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Article ; Online: Ppp6c deficiency accelerates K-ras

2021 Volume 10, Issue 13, Page(s) 4451–4464

Abstract: ... deficiency on tongue tumor development in K (K-rasG12D)- and KP (K-rasG12D + Trp53-deficient)-inducible mice ... Results: Mice of K and KP genotypes developed squamous cell carcinoma in situ in the tongue approximately ... that in the presence of K-rasG12D, Ppp6c deletion enhanced the activation of the ERK-ELK1-FOS, AKT-4EBP1, and AKT-FOXO ...

Abstract	Background: Effective treatments for cancer harboring mutant RAS are lacking. In Drosophila, it was reported that PP6 suppresses tumorigenicity of mutant RAS. However, the information how PP6 regulates oncogenic RAS in mammals is limited. Methods: We examined the effects of PP6 gene (Ppp6c) deficiency on tongue tumor development in K (K-rasG12D)- and KP (K-rasG12D + Trp53-deficient)-inducible mice. Results: Mice of K and KP genotypes developed squamous cell carcinoma in situ in the tongue approximately 2 weeks after the induction of Ppp6c deficiency and was euthanized due to 20% loss of body weight. Transcriptome analysis revealed significantly different gene expressions between tissues of Ppp6c-deficient tongues and those of Ppp6c wild type, while Trp53 deficiency had a relatively smaller effect. We then analyzed genes commonly altered by Ppp6c deficiency, with or without Trp53 deficiency, and identified a group concentrated in KEGG database pathways defined as 'Pathways in Cancer' and 'Cytokine-cytokine receptor interaction'. We then evaluated signals downstream of oncogenic RAS and those regulated by PP6 substrates and found that in the presence of K-rasG12D, Ppp6c deletion enhanced the activation of the ERK-ELK1-FOS, AKT-4EBP1, and AKT-FOXO-CyclinD1 axes. Ppp6c deletion combined with K-rasG12D also enhanced DNA double-strand break (DSB) accumulation and activated NFκB signaling, upregulating IL-1β, COX2, and TNF.
MeSH term(s)	Animals ; Carcinoma in Situ/genetics ; Carcinoma, Squamous Cell/genetics ; DNA Breaks, Double-Stranded ; Gene Deletion ; Genes, ras ; Genotype ; Mice ; Mutation ; Phosphoprotein Phosphatases/deficiency ; Phosphoprotein Phosphatases/genetics ; Tongue Neoplasms/genetics ; Transcriptome ; Tumor Suppressor Protein p53/deficiency ; Tumor Suppressor Protein p53/genetics
Chemical Substances	Trp53 protein, mouse ; Tumor Suppressor Protein p53 ; Phosphoprotein Phosphatases (EC 3.1.3.16) ; protein phosphatase 6 (EC 3.1.3.16)
Language	English
Publishing date	2021-06-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2659751-2
ISSN	2045-7634 ; 2045-7634
ISSN (online)	2045-7634
ISSN	2045-7634
DOI	10.1002/cam4.3962
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Article ; Online: Relationship of matrix Gla protein and vitamin K with vascular calcification in hemodialysis patients.

Mizuiri, Sonoo / Nishizawa, Yoshiko / Yamashita, Kazuomi / Ono, Kyoka / Naito, Takayuki / Tanji, Chie / Usui, Koji / Doi, Shigehiro / Masaki, Takao / Shigemoto, Kenichiro

Renal failure

2019 Volume 41, Issue 1, Page(s) 770–777

Abstract: Objective: ...

