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  1. Artikel: Sterol 27-Hydroxylase Deficiency as a Cause of Neonatal Cholestasis: Report of 2 Cases and Review of the Literature.

    Lipiński, Patryk / Klaudel-Dreszler, Maja / Ciara, Elzbieta / Jurkiewicz, Dorota / Płoski, Rafał / Cielecka-Kuszyk, Joanna / Socha, Piotr / Jankowska, Irena

    Frontiers in pediatrics

    2021  Band 8, Seite(n) 616582

    Abstract: Introduction: ...

    Abstract Introduction:
    Sprache Englisch
    Erscheinungsdatum 2021-01-13
    Erscheinungsland Switzerland
    Dokumenttyp Case Reports
    ZDB-ID 2711999-3
    ISSN 2296-2360
    ISSN 2296-2360
    DOI 10.3389/fped.2020.616582
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Pathogenic Potential of a PCK1 Gene Variant in Cytosolic PEPCK Deficiency: A Compelling Case Study.

    Duś-Żuchowska, Monika / Nowak, Hanna / Kałużny, Łukasz / Rokicki, Dariusz / Ciara, Elżbieta / Piekutowska-Abramczuk, Dorota / Walkowiak, Jarosław

    The American journal of case reports

    2024  Band 25, Seite(n) e943118

    Abstract: BACKGROUND Cytosolic phosphoenolpyruvate carboxykinase (PEPCK-C) deficiency is an extremely rare autosomal recessive inherited error of metabolism in which gluconeogenesis is impaired, resulting in life-threatening episodes of hypoglycemia and metabolic ... ...

    Abstract BACKGROUND Cytosolic phosphoenolpyruvate carboxykinase (PEPCK-C) deficiency is an extremely rare autosomal recessive inherited error of metabolism in which gluconeogenesis is impaired, resulting in life-threatening episodes of hypoglycemia and metabolic acidosis. The diagnosis of gluconeogenesis disorders is challenging. In the diagnostic pathway, the molecular test plays a paramount role. CASE REPORT The aim of the paper is to present the case report of a girl with recurrent episodes of severe hypoglycemia, in whom molecular diagnosis enabled the confirmation of PEPCK - C deficiency. The patient experienced 4 episodes of severe hypoglycemia. Most of them were accompanied by hyperlacticaemia, metabolic acidosis, and elevated liver enzymes. All of the metabolic decompensations were triggered by infectious agents. The episodes resolved after continuous infusion of high-dose glucose. Due to the recurrent character of the disease, a genetic condition was suspected. The differential diagnosis included metabolic and endocrinological causes of hypoglycemia. Two variants in the PCK1 gene were detected: c.265G>A p.(Glu89Lys) in exon 3 and c.925G>A p.(Gly309Arg) in exon 6. As c.925G>A p.(Gly309Arg) is a known pathogenic variant, the second variant was first described in June 2023 in the ClinVar database and described as "with unknown clinical significance". CONCLUSIONS According to the clinical symptoms observed in the presented case, the variant c.265G>A p.(Glu89Lys) in PCK1 gene should be considered likely pathogenic. We suggest considering molecular diagnostics in every patient presented with recurrent, severe hypoglycemia with accompanying liver damage as most accurate, feasible, and reliable method.
    Mesh-Begriff(e) Female ; Humans ; Gluconeogenesis/genetics ; Hypoglycemia/genetics ; Hypoglycemia/etiology ; Intracellular Signaling Peptides and Proteins/genetics ; Phosphoenolpyruvate Carboxykinase (GTP)/deficiency ; Phosphoenolpyruvate Carboxykinase (GTP)/genetics
    Chemische Substanzen Intracellular Signaling Peptides and Proteins ; PCK1 protein, human (EC 4.1.1.32) ; Phosphoenolpyruvate Carboxykinase (GTP) (EC 4.1.1.32)
    Sprache Englisch
    Erscheinungsdatum 2024-04-24
    Erscheinungsland United States
    Dokumenttyp Case Reports ; Journal Article
    ZDB-ID 2517183-5
    ISSN 1941-5923 ; 1941-5923
    ISSN (online) 1941-5923
    ISSN 1941-5923
    DOI 10.12659/AJCR.943118
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel: DCDC2

