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  1. Buch ; Online: Paris Climate Agreement: Beacon of Hope

    Salawitch, Ross J. / Canty, Timothy P. / Hope, Austin P. / Tribett, Walter R. / Bennett, Brian F.

    (Springer Climate)

    2017  

    Verfasserangabe Ross J. Salawitch, Timothy P. Canty, Austin P. Hope, Walter R. Tribett, Brian F. Bennett
    Serientitel Springer Climate
    Schlagwörter Environment ; Climate change ; Energy industries
    Thema/Rubrik (Code) 577.27
    Sprache Englisch
    Umfang 1 Online-Ressource (XVII, 186 p. 58 illus., 54 illus. in color)
    Verlag Springer International Publishing ; Imprint: Springer
    Erscheinungsort Cham
    Dokumenttyp Buch ; Online
    HBZ-ID HT019227505
    ISBN 978-3-319-46939-3 ; 9783319469386 ; 3-319-46939-8 ; 331946938X
    DOI 10.1007/978-3-319-46939-3
    Datenquelle ZB MED Katalog Medizin, Gesundheit, Ernährung, Umwelt, Agrar

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  2. Buch ; Online: Paris Climate Agreement: Beacon of Hope

    Salawitch, Ross J. / Canty, Timothy P. / Hope, Austin P. / Tribett, Walter R. / Bennett, Brian F.

    2017  

    Schlagwörter Environmental economics ; Manufacturing industries ; Pharmaceutical industries ; Earth sciences, geography, environment, planning ; Biochemical engineering ; Climate Change ; Climate Change Management and Policy ; Energy Economics
    Umfang 1 Online-Ressource
    Verlag Springer Nature
    Erscheinungsort Cham
    Dokumenttyp Buch ; Online
    Anmerkung English ; Open Access
    HBZ-ID HT021029034
    ISBN 9783319730370 ; 3319730371
    Datenquelle ZB MED Katalog Medizin, Gesundheit, Ernährung, Umwelt, Agrar

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  3. Artikel ; Online: Proteasome Inhibition Reprograms Chromatin Landscape in Breast Cancer.

    Kinyamu, H Karimi / Bennett, Brian D / Ward, James M / Archer, Trevor K

    Cancer research communications

    2024  Band 4, Heft 4, Seite(n) 1082–1099

    Abstract: The 26S proteasome is the major protein degradation machinery in cells. Cancer cells use the proteasome to modulate gene expression networks that promote tumor growth. Proteasome inhibitors have emerged as effective cancer therapeutics, but how they work ...

    Abstract The 26S proteasome is the major protein degradation machinery in cells. Cancer cells use the proteasome to modulate gene expression networks that promote tumor growth. Proteasome inhibitors have emerged as effective cancer therapeutics, but how they work mechanistically remains unclear. Here, using integrative genomic analysis, we discovered unexpected reprogramming of the chromatin landscape and RNA polymerase II (RNAPII) transcription initiation in breast cancer cells treated with the proteasome inhibitor MG132. The cells acquired dynamic changes in chromatin accessibility at specific genomic loci termed differentially open chromatin regions (DOCR). DOCRs with decreased accessibility were promoter proximal and exhibited unique chromatin architecture associated with divergent RNAPII transcription. Conversely, DOCRs with increased accessibility were primarily distal to transcription start sites and enriched in oncogenic superenhancers predominantly accessible in non-basal breast tumor subtypes. These findings describe the mechanisms by which the proteasome modulates the expression of gene networks intrinsic to breast cancer biology.
    Significance: Our study provides a strong basis for understanding the mechanisms by which proteasome inhibitors exert anticancer effects. We find open chromatin regions that change during proteasome inhibition, are typically accessible in non-basal breast cancers.
    Mesh-Begriff(e) Chromatin/genetics ; Proteasome Endopeptidase Complex/genetics ; Proteasome Inhibitors/pharmacology ; Proteolysis ; Genomics ; Neoplasms
    Chemische Substanzen Chromatin ; Proteasome Endopeptidase Complex (EC 3.4.25.1) ; Proteasome Inhibitors
    Sprache Englisch
    Erscheinungsdatum 2024-04-16
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ISSN 2767-9764
    ISSN (online) 2767-9764
    DOI 10.1158/2767-9764.CRC-23-0476
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel: Persistent gene expression and DNA methylation alterations linked to carcinogenic effects of dichloroacetic acid.