Abstract	Objective:
MeSH term(s)	Adult ; Biomarkers/blood ; Calcium-Binding Proteins/blood ; Cardiovascular Diseases/blood ; Cardiovascular Diseases/epidemiology ; Cardiovascular Diseases/etiology ; Cross-Sectional Studies ; Extracellular Matrix Proteins/blood ; Female ; Healthy Volunteers ; Humans ; Kidney Failure, Chronic/blood ; Kidney Failure, Chronic/complications ; Kidney Failure, Chronic/therapy ; Male ; Middle Aged ; Prevalence ; Renal Dialysis/adverse effects ; Risk Factors ; Vascular Calcification/blood ; Vascular Calcification/epidemiology ; Vascular Calcification/etiology ; Vitamin K/blood ; Matrix Gla Protein
Chemical Substances	Biomarkers ; Calcium-Binding Proteins ; Extracellular Matrix Proteins ; Vitamin K (12001-79-5)
Language	English
Publishing date	2019-09-05
Publishing country	England
Document type	Journal Article
ZDB-ID	632949-4
ISSN	1525-6049 ; 0886-022X
ISSN (online)	1525-6049
ISSN	0886-022X
DOI	10.1080/0886022X.2019.1650065
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Article: [Pathogenesis of MuSK Antibody-positive Myasthenia Gravis].

Shigemoto, Kazuhiro

Brain and nerve = Shinkei kenkyu no shinpo

2024 Volume 76, Issue 1, Page(s) 47–53

Abstract: Long-term remission is rare in patients with myasthenia gravis (MG), and health-related quality of life is lower in patients with MG than in healthy individuals. Approximately 5% of patients with MG show positive results on muscle-specific kinase (MuSK) ... ...

Abstract	Long-term remission is rare in patients with myasthenia gravis (MG), and health-related quality of life is lower in patients with MG than in healthy individuals. Approximately 5% of patients with MG show positive results on muscle-specific kinase (MuSK) antibody testing and usually have severe symptoms, refractory disease, residual muscle atrophy, and poor prognosis. Recent studies that have investigated the pathogenesis of MuSK antibody-positive MG have reported contributors to treatment refractoriness in cases of MG. In this article, we review the most recent findings.
MeSH term(s)	Humans ; Quality of Life ; Muscular Atrophy ; Myasthenia Gravis
Language	Japanese
Publishing date	2024-01-06
Publishing country	Japan
Document type	Review ; English Abstract ; Journal Article
ZDB-ID	390389-8
ISSN	1344-8129 ; 1881-6096 ; 0006-8969
ISSN (online)	1344-8129
ISSN	1881-6096 ; 0006-8969
DOI	10.11477/mf.1416202557
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Article ; Online: Differential expression patterns of K(+) /Cl(-) cotransporter 2 in neurons within the superficial spinal dorsal horn of rats.

Javdani, Fariba / Holló, Krisztina / Hegedűs, Krisztina / Kis, Gréta / Hegyi, Zoltán / Dócs, Klaudia / Kasugai, Yu / Fukazawa, Yugo / Shigemoto, Ryuichi / Antal, Miklós

The Journal of comparative neurology

2015 Volume 523, Issue 13, Page(s) 1967–1983

Abstract: γ-Aminobutyric acid (GABA)- and glycine-mediated hyperpolarizing inhibition is associated with a chloride influx that depends on the inwardly directed chloride electrochemical gradient. In neurons, the extrusion of chloride from the cytosol primarily ... ...

