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Article ; Online: Maxillo-Facial Morphology in Beckwith-Wiedemann Syndrome: A Preliminary Study on (epi)Genotype-Phenotype Association in Caucasians.

Defabianis, Patrizia / Mussa, Alessandro / Ninivaggi, Rossella / Carli, Diana / Romano, Federica

International journal of environmental research and public health

2022 Volume 19, Issue 4

Abstract: Beckwith-Wiedemann syndrome (BWS) is a congenital overgrowth disorder caused by various (epi)genetic alterations affecting the expression of genes on chromosome 11p15. Cardinal features include abdominal wall defects, macroglossia, and cancer ... ...

Abstract	Beckwith-Wiedemann syndrome (BWS) is a congenital overgrowth disorder caused by various (epi)genetic alterations affecting the expression of genes on chromosome 11p15. Cardinal features include abdominal wall defects, macroglossia, and cancer predisposition. Several (epi)genotype-phenotype associations were described so far, but specific studies on the evolution over time of maxillo-facial phenotype in the molecular subtypes still are scanty. The aim of this cross-sectional study was to associate maxillo-facial morphology and growth pattern with genoype in 25 Caucasian children with BWS and macroglossia. Twelve patients experienced a loss of metilation at imprinting center 2 (IC2-LoM), five had mosaic paternal uniparental isodisomy of chromosome 11 (UPD(11)pat), and eight were negative. A more marked tongue enlargement was detected in patients with IC2-LoM and negative genotype, while UPD(11)pat children showed mild macroglossia (
MeSH term(s)	Beckwith-Wiedemann Syndrome/genetics ; Cross-Sectional Studies ; DNA Methylation ; Genetic Association Studies ; Genomic Imprinting ; Humans ; Male ; Phenotype
Language	English
Publishing date	2022-02-20
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2175195-X
ISSN	1660-4601 ; 1661-7827
ISSN (online)	1660-4601
ISSN	1661-7827
DOI	10.3390/ijerph19042448
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Article ; Online: Mosaic RASopathies: A review of disorders caused by somatic pathogenic variants in the genes of the RAS/MAPK pathway.

Carli, Diana / Resta, Nicoletta / Ferrero, Giovanni Battista / Ruggieri, Martino / Mussa, Alessandro

American journal of medical genetics. Part C, Seminars in medical genetics

2022 Volume 190, Issue 4, Page(s) 520–529

Abstract: Mosaic RASopathies are a heterogeneous group of diseases characterized by the presence at birth or early onset of congenital anomalies, cutaneous and vascular anomalies, segmental overgrowth, and increased cancer risk. They are caused by somatic ... ...

Abstract	Mosaic RASopathies are a heterogeneous group of diseases characterized by the presence at birth or early onset of congenital anomalies, cutaneous and vascular anomalies, segmental overgrowth, and increased cancer risk. They are caused by somatic pathogenic variants of the genes belonging the RAt Sarcoma Mitogen-activated protein kinase (RAS/MAPK) pathway causing its hyperactivation. Here, we review the clinical and molecular characteristics of this heterogeneous group of diseases, including the possibilities of molecular diagnosis and new therapeutic perspectives.
MeSH term(s)	Mitogen-Activated Protein Kinases/genetics ; Mitogen-Activated Protein Kinases/metabolism ; ras Proteins/genetics
Chemical Substances	Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; ras Proteins (EC 3.6.5.2)
Language	English
Publishing date	2022-12-02
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2108622-9
ISSN	1552-4876 ; 0148-7299 ; 1552-4868
ISSN (online)	1552-4876
ISSN	0148-7299 ; 1552-4868
DOI	10.1002/ajmg.c.32021
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Article ; Online: Beckwith-Wiedemann Syndrome Negligible Effects on Tumor Risk Associated With In Vitro Fertilization.

Carli, Diana / Ferrero, Giovanni Battista / Mussa, Alessandro

JAMA pediatrics

2019 Volume 173, Issue 10, Page(s) 996

Language	English
Publishing date	2019-10-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	2701223-2
ISSN	2168-6211 ; 2168-6203
ISSN (online)	2168-6211
ISSN	2168-6203
DOI	10.1001/jamapediatrics.2019.2355
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Article: Lateralized and Segmental Overgrowth in Children.