    Carswell, Gleta / Chamberlin, John / Bennett, Brian D / Bushel, Pierre R / Chorley, Brian N

    Frontiers in oncology

    2024  Band 14, Seite(n) 1389634

    Abstract: Background: Mechanistic understanding of transient exposures that lead to adverse health outcomes will enhance our ability to recognize biological signatures of disease. Here, we measured the transcriptomic and epigenomic alterations due to exposure to ... ...

    Abstract Background: Mechanistic understanding of transient exposures that lead to adverse health outcomes will enhance our ability to recognize biological signatures of disease. Here, we measured the transcriptomic and epigenomic alterations due to exposure to the metabolic reprogramming agent, dichloroacetic acid (DCA). Previously, we showed that exposure to DCA increased liver tumor incidence in B6C3F1 mice after continuous or early life exposures significantly over background level.
    Methods: Using archived formalin-fixed liver samples, we utilized modern methodologies to measure gene expression and DNA methylation levels to link to previously generated phenotypic measures. Gene expression was measured by targeted RNA sequencing (TempO-seq 1500+ toxicity panel: 2754 total genes) in liver samples collected from 10-, 32-, 57-, and 78-week old mice exposed to deionized water (controls), 3.5 g/L DCA continuously in drinking water ("Direct" group), or DCA for 10-, 32-, or 57-weeks followed by deionized water until sample collection ("Stop" groups). Genome-scaled alterations in DNA methylation were measured by Reduced Representation Bisulfite Sequencing (RRBS) in 78-week liver samples for control, Direct, 10-week Stop DCA exposed mice.
    Results: Transcriptomic changes were most robust with concurrent or adjacent timepoints after exposure was withdrawn. We observed a similar pattern with DNA methylation alterations where we noted attenuated differentially methylated regions (DMRs) in the 10-week Stop DCA exposure groups compared to the Direct group at 78-weeks. Gene pathway analysis indicated cellular effects linked to increased oxidative metabolism, a primary mechanism of action for DCA, closer to exposure windows especially early in life. Conversely, many gene signatures and pathways reversed patterns later in life and reflected more pro-tumorigenic patterns for both current and prior DCA exposures. DNA methylation patterns correlated to early gene pathway perturbations, such as cellular signaling, regulation and metabolism, suggesting persistence in the epigenome and possible regulatory effects.
    Conclusion: Liver metabolic reprogramming effects of DCA interacted with normal age mechanisms, increasing tumor burden with both continuous and prior DCA exposure in the male B6C3F1 rodent model.
    Sprache Englisch
    Erscheinungsdatum 2024-05-03
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2649216-7
    ISSN 2234-943X
    ISSN 2234-943X
    DOI 10.3389/fonc.2024.1389634
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel: Sequence meets function—microbiota and cardiovascular disease

    Kim, Myungsuk / Huda, Md Nazmul / Bennett, Brian J.

    Cardiovascular Research. 2022 Feb., v. 118, no. 2

    2022  

    Abstract: The discovery that gut-microbiota plays a profound role in human health has opened a new avenue of basic and clinical research. Application of ecological approaches where the bacterial 16S rRNA gene is queried has provided a number of candidate bacteria ... ...

