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  • 1
    Language: English
    In: International journal of molecular sciences, 2021-04-21, Vol.22 (9), p.4321
    Description: Bone development is a tightly regulated process. Several integrated signaling pathways including HH, PTHrP, WNT, NOTCH, TGF-β, BMP, FGF and the transcription factors SOX9, RUNX2 and OSX are essential for proper skeletal development. Misregulation of these signaling pathways can cause a large spectrum of congenital conditions categorized as skeletal dysplasia. Since the signaling pathways involved in skeletal dysplasia interact at multiple levels and have a different role depending on the time of action (early or late in chondrogenesis and osteoblastogenesis), it is still difficult to precisely explain the physiopathological mechanisms of skeletal disorders. However, in recent years, significant progress has been made in elucidating the mechanisms of these signaling pathways and genotype-phenotype correlations have helped to elucidate their role in skeletogenesis. Here, we review the principal signaling pathways involved in bone development and their associated skeletal dysplasia.
    Subject(s): Animals ; Apoptosis ; Biomedical materials ; Bone Development ; Bone dysplasia ; Cartilage ; Cbfa-1 protein ; Chondrogenesis ; Congenital anomalies ; Extracellular matrix ; Fibroblast growth factor ; Genotype & phenotype ; Genotypes ; Growth factors ; Humans ; Kinases ; Ligands ; Mutation ; Osteoblastogenesis ; Osteochondrodysplasias - metabolism ; Osteochondrodysplasias - physiopathology ; Parathyroid hormone-related protein ; Pathways ; Phenotypes ; Proteins ; Review ; Signal Transduction ; Signaling ; signaling pathways ; skeletal dysplasia ; Skeletogenesis ; Skeleton ; Sox9 protein ; Transcription factors ; Wnt protein
    ISSN: 1661-6596
    E-ISSN: 1422-0067
    Source: Academic Search Ultimate
    Source: PubMed Central
    Source: DOAJ Directory of Open Access Journals - Not for CDI Discovery
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  • 2
    Language: English
    In: Therapeutic Advances in Endocrinology and Metabolism, 2020-03, Vol.11, p.2042018820904016-2042018820904016
    Description: The last few decades have been marked by the identification of numerous genes implicated in genetic disorders, helping in the elucidation of the underlying pathophysiology of these conditions. This has allowed new therapeutic approaches to emerge such as cellular therapy, gene therapy, or pharmacological therapy for various conditions. Skeletal dysplasias are good models to illustrate these scientific advances. Indeed, several therapeutic strategies are currently being investigated in osteogenesis imperfecta; there are ongoing clinical trials based on pharmacological approaches, targeting signaling pathways in achondroplasia and fibrodysplasia ossificans progressiva or the endoplasmic reticulum stress in metaphyseal dysplasia type Schmid or pseudoachondroplasia. Moreover, the treatment of hypophosphatasia or Morquio A disease illustrates the efficacy of enzyme drug replacement. To provide a highly specialized multidisciplinary approach, these treatments are managed by reference centers. The emergence of treatments in skeletal dysplasia provides new perspectives on the prognosis of these severe conditions and may change prenatal counseling in these diseases over the coming years.
