Gene expression
Figure 1: 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: flowchart,  gene expression

Gene expression
Figure 2: 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: flowchart,  gene expression

PDK
Figure 3: 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: flowchart,  PDK

PCR - PDK
Figure 4: 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: flowchart,  PCR,  PDK