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  • 1
    In: Wound Repair and Regeneration, September 2011, Vol.19(5), pp.597-607
    Description: The pathophysiology leading to delayed wound healing is complex and efficient therapeutic approaches for accelerated wound healing currently do not exist. We developed a novel drug‐eluting platform for the potential use in wound dressings. Here, we report on the potential of eluting ascorbic acid‐2‐phosphate (‐2), a highly stable variant of ascorbic acid, to induce angiogenesis and to promote collagen synthesis by fibroblasts. The drug‐eluting platform device () consists of biocompatible polymeric layers comprising polyethylene terephtalate, polyvinyl alcohol (), and polyurethane with as the solvent for ‐2. The angiogenic potential of ‐2 was evaluated in the endothelial cell tube formation assay () and in the chorion allantoic membrane () model. Collagen synthesis by ‐2‐stimulated fibroblasts was determined by irius ed staining. ‐2 significantly induced angiogenesis in five independent and assays and induced collagen synthesis in two different fibroblast cell lines. The eluting kinetics of ‐2 was determined by the ultraviolet anorop method and the functional 2,2′‐Azinobis‐(3‐ethylbenzthiazolin‐6‐sulfonic acid) method. Eluting profiles showed a continuous release in the range of biologically effective concentrations 〉10 days. This is the first report showing the proangiogenic‐ and collagen‐promoting features of ‐2. loaded with ‐2 ought to be further evaluated as wound dressings or as supplementary pads for topical treatment of delayed wound healing in preclinical studies.
    Keywords: Drug Delivery Systems ; Angiogenesis Inducing Agents -- Pharmacology ; Ascorbic Acid -- Analogs & Derivatives ; Neovascularization, Physiologic -- Drug Effects ; Wound Healing -- Drug Effects;
    ISSN: 1067-1927
    E-ISSN: 1524-475X
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  • 2
    Language: English
    In: Medicinal Research Reviews, May 2007, Vol.27(3), pp.401-416
    Description: Despite the fact that neutrophils are essential for the protection from invading pathogens, hyperactive neutrophils may elicit detrimental cerebral damage after severe trauma. The neutrophil interactions with the neurovascular unit entail endothelial dysfunction involving endothelial leakage, formation of edema, coagulation abnormalities, disturbed hemodynamics, tissue infiltration etc. These elements of the “whole body inflammation,” designated systemic inflammatory response syndrome (SIRS) in conjunction with intracerebral proinflammatory activities, are important triggers of post‐traumatic cerebral damage and mortality according to the “second hit” concept. From the immunologic point of view, the brain is an immune privileged site, known to resist autodestructive inflammatory activity much more efficiently than other organs because of the highly efficient diverse functions of the blood–brain barrier (BBB). However, both the underlying strategy of the BBB to maintain cerebral protecting functions against the post‐traumatic neutrophil‐mediated “second hit” and how activated neutrophils may overcome the BBB are currently unknown. Therefore, this review summarizes the current understanding of the “second hit,” the BBB physiology, and its role in the maintenance of cerebral immune privilege, and discusses recent findings that may explain the pathophysiologic neutrophil–BBB interactions occurring after severe trauma, thus offering novel therapeutic options to protect from post‐traumatic brain damage. © 2006 Wiley Periodicals, Inc. Med Res Rev, 27, No. 3, 401–416, 2007
    Keywords: Blood–Brain Barrier ; Hyperactive Neutrophils ; Second Hit Concept ; Sirs ; Trauma
    ISSN: 0198-6325
    E-ISSN: 1098-1128
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  • 3
    Language: English
    In: ChemInform, 24 July 2007, Vol.38(30), pp.no-no
    Description: ChemInform is a weekly ing Service, delivering concise information at a glance that was extracted from about 200 leading journals. To access a ChemInform , please click on HTML or PDF.
    Keywords: Biochemistry ; Review ; Pharmacology ; Medicinal Chemistry ; Vaccines ; Serums
    ISSN: 0931-7597
    E-ISSN: 1522-2667
    Source: John Wiley & Sons, Inc.
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