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  • 1
    Keywords: Medicine ; Immunology ; Biotechnology ; Biomedical Engineering ; Biomedicine ; Immunology ; Biotechnology ; Biomedical Engineering ; Springer eBooks
    Description / Table of Contents: Part 1. Mechanisms -- Thromboinflammation in Therapeutic Medicine -- Complement Interactions with Blood Cells, Endothelial Cells and Microvesicles in Thrombotic and Inflammatory Conditions -- Role of Complement on Broken Surfaces after Trauma -- Complement Involvement in Periodontitis: Molecular Mechanisms and Rational Therapeutic Approaches -- Part 2. Biomaterials -- The Lectin Pathway of Complement and Biocompatibility -- Foreign Body Reaction to Subcutaneous Implants -- Molecular Characterization of Macrophage-Biomaterial Interactions -- Heparan Sulfate Proteoglycan Metabolism and the Fate of Grafted Tissues -- Part 3. Transplantation -- Xenotransplantation of Cells, Tissues, Organs and the German Research Foundation Transregio Collaborative Research Centre 127 -- Macro encapsulated Pig Islets Correct Induced Diabetes in Primates up to 6 Months -- Regulation of Instant Blood Mediated Inflammatory Reaction (IBMIR) in Pancreatic Islet Xeno-Transplantatioń€”Points for Therapeutic Interventions -- Cell Surface Engineering for Regulation of Immune Reactions in Cell Therapy -- Complement Interception Across Humoral Incompatibility in Solid Organ Transplantation€“Á Clinical Perspective
    Abstract: The collection of chapters in this proceedings volume brings together research from academic and industry scientists and clinical development experts who are focused on contemporary and emerging aspects of improving treatments employing biosurfaces. Interactions between biomaterial implants, devices, cell therapies, and whole organ transplants frequently trigger activation of body defense systems and responses that negatively affect the clinical outcome. Optimal tissue integration and modulation of foreign body reactions is therefore essential for preserving anticipated functions and avoiding adverse effects. Topics covered include mechanistic and applied research within the fields of extracorporeal devices, soft and hard tissue implants, tissue and biomaterial-targeting, therapeutic modulation of foreign body reactions, cell encapsulations, as well as cell and whole organ transplantation
    Pages: XII, 242 p. 34 illus., 28 illus. in color. : online resource.
    Edition: 1st ed. 2015.
    ISBN: 9783319186030
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  • 2
    Keywords: Life sciences ; Forests and forestry ; Life sciences ; Forestry ; Springer eBooks
    Pages: : digital
    ISBN: 9789048198061
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  • 3
    Call number: 05-MAT-20:19
    Keywords: Artificial intelligence
    Pages: xi, 137 p. : illus.
    ISBN: 0-07-046570-3
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    05-MAT-20:19 departmental collection or stack – please contact the library
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  • 4
    Keywords: Life sciences ; Proteins ; Life sciences ; Protein Science ; Springer eBooks
    Description / Table of Contents: Methods for Structural Analysis of Aggregates Formed by Self-Assembling Peptides -- Solid state NMR Structura -- Characterization of Self-assembled Peptides With Selective 13C and 15N Isotopic LabelsATR-FTIR Analysis of Amyloid Proteins -- Imaging Protein Fibers at the Nanoscale and In Situ -- Replica Exchange Molecular Dynamics: A Practical Application Protocol with Solutions to Common Problems and a Peptide Aggregation and Self-Assembly Example -- An Aggregate Weight-normalized thioflavin-T Measurement Scale For Characterizing Polymorphic Amyloids And Assembly Intermediates -- Nanoparticle Tracking for Protein Aggregation Research -- Peptide Self-assembly Measured using Fluorescence Correlation Spectroscopy -- A General Method to Prepare Peptide-based Supramolecular Hydrogels -- Recursive Directional Ligation Approach for Cloning Recombinant Spider Silks -- Synthesis of Mikto-Arm Star Peptide Conjugates -- Synthesis and Evaluation of Self€”Ássembled Nanostructures of Peptid途π chromophore conjugates -- Programmable Fabrication of Multi-layer Collagen Nanosheets of Defined Composition -- Practical Considerations in the Design and use of Immunologically Active Fibrillar Peptide Assemblies -- Microwave-assisted Synthesis and Immunological Evaluation of Self-Assembling Peptide Vaccines -- Preparation and Screening of Catalytic Amyloid Assemblies.-Self-assembly of Filamentous Cell Penetrating Peptides for Gene Delivery -- Biogelx: Cell Culture on Gels based on Aromatic Peptide Amphiphiles -- Production and use of Recombinant AÎø for Aggregation Studies -- Disaggregation of Ab42 for Structural and Biochemical Studies -- Preparation of Stable Amyloid-Îø Oligomers Without Perturbative Methods -- Discriminating Strains of Self-Propagating Protein Aggregates Using a Conformational Stability Assay -- Model Phospholipid Liposomes to Study the b-Amyloid-Peptide-Induced Membrane Disruption -- Using Molecular Tweezers to Remodel Abnormal Protein Self-assembly and Inhibit the Toxicity of Amyloidogenic Proteins -- Incorporation of an azobenzene b-turn Peptidomimetic into Amyloid-b to Probe Potential Structural Motifs Leading to b-sheet self-assembly -- Solid State NMR Studies of Amyloid Materials: A Protocol to Define an Atomic Model of AÎø(1́€“42) in Amyloid Fibrils -- Experimental and Computational Protocols for Studies of Cross-seeding Amyloid Assemblies
