The Peep of Nanotechnology in Reproductive Medicine: A Mini-review روزنه امید نانوفناوری در پزشکی بازساختی: یک مقاله مروری 2 1 مقدمه: نانوفناوری یک حوزه جدیدی را در پزشکی مانند سایر علوم باز کرده است. هدف این مطالعه بررسی قابلیت نانوفناوری برای درمان بیماری های دستگاه تولید مثل می باشد. مواد و روشها: در این مطالعه ما همه مقالات چاپ شده در گوگل اسکولار، پاب مد و ساینس دایرکت در مورد نانوفناوری و پزشکی تولید مثل بین سال های ۲۰۰۰تا ۲۰۱۵را مورد تجزیه و تحلیل قرار دادیم. نتایج: این مطالعه آشکار ساخت که نانوفناوری بطور گسترده برای کاربردهای مختلف پزشکی از جمله تشخیص بیماری ها، حمل دارو، تصویربرداری تشخیصی و غیره، و بطور اخص در درمان و تشخیص سرطان مورد استفاده قرار گرفته است. در این تحقیق اهمیت حیاتی نانوفناوری در پزشکی بازساختی و بیولوژی تولید مثل مشخص گردید. همچنین شواهد موجود در مورد استفاده از نانومواد برای تشخیص و درمان بیماری های تولید مثل خلاصه شد. نانوذرات پتانسیل کاربردی زیادی در بیولوژی تولید مثل دارد، همچنین درمان و تصویر برداری سرطان های دستگاه تولید مثل می تواند با نانوذرات مهندسی شده انجام گردد. علاوه بر آن تعدادی از بیماری های غیرسرطانی نظیر اندومتریوز با کمک نانوفناوری قابل درمان است. نتیجه گیری: مطالعات فواید و اهمیت استفاده از نانوفناوری را در بافت های حساس تولید مثل و همچنین گامت ها مورد بررسی قرار داده اند. روش های مبتنی بر نانوذرات خلاقانه و البته بحث برانگیز بوده و درعین حال دید مکانیسمی در مورد بیماری های تولید مثل به ما می دهد. 2 Nanotechnology has opened a new field in medicine as well as in other sciences. The aim of this study was to seek the capability of nanotechnology for the treatment of various reproductive diseases. In this study, we analyzed all articles about “nanotechnology and reproductive medicine” published in 2000-2015, indexed in Google Scholar, PubMed and Science Direct. This study indicated that nanotechnology has been extensively used for different biomedical applications, e.g. detection, drug delivery, diagnostic imaging, etc. particularly in cancer diagnostics and treatment. Here, the emerging uses of nanotechnology in reproductive medicine and reproductive biology were found. The available evidence regarding the use of nanomaterials as experimental tools for the detection and treatment of reproductive diseases was summarized. Nanoparticles have potential applications in reproductive biology. Treatment and imaging of reproductive system-related cancers can be performed by engineered nanoparticles. Also, some non-cancerous diseases can be treated by nanotechnology, e.g. endometriosis. The benefits and concerns associated with their use in a highly delicate system of reproductive tissues and gametes have been investigated. Nano-based methods are innovative and potentially controversial approaches in the clinical settings and give us the mechanisms underlying reproductive diseases. 1 15 2015/05/11 1394/2/21 2015/05/11 1394/2/21 محمد رازی Mohammad Razi Department of Medical Genetics, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran. Iran علی دهقان Ali Dehghani Department of Medical Genetics, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran. Iran فهیمه بیگی Fahimeh Beigi Department of Medical Genetics, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran. Iran حمید نجمی نژاد Hamid Najminejad Department of Medical Genetics, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran. Iran کاظم وطن خواه یزدی Kazem Vatankhahyazdi Department of Medical Genetics, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran. Iran محمد آقا آیت اللهی Mohammad Agha Ayatollahi