PO5-138 ENDOTHELIAL NITRIC OXIDE SYNTHASE G894T GENE POLYMORPHISM, BLOOD PRESSURE AND HYPERTENSION IN THE TURKISH ADULT RISK FACTOR STUDY

2007 ◽  
Vol 8 (1) ◽  
pp. 51
Author(s):  
N. Erginel-Unaltuna ◽  
E. Komurcu-Bayrak ◽  
M. Poda ◽  
E. Becer ◽  
A. Onat ◽  
...  
Author(s):  
Rizk Elbaz ◽  
Lamiaa A. A. Barakat ◽  
Ahmed Nageb ◽  
Hewaydah El Sayed

Background and Objective: Endothelial nitric oxide synthase gene polymorphism  (eNOS) is one of three isoforms that synthesize nitric oxide (NO), that participates in several biological processes have been associated with obesity. This study was undertaken to determine if eNOS gene (G894T) was associated with susceptibility of obesity. Materials and Methods: The study was carried out on 200 cases divided into 100 obese patient and 100 healthy as control. The mean age cases was (27.02 ± 10.90) they include 79 female and 21 males. All participants were subjected to an estimation of their body mass index (BMI), weight hip ratio (WHR), in addition to random blood sugar (RBS), total cholesterol, triglyceride (TG), and lactate dehydrogenase enzyme (LDH). DNA was amplified using PCR-SSP for detection of relation between polymorphism and endothelial nitric oxide synthase gene in G894T.   Results: All cases showed that there were  no significant difference between cases and controls regarding to their chemical lab’s  analysis (TG, Cholesterol, LDL and HDL).All cases showed significant frequency of G894T GG, TT and GT (P <0.001) vs. Controls Conclusion: The polymorphism G894T of eNOS considered as a potential risk factor for obesity.


2020 ◽  
Vol 15 (2) ◽  
pp. 145-151
Author(s):  
Kateryna Zaichko ◽  
Nataliia Zaichko ◽  
Oleksandr Maievskyi ◽  
Oleksandr Korotkyi ◽  
Tetyana Falalyeyeva ◽  
...  

Background: Rheumatoid Arthritis (RA) is an autoimmune polygenic disease characterized by rapid disability progression and high prevalence. Progression of RA is closely associated with chronobiological changes in the production of some hormones and inflammatory mediators, influencing the disease course and therapy efficacy. The main pathogenetic mechanism of RA is angiogenesis, which is controlled by biological clock-genes. Further investigation of circadian rhythms of angiogenic mediators production in RA patients may be considered as important and relevant. The aim of this study was to establish daily variability of serum endothelial Nitric Oxide Synthase (NOS3) and toll-like receptors 2 (sTLR2) levels in female RA patients depending on the NOS3 gene polymorphism. Methods: We examined 173 RA patients (100% female) aged 43.7 ± 7.35 years and 34 age-matched healthy women without joint diseases and autoimmune diseases (control). RA was diagnosed by ACR/EULAR 2010 criteria. Blood serum NOS3 and sTLR2 levels were determined at 08:00 and 20:00 using Cloud-Clone Corp kits (USA). NOS3 T-786С (rs2070744) polymorphism was determined by Real-Time PCR (Bio-Rad iCycler IQ5) using SNP-express kits. The SPSS22 software package was used for statistical processing of the results. Results: Females with RA demonstrated oppositely directed serum NOS3 and sTLR2 daily changes: NOS3 level in the morning (08:00) was lower than in the evening (+ 45.5 ± 30.7%), and sTLR2 level in the evening (at 20:00) was lower than in the morning (-21.6 ± 13.1%). RA patients had differences in NOS3 and sTLR2 production depending on NOS3 T786C genotype. CC subjects had NOS3 level at 08:00, 20:00 and day average levels lower (16-25%), and sTLR2 level higher (24-27%) than those of TT subjects. RA patients, carriers of CC genotype, had higher chances of NOS3 and sTLR2 aberrant production compared to TT and TC genotype carriers (OR = 2.99 and 4.79, respectively). Conclusion: RA patients demonstrated oppositely directed circadian changes of serum NOS3 and sTLR2. CC genotype carriers had lower NOS3 and higher sTLR2 production rates than TT and TC genotype carriers.


Neurology ◽  
1997 ◽  
Vol 49 (2) ◽  
pp. 614-617 ◽  
Author(s):  
L. R. Griffiths ◽  
D. R. Nyholt ◽  
R. P. Curtain ◽  
P. J. Goadsby ◽  
P. J. Brimage

Sign in / Sign up

Export Citation Format

Share Document