Mussa, Alessandro / Carli, Diana / Cardaropoli, Simona / Ferrero, Giovanni Battista / Resta, Nicoletta

Cancers

2021 Volume 13, Issue 24

Abstract: Congenital disorders of lateralized or segmental overgrowth (LO) are heterogeneous conditions with increased tissue growth in a body region. LO can affect every region, be localized or extensive, involve one or several embryonic tissues, showing variable ...

Abstract	Congenital disorders of lateralized or segmental overgrowth (LO) are heterogeneous conditions with increased tissue growth in a body region. LO can affect every region, be localized or extensive, involve one or several embryonic tissues, showing variable severity, from mild forms with minor body asymmetry to severe ones with progressive tissue growth and related relevant complications. Recently, next-generation sequencing approaches have increased the knowledge on the molecular defects in LO, allowing classifying them based on the deranged cellular signaling pathway. LO is caused by either genetic or epigenetic somatic anomalies affecting cell proliferation. Most LOs are classifiable in the Beckwith-Wiedemann spectrum (BWSp), PI3KCA/AKT-related overgrowth spectrum (PROS/AROS), mosaic RASopathies, PTEN Hamartoma Tumor Syndrome, mosaic activating variants in angiogenesis pathways, and isolated LO (ILO). These disorders overlap over common phenotypes, making their appraisal and distinction challenging. The latter is crucial, as specific management strategies are key: some LO is associated with increased cancer risk making imperative tumor screening since childhood. Interestingly, some LO shares molecular mechanisms with cancer: recent advances in tumor biological pathway druggability and growth downregulation offer new avenues for the treatment of the most severe and complicated LO.
Language	English
Publishing date	2021-12-07
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13246166
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Article ; Online: Syndromic Disorders Caused by Disturbed Human Imprinting

Carli, Diana / Riberi, Evelise / Ferrero, Giovanni Battista / Mussa, Alessandro

Journal of clinical research in pediatric endocrinology

2019 Volume 12, Issue 1, Page(s) 1–16

Abstract: Imprinting disorders are a group of congenital diseases caused by dysregulation of genomic imprinting, affecting prenatal and postnatal growth, neurocognitive development, metabolism and cancer predisposition. Aberrant expression of imprinted genes can ... ...

Abstract	Imprinting disorders are a group of congenital diseases caused by dysregulation of genomic imprinting, affecting prenatal and postnatal growth, neurocognitive development, metabolism and cancer predisposition. Aberrant expression of imprinted genes can be achieved through different mechanisms, classified into epigenetic - if not involving DNA sequence change - or genetic in the case of altered genomic sequence. Despite the underlying mechanism, the phenotype depends on the parental allele affected and opposite phenotypes may result depending on the involvement of the maternal or the paternal chromosome. Imprinting disorders are largely underdiagnosed because of the broad range of clinical signs, the overlap of presentation among different disorders, the presence of mild phenotypes, the mitigation of the phenotype with age and the limited availability of molecular techniques employed for diagnosis. This review briefly illustrates the currently known human imprinting disorders, highlighting endocrinological aspects of pediatric interest.
MeSH term(s)	Abnormalities, Multiple/genetics ; Child ; Diabetes Mellitus/genetics ; Genomic Imprinting/genetics ; Humans ; Infant, Newborn, Diseases/genetics ; Intellectual Disability/genetics ; Pseudohypoparathyroidism/genetics ; Puberty, Precocious/genetics ; Syndrome ; Uniparental Disomy/genetics
Language	English
Publishing date	2019-04-10
Publishing country	Turkey
Document type	Journal Article ; Review
ZDB-ID	2641608-6
ISSN	1308-5735 ; 1308-5727
ISSN (online)	1308-5735
ISSN	1308-5727
DOI	10.4274/jcrpe.galenos.2019.2018.0249
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Article ; Online: Functional evaluation of a novel nonsense variant of the calcium-sensing receptor gene leading to hypocalcemia.

