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Alle Journale wurden nach Holzwart E durchsucht Treffer 1 - 13 von 13

Medizinische Publikationen (3)  ::   Abbildungen und Graphiken  ::   Volltext (0)

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1. Gasser R; Pätzold S; Holzwart E; Ablasser K; Kraigher-Krainer E; Friehs I; Lewinski D; Pieske B; Mächler H; Trantiner-Yates A; Tscheliessnig KH; Mangge H; Porta S; Gasser S
Immunological Implications in Experimental Myocardial Ischaemia: MPO (Myeloperoxidase) Expression Is Differentially Regulated by Beta-Blockers, While CD80 Expression Remains Unaffected
CD80 Experiments
Journal of Clinical and Basic Cardiology 2011; 14 (1-4): 16-22
It shows the results from real-time PCR measurements of all CD80 experiments (o2ko: well-oxygenated, no ischaemia, no drug; n2ko: experimental ischaemia, no drug; o2at: well-oxygenated, no ischaemia, atenolol present; n2at: experimental ischaemia, atenolol present; o2neb: well-oxygenated, nebivolol present; n2neb: experimental ischaemia, nebivolol present). It can be seen that during experimental ischaemia, there is an up-regulation of CD80 expression. There is also a regulation with and without the influence of beta-blockers during myocardial ischaemia.

Keywords: CD80flowchart
2. Gasser R; Pätzold S; Holzwart E; Ablasser K; Kraigher-Krainer E; Friehs I; Lewinski D; Pieske B; Mächler H; Trantiner-Yates A; Tscheliessnig KH; Mangge H; Porta S; Gasser S
Immunological Implications in Experimental Myocardial Ischaemia: MPO (Myeloperoxidase) Expression Is Differentially Regulated by Beta-Blockers, While CD80 Expression Remains Unaffected
Interleukin Pathway
Journal of Clinical and Basic Cardiology 2011; 14 (1-4): 16-22
Interleukin pathway up-regulated by nebivolol, not by atenolol, during experimental ischaemia.

Keywords: flowchartinterleukin
3. Gasser R; Pätzold S; Holzwart E; Ablasser K; Kraigher-Krainer E; Friehs I; Lewinski D; Pieske B; Mächler H; Trantiner-Yates A; Tscheliessnig KH; Mangge H; Porta S; Gasser S
Immunological Implications in Experimental Myocardial Ischaemia: MPO (Myeloperoxidase) Expression Is Differentially Regulated by Beta-Blockers, While CD80 Expression Remains Unaffected
MPO Experiments
Journal of Clinical and Basic Cardiology 2011; 14 (1-4): 16-22
It shows the results from real-time PCR measurements of all MPO experiments (o2ko: well-oxygenated, no ischaemia, no drug; n2ko: experimental ischaemia, no drug; o2at: well-oxygenated, no ischaemia, atenolol present; n2at: experimental ischaemia, atenolol present; o2neb: well-oxygenated, nebivolol present; n2neb: experimental ischaemia, nebivolol present). Using PCR for validation, we find that during experimental ischaemia, there is an up-regulation of MPO expression. There is a differential regulation between different beta-blockers during myocardial ischaemia, which warrants further investigation.

Keywords: flowchartMPO
4. Holzwart E; Gasser S; Roessl U; Buehner A; Ablasser K; Friehs I; Pieske B; Mächler H; Yates A; Tscheliessnig KH; Mangge H; Porta S; Gasser R
Effect of Betablockers on the Regulation of PDK (Pyruvate Dehydrogenase Kinase) Gene Expression in Both Normoxic and Hypoxic Myocardium
PCR - PDK
Journal of Clinical and Basic Cardiology 2010; 13 (1-4): 12-18
The results from real-time PCR measurements of PDK experiments are illustrated (o2ko: well-oxygenated, no ischemia, no drug; n2ko: experimental ischemia, no drug; o2at: well-oxygenated, no ischemia, atenolol present; n2at: experimental ischemia, atenolol present; o2neb: well-oxygenated, nebivolol present; n2neb: experimental ischemia, nebivolol present). It can be seen that, without the influence of betablockers, there is no significant regulation of PDK expression during myocardial ischemia. There is just a trend towards a decrease in PDK gene expression. There is, however, a significant difference between the expression of PDK during myocardial ischemia in the presence of atenolol (3.62 ± 0. 18) and nebivolol (1.97 ± 0.06; ± SEM; P ≤ 0.05): PDK expression is decreased during normoxia (trend) and ischemia (significant) in the presence of nebivolol.