    Lipiński, Patryk / Ciara, Elżbieta / Jurkiewicz, Dorota / Mekrouda, Magda / Cielecka-Kuszyk, Joanna / Jurkiewicz, Elżbieta / Płoski, Rafał / Pawłowska, Joanna / Jankowska, Irena

    Diagnostics (Basel, Switzerland)

    2023  Band 13, Heft 11

    Abstract: Introduction: The increasing usage of NGS technology has enabled the discovery of new causal genes in ciliopathies, including the : Material and methods: A retrospective chart review of the clinical, biochemical, pathological (liver histology) and ... ...

    Abstract Introduction: The increasing usage of NGS technology has enabled the discovery of new causal genes in ciliopathies, including the
    Material and methods: A retrospective chart review of the clinical, biochemical, pathological (liver histology) and molecular features of the study group was performed. The database PubMed (MEDLINE) was searched for relevant studies.
    Results: All the patients presented with cholestatic jaundice and elevated GGT; the mean age was 2 months. The initial liver biopsy was performed in four children at a mean age of 3 months (age range: 2-5 months). In all of them, features of cholestasis, portal fibrosis and mild portal inflammation were observed; in three of them ductular proliferation was observed. One patient had undergone liver transplantation (LTx) at 8 years of age. At hepatectomy, a biliary-pattern cirrhosis was observed. Only one patient presented with features of renal disease. Whole exome sequencing was performed in all patients at the last follow-up visit (mean age 10 years). Three different variants (one novel) in the
    Conclusions: Our findings expand the molecular spectrum of pathogenic
    Sprache Englisch
    Erscheinungsdatum 2023-05-30
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2662336-5
    ISSN 2075-4418
    ISSN 2075-4418
    DOI 10.3390/diagnostics13111917
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: DCDC2 -Related Ciliopathy

    Patryk Lipiński / Elżbieta Ciara / Dorota Jurkiewicz / Magda Mekrouda / Joanna Cielecka-Kuszyk / Elżbieta Jurkiewicz / Rafał Płoski / Joanna Pawłowska / Irena Jankowska

    Diagnostics, Vol 13, Iss 1917, p

    Report of Six Polish Patients, Novel DCDC2 Variant, and Literature Review of Reported Cases

    2023  Band 1917

    Abstract: Introduction: The increasing usage of NGS technology has enabled the discovery of new causal genes in ciliopathies, including the DCDC2 gene. The aim of our study was to present the clinical, pathological and molecular report of six patients (from three ... ...

    Abstract Introduction: The increasing usage of NGS technology has enabled the discovery of new causal genes in ciliopathies, including the DCDC2 gene. The aim of our study was to present the clinical, pathological and molecular report of six patients (from three unrelated families) with DCDC2 biallelic pathogenic variants. A detailed overview of the reported patients with DCDC2 -related disease was provided. Material and methods: A retrospective chart review of the clinical, biochemical, pathological (liver histology) and molecular features of the study group was performed. The database PubMed (MEDLINE) was searched for relevant studies. Results: All the patients presented with cholestatic jaundice and elevated GGT; the mean age was 2 months. The initial liver biopsy was performed in four children at a mean age of 3 months (age range: 2–5 months). In all of them, features of cholestasis, portal fibrosis and mild portal inflammation were observed; in three of them ductular proliferation was observed. One patient had undergone liver transplantation (LTx) at 8 years of age. At hepatectomy, a biliary-pattern cirrhosis was observed. Only one patient presented with features of renal disease. Whole exome sequencing was performed in all patients at the last follow-up visit (mean age 10 years). Three different variants (one novel) in the DCDC2 gene were identified in the study group. With our six patients, a total of 34 patients with DCDC2 -related hepatic ciliopathy were identified. The main clinical presentation of DCDC2 -related ciliopathy was liver disease in the form of neonatal sclerosing cholangitis. The predominance of early and severe liver disease associated with no or mildly expressed kidney involvement was observed. Conclusions: Our findings expand the molecular spectrum of pathogenic DCDC2 variants, provide a more accurate picture of the phenotypic expression associated with molecular changes in this gene and confirm a loss of functional behaviour as the mechanism of disease.
    Schlagwörter ciliopathy ; DCDC2 ; cholestasis ; liver transplantation ; next generation sequencing ; Medicine (General) ; R5-920
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2023-05-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  5. Artikel ; Online: Fucosidosis-Clinical Manifestation, Long-Term Outcomes, and Genetic Profile-Review and Case Series.

