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  1. Article: [Secondary osteoporosis. Bone quality deterioration in lifestyle-related disease.]

    Kanazawa, Ippei

    Clinical calcium

    2019  Volume 28, Issue 12, Page(s) 1581–1589

    Abstract: Both lifestyle-related disease and ostepoross increase with aging;thus the number of patients with these diseases will increase in future. Because diabetes mellitus, a representative lifestyle-related disease, induces bone fragility due to deterioration ... ...

    Abstract Both lifestyle-related disease and ostepoross increase with aging;thus the number of patients with these diseases will increase in future. Because diabetes mellitus, a representative lifestyle-related disease, induces bone fragility due to deterioration of bone quality, if all of the focus is given only to bone mineral density values, we might underestimate fracture risks in the patients. Previous studies have shown that accumulation of advanced glycation end products in bone matrix, abnormal bone microstructure, and dysfunction of bone remodeling with decreased bone formation are involved in the mechanism of bone quality deterioration. However, there are no specific parameters to evaluate bone quality in clinical settings so far. Therefore, it is necessary to find patients with clinical risk factor of fracture and to perform intensive treatments for osteoporosis.
    MeSH term(s) Bone Density ; Bone Remodeling ; Bone and Bones ; Humans ; Life Style ; Osteoporosis/etiology
    Language Japanese
    Publishing date 2019-02-05
    Publishing country Japan
    Document type Journal Article
    ZDB-ID 2386417-5
    ISSN 0917-5857
    ISSN 0917-5857
    DOI CliCa181215811589
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6536: Show issues Location:
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  2. Article: Autoinflammatory Diseases Due to Defects in Degradation or Transport of Intracellular Proteins.

    Sasaki, Izumi / Kato, Takashi / Kanazawa, Nobuo / Kaisho, Tsuneyasu

    Advances in experimental medicine and biology

    2024  Volume 1444, Page(s) 83–95

    Abstract: The number of human inborn errors of immunity has now gone beyond 430. The responsible gene variants themselves are apparently the cause for the disorders, but the underlying molecular or cellular mechanisms for the pathogenesis are often unclear. In ... ...

    Abstract The number of human inborn errors of immunity has now gone beyond 430. The responsible gene variants themselves are apparently the cause for the disorders, but the underlying molecular or cellular mechanisms for the pathogenesis are often unclear. In order to clarify the pathogenesis, the mutant mice carrying the gene variants are apparently useful and important. Extensive analysis of those mice should contribute to the clarification of novel immunoregulatory mechanisms or development of novel therapeutic maneuvers critical not only for the rare monogenic diseases themselves but also for related common polygenic diseases. We have recently generated novel model mice in which complicated manifestations of human inborn errors of immunity affecting degradation or transport of intracellular proteins were recapitulated. Here, we review outline of these disorders, mainly based on the phenotype of the mutant mice we have generated.
    MeSH term(s) Humans ; Animals ; Mice ; Hereditary Autoinflammatory Diseases/genetics ; Hereditary Autoinflammatory Diseases/therapy ; Cytokines/genetics ; Phenotype ; Syndrome
    Chemical Substances Cytokines
    Language English
    Publishing date 2024-03-11
    Publishing country United States
    Document type Review ; Journal Article
    ZDB-ID 410187-X
    ISSN 0065-2598
    ISSN 0065-2598
    DOI 10.1007/978-981-99-9781-7_6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Next-generation regenerative therapy for ischemic stroke using peripheral blood mononuclear cells.

    Kanazawa, Masato / Ninomiya, Itaru / Otsu, Yutaka / Hatakeyama, Masahiro

    Neural regeneration research

    2024  Volume 19, Issue 11, Page(s) 2341–2342

    Language English
    Publishing date 2024-01-31
    Publishing country India
    Document type Journal Article
    ZDB-ID 2388460-5
    ISSN 1876-7958 ; 1673-5374
    ISSN (online) 1876-7958
    ISSN 1673-5374
    DOI 10.4103/NRR.NRR-D-23-01784
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Corrigendum: Regeneration of the cerebral cortex by direct chemical reprogramming of macrophages into neuronal cells in acute ischemic stroke.

    Ninomiya, Itaru / Koyama, Akihide / Otsu, Yutaka / Onodera, Osamu / Kanazawa, Masato

    Frontiers in cellular neuroscience

    2024  Volume 18, Page(s) 1372045

    Abstract: This corrects the article DOI: 10.3389/fncel.2023.1225504.]. ...

    Abstract [This corrects the article DOI: 10.3389/fncel.2023.1225504.].
    Language English
    Publishing date 2024-02-05
    Publishing country Switzerland
    Document type Published Erratum
    ZDB-ID 2452963-1
    ISSN 1662-5102
    ISSN 1662-5102
    DOI 10.3389/fncel.2024.1372045
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Arthroscopic ankle arthrodesis in two alkaptonuria patients.