Keywords: flowchartPCRPDK
5. Holzwart E; Gasser S; Roessl U; Buehner A; Ablasser K; Friehs I; Pieske B; Mächler H; Yates A; Tscheliessnig KH; Mangge H; Porta S; Gasser R
Effect of Betablockers on the Regulation of PDK (Pyruvate Dehydrogenase Kinase) Gene Expression in Both Normoxic and Hypoxic Myocardium
PDK
Journal of Clinical and Basic Cardiology 2010; 13 (1-4): 12-18
In this figure, the results from microarray measurements of PDK experiments are illustrated. Pooled DNA data: Control experiments: Owo: pool control, well-oxygenated, no ischemia, no drug; Nwo: pool experimental ischemia, no drug; Atenolol experiments: O2At: pool welloxygenated, no ischemia, atenolol present; N2At: pool experimental ischemia, atenolol present; Nebivolol experiments: Ob: pool well-oxygenated, nebivolol present; Nb: pool experimental ischemia, nebivolol present. It can be seen that, without the influence of betablockers, there is no significant regulation of PDK expression during myocardial ischemia. While there is no down-regulation of PDK gene expression by atenolol, there is a decrease in PDK gene expression in the presence of nebivolol both during normoxia and hypoxia. 167Nb, 167Ob, 236N2At and 236O2At are corresponding single-experiment controls.

Keywords: flowchartPDK
6. Holzwart E; Gasser S; Roessl U; Buehner A; Ablasser K; Friehs I; Pieske B; Mächler H; Yates A; Tscheliessnig KH; Mangge H; Porta S; Gasser R
Effect of Betablockers on the Regulation of PDK (Pyruvate Dehydrogenase Kinase) Gene Expression in Both Normoxic and Hypoxic Myocardium
Gene expression
Journal of Clinical and Basic Cardiology 2010; 13 (1-4): 12-18
Gene expression of biological processes associated with glucose metabolism during normoxia and hypoxia is down-regulated in human atrial tissue. Up-regulation of gene-expression associated with glucose metabolism during hypoxia.

Keywords: flowchartgene expression
7. Holzwart E; Gasser S; Roessl U; Buehner A; Ablasser K; Friehs I; Pieske B; Mächler H; Yates A; Tscheliessnig KH; Mangge H; Porta S; Gasser R
Effect of Betablockers on the Regulation of PDK (Pyruvate Dehydrogenase Kinase) Gene Expression in Both Normoxic and Hypoxic Myocardium
Gene expression
Journal of Clinical and Basic Cardiology 2010; 13 (1-4): 12-18
Example of differential regulation of gene expression by atenolol and nebivolol in well-oxygenized preparations: one can see that numerous biochemical processes are affected by nebivolol but not by atenolol. For example, many processes involved in contraction, lipid metabolism, and proliferation are down-regulated by nebivolol only (not by atenolol). Reducing lipid metabolism in exchange for an increased carbohydrate metabolism may render the heart less vulnerable to O2 deficit or ischemia.

Keywords: flowchartgene expression
8. Gasser R; Roessl U; Holzwart E; Ablasser K; Friehs I; Lewinski D; Pieske B; Mächler H; Trantiner-Yates A; Tscheliessnig KH; Mangge H; Gasser S
Shift from Adult to Fetal Metabolic Phenotype During Prolonged Experimental Myocardial Ischemia: A Study on the Effect of Beta Blockers upon Gene Expression of Transmembrane Glucose Transporters
Myocardial Metabolism
Journal of Clinical and Basic Cardiology 2009; 12 (1-4): 11-17
Plasticity of myocardial metabolism: during exercise, hypoxia/ ischemia etc myocardial cells prefer glucose as a substrate. Both fasting and diabetes shift the metabolic substrates to the fatty acid site. Mod. from [29, 33].

Keywords: chartDiagramm
9. Gasser R; Roessl U; Holzwart E; Ablasser K; Friehs I; Lewinski D; Pieske B; Mächler H; Trantiner-Yates A; Tscheliessnig KH; Mangge H; Gasser S
Shift from Adult to Fetal Metabolic Phenotype During Prolonged Experimental Myocardial Ischemia: A Study on the Effect of Beta Blockers upon Gene Expression of Transmembrane Glucose Transporters
Cardiac metabolism
Journal of Clinical and Basic Cardiology 2009; 12 (1-4): 11-17
Shifting cardiac metabolism to its fetal phenotype: as an anti-anginal target (mod. from [32]) of dichloracetate augments cellular glucose metabolism. Etoximir and perhexiline inhibit cellular fatty acid metabolism and both ranolazine as well as trimetazidine slow down beta oxidation. Beta-adrenergic blockade enhances GLUT1 and GLUT4 expressions.

