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  • 1
    Online Resource
    Online Resource
    San Diego :Elsevier Science & Technology,
    Keywords: Peptides. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (392 pages)
    Edition: 1st ed.
    ISBN: 9780081008522
    DDC: 610.28/4
    Language: English
    Note: Front Cover -- Peptides and Proteins as Biomaterials for Tissue Regeneration and Repair -- Copyright -- Contents -- Contributors -- Preface -- Peptides and proteins as biomaterials for tissue regeneration and repair -- Chapter 1: Fundamentals of protein and cell interactions in biomaterials -- 1.1 Fundamentals of protein adsorption on biomaterials -- 1.1.1 Basics of protein adsorption -- 1.1.1.1 Function and structural organization -- 1.1.1.2 Structure and orientation of adsorbed proteins -- 1.1.2 Interactions with the surface: hydrophobic and electrostatic bonding -- 1.1.3 Kinetics of protein adsorption -- 1.1.4 Conformational changes and stability -- 1.1.5 Reversibility of protein adsorption -- 1.1.6 Competitive adsorption behavior -- 1.2 Biomaterial surface properties and their effect on protein adsorption -- 1.2.1 Promoting protein adsorption: Osseointegration -- 1.2.2 Preventing protein adsorption: Hemocompatibility -- 1.3 Quantification of protein adsorption -- 1.3.1 Optical -- 1.3.1.1 Ellipsometry -- 1.3.1.2 Surface plasmon resonance -- 1.3.2 Spectroscopic -- 1.3.2.1 Fluorescent spectroscopy -- 1.3.2.2 Infrared absorption spectroscopy -- 1.3.3 Microscopic -- 1.3.3.1 Atomic force microscopy (AFM) -- 1.3.4 Radiolabeling -- 1.3.5 Quartz crystal microbalance with dissipation monitoring (QCM-D) -- 1.4 The importance of adsorbed proteins in the tissue reaction to biomaterials -- 1.4.1 Effect of adsorbed proteins on cell adhesion -- 1.4.2 Effect of adsorbed proteins on cell activation -- 1.4.3 Effect of adsorbed proteins on the FBR -- 1.5 Quantification/detection of cell adhesion and activation -- 1.5.1 Cell adhesion -- 1.5.1.1 Micropatterning -- 1.5.1.2 Three-dimensional traction force microscopy (3D-TFM) -- 1.5.1.3 QCM-D -- 1.5.1.4 Microfluidic -- 1.5.1.5 AFM -- 1.5.2 Cell activation -- 1.5.2.1 Fluorescence microscopy -- 1.5.2.2 Flow cytometry. , 1.5.2.3 Enzyme-linked immunosorbent assay (ELISA) -- 1.6 Concluding remarks -- References -- Chapter 2: Extracellular matrix constitution and function for tissue regeneration and repair -- 2.1 An overview of ECM structure and function -- 2.1.1 Architectural role -- 2.1.2 Adhesion mediator -- 2.1.3 Mechanosensor -- 2.1.4 Growth factor reservoir and modulator of signaling peptides -- 2.2 Major ECM components -- 2.2.1 Collagen -- 2.2.2 Proteoglycans -- 2.2.3 Other ECM molecules -- 2.2.4 Matrix-degrading enzymes -- 2.3 ECM dynamics in development -- 2.3.1 General aspects/processes -- 2.3.1.1 Embryogenesis -- 2.3.1.2 Branching morphogenesis -- 2.3.1.3 Stem cell niches and stem cell differentiation -- 2.3.1.4 Homeostasis -- 2.3.2 How systems work -- 2.3.2.1 ECM in nervous system development -- 2.3.2.2 Skeletal development -- 2.3.2.3 Skin development -- 2.4 ECM remodeling in regeneration and repair -- 2.4.1 Intervertebral disc regeneration -- 2.4.2 Wound healing -- 2.4.3 Bone remodeling and healing -- 2.4.4 CNS regeneration and repair -- 2.5 Conclusions -- References -- Chapter 3: Surface functionalization of biomaterials for bone tissue regeneration and repair -- 3.1 General introduction and chapter overview -- 3.2 Principles of surface biofunctionalization for bone repair -- 3.2.1 Mimicking bone ECM with peptides and proteins -- 3.2.1.1 Integrin signaling -- 3.2.1.2 Growth factor signaling -- 3.2.2 Ligands used for biofunctionalization -- 3.2.2.1 Limitations of proteins -- 3.2.2.2 Limitations of synthetic peptides -- 3.3 RGD peptidomimetics as surface coating molecules -- 3.3.1 Cyclic peptides and modifications of the peptide structure -- 3.3.2 Design of nonpeptidic integrin-binding ligands -- 3.3.3 Examples of surface functionalization with avß3- or a5ß1-selective peptidomimetics -- 3.4 Multifunctionality on biomaterials. , 