    Subject(s): Achondroplasia ; Biomedical materials ; Bone dysplasia ; Clinical trials ; Dysplasia ; Endoplasmic reticulum ; endoplasmic reticulum stress ; fibrodysplasia ossificans progressiva ; Gene therapy ; Genetic disorders ; Health services ; Hypophosphatasia ; Medical treatment ; Musculoskeletal system ; Myositis ossificans ; Osteogenesis ; Osteogenesis imperfecta ; Pathophysiology ; Pharmacology ; Precision medicine ; Pseudoachondroplasia ; Review ; Skeleton
    ISSN: 2042-0188
    E-ISSN: 2042-0196
    Source: PubMed Central
    Source: DOAJ Directory of Open Access Journals - Not for CDI Discovery
    Source: ProQuest Central
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  • 3
    Language: English
    In: Orphanet journal of rare diseases, 2017-06-30, Vol.12 (1), p.123-123
    Description: Fibrodysplasia ossificans progressiva (FOP) is a rare, severely disabling, and life-shortening genetic disorder that causes the formation of heterotopic bone within soft connective tissue. Previous studies found that the FOP prevalence was about one in every two million lives. The aim of this study is to estimate the FOP prevalence in France by probabilistic record-linkage of 2 national databases: 1) the PMSI (Programme de médicalisation des systèmes d'information), an administrative database that records all hospitalization activities in France and 2) CEMARA, a registry database developed by the French Centres of Reference for Rare Diseases. Using a capture-recapture methodology to adjust the crude number of patients identified in both data sources, 89 FOP patients were identified, which results in a prevalence of 1.36 per million inhabitants (CI95% = [1.10; 1.68]). FOP patients' mean age was 25 years, only 14.9% were above 40 years, and 53% of them were males. The first symptoms - beside toe malformations- occurred after birth for 97.3% of them. Mean age at identified symptoms was 7 years and above 18 years for only 6.9% of patients. Mean age at diagnosis was 10 years, and above 18 years for 14.9% of the patients. FOP patients were distributed across France. Despite the challenge of ascertaining patients with rare diseases, we report a much higher prevalence of FOP in France than in previous studies elsewhere. We suggest that efforts to identify patients and confirm the diagnosis of FOP should be reinforced and extended at both national and European level.
    Subject(s): Adolescent ; Adult ; Age ; Bone diseases ; Bone growth ; Capture-recapture studies ; Child ; Classification ; Data bases ; Databases ; Databases, Factual ; Datasets ; Epidemiology ; Female ; Fibrodysplasia ossificans progressiva ; Fractures ; France - epidemiology ; Genetic disorders ; Humans ; Information systems ; Life Sciences ; Male ; Mutation ; Myositis ossificans ; Myositis Ossificans - epidemiology ; Patients ; Population ; Prevalence ; Prevalence studies (Epidemiology) ; Rare genetic diseases ; Research ; Studies ; Toe ; Young Adult
    ISSN: 1750-1172
    E-ISSN: 1750-1172
    Source: BioMedCentral Open Access
    Source: Academic Search Ultimate
    Source: PubMed Central
    Source: DOAJ Directory of Open Access Journals - Not for CDI Discovery
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  • 4
    Language: English
    In: American journal of human genetics, 2014-03-06, Vol.94 (3), p.405-414
    Description: Desbuquois dysplasia (DBQD) is a severe condition characterized by short stature, joint laxity, and advanced carpal ossification. Based on the presence of additional hand anomalies, we have previously distinguished DBQD type 1 and identified CANT1 (calcium activated nucleotidase 1) mutations as responsible for DBQD type 1. We report here the identification of five distinct homozygous xylosyltransferase 1 (XYLT1) mutations in seven DBQD type 2 subjects from six consanguineous families. Among the five mutations, four were expected to result in loss of function and a drastic reduction of XYLT1 cDNA level was demonstrated in two cultured individual fibroblasts. Because xylosyltransferase 1 (XT-I) catalyzes the very first step in proteoglycan (PG) biosynthesis, we further demonstrated in the two individual fibroblasts a significant reduction of cellular PG content. Our findings of XYLT1 mutations in DBQD type 2 further support a common physiological basis involving PG synthesis in the multiple dislocation group of disorders. This observation sheds light on the key role of the XT-I during the ossification process.
