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  • 1
    Language: English
    In: Langenbeck's Archives of Surgery, 2011, Vol.396(8), pp.1165-1172
    Description: Byline: Patrizia Malkomes (1), Elsie Oppermann (1), Wolf-Otto Bechstein (1), Katharina Holzer (1) Keywords: PDGF; PDGF receptor; Thyroid; Recurrent goitre Abstract: Purpose Platelet-derived growth factor (PDGF) is a critical regulator of cell proliferation and influences the development of tumors. The role of PDGF in benign thyroid diseases is presently not well-determined. The purpose is to evaluate PDGF isoforms and receptors in primary culture of thyrocytes isolated from human thyroid tissue. Methods Forty patients with uninodular (n=11), multinodular (n=15) and recurrent goitre (n=14) were investigated. Nodular and corresponding paranodular thyroid tissues were characterized. RNA and protein were extracted from primary thyrocyte monoculture. RT-PCR, western blot and ELISA were performed to evaluate PDGF isoforms AA, BB, CC, DD and PDGF receptors [alpha] and [beta]. Results Significantly higher mRNA expression of PDGF-AA, -BB, -CC and PDGFR molecules [alpha] and [beta] was measured by RT-PCR in thyrocytes from uninodular and recurrent nodular tissue compared with corresponding paranodular tissue. Elevated PDGF protein and PDGFR-[alpha] and -[beta] were confirmed by western blot. Likewise, higher secretion of PDGF-AA and -BB was detected in the supernatant of thyrocyte culture from all nodular tissue compared with paranodular tissue. Interestingly, comparison of nodular and corresponding paranodular tissues in multinodular goitre did not show significant difference of expression levels of PDGF isoforms or receptors. Conclusion These findings suggest that the overexpression of PDGF isoforms and receptors may play a crucial role in the development of thyroid nodules and recurrent goitre. Author Affiliation: (1) Department of General Surgery, Johann-Wolfgang Goethe University, Universitatsklinikum Frankfurt am Main, Theodor-Stern-Kai 7, 60590, Frankfurt am Main, Germany Article History: Registration Date: 12/04/2011 Received Date: 23/11/2010 Accepted Date: 12/04/2011 Online Date: 08/05/2011
    Keywords: PDGF ; PDGF receptor ; Thyroid ; Recurrent goitre
    ISSN: 1435-2443
    E-ISSN: 1435-2451
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  • 2
    Language: English
    In: Mediators of Inflammation, Annual, 2014
    Description: Chronic ethanol abuse is known to increase susceptibility to infections after injury, in part, by modification of macrophage function. Several intracellular signalling mechanisms are involved in the initiation of inflammatory responses, including the nuclear factor[kappa]B (NF-[kappa]B) pathway In this study, we investigated the systemic and hepatic effect of chronic ethanol feeding on in vivo activation of NF-[kappa]B in [NF-[kappa]B.sup.EGFP] reporter gene mice. Specifically, the study focused on Kupffer cell proinflammatory cytokines IL-6 and TNF-[alpha] and activation of NF-[kappa]B after chronic ethanol feeding followed by in vitro stimulation with lipopolysaccharide (LPS). We found that chronic ethanol upregulated NF-[kappa]B activation and increased hepatic and systemic proinflammatory cytokine levels. Similarly, LPS-stimulated IL-1[beta] release from whole blood was significantly enhanced in ethanol-fed mice. However, LPS significantly increased IL-6 and TNF-[alpha] levels. These results demonstrate that chronic ethanol feeding can improve the responsiveness of macrophage LPSstimulated IL-6 and TNF-[alpha] production and indicate that this effect may result from ethanol-induced alterations in intracellular signalling through NF-[kappa]B. Furthermore, LPS and TNF-[alpha] stimulated the gene expression of different inflammatory mediators, in part, in a NF-[kappa]B-dependent manner.
    Keywords: Kupffer Cells -- Genetic Aspects ; Kupffer Cells -- Health Aspects ; Inflammation -- Genetic Aspects ; Gene Expression -- Identification And Classification ; White Blood Cells -- Health Aspects ; White Blood Cells -- Genetic Aspects ; Tumor Necrosis Factor -- Health Aspects ; Ethanol -- Health Aspects
    ISSN: 0962-9351
    Source: Cengage Learning, Inc.
