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Quoted phrase not found in phrase index: "Anaphylotoxin inactivator deficiency"
Page 1
Paroxysmal nocturnal haemoglobinuria.
Hill A, DeZern AE, Kinoshita T, Brodsky RA. Hill A, et al. Nat Rev Dis Primers. 2017 May 18;3:17028. doi: 10.1038/nrdp.2017.28. Nat Rev Dis Primers. 2017. PMID: 28516949 Free PMC article. Review.
Clinical manifestations of PNH occur when a HSC clone carrying somatic PIGA mutations acquires a growth advantage and differentiates, generating mature blood cells that are deficient of GPI-anchored proteins. The loss of CD55 and CD59 renders PNH erythrocytes suscep …
Clinical manifestations of PNH occur when a HSC clone carrying somatic PIGA mutations acquires a growth advantage and differentiates, …
Complement and periodontitis.
Hajishengallis G. Hajishengallis G. Biochem Pharmacol. 2010 Dec 15;80(12):1992-2001. doi: 10.1016/j.bcp.2010.06.017. Epub 2010 Jun 23. Biochem Pharmacol. 2010. PMID: 20599785 Free PMC article. Review.
This paper reviews evidence linking complement to periodontal inflammation and pathogenesis. Clinical and histological observations show a correlation between periodontal inflammatory activity and local complement activation. Certain genetic polymorphisms or deficiencie …
This paper reviews evidence linking complement to periodontal inflammation and pathogenesis. Clinical and histological observations s …
The Role of Complement C3a Receptor in Stroke.
Ahmad S, Bhatia K, Kindelin A, Ducruet AF. Ahmad S, et al. Neuromolecular Med. 2019 Dec;21(4):467-473. doi: 10.1007/s12017-019-08545-7. Epub 2019 May 17. Neuromolecular Med. 2019. PMID: 31102134 Review.
The C3a anaphylatoxin, via its cognate C3a receptor (C3aR), mediates inflammation by promoting breakdown of the blood-brain barrier and the massive infiltration of leukocytes into ischemic brain in experimental stroke models. Studies utilizing complement deficient mice as …
The C3a anaphylatoxin, via its cognate C3a receptor (C3aR), mediates inflammation by promoting breakdown of the blood-brain barrier and the …
Coagulation inhibitor substitution during sepsis.
Fourrier F, Jourdain M, Tournois A, Caron C, Goudemand J, Chopin C. Fourrier F, et al. Intensive Care Med. 1995 Nov;21 Suppl 2:S264-8. doi: 10.1007/BF01740765. Intensive Care Med. 1995. PMID: 8636534 Review.
Activation of the contact system induces activation of the classical complement pathway with generation of anaphylatoxins, of the kinins pathway and of fibrinolysis. Physiologic inhibition depends on the C1-inhibitor (C1-Inh.). Septic patients exhibit a relative deficie …
Activation of the contact system induces activation of the classical complement pathway with generation of anaphylatoxins, of the kin …
Controlling the complement system in inflammation.
Kirschfink M. Kirschfink M. Immunopharmacology. 1997 Dec;38(1-2):51-62. doi: 10.1016/s0162-3109(97)00057-x. Immunopharmacology. 1997. PMID: 9476114 Review.
These consequences are clinically manifested in various disorders, including septic shock, multiple organ failure and hyperacute graft rejection. Genetic complement deficiencies or complement depletion have been proven to be beneficial in reducing tissue injury in a number …
These consequences are clinically manifested in various disorders, including septic shock, multiple organ failure and hyperacute graft rejec …
Complement inhibition keeps mothers calm and avoids fetal rejection.
Girardi G. Girardi G. Immunol Invest. 2008;37(5):645-59. doi: 10.1080/08820130802191615. Immunol Invest. 2008. PMID: 18716942 Review.
Complement activation caused dysregulation of the angiogenic factors (deficiency of free vascular endothelial growth factor (VEGF) and elevated levels of soluble VEGF receptor 1) required for normal placental development. ...
Complement activation caused dysregulation of the angiogenic factors (deficiency of free vascular endothelial growth factor (VEGF) an …
C1-inhibitor substitution therapy in septic shock and in the vascular leak syndrome induced by high doses of interleukin-2.
Hack CE, Ogilvie AC, Eisele B, Eerenberg AJ, Wagstaff J, Thijs LG. Hack CE, et al. Intensive Care Med. 1993;19 Suppl 1:S19-28. doi: 10.1007/BF01738946. Intensive Care Med. 1993. PMID: 8053997 Review.
Functional levels of C1-INH tend to be normal in septic patients although paradoxically this inhibitor is an acute phase protein. Moreover, levels of proteolytically inactivated C1-INH are increased in sepsis pointing to an increased turn-over. These observations suggest a …
Functional levels of C1-INH tend to be normal in septic patients although paradoxically this inhibitor is an acute phase protein. Moreover, …
C1-Esterase inhibitor: an anti-inflammatory agent and its potential use in the treatment of diseases other than hereditary angioedema.
Caliezi C, Wuillemin WA, Zeerleder S, Redondo M, Eisele B, Hack CE. Caliezi C, et al. Pharmacol Rev. 2000 Mar;52(1):91-112. Pharmacol Rev. 2000. PMID: 10699156 Review.
C1-esterase inhibitor (C1-Inh) therapy was introduced in clinical medicine about 25 years ago as a replacement therapy for patients with hereditary angioedema caused by a deficiency of C1-Inh. ...We will discuss studies addressing therapeutic administration of C1-In …
C1-esterase inhibitor (C1-Inh) therapy was introduced in clinical medicine about 25 years ago as a replacement therapy for patients w …
Attenuation of cGVHD by C5a/C5aR blockade is associated with increased frequency of Treg.
Wang Y, Lai P, Chen X, He C, Huang X, Geng S, Luo C, Wu S, Ling W, Zhong L, Lu Z, Li P, Weng J, Du X. Wang Y, et al. Sci Rep. 2017 Jun 15;7(1):3603. doi: 10.1038/s41598-017-03700-1. Sci Rep. 2017. PMID: 28620195 Free PMC article.
Our data also demonstrated a significant negative correlation between C5aR expression and regulatory T cells (Treg) frequency in cGVHD patients, indicating a potential role of C5aR in the generation and regulation of Treg. In addition, an in vitro experiment revealed C5aR defi …
Our data also demonstrated a significant negative correlation between C5aR expression and regulatory T cells (Treg) frequency in cGVHD patie …
Plasma protease inhibitor and anaphylatoxin inactivator levels in chronic urticaria/angioedema and in patients experiencing anaphylactoid reactions to radiographic contrast media.
Mathews KP, Pan PM, Amendola MA, Lewis FH. Mathews KP, et al. Int Arch Allergy Appl Immunol. 1986;79(2):220-3. doi: 10.1159/000233975. Int Arch Allergy Appl Immunol. 1986. PMID: 3943918
Since a protease inhibitor or anaphylatoxin inactivator deficiency might explain why certain individuals are prone to develop chronic urticaria/angioedema or anaphylactoid reactions to radiographic contrast media, serum alpha 1-protease inhibitor, alpha 1-antichymot …
Since a protease inhibitor or anaphylatoxin inactivator deficiency might explain why certain individuals are prone to develop …
18 results