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Article ; Online: Role of Stromal Fibroblast-Induced WNT7A Associated with Cancer Cell Migration Through the AKT/CLDN1 Signaling Axis in Oral Squamous Cell Carcinoma.

Kayamori, Kou / Katsube, Ken-Ichi / Hirai, Hideaki / Harada, Hiroyuki / Ikeda, Tohru

Laboratory investigation; a journal of technical methods and pathology

2023 Volume 103, Issue 10, Page(s) 100228

Abstract: Wnt signaling plays a crucial role in the progression of various cancers, including oral squamous cell carcinoma (OSCC). However, the tumor microenvironment (TME) regulating Wnt signaling has not yet been fully elucidated. In this study, we investigated ... ...

Abstract	Wnt signaling plays a crucial role in the progression of various cancers, including oral squamous cell carcinoma (OSCC). However, the tumor microenvironment (TME) regulating Wnt signaling has not yet been fully elucidated. In this study, we investigated whether cancer-associated fibroblasts (CAFs), the primary components of the TME, activate Wnt signaling and promote tumor progression in OSCC. We conducted a Transwell coculture assay using human OSCC cell lines and normal human dermal fibroblasts (NHDFs). NHDFs stimulated WNT7A expression in several OSCC cell lines, especially HO-1-N-1 and HSC-5. An immunohistochemical study using 122 human OSCC samples indicated that high WNT7A expression in tumor cells was significantly associated with invasion depth and poor prognosis. Moreover, WNT7A expression in OSCC cells was positively correlated with α-smooth muscle actin expression in CAFs. WNT7A knockdown in OSCC cells demonstrated that OSCC cells cocultured with NHDFs significantly promoted tumor cell migration and invasion, which was dependent on WNT7A expression in OSCC cells. We also isolated HSC-5 cells from the coculture and conducted microarray analysis to investigate the factors that promote tumor progression induced by WNT7A. Among the various differentially expressed genes, we identified a downregulated gene encoding CLDN1 and confirmed that WNT7A negatively regulated CLDN1 expression in OSCC cells and CLDN1 knockdown in OSCC cells promoted their migration. Phosphokinase array analysis showed that WNT7A activates protein kinase B (AKT) phosphorylation. Activating AKT signaling using the SC79 agonist induced CLDN1 downregulation in OSCC cells. In the coculture assay, the AKT inhibitor MK2206 significantly recovered CLDN1 expression downregulated by WNT7A, resulting in OSCC cell migration suppression. These results suggest that CAFs stimulate OSCC cells to produce WNT7A, following CLDN1 expression downregulation by activating AKT signaling, promoting cancer cell migration. These findings highlight the importance of molecular therapies targeting the TME in OSCC.
MeSH term(s)	Humans ; Carcinoma, Squamous Cell/metabolism ; Squamous Cell Carcinoma of Head and Neck/metabolism ; Mouth Neoplasms/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Fibroblasts/metabolism ; Cell Movement/physiology ; Wnt Signaling Pathway ; Cell Line, Tumor ; Head and Neck Neoplasms/genetics ; Cell Proliferation ; Gene Expression Regulation, Neoplastic ; Tumor Microenvironment ; Wnt Proteins/genetics ; Wnt Proteins/metabolism
Chemical Substances	Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; WNT7A protein, human ; Wnt Proteins ; CLDN1 protein, human
Language	English
Publishing date	2023-08-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80178-1
ISSN	1530-0307 ; 0023-6837
ISSN (online)	1530-0307
ISSN	0023-6837
DOI	10.1016/j.labinv.2023.100228
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Article ; Online: Ankle foot orthosis that prevents slippage for tibial rotation in knee osteoarthritis patients.

Katsube, Go / Qi, Song / Itami, Taku / Yano, Ken'ichi / Mori, Ichidai / Kameda, Kazuhiro

Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual International Conference

2021 Volume 2021, Page(s) 4728–4731

Abstract: Knee osteoarthritis (OA) is a disease caused by age-related muscle weakness, obesity, or sports injury that leads to gait disability due to pain during walking. Knee OA is characterized by abnormal knee joint alignment and rotational dyskinesia, which ... ...

