Cluster analysis of the mRNA expression profiles after the citrinin treatment

<p><b>Copyright information:</b></p><p>Taken from "Evaluation of toxicity of the mycotoxin citrinin using yeast ORF DNA microarray and Oligo DNA microarray"</p><p>http://www.biomedcentral.com/1471-2164/8/95</p><p>BMC Genomics 2007;8():95-95.</p><p>Published online 5 Apr 2007</p><p>PMCID:PMC1865386.</p><p></p> Hierarchical cluster analysis was performed using GeneSpring as described in the text

Image1.JPEG

<p>Cardiopulmonary bypass (CPB) induced systemic inflammation significantly contributes to the development of postoperative complications, including respiratory failure, myocardial, renal and neurological dysfunction and ultimately can lead to failure of multiple organs. Ghrelin is a small endogenous peptide with wide ranging physiological effects on metabolism and cardiovascular regulation. Herein, we investigated the protective effects of ghrelin against CPB-induced inflammatory reactions, oxidative stress and acute organ damage. Adult male Sprague Dawley rats randomly received vehicle (n = 5) or a bolus of ghrelin (150 μg/kg, sc, n = 5) and were subjected to CPB for 4 h (protocol 1). In separate rats, ghrelin pre-treatment (protocol 2) was compared to two doses of ghrelin (protocol 3) before and after CPB for 2 h followed by recovery for 2 h. Blood samples were taken prior to CPB, and following CPB at 2 h and 4 h. Organ nitrosative stress (3-nitrotyrosine) was measured by Western blotting. CPB induced leukocytosis with increased plasma levels of tumor necrosis factor-α and interleukin-6 indicating a potent inflammatory response. Ghrelin treatment significantly reduced plasma organ damage markers (lactate dehydrogenase, aspartate aminotransferase, alanine aminotransferase) and protein levels of 3-nitrotyrosine, particularly in the brain, lung and liver, but only partly suppressed inflammatory cell invasion and did not reduce proinflammatory cytokine production. Ghrelin partially attenuated the CPB-induced elevation of epinephrine and to a lesser extent norepinephrine when compared to the CPB saline group, while dopamine levels were completely suppressed. Ghrelin treatment sustained plasma levels of reduced glutathione and decreased glutathione disulphide when compared to CPB saline rats. These results suggest that even though ghrelin only partially inhibited the large CPB induced increase in catecholamines and organ macrophage infiltration, it reduced oxidative stress and subsequent cell damage. Pre-treatment with ghrelin might provide an effective adjunct therapy for preventing widespread CPB induced organ injury.</p

Evaluation of toxicity of the mycotoxin citrinin using yeast ORF DNA microarray and Oligo DNA microarray-2

<p><b>Copyright information:</b></p><p>Taken from "Evaluation of toxicity of the mycotoxin citrinin using yeast ORF DNA microarray and Oligo DNA microarray"</p><p>http://www.biomedcentral.com/1471-2164/8/95</p><p>BMC Genomics 2007;8():95-95.</p><p>Published online 5 Apr 2007</p><p>PMCID:PMC1865386.</p><p></p>Different types of microarray. Dye swap was carried out with the OL-1-1, OL-1-2 and OL-1-3 sheets

Evaluation of toxicity of the mycotoxin citrinin using yeast ORF DNA microarray and Oligo DNA microarray-4

<p><b>Copyright information:</b></p><p>Taken from "Evaluation of toxicity of the mycotoxin citrinin using yeast ORF DNA microarray and Oligo DNA microarray"</p><p>http://www.biomedcentral.com/1471-2164/8/95</p><p>BMC Genomics 2007;8():95-95.</p><p>Published online 5 Apr 2007</p><p>PMCID:PMC1865386.</p><p></p>low the images