    Tomonaga, Seiya / Yoshimura, Ichiro / Kanazawa, Kazuki / Yamamoto, Takuaki

    BMJ case reports

    2023  Volume 16, Issue 10

    Abstract: Alkaptonuria is a very rare disorder in which homogentisic acid accumulates due to a deficiency in the activity of homogentisic acid 1,2 dioxygenase. This deficiency results in deposition of a yellowish-brown pigment in connective tissue. Such deposition ...

    Abstract Alkaptonuria is a very rare disorder in which homogentisic acid accumulates due to a deficiency in the activity of homogentisic acid 1,2 dioxygenase. This deficiency results in deposition of a yellowish-brown pigment in connective tissue. Such deposition is termed 'ochronosis' and leads to deterioration in the formation and structure of proteoglycans in hyaline cartilage. These actions lead to fragmentation and rapid destructive arthritis. Often, ochronotic arthritis appears at 40-60 years of age, and many patients are treated symptomatically. Here, we report two patients (three ankles) with ochronotic arthritis who were treated with ankle arthrodesis. In all cases, the postoperative clinical score improved, but the time needed for fusion was prolonged and symptomatic subtalar arthropathy developed in the early postoperative period.
    MeSH term(s) Humans ; Alkaptonuria/complications ; Alkaptonuria/surgery ; Ankle ; Homogentisic Acid ; Osteoarthritis ; Cartilage Diseases ; Arthrodesis
    Chemical Substances Homogentisic Acid (NP8UE6VF08)
    Language English
    Publishing date 2023-10-25
    Publishing country England
    Document type Case Reports ; Journal Article
    ISSN 1757-790X
    ISSN (online) 1757-790X
    DOI 10.1136/bcr-2022-254300
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Interaction between bone and glucose metabolism [Review].

    Kanazawa, Ippei

    Endocrine journal

    2017  Volume 64, Issue 11, Page(s) 1043–1053

    Abstract: Accumulating evidence has shown that bone and glucose metabolism are closely associated with each other. Since the risk of osteoporotic fractures is increased in patients with diabetes mellitus (DM), osteoporosis is recently recognized as one of diabetic ...

    Abstract Accumulating evidence has shown that bone and glucose metabolism are closely associated with each other. Since the risk of osteoporotic fractures is increased in patients with diabetes mellitus (DM), osteoporosis is recently recognized as one of diabetic complications, called DM-induced bone fragility. Previous studies showed that collagen cross-links of advanced glycation end products (AGEs) and dysfunctions of osteoblast and osteocyte are involved in DM-induced bone fragility. Circulating levels of AGEs and homocysteine are increased in patients with DM, and they directly impair the functions of osteoblast and osteocyte, resulting in decreased bone formation and bone remodeling. On the other hand, bone is recently recognized as an endocrine organ. Previous studies based on in vitro and animal studies showed that osteocalcin, which is specifically expressed in osteoblasts and secreted into the circulation, may regulate glucose homeostasis. Although several clinical studies reported the relationship between osteocalcin and glucose metabolism, further large-scale and intervention studies are necessary to confirm the beneficial effects of osteocalcin on glucose metabolism in human. It has been shown that adenosine monophosphate-activated protein kinase (AMPK), an intracellular energy sensor, is involved in bone metabolism. Adiponectin and metformin stimulate osteocalcin expression and the differentiation of osteoblasts via AMPK activation. Also, AMPK activation protects against oxidative stress-induced apoptosis of osteocytes. These findings suggest that AMPK in osteoblasts and osteocytes may be a therapeutic target for DM-induced bone fragility.
    MeSH term(s) Animals ; Bone and Bones/metabolism ; Bone and Bones/physiology ; Carbohydrate Metabolism/physiology ; Glucose/metabolism ; Humans ; Osteogenesis/physiology
    Chemical Substances Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2017-11-29
    Publishing country Japan
    Document type Journal Article ; Review
    ZDB-ID 1151918-6
    ISSN 1348-4540 ; 0918-8959
    ISSN (online) 1348-4540
    ISSN 0918-8959
    DOI 10.1507/endocrj.EJ17-0323
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: Osteocalcin as a hormone regulating glucose metabolism.

    Kanazawa, Ippei

    World journal of diabetes

    2016  Volume 6, Issue 18, Page(s) 1345–1354

    Abstract: The number of patients with osteoporosis and diabetes is rapidly increasing all over the world. Bone is recently recognized as an endocrine organ. Accumulating evidence has shown that osteocalcin, which is specifically expressed in osteoblasts and ... ...

    Abstract The number of patients with osteoporosis and diabetes is rapidly increasing all over the world. Bone is recently recognized as an endocrine organ. Accumulating evidence has shown that osteocalcin, which is specifically expressed in osteoblasts and secreted into the circulation, regulates glucose homeostasis by stimulating insulin expression in pancreas and adiponectin expression in adipocytes, resulting in improving glucose intolerance. On the other hand, insulin and adiponectin stimulate osteocalcin expression in osteoblasts, suggesting that positive feedforward loops exist among bone, pancreas, and adipose tissue. In addition, recent studies have shown that osteocalcin enhances insulin sensitivity and the differentiation in muscle, while secreted factors from muscle, myokines, regulate bone metabolism. These findings suggest that bone metabolism and glucose metabolism are associated with each other through the action of osteocalcin. In this review, I describe the role of osteocalcin in the interaction among bone, pancreas, brain, adipose tissue, and muscle.
    Language English
    Publishing date 2016-01-01
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2583471-X
    ISSN 1948-9358
    ISSN 1948-9358
    DOI 10.4239/wjd.v6.i18.1345
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Conference proceedings: [Topics for basic and clinical research in ASBMR 2015].