    Subject(s): Adolescent ; Adult ; Biochemistry ; Biochemistry, Molecular Biology ; Biosynthesis ; Bone and Bones - metabolism ; Cell culture ; Child ; Consanguinity ; Craniofacial Abnormalities - genetics ; DNA, Complementary - metabolism ; Dwarfism - genetics ; Dysplasia ; Enzymes ; Exome ; Female ; Fibroblasts - metabolism ; Genes ; Genetic aspects ; Genetic disorders ; Genetic Predisposition to Disease ; Genetics ; Health aspects ; Homozygote ; Human genetics ; Humans ; Joint Instability - genetics ; Life Sciences ; Male ; Microsatellite Repeats - genetics ; Mutation ; Mutation (Biology) ; Ossification, Heterotopic - genetics ; Pentosyltransferases - genetics ; Pentosyltransferases - metabolism ; Polydactyly - genetics ; Proteoglycans - metabolism ; Sequence Analysis, DNA
    ISSN: 0002-9297
    E-ISSN: 1537-6605
    Source: PubMed Central
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  • 5
    Language: English
    In: Journal of bone and mineral research, 2020-08, Vol.35 (8), p.1470-1480
    Description: ABSTRACT Osteogenesis imperfecta (OI) is a primary bone fragility disorder with an estimated prevalence of 1 in 15,000 births. The majority of OI cases are inherited in an autosomal‐dominant manner, while 5% to 10% have recessive or X‐linked inheritance. Up to now, approximately 5% of OI cases remain without mutation demonstrated, supporting the involvement of other genes in the disease spectrum. By whole‐exome sequencing, we identified a homozygous variant (c.2T〉C) in CCDC134 gene in three patients from two unrelated families with severe bone fragility that did not respond to bisphosphonate treatment, short stature, and gracile long bones with pseudarthroses but no dentinogenesis imperfecta. CCDC134 encodes a secreted protein widely expressed and implicated in the regulation of some mitogen‐activated protein kinases (MAPK) signaling pathway. Western blot and immunofluorescence analyses confirmed the absence of CCDC134 protein in patient cells compared with controls. Furthermore, we demonstrated that CCDC134 mutations are associated with increased Erk1/2 phosphorylation, decreased OPN mRNA and COL1A1 expression and reduced mineralization in patient osteoblasts compared with controls. These data support that CCDC134 is a new gene involved in severe progressive deforming recessive osteogenesis imperfecta (type III). © 2020 American Society for Bone and Mineral Research.
    Subject(s): CCDC134 ; Collagen (type I) ; Dentinogenesis ; Dentinogenesis imperfecta ; Extracellular signal-regulated kinase ; Gene expression ; Heredity ; Immunofluorescence ; Kinases ; MAP kinase ; MAPK PATHWAYS ; Mineralization ; mRNA ; Mutation ; OSTEOBLAST ; Osteoblasts ; Osteogenesis ; OSTEOGENESIS IMPERFECTA ; Phosphorylation ; Proteins ; Signal transduction ; WHOLE‐EXOME SEQUENCING
    ISSN: 0884-0431
    E-ISSN: 1523-4681
    Source: Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
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  • 6
    Language: English
    In: American journal of human genetics, 2009-05-15, Vol.84 (5), p.706-711
    Description: Jeune asphyxiating thoracic dystrophy (ATD) is an autosomal-recessive chondrodysplasia characterized by short ribs and a narrow thorax, short long bones, inconstant polydactyly, and trident acetabular roof. ATD is closely related to the short rib polydactyly syndrome (SRP) type III, which is a more severe condition characterized by early prenatal expression and lethality and variable malformations. We first excluded IFT80 in a series of 26 fetuses and children belonging to 14 families diagnosed with either ATD or SRP type III. Studying a consanguineous family from Morocco, we mapped an ATD gene to chromosome 11q14.3-q23.1 in a 20.4 Mb region and identified homozygous mutations in the cytoplasmic dynein 2 heavy chain 1 (DYNC2H1) gene in the affected children. Compound heterozygosity for DYNC2H1 mutations was also identified in four additional families. Among the five families, 3/5 were diagnosed with ATD and 2/5 included pregnancies terminated for SRP type III. DYNC2H1 is a component of a cytoplasmic dynein complex and is directly involved in the generation and maintenance of cilia. From this study, we conclude that ATD and SRP type III are variants of a single disorder belonging to the ciliopathy group.
