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Article ; Online: Primary mouse osteoblast and osteoclast culturing and analysis.

Chevalier, Claire / Çolakoğlu, Melis / Brun, Julia / Thouverey, Cyril / Bonnet, Nicolas / Ferrari, Serge / Trajkovski, Mirko

STAR protocols

2021 Volume 2, Issue 2, Page(s) 100452

Abstract: Mesenchymal-derived osteoblasts play a key role in bone formation via synthesis and mineralization of the bone and bone remodeling. Osteoclasts are multinucleated cells of hematopoietic origin with a role in bone resorption. Here, we describe a protocol ... ...

Abstract	Mesenchymal-derived osteoblasts play a key role in bone formation via synthesis and mineralization of the bone and bone remodeling. Osteoclasts are multinucleated cells of hematopoietic origin with a role in bone resorption. Here, we describe a protocol for generating primary cultures of these two cell types from bone tissue including the femur, tibia, and humerus of young mice. We describe methods for addressing their activity and/or differentiation, enabling studying the effects of various treatments during or following differentiation
MeSH term(s)	Animals ; Mice ; Osteoblasts/cytology ; Osteoblasts/metabolism ; Osteoclasts/cytology ; Osteoclasts/metabolism ; Primary Cell Culture
Language	English
Publishing date	2021-04-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2666-1667
ISSN (online)	2666-1667
DOI	10.1016/j.xpro.2021.100452
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Article ; Online: Suppression of p38α MAPK Signaling in Osteoblast Lineage Cells Impairs Bone Anabolic Action of Parathyroid Hormone.

Thouverey, Cyril / Caverzasio, Joseph

Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

2016 Volume 31, Issue 5, Page(s) 985–993

Abstract: Intermittent parathyroid hormone administration (iPTH) increases bone mass and strength by stimulating osteoblast number and activity. PTH exerts its anabolic effects through cAMP/protein kinase A (PKA) signaling pathway in mature osteoblasts and ... ...

Abstract	Intermittent parathyroid hormone administration (iPTH) increases bone mass and strength by stimulating osteoblast number and activity. PTH exerts its anabolic effects through cAMP/protein kinase A (PKA) signaling pathway in mature osteoblasts and osteocytes. Here, we show that inactivation of the p38α MAPK-encoding gene with the use of an osteocalcin-cre transgene prevents iPTH bone anabolic action. Indeed, iPTH fails to increase insulin-like growth factor 1 expression, osteoblast number and activity, and bone formation in mice lacking p38α in osteoblasts and osteocytes. Moreover, iPTH-induced expression of receptor activator of NF-κB ligand (RANKL) and subsequent increased bone resorption are suppressed in those mice. Finally, we found that PTH activates p38α MAPK downstream of cAMP/PKA signaling pathway in mature osteoblasts. Our findings identify p38α MAPK as a key component of PTH signaling in osteoblast lineage cells and highlight its requirement in iPTH osteoanabolic activity. © 2015 American Society for Bone and Mineral Research.
Language	English
Publishing date	2016-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	632783-7
ISSN	1523-4681 ; 0884-0431
ISSN (online)	1523-4681
ISSN	0884-0431
DOI	10.1002/jbmr.2762
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Article ; Online: Selective inhibition of Src family kinases by SU6656 increases bone mass by uncoupling bone formation from resorption in mice.

Thouverey, Cyril / Ferrari, Serge / Caverzasio, Joseph

Bone

2018 Volume 113, Page(s) 95–104

Abstract: Mice deficient in the non-receptor tyrosine kinase Src exhibit high bone mass due to impaired bone resorption and increased bone formation. Although several Src family kinase inhibitors inhibit bone resorption in vivo, they display variable effects on ... ...

