Receptor for advanced glycation end products (RAGE) protein expression in lung tissue from individual RAGE(lanes 1 to 3), RAGE(lanes 4 to 6), and RAGE(lanes 7 to 9) animals

<p><b>Copyright information:</b></p><p>Taken from "Inhibition of the RAGE products increases survival in experimental models of severe sepsis and systemic infection"</p><p>http://ccforum.com/content/11/6/R122</p><p>Critical Care 2007;11(6):R122-R122.</p><p>Published online 6 Nov 2007</p><p>PMCID:PMC2246216.</p><p></p> Actin was used to demonstrate equal loading

Lethality from cecal ligation and puncture (CLP) is decreased in BALB/c mice administered an anti-RAGE monoclonal antibody (mAb)

<p><b>Copyright information:</b></p><p>Taken from "Inhibition of the RAGE products increases survival in experimental models of severe sepsis and systemic infection"</p><p>http://ccforum.com/content/11/6/R122</p><p>Critical Care 2007;11(6):R122-R122.</p><p>Published online 6 Nov 2007</p><p>PMCID:PMC2246216.</p><p></p> The Kaplan-Meier survival analysis following CLP compares anti-RAGE mAb-treated animals given 7.5 mg/kg (= 15) or 15 mg/kg (= 15) intravenously 30 to 60 minutes before CLP with serum control animals (= 15). The group given 15 mg/kg had a significantly greater survival than the group given 7.5 mg/kg (< 0.05) or serum control (< 0.001). RAGE, receptor for advanced glycation end products

Delayed administration of the anti-RAGE antibody is protective in cecal ligation and puncture (CLP)

<p><b>Copyright information:</b></p><p>Taken from "Inhibition of the RAGE products increases survival in experimental models of severe sepsis and systemic infection"</p><p>http://ccforum.com/content/11/6/R122</p><p>Critical Care 2007;11(6):R122-R122.</p><p>Published online 6 Nov 2007</p><p>PMCID:PMC2246216.</p><p></p> The Kaplan-Meier survival analysis following CLP in BALB/c mice compares delayed anti-RAGE monoclonal antibody (mAb) treatment given at various time intervals after CLP with serum control. Each group had a significantly greater survival than the control group (< 0.01), except for the 36-hour delayed treatment group (= 0.12). RAGE, receptor for advanced glycation end products

Modulation of receptor for advanced glycation end products (RAGE) protects mice from the effects of cecal ligation and puncture (CLP)

<p><b>Copyright information:</b></p><p>Taken from "Inhibition of the RAGE products increases survival in experimental models of severe sepsis and systemic infection"</p><p>http://ccforum.com/content/11/6/R122</p><p>Critical Care 2007;11(6):R122-R122.</p><p>Published online 6 Nov 2007</p><p>PMCID:PMC2246216.</p><p></p> Kaplan-Meier survival analysis following CLP comparing wild-type RAGE129SvEvBrd mice (= 15), RAGEmice (= 15), RAGEmice (= 23), and anti-RAGE monoclonal antibody-treated (15 mg/kg intravenously 30 to 60 minutes before CLP) wild-type mice (= 15). < 0.001 for each group in comparison with the wild-type CLP control group. Sham surgery-treated wild-type 129SvEvBrd mice (= 5) were used as an additional control group. WT, wild-type

Inhibition or deletion of receptor for advanced glycation end products (RAGE) does not disrupt the host mechanism for clearance of

<p><b>Copyright information:</b></p><p>Taken from "Inhibition of the RAGE products increases survival in experimental models of severe sepsis and systemic infection"</p><p>http://ccforum.com/content/11/6/R122</p><p>Critical Care 2007;11(6):R122-R122.</p><p>Published online 6 Nov 2007</p><p>PMCID:PMC2246216.</p><p></p> Quantitative levels of in organ samples (liver and spleen, = 10 per group) 48 hours after an intraperitoneal injection of 10colony-forming units (CFU) per animal (< 0.001 anti-tumor necrosis factor [TNF] monoclonal antibody [mAb] group versus all other groups)