Risk Predictor: Individual SUDEP Risk Factor Cluster IDs

2015 ◽  
pp. 117-120
Author(s):  
Claire Lathers ◽  
Steven Schachter ◽  
Braxton Wannamaker ◽  
Jan Leestma
Keyword(s):  
Author(s):  
Н. Воробьева ◽  
А. Воробьева ◽  
Н. Юрьев ◽  
А. Валькова

Цель исследования: анализ особенностей фолатного обмена в популяции ненцев острова Вайгач. Исследование выполнено в рамках трансширотной морской научной экспедиции «Арктический плавучий университет-2016». Материалы и методы. Обследовано 42 ненца (27 женщин и 15 мужчин), постоянно проживающих на острове Вайгач. Исследованы основные маркеры фолатного обмена: содержание фолатов и гомоцистеина, полиморфизм генов фолатного обмена у коренных жителей (ненцев) Арктики. Результаты. Выявлен фактор риска развития гипергомоцистеинемии — низкий уровень фолатов. Заключение. В изученной выборке преобладал аллель «дикого типа» в генах MTHFR677 C]>]T, MTHFR1298 А]>]С, MTR2756 A]>]G, за исключением аллеля A66G в гене MTRR. Aim: to analyze the peculiarities of folate metabolism in Nenets population of Vaigach Island. The study was performed during trans-latitudinal marine research expedition «Arctic Floating University-2016». Materials and methods. We examined 42 Nenets (27 women and 15 men) — permanent residents on Vaigach Island. We studied the main markers of folate metabolism: levels of folate and homocysteine, polymorphism of folate metabolism genes in indigenous Arctic ethnos (Nenets). Results. We revealed risk factor for hyperhomocysteinemia development — a low folate level. Conclusion. The «wild-type» allele of genes MTHFR677 C]>]T, MTHFR1298 A]>]C, MTR2756 A]>]G was prevalent among examined population except A66G allele in MTRR gene.


2009 ◽  
Vol 26 (6) ◽  
pp. 1069-1074 ◽  
Author(s):  
Thomas Kantermann ◽  
Till Roenneberg

2009 ◽  
Vol 26 (6) ◽  
pp. 1069-1074 ◽  
Author(s):  
Thomas Kantermann ◽  
Till Roenneberg

VASA ◽  
2004 ◽  
Vol 33 (4) ◽  
pp. 191-203 ◽  
Author(s):  
Weiss ◽  
Hilge ◽  
Hoffmann

Elevated plasma levels of homocysteine (hyperhomocysteinemia) are increasingly recognized as a potential risk for atherothrombotic vascular diseases by numerous epidemiological and clinical studies. There are increasing experimental data that indicate mechanisms by which homocysteine may alter the vasculature in a way that predisposes to atherosclerotic vascular disease. A key event in the vascular pathobiology of hyperhomocysteinemia seems to involve the induction of endothelial dysfunction due to a reduction of the endogenous antiatherothrombotic molecular nitric oxide. Elevated homocysteine levels can be efficiently and safely reduced in most of hyperhomocysteinemic patients by supplementation of folic acid and cobalamin. This reduction is associated with an improvement in endothelial function and other surrogate markers of atherothrombosis, like carotid plaque area and the rate of abnormal stress electrocardiograms. Whether or not this translates into clinical benefits, is still under investigation. The first clinical study on homocysteine-lowering vitamin supplementation in patients that had undergone coronary intervention showed a benefitial effect on the rate on restenosis and the need for revascularization which translated into a reduction of major coronary events. In contrast, in three larger scaled secondary intervention trials in patients with stable coronary disease or post non-disabling stroke, vitamin supplementation had no effect on future vascular events although baseline homocysteine levels were significantly associated with a worse prognosis. Until the results of more clinical trials are available, the clinical relevant question whether or not homocysteine is just a risk predictor or a modifiable risk factor can not definitely be answered.


2004 ◽  
Vol 71 ◽  
pp. 121-133 ◽  
Author(s):  
Ascan Warnholtz ◽  
Maria Wendt ◽  
Michael August ◽  
Thomas Münzel

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.


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