scholarly journals Fcγ Receptor IIIA Polymorphism as a Risk Factor for Acute Poliomyelitis

2002 ◽  
Vol 186 (12) ◽  
pp. 1840-1843 ◽  
Author(s):  
Tiina Rekand ◽  
Nina Langeland ◽  
Johan A. Aarli ◽  
Christian A. Vedeler
Keyword(s):  
Risk Factor ◽  
Fcγ Receptor ◽  
Acute Poliomyelitis

Fcγ receptor IIIA polymorphism as a risk-factor for coronary artery disease

2005 ◽  
Vol 180 (2) ◽  
pp. 277-282 ◽  
Author(s):  
Sonia Gavasso ◽  
Ottar Nygård ◽  
Eva Ringdal Pedersen ◽  
Jan H. Aarseth ◽  
Øyvind Bleie ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Risk Factor ◽  
Coronary Artery ◽  
Fcγ Receptor ◽  
Artery Disease

scholarly journals The Fcγ receptor III genotype as a risk factor for aggressive periodontitis in Korean patients

2006 ◽  
Vol 36 (1) ◽  
pp. 113
Author(s):  
Myung Hyun Kim ◽  
Seung Yun Shin ◽  
Tae Il Kim ◽  
Yang Jo Seol ◽  
Yong Moo Lee ◽  
...  
Keyword(s):  
Risk Factor ◽  
Aggressive Periodontitis ◽  
Fcγ Receptor ◽  
Korean Patients

The homozygous FcγRIIIa-158V genotype is a risk factor for heparin-induced thrombocytopenia in patients with antibodies to heparin-platelet factor 4 complexes

Blood ◽  
2004 ◽  
Vol 104 (9) ◽  
pp. 2791-2793 ◽  
Author(s):  
Yves Gruel ◽  
Claire Pouplard ◽  
Dominique Lasne ◽  
Charlotte Magdelaine-Beuzelin ◽  
Chloé Charroing ◽  
...  
Keyword(s):  
Risk Factor ◽  
Immunoglobulin G ◽  
Platelet Factor 4 ◽  
Allele Frequencies ◽  
Genotype Distribution ◽  
Fcγ Receptor ◽  
Control Groups ◽  
Platelet Factor ◽  
Heparin Induced Thrombocytopenia

Abstract We hypothesized that Fcγ receptor IIIa (FcγRIIIa), a polymorphic receptor for the Fc portion of immunoglobulin G (IgG) other than FcγRIIa, was involved in heparin-induced thrombocytopenia (HIT). FcγRIIa-131 and FcγRIIIa-158 genotypes were determined in 102 patients with definite HIT and in 2 control groups of patients treated by heparin (86 subjects without detectable antibodies [Abs] to heparin-platelet factor 4 [H/PF4], Ab- group; 84 patients with Abs to H/PF4 without HIT, Ab+ group). There were no significant differences in genotype distribution or allele frequencies between the 3 groups for FcγRIIa-131H/R polymorphism. In contrast, FcγRIIIa-158V homozygotes were more frequent in the HIT group than in the Ab+ group (P = .02), a difference that was more pronounced in patients with high levels of anti-H/PF4 Abs (P = .01). Since anti-H/PF4 Abs are mainly IgG1 and IgG3, clearance of sensitized platelets may be increased in patients homozygous for the FcγRIIIa-158V allotype, thus contributing to the development of thrombocytopenia. (Blood. 2004;104:2791-2793)

The Fcγ Receptor Genotype as a Risk Factor for Generalized Early-Onset Periodontitis in Japanese Patients

2000 ◽  
Vol 71 (9) ◽  
pp. 1425-1432 ◽  
Author(s):  
Tetsuo Kobayashi ◽  
Noriko Sugita ◽  
W-Ludo van der Pol ◽  
Yasuko Nunokawa ◽  
Nomdo A.C. Westerdaal ◽  
...  
Keyword(s):  
Risk Factor ◽  
Early Onset ◽  
Japanese Patients ◽  
Fcγ Receptor

Clinical aspects of reactive oxygen and nitrogen species

2004 ◽  
Vol 71 ◽  
pp. 121-133 ◽  
Author(s):  
Ascan Warnholtz ◽  
Maria Wendt ◽  
Michael August ◽  
Thomas Münzel
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Risk Factor ◽  
Endothelial Dysfunction ◽  
Vascular Tissue ◽  
Rapid Development ◽  
Reactive Oxygen ◽  
Clinical Aspects ◽  
No Production ◽  
Oxygen Species

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.

Parental Mental Illness in Childhood as a Risk Factor for Suicidal and Self-Harm Ideations in Adults Seeking Help for Tinnitus and/or Hyperacusis

2019 ◽  
Vol 28 (3) ◽  
pp. 527-533
Author(s):  
Hashir Aazh ◽  
Michael Landgrebe ◽  
Ali A. Danesh
Keyword(s):  
Mental Illness ◽  
Risk Factor ◽  
Parental Mental Illness ◽  
Seeking Help ◽  
Self Harm

Functional interaction of calmodulin with the Fcγ-receptor FcRn

2001 ◽  
Vol 120 (5) ◽  
pp. A698-A698
Author(s):  
B DICKINSON ◽  
S CLAYPOOL ◽  
R BLUMBERG ◽  
W LENCER
Keyword(s):  
Fcγ Receptor ◽  
Functional Interaction

M.614 Homocysteine as an independent risk factor for cardiovascular disease

2004 ◽  
Vol 5 (1) ◽  
pp. 142
Author(s):  
S PAXIMADAS
Keyword(s):  
Cardiovascular Disease ◽  
Risk Factor ◽  
Independent Risk Factor
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