Abstract	Knee osteoarthritis (OA) is a disease caused by age-related muscle weakness, obesity, or sports injury that leads to gait disability due to pain during walking. Knee OA is characterized by abnormal knee joint alignment and rotational dyskinesia, which are believed to worsen the symptoms. We previously developed an ankle orthosis that mechanically induces the rotation of the lower limb in conjunction with that of the ankle joint. This orthosis can effectively correct the alignment of the knee joint. However, slippage between the orthosis and leg can occur during walking, decreasing the corrective force. In this study, we clarify the effect of slippage between the orthosis and body on the correction force of the orthosis, and develop a lower leg tracking mechanism to suppress slippage and minimize reduction of force. The effectiveness of the proposed mechanism was evaluated by three-dimensional motion analysis of gait. Analysis results confirmed that the proposed mechanism was effective in suppressing slippage and improving correction force, demonstrating the effectiveness of the mechanism for knee OA.
MeSH term(s)	Ankle ; Biomechanical Phenomena ; Foot Orthoses ; Humans ; Osteoarthritis, Knee/therapy ; Rotation
Language	English
Publishing date	2021-12-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2694-0604
ISSN (online)	2694-0604
DOI	10.1109/EMBC46164.2021.9631003
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Article ; Online: Notch signaling is involved in Fgf23 upregulation in osteocytes.

Tamamura, Yoshihiro / Sakamoto, Kei / Katsube, Ken-Ichi / Yamaguchi, Akira

Biochemical and biophysical research communications

2019 Volume 518, Issue 2, Page(s) 233–238

Abstract: Fgf23 acts as a phosphaturic factor secreted from osteocytes in bone, but the mechanism regulating Fgf23 is not fully understood. Here, we showed the colocalization of Fgf23, Notch, and Hes1, a downstream target of Notch signaling, in numerous osteocytes ...

Abstract	Fgf23 acts as a phosphaturic factor secreted from osteocytes in bone, but the mechanism regulating Fgf23 is not fully understood. Here, we showed the colocalization of Fgf23, Notch, and Hes1, a downstream target of Notch signaling, in numerous osteocytes in cortical bone of femur in wild-type mice. We generated NICD (Notch intracellular domain)-transgenic mice driven by a 2.3 kb collagenα1 (I) (Col1a1) promoter fragment. Western blot and RT-PCR analyses revealed upregulation of Notch protein and mRNA levels in the bones of transgenic mice compared with those in wild-type mice. In the transgenic mice, immunohistochemical studies demonstrated that numerous osteocytes and osteoblasts express Notch in the rib, whereas only osteoblasts exhibit Notch in the femur. NICD-transgenic mice were characterized by upregulation of Fgf23 mRNA levels in the rib but not in the femur compared with that in wild type mice. These mice exhibited dwarfism associated with an osteomalacia phenotype. The expression of Alpl, Col1a1, and Bglap decreased in NICD-transgenic mice compared with wild-type mice. UMR-106 cells cultured on Jagged1-immobilized wells significantly increased Fgf23 expressions associating with upregulation of Hes1 and Hey1. These results imply that Notch signaling is a positive regulator for Fgf23 expression in osteocytes.
MeSH term(s)	Animals ; Cell Line, Tumor ; Female ; Fibroblast Growth Factors/analysis ; Fibroblast Growth Factors/metabolism ; Mice, Inbred C57BL ; Mice, Transgenic ; Osteocytes/cytology ; Osteocytes/metabolism ; Rats ; Receptors, Notch/analysis ; Receptors, Notch/metabolism ; Signal Transduction ; Up-Regulation
Chemical Substances	Receptors, Notch ; Fibroblast Growth Factors (62031-54-3) ; fibroblast growth factor 23 (7Q7P4S7RRE)
Language	English
Publishing date	2019-08-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2019.08.038
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Article: Notch signaling is involved in Fgf23 upregulation in osteocytes

