Muslime in Europa zwischen Globalisierung und Lokalisierung. Gesellschaftspolitische und theologische Perspektiven im Anschluss an Enes Karic und Tariq Ramadan

). Culture media was collected from hyperoxic conditions (open bars) or normoxic conditions (filled bars) at 24 hours intervals. Final concentrations were estimated from individual standard curves. Generation of endogenous HOwas monitored in separate experiments at the indicated time-points in LSEC cultures by HO-mediated oxidation of DCFH-DA into DFC during 6 h (b). Values are total fluorescence emitted at 545 nm.<p><b>Copyright information:</b></p><p>Taken from "The influence of oxygen tension on the structure and function of isolated liver sinusoidal endothelial cells"</p><p>http://www.comparative-hepatology.com/content/7/1/4</p><p>Comparative Hepatology 2008;7():4-4.</p><p>Published online 5 May 2008</p><p>PMCID:PMC2408922.</p><p></p

The influence of oxygen tension on the structure and function of isolated liver sinusoidal endothelial cells-1

maintained in either high (a) or low (b) oxygen tension. Separately, viability was determined at the indicated time points by MTT colorimetric assay (c). Freshly isolated LSECs cultures were established on 24 well-plates and incubated either at hyperoxia (open bars) or at normoxia (filled bars). The obtained results demonstrate a faster decay of loss of cells in cultures maintained at hyperoxic conditions. Statistical analyses by t-student test: *P < 0.05, **P < 0.001.<p><b>Copyright information:</b></p><p>Taken from "The influence of oxygen tension on the structure and function of isolated liver sinusoidal endothelial cells"</p><p>http://www.comparative-hepatology.com/content/7/1/4</p><p>Comparative Hepatology 2008;7():4-4.</p><p>Published online 5 May 2008</p><p>PMCID:PMC2408922.</p><p></p

The influence of oxygen tension on the structure and function of isolated liver sinusoidal endothelial cells-5

Nt time-points. Conditioned media were collected from LSECs cultured at hyperoxia (open bars) or normoxia (filled bars) at 24 hours intervals. Final concentrations were estimated from individual standard curves. Values are means of triplicate measurements. The results are representative data obtained from three independent experiments. Statistical analyses by t-student test: *P < 0.001.<p><b>Copyright information:</b></p><p>Taken from "The influence of oxygen tension on the structure and function of isolated liver sinusoidal endothelial cells"</p><p>http://www.comparative-hepatology.com/content/7/1/4</p><p>Comparative Hepatology 2008;7():4-4.</p><p>Published online 5 May 2008</p><p>PMCID:PMC2408922.</p><p></p

The influence of oxygen tension on the structure and function of isolated liver sinusoidal endothelial cells-4

Ncubation of cells at normoxic or hyperoxic conditions. Each column represents separate values of cell-associated (lower part) and degraded (upper part) I-FSA. Total endocytosis is the result of adding cell associated and degraded ligand (full column size), calculated as percentage of total I-FSA added to cultures. Values are means of triplicate measurements. The results are representative data obtained from three independent experiments. Statistical analyses by Student's -test: *P < 0.05, **P < 0.001.<p><b>Copyright information:</b></p><p>Taken from "The influence of oxygen tension on the structure and function of isolated liver sinusoidal endothelial cells"</p><p>http://www.comparative-hepatology.com/content/7/1/4</p><p>Comparative Hepatology 2008;7():4-4.</p><p>Published online 5 May 2008</p><p>PMCID:PMC2408922.</p><p></p

The influence of oxygen tension on the structure and function of isolated liver sinusoidal endothelial cells-3

E excluded from the analysis. Porosity measurements are expressed as percentage of the total area covered by cells in each coverslip. Black columns: 20% oxygen. White columns: 5% oxygen.<p><b>Copyright information:</b></p><p>Taken from "The influence of oxygen tension on the structure and function of isolated liver sinusoidal endothelial cells"</p><p>http://www.comparative-hepatology.com/content/7/1/4</p><p>Comparative Hepatology 2008;7():4-4.</p><p>Published online 5 May 2008</p><p>PMCID:PMC2408922.</p><p></p

The influence of oxygen tension on the structure and function of isolated liver sinusoidal endothelial cells-0

at normoxia (d-f). The general morphology of the cultures was monitored by light microscopy at day 1 (a, d), day 3 (b, d) and day 5 (c, f) after isolation. Decline of LSECs cultures may be observed in dishes maintained at atmospheric oxygen levels (a-c) after several days of culture.<p><b>Copyright information:</b></p><p>Taken from "The influence of oxygen tension on the structure and function of isolated liver sinusoidal endothelial cells"</p><p>http://www.comparative-hepatology.com/content/7/1/4</p><p>Comparative Hepatology 2008;7():4-4.</p><p>Published online 5 May 2008</p><p>PMCID:PMC2408922.</p><p></p

The influence of oxygen tension on the structure and function of isolated liver sinusoidal endothelial cells-2