Saglia, Claudia / Arruga, Francesca / Scolari, Caterina / Kalantari, Silvia / Albanese, Serena / Bracciamà, Valeria / Corso Faini, Angelo / Brach Del Prever, Giulia / Luca, Maria / Romeo, Carmelo / Mioli, Fiorenza / Migliorero, Martina / Tessaris, Daniele / Carli, Diana / Amoroso, Antonio / Vaisitti, Tiziana / De Sanctis, Luisa / Deaglio, Silvia

European journal of endocrinology

2024 Volume 190, Issue 4, Page(s) 296–306

Abstract: Objective: The calcium-sensing receptor (CASR) gene encodes a G protein-coupled receptor crucial for calcium homeostasis. Gain-of-function CASR variants result in hypocalcemia, while loss-of-function variants lead to hypercalcemia. This study aims to ... ...

Abstract	Objective: The calcium-sensing receptor (CASR) gene encodes a G protein-coupled receptor crucial for calcium homeostasis. Gain-of-function CASR variants result in hypocalcemia, while loss-of-function variants lead to hypercalcemia. This study aims to assess the functional consequences of the novel nonsense CASR variant [c.2897_2898insCTGA, p.(Gln967) (Q967)] identified in adolescent patient with chronic hypocalcemia, a phenotype expected for a gain-of-function variants. Design and methods: To functionally characterize the Q967* mutant receptor, both wild-type (WT) and mutant CASR were transiently transfected into HEK293T cells and calcium-sensing receptor (CaSR) protein expression and functions were comparatively evaluated using multiple read-outs. Results: Western blot analysis revealed that the CaSR mutant protein displayed a lower molecular weight compared with the WT, consistent with the loss of the last 122 amino acids in the intracellular domain. Mitogen-activated protein kinase activation and serum responsive element luciferase assays demonstrated that the mutant receptor had higher baseline activity than the WT. Extracellular-signal-regulated kinase/c-Jun N-terminal kinase phosphorylation, however, remained consistently high in the mutant, without significant modulations following exposure to increasing extracellular calcium (Ca2+o) levels, suggesting that the mutant receptor is more sensitive to Ca2+o compared with the WT. Conclusions: This study provides functional validation of the pathogenicity of a novel nonsense CASR variant, resulting in an abnormally hyperfunctioning protein consistent with the patient's phenotype. Functional analyses indicate that mutant receptor is constitutively active and poorly sensitive to increasing concentrations of extracellular calcium, suggesting that the cytoplasmic tail may contain elements regulating signal transduction.
MeSH term(s)	Adolescent ; Humans ; Hypocalcemia/genetics ; Calcium ; Receptors, Calcium-Sensing/genetics ; HEK293 Cells ; Hypercalcemia/genetics ; Mutation/genetics
Chemical Substances	Calcium (SY7Q814VUP) ; Receptors, Calcium-Sensing
Language	English
Publishing date	2024-04-01
Publishing country	England
Document type	Journal Article
ZDB-ID	1183856-5
ISSN	1479-683X ; 0804-4643
ISSN (online)	1479-683X
ISSN	0804-4643
DOI	10.1093/ejendo/lvae035
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Article: Implications of an Underlying Beckwith-Wiedemann Syndrome for Wilms Tumor Treatment Strategies.

Quarello, Paola / Carli, Diana / Biasoni, Davide / Gerocarni Nappo, Simona / Morosi, Carlo / Cotti, Roberta / Garelli, Emanuela / Zucchetti, Giulia / Spadea, Manuela / Tirtei, Elisa / Spreafico, Filippo / Fagioli, Franca

Cancers

2023 Volume 15, Issue 4

Abstract: Beckwith-Wiedemann Syndrome (BWS) is a pediatric overgrowth disorder involving a predisposition to embryonal tumors. Most of the tumors associated with BWS occur in the first 8-10 years of life, and the most common is Wilms tumor (WT). BWS clinical ... ...

