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  • 1
    Online Resource
    Online Resource
    Hematopoietic loss of Y chromosome leads to cardiac fibrosis and heart failure mortality
    American Association for the Advancement of Science (AAAS) ; 2022
    In:  Science Vol. 377, No. 6603 ( 2022-07-15), p. 292-297
    Details
    In: Science, American Association for the Advancement of Science (AAAS), Vol. 377, No. 6603 ( 2022-07-15), p. 292-297
    Abstract: Mosaic loss of the Y chromosome in blood cells is linked to heart failure mediated by accelerated tissue fibrosis.
    Type of Medium: Online Resource
    ISSN: 0036-8075 , 1095-9203
    URL: Article
    DOI: 10.1126/science.abn3100
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2022
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    detail.hit.zdb_id: 2066996-3
    detail.hit.zdb_id: 2060783-0
    SSG: 11
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  • 2
    Online Resource
    Online Resource
    The Cancer Therapy-Related Clonal Hematopoiesis Driver Gene Ppm1d Promotes Inflammation and Non-Ischemic Heart Failure in Mice
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Circulation Research Vol. 129, No. 6 ( 2021-09-03), p. 684-698
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 129, No. 6 ( 2021-09-03), p. 684-698
    Abstract: Cancer therapy can be associated with short- and long-term cardiac dysfunction. Patients with cancer often exhibit therapy-related clonal hematopoiesis (t-CH), an aggressive form of clonal hematopoiesis that can result from somatic mutations in genes encoding regulators of the DNA-damage response (DDR) pathway. Gain-of-function mutations in exon 6 of the protein phosphatase Mg2+/Mn2+ dependent 1D ( PPM1D ) gene are the most frequently mutated DNA-damage response gene associated with t-CH. Whether t-CH can contribute to cardiac dysfunction is unknown. Objective: We evaluated the causal and mechanistic relationships between Ppm1d -mediated t-CH and nonischemic heart failure in an experimental system. Methods and Results: To test whether gain-of-function hematopoietic cell mutations in Ppm1d can increase susceptibility to cardiac stress, we evaluated cardiac dysfunction in a mouse model where clonal hematopoiesis-associated mutations in exon 6 of Ppm1d were produced by CRISPR-Cas9 technology. Mice transplanted with hematopoietic stem cells containing the mutated Ppm1d gene exhibited augmented cardiac remodeling following the continuous infusion of Ang II (angiotensin II). Ppm1d -mutant macrophages were impaired in DDR pathway activation and displayed greater DNA damage, higher reactive oxygen species generation, and an augmented proinflammatory profile with elevations in IL (interleukin)-1β and IL-18. The administration of an NLRP3 (NLR family pyrin domain containing 3) inflammasome inhibitor to mice reversed the cardiac phenotype induced by the Ppm1d -mutated hematopoietic stem cells under conditions of Ang II–induced stress. Conclusions: A mouse model of Ppm1d -mediated t-CH was more susceptible to cardiac stress. Mechanistically, disruption of the DDR pathway led to elevations in inflammatory cytokine production, and the NLRP3 inflammasome was shown to be essential for this augmented cardiac stress response. These data indicate that t-CH involving activating mutations in PPM1D can contribute to the cardiac dysfunction observed in cancer survivors, and that anti-inflammatory therapy may have utility in treating this condition.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/CIRCRESAHA.121.319314
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 1467838-X
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  • 3
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    Online Resource
    Abstract 12653: The Therapy-related Clonal Hematopoiesis Driver Gene Ppm1d Promotes Inflammation and Non-ischemic Heart Failure in a Murine Model
    Ovid Technologies (Wolters Kluwer Health) ; 2020
    In:  Circulation Vol. 142, No. Suppl_3 ( 2020-11-17)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 142, No. Suppl_3 ( 2020-11-17)