    Abstract The discovery that gut-microbiota plays a profound role in human health has opened a new avenue of basic and clinical research. Application of ecological approaches where the bacterial 16S rRNA gene is queried has provided a number of candidate bacteria associated with coronary artery disease and hypertension. We examine the associations between gut microbiota and a variety of cardiovascular disease (CVD) including atherosclerosis, coronary artery disease, and blood pressure. These approaches are associative in nature and there is now increasing interest in identifying the mechanisms underlying these associations. We discuss three potential mechanisms including: gut permeability and endotoxemia, increased immune system activation, and microbial derived metabolites. In addition to discussing these potential mechanisms we highlight current studies manipulating the gut microbiota or microbial metabolites to move beyond sequence-based association studies. The goal of these mechanistic studies is to determine the mode of action by which the gut microbiota may affect disease susceptibility and severity. Importantly, the gut microbiota appears to have a significant effect on host metabolism and CVD by producing metabolites entering the host circulatory system such as short-chain fatty acids and trimethylamine N-Oxide. Therefore, the intersection of metabolomics and microbiota research may yield novel targets to reduce disease susceptibility. Finally, we discuss approaches to demonstrate causality such as specific diet changes, inhibition of microbial pathways, and fecal microbiota transplant.
    Schlagwörter atherosclerosis ; biomedical research ; blood pressure ; circulatory system ; coronary artery disease ; diet ; digestive system ; disease susceptibility ; endotoxemia ; genes ; human health ; hypertension ; immune system ; intestinal microorganisms ; mechanism of action ; metabolism ; metabolites ; metabolomics ; permeability ; trimethylamine
    Sprache Englisch
    Erscheinungsverlauf 2022-02
    Umfang p. 399-412.
    Erscheinungsort Oxford University Press (OUP)
    Dokumenttyp Artikel
    ZDB-ID 80340-6
    ISSN 1755-3245 ; 0008-6363
    ISSN (online) 1755-3245
    ISSN 0008-6363
    DOI 10.1093/cvr/cvab030
    Datenquelle NAL Katalog (AGRICOLA)

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    Verfügbar in ZB MED Bonn

    Z 71/513: Hefte anzeigen

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  6. Artikel: Proteasome inhibition reprograms chromatin landscape in breast cancer.

    Kinyamu, H Karimi / Bennett, Brian D / Ward, James M / Archer, Trevor

    bioRxiv : the preprint server for biology

    2023  

    Abstract: The 26S proteasome is the major protein degradation machinery in cells. Cancer cells use the proteasome to modulate gene expression networks that promote tumor growth. Proteasome inhibitors have emerged as effective cancer therapeutics, but how they work ...

    Abstract The 26S proteasome is the major protein degradation machinery in cells. Cancer cells use the proteasome to modulate gene expression networks that promote tumor growth. Proteasome inhibitors have emerged as effective cancer therapeutics, but how they work mechanistically remains unclear. Here, using integrative genomic analysis, we discovered unexpected reprogramming of the chromatin landscape and RNAPII transcription initiation in breast cancer cells treated with the proteasome inhibitor MG132. The cells acquired dynamic changes in chromatin accessibility at specific genomic loci termed Differentially Open Chromatin Regions (DOCRs). DOCRs with decreased accessibility were promoter proximal and exhibited unique chromatin architecture associated with divergent RNAPII transcription. Conversely, DOCRs with increased accessibility were primarily distal to transcription start sites and enriched in oncogenic super enhancers predominantly accessible in non-basal breast tumor subtypes. These findings describe the mechanisms by which the proteasome modulates the expression of gene networks intrinsic to breast cancer biology.
    Highlights: Proteasome inhibition uncovers
    Sprache Englisch
    Erscheinungsdatum 2023-10-17
    Erscheinungsland United States
    Dokumenttyp Preprint
    DOI 10.1101/2023.10.13.562284
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: Genetic screen identified PRMT5 as a neuroprotection target against cerebral ischemia.

    Wu, Haoyang / Lv, Peiyuan / Wang, Jinyu / Bennett, Brian / Wang, Jiajia / Li, Pishun / Peng, Yi / Hu, Guang / Lin, Jiaji

    eLife

    2024  Band 12

    Abstract: Epigenetic regulators present novel opportunities for both ischemic stroke research and therapeutic interventions. While previous work has implicated that they may provide neuroprotection by potentially influencing coordinated sets of genes and pathways, ...