Tamamura, Yoshihiro / Sakamoto, Kei / Katsube, Ken-ichi / Yamaguchi, Akira

Biochemical and biophysical research communications. 2019 Oct. 15, v. 518, no. 2

2019

Abstract	Fgf23 acts as a phosphaturic factor secreted from osteocytes in bone, but the mechanism regulating Fgf23 is not fully understood. Here, we showed the colocalization of Fgf23, Notch, and Hes1, a downstream target of Notch signaling, in numerous osteocytes in cortical bone of femur in wild-type mice. We generated NICD (Notch intracellular domain)-transgenic mice driven by a 2.3 kb collagenα1 (I) (Col1a1) promoter fragment. Western blot and RT-PCR analyses revealed upregulation of Notch protein and mRNA levels in the bones of transgenic mice compared with those in wild-type mice. In the transgenic mice, immunohistochemical studies demonstrated that numerous osteocytes and osteoblasts express Notch in the rib, whereas only osteoblasts exhibit Notch in the femur. NICD-transgenic mice were characterized by upregulation of Fgf23 mRNA levels in the rib but not in the femur compared with that in wild type mice. These mice exhibited dwarfism associated with an osteomalacia phenotype. The expression of Alpl, Col1a1, and Bglap decreased in NICD-transgenic mice compared with wild-type mice. UMR-106 cells cultured on Jagged1-immobilized wells significantly increased Fgf23 expressions associating with upregulation of Hes1 and Hey1. These results imply that Notch signaling is a positive regulator for Fgf23 expression in osteocytes.
Keywords	Western blotting ; dwarfing ; femur ; immunohistochemistry ; osteoblasts ; osteomalacia ; phenotype ; research
Language	English
Dates of publication	2019-1015
Size	p. 233-238.
Publishing place	Elsevier Inc.
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2019.08.038
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Article ; Online: The Bone Regeneration Model and Primary Osteoblastic Cell Culture Used in the Analysis of Ccn3 Transgenic and Knockout Mice.

Sakamoto, Kei / Matsushita, Yuki / Minamizato, Tokutaro / Katsuki, Yuko / Katsube, Ken-Ichi / Yamaguchi, Akira

Methods in molecular biology (Clifton, N.J.)

2017 Volume 1489, Page(s) 309–324

Abstract: Bone tissue is intrinsically hard and thus, it is more difficult to handle, process, and examine than soft tissues. Here, we describe an experimental model of bone regeneration and several selected protocols useful for investigating mRNA and protein ... ...

Abstract	Bone tissue is intrinsically hard and thus, it is more difficult to handle, process, and examine than soft tissues. Here, we describe an experimental model of bone regeneration and several selected protocols useful for investigating mRNA and protein expression in bone. The inhibitory function of CCN3 on membranous bone formation has been confirmed by following the protocols described herein (Fig. 1).
Language	English
Publishing date	2017
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-6430-7_27
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Article ; Online: Pulp inflammation induces Kv1.1 K

Murano, Hiroki / Kaneko, Tomoatsu / Zaw, Su Yee Myo / Sone, Phyo Pyai / Zaw, Zar Chi Thein / Okada, Yamato / Sunakawa, Mitsuhiro / Katsube, Ken-Ichi / Okiji, Takashi

Oral diseases

2021 Volume 28, Issue 6, Page(s) 1674–1681

Abstract: Objectives: Signals from inflamed tooth pulp activate thalamic neurons to evoke central sensitization. We aimed to gain insights into the mechanisms mediating the early phase of pulpal inflammation-induced thalamic neural and glial activation.: ... ...