Abstract	γ-Aminobutyric acid (GABA)- and glycine-mediated hyperpolarizing inhibition is associated with a chloride influx that depends on the inwardly directed chloride electrochemical gradient. In neurons, the extrusion of chloride from the cytosol primarily depends on the expression of an isoform of potassium-chloride cotransporters (KCC2s). KCC2 is crucial in the regulation of the inhibitory tone of neural circuits, including pain processing neural assemblies. Thus we investigated the cellular distribution of KCC2 in neurons underlying pain processing in the superficial spinal dorsal horn of rats by using high-resolution immunocytochemical methods. We demonstrated that perikarya and dendrites widely expressed KCC2, but axon terminals proved to be negative for KCC2. In single ultrathin sections, silver deposits labeling KCC2 molecules showed different densities on the surface of dendritic profiles, some of which were negative for KCC2. In freeze fracture replicas and tissue sections double stained for the β3-subunit of GABAA receptors and KCC2, GABAA receptors were revealed on dendritic segments with high and also with low KCC2 densities. By measuring the distances between spots immunoreactive for gephyrin (a scaffolding protein of GABAA and glycine receptors) and KCC2 on the surface of neurokinin 1 (NK1) receptor-immunoreactive dendrites, we found that gephyrin-immunoreactive spots were located at various distances from KCC2 cotransporters; 5.7 % of them were recovered in the middle of 4-10-µm-long dendritic segments that were free of KCC2 immunostaining. The variable local densities of KCC2 may result in variable postsynaptic potentials evoked by the activation of GABAA and glycine receptors along the dendrites of spinal neurons.
MeSH term(s)	Animals ; Calcitonin Gene-Related Peptide/metabolism ; Carrier Proteins/metabolism ; Glutamate Decarboxylase/metabolism ; Male ; Membrane Proteins/metabolism ; Microscopy, Immunoelectron ; Posterior Horn Cells/cytology ; Posterior Horn Cells/diagnostic imaging ; Posterior Horn Cells/metabolism ; Presynaptic Terminals/metabolism ; Presynaptic Terminals/ultrastructure ; Rats ; Rats, Wistar ; Receptors, GABA-A/metabolism ; Receptors, Neurokinin-1/metabolism ; Spinal Cord Dorsal Horn/cytology ; Symporters/metabolism ; Ultrasonography ; Vesicular Glutamate Transport Protein 2/metabolism ; Vesicular Glutamate Transport Protein 2/ultrastructure ; K Cl- Cotransporters
Chemical Substances	Carrier Proteins ; Membrane Proteins ; Receptors, GABA-A ; Receptors, Neurokinin-1 ; Slc17a6 protein, rat ; Symporters ; Vesicular Glutamate Transport Protein 2 ; gephyrin ; Glutamate Decarboxylase (EC 4.1.1.15) ; glutamate decarboxylase 1 (EC 4.1.1.15) ; glutamate decarboxylase 2 (EC 4.1.1.15) ; Calcitonin Gene-Related Peptide (JHB2QIZ69Z)
Language	English
Publishing date	2015-04-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3086-7
ISSN	1096-9861 ; 0021-9967 ; 0092-7317
ISSN (online)	1096-9861
ISSN	0021-9967 ; 0092-7317
DOI	10.1002/cne.23774
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Article ; Online: Retrograde synaptic signaling mediated by K+ efflux through postsynaptic NMDA receptors.

Shih, Pei-Yu / Savtchenko, Leonid P / Kamasawa, Naomi / Dembitskaya, Yulia / McHugh, Thomas J / Rusakov, Dmitri A / Shigemoto, Ryuichi / Semyanov, Alexey

Cell reports

2013 Volume 5, Issue 4, Page(s) 941–951

Abstract: ... and plasticity in dendritic spines. Whether the concurrent K(+) efflux through the same receptors ... into the synaptic cleft has a physiological role is not known. Here, we report that NMDAR-dependent K(+) efflux ... can provide a retrograde signal in the synapse. In hippocampal CA3-CA1 synapses, the bulk of astrocytic K ...

Abstract	Synaptic NMDA receptors (NMDARs) carry inward Ca(2+) current responsible for postsynaptic signaling and plasticity in dendritic spines. Whether the concurrent K(+) efflux through the same receptors into the synaptic cleft has a physiological role is not known. Here, we report that NMDAR-dependent K(+) efflux can provide a retrograde signal in the synapse. In hippocampal CA3-CA1 synapses, the bulk of astrocytic K(+) current triggered by synaptic activity reflected K(+) efflux through local postsynaptic NMDARs. The local extracellular K(+) rise produced by activation of postsynaptic NMDARs boosted action potential-evoked presynaptic Ca(2+) transients and neurotransmitter release from Schaffer collaterals. Our findings indicate that postsynaptic NMDAR-mediated K(+) efflux contributes to use-dependent synaptic facilitation, thus revealing a fundamental form of retrograde synaptic signaling.
MeSH term(s)	Action Potentials ; Animals ; Astrocytes/metabolism ; Calcium/chemistry ; Glutamic Acid/metabolism ; Hippocampus/metabolism ; Ion Transport/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Potassium/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/metabolism ; Receptors, Neurotransmitter/metabolism ; Signal Transduction
Chemical Substances	Receptors, N-Methyl-D-Aspartate ; Receptors, Neurotransmitter ; Glutamic Acid (3KX376GY7L) ; Potassium (RWP5GA015D) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2013-11-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2013.10.026
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Article ; Online: Vitamin K₂ alters bone metabolism markers in hemodialysis patients with a low serum parathyroid hormone level.