Image2.PDF

<p>Cardiopulmonary bypass (CPB) induced systemic inflammation significantly contributes to the development of postoperative complications, including respiratory failure, myocardial, renal and neurological dysfunction and ultimately can lead to failure of multiple organs. Ghrelin is a small endogenous peptide with wide ranging physiological effects on metabolism and cardiovascular regulation. Herein, we investigated the protective effects of ghrelin against CPB-induced inflammatory reactions, oxidative stress and acute organ damage. Adult male Sprague Dawley rats randomly received vehicle (n = 5) or a bolus of ghrelin (150 μg/kg, sc, n = 5) and were subjected to CPB for 4 h (protocol 1). In separate rats, ghrelin pre-treatment (protocol 2) was compared to two doses of ghrelin (protocol 3) before and after CPB for 2 h followed by recovery for 2 h. Blood samples were taken prior to CPB, and following CPB at 2 h and 4 h. Organ nitrosative stress (3-nitrotyrosine) was measured by Western blotting. CPB induced leukocytosis with increased plasma levels of tumor necrosis factor-α and interleukin-6 indicating a potent inflammatory response. Ghrelin treatment significantly reduced plasma organ damage markers (lactate dehydrogenase, aspartate aminotransferase, alanine aminotransferase) and protein levels of 3-nitrotyrosine, particularly in the brain, lung and liver, but only partly suppressed inflammatory cell invasion and did not reduce proinflammatory cytokine production. Ghrelin partially attenuated the CPB-induced elevation of epinephrine and to a lesser extent norepinephrine when compared to the CPB saline group, while dopamine levels were completely suppressed. Ghrelin treatment sustained plasma levels of reduced glutathione and decreased glutathione disulphide when compared to CPB saline rats. These results suggest that even though ghrelin only partially inhibited the large CPB induced increase in catecholamines and organ macrophage infiltration, it reduced oxidative stress and subsequent cell damage. Pre-treatment with ghrelin might provide an effective adjunct therapy for preventing widespread CPB induced organ injury.</p

Evaluation of toxicity of the mycotoxin citrinin using yeast ORF DNA microarray and Oligo DNA microarray-1

<p><b>Copyright information:</b></p><p>Taken from "Evaluation of toxicity of the mycotoxin citrinin using yeast ORF DNA microarray and Oligo DNA microarray"</p><p>http://www.biomedcentral.com/1471-2164/8/95</p><p>BMC Genomics 2007;8():95-95.</p><p>Published online 5 Apr 2007</p><p>PMCID:PMC1865386.</p><p></p>icated concentration. The stock solution was added directly to the yeast cells grown for 2–3 days such that they were diluted more than 100-fold

Cytotoxic T cell assay against GFP in ICVI mice (N = 4) and GFP-immunized mice (N = 4).

<p>CTL reactivity against GFP-BMCs were measured using ELISPOT which Indicated spot counts per 2.5 x 10⁵ effector cells. ICVI mice had a tendency to generate less response than immunized controls (P = 0.13).</p

Successful delivery of GFP-BMCs to mouse embryos by ICVI at E10.

<p>A: GFP positive cells were detected in the fetal body and heart at 30 minutes after injection (x10). B: Naïve fetus at E10 (x10). C-D: E17 mouse liver and thymus at 1 week after ICVI (x40).</p

E10 embryo imaged by power Doppler mode.

<p>The two layers of the placenta, which consist of the labyrinth and spongiotrophoblasts layer and the maternal decidua. The white dotted line indicates the border between these two layers.</p

Generation of antibodies against GFP after GFP-skin grafting.

<p>Antibodies against GFP were measured using ELISA 4 weeks after skin grafting. Non ICVI control mice (N = 5) produced significant amounts of antibodies, whereas ICVI mice (N = 5) did not. The no treatment group consisted of naïve mice that did not undergo ICVI or skin grafting as a negative control (N = 4). *Statistical significance was assessed if P<0.0167 with Bonferroni correction. P = 0.008 from Kruscal-Wallis test indicating a global difference.</p