    Subject(s): Biological and medical sciences ; Bone diseases ; Bones ; Carrier Proteins - genetics ; Carrier Proteins - metabolism ; Chromosomes, Human, Pair 11 - genetics ; Cytoplasmic Dyneins ; Diseases of the osteoarticular system ; Dynein ; Dyneins - chemistry ; Dyneins - genetics ; Family ; Fetuses ; Fundamental and applied biological sciences. Psychology ; General aspects. Genetic counseling ; Genes ; Genetic aspects ; Genetic research ; Genetics of eukaryotes. Biological and molecular evolution ; Genomics ; Humans ; Malformations and congenital and or hereditary diseases involving bones. Joint deformations ; Medical genetics ; Medical sciences ; Models, Molecular ; Molecular and cellular biology ; Mutation ; Pedigree ; Pregnant women ; Report ; Respiratory Insufficiency - genetics ; Short Rib-Polydactyly Syndrome - genetics ; Studies
    ISSN: 0002-9297
    E-ISSN: 1537-6605
    Source: Cell Press Collection [ECCPC]
    Source: PubMed Central
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  • 7
    Language: English
    In: American journal of human genetics, 2012-04-06, Vol.90 (4), p.740-745
    Description: Acrodysostosis is a rare autosomal-dominant condition characterized by facial dysostosis, severe brachydactyly with cone-shaped epiphyses, and short stature. Moderate intellectual disability and resistance to multiple hormones might also be present. Recently, a recurrent mutation (c.1102C〉T [p.Arg368∗]) in PRKAR1A has been identified in three individuals with acrodysostosis and resistance to multiple hormones. After studying ten unrelated acrodysostosis cases, we report here de novo PRKAR1A mutations in five out of the ten individuals (we found c.1102C〉T [p.Arg368∗] in four of the ten and c.1117T〉C [p.Tyr373His] in one of the ten). We performed exome sequencing in two of the five remaining individuals and selected phosphodiesterase 4D (PDE4D) as a candidate gene. PDE4D encodes a class IV cyclic AMP (cAMP)-specific phosphodiesterase that regulates cAMP concentration. Exome analysis detected heterozygous PDE4D mutations (c.673C〉A [p.Pro225Thr] and c.677T〉C [p.Phe226Ser]) in these two individuals. Screening of PDE4D identified heterozygous mutations (c.568T〉G [p.Ser190Ala] and c.1759A〉C [p.Thr587Pro]) in two additional acrodysostosis cases. These mutations occurred de novo in all four cases. The four individuals with PDE4D mutations shared common clinical features, namely characteristic midface and nasal hypoplasia and moderate intellectual disability. Metabolic screening was normal in three of these four individuals. However, resistance to parathyroid hormone and thyrotropin was consistently observed in the five cases with PRKAR1A mutations. Finally, our study further supports the key role of the cAMP signaling pathway in skeletogenesis.
    Subject(s): Adolescent ; Adult ; Analysis ; Base Sequence ; Biological and medical sciences ; Body height ; Brachydactyly ; Causes of ; Child ; Child, Preschool ; Congenital diseases ; Cyclic AMP ; Cyclic AMP-Dependent Protein Kinase RIalpha Subunit - genetics ; Cyclic Nucleotide Phosphodiesterases, Type 3 - genetics ; Cyclic Nucleotide Phosphodiesterases, Type 4 ; DNA sequencing ; Dwarfism ; Dysostoses - genetics ; Dysostosis ; Enzymes ; Epiphysis ; Exome - genetics ; Female ; Fundamental and applied biological sciences. Psychology ; Gene mutations ; General aspects. Genetic counseling ; Genetic aspects ; Genetics of eukaryotes. Biological and molecular evolution ; Genomics ; Hormones ; Humans ; Hypoplasia ; Intellectual Disability - genetics ; Male ; Medical genetics ; Medical sciences ; Mental retardation ; Molecular and cellular biology ; Molecular Sequence Data ; Mutation ; Nucleotide sequencing ; Osteochondrodysplasias - genetics ; Parathyroid hormone ; Parathyroid Hormone - metabolism ; phosphodiesterase ; Prosopagnosia ; Report ; Research ; Sequence Analysis, DNA ; Signal transduction ; Signal Transduction - genetics ; Skeletogenesis ; Thyroid-stimulating hormone ; Thyrotropin - metabolism ; Young Adult
    ISSN: 0002-9297
    E-ISSN: 1537-6605
    Source: Cell Press Collection [ECCPC]
    Source: PubMed Central
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  • 8
    Language: English
