Genomes and Genes
Jon A Buras
Affiliation: Harvard University
- Inhibition of C5 or absence of C6 protects from sepsis mortalityJon A Buras
Department of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA
Immunobiology 209:629-35. 2004..Inhibition of the complement MAC does not increase bacterial load or mortality, therefore, the use of anti-C5 therapy may be beneficial rather than detrimental in sepsis...
- Animal models of sepsis: setting the stageJon A Buras
Department of Emergency Medicine, Beth Israel Deaconess Medical Center, 1 Deaconess Road, Boston, Massachusetts 02215, USA
Nat Rev Drug Discov 4:854-65. 2005..This review summarizes the common animal sepsis models and highlights how results of recent human clinical trials might affect their use...
- Hyperbaric oxygen protects from sepsis mortality via an interleukin-10-dependent mechanismJon A Buras
New England Inflammation and Tissue Protection Institute Consortium at Northeastern University, Boston, MA, USA
Crit Care Med 34:2624-9. 2006..Finally, we wished to determine whether the mechanism of HBO2 protection in sepsis was dependent on IL-10 production...
- Hyperbaric oxygen reduces acetaminophen toxicity and increases HIF-1alpha expressionSteven D Salhanick
Program in Toxicology, Division of Emergency Medicine, Children s Hospital, Boston, MA, USA
Acad Emerg Med 13:707-14. 2006..In vitro assays were performed to better understand the effects of HBO2 on HIF-1alpha function...
- CpG oligodeoxynucleotide protection in polymicrobial sepsis is dependent on interleukin-17Lauren Rice
Department of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA
J Infect Dis 191:1368-76. 2005..Anti-IL-17 antibody inhibited the CpG-mediated prevention of mortality. These data suggest that IL-17 may mediate CpG-inducible host defenses during intraabdominal sepsis...
- Endothelially derived nitric oxide affects the severity of early acetaminophen-induced hepatic injury in miceSteven D Salhanick
Department of Emergency Medicine, Beth Israel Deaconess Hospital, Boston, MA, USA
Acad Emerg Med 13:479-85. 2006..The authors sought to evaluate the effect of eNOS-derived NO during APAP toxicity...
- Gastrointestinal ischemia-reperfusion injury is lectin complement pathway dependent without involving C1qMelanie L Hart
Center for Experimental Therapeutics and Reperfusion Injury, Anesthesiology, Perioperative and Pain Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
J Immunol 174:6373-80. 2005..These data demonstrate that C2 and MBL, but not C1q, are necessary for gut injury after GI/R. Lung injury in mice after GI/R is MBL and C1q independent, but C2 dependent, suggesting a potential role for ficolins in this model...
- Role for the alternative complement pathway in ischemia/reperfusion injuryGregory L Stahl
Department of Anesthesiology, Perioperative, and Pain Medicine, Center for Experimental Therapeutics and Reperfusion Injury, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
Am J Pathol 162:449-55. 2003..These data suggest that the alternative complement pathway plays an important role in local and remote tissue injury after GI/R. Inhibition of factor D may represent an effective therapeutic approach for GI/R injury...
- A2B adenosine receptor blockade enhances macrophage-mediated bacterial phagocytosis and improves polymicrobial sepsis survival in miceBryan G Belikoff
Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA 02118, USA
J Immunol 186:2444-53. 2011..Our findings of enhanced bacterial clearance and host survival suggest that antagonism of A2BRs offers a therapeutic target to improve macrophage function in a late treatment protocol that improves sepsis survival...