    Abstract Epigenetic regulators present novel opportunities for both ischemic stroke research and therapeutic interventions. While previous work has implicated that they may provide neuroprotection by potentially influencing coordinated sets of genes and pathways, most of them remain largely uncharacterized in ischemic conditions. In this study, we used the oxygen-glucose deprivation (OGD) model in the immortalized mouse hippocampal neuronal cell line HT-22 and carried out an RNAi screen on epigenetic regulators. PRMT5 was identified as a novel negative regulator of neuronal cell survival after OGD, which presented a phenotype of translocation from the cytosol to the nucleus upon oxygen and energy depletion both in vitro and in vivo. PRMT5 bound to the chromatin and a large number of promoter regions to repress downstream gene expression. Silencing
    Mesh-Begriff(e) Animals ; Mice ; Brain Ischemia/genetics ; Glucose ; Hedgehog Proteins ; Neuroprotection/genetics ; Oxygen ; Phenotype ; Protein-Arginine N-Methyltransferases/genetics
    Chemische Substanzen Glucose (IY9XDZ35W2) ; Hedgehog Proteins ; Oxygen (S88TT14065) ; Prmt5 protein, mouse (EC 2.1.1.319) ; Protein-Arginine N-Methyltransferases (EC 2.1.1.319)
    Sprache Englisch
    Erscheinungsdatum 2024-02-19
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 2687154-3
    ISSN 2050-084X ; 2050-084X
    ISSN (online) 2050-084X
    ISSN 2050-084X
    DOI 10.7554/eLife.89754
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel ; Online: Role of second-sphere arginine residues in metal binding and metallocentre assembly in nitrile hydratases.

    Miller, Callie / Huntoon, Delanie / Kaley, Nicholas / Ogutu, Irene / Fiedler, Adam T / Bennett, Brian / Liu, Dali / Holz, Richard

    Journal of inorganic biochemistry

    2024  Band 256, Seite(n) 112565

    Abstract: Two conserved second-sphere βArg (R) residues in nitrile hydratases (NHase), that form hydrogen bonds with the catalytically essential sulfenic and sulfinic acid ligands, were mutated to Lys and Ala residues in the Co-type NHase from Pseudonocardia ... ...

    Abstract Two conserved second-sphere βArg (R) residues in nitrile hydratases (NHase), that form hydrogen bonds with the catalytically essential sulfenic and sulfinic acid ligands, were mutated to Lys and Ala residues in the Co-type NHase from Pseudonocardia thermophila JCM 3095 (PtNHase) and the Fe-type NHase from Rhodococcus equi TG328-2 (ReNHase). Only five of the eight mutants (PtNHase βR52A, βR52K, βR157A, βR157K and ReNHase βR61A) were successfully expressed and purified. Apart from the PtNHase βR52A mutant that exhibited no detectable activity, the k
    Mesh-Begriff(e) Hydro-Lyases/chemistry ; Hydro-Lyases/metabolism ; Hydro-Lyases/genetics ; Arginine/chemistry ; Rhodococcus equi/enzymology ; Rhodococcus equi/genetics ; Bacterial Proteins/chemistry ; Bacterial Proteins/genetics ; Bacterial Proteins/metabolism ; Actinomycetales/enzymology ; Actinomycetales/genetics ; Catalytic Domain
    Chemische Substanzen Hydro-Lyases (EC 4.2.1.-) ; nitrile hydratase (EC 4.2.1.-) ; Arginine (94ZLA3W45F) ; Bacterial Proteins
    Sprache Englisch
    Erscheinungsdatum 2024-04-16
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 162843-4
    ISSN 1873-3344 ; 0162-0134
    ISSN (online) 1873-3344
    ISSN 0162-0134
    DOI 10.1016/j.jinorgbio.2024.112565
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Volltext online

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    Zs.B 1730: Hefte anzeigen Standort:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  9. Artikel ; Online: Catalytic role of histidine-114 in the hydrolytic dehalogenation of chlorothalonil by Pseudomonas sp. CTN-3.

