Showing 3 results for Nourazarian
H Dolatkhah, Mh Somi, R Estakhri, N Dolatkhah, A Mirza-Aghazadeh, M Nourazarian, B Pourasghari, E Fattahi,
Volume 4, Issue 1 (Spring - Summer 2010[PERSIAN] 2010)
Abstract
Spring summer 2010, Vol.4, No.1 /74 Medical Laboratory Journal Severity of Oxidative DNA Damage in Gastric Tissue of Smoker and Non-smoker Patients with Dyspepsia Abstract Background and Objectives: Cigarette smoking is associated with an increase in risk of peptic ulcer and Gastro-Intestinal cancer. Toxic materials in smoke and tar have a significant role in production of carcinogenic complexes, injury to DNA and cellular proliferation in gastric cancer. The study was designed to compare the rate of injury to DNA in gastric tissue of smoker and non-smoker patients with active peptic ulcer. Material and Methods: In this Case-Control study, the case group composed of 43 smoker patients aged 45.30±13.16 with active peptic ulcer (14 female & 29 male) referred to gastroenterology clinic. The first control group consisted of 43 non-smokers without peptic ulcer (13 female & 30 male) with mean age of 42.67±16.04, and the second control group included 43 smokers without peptic ulcer (16 female & 27 male) with mean age of 44.58±12.07, and the third ones had 43 non-smoker patients with active peptic ulcer (20 female & 23 male) with mean age of 45.37±13.39. The rate of gastric mucosa DNA damage in the four groups was measured by calorimetrically method. Results: The DNA damage in gastric mucosa of smoker patients with active peptic ulcer(28.05±5.54 AP/100000bp) is higher than those of the three control groups (p<0.0001 in all case). Conclusion: Results of this study approve the direct relation between increase in DNA damage and toxic complexes existing in smoke and tar of cigarette. Key Words:Cigarette Smoking, DNA Damage, Active Peptic Ulcer Dolatkhah H Research Center of Gastroenterology and Hepatology, Tabriz University of Medical Sciences Somi MH Research Center of Gastroenterology and Hepatology, Tabriz University of Medical Sciences Fattahi E Research Center of Gastroenterology and Hepatology, Tabriz University of Medical Sciences Estakhri R Research Center of Gastroenterology and Hepatology, Tabriz University of Medical Sciences Dolatkhah N Talegani Hospital, Tabriz University of Medical Sciences Mirza-Aghazadeh A Dept. of Basic Sciences, Paramedical Faculty , Tabriz University of Medical Sciences Nourazarian,M Clinical Laboratory of Emam Reza Hospital, Tabriz University of Medical Sciences Pourasghari B Clinical Laboratory of Emam Reza Hospital,Tabriz University of Medical Sciences Corresponding: Dolatkhah, H E-mail: dolatkhahh@gmail.com
M Rahbani-Nobar, Mh Somi, A Fattahi, N Dolatkhah, M Nourazarian, S J Seyedi-Khoshknab, B Pourasghari, H Dolatkhah,
Volume 4, Issue 2 (Autumn – Winter 2011[PERSIAN] 2010)
Abstract
Abstract Bachground and objectives: Epidemiological studies have shown that using tobacco products is one of the main factors in forming malignancies in various tissues of the body. There is more than 600 μgr nitric oxide radical (NO°) in gas phase in each cigarette with fresh smoke. Hence, oxidation of nitrogen components in tobacco, more than 100 μgr of atmospheric NO°is produced by smoking, would be transferred to the body without any filtration. We studied nitric oxide levels in the gastric juice of smokers and non-smokers patients with active peptic ulcer. Material and Methods: In this study, 43 smoker patients with active peptic ulcer (14 female & 29 male) referred to gastroenterology clinic with mean age of 45.30±13.16 as case group.Forthy-three non-smokers without peptic ulcer (13 female & 30 male) aged 42.67±16.04, 43 smoker without peptic ulcer (16 female & 27 male) with mean age of 44.58±12.07 and 43 non-smoker with active peptic ulcer (20 female & 23 male) with mean age of 45.37±13.39 were selected as control groups of 1, 2 and 3 ,respectively. The level of Nitric oxide in gastric juice was measured by using Greiss colorimetric method. Results: Comparing with control group one and two, meaningful rise is noticed in mean level of nitric oxide case group (p<0.0001). Mean levels of NO in control group 1, 3 and case group are 4.21±1.13, 5.37±2.26, 7.90±2.12 μmol/L, respectively. Nitric oxide level in case group in comparison with control group 2 dose not show Significant difference (p=0.656). Mean levels of NO in control 2 and case groups are 7.45±1.54 and 7.90±2.12 μmol/L, respectively. Conclusion: It can be concluded that cigarette smoking may be one of the cause of increased level of gastric juice nitric oxide. This increase may be due to component in cigarette smoke and tar. These components can cause DNA damage through oxidation-reduction cycle and consequently increase the risk of malignancies in gastric tissues. Key words: Cigarette Smoking, Nitric Oxide, Nitrosative Stress, Active Peptic Ulcer
Seyyed Manuchehr Nourazarian , Mojtaba Ghaffarian , Homayun Dolatkhah ,
Volume 10, Issue 3 (May-Jun 2016 2016)
Abstract
ABSTRACT
Background and Objective: The relationship between diabetes mellitus and increased risk of cardiovascular diseases has been demonstrated. The aim of this study was to determine the fatty acid profile of epicardial adipose tissue in diabetic and non-diabetic patients with cardiovascular disease.
Methods: In this study, 28 diabetic and 40 nondiabetic patients were evaluated. The epicardial adipose tissue and blood samples of patients were collected during surgery. Non‐esterified fatty acids and phospholipids were measured by the thin layer chromatography and gas chromatography.
Results: Saturated free fatty acids (12: 0) level was higher in diabetic patients compared to nondiabetic patients (P=0.038), while saturated free fatty acids (16: 0) was significantly lower in diabetics (P=0.011). Unsaturated fatty acid (20: 3n-9) was higher in nondiabetics compared to diabetics (P=0.015). There was a significant decrease in level of monounsaturated fatty acids in diabetic patients. The epicardial adipose tissue of diabetics showed a significant increase in free fatty acid (18: 0) and conjugated linoleic acid levels, while there was a significant decrease in the level of free fatty acid (18: 1n-11). Level of epicardial omega-3 free fatty acid (20: 5 n-3) and 22: 6 n -3 was significantly reduced in these patients.
Conclusion: Differences in the serum free fatty acid profile of the two groups may be due to differences in their diet, while changes in the fatty acid composition of epicardial adipose tissue in these two groups could be due to impaired metabolism of fatty acids such as uptake, movement and androgen synthesis as a result of diabetes. These changes increase the risk of developing atherosclerosis in diabetic patients.