Nt time points by SEM. LSECs cultures were maintained at high (a-c) or low (d-f) oxygen levels. Highly fenestrated cells can be observed during early time points of culture. Fenestration is gradually lost over time in both normoxic or hypoxic conditions.<p><b>Copyright information:</b></p><p>Taken from "The influence of oxygen tension on the structure and function of isolated liver sinusoidal endothelial cells"</p><p>http://www.comparative-hepatology.com/content/7/1/4</p><p>Comparative Hepatology 2008;7():4-4.</p><p>Published online 5 May 2008</p><p>PMCID:PMC2408922.</p><p></p

Calculation of the pole-face windings compensation at injection

<div><p>Background</p><p>Hydrogen sulfide (H₂S), produced by the activity of cystathionine-gamma-lyase (CSE), is a key mediator of inflammation in sepsis. The liver sinusoidal endothelial cells (LSECs) are important target and mediator of sepsis. The aim of this study was to investigate the role of CSE-derived H₂S on inflammation and LSECs fenestrae in caecal-ligation and puncture (CLP)-induced sepsis using CSE KO mice.</p><p>Methods</p><p>Sepsis was induced by CLP, and mice (C57BL/6J, male) were sacrificed after 8 hours. Liver, lung, and blood were collected and processed to measure CSE expression, H₂S synthesis, MPO activity, NF-κB p65, ERK1/2, and cytokines/chemokines levels. Diameter, frequency, porosity and gap area of the liver sieve were calculated from scanning electron micrographs of the LSECs.</p><p>Results</p><p>An increased CSE expression and H₂S synthesizing activity in the liver and lung of wild-type mice following CLP-induced sepsis. This was associated with an increased liver and lung MPO activity, and increased liver and lung and plasma levels of the pro-inflammatory cytokines TNF-α, IL-6, and IL-1β, and the chemokines MCP-1 and MIP-2α. Conversely, CSE KO mice had less liver and lung injury and reduced inflammation following CLP-induced sepsis as evidenced by decreased levels of H₂S synthesizing activity, MPO activity, and pro-inflammatory cytokines/chemokines production. Extracellular-regulated kinase (ERK1/2) and nuclear factor-κB p65 (NF-κB) became significantly activated after the CLP in WT mice but not in CSE KO mice. In addition, CLP-induced damage to the LSECs, as indicated by increased defenestration and gaps formation in the LSECs compared to WT sham control. CSE KO mice showed decreased defenestration and gaps formation following sepsis.</p><p>Conclusions</p><p>Mice with CSE (an H₂S synthesising enzyme) gene deletion are less susceptible to CLP-induced sepsis and associated inflammatory response through ERK1/2-NF-κB p65 pathway as evidenced by reduced inflammation, tissue damage, and LSECs defenestration and gaps formation.</p></div

CSE Protein Expression and H₂S-Synthesizing Activity Following CLP Induced Sepsis.

<p>(A-B) Liver CSE protein expression and (C-D) lung CSE protein expression. Liver and lung CSE protein expression was increased following CLP induced sepsis compared to sham control (liver: P<0.001 vs. sham control; lung P<0.01 vs. sham control) and no CSE protein expression was detected in CSE KO mice. Results were normalized with GAPDH and expressed as the relative fold increase of CSE protein expression compared with sham control. For western blot results, each lane represents a separate animal. The blots shown were representative of all animals in each group with similar results. (E) Liver H₂S synthesizing activity. H₂S synthesizing activity was increased following increased CSE protein expression in WT CLP induced sepsis mice compared to sham controls and CSE KO mice had significantly lower H₂S synthesizing activity compared to WT sepsis mice. Data represent the mean±standard deviation (n = 8). Data were analysed for Gaussian or Normal distribution using Shapiro-Wilk test. One-way ANOVA with post hoc Tukey’s test was performed to compare multiple groups. Statistical significance was assigned as *P<0.05; **P<0.01; ***P<0.001; and ****P<0.0001.</p

Effect of CSE Gene Deletion on Lung Pro-inflammatory Cytokines and Chemokines.

<p>(A) Lung TNF-α, (B) Lung IL-6, (C) Lung IL-1β, (D) Lung MCP-1 and (E) Lung MIP-2α. CLP induced sepsis significantly increased the lung cytokines TNF-α (P<0.05), IL-6 (P<0.001) and IL-1β (P<0.001) and the chemokines MCP-1 (P<0.001) and MIP-2α (P<0.01) in WT mice compared to sham operation controls. Knockdown of the CSE gene protects mice against lung injury by reducing pro-inflammatory TNF-α (P<0.01), IL-6 (P<0.05), IL-1β (P<0.05), MCP-1 (P<0.05) and MIP-2α (P<0.05) following CLP induced sepsis compared to WT sepsis mice. Results were expressed in ng/mg of protein. Data represent the mean±standard deviation (n = 8). Data were analysed for Gaussian or Normal distribution using Shapiro-Wilk test. One-way ANOVA with post hoc Tukey’s test was performed to compare multiple groups. Statistical significance was assigned as *P<0.05; **P<0.01: and ***P<0.001.</p