Abstract	Objectives: Signals from inflamed tooth pulp activate thalamic neurons to evoke central sensitization. We aimed to gain insights into the mechanisms mediating the early phase of pulpal inflammation-induced thalamic neural and glial activation. Materials and methods: Pulpal inflammation was induced via the application of mustard oil (MO) to the upper first molar of Wistar rats with local anesthesia (LA) or saline injection. After 0.5, 1, 2, and 24 hr, contralateral thalami were subjected to microarrays, a real-time polymerase chain reaction and immunohistochemistry to identify differentially expressed genes and assess potassium voltage-gated channel subfamily A member 1 (Kv1.1)-expressing axons and glial fibrillary acidic protein (GFAP)-expressing astrocytes. Results: The Kv1.1 gene (Kcna1) was down-regulated and the density of Kv1.1-expressing axons decreased in non-anesthetized rats, but not in anesthetized rats 1 hr after the MO treatment. The density of GFAP-expressing astrocytes increased in both groups until 24 hr after the MO treatment, with a greater increase being observed in the saline-injection group than in the LA group. Conclusions: MO induced the transient down-regulation of Kcna1, transiently reduced the density of Kv1.1-expressing axons, and increased astrocytes in thalami within 1 hr of pulpal application. These results suggest central sensitization represented by neuronal hyperexcitability and astrocyte activation.
MeSH term(s)	Animals ; Dental Pulp ; Down-Regulation ; Inflammation ; Rats ; Rats, Wistar ; Thalamus
Language	English
Publishing date	2021-04-19
Publishing country	Denmark
Document type	Journal Article
ZDB-ID	1290529-x
ISSN	1601-0825 ; 1354-523X
ISSN (online)	1601-0825
ISSN	1354-523X
DOI	10.1111/odi.13866
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Article ; Online: A facile one-step strategy for the generation of conditional knockout mice to explore the role of Notch1 in oroesophageal tumorigenesis.

Mandasari, Masita / Sawangarun, Wanlada / Katsube, Ken-ichi / Kayamori, Kou / Yamaguchi, Akira / Sakamoto, Kei

Biochemical and biophysical research communications

2016 Volume 469, Issue 3, Page(s) 761–767

Abstract: NOTCH1 plays an important role in epithelial differentiation and carcinogenesis. To investigate the impact of Notch1 inactivation in oroesophageal epithelium, we generated conditional knockout (cKO) mice, using a combined construct which induces the ... ...

Abstract	NOTCH1 plays an important role in epithelial differentiation and carcinogenesis. To investigate the impact of Notch1 inactivation in oroesophageal epithelium, we generated conditional knockout (cKO) mice, using a combined construct which induces the expression of single guide RNA targeting Notch1 and Cas9 by the KRT14 promoter. The cKO mice exhibited patchy hair loss and multiple NOTCH1-negative areas in the tongue epithelium, indicative of heterogeneous knockout. The cKO mice showed susceptibility to esophageal tumorigenesis, underscoring Notch1 as a tumor suppressor. Our one-step strategy for generation of cKO mice provides a versatile method to examine a gene function in vivo.
MeSH term(s)	Animals ; Carcinogenesis/metabolism ; Carcinogenesis/pathology ; Cell Line, Tumor ; Disease Models, Animal ; Esophageal Neoplasms/genetics ; Esophageal Neoplasms/metabolism ; Esophageal Neoplasms/pathology ; Mice ; Mice, Knockout/genetics ; Mice, Knockout/immunology ; Mice, Knockout/metabolism ; Receptor, Notch1/genetics ; Receptor, Notch1/metabolism
Chemical Substances	Notch1 protein, mouse ; Receptor, Notch1
Language	English
Publishing date	2016-01-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2015.12.006
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Article ; Online: Crosstalk between dental pulp stem cells and endothelial cells augments angiogenic factor expression.

Zaw, Su Yee Myo / Kaneko, Tomoatsu / Zaw, Zar Chi Thein / Sone, Phyo Pyai / Murano, Hiroki / Gu, Bin / Okada, Yamato / Han, Peifeng / Katsube, Ken-Ichi / Okiji, Takashi

Oral diseases

2020 Volume 26, Issue 6, Page(s) 1275–1283

Abstract: Objectives: We aimed to investigate whether the mesenchymal stem cell-endothelial cell crosstalk enhances angiogenic factor expression via nuclear factor-kappa B (NF-κB)-dependent mechanisms.: Materials and methods: Human dermal microvascular ... ...