3.4.1 Combining multiple biological cues-toward highly bioactive biomaterials -- 3.4.1.1 Multifunctional approaches (I): Improving cell adhesion -- 3.4.1.2 Multifunctional approaches (II): Mimicking the ECM microenvironment -- 3.4.1.3 Multifunctional approaches (III): Winning the race for the surface -- 3.4.2 Systems of presentation -- 3.4.2.1 Peptide mixtures -- 3.4.2.2 Peptide oligomers and constructs -- 3.4.2.3 Engineered protein fragments -- 3.4.2.4 Growth factor recruiting systems -- 3.4.2.5 Functionalized (antifouling) polymers -- 3.4.2.6 Functionalized drug-releasing polymers -- 3.4 Conclusions and future perspectives -- References -- Chapter 4: Bioengineered peptide-functionalized hydrogels for tissue regeneration and repair -- 4.1 Introduction -- 4.1.1 Structural and compositional features of the native extracellular matrix -- 4.2 Hydrogels as ECM mimics -- 4.2.1 Bioactive and bioinert hydrogels -- 4.3 Bioengineered hydrogels -- 4.3.1 Biofunctionalization of hydrogels with bioactive peptides -- 4.3.1.1 Hydrogel conjugation with integrin-binding peptides -- 4.3.1.2 Hydrogel conjugation with protease-sensitive peptides -- 4.3.1.3 Hydrogel conjugation with proangiogenic peptides -- 4.3.1.4 Hydrogel conjugation with differentiation-inducer peptides -- 4.3.1.5 Hydrogel conjugation with GAG-binding peptides -- 4.4 Balancing biochemical and biomechanical cues in hydrogel-based matrices -- 4.5 Dynamically switchable peptide-functionalized hydrogels -- 4.6 General conclusions and future directions -- Acknowledgments -- References -- Chapter 5: Collagen-based biomaterials for tissue regeneration and repair -- 5.1 Introduction -- 5.2 Structure and function of collagen -- 5.3 Manufacturing and fabrication of collagen-based biomaterials -- 5.3.1 Isolation of collagen -- 5.3.2 Freeze-drying -- 5.3.3 Electrospinning -- 5.3.4 3D bioprinting. , 5.3.5 Cross-linking -- 5.3.5.1 Dehydrothermal treatment -- 5.3.5.2 Ultraviolet radiation -- 5.3.5.3 Glutaraldehyde -- 5.3.5.4 Carbodiimides -- 5.3.5.5 Microbial transglutaminase -- 5.4 Functionalized collagen-based biomaterials for tissue regeneration -- 5.4.1 Composite scaffolds -- 5.4.2 Cell-based therapies -- 5.4.3 Growth factor and recombinant protein delivery -- 5.4.4 Gene-activated matrices -- 5.5 State of the art and future trends -- References -- Chapter 6: Fibrin biomaterials for tissue regeneration and repair -- 6.1 Introduction -- 6.2 Fibrin(ogen) structure -- 6.3 Fibrin polymerization -- 6.4 Overview of fibrin's role in promoting cell infiltration during wound repair -- 6.5 Fibrin-cell interactions -- 6.6 Impact of cells on fibrin network formation and properties -- 6.7 Fibrin and inflammation -- 6.8 Fibrin and angiogenesis -- 6.9 Overview of fibrin biomaterials and current clinical uses -- 6.10 Fibrin as a tissue sealant -- 6.11 Engineering the properties of fibrin networks -- 6.12 Mechanical modification of stiffness/elasticity -- 6.13 Modification of degradation properties -- 6.14 Modification with growth factors -- 6.15 Summary and future outlooks -- References -- Chapter 7: Fibrous protein-based biomaterials (silk, keratin, elastin, and resilin proteins) for tissue regeneration and repair -- 7.1 Introduction -- 7.2 Biopolymer-gels based on fibrous proteins: General considerations -- 7.3 Silk fibroin -- 7.3.1 Protein structure -- 7.3.2 Extraction and purification -- 7.3.3 Hydrogels formation -- 7.3.4 Applications in tissue repair and regeneration -- 7.4 Keratins -- 7.4.1 Protein structure -- 7.4.2 Extraction and purification -- 7.4.3 Hydrogel formation -- 7.4.4 Applications in tissue repair and regeneration -- 7.4.4.1 Nerve regeneration -- 7.4.4.2 Wound dressing -- 7.4.4.3 Hemostatic agent -- 7.4.4.4 Cartilage tissue engineering. , 7.4.4.5 Controlled drug delivery system -- 7.4.4.6 Cell culture systems -- 7.5 Elastin -- 7.5.1 Protein structure -- 7.5.2 Extraction and purification -- 7.5.3 Hydrogel formation -- 7.5.4 Application in tissue repair and regeneration -- 7.6 Resilin -- 7.6.1 Protein structure -- 7.6.2 Protein extraction