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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
S H Alizadeh Shargh, A Ghazanchaei, A A Ayetollahi, A Khandan Del, B Pourasghari, R Estakhri,
Volume 4, Issue 2 (Autumn – Winter 2011[PERSIAN] 2010)
Abstract

Abstract Bachground and objectives: Dientamoeba fragilis is a habitant protozoa in human colon causing clinical symptoms, such as local stomach pain, weight loss, lack of appetite and flatulence. It is important to diagnose this infection correctly and differentiate it from other Protozoa. In this study PCR and Iron Hematoxylin methods were used to detection of this protozoa in Chalous Medical centers refers in 2010. Material and Methods: The stool samples (n=302) of this cross-sectional study were selected via cluster random sampling. After wet mount study the samples were preserved in PVA (for staining) and Ethanol (for molecular). The samples were studied both Staining and Molecular methods. Sensitivity and specificity were assessed. Results: Of 302 samples, six of them are positive via staining method (1.99%) and five by molecular method. All negative results with staining method are also negative with PCR. Contamination with E.coli in 2 samples and with Balstocystis homonis were seen in one sample. Sensitivity and specificity of PCR was 85% and 100% respectively. Conclusion: The discrepancy between two methods maybe caused by observer errors in staining method and unsynchronized molecular and microscopic studies. Key words: Dientamoeba fragilis, PCR, Iron Hematoxylin, Chalous region

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