    Abstract: Background: Therapy-related clonal hematopoiesis in cancer patients is typically associated with somatic mutations in hematopoietic cell genes that encode regulators of the DNA-damage response (DDR) pathway. The Protein Phosphatase Mg2+/Mn2+ Dependent 1D ( PPM1D ) gene is the most frequently mutated DDR gene associated with therapy-related clonal hematopoiesis. While epidemiological evidence suggests an association between therapy-related clonal hematopoiesis and cardiovascular disease in cancer patients, causal and mechanistic relationships have never been evaluated in an experimental system. Methods: To test whether hematopoietic cell mutations in PPM1D can increase the susceptibility to cardiac stress, we evaluated cardiac dysfunction in response to angiotensin II infusion in a mouse model where clonal-hematopoiesis-associated mutations in Ppm1d were produced by CRISPR-Cas9 technology. Results: Mice transplanted with hematopoietic stem cells containing clinically relevant mutations in exon 6 of Ppm1d exhibited augmented cardiac remodeling following the continuous infusion of angiotensin II. Ppm1d -mutated macrophages showed impairments in the DDR pathway and had an augmented proinflammatory profile. Mice transplanted with Ppm1d mutated cells exhibited elevated IL-1β in the stressed myocardium, and bone marrow derived macrophages produced more IL-1β in response to LPS stimulation. The administration of an NLRP3 inflammasome inhibitor to mice reversed the cardiac phenotype induced by the Ppm1d -mutated hematopoietic stem cells under conditions of Angiotensin II-induced stress. Conclusions: A mouse model of Ppm1d -mediated clonal hematopoiesis was more susceptible to cardiac stress following of angiotensin II infusion. Mechanistically, disruption of the DDR pathway led to elevations in inflammatory cytokine production, and the NLRP3 inflammasome was shown to be essential for this augmented cardiac stress response. These data indicate that therapy-related clonal hematopoiesis involving mutations in PPM1D could contribute to the cardiac dysfunction observed in cancer survivors.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.142.suppl_3.12653
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
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  • 4
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    Online Resource
    Murine models of clonal haematopoiesis to assess mechanisms of cardiovascular disease
    Oxford University Press (OUP) ; 2022
    In:  Cardiovascular Research Vol. 118, No. 6 ( 2022-05-06), p. 1413-1432
    Details
    In: Cardiovascular Research, Oxford University Press (OUP), Vol. 118, No. 6 ( 2022-05-06), p. 1413-1432
    Abstract: Clonal haematopoiesis (CH) is a phenomenon whereby somatic mutations confer a fitness advantage to haematopoietic stem and progenitor cells (HSPCs) and thus facilitate their aberrant clonal expansion. These mutations are carried into progeny leucocytes leading to a situation whereby a substantial fraction of an individual’s blood cells originate from the HSPC mutant clone. Although this condition rarely progresses to a haematological malignancy, circulating blood cells bearing the mutation have the potential to affect other organ systems as they infiltrate into tissues under both homeostatic and disease conditions. Epidemiological and clinical studies have revealed that CH is highly prevalent in the elderly and is associated with an increased risk of cardiovascular disease and mortality. Recent experimental studies in murine models have assessed the most commonly mutated ‘driver’ genes associated with CH, and have provided evidence for mechanistic connections between CH and cardiovascular disease. A deeper understanding of the mechanisms by which specific CH mutations promote disease pathogenesis is of importance, as it could pave the way for individualized therapeutic strategies targeting the pathogenic CH gene mutations in the future. Here, we review the epidemiology of CH and the mechanistic work from studies using murine disease models, with a particular focus on the strengths and limitations of these experimental systems. We intend for this review to help investigators select the most appropriate models to study CH in the setting of cardiovascular disease.