Abstract	Beckwith-Wiedemann Syndrome (BWS) is a pediatric overgrowth disorder involving a predisposition to embryonal tumors. Most of the tumors associated with BWS occur in the first 8-10 years of life, and the most common is Wilms tumor (WT). BWS clinical heterogeneity includes subtle overgrowth features or even silent phenotypes, and WT may be the presenting symptom of BWS. WT in BWS individuals exhibit distinct characteristics from those of sporadic WT, and the management of these patients needs a peculiar approach. The most important feature is a higher risk of developing bilateral disease at some time in the course of the illness (synchronous bilateral disease at diagnosis or metachronous recurrence after initial presentation with unilateral disease). Accordingly, neoadjuvant chemotherapy is the recommended approach also for BWS patients with unilateral WT to facilitate nephron-sparing surgical approaches. This review emphasizes the importance of early BWS recognition, particularly if a WT has already occurred, as this will result in an urgent consideration of first-line cancer therapy.
Language	English
Publishing date	2023-02-17
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers15041292
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Article ; Online: Mulibrey nanism and immunological complications: a comprehensive case report and literature review.

Gazzin, Andrea / Pala, Francesca / Bosticardo, Marita / Niemela, Julie / Stoddard, Jennifer / Biasin, Eleonora / Quarello, Paola / Carli, Diana / Ferroni, Francesca / Delmonte, Ottavia M / Montin, Davide / Rosenzweig, Sergio D / Licciardi, Francesco / Notarangelo, Luigi D

Frontiers in immunology

2023 Volume 14, Page(s) 1303251

Abstract: Introduction: Mulibrey nanism (MUL) is a rare disorder caused by : Methods: We present a case of MUL with progressive lymphopenia and review similar cases from the literature.: Results: Our patient presented with prenatal onset growth restriction, ...

Abstract	Introduction: Mulibrey nanism (MUL) is a rare disorder caused by Methods: We present a case of MUL with progressive lymphopenia and review similar cases from the literature. Results: Our patient presented with prenatal onset growth restriction, characteristic dysmorphic features, and Wilms' tumor. She developed progressive lymphopenia starting at 10 years of age, leading to the initiation of intravenous immunoglobulin (IVIG) replacement therapy and infection prophylaxis. Genetic analysis detected a likely pathogenic variant on the maternal allele and copy number loss on the paternal allele in Discussion: The immunological profile of MUL patients reported so far shares similarities with that described in protein-losing enteropathy secondary to CHF in Fontan circulation and primary intestinal lymphangiectasia. These similarities include hypogammaglobulinemia, significant T-cell deficiency with decreased CD4+ and CD8+ counts, altered CD4+/CD8+ ratios, and significantly modified CD4+ and CD8+ T-cell phenotypes toward effector and terminal differentiated T cells, accompanied by a loss of naïve CD45RA+ T lymphocytes. In MUL, CHF is a cardinal feature, occurring in a significant proportion of patients and influencing prognosis. Signs of CHF or constrictive pericarditis have been evident in the case reported here and in all cases of MUL with documented immune dysfunction reported so far. These observations raise intriguing connections between these conditions. However, further investigation is warranted to in-depth define the immunological defect, providing valuable insights into the pathophysiology and treatment strategies for this condition.
MeSH term(s)	Female ; Humans ; Agammaglobulinemia/complications ; Heart Failure/etiology ; Heart Failure/therapy ; Immunoglobulins, Intravenous/therapeutic use ; Kidney Neoplasms/genetics ; Lymphopenia/complications ; Mulibrey Nanism/genetics ; Mutation ; Nuclear Proteins/genetics ; Tripartite Motif Proteins/genetics ; Ubiquitin-Protein Ligases/genetics ; Wilms Tumor/complications
Chemical Substances	Immunoglobulins, Intravenous ; Nuclear Proteins ; TRIM37 protein, human (EC 2.3.2.27) ; Tripartite Motif Proteins ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
Language	English
Publishing date	2023-12-05
Publishing country	Switzerland
Document type	Case Reports ; Journal Article ; Review ; Research Support, N.I.H., Intramural
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.1303251
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Article ; Online: Epidemiology of the disorders of the Pik3ca-related overgrowth spectrum (Pros).

Reynolds, Giuseppe / Cardaropoli, Simona / Carli, Diana / Luca, Maria / Gazzin, Andrea / Coppo, Paola / La Selva, Roberta / Piglionica, Marilidia / Bagnulo, Rosanna / Turchiano, Antonella / Ranieri, Carlotta / Resta, Nicoletta / Mussa, Alessandro

European journal of human genetics : EJHG

2023 Volume 31, Issue 11, Page(s) 1333–1336

Abstract: PIK3CA pathogenic variants are responsible for a group of overgrowth syndromes, collectively known as PIK3CA-Related Overgrowth Spectrum (PROS). These gain-of-function variants arise postzygotically, and, according to time of onset, kind of embryonal ... ...