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  • 3
    Language: English
    In: Mediators of Inflammation, 2014
    Description: Chronic ethanol abuse is known to increase susceptibility to infections after injury, in part, by modification of macrophage function. Several intracellular signalling mechanisms are involved in the initiation of inflammatory responses, including the nuclear factor[kappa]B (NF-[kappa]B) pathway In this study, we investigated the systemic and hepatic effect of chronic ethanol feeding on in vivo activation of NF-[kappa]B in [NF-[kappa]B.sup.EGFP] reporter gene mice. Specifically, the study focused on Kupffer cell proinflammatory cytokines IL-6 and TNF-[alpha] and activation of NF-[kappa]B after chronic ethanol feeding followed by in vitro stimulation with lipopolysaccharide (LPS). We found that chronic ethanol upregulated NF-[kappa]B activation and increased hepatic and systemic proinflammatory cytokine levels. Similarly, LPS-stimulated IL-1[beta] release from whole blood was significantly enhanced in ethanol-fed mice. However, LPS significantly increased IL-6 and TNF-[alpha] levels. These results demonstrate that chronic ethanol feeding can improve the responsiveness of macrophage LPSstimulated IL-6 and TNF-[alpha] production and indicate that this effect may result from ethanol-induced alterations in intracellular signalling through NF-[kappa]B. Furthermore, LPS and TNF-[alpha] stimulated the gene expression of different inflammatory mediators, in part, in a NF-[kappa]B-dependent manner.
    Keywords: Kupffer Cells – Genetic Aspects ; Kupffer Cells – Health Aspects ; Inflammation – Genetic Aspects ; Gene Expression – Identification and Classification ; White Blood Cells – Health Aspects ; White Blood Cells – Genetic Aspects ; Tumor Necrosis Factor – Health Aspects ; Ethanol – Health Aspects
    ISSN: 0962-9351
    Source: Cengage Learning, Inc.
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  • 4
    Language: English
    In: Molecular Medicine Reports, 8/2015, Vol.12(2), pp.2991-2998
    Description: Increased local and systemic levels of interleukin (IL)-6 are associated with inflammatory processes, including neutrophil infiltration of the alveolar space, resulting in lung injury. Our previous study demonstrated the beneficial anti-inflammatory effects of acute exposure to ethanol (EtOH) in an acute in vivo model of inflammation. However, due to its side-effects, EtOH is not used clinically. In the present study, the effects of EtOH and ethyl pyruvate (EtP) as an alternative anti-inflammatory drug prior to and following application of an IL-6 stimulus on cultured A549 lung epithelial cells were compared, and it was hypothesized that treatment with EtOH and EtP reduces the inflammatory potential of the A549 cells. Time- and dose-dependent release of IL-8 from the A549 cells was observed following stimulation with IL-6. The release of IL-8 from the A549 cells was assessed following treatment with EtP (2.5–10 mM), sodium pyruvate (NaP; 10 mM) or EtOH (85–170 mM) for 1, 24 or 72 h, prior to and following IL-6 stimulation. The adhesion capacities of neutrophils to the treated A549 cells, and the expression levels of cluster of differentiation (CD)54 by the epithelial cells were measured. Treatment of the A549 cells with either EtOH or EtP significantly reduced the IL-6-induced release of IL-8. This effect was observed in the pre- and post-stimulatory conditions, which is of therapeutic importance. Similar data was revealed regarding the IL-6-induced neutrophil adhesion to the treated A549 cells, in which pre- and post-treatment with EtOH or EtP decreased the adhesion capacity, however, the results were dependent on the duration of incubation. Incubation durations of 1 and 24 h decreased the adhesion rates of neutrophils to the stimulated A549 cells, however, the reduction was only significant at 72 h post-treatment. The expression of CD54 was reduced only following treatment for 24 h with either EtOH or EtP, prior to IL-6 stimulation. Therefore, EtOH and EtP reduced the inflammatory response of lung epithelial cells, and the potential of EtP to mimic EtOH was observed in the pre- and post-treatment conditions.