    Stepien, Karolina M / Ciara, Elżbieta / Jezela-Stanek, Aleksandra

    Genes

    2020  Band 11, Heft 11

    Abstract: Fucosidosis is a neurodegenerative disorder which progresses inexorably. Clinical features include coarse facial features, growth retardation, recurrent upper respiratory infections, dysostosis multiplex, and angiokeratoma corporis diffusum. Fucosidosis ... ...

    Abstract Fucosidosis is a neurodegenerative disorder which progresses inexorably. Clinical features include coarse facial features, growth retardation, recurrent upper respiratory infections, dysostosis multiplex, and angiokeratoma corporis diffusum. Fucosidosis is caused by mutations in the
    Mesh-Begriff(e) Animals ; Disease Models, Animal ; Enzyme Replacement Therapy ; Fucosidosis/diagnosis ; Fucosidosis/etiology ; Fucosidosis/genetics ; Fucosidosis/therapy ; Genetic Association Studies ; Hematopoietic Stem Cell Transplantation ; Humans ; Molecular Diagnostic Techniques/methods ; Prenatal Diagnosis ; alpha-L-Fucosidase/genetics
    Chemische Substanzen FUCA1 protein, human ; alpha-L-Fucosidase (EC 3.2.1.51)
    Sprache Englisch
    Erscheinungsdatum 2020-11-22
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2527218-4
    ISSN 2073-4425 ; 2073-4425
    ISSN (online) 2073-4425
    ISSN 2073-4425
    DOI 10.3390/genes11111383
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Neuropathophysiology, Genetic Profile, and Clinical Manifestation of Mucolipidosis IV-A Review and Case Series.

    Jezela-Stanek, Aleksandra / Ciara, Elżbieta / Stepien, Karolina M

    International journal of molecular sciences

    2020  Band 21, Heft 12

    Abstract: Mucolipidosis type IV (MLIV) is an ultra-rare lysosomal storage disorder caused by biallelic mutations ... ...

    Abstract Mucolipidosis type IV (MLIV) is an ultra-rare lysosomal storage disorder caused by biallelic mutations in
    Mesh-Begriff(e) Adult ; Female ; Genetic Association Studies ; Genetic Profile ; Humans ; Male ; Mucolipidoses/genetics ; Mucolipidoses/physiopathology ; Mutation ; TRPM Cation Channels/genetics ; Young Adult
    Chemische Substanzen TRPM Cation Channels
    Sprache Englisch
    Erscheinungsdatum 2020-06-26
    Erscheinungsland Switzerland
    Dokumenttyp Case Reports ; Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms21124564
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: Neuropathophysiology, Genetic Profile, and Clinical Manifestation of Mucolipidosis IV—A Review and Case Series

    Aleksandra Jezela-Stanek / Elżbieta Ciara / Karolina M. Stepien

    International Journal of Molecular Sciences, Vol 21, Iss 4564, p

    2020  Band 4564

    Abstract: Mucolipidosis type IV (MLIV) is an ultra-rare lysosomal storage disorder caused by biallelic mutations in MCOLN1 gene encoding the transient receptor potential channel mucolipin-1. So far, 35 pathogenic or likely pathogenic MLIV-related variants have ... ...

