LIVIVO - Search results -

Search results

Result 1 - 10 of total 26

Search options

Article ; Online: SOXC are critical regulators of adult bone mass.

Angelozzi, Marco / Karvande, Anirudha / Lefebvre, Véronique

2024 Volume 15, Issue 1, Page(s) 2956

Abstract: Pivotal in many ways for human health, the control of adult bone mass is governed by complex, incompletely understood crosstalk namely between mesenchymal stem cells, osteoblasts and osteoclasts. The SOX4, SOX11 and SOX12 (SOXC) transcription factors ... ...

Abstract	Pivotal in many ways for human health, the control of adult bone mass is governed by complex, incompletely understood crosstalk namely between mesenchymal stem cells, osteoblasts and osteoclasts. The SOX4, SOX11 and SOX12 (SOXC) transcription factors were previously shown to control many developmental processes, including skeletogenesis, and SOX4 was linked to osteoporosis, but how SOXC control adult bone mass remains unknown. Using SOXC loss- and gain-of-function mouse models, we show here that SOXC redundantly promote prepubertal cortical bone mass strengthening whereas only SOX4 mitigates adult trabecular bone mass accrual in early adulthood and subsequent maintenance. SOX4 favors bone resorption over formation by lowering osteoblastogenesis and increasing osteoclastogenesis. Single-cell transcriptomics reveals its prevalent expression in Lepr
MeSH term(s)	Mice ; Animals ; Humans ; Adult ; Mesenchymal Stem Cells/metabolism ; SOXC Transcription Factors/genetics ; SOXC Transcription Factors/metabolism
Chemical Substances	SOXC Transcription Factors ; SOX4 protein, human ; SOX12 protein, human
Language	English
Publishing date	2024-04-05
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-024-47413-2
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Article ; Online: Skeletal growth is enhanced by a shared role for SOX8 and SOX9 in promoting reserve chondrocyte commitment to columnar proliferation.

Molin, Arnaud N / Contentin, Romain / Angelozzi, Marco / Karvande, Anirudha / Kc, Ranjan / Haseeb, Abdul / Voskamp, Chantal / de Charleroy, Charles / Lefebvre, Véronique

Proceedings of the National Academy of Sciences of the United States of America

2024 Volume 121, Issue 8, Page(s) e2316969121

Abstract: SOX8 was linked in a genome-wide association study to human height heritability, but roles in chondrocytes for this close relative of the master chondrogenic transcription factor SOX9 remain unknown. We undertook here to fill this knowledge gap. High- ... ...

Abstract	SOX8 was linked in a genome-wide association study to human height heritability, but roles in chondrocytes for this close relative of the master chondrogenic transcription factor SOX9 remain unknown. We undertook here to fill this knowledge gap. High-throughput assays demonstrate expression of human
MeSH term(s)	Mice ; Humans ; Animals ; Chondrocytes/metabolism ; Genome-Wide Association Study ; SOX9 Transcription Factor/genetics ; SOX9 Transcription Factor/metabolism ; Gene Expression Regulation ; Cell Differentiation ; Cell Proliferation ; SOXE Transcription Factors/genetics ; SOXE Transcription Factors/metabolism
Chemical Substances	SOX9 Transcription Factor ; SOX8 protein, human ; SOXE Transcription Factors ; SOX9 protein, human
Language	English
Publishing date	2024-02-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2316969121
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1148: 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)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: SOXopathies: Growing Family of Developmental Disorders Due to SOX Mutations.

Angelozzi, Marco / Lefebvre, Véronique

Trends in genetics : TIG

2019 Volume 35, Issue 9, Page(s) 658–671

Abstract: The SRY-related (SOX) transcription factor family pivotally contributes to determining cell fate and identity in many lineages. Since the original discovery that SRY deletions cause sex reversal, mutations in half of the 20 human SOX genes have been ... ...

