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  • English  (16)
  • Cinatl, Jindrich  (16)
  • Wiley Online Library  (16)
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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: ChemInform, 12 July 2005, Vol.36(28), pp.no-no
    Description: For see ChemInform in Full Text.
    Keywords: Biochemistry ; Review ; Pharmacology ; Medicinal Chemistry ; Vaccines ; Serums
    ISSN: 0931-7597
    E-ISSN: 1522-2667
    Source: John Wiley & Sons, Inc.
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  • 6
    Language: English
    In: Medicinal Research Reviews, September 2002, Vol.22(5), pp.492-511
    Description: Valproic acid (VPA, 2‐propylpentanoic acid) is an established drug in the long‐term therapy of epilepsy. During the past years, it has become evident that VPA is also associated with anti‐cancer activity. VPA not only suppresses tumor growth and metastasis, but also induces tumor differentiation in vitro and in vivo. Several modes of action might be relevant for the biological activity of VPA: (1) VPA increases the DNA binding of activating protein‐1 (AP‐1) transcription factor, and the expression of genes regulated by the extracellular‐regulated kinase (ERK)‐AP‐1 pathway; (2) VPA downregulates protein kinase C (PKC) activity; (3) VPA inhibits glycogen synthase kinase‐3β (GSK‐3β), a negative regulator of the Wnt signaling pathway; (4) VPA activates the peroxisome proliferator‐activated receptors PPARγ and †; (5) VPA blocks HDAC (histone deacetylase), causing hyperacetylation. The findings elucidate an important role of VPA for cancer therapy. VPA might also be useful as low toxicity agent given over long time periods for chemoprevention and/or for control of residual minimal disease. © 2002 Wiley Periodicals, Inc. Med Res Rev, 22, No. 5, 492–511, 2002; Published online in Wiley InterScience (). DOI 10.1002/med.10017
    Keywords: Valproic Acid ; Tumor Differentiation ; Tumor Growth ; Signaling Cascade
    ISSN: 0198-6325
    E-ISSN: 1098-1128
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  • 7
    Language: English
    In: International Journal of Cancer, 10 March 2003, Vol.104(1), pp.36-43
    Description: Cytotoxic drug treatment of neuroblastoma often leads to the development of drug resistance and may be associated with increased malignancy. To study the effects of long‐term cytotoxic treatment on malignant properties of tumor cells, we established 2 neuroblastoma cell sublines resistant to vincristine (VCR) and doxorubicin (DOX). Both established cell lines (UKF‐NB‐2VCR and UKF‐NB‐2DOX) were highly resistant to VCR, DOX and vice‐versa but retained their sensitivity to cisplatin. UKF‐NB‐2VCR and UKF‐NB‐2DOX expressed significant amounts of P‐glycoprotein, while parental cells were P‐glycoprotein negative. GD2 expression was upregulated, whereas NCAM expression was decreased in both resistant cells. Spectral karyotype (SKY) analysis revealed complex aberrant karyotypes in all cell lines and additional acquired karyotype changes in both resistant cells. All cell lines harbored high levels of N‐myc amplification. Compared to parental cells, UKF‐NB‐2VCR and UKF‐NB‐2DOX exhibited more than 2‐fold increase in clonal growth , accelerated adhesion and transendothelial penetration and higher tumorigenicity . We conclude that development of drug resistance and acquisition of certain karyotypic alterations is associated with an increase of additional malignant properties that may contribute to the poor prognosis in advanced forms of NB. The 2 novel neuroblastoma cell sublines also provide useful models for the study of drug resistance in aggressive forms of neuroblastoma. © 2002 Wiley‐Liss, Inc.
    Keywords: Neuroblastoma ; Drug Resistance ; Mdr‐1 ; Ncam ; Gd2 ; Karyotype
    ISSN: 0020-7136
    E-ISSN: 1097-0215
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  • 8
    In: Journal of the European Academy of Dermatology and Venereology, March 1996, Vol.6(2), pp.112-126
    Description: Since 1981, the standard therapy of herpes simplex virus infections has been based on acyclovir. Valaciclovir, the ‐valine ester of acyclovir and famciclovir, a pro‐drug of penciclovir with an improved oral bioavailability have been recently licensed. HPMPC, an acyclic nucleoside phosponate, is highly active and shows a broad range of activity against all the herpes viruses, and it is far more efficient than ganciclovir against cytomegalovirus. Ribonucleotidase inhibitors have so far been unsuccessful in the treatment of acyclovir‐resistant HSV infections. In the future, anti‐sense oligonucleotides may play a role in the therapy of herpes virus infections and many efforts continue to be made to develop vaccines which may prevent recurrences in already infected individuals. Resistance to anti‐HSV agents is almost exclusively encountered in immunocompromised patients. Failure of acyclovir therapy is mostly due to viral thymidine kinase (TK) deficiency as a result of mutation in the TK gene. Until now, the only alternatives for the treatment of acyclovir‐resistant infections have been the intravenous administration of foscarnet, frequently associated with relatively severe side effects, or the topical application of trifluridine either as single agent or in combination with interferon alpha. In vitro observations suggest that the failure of antiviral therapy is not directly due to the emergence of resistant virus isolates. Reduced uptake or activation of acyclovir may represent a selective pressure for resistant isolates in immunocompromised patients. New prodrugs with increased bioavailability, such as valaciclovir and famciclovir will perhaps prevent or delay the emergence of drug resistant isolates in immunocompromised patients since higher intracellular levels of the active compound can be achieved.
    Keywords: Acyclovir ; Famciclovir ; Valaciclovir ; Mechanism Of Action ; Antiviral Resistance
    ISSN: 0926-9959
    E-ISSN: 1468-3083
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  • 9
    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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  • 10
    Language: English
    In: Medicinal Research Reviews, July 2005, Vol.25(4), pp.383-397
    Description: The short chain fatty acid valproic acid (VPA) and VPA‐analogs modulate the biology of diverse tumor cell entities by inducing differentiation, inhibiting proliferation, increasing apoptosis, and immunogenicity and by decreasing metastatic and angiogenetic potential. This review updates an earlier one in 2002, reflecting the interest in VPA as a potent anticancer drug. A number of studies show that the types of known tumor cells susceptible to VPA is steadily increasing. Of special note is the strong antineoplastic activity of VPA in chemoresistant cancer cells. A novel and promising approach is combining VPA with other drugs to achieve a broad therapeutic index. Clinical studies are underway and the preliminary results indicate that VPA alone or in combination offers a promising avenue of treatment, both in solid and hematopoetic malignancies. © 2005 Wiley Periodicals, Inc.
    Keywords: Valproic Acid ; Hdac ; Differentiation ; Angiogenesis ; Combination Therapy ; Clinical Studies
    ISSN: 0198-6325
    E-ISSN: 1098-1128
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