and purification -- 7.6.3 Hydrogel formation -- 7.6.4 Application on tissue repair and regeneration -- 7.7 Final remarks and future perspectives -- References -- Further reading -- Chapter 8: Fabrication of nanofibers and nanotubes for tissue regeneration and repair -- 8.1 Introduction -- 8.2 Nanofibers from organic materials -- 8.2.1 Electrospinning -- 8.2.2 Self-assembly -- 8.2.3 Phase separation -- 8.2.4 Other processing techniques -- 8.3 Inorganic nanofibers -- 8.4 Nanotubes -- 8.5 Nanocomposites -- 8.6 Conclusions -- References -- Further reading -- Chapter 9: Peptide and protein printing for tissue regeneration and repair -- 9.1 Introduction -- 9.2 Contact printing technologies -- 9.2.1 Reactive microcontact printing -- 9.2.2 Supramolecular microcontact printing -- 9.2.3 Dip pen nanolithography -- 9.2.4 Polymer pen lithography -- 9.2.5 Transfer printing -- 9.3 Printing applications in biology and medicine -- 9.3.1 Biomaterial microarrays -- 9.3.2 ECM microarrays to control cell shape -- 9.3.3 Shape-induced stem cell differentiation -- 9.3.4 Printed arrays for neurons -- 9.3.5 Peptide arrays in cartilage research -- 9.3.6 Antiinflammation by printed micropatterns -- 9.3.7 Drug delivery from arrays -- 9.3.8 Biomembrane modeling -- 9.4 Conclusion and outlook -- Acknowledgments -- References -- Chapter 10: Self-assembling peptides and their application in tissue engineering and regenerative medicine -- 10.1 Introduction -- 10.2 Common secondary structure of proteins and peptides -- 10.2.1 α-Helix -- 10.2.2 Coiled-coil helix -- 10.2.3 ß-Sheet. , 10.2.4 ß-Hairpins.
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  • 2
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Analytical chemistry 50 (1978), S. 229-231 
    ISSN: 1520-6882
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    [S.l.] : American Institute of Physics (AIP)
    Journal of Applied Physics 89 (2001), S. 6680-6682 
    ISSN: 1089-7550
    Source: AIP Digital Archive
    Topics: Physics
    Notes: We present experimental results on the growth and structure of Fe overlayers deposited on Cu84Al16(100) and discuss the correlation between the structural and magnetic properties of this system. Fe films 1–6 monolayers (ML) thick were grown under molecular beam epitaxy conditions onto the clean substrate at 160 K. Electron diffraction was applied to investigate the structure of the Fe films. The magnetic properties were investigated in situ by surface magneto-optical Kerr effect in the longitudinal geometry. Our results show that the onset of in-plane ferromagnetism around 3.5 ML of Fe coincides with structural changes that suggest a transformation within the Fe films from a fcc-like (100) to a bcc-like (110) structure with increasing Fe thickness, starting from 2.5 ML. © 2001 American Institute of Physics.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The aim of this study was to investigate the role of immunoglobulin E (IgE) in the late phase reaction (LPR) of murine experimental asthma. Our model consisted of an implant of DNP-conjugated, heat-coagulated hen's egg white (DNP-EWI), followed 14 days later by an intratracheal challenge with aggregated DNP-ovalbumin. Airway inflammation was analyzed 48 h after challenge and compared with a similarly immunized group of mice with highly suppressed humoral response due to anti-μ and anti-δ antibody treatment. Total number of cells in the bronchoalveolar lavage (BAL) (with predominance of eosinophils) and EPO activity in the lung homogenate were increased in the DNP-EWI-immunized group compared with immunosuppressed or nonimmunized mice. However, the cellular infiltration and EPO activity observed in the immunosuppressed group were still significantly above those obtained in the nonimmunized group, indicating that inhibition of antibody production did not completely prevent the inflammatory manifestations in BAL and lung. Airway hyperresponsiveness to methacoline was obtained in DNP-EWI-immunized mice, but the respiratory mechanical parameters returned to normal levels in the immunosuppressed group. When these mice were reconstituted with monoclonal anti-DNP antibodies, only IgE, but not IgG1, restored lung inflammation and decreased the conductance of the respiratory system, therefore, increasing hyperresponsiveness. These results indicate that antibodies are not essential for induction of LPR in the lung. However, IgE enhances pulmonary inflammation and hyperresponsiveness.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1520-5827