    Abstract Mucolipidosis type IV (MLIV) is an ultra-rare lysosomal storage disorder caused by biallelic mutations in MCOLN1 gene encoding the transient receptor potential channel mucolipin-1. So far, 35 pathogenic or likely pathogenic MLIV-related variants have been described. Clinical manifestations include severe intellectual disability, speech deficit, progressive visual impairment leading to blindness, and myopathy. The severity of the condition may vary, including less severe psychomotor delay and/or ocular findings. As no striking recognizable facial dysmorphism, skeletal anomalies, organomegaly, or lysosomal enzyme abnormalities in serum are common features of MLIV, the clinical diagnosis may be significantly improved because of characteristic ophthalmological anomalies. This review aims to outline the pathophysiology and genetic defects of this condition with a focus on the genotype–phenotype correlation amongst cases published in the literature. The authors will present their own clinical observations and long-term outcomes in adult MLIV cases.
    Schlagwörter mucolipidosis type IV ; MCOLN1 ; corneal clouding ; gastrin ; myopathy ; neurodegenerative ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2020-06-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  8. Artikel ; Online: Clinical heterogeneity of polish patients with KAT6B-related disorder.

    Klaniewska, Magdalena / Bolanowska-Tyszko, Anna / Latos-Bielenska, Anna / Jezela-Stanek, Aleksandra / Szczaluba, Krzysztof / Krajewska-Walasek, Malgorzata / Ciara, Elzbieta / Pelc, Magdalena / Jurkiewicz, Dorota / Stawinski, Piotr / Zubkiewicz-Kucharska, Agnieszka / Rydzanicz, Małgorzata / Ploski, Rafal / Smigiel, Robert

    Molecular genetics & genomic medicine

    2023  Band 11, Heft 12, Seite(n) e2265

    Abstract: Background: Say-Barber-Biesecker-Young-Simpson (SBBYSS) variant of Ohdo syndrome is a rare, autosomal dominant and clinically heterogenous disorder, caused by pathogenic variants in the KAT6B gene located on chromosome 10q22.2. KAT6B encodes a highly ... ...

    Abstract Background: Say-Barber-Biesecker-Young-Simpson (SBBYSS) variant of Ohdo syndrome is a rare, autosomal dominant and clinically heterogenous disorder, caused by pathogenic variants in the KAT6B gene located on chromosome 10q22.2. KAT6B encodes a highly conserved histone acetyltransferase belonging to the MYST family. Currently, diseases caused by pathogenic variants in KAT6B (KAT6B-related disorders) comprise two allelic entities: SBBYSS variant of Ohdo syndrome and genitopatellar syndrome (GPS). Increase in the number of cases with overlapping GPS/SBBYSS phenotype which makes it necessary to redefine this group of phenotypes as KAT6B-related disorders or KAT6B spectrum disorders. Individuals with SBBYSS usually present with facial abnormalities, hypotonia, joint laxity, feeding problems, and long thumbs/great toes. This syndrome also typically involves skeletal problems including patellar hypoplasia/agenesis.
    Methods: Here we report six SBBYS syndrome patients with the same dysmorphic features but a different course of the disease. One known and five novel KATB6 pathogenic variants were identified by molecular diagnostics using Next Generation Sequencing (NGS).
    Results: We present a detailed phenotypic analysis of six individuals with KAT6B-related disorders, in whom a heterozygous pathogenic variant in KAT6B gene was found. In all of our patients facial dysmorphism as well as developmental and speech delay were present. Additionally, all but one patients presented with hypotonia, ocular abnormalities and long thumbs. Most of our probands showed blepharophimosis and skeletal (mainly knee) defects. Contrary to previously reported severe patellar defects (hypoplasia/agenesis) anomalies presented by our patients were less severe (dysplasia, habitual dislocation, subluxation) referring to KAT6B-related disorders.
    Conclusion: While most of the anomalies found in our patients comply with SBBYSS criteria, phenotypic differences in our probands support a broader spectrum of the disease phenotype. To establish the range of this spectrum, a detailed analysis of clinical variability among patients with SBBYSS requires further investigation.
    Mesh-Begriff(e) Male ; Humans ; Mutation ; Muscle Hypotonia/genetics ; Poland ; Intellectual Disability/genetics ; Histone Acetyltransferases/genetics
    Chemische Substanzen KAT6B protein, human (EC 2.3.1.48) ; Histone Acetyltransferases (EC 2.3.1.48)
    Sprache Englisch
    Erscheinungsdatum 2023-09-01
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2734884-2
    ISSN 2324-9269 ; 2324-9269
    ISSN (online) 2324-9269
    ISSN 2324-9269
    DOI 10.1002/mgg3.2265
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  9. Artikel ; Online: Biochemical, Genetic and Clinical Diagnostic Approaches to Autism-Associated Inherited Metabolic Disorders.