Ochiai, Mariko / Nakashima, Ayumu / Takasugi, Norihisa / Kiribayashi, Kei / Kawai, Toru / Usui, Koji / Shigemoto, Kenichiro / Hamaguchi, Naoki / Kohno, Nobuoki / Yorioka, Noriaki

Nephron. Clinical practice

2011 Volume 117, Issue 1, Page(s) c15–9

Abstract: ... K₂ on adynamic bone disease. In this study, we assessed the efficacy of oral vitamin K₂ ... randomly divided into two groups, which were a vitamin K₂ group receiving oral menatetrenone (45 mg/day ... for 1 year and a control group without vitamin K₂. Venous blood samples were collected at baseline and ...

Abstract	Background: A low level of intact parathyroid hormone (PTH) is an indicator of adynamic bone disease in hemodialysis patients, and is associated with a significant increase of all-cause mortality. Thus, effective treatment for adynamic bone disease is required. We previously investigated the effect of vitamin K₂ on adynamic bone disease. In this study, we assessed the efficacy of oral vitamin K₂ in a controlled trial. Methods: Forty hemodialysis patients with low intact PTH levels (<100 pg/ml) were randomly divided into two groups, which were a vitamin K₂ group receiving oral menatetrenone (45 mg/day) for 1 year and a control group without vitamin K₂. Venous blood samples were collected at baseline and during the study for measurement of bone metabolism parameters. Results: Thirty-three patients completed follow-up. There was a significant increase of the serum intact osteocalcin level after 1 month of vitamin K₂ administration. Serum levels of intact PTH, bone alkaline phosphatase, and cross-linked N-terminal telopeptide of type I collagen increased significantly after 12 months in the vitamin K₂ group. The serum osteoprotegerin level was decreased after 12 months in the vitamin K₂ group, but the change was not significant. Conclusion: Vitamin K₂ therapy improves bone remodeling in hemodialysis patients with a low intact PTH level.
MeSH term(s)	Aged ; Alkaline Phosphatase/blood ; Biomarkers/blood ; Bone Diseases/etiology ; Bone Diseases/metabolism ; Bone Remodeling/drug effects ; Collagen Type I/blood ; Female ; Humans ; Male ; Middle Aged ; Osteocalcin/blood ; Parathyroid Hormone/blood ; Peptides/blood ; Renal Dialysis/adverse effects ; Statistics, Nonparametric ; Vitamin K 2/analogs & derivatives ; Vitamin K 2/pharmacology ; Vitamin K 2/therapeutic use
Chemical Substances	Biomarkers ; Collagen Type I ; Parathyroid Hormone ; Peptides ; collagen type I trimeric cross-linked peptide ; Osteocalcin (104982-03-8) ; Vitamin K 2 (11032-49-8) ; menatetrenone (27Y876D139) ; Alkaline Phosphatase (EC 3.1.3.1)
Language	English
Publishing date	2011
Publishing country	Switzerland
Document type	Journal Article ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
ZDB-ID	207121-6
ISSN	1660-2110 ; 1423-0186 ; 2235-3186 ; 1660-8151 ; 0028-2766
ISSN (online)	1660-2110 ; 1423-0186 ; 2235-3186
ISSN	1660-8151 ; 0028-2766
DOI	10.1159/000319642
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Book ; Online: Various Logistic Curves in SIS and SIR Models

Shigemoto, Kazuyasu

2022

Abstract: In our previous paper, the logistic curve of the removed number was derived from SIR and SEIR models in the case of the small basic reproduction number. In this paper, we derive various logistic curves of the removed, unsusceptible and infectious numbers ...

Abstract	In our previous paper, the logistic curve of the removed number was derived from SIR and SEIR models in the case of the small basic reproduction number. In this paper, we derive various logistic curves of the removed, unsusceptible and infectious numbers respectively from SIS and SIR models in the case of small and large basic reproduction numbers. Comment: 9 pages, 6 fugures
Keywords	Physics - Biological Physics ; Physics - Physics and Society ; Quantitative Biology - Populations and Evolution
Publishing date	2022-11-08
Publishing country	us
Document type	Book ; Online
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Article ; Online: Cell type-specific spatial and functional coupling between mammalian brain Kv2.1 K+ channels and ryanodine receptors.

