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Fereydon Azizi , Farid Raiszadeh, Payam Salehi, Maziar Rahmani, Habib Emami, Arash Ghanbarian , Rambod Hajipoor,
Volume 24, Issue 3 (Autumn 2000)
Abstract

Decreased serum HDL is one one of the most lonmon lipiu disoides in paterts with colonary disease and the existing enidenie svggests that every lmg/dl decreaie in servn HDL inveases CAD risk by 2-3 % . This study was performed in 2000 to study HDL deterninants in tehran popolation. westudied 9514 individvais, 20-69 yers old who have participated in tehran lipid and gwcose study (tl62), inclvding 3942 men and 5571 woman. in all subjects a personal history questionnaire especially on physical activity and cigarette smoking, was filled out and clinical examination inclvding anthroponetic
measurements were performed. Serum levels of total cholesterol, trig;ucerides, and HDL were ,easured. Women had a significantly hoher mear HDL than in men (45± 11 vs 38±9 mg/dl; P<0.001); low HDL level (HDL < 35 mg/dl) was observed in 31 % of men and 13 % of women (P < 0. 00 I). Obese subjects (BMI 30 Kg/m2) had a significantly lower HDL level than normal subjects(42± 11 vs 44± 1 I: P < 0.0001). Subjects with truncal obesity (WHR0.95 in ,en and WHR 0.8 in women) had lower HDL level than normal subjects (37 ±9 vs 39± 10 in mean and 44± 11 vs 48± 11 in women  P < 0.001 in both). Smokers had a significantly lower HDL level than nonsmokers (38± 10 vs 43±11; P<0.001) and low HDL level was two ties more common in smokers than in nonsmokers (36.4 vs two times more common in smokers than in nonsmokers (36.4 vs 18.2 pecent). Passive smokers had also lower wean HDL levels ( 42 ± 11 vs 43 ± 11; P<0.001). Mean HDL level was not different in subjects with different degrees of physical acfiuity. In multiple stepwise logistic regression, deferminarts of serum HDL level, in order of entering the model, were: Sex (OR 3.03, P<0.001), high WHR (OR 1.56; P<0.001), Cigarethe smoking (OR 1.63; P<0.0001), age (OR 0.99; P<0.001), obesity (OR I. 21; P < 0. 005), and possive smoking (OR 1.17; P < 0. 04). Physical activity did not enter the predictive model apart from age and sex which are constitutional, nonmodifiable variables, other modifiable determinarts of HDL level (obesity, truncal obesity, cigareth smoking, and passive smoking) can be used in community prevention programs in control of CAD.

S Seyedmousavi, A Ghanbarian, M Seyedahadi, N Saadat, F , Azizi,
Volume 30, Issue 4 (12-2006)
Abstract

Background: The aim of this study was to assess non-communicable disease risk factors in children of parents with an ECG evidence of myocardial infarction (MI), and compare them with children from families with no such parental history. Materials and methods: Of 15005 participants in the Tehran Lipid and Glucose Study, all individuals over the age of 30 years underwent routine ECG exams. Among these, 303 off springs aged 3-30 years, who had one or two parents with possible or probable myocardial infarction (MI) according to the Minnesota coding were selected. An age and sex-matched sample of 601 off springs who had no parental evidence of ECG-defined MI were randomly selected as the control group. Risk factors studied were: BMI, blood pressure, FBS, total cholesterol, HDL-C, LDL-C, triglycerides and the metabolic syndrome. Results: A "paternal" and "parental" history of MI was associated with a higher prevalence of overweight and obesity, respectively, (34.9% vs. 24.8 %) and a lower prevalence of high blood pressure, (12.2% vs. 18.1%), in their off springs. Likewise, in male children of fathers or both parents with ECG evidence of MI, a lower prevalence of hypertension was noticed, Compared with the control group, in female children of mothers with a history of MI,a higher prevalence of elevated serum LDL-C was found (28.0% vs. 10.7%) (p<0.05). Paternal MI was associated with increased prevalence of higher body mass indices (BMI) in their off springs (OR=1.6 95% CI: 1.1-2.4p<0.05). Conclusion: There is a significant familial correlation between paternal history of MI and overweight and obesity in their offspring.
Zohre Bolandi, Hosein Ghanbarian,
Volume 41, Issue 3 (9-2017)
Abstract