    Keywords: Ethanol ; Ethyl Pyruvate ; Lung ; Inflammation ; In Vitro
    ISSN: 1791-2997
    E-ISSN: 1791-3004
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  • 5
    Language: English
    In: International Journal of Molecular Medicine, March 2011, Vol.27(3), pp.447-454
    Description: Identification of patients at risk of a complicated course after liver resection is crucial for adapting post-operative care. In the present study, we investigated the diagnostic value of the plasma levels of various cytokines obtained immediately after surgery. IL-6, IL-10, IL-8, monokine induced by interferon-γ (MIG), monocyte chemotactic protein-1 (MCP-1) and interferon-inducible protein-10 (IP-10) concentrations were measured in 26 patients after liver resection using a cytometric bead assay and were correlated with liver function, resectate weight, surgery duration, ischemia/reperfusion, hospitalization time and occurrence of complications. Patients with post-surgical complications showed distinctive patterns of IL-6 and IL-8 as early as minutes to hours after surgery. In addition, although pre-operative bilirubin in most patients remained within the normal range, a cut-off of 1 mg/dl separated the patients into groups with different profiles of IL-6, IL-8, and MCP-1 secretion and different likelihoods of experiencing post-operative complications (bilirubin levels ≥1.0 vs. 〈1.0 mg/dl; IL-6 (4 h): 701 vs. 265; IL-8 (6 h): 262 vs. 97 pg/ml; p〈0.05 for both). Extended hospitalization, related to delayed recovery, was correlated with increased IL-8 and MCP-1 immediately after surgery. In conclusion, on the basis of these observations, we suggest that early measurement of post-operative levels of MCP-1, IL-6, and IL-8 can be used to identify individuals at risk of post-operative complications immediately after liver surgery.
    Keywords: Surgical Stapler;
    ISSN: 1107-3756
    E-ISSN: 1791244X
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  • 6
    Language: English
    In: Experimental and Therapeutic Medicine/2011, Vol.2(2), pp.301-307
    Description: Valproate (VPA) is a well-characterized histone deacetylase inhibitor with anti-neoplastic properties. We analyzed the growth blocking effects and the molecular mode of action of this compound in colorectal cancer cells in vitro and in vivo . Caco-2, SW-480, CX-1 or WIDR cell lines were exposed to VPA (0.25–2 mM) for various time periods. Cell growth, cell cycle progression and apoptosis were analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide dye reduction assay and flow cytometry. Cell cycle- and apoptosis-regulating proteins and histone acetylation were assessed by Western blotting. In vivo tumor growth and regulating protein expression under VPA were investigated in a subcutaneous xenograft tumor model. VPA inhibited the growth of all cell lines with cell cycle arrest paralleled by the up-regulation of H3 and H4 acetylation. In vivo tumor growth was substantially depressed by VPA (200 mg/kg bw). Cell cycle proteins (cdk1, cdk2, cdk4, cyclin D, cyclin E, p19, p21 and p27) were differentially altered by VPA. Predominantly cdk1 was decreased and p27 was up-regulated in all models. Apoptosis-related proteins were altered in vivo with up-regulation of bax and down-regulation of bcl-2. VPA exerts anti-neoplastic activity in colorectal tumor cell lines in vitro and in vivo by altering cell cycle regulation.
    Keywords: Valproic Acid ; Tumor Cell Lines ; Histone Deacetylase Inhibition ; Colorectal Cancer
    ISSN: 1792-0981
    E-ISSN: 1792-1015
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  • 7
    Language: English
    In: Cancer Letters, Oct 28, 2010, Vol.296(2), p.160(8)
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.canlet.2010.04.010 Byline: Wolf-Dietrich C. Beecken (a), Eva Maria Ringel (a), Jan Babica (b), Elsie Oppermann (c), Dietger Jonas (a), Roman A. Blaheta (a) Keywords: Angiogenesis; [beta].sub.2-Glycoprotein-I; Cell cycle; Cyclins; HUVEC Abstract: [beta].sub.2-Glycoprotein-I ([beta].sub.2gpI), an abundant plasma glycoprotein, functions as a regulator of thrombosis. Previously, we demonstrated that plasmin-clipped [beta].sub.2gpI (c[beta].sub.2gpI) exerts an anti-angiogenic effect on human umbilical vein endothelial cells (HUVEC). The present study was focused on the molecular background responsible for this phenomenon. c[beta].sub.2gpI strongly reduced HUVEC growth and proliferation as evidenced by the MTT and BrdU assay and delayed cell cycle progression arresting HUVEC in the S-and G2/M-phase. Western blot analysis indicated that c[beta].sub.2gpI inhibited cyclin A, B and D1, and enhanced p21 and p27 expression. Activity of p38 was down-regulated independently from the c[beta].sub.2gpI incubation time. Phosphorylation of ERK1/2 was not changed early (30 and 60min) but became enhanced later (90min, 4h). JNK activity was reduced rapidly after c[beta].sub.2gpI treatment but compared to controls, increased thereafter. Annexin II blockade prevented growth inhibition and cell cycle delay evoked by c[beta].sub.2gpI. We assume that c[beta].sub.2gpI's effects on HUVEC growth is mediated via cyclin A, B and D1 suppression, up-regulation of p21 and p27 and coupled to modifications of the mitogen-activated protein (MAP) kinase signalling pathway. c[beta].sub.2gpI may represent a potential endogenous angiogenesis-targeted compound, opening the possibility of a novel tool to treat cancer. Author Affiliation: (a) Department of Urology, J.W. Goethe-University, Frankfurt am Main, Germany (b) Institute of Biochemistry II, J.W. Goethe-University, Frankfurt am Main, Germany (c) Department of General and Visceral Surgery, J.W. Goethe-University, Frankfurt am Main, Germany Article History: Received 3 September 2009; Revised 19 March 2010; Accepted 6 April 2010
    Keywords: Endothelium -- Growth ; Endothelium -- Analysis
    ISSN: 0304-3835
    Source: Cengage Learning, Inc.
