|1.||Wetsel, Rick A: 14 articles (11/2014 - 11/2002)|
|2.||Ward, Peter A: 11 articles (09/2015 - 05/2002)|
|3.||Lambris, John D: 9 articles (11/2012 - 10/2002)|
|4.||Köhl, Jörg: 8 articles (12/2014 - 03/2003)|
|5.||Gerard, Craig: 6 articles (01/2014 - 12/2002)|
|6.||Sarma, J Vidya: 6 articles (04/2013 - 05/2002)|
|7.||Zwirner, Jörg: 6 articles (08/2007 - 12/2002)|
|8.||Huber-Lang, Markus: 5 articles (04/2013 - 05/2002)|
|9.||Drouin, Scott M: 5 articles (01/2012 - 11/2002)|
|10.||Mazor, Moshe: 5 articles (07/2010 - 01/2005)|
12/01/1996 - "HF effectively eliminated the anaphylatoxins C3adesArg and C5adesArg during sepsis. "
04/15/2013 - "During experimental sepsis, excessive generation of the anaphylatoxin C5a results in reduction of the C5a receptor (C5aR) on neutrophils. "
01/01/2008 - "Especially the anaphylatoxin C5a has been shown to have numerous harmful effects during sepsis. "
06/15/2007 - "We previously reported that generation of the anaphylatoxin C5a is linked to the development of cardiac dysfunction in sepsis due to C5a interaction with its receptor (C5aR) on cardiomyocytes. "
10/01/2002 - "There is also evidence in rats that sepsis is associated with excessive complement activation and generation of the potent anaphylatoxin C5a. "
|2.||Wounds and Injuries (Trauma)
12/01/1984 - "Consequently, longitudinal monitoring of anaphylatoxin levels may prove helpful in diagnosing the status of trauma patients."
09/01/1997 - "The expression of the C5aR by astrocytes suggests new roles for the C5a anaphylatoxin in reactive astrogliosis to CNS injuries."
07/01/1992 - "The anaphylatoxin C3a or its desArg form (C3a/desArg) generated during complement activation could be detected in the vicinity of incised skin wounds of guinea pigs using immunoblotting methods. "
09/01/1986 - "This raises a note of caution with regard to diagnostic and/or therapeutic decisions based on anaphylatoxin assessment of neurosurgical trauma patients at risk of ARDS."
04/01/1992 - "To determine the generation of anaphylatoxin C3a in plasma and bronchoalveolar lavage fluid in trauma patients at risk for the adult respiratory distress syndrome (ARDS). "
|3.||Acute Lung Injury
12/01/2009 - "Importantly, however, blockade of FcgammaRIV is also effective in inhibiting phagocytosis and cytokine production in IgG2b-induced anemia and acute lung injury, processes that display a further dependence on C5a anaphylatoxin receptor. "
01/01/2012 - "Role of C3, C5 and anaphylatoxin receptors in acute lung injury and in sepsis."
01/01/2014 - "We have studied experimental acute lung injury (ALI) in mice following airway deposition of bacterial lipopolysaccharide (LPS) or the recombinant mouse complement anaphylatoxin, C5a. "
09/01/2015 - "In this study, we analyzed the role of complement-derived anaphylatoxins in the pathogenesis of experimental acute lung injury/acute respiratory distress syndrome (ALI/ARDS) in C57BL/6J mice. "
09/01/2015 - "Experimental design of complement component 5a-induced acute lung injury (C5a-ALI): a role of CC-chemokine receptor type 5 during immune activation by anaphylatoxin."
01/01/2011 - "The complement activation product, C5a (anaphylatoxin) has been reported to be a contributing factor leading to mesenteric ischemia/reperfusion injury which is a predisposing factor in the pathogenesis of NEC. "
01/01/2007 - "C5a levels in particular are predictive of overall injury, and we suggest this anaphylatoxin causes most of reperfusion injury via both direct toxic effects and a generalised immune activation. "
04/01/2014 - "Endothelial-to-mesenchymal transition and renal fibrosis in ischaemia/reperfusion injury are mediated by complement anaphylatoxins and Akt pathway."
04/01/2013 - "Blocking properdin, the alternative pathway, and anaphylatoxin receptors ameliorates renal ischemia-reperfusion injury in decay-accelerating factor and CD59 double-knockout mice."
02/01/2006 - "Complement C5a, a potent anaphylatoxin, is a candidate target molecule for the treatment of inflammatory diseases, such as myocardial ischemia/reperfusion injury, RA, and the antiphospholipid syndrome. "
|5.||Otitis Media with Effusion
01/01/1985 - "The above results revealed that an extremely intensive inflammatory reaction may take place in the middle ear, and that anaphylatoxin might play an important role as a delayed factor in otitis media with effusion."
05/01/1992 - "Tranilast may be effective for treating secretory otitis media because it directly suppresses anaphylatoxin present in middle ear effusion."
01/01/1985 - "Complement anaphylatoxins activity in middle ear effusion."
10/01/2000 - "To analyze whether complement C3a anaphylatoxin, other C3 fragments, interleukin-1beta (IL-1beta), or tumor necrosis factor-alpha (TNF-alpha) contributes to inflammation in chronic otitis media with effusion (OME). "
|1.||Complement System Proteins (Complement)
|2.||Immunoglobulin G (IgG)
|3.||Lysine Carboxypeptidase (Carboxypeptidase N)
|5.||tranilast (N 5')
|6.||CD55 Antigens (Decay Accelerating Factor)
|7.||cobra venom factor
|9.||Histamine (Histamine Dihydrochloride)
|10.||Complement Membrane Attack Complex (Membrane Attack Complex)
|3.||Renal Dialysis (Hemodialysis)