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Scandinavian journal of immunology 55 (2002), S. 0 
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Toxoplasma gondii is an intracellular parasite whose life cycle may include the man as an intermediate host. Close to a billion people are infected with this parasite worldwide. Ocular lesions may occur in up to 25% of those individuals infected. The infection may occur intra-uterus, through the placenta when the mother is infected during pregnancy. The parasite may also infect adults after the ingestion of contaminated food products, most notably meats or water. We have shown that although congenital and post-natal (acquired) infection results in similar ocular lesions, the immunological mechanisms behind the development of disease are different. On the other hand, contrary to published data obtained in mice, we were unable to find evidence that the T. gondii express superantigen activity for human lymphocytes. Our findings are important because they suggest that superantigen activity is not important as a pathological mechanism in human disease. Our data also suggest that, whereas the ocular lesion caused by infection after birth is the result of an excessive or dysfunctional immune response, the lesions caused by congenital infection may be due to a lack of an appropriate response to the parasite.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Clinical & experimental allergy 35 (2005), S. 0 
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background We have recently isolated two distinct components from Ascaris suum adult worms with different effects on the immune system: the allergenic protein of A. suum (APAS-3), which induces IgE antibody production, and suppressive protein of A. suum (PAS-1), which inhibits humoral and cellular immune responses induced by unrelated antigens. In this study, we investigated the immunomodulatory effect of PAS-1 on a murine model of asthma induced by APAS-3.Methods BALB/c mice were immunized twice with APAS-3 or APAS-3 plus PAS-1 by the intraperitoneal and subcutaneous route (on days 0 and 7) and challenged twice with the same antigens intranasally (days 14 and 21). Two days after the last challenge, the allergic airway inflammation was evaluated by cellular migration, eosinophil peroxidase (EPO) activity, cytokine and chemokine production and pulmonary mechanical parameters.Results The allergenic properties of APAS-3 were confirmed by the stimulation of anaphylactic IgE and IgG1 antibody production and eosinophilic airway inflammation and hyper-responsiveness. On the other hand, PAS-1-treated mice showed a marked suppression of cellular migration and EPO activity that correlated well with a significant reduction in the levels of IL-4, IL-5, eotaxin and RANTES in the bronchoalveolar lavage (BAL) fluid. In contrast, considerable amounts of IL-10 were observed in the BAL fluid of PAS-1-treated mice. Airway hyper-responsiveness was obtained in APAS-3-immunized mice, but the conductance of the respiratory system was restored to normal values in the presence of PAS-1.Conclusion These results indicate that A. suum allergenic protein APAS-3 induces a T helper 2-type immune response and, consequently, eosinophilic airway inflammation and hyper-responsiveness. Moreover, the modulatory protein PAS-1 has a marked suppressive effect on this response, and the inhibition of cytokine (IL-4, IL-5) and chemokine (eotaxin and RANTES) release, probably because of the presence of IL-10, may contribute to this effect.