    Abstract: This volume details methods and protocols on b-sheet assemblies and collagen. Divided into three parts chapters focus on expanding use of solid-state NMR as a powerful method to enhance structural understanding of self-assembled peptide materials, methods for the design, synthesis, and application of self-assembled peptide materials, and structural and mechanistic analyses of pathological amyloid systems that provide novel ways to assess function of the various possible aggregates as well to determine how the structure of these materials correlates to function/dysfunction in the biological context. Written in the highly successful Methods in Molecular Biology series format, chapters include introductions to their respective topics, lists of the necessary materials and reagents, step-by-step, readily reproducible laboratory protocols, and tips on troubleshooting and avoiding known pitfalls. Authoritative and cutting-edge, Computational Drug Discovery and Design aims to capture modern methods that span the breadth of the exciting and expanding field of peptide self-assembly
    Pages: XV, 452 p. 130 illus., 53 illus. in color. : online resource.
    ISBN: 9781493978113
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  • 5
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The human leukaemia cell line KU812 has previously been used to study basophil differentiation. In this study the authors analysed the capacity of KU812 to produce the mast cell proteinase tryptase and to synthesize factor(s) mitogenic for fibroblasts. KU812 cells were treated with tetradecanoyl-phorbol-13-acetate (TPA), conditioned medium from the human T-cell line Mo (Mo-CM), or cultured under serum free conditions. After 4 days the cells were analysed for cell growth, differentiation, content of tryptase, and secretion of fibroblast mitogenic activity. Mo-CM and serum starvation increased the expression while TPA treatment down-regulated the expression of FcεRI-α chain. An increase in tryptase content in cell extracts was detected after 4 days of culture in serum-free medium or in the presence of Mo-CM. KU812 conditioned media was found to have a baseline expression of mitogenic activity on normal human foreskin fibroblasts that was increased after serum starvation or after treatment with TPA. Mast cell-derived tryptase has previously been reported to be mitogenic for fibroblasts, but in this study the expression of tryptase did not correlate with the expression of fibroblast mitogenic activity in KU812 cells. Furthermore, affinity-purified lung tryptase did not show any mitogenic activity. Platelet-derived growth factor was also excluded. Although the factor(s) from KU812 cells stimulating fibroblast proliferation have not been identified, our results indicate that basophils may be potential producers of growth factors inducing fibroblast proliferation.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In recent years, conjugation of heparin to biomaterials has been shown to improve its biocompatibility. The purpose of the present work was to compare complement activation and binding of C3 to unmodified and heparin-treated polystyrene surfaces of microtitre plates. When polystyrene was incubated with human serum, C3 was deposited on the surface by both adsorption and binding dependent on activation of the classical (CPW) and alternative (APW) pathways After end-point attachment of heparin, significant C3 deposition, although at reduced levels, occurred only by CPW-mediated mechanisms. while adsorption and APW -mediated binding were strongly reduced. Generally, the modified surface bound lower amounts of protein, e.g. serum albumin and IgG, than the unmodified. By contrast, it had increased affinity for Clq which leads to binding of Cl and activation of complement via the CPW. Nevertheless, the net effect of the surface modification on the complement reaction was an overall reduction of C3 binding due to obliteration of APW. This can be related to an enhanced factor H/I-dependent down-regulation of C3b and to the lowered protein-adsorbing property of the surface, both of which have inhibitory effects on APW and on the C3 shunt-dependent activation of the complement system.