Abstract	Mice deficient in the non-receptor tyrosine kinase Src exhibit high bone mass due to impaired bone resorption and increased bone formation. Although several Src family kinase inhibitors inhibit bone resorption in vivo, they display variable effects on bone formation. SU6656 is a selective Src family kinase inhibitor with weaker activity towards the non-receptor tyrosine kinase Abl and receptor tyrosine kinases which are required for appropriate osteoblast proliferation, differentiation and function. Therefore, we sought to determine whether SU6656 could increase bone mass by inhibiting bone resorption and by stimulating bone formation, and to explore its mechanisms of action. Four-month-old female C57Bl/6J mice received intraperitoneal injections of either 25 mg/kg SU6656 or its vehicle every other day for 12 weeks. SU6656-treated mice exhibited increased bone mineral density, cortical thickness, cancellous bone volume and trabecular thickness. SU6656 inhibited bone resorption in mice as shown by reduced osteoclast number, and diminished expressions of Oscar, Trap5b and CtsK. SU6656 did not affect Rankl or Opg expressions. However, it blocked c-fms signaling, osteoclastogenesis and matrix resorption, and induced osteoclast apoptosis in vitro. In addition, SU6656 stimulated bone formation rates at trabecular, endosteal and periosteal bone envelopes, and increased osteoblast number in trabecular bone. SU6656 did not affect expressions of clastokines favoring bone formation in mice. However, it stimulated osteoblast differentiation and matrix mineralization by specifically facilitating BMP-SMAD signaling pathway in vitro. Knockdown of Src and Yes mimicked the stimulatory effect of SU6656 on osteoblast differentiation. In conclusion, SU6656 uncouples bone formation from resorption by inhibiting osteoclast development, function and survival, and by enhancing BMP-mediated osteoblast differentiation.
MeSH term(s)	Animals ; Bone Density/drug effects ; Bone Resorption/metabolism ; Female ; Indoles/pharmacology ; Mice ; Mice, Inbred C57BL ; Osteoblasts/drug effects ; Osteoclasts/drug effects ; Osteogenesis/drug effects ; Protein Kinase Inhibitors/pharmacology ; Sulfonamides/pharmacology ; src-Family Kinases/antagonists & inhibitors
Chemical Substances	Indoles ; Protein Kinase Inhibitors ; SU 6656 ; Sulfonamides ; src-Family Kinases (EC 2.7.10.2)
Language	English
Publishing date	2018-05-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	632515-4
ISSN	1873-2763 ; 8756-3282
ISSN (online)	1873-2763
ISSN	8756-3282
DOI	10.1016/j.bone.2018.05.006
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Zs.A 1571: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article: Focus on the p38 MAPK signaling pathway in bone development and maintenance.

Thouverey, Cyril / Caverzasio, Joseph

BoneKEy reports

2015 Volume 4, Page(s) 711

Abstract: The p38 mitogen-activated protein kinase (MAPK) signaling pathway can be activated in response to a wide range of extracellular signals. As a consequence, it can generate many different biological effects that depend on the stimulus and on the activated ... ...

Abstract	The p38 mitogen-activated protein kinase (MAPK) signaling pathway can be activated in response to a wide range of extracellular signals. As a consequence, it can generate many different biological effects that depend on the stimulus and on the activated cell type. Therefore, this pathway has been found to regulate many aspects of tissue development and homeostasis. Recent work with the aid of genetically modified mice has highlighted the physiological functions of this pathway in skeletogenesis and postnatal bone maintenance. In this review, emphasis is given to the roles of the p38 MAPK pathway in chondrocyte, osteoblast and osteoclast biology. In particular, we describe the molecular mechanisms of p38 MAPK activation and downstream targets. The requirement of this pathway in physiological bone development and homeostasis is demonstrated by the ability of p38 MAPK to regulate master transcription factors controlling geneses and functions of chondrocytes, osteoblasts and osteoclasts.
Language	English
Publishing date	2015-06-10
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2816308-4
ISSN	2047-6396
ISSN	2047-6396
DOI	10.1038/bonekey.2015.80
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Article ; Online: Ablation of p38α MAPK Signaling in Osteoblast Lineage Cells Protects Mice From Bone Loss Induced by Estrogen Deficiency.