    Type of Medium: Online Resource
    ISSN: 0008-6363 , 1755-3245
    URL: Article
    DOI: 10.1093/cvr/cvab215
    RVK:
    WA 15000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
    detail.hit.zdb_id: 1499917-1
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  • 5
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    Tet2-mediated clonal hematopoiesis in nonconditioned mice accelerates age-associated cardiac dysfunction
    American Society for Clinical Investigation ; 2020
    In:  JCI Insight Vol. 5, No. 6 ( 2020-3-26)
    Details
    In: JCI Insight, American Society for Clinical Investigation, Vol. 5, No. 6 ( 2020-3-26)
    Type of Medium: Online Resource
    ISSN: 2379-3708
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.1172/jci.insight.135204
    DOI: 10.1172/jci.insight.135204DS1
    DOI: 10.1172/jci.insight.135204DS2
    Language: English
    Publisher: American Society for Clinical Investigation
    Publication Date: 2020
    detail.hit.zdb_id: 2874757-4
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  • 6
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    564-P: Secreted Factors from Dental Pulp Stem Cells Ameliorated Neural Functions in Streptozotocin-Induced Diabetic Mice
    American Diabetes Association ; 2019
    In:  Diabetes Vol. 68, No. Supplement_1 ( 2019-06-01)
    Details
    In: Diabetes, American Diabetes Association, Vol. 68, No. Supplement_1 ( 2019-06-01)
    Abstract: Aims/Introduction: We previously reported that stem cell transplantation into limb skeletal muscle improved diabetic polyneuropathy (DPN) in diabetic animal models. In this study, we examined whether the secreted factors from stem cells from human exfoliated deciduous teeth (SHED) had beneficial effects on DPN. Materials and Methods: The conditioned medium from SHED(SHED-CM) was collected 48 hours after culturing in serum-free DMEM and was separated into four fractions according to molecular weight. Dorsal root ganglion (DRG) neurons isolated from C57BL/6J mice were cultured with SHED-CM, each fraction of SHED-CM or DMEM. Streptozotocin induced diabetic mice were injected with 100µl of SHED-CM or DMEM into unilateral hindlimb muscles twice a week over 4 weeks. Peripheral nerve functions were evaluated by the plantar test and motor and sensory nerve conduction velocities (MNCV and SNCV). Intraepidermal nerve fiber densities (IENFDs), capillary number-to-muscle fiber ratio (CNMFR) and morphometry of sural nerves were also evaluated. The angiogenic profile of SHED-CM was evaluated by MTT, transwell migration, and wound healing assay using human umbilical vein endothelial cells (HUVECs). Results: SHED-CM significantly promoted neurite outgrowth of DRG neurons. Only less than 6 kDa of SHED-CM promoted the neurite outgrowth. SHED-CM significantly prevented decline in SNCVs compared with DMEM in diabetic mice. SHED-CM did not cause any change in MNCVs or sensory functions. Though SHED-CM did not improve IENFDs or morphometry of sural nerves, CNMFR was ameliorated by the administration of SHED-CM. SHED-CM significantly increased the proliferation and the migration of HUVECs. Conclusions: These results suggested that SHED-CM had the therapeutic effect on DPN by promoting neurite outgrowths and improving microcirculation in peripheral nerves. Disclosure E. Miura-Yura: None. S. Tsunekawa: None. K. Naruse: None. M. Kawai: None. M. Kato: None. H. Shimoda: None. Y. Yamada: None. M. Motegi: None. S. Asano: None. T. Himeno: None. M. Kondo: None. Y. Kato: Speaker's Bureau; Self; Merck & Co., Inc. J. Nakamura: Research Support; Self; Astellas Pharma Inc., Boehringer Ingelheim Pharmaceuticals, Inc., Daiichi Sankyo Company, Limited, Eli Lilly and Company, Japan Tobacco Inc., Kissei Pharmaceutical Co., Ltd., Merck Sharp & Dohme Corp., Novartis Pharmaceuticals Corporation, Novo Nordisk Inc., Ono Pharmaceutical Co., Ltd., Sanofi K.K., Sumitomo Dainippon Pharma Co., Ltd., Taisho Pharmaceutical Co., Ltd., Takeda Pharmaceutical Company Limited. Speaker's Bureau; Self; Astellas Pharma Inc., AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Daiichi Sankyo Company, Limited, Eli Lilly and Company, Kowa Pharmaceu. Co. Ltd., Merck Sharp & Dohme Corp., Mitsubishi Tanabe Pharma Corporation, Novartis Pharmaceuticals Corporation, Novo Nordisk Inc., Ono Pharmaceutical Co., Ltd., Sanofi K.K., Takeda Pharmaceutical Company Limited, Terumo Medical Corporation. H. Kamiya: Speaker's Bureau; Self; Astellas Pharma Inc., Eli Lilly Japan K.K., MSD K.K., Novartis Pharma K.K., Novo Nordisk Oharma Ltd., Ono Pharmaceutical Co., Ltd., Sanofi K.K.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db19-564-P