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  • 8
    Language: English
    In: Langenbeck's Archives of Surgery, 2010, Vol.395(6), pp.643-653
    Description: Byline: Katharina Holzer (1), Dennis Hofmann (1), Elsie Oppermann (1), Stefan Zeuzem (2), Christian Monch (1), Dirk Henrich (3), Wolf-Otto Bechstein (1) Keywords: Neutrophils; Partial hepatectomy; Adhesion molecule; Fcy receptor; Oxygen radical production; Phagocytosis Abstract: Purpose Hepatic resections are still associated with considerable morbidity mainly because of postoperative infection. Adequate function of neutrophils is a crucial element in host defense. The aim of the study was to characterize neutrophils during partial hepatectomy. Methods Fourteen patients undergoing partial liver resection were enrolled. Twenty-four hours pre-, intra- (after induction of anesthesia, after preparation of the liver, and 15 min after release of the Pringle maneuver), as well as postoperatively (3 h after Pringle 24, 48, and 120 h after surgery), blood samples were obtained. In addition, healthy volunteers (n=5) were investigated. Adhesion molecules (CD 62, CD 18), Fcy receptors (CD 16, CD 32), and phagocytosis by neutrophils were characterized by fluorescence-activated cell sorter analysis. Spontaneous and stimulated (formyl-methionyl-leucyl-phenylalanine) oxygen radical generation was measured by lucigenin-enhanced chemiluminescence. Results Numeric upregulation of CD 62 and CD 18 on neutrophils was seen before the use of Pringle maneuver and persisted thereafter (p〈0.05). Spontaneous numeric expression of Fcy receptors (CD16 and CD 32) was unchanged during liver dissection but downregulated after Pringle maneuver was opened (p〈0.05). Although numeric Fcy receptors were downregulated, phagocytosis of heterologous opsonized Escherichia coli bacteria by neutrophils was unaffected. Spontaneous oxygen radical production peaked sharply 15 min after release of the Pringle maneuver (p〈0.05), contrary to stimulated oxygen radical production, which was depressed 3 h after the release of the Pringle maneuver (ns). Conclusions Uneventful partial hepatectomy in man resulted already in a significant change in the phenotype but in less significant changes in the functions of neutrophils. Author Affiliation: (1) Department of General Surgery, Johann-Wolfgang Goethe-University, Theodor- Stern- Kai 7, 60590, Frankfurt, Germany (2) Department of Internal Medicine, Johann-Wolfgang Goethe-University, Frankfurt, Germany (3) Department of Trauma Surgery, Johann-Wolfgang Goethe-University, Frankfurt, Germany Article History: Registration Date: 18/09/2009 Received Date: 30/06/2009 Accepted Date: 16/09/2009 Online Date: 13/02/2010
    Keywords: Neutrophils ; Partial hepatectomy ; Adhesion molecule ; Fcy receptor ; Oxygen radical production ; Phagocytosis
    ISSN: 1435-2443
    E-ISSN: 1435-2451
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  • 9
    Language: English
    In: Cancer biomarkers : section A of Disease markers, 2015, Vol.15(3), pp.311-6
    Description: Extent of pelvic lymph node (LN) dissemination is a critical prognostic feature for patients with prostate cancer (PCa) maintaining extended pelvic lymphadenectomy (LAD) as the gold standard for LN-staging. Unfortunately, conventional histopathological assessment may miss micrometastasis and recently presented immunocytochemical approach of the single cell analysis is still intricate. To comparatively assess the potential of Prostate cancer gene 3 (PCA3) and prostate specific antigene (PSA) to perform as markers for tumor cell load. Patients with high risk PCa for LN metastasis undergoing either a sentinel LN-guided staging LAD or retropubic radical prostatectomy with sentinel-guided pelvic LN dissection were included. LNs were investigated by routine histopathology. Tumor cell load was quantified by %immunocytochemistry. immunocytochemical single cell analysis. Gene activity was determined by qRT-PCR. Twenty four out of 226 LNs were positive in routine histopathology and 51 in single cell analysis. PSA mRNA level correlated with tumor cell density in patients with a positive immunocytochemistry. Gene activity of PCA3 was upregulated in metastatic LNs and correlated with tumor cell density in patients with tumor-invaded LNs as detected by immunocytochemistry. PCA3 gene expression discriminates LN metastasis and might outperform PSA gene activity in reflecting tumor cell burden in pelvic LNs of PCa patients.