    Gerlich, Grayson / Miller, Callie / Yang, Xinhang / Diviesti, Karla / Bennett, Brian / Klein-Seetharaman, Judith / Holz, Richard C

    Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry

    2024  

    Abstract: Chlorothalonil (2,4,5,6-tetrachloroisophthalonitrile; TPN) is an environmentally persistent fungicide that sees heavy use in the USA and is highly toxic to aquatic species and birds, as well as a probable human carcinogen. The chlorothalonil dehalogenase ...

    Abstract Chlorothalonil (2,4,5,6-tetrachloroisophthalonitrile; TPN) is an environmentally persistent fungicide that sees heavy use in the USA and is highly toxic to aquatic species and birds, as well as a probable human carcinogen. The chlorothalonil dehalogenase from Pseudomonas sp. CTN-3 (Chd, UniProtKB C9EBR5) degrades TPN to its less toxic 4-OH-TPN analog making it an exciting candidate for the development of a bioremediation process for TPN; however, little is currently known about its catalytic mechanism. Therefore, an active site residue histidine-114 (His114) which forms a hydrogen bond with the Zn(II)-bound water/hydroxide and has been suggested to be the active site acid/base, was substituted by an Ala residue. Surprisingly, Chd
    Sprache Englisch
    Erscheinungsdatum 2024-05-26
    Erscheinungsland Germany
    Dokumenttyp Journal Article
    ZDB-ID 1464026-0
    ISSN 1432-1327 ; 0949-8257
    ISSN (online) 1432-1327
    ISSN 0949-8257
    DOI 10.1007/s00775-024-02053-1
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  10. Artikel: Modulating the Microbiota as a Therapeutic Intervention for Type 2 Diabetes.

    Huda, M Nazmul / Kim, Myungsuk / Bennett, Brian J

    Frontiers in endocrinology

    2021  Band 12, Seite(n) 632335

    Abstract: Mounting evidence suggested that the gut microbiota has a significant role in the metabolism and disease status of the host. In particular, Type 2 Diabetes (T2D), which has a complex etiology that includes obesity and chronic low-grade inflammation, is ... ...

    Abstract Mounting evidence suggested that the gut microbiota has a significant role in the metabolism and disease status of the host. In particular, Type 2 Diabetes (T2D), which has a complex etiology that includes obesity and chronic low-grade inflammation, is modulated by the gut microbiota and microbial metabolites. Current literature supports that unbalanced gut microbial composition (dysbiosis) is a risk factor for T2D. In this review, we critically summarize the recent findings regarding the role of gut microbiota in T2D. Beyond these associative studies, we focus on the causal relationship between microbiota and T2D established using fecal microbiota transplantation (FMT) or probiotic supplementation, and the potential underlying mechanisms such as byproducts of microbial metabolism. These microbial metabolites are small molecules that establish communication between microbiota and host cells. We critically summarize the associations between T2D and microbial metabolites such as short-chain fatty acids (SCFAs) and trimethylamine N-Oxide (TMAO). Additionally, we comment on how host genetic architecture and the epigenome influence the microbial composition and thus how the gut microbiota may explain part of the missing heritability of T2D found by GWAS analysis. We also discuss future directions in this field and how approaches such as FMT, prebiotics, and probiotics supplementation are being considered as potential therapeutics for T2D.
    Mesh-Begriff(e) Diabetes Mellitus, Type 2/etiology ; Diabetes Mellitus, Type 2/therapy ; Dysbiosis/complications ; Dysbiosis/therapy ; Fecal Microbiota Transplantation ; Gastrointestinal Microbiome/physiology ; Humans ; Prebiotics ; Probiotics/therapeutic use
    Chemische Substanzen Prebiotics
    Sprache Englisch
    Erscheinungsdatum 2021-04-07
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 2592084-4
    ISSN 1664-2392
    ISSN 1664-2392
    DOI 10.3389/fendo.2021.632335
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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