Abstract	Objectives: We aimed to investigate whether the mesenchymal stem cell-endothelial cell crosstalk enhances angiogenic factor expression via nuclear factor-kappa B (NF-κB)-dependent mechanisms. Materials and methods: Human dermal microvascular endothelial cells (HDMECs) and stem cells from human exfoliated deciduous teeth (SHEDs) were cocultured for 96 hr, in the presence of NF-κB decoy oligodeoxynucleotides (ODNs) or scramble (control). Vascular endothelial cell growth factor (VEGF) and phospho-NF-κB p65 were measured with enzyme-linked immunosorbent assay. Angiogenesis-related gene expression was analyzed with microarray analysis followed by real-time polymerase chain reaction. Tube formation assay was conducted in the presence of NF-κB decoy. Results: The VEGF and phospho-NF-κB p65 levels were significantly higher in the coculture with NF-κB decoy scramble than in single culture and coculture with NF-κB decoy ODN. Microarray analysis of SHEDs and HDMECs with NF-κB decoy scramble showed higher expression of proangiogenic genes, Bcl-2, NF-κB1, VEGFA, CXCL8, and CXCR1, and lower expression of proapoptotic genes, Bax and Caspase 9, compared to cells with NF-κB decoy ODN. Real-time PCR results for Bcl-2 and CXCL8 showed a similar trend. Tube formation assay showed more tube development in the presence of NF-κB decoy scramble. Conclusion: The SHED-HDMEC crosstalk enhanced proangiogenic factor expression via NF-κB-dependent pathways.
Language	English
Publishing date	2020-04-20
Publishing country	Denmark
Document type	Journal Article
ZDB-ID	1290529-x
ISSN	1601-0825 ; 1354-523X
ISSN (online)	1601-0825
ISSN	1354-523X
DOI	10.1111/odi.13341
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Article ; Online: Neural Regeneration/Remodeling in Engineered Coronal Pulp Tissue in the Rat Molar.

Sone, Phyo Pyai / Kaneko, Tomoatsu / Zaw, Su Yee Myo / Sueyama, Yukiko / Gu, Bin / Murano, Hiroki / Zaw, Zar Chi Thein / Okada, Yamato / Han, Peifeng / Katsube, Ken-Ichi / Okiji, Takashi

Journal of endodontics

2020 Volume 46, Issue 7, Page(s) 943–949

Abstract: Introduction: This study aimed to examine the process of reinnervation during coronal pulp tissue regeneration in a rat model in which rat bone marrow mesenchymal stem cells were implanted in pulpotomized molars.: Methods: The maxillary first molars ... ...

Abstract	Introduction: This study aimed to examine the process of reinnervation during coronal pulp tissue regeneration in a rat model in which rat bone marrow mesenchymal stem cells were implanted in pulpotomized molars. Methods: The maxillary first molars of Wistar rats were pulpotomized, and preformed biodegradable porous poly L-lactic acid scaffolds and hydrogel carrying rat bone marrow mesenchymal stem cells were implanted in the pulp chamber. After 3, 7, and 14 days, the implanted teeth were processed for histologic analysis; immunoperoxidase staining for protein gene product 9.5 (a general neuronal marker), calcitonin gene-related peptide (CGRP), or substance P (SP); and real-time polymerase chain reaction for nerve growth factor (NGF) and growth-associated protein 43 (GAP-43) messenger RNA (mRNA) expression. Results: Histologic analysis of the implanted region revealed sparse cellular distribution at 3 days, pulplike tissue with a thin dentin bridge-like structure at 7 days, and dentin bridge-like mineralized tissue formation and resorption of most scaffolds at 14 days. Protein gene product 9.5 and CGRP-immunoreactive nerve fibers showed the lowest density at 3 days and significantly increased until 14 days when the CGRP-immunoreactive fibers reached normal levels. SP-immunoreactive nerve fibers showed the highest density at 7 days and decreased to normal levels at 14 days. NGF mRNA increased with time, whereas GAP-43 mRNA levels peaked at 3 days and subsequently dropped until 14 days. Conclusions: Regeneration/remodeling of SP-immunoreactive and CGRP-immunoreactive nerve fibers with increased mRNA expression of NGF and GAP-43 occurred in a rat model of coronal pulp tissue engineering with bone marrow mesenchymal stem cells.
MeSH term(s)	Animals ; Dental Pulp ; Molar ; Nerve Regeneration ; Rats ; Rats, Wistar ; Tissue Engineering
Language	English
Publishing date	2020-05-25
Publishing country	United States
Document type	Journal Article
ZDB-ID	752412-2
ISSN	1878-3554 ; 0099-2399
ISSN (online)	1878-3554
ISSN	0099-2399
DOI	10.1016/j.joen.2020.04.002
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Article ; Online: Inhibition of Nuclear Factor Kappa B Prevents the Development of Experimental Periapical Lesions.