Thouverey, Cyril / Caverzasio, Joseph

Endocrinology

2015 Volume 156, Issue 12, Page(s) 4377–4387

Abstract: Estrogen deficiency causes bone loss by increasing the number of bone-resorbing osteoclasts. Selective p38α MAPK inhibitors prevent bone-wasting effects of estrogen withdrawal but implicated mechanisms remain to be identified. Here, we show that ... ...

Abstract	Estrogen deficiency causes bone loss by increasing the number of bone-resorbing osteoclasts. Selective p38α MAPK inhibitors prevent bone-wasting effects of estrogen withdrawal but implicated mechanisms remain to be identified. Here, we show that inactivation of the p38α-encoding gene in osteoblast lineage cells with the use of an osteocalcin-cre transgene protects mice from ovariectomy-induced bone loss (a murine model of postmenopausal osteoporosis). Ovariectomy fails to induce bone loss, increase bone resorption, and stimulate receptor activator of nuclear factor κB ligand and IL-6 expression in mice lacking p38α in osteoblasts and osteocytes. Finally, TNFα or IL-1, which are osteoclastogenic cytokines overproduced in the bone marrow under estrogen deficiency, can activate p38α signaling in osteoblasts, but those cytokines cannot enhance Rankl and Il6 expressions or increase osteoclast formation in p38a-deficient osteoblast cultures. These findings demonstrate that p38α MAPK signaling in osteoblast lineage cells mediates ovariectomy-induced bone loss by up-regulating receptor activator of nuclear factor κB ligand and IL-6 production.
MeSH term(s)	Absorptiometry, Photon ; Animals ; Blotting, Western ; Bone Resorption/genetics ; Bone Resorption/metabolism ; Cells, Cultured ; Coculture Techniques ; Collagen Type I/metabolism ; Disease Models, Animal ; Estrogens/deficiency ; Gene Knockdown Techniques ; Humans ; Interleukin-1/metabolism ; Interleukin-6/metabolism ; Mice ; Mitogen-Activated Protein Kinase 14/genetics ; Osteoblasts/metabolism ; Osteoclasts/metabolism ; Osteocytes/metabolism ; Osteoporosis, Postmenopausal/genetics ; Osteoporosis, Postmenopausal/metabolism ; Ovariectomy ; RANK Ligand/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; Tumor Necrosis Factor-alpha/metabolism ; Up-Regulation ; X-Ray Microtomography
Chemical Substances	Collagen Type I ; Estrogens ; Interleukin-1 ; Interleukin-6 ; RANK Ligand ; Tnfsf11 protein, mouse ; Tumor Necrosis Factor-alpha ; interleukin-6, mouse ; Mitogen-Activated Protein Kinase 14 (EC 2.7.11.24)
Language	English
Publishing date	2015-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2015-1669
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Article: Sclerostin inhibits osteoblast differentiation without affecting BMP2/SMAD1/5 or Wnt3a/β-catenin signaling but through activation of platelet-derived growth factor receptor signaling in vitro.

Thouverey, Cyril / Caverzasio, Joseph

BoneKEy reports

2015 Volume 4, Page(s) 757

Abstract: Sclerostin inhibits bone formation mostly by antagonizing LRP5/6, thus inhibiting Wnt signaling. However, experiments with genetically modified mouse models suggest that a significant part of sclerostin-mediated inhibition of bone formation is due to ... ...