Abstract
Background: MicroRNAs (miRNAs) are endogenous, non-coding short RNAs (~22 nt) that can downregulate gene expression by translational repression, mRNA degradation, or transcriptional repression. miRNA misregulation has been implicated in pathogenic alterations such as cancer. In order to investigate microRNA functions in gene regulation and/or to modulate their expression in pathogenic conditions, microRNAs are overexpressed by using plasmid or synthetic RNA duplexes designed to mimic the miRNA of interest. 
Methods: Mouse fibroblast cells were cultured in DMEM containing 10% FBS, 100 U/ml penicillin, and 0.1 mg/ml streptomycin. Lipofectamine 2000 reagent (Invitrogen, 11668-027) was used for transfection according to the manufacturer’s instructions. RNA was extracted from cells and tissues using Qiazol (Qiagen, Germany), according to the manufacturer’s protocol. 2 µg RNA samples were reverse transcribed to cDNA using microRNA-1 specific stem loop and random hexamer primers and MLV reverse transcriptase.q-PCR was performed with the ‘SYBR Green I Master Mix’ kit. 
Results: miR-1-expressing plasmid (pPRO-miR-1) was transfected into fibroblast cells. Quantitative real time PCR determination showed that Cdk9 expression was inhibited in transfected cells compared to control. Similarly, downregulation of Cdk9 was also observed following transfection of 22 nucleotide mature double stranded miR-1. Interestingly, transfection of synthetic 22 nucleotide mature single stranded miR-1 (miR-1-3p) induced Cdk9 expression in the fibroblast cells. 
Conclusion: Unlike miR-expressing vector or synthetic RNA duplexes designed to mimic the miRNA of interest that can downregulate gene expression, synthetic 22 nucleotide mature single stranded microRNA probably induces gene expression in a locus-specific manner. 
 


Maryam Ghahremani Piraghaj, Seyed Mahmoud Hashemi, Sara Soudi, Hossein Ghanbarian,
Volume 42, Issue 3 (9-2018)
Abstract

Background: Macrophages are one of the most important immune cells. Macrophages can be divided into two main subgroups of classical or inflammatory macrophages(M1) and alternative or non -inflammatory macrophages or (M2), due to different stimuli. One of the factors that causes the macrophage to orient towards M2, is the phagocytosis of apoptosis cells (efferocytosis). The phagocytosis of mesenchymal stem cells, can be very important in cell therapy due to immunomedulatory   properties and their ability to modulate macrophage function.
Materials and Methods: Mesenchymal stem cells were  isolated  from Wharton's  jelly and characterized by flow cytometry as well as differentiation to Osteoblasts and adipocytes. MSCs in the passage 2 exposed to UV light for induction of apoptosis for thirty minutes and followed by incubation for two hours. The cells were then isolated and added to macrophages in a ratio of 4 to 1. After that cells were incubated for 48 hours, after incubation time the production of TNFα and IL10 cytokines was measured by ELISA and nitric oxide production was measured. Macrophages phagocytosis ability was also measured by yeast and apoptotic thymocytes phagocytosis in different groups.
Results: The phagocytosis of Wharton's jelly–Mesenchymal stem cells (WJ–MSCs) by macrophages reduces the production of inflammatory cytokine TNFα and increases the production of inhibitory cytokine IL-10. Nitric oxide production has decreased in these macrophages. Also, after phagocytosis of apoptotic WJ–MSCs, the ability of yeast phagocytosis in these macrophages was reduced and phagocytosis of apoptotic thymocyte was increased.
 Conclusion: The phagocytosis of apoptotic WJ–MSCs, induce non-inflammatory phenotype in macrophages. So, injected WJ–MSCs maintain their immunomodulatory properties even if they get apoptosed in the body.

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