Mandikian, Danielle / Bocksteins, Elke / Parajuli, Laxmi Kumar / Bishop, Hannah I / Cerda, Oscar / Shigemoto, Ryuichi / Trimmer, James S

The Journal of comparative neurology

2014 Volume 522, Issue 15, Page(s) 3555–3574

Abstract: The Kv2.1 voltage-gated K+ channel is widely expressed throughout mammalian brain ...

Abstract	The Kv2.1 voltage-gated K+ channel is widely expressed throughout mammalian brain, where it contributes to dynamic activity-dependent regulation of intrinsic neuronal excitability. Here we show that somatic plasma membrane Kv2.1 clusters are juxtaposed to clusters of intracellular ryanodine receptor (RyR) Ca2+ -release channels in mouse brain neurons, most prominently in medium spiny neurons (MSNs) of the striatum. Electron microscopy-immunogold labeling shows that in MSNs, plasma membrane Kv2.1 clusters are adjacent to subsurface cisternae, placing Kv2.1 in close proximity to sites of RyR-mediated Ca2+ release. Immunofluorescence labeling in transgenic mice expressing green fluorescent protein in specific MSN populations reveals the most prominent juxtaposed Kv2.1:RyR clusters in indirect pathway MSNs. Kv2.1 in both direct and indirect pathway MSNs exhibits markedly lower levels of labeling with phosphospecific antibodies directed against the S453, S563, and S603 phosphorylation site compared with levels observed in neocortical neurons, although labeling for Kv2.1 phosphorylation at S563 was significantly lower in indirect pathway MSNs compared with those in the direct pathway. Finally, acute stimulation of RyRs in heterologous cells causes a rapid hyperpolarizing shift in the voltage dependence of activation of Kv2.1, typical of Ca2+ /calcineurin-dependent Kv2.1 dephosphorylation. Together, these studies reveal that striatal MSNs are distinct in their expression of clustered Kv2.1 at plasma membrane sites juxtaposed to intracellular RyRs, as well as in Kv2.1 phosphorylation state. Differences in Kv2.1 expression and phosphorylation between MSNs in direct and indirect pathways provide a cell- and circuit-specific mechanism for coupling intracellular Ca2+ release to phosphorylation-dependent regulation of Kv2.1 to dynamically impact intrinsic excitability.
MeSH term(s)	Animals ; Brain/cytology ; Brain/physiology ; Brain/ultrastructure ; Cell Membrane/physiology ; Cell Membrane/ultrastructure ; Female ; HEK293 Cells ; Humans ; Membrane Potentials/physiology ; Mice, Knockout ; Mice, Transgenic ; Neurons/cytology ; Neurons/physiology ; Neurons/ultrastructure ; Phosphorylation ; Ryanodine Receptor Calcium Release Channel/genetics ; Ryanodine Receptor Calcium Release Channel/metabolism ; Shab Potassium Channels/genetics ; Shab Potassium Channels/metabolism
Chemical Substances	Ryanodine Receptor Calcium Release Channel ; Shab Potassium Channels
Language	English
Publishing date	2014-07-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3086-7
ISSN	1096-9861 ; 0021-9967 ; 0092-7317
ISSN (online)	1096-9861
ISSN	0021-9967 ; 0092-7317
DOI	10.1002/cne.23641
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Article ; Online: Retrograde Synaptic Signaling Mediated by K+ Efflux through Postsynaptic NMDA Receptors

Pei-Yu Shih / Leonid P. Savtchenko / Naomi Kamasawa / Yulia Dembitskaya / Thomas J. McHugh / Dmitri A. Rusakov / Ryuichi Shigemoto / Alexey Semyanov

Cell Reports, Vol 5, Iss 4, Pp 941-

2013 Volume 951

Abstract: ... and plasticity in dendritic spines. Whether the concurrent K+ efflux through the same receptors ... into the synaptic cleft has a physiological role is not known. Here, we report that NMDAR-dependent K+ efflux ... can provide a retrograde signal in the synapse. In hippocampal CA3-CA1 synapses, the bulk of astrocytic K+ ...

