Mammalian DNA is an endogenous danger signal that stimulates local synthesis and release of complement factor B.

Complement factor B plays a critical role in ischemic tissue injury and autoimmunity. Factor B is dynamically synthesized and released by cells outside of the liver, but the molecules that trigger local factor B synthesis and release during endogenous tissue injury have not been identified. We determined that factor B is upregulated early after cold ischemia-reperfusion in mice, using a heterotopic heart transplant model.

Transcriptomic response of murine liver to severe injury and hemorrhagic shock: a dual-platform microarray analysis.

Trauma-hemorrhagic shock (HS/T) is a complex process that elicits numerous molecular pathways. We hypothesized that a dual-platform microarray analysis of the liver, an organ that integrates immunology and metabolism, would reveal key pathways engaged following HS/T. C57BL/6 mice were divided into five groups (n = 4/group), anesthetized, and surgically treated to simulate a time course and trauma severity model: 1) nonmanipulated animals, 2) minor trauma, 3) 1.

Body adipose content is independently associated with a higher risk of organ failure and nosocomial infection in the nonobese patient postinjury.

Objective: Obesity defined by a body mass index (BMI) >30 kg/m is associated with increased morbidity and mortality following trauma. Evidence suggests that obesity represents a state of chronic inflammation and that the adipose tissue content may affect the intensity and resolution of inflammatory response. We sought to avoid the confounding effects attributable to obesity and determine the association of BMI and outcomes following injury in nonobese patients.

Complement factor 3 deficiency attenuates hemorrhagic shock-related hepatic injury and systemic inflammatory response syndrome.

Although complement activation is known to occur in the setting of severe hemorrhagic shock and tissue trauma (HS/T), the extent to which complement drives the initial inflammatory response and end-organ damage is uncertain. In this study, complement factor 3-deficient (C3(-/-)) mice and wild-type control mice were subjected to 1.5-h hemorrhagic shock, bilateral femur fracture, and soft tissue injury, followed by 4.

Pivotal advance: The pattern recognition receptor ligands lipopolysaccharide and polyinosine-polycytidylic acid stimulate factor B synthesis by the macrophage through distinct but overlapping mechanisms.

TLRs and complement are critical to the host response in sepsis, trauma, and ischemia/reperfusion. We hypothesize that TLR stimulation leads to synthesis and release of complement components by macrophages, an important source of extrahepatic complement. RAW264.

Staged endourologic and endovascular repair of an infrarenal inflammatory abdominal aortic aneurysm presenting with forniceal rupture.

We present the case of a 79-year-old female who presented with severe left flank pain and a pulsatile abdominal mass. She was diagnosed with left peripelvic urinary extravasation and forniceal rupture secondary to an intact infrarenal inflammatory abdominal aortic aneurysm with extensive periaortic fibrosis. Successful operative repair was performed with staged ureteral and endovascular stenting with subsequent resolution of periaortic inflammation and ureteral obstruction, and shrinkage of the aneurysm sac.

ClC-5: ontogeny of an alternative chloride channel in respiratory epithelia.

Chloride transport is critical to many functions of the lung. Molecular defects in the best-known chloride channel, cystic fibrosis transmembrane conductance regulator (CFTR), lead to impaired function of airway defensins, hydration of airway surface fluid, and mucociliary clearance leading to chronic lung disease, and premature death, but do not cause defects in lung development. We examined the expression of one member of the ClC family of volume- and voltage-regulated channels using the ribonuclease protection assay and Western blot analysis in rats.