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  • 8
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background The site and distribution of inflammation in the airways of asthmatic patients has been largely investigated. Inflammatory cells are distributed in both large and small airways in asthma. It has been demonstrated that distal lung inflammation in asthma may significantly contribute to the pathophysiology of the disease. The upper airways have also been implicated in the overall asthmatic inflammation. Although it is now accepted that lung inflammation is not restricted to the intrapulmonary airways in asthma, little is known about cell distribution in the other lung compartments and their relation to the intrapulmonary airways.Objective We aimed to map the inflammatory process in fatal asthma (FA), from the upper airways to the lung parenchyma.Methods Eosinophil, neutrophil, mast cell and lymphocyte content were determined in nasal mucosa, the trachea, intrapulmonary airways and parenchyma (peribronchiolar and distal) of 20 patients with FA and 10 controls.Results Eosinophil content was higher in all studied areas in FA compared with controls (P〈0.02). Mast cell content was higher in the outer area of larger airways, small membranous bronchioles and in peribronchiolar parenchyma of FA compared with controls (P〈0.04). CD3+, CD4+and CD20+cells showed increased content in FA intrapulmonary airways compared with controls (P〈0.05). There was a positive correlation between CD4+cell content in nasal mucosa and larger airways in asthmatics. Increased neutrophil content was observed only in peribronchiolar parenchyma of FA (P=0.028).Conclusion Eosinophils present a widespread distribution within the respiratory tract in FA, from the nasal mucosa to the distal lung. The outer wall of small membranous bronchioles is the main site of inflammatory changes in FA. There is a localized distribution of alveolar inflammation at the peribronchiolar region for mast cells and neutrophils. Our findings provide further evidence of the importance of the lung periphery in the pathophysiology of FA.
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  • 9
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Leukotriene receptor antagonists have been demonstrated in several studies to possess bronchodilating and anti-inflammatory properties in asthma. However, there are few experimental studies performed to compare the effects of anti-leukotrienes and glucocorticoids, most used anti-inflammatory agents in asthma. In the present study, we evaluated the effects of treatment with dexamethasone or montelukast on eosinophil and mononuclear cell recruitment in an experimental model of allergen-induced chronic airway inflammation in guinea-pigs (GP).Methods GP were submitted to increasing concentrations of aerosols of ovalbumin (OVA) twice a week for 4 weeks. After 2 weeks, animals were treated daily with dexamethasone, montelukast or saline solution. After this period, GP were anaesthetized, tracheostomized, mechanically ventilated and challenged with OVA aerosol.Results Maximal changes of respiratory system resistance and elastance induced by OVA challenge were attenuated by dexamethasone (P〈0.001), but not by montelukast treatment. Neither dexamethasone nor montelukast significantly influenced bronchial oedema formation. Dexamethasone but not montelukast induced a decrease in mononuclear cells in airways (P〈0.001). Eosinophil infiltration in the bronchial wall was reduced by both dexamethasone and montelukast (P〈0.005). Only dexamethasone treatment reduced the levels of exhaled nitric oxide (P〈0.025).Conclusion Although leukotriene receptor antagonist treatment reduces eosinophil accumulation induced by multiple antigen challenges, glucocorticoid treatment attenuates both eosinophil and mononuclear cell infiltration.
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  • 10
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background The increase of atopic disorders in developed countries has been associated with the decline of infectious diseases, including helminthic infections. We have already demonstrated that adult worm extracts from Ascaris suum (ASC) suppress the IgE antibody production against unrelated antigens.Objective Here we investigated the influence of ASC on the development of pulmonary eosinophilic inflammation in a murine model of asthma.Methods Heat-coagulated egg white alone (EWI) or mixed with ASC (EWI + ASC) was implanted subcutaneously in B10.A or C57BL/6 mice, and 14 days later they were challenged intratracheally with OVA or exposed to aerosolized OVA for 4 days.Results The suppressive effect of ASC was demonstrated on the accumulation of cells into airways, with reduction of eosinophil numbers and of eosinophil peroxidase activity in EWI + ASC- immunized mice. This effect correlated with a marked reduction of IL-5 and IL-4 levels in the BAL from C57BL/6 and B10.A mice, respectively, and of eotaxin in BAL and lung tissue from both strains. OVA-specific IgG1 and IgE levels were also impaired in serum and BAL from these mice. Airway hyper-reactivity to methacholine was obtained in B10.A mice sensitized with EWI, but the respiratory mechanical parameters returned to normal levels in EWI + ASC-immunized mice.Conclusion These results indicate that ASC has a profound inhibitory effect on lung inflammation and hyper-responsiveness and that suppression of IL-5 or IL-4 and of eotaxin contributes to this effect.
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