Abstract	Synaptic NMDA receptors (NMDARs) carry inward Ca2+ current responsible for postsynaptic signaling and plasticity in dendritic spines. Whether the concurrent K+ efflux through the same receptors into the synaptic cleft has a physiological role is not known. Here, we report that NMDAR-dependent K+ efflux can provide a retrograde signal in the synapse. In hippocampal CA3-CA1 synapses, the bulk of astrocytic K+ current triggered by synaptic activity reflected K+ efflux through local postsynaptic NMDARs. The local extracellular K+ rise produced by activation of postsynaptic NMDARs boosted action potential-evoked presynaptic Ca2+ transients and neurotransmitter release from Schaffer collaterals. Our findings indicate that postsynaptic NMDAR-mediated K+ efflux contributes to use-dependent synaptic facilitation, thus revealing a fundamental form of retrograde synaptic signaling.
Keywords	Biology (General) ; QH301-705.5
Subject code	571 ; 572
Language	English
Publishing date	2013-11-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article: Vitamin K ; Alters Bone Metabolism Markers in Hemodialysis Patients with a Low Serum Parathyroid Hormone Level

Ochiai, Mariko / Nakashima, Ayumu / Takasugi, Norihisa / Kiribayashi, Kei / Kawai, Toru / Usui, Koji / Shigemoto, Kenichiro / Hamaguchi, Naoki / Kohno, Nobuoki / Yorioka, Noriaki

Nephron Clinical Practice

2010 Volume 117, Issue 1, Page(s) c15–c19

Abstract: Background: A low level of intact parathyroid hormone (PTH) is an indicator of adynamic bone disease in hemodialysis patients, and is associated with a significant increase of all-cause mortality. Thus, effective treatment for adynamic bone disease is ... ...

Institution	Departments of Advanced Nephrology and Molecular and Internal Medicine, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Departments of Internal Medicine Onomichi Clinic, Onomichi Hakuai Clinic Clear Yakeyama Clinic, and Chuonaika Clinic, Kure, and Harada Hospital, Saeki, Japan
Abstract	Background: A low level of intact parathyroid hormone (PTH) is an indicator of adynamic bone disease in hemodialysis patients, and is associated with a significant increase of all-cause mortality. Thus, effective treatment for adynamic bone disease is required. We previously investigated the effect of vitamin K2 on adynamic bone disease. In this study, we assessed the efficacy of oral vitamin K2 in a controlled trial. Methods: Forty hemodialysis patients with low intact PTH levels (<100 pg/ml) were randomly divided into two groups, which were a vitamin K2 group receiving oral menatetrenone (45 mg/day) for 1 year and a control group without vitamin K2. Venous blood samples were collected at baseline and during the study for measurement of bone metabolism parameters. Results: Thirty-three patients completed follow-up. There was a significant increase of the serum intact osteocalcin level after 1 month of vitamin K2 administration. Serum levels of intact PTH, bone alkaline phosphatase, and cross-linked N-terminal telopeptide of type I collagen increased significantly after 12 months in the vitamin K2 group. The serum osteoprotegerin level was decreased after 12 months in the vitamin K2 group, but the change was not significant. Conclusion: Vitamin K2 therapy improves bone remodeling in hemodialysis patients with a low intact PTH level.
Keywords	Vitamin K ; Bone metabolism markers ; Intact parathyroid hormone ; Hemodialysis
Language	English
Publishing date	2010-08-03
Publisher	S. Karger AG
Publishing place	Basel, Switzerland
Document type	Article
Note	Original Paper
ZDB-ID	207121-6
ISSN	1660-2110 ; 1423-0186 ; 2235-3186 ; 1660-8151 ; 0028-2766
ISSN (online)	1660-2110 ; 1423-0186 ; 2235-3186
ISSN	1660-8151 ; 0028-2766
DOI	10.1159/000319642
Database	Karger publisher's database

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