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2019
    detail.hit.zdb_id: 1501252-9
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  • 7
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    Online Resource
    454-P: Conditioned Medium from Dental Pulp Stem Cells Promotes Angiogenesis
    American Diabetes Association ; 2020
    In:  Diabetes Vol. 69, No. Supplement_1 ( 2020-06-01)
    Details
    In: Diabetes, American Diabetes Association, Vol. 69, No. Supplement_1 ( 2020-06-01)
    Abstract: Background/Aim: We previously reported that conditioned medium (CM) of stem cells from human exfoliated deciduous teeth (SHED) improved diabetic polyneuropathy in diabetic mice due to an increase of capillary blood flow in the vasa nervorum, and in in vitro study only secreted factors of less than 6 kDa fraction of SHED-CM promoted neurite outgrowth of mouse dorsal root ganglion neurons. In this study, we examined whether SHED-CM had beneficial effects on angiogenesis. Methods: SHED-CM was collected 48 hours after culturing in serum-free DMEM, and was separated into two fractions according to molecular weight (less than 6 kDa and more than 6 kDa). Exosomes were isolated from SHED-CM by ultracentrifugation. Human umbilical-vein endothelial cells (HUVECs) were cultured with six different media (DMEM, DMEM with VEGF, SHED-CM, less than 6 kDa, more than 6 kDa or DMEM with exosomes) for 12-48 hours, then MTT assay, wound healing assay, Boyden chamber assay and tube formation assay were performed to evaluate the cell viability, migration ability and tube formation ability in HUVECs. Rat aortic ring assay and mouse Matrigel plug assay were performed to assess neovascularization and endothelial cell migration. Results: SHED-CM, especially more than 6 kDa fraction, significantly promoted cell viability, migration and tube formation in HUVECs, compared with DMEM. Meanwhile, less than 6 kDa fraction promoted only tube formation, and the effects of exosomes were negligible. In aortic ring assay and Matrigel plug assay, SHED-CM accelerated neovascularization and increased endothelial cell migration in HUVECs, and the effects of more than 6 kDa fraction were stronger than that of less than 6 kDa fraction. These data suggested that the secreted factors in more than 6 kDa fraction played an essential role in promoting angiogenesis. Conclusion: Soluble factors from SHED might have angiogenesis-promoting effects and hold promise for comprehensive clinical applications in vascular diseases and diabetic complications. Disclosure M. Kato: None. S. Tsunekawa: None. N. Nakamura: None. E. Miura-Yura: None. Y. Yamada: None. Y. Hayashi: None. R. Inoue: None. M. Mohiuddin: Other Relationship; Self; Abbott Japan Co. Ltd, ARKRAY, Astellas Pharma Inc., Astellas Pharma Inc., AstraZeneca K.K., Boehlinger Ingelheim Japan Co. Ltd., Boehringer Ingelheim Pharmaceuticals, Inc., Daiichi Sankyo, Daiichi Sankyo, Eli Lilly Japan K.K., Eli Lilly Japan K.K., Fukuda Denshi, Japan Tobacco Inc., Kaken Pharmaceutical Co., Ltd., Kissei Pharmaceutical Co., Ltd., Kowa pharmaceu. co. Ltd., Kowa Pharmaceu. Co., Ltd., Kyowa Kirin Co., Ltd., Mitsubishi Tanabe Pharma Corporation, Mitsubishi Tanabe Pharma Corporation, MSD K.K., MSD K.K., Mylan N. V., Novartis Pharma K.K., Novartis Pharma K.K., Novo Nordisk Pharma Ltd., Novo Nordisk Pharma Ltd., Ono Pharmaceu. Co., Ltd., Ono Pharmaceutical Co., Ltd., Otsuka Pharmaceutical Co., Ltd., Pfizer Japan Inc., Sanofi K.K., Sanofi K.K., Sanwa Kagaku Kenkyusho, Sanwa Kagaku Kenkyusho, Shionogi & Co., Ltd., Sumitomo Dainippon Pharma Co., Ltd., Sumitomo Dainippon Pharma Co., Ltd., Taisho Pharmaceutical Co., Ltd., Taisho Pharmaceutical Co., Ltd., Takeda Pharmaceutical Company Limited, Takeda Pharmaceutical Company Limited, Terumo Co. Ltd. Y. Morishita: None. T. Himeno: None. M. Kondo: None. Y. Kato: None. H. Kamiya: Speaker’s Bureau; Self; Astellas Pharma Inc., AstraZeneca K.K., Boehringer Ingelheim K.K., Daiichi Sankyo, Eli Lilly Japan K.K., Fukuda Denshi, Kissei Pharmaceutical Co., Ltd., Kowa Company, Ltd., Kyowa Hakko Kirin Co., Ltd., Mitsubishi Tanabe Pharma Corporation, MSD K.K., Novartis