    Kanazawa, Ippei

    Clinical calcium

    2016  Volume 26, Issue 1, Page(s) 133–135

    Abstract: This is a brief report on selected topics in 37th Annual meeting of ASBMR held in Seattle on October 9-12, 2015. I focused on several interesting presentations of basic and clinical research. ...

    Abstract This is a brief report on selected topics in 37th Annual meeting of ASBMR held in Seattle on October 9-12, 2015. I focused on several interesting presentations of basic and clinical research.
    MeSH term(s) Animals ; Bone Morphogenetic Proteins/physiology ; Diabetes Complications ; Humans ; Mice ; Osteogenesis/genetics ; Osteoporosis/etiology ; Research ; Societies, Scientific/organization & administration ; United States ; Wnt Signaling Pathway/physiology
    Chemical Substances Bone Morphogenetic Proteins
    Language Japanese
    Publishing date 2016-01
    Publishing country Japan
    Document type Congresses ; English Abstract
    ZDB-ID 2386417-5
    ISSN 0917-5857
    ISSN 0917-5857
    DOI CliCa1601133135
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  9. Article: Regeneration of the cerebral cortex by direct chemical reprogramming of macrophages into neuronal cells in acute ischemic stroke.

    Ninomiya, Itaru / Koyama, Akihide / Otsu, Yutaka / Onodera, Osamu / Kanazawa, Masato

    Frontiers in cellular neuroscience

    2023  Volume 17, Page(s) 1225504

    Abstract: Theoretically, direct chemical reprogramming of somatic cells into neurons in the infarct area represents a promising regenerative therapy for ischemic stroke. Previous studies have reported that human fibroblasts and astrocytes transdifferentiate into ... ...

    Abstract Theoretically, direct chemical reprogramming of somatic cells into neurons in the infarct area represents a promising regenerative therapy for ischemic stroke. Previous studies have reported that human fibroblasts and astrocytes transdifferentiate into neuronal cells in the presence of small molecules without introducing ectopic transgenes. However, the optimal combination of small molecules for the transdifferentiation of macrophages into neurons has not yet been determined. The authors hypothesized that a combination of small molecules could induce the transdifferentiation of monocyte-derived macrophages into neurons and that the administration of this combination may be a regenerative therapy for ischemic stroke because monocytes and macrophages are directly involved in the ischemic area. Transcriptomes and morphologies of the cells were compared before and after stimulation using RNA sequencing and immunofluorescence staining. Microscopic analyses were also performed to identify cell markers and evaluate functional recovery by blinded examination following the administration of small molecules after ischemic stroke in CB-17 mice. In this study, an essential combination of six small molecules [CHIR99021, Dorsomorphin, Forskolin, isoxazole-9 (ISX-9), Y27632, and DB2313] that transdifferentiated monocyte-derived macrophages into neurons
    Language English
    Publishing date 2023-08-11
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2452963-1
    ISSN 1662-5102
    ISSN 1662-5102
    DOI 10.3389/fncel.2023.1225504
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: [Diabetes-related osteoporosis].

    Kanazawa, Ippei

    Nihon rinsho. Japanese journal of clinical medicine

    2015  Volume 73, Issue 10, Page(s) 1718–1722

    Abstract: Accumulating evidence has shown that the risk of osteoporotic fracture is increased in patients with type 1 and 2 diabetes mellitus. Measurement of bone mineral density is not a good evaluation tool for diabetes-related osteoporosis because the ... ...

    Abstract Accumulating evidence has shown that the risk of osteoporotic fracture is increased in patients with type 1 and 2 diabetes mellitus. Measurement of bone mineral density is not a good evaluation tool for diabetes-related osteoporosis because the underlying mechanism is based on the deterioration of bone quality with accumulation of collagen cross-links of advanced glycation end products, decreased bone formation, and cortical porosity. Thus, we should choose the anti-osteoporosis drug while taking the mechanism into consideration. However, the evidence of treatments for diabetes-related osteoporosis is not sufficient so far. Therefore, further studies are necessary to solve this issue in future.
    MeSH term(s) Bone Density ; Diabetes Complications ; Diabetes Mellitus ; Humans ; Osteoporosis/drug therapy ; Osteoporosis/etiology ; Osteoporotic Fractures/prevention & control ; Risk Factors
    Language Japanese
    Publishing date 2015-10
    Publishing country Japan
    Document type English Abstract ; Journal Article
    ZDB-ID 390903-7
    ISSN 0047-1852
    ISSN 0047-1852
    Database MEDical Literature Analysis and Retrieval System OnLINE

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