Abstract	The SRY-related (SOX) transcription factor family pivotally contributes to determining cell fate and identity in many lineages. Since the original discovery that SRY deletions cause sex reversal, mutations in half of the 20 human SOX genes have been associated with rare congenital disorders, henceforward called SOXopathies. Mutations are generally de novo, heterozygous, and inactivating, revealing gene haploinsufficiency, but other types, including duplications, have been reported too. Missense variants primarily target the HMG domain, the SOX hallmark that mediates DNA binding and bending, nuclear trafficking, and protein-protein interactions. We here review key clinical and molecular features of SOXopathies and discuss the prospect that the disease family likely involves more SOX genes and larger clinical and genetic spectrums than currently appreciated.
MeSH term(s)	Developmental Disabilities/etiology ; Developmental Disabilities/genetics ; Gene Expression Regulation, Developmental ; Haploinsufficiency ; Humans ; Mutation ; SOX Transcription Factors/chemistry ; SOX Transcription Factors/genetics ; SOX Transcription Factors/metabolism ; SOXD Transcription Factors/genetics ; Sex-Determining Region Y Protein/genetics
Chemical Substances	SOX Transcription Factors ; SOXD Transcription Factors ; SRY protein, human ; Sex-Determining Region Y Protein
Language	English
Publishing date	2019-07-06
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	619240-3
ISSN	1362-4555 ; 0168-9525 ; 0168-9479
ISSN (online)	1362-4555
ISSN	0168-9525 ; 0168-9479
DOI	10.1016/j.tig.2019.06.003
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 2272: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: EdU-Based Assay of Cell Proliferation and Stem Cell Quiescence in Skeletal Tissue Sections.

Angelozzi, Marco / de Charleroy, Charles R / Lefebvre, Véronique

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

2020 Volume 2230, Page(s) 357–365

Abstract: Identifying and tracking proliferating and quiescent cells in situ is an important phenotyping component of skeletal tissues in development, physiology and disease. Among all the methods that exist, which include immunostaining for cell cycle-specific ... ...

Abstract	Identifying and tracking proliferating and quiescent cells in situ is an important phenotyping component of skeletal tissues in development, physiology and disease. Among all the methods that exist, which include immunostaining for cell cycle-specific proteins, the gold standards use thymidine analogs. These compounds label proliferating cells by being incorporated into de novo-synthesized genomic DNA. 5-bromo-2'-deoxyuridine (BrdU) has traditionally been used for this purpose, but its detection is lengthy and requires harsh treatment of tissue sections to give access of anti-BrdU antibody to DNA. An alternative, more recently developed, uses 5-ethynyl-2'-deoxyuridine (EdU). This thymidine analog is detected by click chemistry, that is, covalent cross-linking of its ethynyl group with a fluorescent azide that is small enough to easily penetrate native tissues and reach DNA. In addition to being simple and quick, this EdU-based assay is compatible with other protocols, such as immunostaining, on the same tissue sections. We here describe an EdU-based protocol optimized to label and functionally assess actively proliferating cells as well as slowly dividing cells, including stem cells, in mouse skeletal tissues.
MeSH term(s)	Animals ; Bone Development/drug effects ; Bone and Bones/drug effects ; Bone and Bones/ultrastructure ; Cell Proliferation/drug effects ; Click Chemistry/methods ; Deoxyuridine/analogs & derivatives ; Deoxyuridine/pharmacology ; Flow Cytometry/methods ; Mice ; Staining and Labeling/methods
Chemical Substances	5-ethynyl-2'-deoxyuridine (G373S00W2J) ; Deoxyuridine (W78I7AY22C)
Language	English
Publishing date	2020-11-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-1028-2_21
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Single-cell atlas of craniogenesis uncovers SOXC-dependent, highly proliferative, and myofibroblast-like osteodermal progenitors.

Angelozzi, Marco / Pellegrino da Silva, Renata / Gonzalez, Michael V / Lefebvre, Véronique

Cell reports

2022 Volume 40, Issue 2, Page(s) 111045

Abstract: The mammalian skull vault is essential to shape the head and protect the brain, but the cellular and molecular events underlying its development remain incompletely understood. Single-cell transcriptomic profiling from early to late mouse embryonic ... ...