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Earlier studies have shown that C3 can be denatured when blood comes in contact with a polystyrene surface. This study was undertaken to sec if similar denaturation of C3 occurs at the gas plasma interface which is found in all kinds of oxygenator used during cardio-pulmonary operations. An in vitro system consisting of gas bubbling through human blood, serum or plasma was used. The generation of C3a, as an indicator of complement activation, and iC3 and iC3 fragments were monitored. Both C3a and iC3/iC3 fragments levels were increased during bubbling. In contrast to the C3a level, no reduction in iC3/iC3 fragments formation was seen in the presence of EDTA, indicating that il was independent of complement activation. The rate of iC3/iC3 fragments generation was unaffected by the composition of the gas (pure oxygen, pure nitrogen or air), suggesting that the denaturation of C3 indeed occurred at the serum gas interface. C3 and iC3/iC3 fragments were isolated from bubbled EDTA-chelated serum by PEG precipitation and chromatography on FPLC, using a Mono S column and detected by two ELISAs, specific for native C3 and iC3/iC3 fragments. After 240 min approximately 20% of the total amount of C3 consisted of intact iC3 and it was confirmed that this population bound to human erythrocytes.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1573-2592
    Keywords: Complement activation ; C3a ; terminal sC5b-9 ; cardiopulmonary bypass ; heparin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We describe here a model for the study of blood/surface and blood/air interaction as encountered in cardiopulmonary bypass (CPB) circuits. Polyethylene tubing was filled with serum or blood and closed end to end into loops whereby the volume of the remaining air bubble was inversely varied with respect to that of the fluid. The loops were rotated vertically in a water bath at 37°C. The profiles of C3a, iC3, and TCC generation were similar to those observed at surgery, involving CPB. Soluble heparin and heparan sulfate inhibited both C3a and TCC formation, but surface-conjugated heparin had only a minor effect. Binding of C3 and/or C3 fragments to the heparin surface was much reduced compared to the amine matrix to which heparin was linked, but compared with the polyethylene surface the effect was less pronounced. These data suggest that, in addition to the biomaterial surface, the blood-gas interface seems to play an important role in the activation of complement and that this activation is inhibitable by high concentrations of soluble glucose aminoglycans.
    Type of Medium: Electronic Resource
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  • 9
    Keywords: CANCER ; INHIBITION ; KINASE ; PATHWAY ; GENE-EXPRESSION ; C-MYC ; TUMOR SUPPRESSION ; PROTEIN-SYNTHESIS ; DRIVEN ; SYNTHETIC LETHALITY
    Abstract: Myc oncogenic transcription factors (c-Myc, N-Myc, and L-Myc) coordinate the control of cell growth, division, and metabolism. In cancer, Myc overexpression is often associated with aggressive disease, which is in part due to the destruction of select targets by the ubiquitin-proteasome system (eg, SCF(Skp2)-directed destruction of the Cdk inhibitor p27(Kip1)). We reasoned that Myc would also regulate SUMOylation, a related means of posttranslational modification of proteins, and that this circuit would play essential roles in Myc-dependent tumorigenesis. Here, we report marked increases in the expression of genes that encode regulators and components of the SUMOylation machinery in mouse and human Myc-driven lymphomas, resulting in hyper-SUMOylation in these tumors. Further, inhibition of SUMOylation by genetic means disables Myc-induced proliferation, triggering G2/M cell-cycle arrest, polyploidy, and apoptosis. Using genetically defined cell models and conditional expression systems, this response was shown to be Myc specific. Finally, in vivo loss-of-function and pharmacologic studies demonstrated that inhibition of SUMOylation provokes rapid regression of Myc-driven lymphoma. Thus, targeting SUMOylation represents an attractive therapeutic option for lymphomas with MYC involvement.
    Type of Publication: Journal article published
    PubMed ID: 25143484
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  • 10
    Abstract: Immune checkpoint inhibitors and adoptive cell transfer (ACT) of autologous tumor-infiltrating T cells have shown durable responses in patients with melanoma. To study ACT and immunotherapies in a humanized model, we have developed PDXv2.0 - a melanoma PDX model where tumor cells and tumor-infiltrating T cells from the same patient are transplanted sequentially in non-obese diabetic/severe combined immune-deficient/common gamma chain (NOG/NSG) knockout mouse. Key to T-cell survival/effect in this model is the continuous presence of interleukin-2 (IL-2). Tumors that grow in PDXv2.0 are eradicated if the autologous tumor cells and T cells come from a patient that exhibited an objective response to ACT in the clinic. However, T cells from patients that are non-responders to ACT cannot kill tumor cells in PDXv2.0. Taken together, PDXv2.0 provides the potential framework to further model genetically diverse human cancers for assessing the efficacy of immunotherapies as well as combination therapies.Combining different types of immune therapies might benefit certain patients. Here, the authors develop an autologous immune-humanized melanoma mouse model that allows the preclinical assessment of cancer cell-T cell interactions from each individual patient and the benefits of immunotherapies combinations.
    Type of Publication: Journal article published
    PubMed ID: 28955032
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