid Fibril Formation of β2-Microglobulin. J. Biol. Chem. 2005; 280, 32843-32848. © the American Society for Biochemistry and Molecular Biolog

    Polymorphism of β2-Microglobulin Amyloid Fibrils Manifested by Ultrasonication-enhanced Fibril Formation in Trifluoroethanol

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    This research was originally published in the Journal of Biological Chemistry. Eri Chatani, Hisashi Yagi, Hironobu Naiki and Yuji Goto. Polymorphism of β2-Microglobulin Amyloid Fibrils Manifested by Ultrasonication-enhanced Fibril Formation in Trifluoroethanol. J. Biol. Chem. 2012; 287, 22827-22837. © the American Society for Biochemistry and Molecular Biolog

    Direct Measurement of the Thermodynamic Parameters of Amyloid Formation by Isothermal Titration Calorimetry

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    This research was originally published in the Journal of Biological Chemistry. József Kardos, Kaori Yamamoto, Kazuhiro Hasegawa, Hironobu Naiki and Yuji Goto. Direct Measurement of the Thermodynamic Parameters of Amyloid Formation by Isothermal Titration Calorimetry. J. Biol. Chem. 2004; 279, 55308-55314. © the American Society for Biochemistry and Molecular Biolog

    A Comprehensive Model for Packing and Hydration for Amyloid Fibrils of β2-Microglobulin

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    This research was originally published in the Journal of Biological Chemistry. Young-Ho Lee, Eri Chatani, Kenji Sasahara, Hironobu Naiki and Yuji Goto. A Comprehensive Model for Packing and Hydration for Amyloid Fibrils of β2-Microglobulin. J. Biol. Chem. 2009; 284, 2169-2175. © the American Society for Biochemistry and Molecular Biolog

    Esophageal erosion as a possible bacterial entry site in an acute lymphoblastic leukemia patient with sepsis

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    A 69-year-old man with relapsed acute lymphoid leukemia was treated with adriamycin, vincristine, and prednisolone. During this chemotherapy, the patient developed sepsis and meningitis. Although many kinds of antimicrobial drugs, including imipenem, meropenem, amphotericin-B, and γ-globulin were administered, the patient died of respiratory failure. A positive result for Enterococcus faecalis was obtained in both blood and cerebrospinal fluid culture. Autopsy revealed multiple small erosions in the lower esophagus. Histopathological examination showed multiple nuclear inclusion bodies of herpes simplex virus in the squamous epithelial cells at the edge of the erosions. Moreover, proliferation of micrococci was observed at the base of the erosions and in the lumina of the submucosal small vessels. These findings suggested that E faecalis entered the blood circulation from this lesion. In many patients with febrile neutropenia, the pathogenesis of infection remains unclear. Our case seems significant for clarifying the focus and pathogenesis of febrile neutropenia

    Investigation of a Peptide Responsible for Amyloid Fibril Formation of β2-Microglobulin by Achromobacter Protease I

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    This research was originally published in the Journal of Biological Chemistry. Gennady V. Kozhukh, Yoshihisa Hagihara, Toru Kawakami, Kazuhiro Hasegawa, Hironobu Naiki and Yuji Goto. Investigation of a Peptide Responsible for Amyloid Fibril Formation of β2-Microglobulin by Achromobacter Protease I. J. Biol. Chem. 2002; 277, 1310-1315. © the American Society for Biochemistry and Molecular Biolog

    Flow-induced Alignment of Amyloid Protofilaments Revealed by Linear Dichroism

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    This research was originally published in the Journal of Biological Chemistry. Rumi Adachi, Kei-ichi Yamaguchi, Hisashi Yagi, Kazumasa Sakurai, Hironobu Naiki and Yuji Goto. Flow-induced Alignment of Amyloid Protofilaments Revealed by Linear Dichroism. J. Biol. Chem. 2007; 282, 8978-8983. © the American Society for Biochemistry and Molecular Biolog

    Non-steroidal anti-inflammatory drugs have anti-amyloidogenic effects for Alzheimer\u27s β-amyloid fibrils in vitro

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    金沢大学医学部附属病院放射線部The pathogenesis of Alzheimer\u27s disease (AD) is characterized by cerebral deposits of amyloid β-peptides (Aβ) and neurofibrillary tangles which are surrounded by inflammatory cells. Long-term use of non-steroidal anti-inflammatory drugs (NSAIDs) reduces the risk of developing AD and delays the onset of the disease. In the present study, we used fluorescence spectroscopy with thioflavin T and electron microscopy to examine the effects of NSAIDs such as ibuprofen, aspirin, meclofenamic acid sodium salt, diclofenac sodium salt, ketoprofen, flurbiprofen, naproxen, sulindac sulfide and indomethacin on the formation, extension, and destabilization of β-amyloid fibrils (fAβ) at pH 7.5 at 37°C in vitro. All examined NSAIDs dose-dependently inhibited formation of fAβ from fresh Aβ(1-40) and Aβ(1-42), as well as their extension. Moreover, these NSAIDs dose-dependently destabilized preformed fAβs. The overall activity of the molecules examined was in the following order: ibuprofen ≈ sulindac sulfide ≥ meclofenamic acid sodium salt > aspirin ≈ ketoprofen ≥ flurbiprofen ≈ diclofenac sodium salt > naproxen ≈ indomethacin. Although the mechanisms by which these NSAIDs inhibit fAβ formation from Aβ, and destabilize preformed fAβ in vitro are still unclear, NSAIDs may be promising for the prevention and treatment of AD. © 2005 Elsevier Ltd. All rights reserved

    Development of congenic strains of mice carrying amyloidogenic apolipoprotein A-II (Apoa2c) Apoa2c reduces the plasma level and the size of high density lipoprotein

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    AbstractA congenic strain of mice with amyloidogenic apolipoprotein A-II (Apoa2c) on the genetic background of the amyloidosis-resistant SAM-R/1 strain was produced by 12 generations of backcrossing. Genome mapping using endogenous murine leukemia proviral markers was done in the congenic strain, termed R1·P1-Apoa2c. We confirmed that only a small region surrounding the apoA-II gene on chromosome 1 was transferred from the genome of the donor SAM-P/1 strain. The level and particle size of plasma high density lipoprotein were decreased in RI · Pl-Apoa2c mice compared to those in the progenitor SAM-R/1 mice. The function of apoA-II can be studied using this strain of mice
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