Abstract	The mammalian skull vault is essential to shape the head and protect the brain, but the cellular and molecular events underlying its development remain incompletely understood. Single-cell transcriptomic profiling from early to late mouse embryonic stages provides a detailed atlas of cranial lineages. It distinguishes various populations of progenitors and reveals a high expression of SOXC genes (encoding the SOX4, SOX11, and SOX12 transcription factors) early in development in actively proliferating and myofibroblast-like osteodermal progenitors. SOXC inactivation in these cells causes severe skull and skin underdevelopment due to the limited expansion of cell populations before and upon lineage commitment. SOXC genes enhance the expression of gene signatures conferring dynamic cellular and molecular properties, including actin cytoskeleton assembly, chromatin remodeling, and signaling pathway induction and responsiveness. These findings shed light onto craniogenic mechanisms and SOXC functions and suggest that similar mechanisms could decisively control many developmental, adult, pathological, and regenerative processes.
MeSH term(s)	Animals ; Gene Expression Regulation, Developmental ; Mammals/metabolism ; Mice ; Myofibroblasts/metabolism ; SOXC Transcription Factors/genetics ; SOXC Transcription Factors/metabolism
Chemical Substances	SOXC Transcription Factors
Language	English
Publishing date	2022-07-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2022.111045
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: SOX9 in cartilage development and disease.

Lefebvre, Véronique / Angelozzi, Marco / Haseeb, Abdul

Current opinion in cell biology

2019 Volume 61, Page(s) 39–47

Abstract: SOX9 is a pivotal transcription factor in chondrocytes, a lineage essential in skeletogenesis. Its mandatory role in transactivating many cartilage-specific genes is well established, whereas its pioneer role in lineage specification, which along with ... ...

Abstract	SOX9 is a pivotal transcription factor in chondrocytes, a lineage essential in skeletogenesis. Its mandatory role in transactivating many cartilage-specific genes is well established, whereas its pioneer role in lineage specification, which along with transactivation defines master transcription factors, remains to be better defined. Abundant, but yet incomplete evidence exists that intricate molecular networks control SOX9 activity during the multi-step chondrogenesis pathway. They include a highly modular genetic regulation, post-transcriptional and post-translational modifications, and varying sets of functional partners. Fully uncovering SOX9 actions and regulation is fundamental to explain mechanisms underlying many diseases that directly or indirectly affect SOX9 activities and to design effective disease treatments. We here review current knowledge, highlight recent discoveries, and propose new research directions to answer remaining questions.
MeSH term(s)	Animals ; Cartilage/metabolism ; Cartilage/pathology ; Chondrocytes/metabolism ; Chondrogenesis ; Gene Expression Regulation ; Humans ; Protein Processing, Post-Translational ; SOX9 Transcription Factor/chemistry ; SOX9 Transcription Factor/genetics ; SOX9 Transcription Factor/metabolism
Chemical Substances	SOX9 Transcription Factor
Language	English
Publishing date	2019-08-02
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1026381-0
ISSN	1879-0410 ; 0955-0674
ISSN (online)	1879-0410
ISSN	0955-0674
DOI	10.1016/j.ceb.2019.07.008
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 2963: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: SOX9 keeps growth plates and articular cartilage healthy by inhibiting chondrocyte dedifferentiation/osteoblastic redifferentiation.

Haseeb, Abdul / Kc, Ranjan / Angelozzi, Marco / de Charleroy, Charles / Rux, Danielle / Tower, Robert J / Yao, Lutian / Pellegrino da Silva, Renata / Pacifici, Maurizio / Qin, Ling / Lefebvre, Véronique

Proceedings of the National Academy of Sciences of the United States of America

2023 Volume 118, Issue 8

Abstract: Cartilage is essential throughout vertebrate life. It starts developing in embryos when osteochondroprogenitor cells commit to chondrogenesis, activate a pancartilaginous program to form cartilaginous skeletal primordia, and also embrace a growth-plate ... ...