Pharma K.K., Novo Nordisk Pharma Ltd., Ono Pharmaceutical Co., Ltd., Sanofi K.K., Sumitomo Dainippon Pharma Co., Ltd., Taisho Pharmaceutical Co., Ltd., Takeda Pharmaceutical Company Limited. K. Naruse: None. J. Nakamura: Research Support; Self; Astellas Pharma Inc., Boehlinger Ingelheim Japan Co., Ltd., Daiichi Sankyo, Eli Lilly Japan K.K., Japan Tobacco Inc., Kaken Pharmaceutical Co., Ltd., Kowa Company, Ltd., Kyowa Hakko Kirin Co., Ltd., Mitsubishi Tanabe Pharma Corporation, MSD K.K., Novartis Pharma K.K., Novo Nordisk Pharma Ltd., Ono Pharmaceutical Co., Ltd., Otsuka Pharmaceutical Co., Ltd., Pfizer Japan Inc., Sanofi K.K., Sanwa Kagaku Kenkyusho, Shionogi & Co., Ltd., Sumitomo Dainippon Pharma Co., Ltd., Taisho Pharmaceutical Co., Ltd., Takeda Pharmaceutical Company Limited. Speaker’s Bureau; Self; Abbott Japan Co., Ltd., ARKRAY, Astellas Pharma Inc., AstraZeneca K.K., Boehlinger Ingelheim Japan Co., Ltd.,, Daiichi Sankyo, Eli Lilly Japan K.K., Fukuda Denshi, Kissei Pharmaceutical Co., Ltd., Kowa Company, Ltd., Mitsubishi Tanabe Pharma Corporation, MSD K.K., Mylan, Novartis Pharma K.K., Novo Nordisk Pharma Ltd, Ono Pharmaceutical Co., Ltd., Sanofi, Sanwa Kagaku Kenkyusho, Sumitomo Dainippon Pharma Co., Ltd., Taisho Pharmaceutical Co., Ltd., Takeda Pharmaceutical Company Limited, Terumo Medical Corporation.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db20-454-P
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2020
    detail.hit.zdb_id: 1501252-9
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  • 8
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    The efficacy of switching basal–bolus insulin therapy to basal insulin-supported oral therapy with a glinide and an α-glucosidase inhibitor in patients with type 2 diabetes depends on insulin secretory capacity, but not on blood glucose profiles and insulin dosages prior to the switching
    Springer Science and Business Media LLC ; 2023
    In:  Diabetology International
    Details
    In: Diabetology International, Springer Science and Business Media LLC
    Type of Medium: Online Resource
    ISSN: 2190-1678 , 2190-1686
    URL: Article
    DOI: 10.1007/s13340-023-00651-z
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 2574501-3
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  • 9
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    Kir6.2-deficient mice develop somatosensory dysfunction and axonal loss in the peripheral nerves
    Elsevier BV ; 2022
    In:  iScience Vol. 25, No. 1 ( 2022-01), p. 103609-
    Details
    In: iScience, Elsevier BV, Vol. 25, No. 1 ( 2022-01), p. 103609-
    Type of Medium: Online Resource
    ISSN: 2589-0042
    URL: Article
    DOI: 10.1016/j.isci.2021.103609
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2022
    detail.hit.zdb_id: 2927064-9
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  • 10
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    Thermal gradient ring reveals thermosensory changes in diabetic peripheral neuropathy in mice
    Springer Science and Business Media LLC ; 2022
    In:  Scientific Reports Vol. 12, No. 1 ( 2022-06-13)
    Details
    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 12, No. 1 ( 2022-06-13)
    Abstract: Diabetic peripheral neuropathy (DPN) includes symptoms of thermosensory impairment, which are reported to involve changes in the expression or function, or both, of nociceptive TRPV1 and TRPA1 channels in rodents. In the present study, we did not find changes in the expression or function of TRPV1 or TRPA1 in DPN mice caused by STZ, although thermal hypoalgesia was observed in a murine model of DPN or TRPV1 −/− mice with a Plantar test, which specifically detects temperature avoidance. With a Thermal Gradient Ring in which mice can move freely in a temperature gradient, temperature preference can be analyzed, and we clearly discriminated the temperature-dependent phenotype between DPN and TRPV1 −/− mice. Accordingly, we propose approaches with multiple behavioral methods to analyze the progression of DPN by response to thermal stimuli. Attention to both thermal avoidance and preference may provide insight into the symptoms of DPN.
    Type of Medium: Online Resource
    ISSN: 2045-2322
    URL: Article
    DOI: 10.1038/s41598-022-14186-x
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 2615211-3
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