Keywords: Schemascheme
10. Gasser R; Roessl U; Holzwart E; Ablasser K; Friehs I; Lewinski D; Pieske B; Mächler H; Trantiner-Yates A; Tscheliessnig KH; Mangge H; Gasser S
Shift from Adult to Fetal Metabolic Phenotype During Prolonged Experimental Myocardial Ischemia: A Study on the Effect of Beta Blockers upon Gene Expression of Transmembrane Glucose Transporters
Glucose metabolism
Journal of Clinical and Basic Cardiology 2009; 12 (1-4): 11-17
(a) Gene expression of biological processes associated with glucose metabolism during normoxia and hypoxia. Up-regulation of glucose metabolism. (b) Down-regulation of gene expression of biological processes associated with fatty acid and amino acid metabolism – (a) and (b) indicate a conversion to the fetal type of metabolism. Based on data from [4–9, 32–35].

Keywords: chartDiagramm
11. Gasser R; Roessl U; Holzwart E; Ablasser K; Friehs I; Lewinski D; Pieske B; Mächler H; Trantiner-Yates A; Tscheliessnig KH; Mangge H; Gasser S
Shift from Adult to Fetal Metabolic Phenotype During Prolonged Experimental Myocardial Ischemia: A Study on the Effect of Beta Blockers upon Gene Expression of Transmembrane Glucose Transporters
Myocardial Metabolism
Journal of Clinical and Basic Cardiology 2009; 12 (1-4): 11-17
Substrates of myocardial metabolism. Mod. from [29, 32]. The fetal myocardial phenotype uses predominantly glucose for its metabolism, whereas the adult individual mainly metabolises fatty acids. During special conditions, like hypoxia, the adult phenotype of myocardial metabolism converts to the fetal phenotype, again preferably using glucose for its metabolism (Fig. 4). It has been shown that a preferentially glucose-oriented cardiac metabolism is beneficial in myocardial ischemia. However, knockout experiments have shown that successful transfer to the fetal metabolism is possible only under adequate/increased GLUT1 expression [33–35].

Keywords: chartDiagramm
12. Gasser R; Roessl U; Holzwart E; Ablasser K; Friehs I; Lewinski D; Pieske B; Mächler H; Trantiner-Yates A; Tscheliessnig KH; Mangge H; Gasser S
Shift from Adult to Fetal Metabolic Phenotype During Prolonged Experimental Myocardial Ischemia: A Study on the Effect of Beta Blockers upon Gene Expression of Transmembrane Glucose Transporters
Real-time PCR
Journal of Clinical and Basic Cardiology 2009; 12 (1-4): 11-17
Results from real-time PCR measurements of all GLUT4 experiments (o2ko = well-oxygenated, no ischemia, no drug; n2ko = experimental ischemia, no drug; o2at = well-oxygenated, no ischemia, atenolol present; n2at = experimental ischemia, atenolol present; o2neb = well-oxygenated, nebivolol present; n2neb = experimental ischemia, nebivolol present). It can be seen that during experimental ischemia, there is an up-regulation of GLUT4 (SLC2A4) expression, however not statistically significant.

Keywords: chartDiagramm
13. Gasser R; Roessl U; Holzwart E; Ablasser K; Friehs I; Lewinski D; Pieske B; Mächler H; Trantiner-Yates A; Tscheliessnig KH; Mangge H; Gasser S
Shift from Adult to Fetal Metabolic Phenotype During Prolonged Experimental Myocardial Ischemia: A Study on the Effect of Beta Blockers upon Gene Expression of Transmembrane Glucose Transporters
Real-time PCR
Journal of Clinical and Basic Cardiology 2009; 12 (1-4): 11-17
Results from real-time PCR measurements of 72 experiments (n = 12 in each group; o2ko = well-oxygenated, no ischemia, no drug; n2ko = experimental ischemia, no drug; o2at = well-oxygenated, no ischemia, atenolol present; n2at = experimental ischemia, atenolol present; o2neb = well-oxygenated, nebivolol present; n2neb = experimental ischemia, nebivolol present). It can be seen that during experimental ischemia, there is an up-regulation of GLUT1 expression, however, not statistically significant. This confirms earlier data by our group. While there is no significant regulation with and without the influence of beta blockers during myocardial ischemia either, there is, however, a significant difference between the expression of GLUT1 in well-oxygenized preparations with (0.87 ± 0.02) and without nebivolol (0.62 ± 0.02; ± SEM; p ≤ 0.05). Similarly, atenolol led to an increase of GLUT1 expression in welloxygenated preparations compared to controls: 1.18 ± 0.08 and 0.62 ± 0.02, respectively (+ SEM; p < 0.05)

Keywords: chartDiagramm
 

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