Abstract	Cartilage is essential throughout vertebrate life. It starts developing in embryos when osteochondroprogenitor cells commit to chondrogenesis, activate a pancartilaginous program to form cartilaginous skeletal primordia, and also embrace a growth-plate program to drive skeletal growth or an articular program to build permanent joint cartilage. Various forms of cartilage malformation and degeneration diseases afflict humans, but underlying mechanisms are still incompletely understood and treatment options suboptimal. The transcription factor SOX9 is required for embryonic chondrogenesis, but its postnatal roles remain unclear, despite evidence that it is down-regulated in osteoarthritis and heterozygously inactivated in campomelic dysplasia, a severe skeletal dysplasia characterized postnatally by small stature and kyphoscoliosis. Using conditional knockout mice and high-throughput sequencing assays, we show here that SOX9 is required postnatally to prevent growth-plate closure and preosteoarthritic deterioration of articular cartilage. Its deficiency prompts growth-plate chondrocytes at all stages to swiftly reach a terminal/dedifferentiated stage marked by expression of chondrocyte-specific (
MeSH term(s)	Animals ; Cartilage, Articular/cytology ; Cartilage, Articular/metabolism ; Cell Differentiation ; Cell Lineage ; Chondrocytes/cytology ; Chondrocytes/metabolism ; Chondrogenesis ; Growth Plate/cytology ; Growth Plate/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Osteoblasts/cytology ; Osteoblasts/metabolism ; Osteogenesis ; SOX9 Transcription Factor/physiology
Chemical Substances	SOX9 Transcription Factor ; Sox9 protein, mouse
Language	English
Publishing date	2023-12-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2019152118
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1148: 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)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Genetic activation of glycolysis in osteoblasts preserves bone mass in type I diabetes.

Ji, Xing / Seeley, Rebecca / Li, Ke / Song, Fangfang / Liao, Xueyang / Song, Chao / Angelozzi, Marco / Valeri, Arianna / Marmo, Tyler / Lee, Wen-Chih / Shi, Yu / Long, Fanxin

Cell chemical biology

2023 Volume 30, Issue 9, Page(s) 1053–1063.e5

Abstract: Type I diabetes (T1D) impairs bone accrual in patients, but the mechanism is unclear. Here in a murine monogenic model for T1D, we demonstrate that diabetes suppresses bone formation resulting in a rapid loss of both cortical and trabecular bone. Single- ... ...

Abstract	Type I diabetes (T1D) impairs bone accrual in patients, but the mechanism is unclear. Here in a murine monogenic model for T1D, we demonstrate that diabetes suppresses bone formation resulting in a rapid loss of both cortical and trabecular bone. Single-cell RNA sequencing uncovers metabolic dysregulation in bone marrow osteogenic cells of diabetic mice. In vivo stable isotope tracing reveals impaired glycolysis in diabetic bone that is highly responsive to insulin stimulation. Remarkably, deletion of the insulin receptor reduces cortical but not trabecular bone. Increasing glucose uptake by overexpressing Glut1 in osteoblasts exacerbates bone defects in T1D mice. Conversely, activation of glycolysis by Pfkfb3 overexpression preserves both trabecular and cortical bone mass in the face of diabetes. The study identifies defective glucose metabolism in osteoblasts as a pathogenic mechanism for osteopenia in T1D, and furthermore implicates boosting osteoblast glycolysis as a potential bone anabolic therapy.
MeSH term(s)	Humans ; Mice ; Animals ; Diabetes Mellitus, Type 1/complications ; Diabetes Mellitus, Type 1/genetics ; Diabetes Mellitus, Type 1/metabolism ; Diabetes Mellitus, Experimental ; Osteoblasts/metabolism ; Bone Density ; Glycolysis
Language	English
Publishing date	2023-08-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	2451-9448
ISSN (online)	2451-9448
DOI	10.1016/j.chembiol.2023.07.003
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Details ▾
- Full text online
- Order with fees

Article ; Online: SOX9 is dispensable for the initiation of epigenetic remodeling and the activation of marker genes at the onset of chondrogenesis.

Liu, Chia-Feng / Angelozzi, Marco / Haseeb, Abdul / Lefebvre, Véronique

Development (Cambridge, England)

2018 Volume 145, Issue 14

Abstract: SOX9 controls cell lineage fate and differentiation in major biological processes. It is known as a potent transcriptional activator of differentiation-specific genes, but its earliest targets and its contribution to priming chromatin for gene activation ...