    In: Journal of medical genetics, 2014-08, Vol.51 (8), p.512-517
    Description: Background Overgrowth conditions are a heterogeneous group of disorders characterised by increased growth and variable features, including macrocephaly, distinctive facial appearance and various degrees of learning difficulties and intellectual disability. Among them, Sotos and Weaver syndromes are clinically well defined and due to heterozygous mutations in NSD1 and EZH2, respectively. NSD1 and EZH2 are both histone-modifying enzymes. These two epigenetic writers catalyse two specific post-translational modifications of histones: methylation of histone 3 lysine 36 (H3K36) and lysine 27 (H3K27). We postulated that mutations in writers of these two chromatin marks could cause overgrowth conditions, resembling Sotos or Weaver syndromes, in patients with no NSD1 or EZH2 abnormalities. Methods We analysed the coding sequences of 14 H3K27 methylation-related genes and eight H3K36 methylation-related genes using a targeted next-generation sequencing approach in three Sotos, 11 ‘Sotos-like’ and two Weaver syndrome patients. Results We identified two heterozygous mutations in the SETD2 gene in two patients with ‘Sotos-like’ syndrome: one missense p.Leu1815Trp de novo mutation in a boy and one nonsense p.Gln274* mutation in an adopted girl. SETD2 is non-redundantly responsible for H3K36 trimethylation. The two probands shared similar clinical features, including postnatal overgrowth, macrocephaly, obesity, speech delay and advanced carpal ossification. Conclusions Our results illustrate the power of targeted next-generation sequencing to identify rare disease-causing variants. We provide a compelling argument for Sotos and Sotos-like syndromes as epigenetic diseases caused by loss-of-function mutations of epigenetic writers of the H3K36 histone mark.
    Subject(s): Abnormalities, Multiple - genetics ; Analysis ; Care and treatment ; Congenital Hypothyroidism - genetics ; Craniofacial Abnormalities - genetics ; Diagnosis ; DNA Mutational Analysis ; Female ; Genetics ; Hand Deformities, Congenital - genetics ; Histone-Lysine N-Methyltransferase - genetics ; Humans ; Life Sciences ; Male ; Methylation ; Obesity ; Sotos Syndrome - genetics ; Weaver syndrome
    ISSN: 0022-2593
    E-ISSN: 1468-6244
    Source: Hellenic Academic Libraries Link
    Source: BMJ Journals - NESLi2
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  • 9
    Language: English
    In: The FASEB journal, 2019-02, Vol.33 (2), p.2707-2718
    Description: ABSTRACT Mutations in the a disintegrin and metalloproteinase with thrombospondin motif–like 2 (ADAMTSL2) gene are responsible for the autosomal recessive form of geleophysic dysplasia, which is characterized by short stature, short extremities, and skeletal abnormalities. However, the exact function of ADAMTSL2 is unknown. To elucidate the role of this protein in skeletal development, we generated complementary knockout (KO) mouse models with either total or chondrocyte Adamtsl2 deficiency. We observed that the Adamtsl2 KO mice displayed skeletal abnormalities reminiscent of the human phenotype. Adamtsl2 deletion affected the growth plate formation with abnormal differentiation and proliferation of chondrocytes. In addition, a TGF‐β signaling impairment in limbs lacking Adamtsl2 was demonstrated. Further investigations revealed that Adamtsl2 KO chondrocytes failed to establish a microfibrillar network composed by fibrillin1 and latent TGF‐β binding protein 1 fibrils. Chondrocyte Adamtsl2 KO mice also exhibited dwarfism. These studies uncover the function of Adamtsl2 in the maintenance of the growth plate ECM by modulating the microfibrillar network.—Delhon, L., Mahaut, C., Goudin, N., Gaudas, E., Piquand, K., Le Goff, W., Cormier‐Daire, V., Le Goff, C. Impairment of chondrogenesis and microfibrillar network in Adamtsl2 deficiency. FASEB J. 33, 2707–2718 (2019). www.fasebj.org
    Subject(s): Biochemistry & Molecular Biology ; Biology ; cartilage ; Cell Biology ; extracellular matrix ; geleophysic dysplasia ; Life Sciences ; Life Sciences & Biomedicine ; Life Sciences & Biomedicine - Other Topics ; mouse model ; Science & Technology
    ISSN: 0892-6638