Abstract	Sclerostin inhibits bone formation mostly by antagonizing LRP5/6, thus inhibiting Wnt signaling. However, experiments with genetically modified mouse models suggest that a significant part of sclerostin-mediated inhibition of bone formation is due to interactions with other binding partners. The objective of the present work was to identify signaling pathways affected by sclerostin in relation with its inhibitory action on osteogenic differentiation of C3H10T1/2 cells, MC3T3-E1 cells and primary osteoblasts. Sclerostin inhibited BMP2-induced osteoblast differentiation without altering SMAD1/5 phosphorylation and transcriptional activity. Moreover, sclerostin prevented Wnt3a-mediated osteoblastogenesis without affecting LRP5/6 phosphorylation or β-catenin transcriptional activity. In addition, sclerostin inhibited mineralization promoted by GSK3 inhibition, which mimics canonical Wnt signaling without activation of LRP5/6, suggesting that sclerostin can prevent osteoblast differentiation without antagonizing LRP5/6. Finally, we found that sclerostin could activate platelet-derived growth factor receptor (PDGFR) and its downstream signaling pathways PLCγ, PKC, Akt and ERK1/2. PDGFR inhibition could reverse sclerostin-mediated inhibitory activity on BMP2-induced osteoblast differentiation. Therefore, our data suggest that sclerostin can activate PDGFR signaling by itself, and this functional interaction may be involved in the negative effect of sclerostin on osteoblast differentiation.
Language	English
Publishing date	2015-11-04
Publishing country	England
Document type	Journal Article
ZDB-ID	2816308-4
ISSN	2047-6396
ISSN	2047-6396
DOI	10.1038/bonekey.2015.126
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Article ; Online: Primary mouse osteoblast and osteoclast culturing and analysis

Claire Chevalier / Melis Çolakoğlu / Julia Brun / Cyril Thouverey / Nicolas Bonnet / Serge Ferrari / Mirko Trajkovski

STAR Protocols, Vol 2, Iss 2, Pp 100452- (2021)

2021

Abstract: Summary: Mesenchymal-derived osteoblasts play a key role in bone formation via synthesis and mineralization of the bone and bone remodeling. Osteoclasts are multinucleated cells of hematopoietic origin with a role in bone resorption. Here, we describe a ... ...

Abstract	Summary: Mesenchymal-derived osteoblasts play a key role in bone formation via synthesis and mineralization of the bone and bone remodeling. Osteoclasts are multinucleated cells of hematopoietic origin with a role in bone resorption. Here, we describe a protocol for generating primary cultures of these two cell types from bone tissue including the femur, tibia, and humerus of young mice. We describe methods for addressing their activity and/or differentiation, enabling studying the effects of various treatments during or following differentiation ex vivo.For further practical example of using these protocols, please refer to Chevalier et al. (2020).
Keywords	Cell Biology ; Cell culture ; Cell isolation ; Metabolism ; Cell Differentiation ; Science (General) ; Q1-390
Language	English
Publishing date	2021-06-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: PDGF Receptor Signaling in Osteoblast Lineage Cells Controls Bone Resorption Through Upregulation of Csf1 Expression.

Brun, Julia / Andreasen, Christina Møller / Ejersted, Charlotte / Andersen, Thomas Levin / Caverzasio, Joseph / Thouverey, Cyril

Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

2020 Volume 35, Issue 12, Page(s) 2458–2469

Abstract: The physiological functions of platelet-derived growth factor receptors (PDGFRs) α and β in osteoblast biology and bone metabolism remain to be established. Here, we show that PDGFRA and PDGFRB genes are expressed by osteoblast-lineage canopy and ... ...