Pharmaceutics Research Center, Faculty of Pharmacy, Kerman University of Medical Sciences, Kerman, Iran Iran علی جبالی Ali Jebali 3Department of Laboratory Sciences, School of Paramedicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran. Reproductive Immunology Research Center, Shahid Sadoughi University of Medical Sciences, Yazd, Iran. Iran 3Department of Laboratory Sciences, School of Paramedicine, Shahid Sadoughi University of Medical Sc Drug Delivery Nanomaterials Nanoparticles Nanotechnology Reproductive Biology Reproductive Medicine حمل دارو بیولوژی تولید مثل نانوتکنولوژی نانومواد نانوذرات [1]. 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The Comparison of Active and Passive Recovery after an Intense Exhaustive Training Session on the Level of Serum Serotonin of Male Runners مقایسه اثر ریکاوری فعال و غیرفعال پس از یک جلسه تمرین فزاینده درمانده ساز بر سطح سروتونین سرم دوندگان مرد 2 1 مقدمه: هدف این مطالعه مقایسه تاثیر ریکاوری فعال و غیر فعال بعد از یک جلسه تمرین فزاینده درمانده ساز بر سطح سرمی سروتونین در دوندگان مرد بود. مواد و روش ها: در این پژوهش نیمه تجربی ۲۶ دونده نخبه سالم مرد بصورت تصادفی در دو گروه فعال (۱۲ نفر) و غیر فعال (۱۴ نفر)، قرار گرفتند. نیم ساعت قبل از شروع تمرین میزان 5 میلی لیتر خون از افراد گرفته شد سپس هر آزمودنی آزمون بروس را تا حد خستگی روی تریدمیل انجام داد، بلافاصله و 10 دقیقه پس از اجرای آزمون بروس مجددا مقدار 5 میلی لیترخون از افراد تهیه و سطح سرمی سروتونین در نمونه ها تعیین گردید. نتایج و نتیجه گیری: میانگین و انحراف معیار سروتونین در سه مرحله قبل، بلافاصله و 10دقیقه پس از ریکاوری در گروه ریکاوری فعال به ترتیب ۲۵۰/۰۵±۳۶۰/۸۳ ، ۳۰۲/۱۳±۴۵۹/۶۷ ، ۴۴۰/۴۸±۵۱۴/۵۰ نانوگرم بر میلی لیتر بود و در گروه ریکاوری غیرفعال به ترتیب ۹۲/۴۱±۱۴۱/۲۶ ، ۱۰۴/۷۸±۲۴۱/۰۴، ۱۲۰/۰۳±۲۱۴/۳۴ نانوگرم بر میلی لیتر بود. بین غلظت سروتونین قبل و بعد از ریکاوری تفاوت معنی داری وجود داشت اما نوع ریکاوری بر روی غلظت سروتونین سرم دوندگان تاثیری نداشت. 2 Introduction: The aim of this research was to compare active and passive recovery after a session of intense exhaustive training on the level of serotonin in the serum of the runners. Materials and Methods: In this semi-experimental study, 26 male elite runners were randomly assigned to two groups of active (n=12) and passive (n=14) recovery. Half an hour before the start of the training, 5 ml blood was drawn from the sample and then each subject was tested starting training on treadmill for Bruce test until reaching exhaustion. Immediately and then 10 minutes after the Bruce test, 5 ml of blood was drawn again for measuring serotonin. Results and Conclusions:The mean of serotonin in three steps of before, immediately after and 10 minutes after recovery were respectively 360.83 ± 250.05, 459.67±302.13, 514.5±440.48 ng/ml in the active recovery group and 141.26 ± 92.41, 241.04 ± 104.78, 214.34 ± 120.03 ng/ml in the passive recovery group. There was a significant difference between the amount of serotonin after recovery compared to that of before. However, the type of recovery program after that had no effect on the serum serotonin of the blood of the runners 16 20 2015/05/112015/05/6 1394/2/16 2015/05/112015/05/6 1394/2/16 علیرضا بابایی مزرعه نو Alireza Babaei Mazreno Department of Physiology, Islamic Azad University, Khorasgan Branch, Isfahan, Iran. Iran allireza.babaei.m@gmail.com غلامرضا شریفی Gholamreza Sharifi Department of Physiology, Islamic Azad University, Khorasgan Branch, Isfahan, Iran. Iran محمد طلابی Mohammad Tollabi Department of Psychometrics, Allameh Tabatabaei University, Tehran, Iran. Iran Active Recovery Bruce Test Passive Recovery Serotonin ریکاوری فعال ریکاوری غیرفعال آزمون بروس سروتونین [1]. Artigas F, Romero L, DE Montigny C, Blier P. Acceleration of the effect of selected antidepressant drugs in major depression by 5-HT1A antagonists. Trends in Neuroscience 2006; 19: 378-383. ##[2]. Alberghina D, Giannetto C, Piccion G. Peripheral serotoninergic response to physical exercise in athletic horses. 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International Medical Society of Paraplegia 1988; 36: 18-20. ##[8]. Langfort J, Baranczuk E, Pawlak D, Chalimoniuk M, Lukacova N, Marsala J, Gorski J. The effect of endurance training on regional serotonin. Cell Mol Neurobiol. 2006;26(7-8):1327-42.##[9]. Caperuto E.C, dos Santos R.V.T, Mello M.T , Costa Rosa L.F. Effect of Endurance Training on Hypothalamic Serotonin Concentration and Performance. Clinical and Experimental Pharmacology and Physiology 2009; 36: 189–191.##[10]. Marius R, Roeykens J, Magnus L, Keizer H, DE Meirleir K. Endurance performance in humans: the effect of a dopamine precursor or a specific serotonin (5-HT2A/2C) antagonist. Int J Sports Med 2008; 18: 571-577. ##[11]. Kiris M, Haussinger D. Mammalian. Amino Acid Transport, Mechanisms and Control. New York: Plenum Pr. 2007; 35(5): 1215–1217. ## ##

Uremia Effect on White Blood Cell Count in Patients with Renal Failure اثرات اورمی بر تعداد گلبول های سفید خون در بیماران با نارسایی کلیوی 2 1 مقدمه: بنظر می رسد که اورمی باعث تخریب گلبول های سفید خون شده و لکوپنی را موجب می گردد. از اینرو این مطالعه با هدف تاثیر اورمی بر تعداد گلبول های سفید خون طراحی شد. مواد و روش ها: این مطالعه مورد-شاهدی بر روی ۱۲۰بیمار مبتلا به اورمی و ۱۰۰فرد بعنوان گروه کنترل انجام شد. میزان اوره و کراتینین سرم و تعداد سلولهای خون در تمام نمونه های مورد مطالعه تعیین گردید. نتایج و نتیجه گیری: در گروه شاهد، میانگین میزان اوره سرم ۱/۹±۱۴/۵ میلی گرم در دسی لیتر و میانگین مقدار کراتینین ۰/۲±۰/۹در مردان و ۳/۲±۰/۶۶ میلی گرم در دسی لیتر در زنان بود. در گروه بیماران، میانگین مقادیر اوره 4/2±83 میلی گرم در دسی لیتر و میانگین کراتینین درمردان و زنان به ترتیب ۱/۳±۲/۴ و ۱/۷±۲/۱ میلی گرم در دسی لیتر بود. میانگین تعداد گلبولهای سفید در گروه مورد ۲/۲±۶/۰۸و در گروه شاهد ۲/۴۳±۶/۱۷ با واحد ۱۰۹در لیتر بود(۰/۱۷=p ) نتایج ما نشان داد که اورمی نمی تواند باعث تغییر در تعداد گلبولهای سفید شود. 2 Introduction: It is believed that uremia causes destruction of white blood cells (WBC) and thus causes leukopenia. Therefore this study had an attempt to assess the effect of uremia on WBC count. Materials and Methods: This case control study was conducted on 120 uremic patients and 100 samples as control group. All samples were examined for determination of urea and creatinine in their serum and complete blood counts were determined. Results and Conclusions: In healthy individuals, the mean value of urea was 14.5±1.9 mg/dL and the mean value of creatinine was 0.9±0.2 mg/dL (male) and 0.66±3.2 mg/dL (female). In the patient group, the mean value of urea was 83±2.4 mg/dL. The mean value of creatinin in male and female were 2.4±1.3 mg/dL and 2.1±1.7 mg/dL respectively. The mean of WBC count in case and control groups were 6.08± 2.24 and 6.17± 2.43x109/L respectively (p=0.71). Our results indicate that uremia cannot change leukocyte count. 21 24 2015/05/112015/05/62015/05/11 1394/2/21 2015/05/112015/05/62015/05/11 1394/2/21 افسانه سرابندی نو Afsaneh Sarabandi Department of Nursing, Faculty of Medical Sciences, Islamic Azad University, Zahedan Branch, Zahedan, Iran. Iran ریما منافی شبستری Rima Manafi Shabestari Department of Hematology and Blood Transfusion, Scientific Research Center, Tehran University of Medical Sciences, Tehran, Iran. Iran یداله فرشی Yadolah Farshi Department of Hematology and Blood Transfusion, Scientific Research Center, Tehran University of Medical Sciences, Tehran, Iran. Iran شادی طبیبیان Shadi Tabibian Department of Hematology and Blood Transfusion, Scientific Research Center, Tehran University of Medical Sciences, Tehran, Iran. Iran اکبر درگلاله Akbar Dorgalaleh Department of Hematology and Blood Transfusion, Iran University of Medical Sciences, Tehran, Iran Iran سمیرا اسماعیلی ری کنده Samira Esmaeili Reykande Department of Hematology and Blood Transfusion, Scientific Research Center, Tehran University of Medical Sciences, Tehran, Iran. Iran سید حسین کیا Seyyed Hossein Kia Tehran Heart Centre, Tehran University of Medical Sciences, Tehran, Iran. Iran بیژن ورمقانی Bijan Varmaghani Department of Hematology and Blood Transfusion, Scientific Research Center, Tehran University of Medical Sciences, Tehran, Iran. Iran جمال رشیدپناه Jamal Rashidpanah Tehran Heart Centre, Tehran University of Medical Sciences, Tehran, Iran. Iran Leukopenia Uremia White blood cells Renal failure اورمی گلبول سفید خون لکوپنی [1]. Meyer T.W. Uremia. New England Journal of Medicine. New England Journal of Medicine 2007;357(13):1316-25.##[2]. Janson P.A, Jubelirer S.J, Weinstein M.J, Deykin D. Treatment of the bleeding tendency in uremia with cryoprecipitate. New England Journal of Medicine 1980;303(23):1318-22.##[3]. Bagdasarian N, Heung M, Malani P.N. Infectious complications of dialysis access devices. Infectious disease clinics of North America 2012;26(1):127-41.##[4]. Cohen G, Hörl W.H. Immune dysfunction in uremia—an update. Toxins Journal 2012;4(11):962-90.##[5]. Alexiewicz J, Smogorzewski M, Fadda G, Massry S. Impaired phagocytosis in dialysis patients: studies on mechanisms. American journal of nephrology 1991;11(2):102-11.##[6]. Mowat A.G, Baum J. Chemotaxis of polymorphonuclear leukocytes from patients with diabetes mellitus. New England journal of medicine 1971;284(12):621-7.##[7]. Hosseini H, Dorgalaleh A, Tabibian S, Kashiri M, Sanei E. Biochemical Interfering Factors and Blood Cells Indices. Thrita 2014; 3(1): e15516.##[8]. Minnaganti V.R, Cunha B.A. Infections associated with uremia and dialysis. Infectious disease clinics of North America 2001;15(2):385-406.##[9]. Agrawal S, Gollapudi P, Elahimehr R, Pahl M.V, Vaziri N.D. Effects of end-stage renal disease and haemodialysis on dendritic cell subsets and basal and LPS-stimulated cytokine production. Nephrology Dialysis Transplantation 2009; 25:737-746.##[10]. Pahl M.V, Gollapudi S, Sepassi L, Gollapudi P, Elahimehr R, Vaziri N.D. Effect of end-stage renal disease on B-lymphocyte subpopulations, IL-7, BAFF and BAFF receptor expression. Nephrology Dialysis Transplantation 2010;25(1):205-12.##[11]. Moser B, Roth G, Brunner M, Lilaj T, Deicher R, Wolner E, et al. Aberrant T cell activation and heightened apoptotic turnover in end-stage renal failure patients: a comparative evaluation between non-dialysis, haemodialysis, and peritoneal dialysis. Biochemical and biophysical research communications 2003;308(3):581-5.## ##

Serum levels of IL-17A increase in Asthma but not in accordance with Serum level of IgE and Asthma Severity سطح سرمی اینترلوکین 17 در افراد مبتلا به آسم افزایش می یابداما میزان آن با سطح سرمی IgE و شدت آسم متناسب نیست 2 1 مقدمه: شواهد اخیر نشان می دهد سلول‌های T یاریگر ۱۷ (Th17) در آسم نقش دارند. سلول‌های Th17 نقشی اساسی در تحریک التهاب در مجاری هوایی مبتلا به آسم دارند، بنابراین اینترلوکین (17A (IL-17A، سایتوکاین اصلی Th17 نیز در التهاب مجاری هوایی شرکت دارد. مواد و روشها: ما سطح سرمی IL-17A و ایمونوگلوبولینE تام (IgE) را در ۱۰۰بیمار مبتلا به آسم و ۸۱کنترل سالم به روش الایزا سنجیدیم. برای تعیین چگونگی ارتباط بین IL-17A با شدت بیماری، بیماران را در سه گروه دسته بندی کردیم: خفیف (۲۸=N)، متوسط (۳۳=N) و شدید (۳۹=N). نتایج: غلظت سرمی IL-17A و IgE تام در بیماران مبتلا به آسم بطور قابل ملاحظه ای بالاتر از گروه کنترل سالم بود ( به ترتیب ۰/۰۲۶=p و 01/ نتیجه گیری: ما در این مطالعه دریافتیم که IL-17A ، همانند IgE تام، در سرم بیماران مبتلا به آسم افزایش می یابد، ولی با الگویی متفاوت. افزایش IgE تام در سرم هماهنگ با شدت بیماری است در حالی که افزایش IL-17A در سرم بر خلاف IgE است. 2 Background and Aims: Recent evidence suggests that T helper (Th) 17 cells are involved in the emergence of asthma. Th17 cells have a key role in inducing inflammation in asthmatic airways thus Interleukin (IL)-17A, the main cytokine of Th17, contributes to airways inflammation. Materials and Methods: We evaluated the level of IL-17A and total immunoglobulin E (IgE) in sera of 100 asthmatic patients and 81 healthy controls by ELISA to determine how serum concentration of IL-17A is associated with asthma severity. We classified patients into three groups mild (n=28), moderate (n=33) and severe cases (n=39). Results: Respectively, serum IL-17A and IgE concentrations were significantly higher in the asthmatic patients than the control group (p=0.026 and p<0.01). Mean of serum IL-17A and IgE values were 37.73 pg/ml and 39.02 IU/ml in the control group and 68.55 pg/ml and 295.87 IU/ml in the patients group. Nevertheless there were non-significant differences between the three groups of asthmatic patients. Respectively, mean of serum IL-17A and IgE values were 94.17 pg/ml and 255.07 IU/ml in the mild group, 71.29 pg/ml and 271.27 IU/ml in the moderate group, and 47.85 pg/ml and 345.97 IU/ml in the severe group. Moreover, there was no correlation between serum levels of IL-17A and IgE. Conclusions: In this study we found that IL-17A, like IgE, rises in sera of asthmatic patients though in a different manner. IgE increases in serum consistent with disease severity though the increases of IL-17A in serum has an inverse relationship with IgE rising. 25 33 2015/05/112015/05/62015/05/112015/05/11 1394/2/21 2015/05/112015/05/62015/05/112015/05/11 1394/2/21 معصومه موحدی Masouma Mowahedi Department of Immunology, International Campus, Shahid Sadoughi University of Medical Sciences, Yazd, Iran. Iran محمد صامت Mohammad Samet Department of Pulmonology, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran. Iran فاطمه زارع Fateme Zare Department of Immunology, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran Iran مرتضی صمدی Morteza Samadi Department of Immunology, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran Iran samadi.for@gmail.com Allergy Asthma IgE IL-17A Th17 آسم آلرژی اینترلوکین 17A ایمونوگلوبولینE (IgE) سلول‌های T یاریگر 17 [1]. Kim H.Y, DeKruyff R.H, Umetsu D.T. The many paths to asthma: phenotype shaped by innate and adaptive immunity. Nature immunology 2010; 11(7): 577-584.##[2]. Lloyd C.M and Hessel E.M. Functions of T cells in asthma: more than just TH2 cells. Nature Reviews Immunology 2010; 10(12): 838-848.