    E-ISSN: 1530-6860
    Source: Federation of American Societies for Experimental Biology
    Source: Web of Science - Science Citation Index Expanded - 2019〈img src="http://exlibris-pub.s3.amazonaws.com/fromwos-v2.jpg" /〉
    Source: Get It Now
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  • 10
    Article
    Article
    2012
    ISSN: 1552-4868  ISSN: 0148-7299  ISSN: 1096-8628 
    Language: English
    In: American Journal of Medical Genetics Part C: Seminars in Medical Genetics, 2012-08-15, Vol.160C (3), p.145-153
    Description: The acromelic dysplasia group is characterized by short stature, short hands and feet, stiff joint, and “muscular” build. Four disorders can now be ascribed to this group, namely Weill–Marchesani syndrome (WMS), geleophysic dysplasia (GD), acromicric dysplasia (AD), and Myhre syndrome (MS). Although closely similar, they can be distinguished by subtle clinical features and their pattern inheritance. WMS is characterized by the presence of dislocation of microspherophakia and has autosomal dominant or recessive mode of inheritance. GD is the more severe one, with a progressive cardiac valvular thickening, tracheal stenosis, bronchopulmonary insufficiency, often leading to an early death. AD has an autosomal dominant mode of inheritance, distinct facial and skeleton features (a hoarse voice and internal notch of the femoral head). Finally, MS is sporadic, characterized by prognathism, deafness, developmental delay, thickened calvarium, and large vertebrae with short and large pedicles. We first identified mutations in Fibrillin‐1 (FBN1) in the dominant form of WMS and then mutations in A Disintegrin‐like And Metalloproteinase domain with ThromboSpondin type 1 repeats 10 (ADAMTS10) in the recessive form of WMS. The function of ADAMTS10 is unknown but these findings support a direct interaction between ADAMTS10 and FBN1. We then identified mutations in ADAMTSL2 in the recessive form of GD and a hotspot of mutations in FBN1 in the dominant form of GD and in AD (exon 41–42, encoding TGFβ binding protein‐like domain 5 (TB5) of FBN1). The function of ADAMTSL2 is unknown. Using a yeast double hybrid screen, we identified latent transforming growth factor‐β (TGFβ) binding protein 1 as a partner of ADAMTSL2. We found an increased level of active TGFβ in the fibroblast medium from patients with FBN1 or ADAMTSL2 mutations and an enhanced phosphorylated SMAD2 level, allowing us to conclude at an enhanced TGFβ signaling in GD and AD. Finally, a direct interaction between ADAMTSL2 and FBN1 was demonstrated suggesting a dysregulation of FBN1/ADAMTSL2 interrelationship as the underlying mechanism of the short stature phenotypes. Using exome sequencing in MS probands, we identified de novo SMAD4 missense mutations, all involving isoleucine residue at position 500, in the MH2 domain. In MS fibroblasts, we found decreased ubiquitination level of SMAD4 and increased level of SMAD4 supporting a stabilization of SMAD4 protein. Functional SMAD4 is required for canonical signal transduction through the oligomerization with phosphorylated SMAD2/3 and SMAD1/5/8. We therefore studied the nuclear localization of mutant SMAD complexes and found that the complexes translocate to the nucleus. We finally observed a decreased expression of downstream TGFβ target genes supporting impaired TGFβ driven transcriptional control in MS. Our findings support a direct link between the short stature phenotypes and the TGFβ signaling. However, the finding of enhanced TGFβ signaling in Marfan phenotypes supports the existence of yet unknown mechanisms regulating TGFβ action. © 2012 Wiley Periodicals, Inc.
    Subject(s): Body Height - physiology ; Bone Diseases, Developmental - metabolism ; Bone Diseases, Developmental - physiopathology ; Growth and Development - physiology ; Humans ; Marfan syndrome ; Signal Transduction ; Transforming Growth Factor beta - metabolism ; transforming growth factor-β
    ISSN: 1552-4868
    ISSN: 0148-7299
    ISSN: 1096-8628
    E-ISSN: 1096-8628
    E-ISSN: 1552-4876
    Source: Hellenic Academic Libraries Link
    Source: Wiley Online Library All Journals
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