Abstract	SOX9 controls cell lineage fate and differentiation in major biological processes. It is known as a potent transcriptional activator of differentiation-specific genes, but its earliest targets and its contribution to priming chromatin for gene activation remain unknown. Here, we address this knowledge gap using chondrogenesis as a model system. By profiling the whole transcriptome and the whole epigenome of wild-type and
MeSH term(s)	Animals ; Chondrogenesis/physiology ; Chromatin Assembly and Disassembly/physiology ; Embryo, Mammalian/cytology ; Embryo, Mammalian/embryology ; Epigenesis, Genetic/physiology ; Gene Expression Regulation, Developmental/physiology ; Limb Buds/cytology ; Limb Buds/embryology ; Mice ; Mice, Transgenic ; Microfilament Proteins/biosynthesis ; Microfilament Proteins/genetics ; Myosin Heavy Chains/biosynthesis ; Myosin Heavy Chains/genetics ; Myosin Type II/biosynthesis ; Myosin Type II/genetics ; Nerve Tissue Proteins/biosynthesis ; Nerve Tissue Proteins/genetics ; SOX9 Transcription Factor/genetics ; SOX9 Transcription Factor/metabolism
Chemical Substances	FAM101A protein, mouse ; Microfilament Proteins ; Myh14 protein, mouse ; Nerve Tissue Proteins ; SOX9 Transcription Factor ; Sox9 protein, mouse ; Myosin Type II (EC 3.6.1.-) ; Myosin Heavy Chains (EC 3.6.4.1)
Language	English
Publishing date	2018-07-18
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	90607-4
ISSN	1477-9129 ; 0950-1991
ISSN (online)	1477-9129
ISSN	0950-1991
DOI	10.1242/dev.164459
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Ub I Zs.183: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 91: Show issues

Order via subito

Details ▾

Article ; Online: Human Adult Fibroblast-like Synoviocytes and Articular Chondrocytes Exhibit Prominent Overlap in Their Transcriptomic Signatures.

Jones, Kyle / Angelozzi, Marco / Gangishetti, Umesh / Haseeb, Abdul / de Charleroy, Charles / Lefebvre, Véronique / Bhattaram, Pallavi

ACR open rheumatology

2021 Volume 3, Issue 6, Page(s) 359–370

Abstract: Objectives: Fibroblast-like synoviocytes (FLS) and articular chondrocytes (AC) derive from a common pool of embryonic precursor cells. They are currently believed to engage in largely distinct differentiation programs to build synovium and articular ... ...

Abstract	Objectives: Fibroblast-like synoviocytes (FLS) and articular chondrocytes (AC) derive from a common pool of embryonic precursor cells. They are currently believed to engage in largely distinct differentiation programs to build synovium and articular cartilage and maintain healthy tissues throughout life. We tested this hypothesis by deeply characterizing and comparing their transcriptomic attributes. Methods: We profiled the transcriptomes of freshly isolated AC, synovium, primary FLS, and dermal fibroblasts from healthy adult humans using bulk RNA sequencing assays and downloaded published single-cell RNA sequencing data from freshly isolated human FLS. We integrated all data to define cell-specific signatures and validated findings with quantitative reverse transcription PCR of human samples and RNA hybridization of mouse joint sections. Results: We identified 212 AC and 168 FLS markers on the basis of exclusive or enriched expression in either cell and 294 AC/FLS markers on the basis of similar expression in both cells. AC markers included joint-specific and pan-cartilaginous genes. FLS and AC/FLS markers featured 37 and 55 joint-specific genes, respectively, and 131 and 239 pan-fibroblastic genes, respectively. These signatures included many previously unrecognized markers with potentially important joint-specific roles. AC/FLS markers overlapped in their expression patterns among all FLS and AC subpopulations, suggesting that they fulfill joint-specific properties in all, rather than in discrete, AC and FLS subpopulations. Conclusion: This study broadens knowledge and identifies a prominent overlap of the human adult AC and FLS transcriptomic signatures. It also provides data resources to help further decipher mechanisms underlying joint homeostasis and degeneration and to improve the quality control of tissues engineered for regenerative treatments.
Language	English
Publishing date	2021-05-01
Publishing country	United States
Document type	Journal Article
ISSN	2578-5745
ISSN (online)	2578-5745
DOI	10.1002/acr2.11255
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

To top

Your last searches

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED