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  • Wiley Online Library  (7)
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  • 1
    In: Acta Ophthalmologica, March 2012, Vol.90(2), pp.e98-e103
    Description: To compare cytokines in undiluted vitreous of treatment‐naïve patients with macular oedema without vitreomacular traction secondary to branch (BRVO), central (CRVO) and hemi‐central (H‐CRVO) retinal vein occlusion. Ninety‐four patients (median age 72 years, 42 men) underwent an intravitreal combination therapy, including a single‐site 23‐gauge core vitrectomy and the application of bevacizumab and dexamethasone due to vision‐decreasing macular oedema. Among these were 43 patients with BRVO, 35 with CRVO and 16 patients with hemi‐CRVO, which were distributed in a fresh or old retinal vein occlusion type (seven or more months after onset). Undiluted vitreous samples were analysed for interleukin 6 (IL‐6), monocyte chemoattractant protein‐1 (MCP‐1) and vascular endothelial growth factor (VEGF‐A) with cytometric BEAD assay. Vitreous samples from patients with idiopathic epiretinal membrane served as controls ( = 14). The mean cytokine values were highest in the CRVO group with IL‐6 = 64.7 pg/ml (SD ± 115.8), MCP‐1 = 1015.8 pg/ml (±970.1) and VEGF‐A = 278.4 pg/ml (±512.8), followed by the H‐CRVO group with IL‐6 = 59.9 pg/ml (SD ± 97.5), MCP‐1 = 938.8 pg/ml (±561.1) and VEGF‐A = 211.5 pg/ml (±232.4). The BRVO group had IL‐6 = 23.2 pg/ml (SD ± 48.8), MCP‐1 = 602.6 pg/ml (±490.3) and VEGF‐A = 161.8 pg/ml (±314.4). The values of MCP‐1 and VEGF‐A were significantly different for CRVO or H‐CRVO versus BRVO. All values were significantly higher than in the control samples, which had 6.2 ± 3.4 pg/ml (IL‐6), 253 ± 74 pg/ml (MCP‐1) and 7 ± 4.9 pg/ml (VEGF‐A). Within the old RVO type, only MCP‐1 was significantly different for CRVO or H‐CRVO versus BRVO. Both inflammatory markers and VEGF‐A were higher in CRVO and H‐CRVO than in BRVO undiluted vitreous samples. It seems that monocyte recruitment to the vessel wall, which might underlie the importance of eosinophils in tissue remodelling after RVO, is of special interest owing to the significant difference in MCP‐1 in the older RVO types.
    Keywords: Cytometric Bead Array ; Interleukin 6 ; Monocyte Chemoattractant Protein ; Retinal Vein Occlusion ; Vascular Endothelial Growth Factor ; Vitreous Samples
    ISSN: 1755-375X
    E-ISSN: 1755-3768
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  • 2
    Language: English
    In: FEBS Letters, 03 April 2007, Vol.581(7), pp.1317-1322
    Description: Treatment of transformed cells from leukemia or solid tumors with histone deacetylase inhibitors (HDACi) was shown to increase their sensitivity to NK cell lysis. In this study, treatment of IL-2-activated NK cells with HDACi including suberoylanilide hydroxamic acid and valproic acid was studied. Both drugs at therapeutic concentrations inhibited NK cell cytotoxicity on human leukemic cells. This inhibition was associated with decreased expression and function of NK cell activating receptors NKp46 and NKp30 as well as impaired granule exocytosis. NFκB activation in IL-2-activated NK cells was inhibited by both HDACi. Pharmacologic inhibition of NFκB activity resulted in similar effects on NK cell activity like those observed for HDACi. These results demonstrate for the first time that HDACi prevent NK cytotoxicity by downregulation of NK cell activating receptors probably through the inhibition of NFκB activation.
    Keywords: Cytotoxicity ; Nk Cells ; Histone Deacetylase Inhibitors ; Nk Cell Activating and Inhibitory Receptors ; Nuclear Factor Kappa B ; Biology ; Chemistry ; Anatomy & Physiology
    ISSN: 0014-5793
    E-ISSN: 1873-3468
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  • 3
    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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  • 4
    Language: English
    In: Medicinal Research Reviews, May 2005, Vol.25(3), pp.331-342
    Description: Systemically applied agents to modulate the Fas/FasL system, e.g., by stimulation of Fas on activated leukocytes or tumor cells failed as strategies in immune therapy due to severe toxic effects in the host. Recently, a novel strategy has been developed by using immobilized immune active biologicals in a medical device that may allow immune management without expensive systemic therapy. This review reports on the potential role of Fas/FasL in immune therapy and summarizes current experimental and clinical data with the leukocyte inhibition module (LIM), an immobilized anti‐Fas antibody containing device yet used in extracorporeal blood circulation. This proof of principal may stimulate the development of other devices based on the regulation of Fas/FasL or other targets relevant for immune disorders. © 2004 Wiley Periodicals, Inc.
    Keywords: Novel Therapeutic Strategies ; Immune Management ; Apoptosis
    ISSN: 0198-6325
    E-ISSN: 1098-1128
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  • 5
    Language: English
    In: Cell Biology International, April 1994, Vol.18(4), pp.271-278
    Description: The effects of aphidicolin, a specific inhibitor of DNA polymerase alpha, on cell growth, DNA synthesis and myogenic differentiation in the human alveolar rhabdomyosarcoma cell line KFR were studied. The treatment with aphidicolin at 5 x 10(-6) M concentration, which completely inhibited DNA synthesis and cell growth, induced morphological differentiation of small mononuclear cells to elongated, multinucleated (myotube-like) structures. The morphological differentiation was accompanied by the expression of skeletal muscle myosin; about 30% myosin-positive cells were observed after 14 days of treatment, compared to 2.3% in untreated cultures. The results showed that aphidicolin induces differentiation of human rhabdomyosarcoma cells and that multinucleated myotube-like elements may develop simply by cell fusion without cell division and DNA synthesis.
    Keywords: Biology
    ISSN: 1065-6995
    E-ISSN: 1095-8355
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  • 6
    Language: English
    In: Medicinal Research Reviews, March 2005, Vol.25(2), pp.167-185
    Description: It has been known for a long time that cytomegalovirus (CMV) has evolved mechanisms that allow the escape from the host immune surveillance. In the past, many efforts have been done to elucidate the molecular mechanisms underlying this virus‐mediated immune escape and thus virus persistence. However, it is unknown, whether CMV may also impair immune responses directed against tumor cells. This might have severe consequences on tumor progression and may explain the growing evidence for CMV‐mediated oncomodulation. This review summarizes recent work on CMV‐mediated immune escape mechanisms of tumor cells and oncomodulation and proposes novel aspects that may be important for understanding the CMV‐associated tumor progression. © 2004 Wiley Periodicals, Inc.
    Keywords: Human Cytomegalovirus Hcmv ; Oncomodulation ; Tumor ; Dna‐Virus ; Apoptosis ; Angiogenesis
    ISSN: 0198-6325
    E-ISSN: 1098-1128
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  • 7
    In: FEMS Microbiology Reviews, February 2004, Vol.28(1), pp.59-77
    Description: A high frequency of human cytomegalovirus (HCMV) genome and antigens in tumor samples of patients with different malignancies is now well documented, although the causative role for HCMV in the development of the neoplasias remains to be established. HCMV infection can modulate multiple cellular regulatory and signalling pathways in a manner similar to that of oncoproteins of small DNA tumor viruses such as human papilloma virus or adenoviruses. However, in contrast to these DNA tumor viruses, HCMV infection fails to transform susceptible normal human cells. There is now growing evidence that tumor cells with disrupted regulatory and signalling pathways enable HCMV to modulate their properties including stimulation of cell proliferation, survival, invasion, production of angiogenic factors, and immunogenic properties. In contrast to previously suggested “hit and run” transformation we suggest that persistence in tumor cells is essential for HCMV to fully express its oncomodulatory effects. These effects are observed particularly in persistent HCMV infection and are mediated mainly by activity of HCMV regulatory proteins. In persistently HCMV‐infected tumor cell lines – a selection of novel, slowly growing virus variants with changes in coding sequences for virus regulatory proteins takes place. As a result, oncomodulatory effects of HCMV infection may lead to a shift to more malignant phenotype of tumor cells contributing to tumor progression.
    Keywords: Human Cytomegalovirus ; Oncomodulation ; Tumor ; Dna‐Virus ; Apoptosis ; Angiogenesis
    ISSN: 0168-6445
    E-ISSN: 1574-6976
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