Abstract	The physiological functions of platelet-derived growth factor receptors (PDGFRs) α and β in osteoblast biology and bone metabolism remain to be established. Here, we show that PDGFRA and PDGFRB genes are expressed by osteoblast-lineage canopy and reversal cells in close proximity to PDGFB-expressing osteoclasts within human trabecular bone remodeling units. We also report that, although removal of only one of the two PDGFRs in Osterix-positive cells does not affect bone phenotype, suppression of both PDGFRs in those osteoblast lineage cells increases trabecular bone volume in male mice as well as in female gonad-intact and ovariectomized mice. Furthermore, osteoblast lineage-specific suppression of PDGFRs reduces Csf1 expression, bone marrow level of macrophage colony-stimulating factor (M-CSF), number of osteoclasts, and, therefore, bone resorption, but does not change bone formation. Finally, abrogation of PDGFR signaling in osteoblasts blocks PDGF-induced ERK1/2-mediated Csf1 expression and M-CSF secretion in osteoblast cultures and calcitriol-mediated osteoclastogenesis in co-cultures. In conclusion, our results indicate that PDGFR signaling in osteoblast lineage cells controls bone resorption through ERK1/2-mediated Csf1 expression. © 2020 American Society for Bone and Mineral Research (ASBMR).
MeSH term(s)	Animals ; Bone Resorption ; Cell Differentiation ; Female ; Macrophage Colony-Stimulating Factor/metabolism ; Male ; Mice ; Osteoblasts/metabolism ; Osteoclasts/metabolism ; Receptors, Platelet-Derived Growth Factor ; Up-Regulation
Chemical Substances	CSF1 protein, mouse ; Macrophage Colony-Stimulating Factor (81627-83-0) ; Receptors, Platelet-Derived Growth Factor (EC 2.7.10.1)
Language	English
Publishing date	2020-09-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	632783-7
ISSN	1523-4681 ; 0884-0431
ISSN (online)	1523-4681
ISSN	0884-0431
DOI	10.1002/jbmr.4150
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Zs.A 2142: Show issues

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Article ; Online: The p38α MAPK positively regulates osteoblast function and postnatal bone acquisition.

Thouverey, Cyril / Caverzasio, Joseph

Cellular and molecular life sciences : CMLS

2012 Volume 69, Issue 18, Page(s) 3115–3125

Abstract: Bone continuously remodels throughout life by coordinated actions of osteoclasts and osteoblasts. Abnormalities in either osteoclast or osteoblast functions lead to bone disorders. The p38 MAPK pathway has been shown to be essential in controlling ... ...

Abstract	Bone continuously remodels throughout life by coordinated actions of osteoclasts and osteoblasts. Abnormalities in either osteoclast or osteoblast functions lead to bone disorders. The p38 MAPK pathway has been shown to be essential in controlling osteoblast differentiation and skeletogenesis. Although p38α is the most abundant p38 member in osteoblasts, its specific individual contribution in regulating postnatal osteoblast activity and bone metabolism is unknown. To elucidate the specific role of p38α in regulating osteoblast function and bone homeostasis, we generated mice lacking p38α in differentiated osteoblasts. Osteoblast-specific p38a knockout mice were of normal weight and size. Despite non-significant bone alterations until 5 weeks of age, mutant mice demonstrated significant and progressive decrease in bone mineral density from that age. Adult mice deficient in p38a in osteoblasts displayed a striking reduction in cancellous bone volume at both axial and appendicular skeletal sites. At 6 months of age, trabecular bone volume was reduced by 62% in those mice. Mutant mice also exhibited progressive decrease in cortical thickness of long bones. These abnormalities correlated with decreased endocortical and trabecular bone formation rate and reduced expressions of type 1 collagen, alkaline phosphatase, osteopontin and osteocalcin whereas bone resorption and osteoclasts remained unaffected. Finally, osteoblasts lacking p38α showed impaired marker gene expressions and defective mineralization in vitro. These findings indicate that p38α is an essential positive regulator of osteoblast function and postnatal bone formation in vivo.
MeSH term(s)	Age Factors ; Alkaline Phosphatase/genetics ; Animals ; Animals, Newborn ; Bone Density/genetics ; Bone Development/physiology ; Bone Resorption/genetics ; Collagen Type I/genetics ; Female ; Gene Expression Regulation, Developmental ; Mice ; Mice, Knockout ; Mitogen-Activated Protein Kinase 14/genetics ; Mitogen-Activated Protein Kinase 14/metabolism ; Osteoblasts/physiology ; Osteocalcin/genetics ; Osteogenesis/physiology ; Osteopontin/genetics
Chemical Substances	Collagen Type I ; Spp1 protein, mouse ; Osteocalcin (104982-03-8) ; Osteopontin (106441-73-0) ; Mitogen-Activated Protein Kinase 14 (EC 2.7.11.24) ; Alkaline Phosphatase (EC 3.1.3.1)
Language	English
Publishing date	2012-04-20
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-012-0983-8
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Zs.A 195: Show issues