    Senarathne, Udara D / Indika, Neluwa-Liyanage R / Jezela-Stanek, Aleksandra / Ciara, Elżbieta / Frye, Richard E / Chen, Cliff / Stepien, Karolina M

    Genes

    2023  Band 14, Heft 4

    Abstract: Autism spectrum disorders (ASD) are a heterogeneous group of neurodevelopmental disorders characterized by impaired social interaction, limited communication skills, and restrictive and repetitive behaviours. The pathophysiology of ASD is multifactorial ... ...

    Abstract Autism spectrum disorders (ASD) are a heterogeneous group of neurodevelopmental disorders characterized by impaired social interaction, limited communication skills, and restrictive and repetitive behaviours. The pathophysiology of ASD is multifactorial and includes genetic, epigenetic, and environmental factors, whereas a causal relationship has been described between ASD and inherited metabolic disorders (IMDs). This review describes biochemical, genetic, and clinical approaches to investigating IMDs associated with ASD. The biochemical work-up includes body fluid analysis to confirm general metabolic and/or lysosomal storage diseases, while the advances and applications of genomic testing technology would assist with identifying molecular defects. An IMD is considered likely underlying pathophysiology in ASD patients with suggestive clinical symptoms and multiorgan involvement, of which early recognition and treatment increase their likelihood of achieving optimal care and a better quality of life.
    Mesh-Begriff(e) Humans ; Autistic Disorder/genetics ; Quality of Life ; Autism Spectrum Disorder/diagnosis ; Autism Spectrum Disorder/genetics ; Metabolic Diseases/diagnosis ; Metabolic Diseases/genetics ; Neurodevelopmental Disorders
    Sprache Englisch
    Erscheinungsdatum 2023-03-27
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2527218-4
    ISSN 2073-4425 ; 2073-4425
    ISSN (online) 2073-4425
    ISSN 2073-4425
    DOI 10.3390/genes14040803
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  10. Artikel ; Online: X-linked myxomatous valvular dystrophy in a patient with a novel mutation in the FLNA gene.

    Madej-Pilarczyk, Agnieszka / Piekutowska-Abramczuk, Dorota / Kucińska, Beata / Furmanek, Mariusz / Gwiazda, Anna / Ciara, Elżbieta / Chrzanowska, Krystyna H / Werner, Bożena

    Kardiologia polska

    2023  Band 81, Heft 3, Seite(n) 306–307

    Mesh-Begriff(e) Humans ; Mitral Valve Prolapse ; Genetic Diseases, X-Linked/genetics ; Heart Defects, Congenital ; Mutation ; Filamins/genetics
    Chemische Substanzen FLNA protein, human ; Filamins
    Sprache Englisch
    Erscheinungsdatum 2023-01-14
    Erscheinungsland Poland
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 411492-9
    ISSN 1897-4279 ; 0022-9032
    ISSN (online) 1897-4279
    ISSN 0022-9032
    DOI 10.33963/KP.a2023.0017
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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