    Keywords: Pca3 ; PSA ; Prostate Cancer ; Lymph Node Metastases ; Molecular Marker ; Tumor Cell Load ; Adenocarcinoma -- Genetics ; Antigens, Neoplasm -- Genetics ; Biomarkers, Tumor -- Genetics ; Prostate-Specific Antigen -- Genetics ; Prostatic Neoplasms -- Genetics
    ISSN: 15740153
    E-ISSN: 1875-8592
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  • 10
    Language: English
    In: World journal of gastroenterology, 07 June 2016, Vol.22(21), pp.5042-9
    Description: To compare the effect of transarterial chemoembolization (TACE) plus GRGDSP (Gly-Arg-Gly-Asp-Ser-Pro, integrin-inhibitor) loaded nanoparticles with TACE alone or TACE + GRGDSP in a rat model of liver tumor. Morris hepatoma 3924A tumors were implanted in the livers of 30 ACI rats. The ACI rats were divided randomly into three groups (10 animals each). Tumor volume before treatment (V1) was examined by magnetic resonance imaging (MRI), and then, after laparotomy and placement of a PE-10 catheter into the hepatic artery, the following interventional protocols were performed: TACE (mitomycin C + lipiodol + degradable starch microspheres) + GRGDSP loaded nanoparticles for group A; TACE + GRGDSP for group B (control group 1); TACE alone for group C (control group 2). Tumor volume (V2) was assessed by MRI and the mean ratio of the post-treatment to pretreatment tumor volumes (V2/V1) was calculated. Immunohistochemical analysis was performed to assess the quantification of matrix metalloprotein 9 (MMP-9) and vascular endothelial growth factor (VEGF) positive tumor cells in each treatment group. The mean tumor growth ratios (V2/V1) were 1.3649 ± 0.1194 in group A, 2.0770 ± 0.1595 in group B, and 3.2148 ± 0.1075 in group C. Compared with groups B and C, group A showed a significant reduction in tumor volume. Lower expression of MMP-9 and VEGF in hepatocellular carcinoma was observed in group A than in groups B and C. The angiogenesis of tumor was evaluated using anti-VEGF antibodies, and the metastasis of tumor was assessed using anti-MMP-9 antibody. MMP-9 and VEGF were expressed in all specimens. The immunoexpression of these proteins was confirmed by the presence of red cytoplasmic staining in tumor cells. Lower expression of MMP-9 and VEGF in hepatocellular carcinoma was observed in group A than in groups B and C. Transarterial administration of integrin inhibitor loaded nanoparticles combined with TACE evidently retards tumor growth and intrahepatic metastases compared with TACE alone or TACE plus integrin inhibitor in an animal model of hepatocellular carcinoma.
    Keywords: Aci Rats ; Hepatocellular Carcinoma ; Integrin Inhibitor ; Matrix Metalloprotein 9 ; Nanoparticles ; Transarterial Chemoembolization ; Vascular Endothelial Growth Factor ; Nanoparticles ; Antineoplastic Agents -- Administration & Dosage ; Carcinoma, Hepatocellular -- Therapy ; Chemoembolization, Therapeutic -- Methods ; Integrins -- Antagonists & Inhibitors ; Liver Neoplasms, Experimental -- Therapy ; Nanomedicine -- Methods ; Oligopeptides -- Administration & Dosage
    ISSN: 10079327
    E-ISSN: 2219-2840
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