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Article ; Online: Activation of FGF receptors is a new mechanism by which strontium ranelate induces osteoblastic cell growth.

Caverzasio, Joseph / Thouverey, Cyril

Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology

2011 Volume 27, Issue 3-4, Page(s) 243–250

Abstract: Background/aims: Strontium ranelate (SrRan) is an anti-osteoporotic treatment that reduces the risk of vertebral and hip fractures. Recent in vitro studies suggest that the effect of strontium ranelate on osteoblastic cell growth likely involves two ... ...

Abstract	Background/aims: Strontium ranelate (SrRan) is an anti-osteoporotic treatment that reduces the risk of vertebral and hip fractures. Recent in vitro studies suggest that the effect of strontium ranelate on osteoblastic cell growth likely involves two processes including activation of the calcium sensing receptor (CaSR) and a yet undefined mechanism. In the present study, we investigated the CaSR-independent molecular mechanism by which SrRan stimulates osteoblast growth. Methods: MC3T3-E1 and primary osteoblastic cells, specific inhibitors of receptor tyrosine kinases (RTK) and western blot analysis were used to characterize the CaSR-independent mechanism in osteoblastic cells. Results: A selective inhibitor of FGF receptor but not other RTK inhibitors markedly blunted cell growth induced by SrRan in osteoblastic cells. Associated with this observation, SrRan induced rapid activation of FGFR signaling pathways such as PLCγ, FRS2, Akt, ERK1,2 and p38. FGFR-dependent stimulation of osteogenic cell growth was also observed with other cations but not with neomycin, a selective CaSR agonist. Also, in cultured conditions used in this study, MC3T3-E1 cells and primary osteoblasts did not express the CaSR. Conclusion: data presented in this study suggest that activation of FGFRs is a new potential mechanism by which strontium can stimulate osteoblastic cell growth. Activation of FGFR-dependent cell growth is also observed in response to other cations suggesting that activation of FGF receptors is a new cation sensing mechanism in osteoblasts.
MeSH term(s)	Animals ; Bone Density Conservation Agents/pharmacology ; Cell Proliferation/drug effects ; Cells, Cultured ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Mitogen-Activated Protein Kinase 1/genetics ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3/genetics ; Mitogen-Activated Protein Kinase 3/metabolism ; Organometallic Compounds/pharmacology ; Osteoblasts/cytology ; Osteoblasts/drug effects ; Osteoblasts/metabolism ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; Receptors, Calcium-Sensing/agonists ; Receptors, Calcium-Sensing/metabolism ; Receptors, Fibroblast Growth Factor/antagonists & inhibitors ; Receptors, Fibroblast Growth Factor/metabolism ; Signal Transduction ; Thiophenes/pharmacology ; p38 Mitogen-Activated Protein Kinases/genetics ; p38 Mitogen-Activated Protein Kinases/metabolism
Chemical Substances	Bone Density Conservation Agents ; FRS2alpha protein, mouse ; Membrane Proteins ; Organometallic Compounds ; Receptors, Calcium-Sensing ; Receptors, Fibroblast Growth Factor ; Thiophenes ; strontium ranelate (04NQ160FRU) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Mitogen-Activated Protein Kinase 1 (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase 3 (EC 2.7.11.24) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2011-04-01
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1067572-3
ISSN	1421-9778 ; 1015-8987
ISSN (online)	1421-9778
ISSN	1015-8987
DOI	10.1159/000327950
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