Abstract	PIK3CA pathogenic variants are responsible for a group of overgrowth syndromes, collectively known as PIK3CA-Related Overgrowth Spectrum (PROS). These gain-of-function variants arise postzygotically, and, according to time of onset, kind of embryonal tissue affected and regional body extension, give rise to heterogeneous phenotypes. PROS rarity and heterogeneity hamper the correct estimation of its epidemiology. Our work represents the first attempt to define the prevalence of PROS according to the established diagnostic criteria and molecular analysis and based on solid demographic data. We assessed the prevalence in Piedmont Region (Italy), including in the study all participants diagnosed with PROS born there from 1998 to 2021. The search identified 37 cases of PROS born across the 25-year period, providing a prevalence of 1:22,313 live births. Molecular analysis was positive in 81.0% of participants. Taking into account the cases with a detected variant in PIK3CA (n = 30), prevalence of molecularly positive PROS was 1:27,519.
MeSH term(s)	Humans ; Mutation ; Growth Disorders/epidemiology ; Growth Disorders/genetics ; Growth Disorders/diagnosis ; Phenotype ; Class I Phosphatidylinositol 3-Kinases/genetics ; Syndrome
Chemical Substances	Class I Phosphatidylinositol 3-Kinases (EC 2.7.1.137)
Language	English
Publishing date	2023-06-26
Publishing country	England
Document type	Journal Article
ZDB-ID	1141470-4
ISSN	1476-5438 ; 1018-4813
ISSN (online)	1476-5438
ISSN	1018-4813
DOI	10.1038/s41431-023-01414-9
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Article ; Online: Chronic subdural hematoma: A previously unreported life-threatening complication in adult with Sotos syndrome.

Carli, Diana / Gazzin, Andrea / Bongioanni, Maria Roberta / Bergui, Mauro / Mussa, Alessandro / Ferrero, Giovanni Battista

American journal of medical genetics. Part A

2020 Volume 182, Issue 12, Page(s) 3052–3055

Abstract: Macrocephaly, defined as head circumference ≥ 2 SDs, is a cardinal feature of Sotos syndrome (SS) and generally persists in adulthood. Subdural fluid collection, typically associated with macrocephaly, is described in children due to anatomical ... ...

Abstract	Macrocephaly, defined as head circumference ≥ 2 SDs, is a cardinal feature of Sotos syndrome (SS) and generally persists in adulthood. Subdural fluid collection, typically associated with macrocephaly, is described in children due to anatomical conformation, and in adulthood due to brain atrophy and ex-vacuo hydrocephalus. On the other hand, a true, symptomatic, chronic subdural hematoma (CSH) is a previously unreported complication of SS in adulthood. Here we describe the first SS patient presenting symptomatic CSH, leading to frequent hospitalizations for surgical evacuations that consistently recurred. Middle meningeal artery (MMA) embolization and epidural blood patch (EBP) allowed to resolve the CSH with complete resolution of clinical signs and symptoms. We hypothesize that appearance and recurrences of CSH may be related to pathological biomechanics of brain, cerebro-spinal fluid and skull, secondary to anatomical features of SS. In this context, surgical evacuation may be less efficient than usual to cure CSH. Alternative treatment to avoid blood extravasation, as MMA embolization, or to cure concurrent causes of the pathology, as EBP, may be considered.
MeSH term(s)	Adult ; Embolization, Therapeutic/methods ; Female ; Hematoma, Subdural, Chronic/etiology ; Hematoma, Subdural, Chronic/pathology ; Hematoma, Subdural, Chronic/therapy ; Humans ; Meningeal Arteries/surgery ; Sotos Syndrome/complications ; Treatment Outcome
Language	English
Publishing date	2020-10-14
Publishing country	United States
Document type	Case Reports ; Journal Article
ZDB-ID	2108614-X
ISSN	1552-4833 ; 0148-7299 ; 1552-4825
ISSN (online)	1552-4833
ISSN	0148-7299 ; 1552-4825
DOI	10.1002/ajmg.a.61900
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