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Verfasst von:Peters, Andreas [VerfasserIn]   i
 Hakimi, Maani [VerfasserIn]   i
 Vittas, Spiros [VerfasserIn]   i
 Fleming, Thomas [VerfasserIn]   i
 Nawroth, Peter Paul [VerfasserIn]   i
 Böckler, Dittmar [VerfasserIn]   i
 Dihlmann, Susanne [VerfasserIn]   i
Titel:Gender difference in glyoxalase 1 activity of atherosclerotic carotid artery lesions
Verf.angabe:Andreas S. Peters, MD, Maani Hakimi, MD, Spiros Vittas, PhD, Thomas H. Fleming, PhD, Peter P. Nawroth, MD, Dittmar Böckler, MD, and Susanne Dihlmann, PhD
Jahr:2015
Jahr des Originals:2014
Umfang:6 S.
Fussnoten:Available online 21 April 2014 ; Gesehen am 02.07.2020
Titel Quelle:Enthalten in: Journal of vascular surgery
Ort Quelle:Amsterdam [u.a.] : Elsevier, 1984
Jahr Quelle:2015
Band/Heft Quelle:62(2015), 2, Seite 471-476
ISSN Quelle:1097-6809
Abstract:Objective - Age and gender are two factors that determine the risk of atherosclerosis. The latter effect is only partly understood. Dicarbonyls, in particular methylglyoxal, participate in the development of atherosclerosis, and their major detoxification route is the enzyme glyoxalase 1 (GLO1), which is known to decrease during aging. - Methods - GLO1 expression and activity were studied in atherosclerotic carotid artery lesions of 71 patients with respect to demographic and clinical characteristics. - Results - GLO1 activity was nonsignificantly reduced by >50% in individuals with carotid artery disease compared with control individuals. There was no significant difference in GLO1 expression between the groups; however, the GLO1 activity-to-protein ratio showed a significant reduction for the carotid artery disease patients compared with the controls. The reduction in the GLO1 activity-to-protein ratio was more pronounced in men and was associated with increased inflammation shown by a significant elevation in the expression-level of interleukin-1β. - Conclusions - These data suggest that GLO1 is regulated on the post-translational level by factors such as gender as well as factors that affect the overall burden of atherosclerosis.
DOI:doi:10.1016/j.jvs.2014.02.058
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext ; Verlag: https://doi.org/10.1016/j.jvs.2014.02.058
 Volltext: http://www.sciencedirect.com/science/article/pii/S0741521414003310
 DOI: https://doi.org/10.1016/j.jvs.2014.02.058
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1703272765
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