Kaneko, Tomoatsu / Myo Zaw, Su Yee / Sueyama, Yukiko / Katsube, Ken-Ichi / Kaneko, Reika / Nör, Jacques E / Okiji, Takashi

Journal of endodontics

2018 Volume 45, Issue 2, Page(s) 168–173

Abstract: Introduction: Nuclear factor kappa B (NF-κB) is an important transcriptional regulator of angiogenesis involving B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X protein (Bax) signaling pathways. Thus, inhibition of NF-κB may suppress the development of ...

Abstract	Introduction: Nuclear factor kappa B (NF-κB) is an important transcriptional regulator of angiogenesis involving B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X protein (Bax) signaling pathways. Thus, inhibition of NF-κB may suppress the development of periapical lesions via blockage of angiogenesis. Accordingly, we examined the effects of NF-κB decoy oligodeoxynucleotide (ODN) treatment on experimentally induced periapical lesions. Methods: Periapical lesions were induced in the mandibular first molars of 5-week-old male Wistar rats by the application of lipopolysaccharide to the pulp. NF-κB decoy ODN or NF-κB decoy scramble (control) was injected intraperitoneally every 7 days, starting 1 day before pulp exposure. After 28 days, the samples were retrieved, and digital radiographs were taken for radiomorphometry. Samples were processed for (1) immunohistochemistry of CD31, Bcl-2, and Bax; (2) laser capture microdissection to analyze Bcl-2, Bax, chemokine (C-X-C motif) ligand 1 (CXCL1), CXC receptor 2 (CXCR2), and vascular endothelial cell growth factor receptor 2 (VEGFR2) messenger RNA (mRNA) expression in CD31+ endothelial cells; (3) enzyme-linked immunosorbent assay to determine NF-κB/p65 activity; and (4) Western blotting for vascular endothelial growth factor expression. Results: NF-κB decoy ODN treatment significantly reduced lesion size, NF-κB/p65 activity, and the density of CD31+ endothelial cells in the lesion. NF-κB decoy ODNs also down-regulated CXCL1, CXCR2, and VEGFR2 mRNAs and up-regulated Bax mRNA in endothelial cells but did not affect Bcl2 mRNA in endothelial cells. Vascular endothelial growth factor protein expression in the lesions was significantly decreased. Conclusions: The inhibition of NF-κB activity by decoy ODN treatment suppressed the development of experimentally induced periapical lesions with a concomitant reduction in angiogenic responses in endothelial cells.
MeSH term(s)	Animals ; Injections, Intraperitoneal ; Lipopolysaccharides/adverse effects ; Male ; NF-kappa B/antagonists & inhibitors ; NF-kappa B/metabolism ; Neovascularization, Pathologic/genetics ; Oligodeoxyribonucleotides/administration & dosage ; Oligodeoxyribonucleotides/pharmacology ; Periapical Diseases/chemically induced ; Periapical Diseases/genetics ; Periapical Diseases/prevention & control ; Rats, Wistar
Chemical Substances	Lipopolysaccharides ; NF-kappa B ; Oligodeoxyribonucleotides
Language	English
Publishing date	2018-08-31
Publishing country	United States
Document type	Journal Article
ZDB-ID	752412-2
ISSN	1878-3554 ; 0099-2399
ISSN (online)	1878-3554
ISSN	0099-2399
DOI	10.1016/j.joen.2018.10.006
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