##[3]. Zhao Y, Yang J, Gao YD, Guo W. Th17 Immunity in Patients with Allergic Asthma. Int Arch Allergy Immunol 2010; 151: 297-307.##[4]. Shean J.A and John F.A. TH17 cells in asthma and inflammation. Biochimica et Biophysica Acta 2011; 1066-1079.##[5]. Pierre M.K and Vijay K.K. Mechanisms of Disease Interleukin-17 and Type 17 Helper T Cells. The New England journal of medicine 2009; 361(9): 888-898.##[6]. Doe C, Bafadhel M, Siddiqui S, Desai D, Mistry V, Rugman P, et al. Expression of the T helper 17-associated cytokines IL-17A and IL-17F in asthma and COPD. CHEST Journal 2010; 138(5): 1140-1147.##[7]. Kudo M, Melton AC, Chen C, Engler MB, Huang KE, Ren X,, et al. IL-17A produced by alphabeta T cells drives airway hyper-responsiveness in mice and enhances mouse and human airway smooth muscle contraction. Nat Med 2012; 18(4): 547-54.##[8]. Pocket Guide for Asthma Management and Prevention. 2012. Available from www.ginasthma.org##[9]. Wenzel S.E. Asthma phenotypes: the evolution from clinical to molecular approaches. Nature medicine 2012; 18(5): 716-725.##[10]. Robinson D.S. The role of the T cell in asthma. J Allergy Clin Immunol 2010; 126(6): 1081-91; quiz 1092-3.##[11]. Iwakura Y, Nakae S, Saijo S, Ishigame H. The roles of IL-17A in inflammatory immune responses and host defense against pathogens. Immunological Reviews 2008; 226: 57-79.##[12]. Shalaby K.H and J.G Martin. Overview of asthma; the place of the T cell. Curr Opin Pharmacol 2010; 10(3): 218-25.##[13]. You L, Carina M, Margareta S, Madeleine R, Serena E, et al. Expansion of CD4+CD25+ and CD25- T-Bet, GATA-3, Foxp3 and RORct Cells in Allergic Inflammation, Local Lung Distribution and Chemokine Gene Expression. PLoS ONE 2011;6(5).##[14]. Wakashin H, Hirose K, Maezawa Y, Kagami S, Suto A, Watanabe N, et al. IL-23 and Th17 cells enhance Th2-cell-mediated eosinophilic airway inflammation in mice. Am J Respir Crit Care Med 2008; 178(10): 1023-32.##[15]. Schnyder-Candrian S1, Togbe D, Couillin I, Mercier I, Brombacher F, Quesniaux V, et al. Interleukin-17 is a negative regulator of established allergic asthma. The Journal of Experimental Medicine 2006; 203(12): 2715-2725.##[16]. Yoshiki Y,Takaharu N, Akiko W, Akane H, Alison H, Giovanna R, et al. Participation of Th17 and Treg Cells in Pediatric Bronchial Asthma. Journal of Health Science 2010; 56(5): 589-597.##[17]. Herbert C, Shadie A.M and Kumar R.K, Interleukin-17 signalling in a murine model of mild chronic asthma. Int Arch Allergy Immunol 2013; 162(3): 253-62.##[18]. Woodruff P.G, et al. T-helper type 2-driven inflammation defines major subphenotypes of asthma. Am J Respir Crit Care Med 2009; 180(5): 388-95.##[19]. Irvin C, Zafar I, Good J, Rollins D2, Christianson C, Gorska MM, et al. Increased frequency of dual-positive T2/T17 cells in bronchoalveolar lavage fluid characterizes a population of patients with severe asthma. J Allergy Clin Immunol 2014; 134(5):1175-1186.## ##

Frequency of FLT3 ITD and FLT3 TKD Mutations in Multiple Myeloma Patients (A Case Control Study) میزان موتاسیون های ژنهای FLT3 ITD و FLT3 TKD در بیماران مبتلا به میلوم مالتیپل (مطالعه شاهد-مورد) 2 1 مقدمه: میلوم مالتیپل تکثیر بی رویه ی پلاسما سل ها از یک کلون بدخیم است. تومور ، محصولات ناشی از آن و پاسخ ایمنی میزبان منجر به آسیب ارگان ها می شود. بعضی فاکتورهای مرتبط با پاتوژنر بیماری شناخته شده اند. از آنجایی که موتاسیون های FLT3 در لوسمی ها به عنوان یک فاکتور تعیین کننده شناخته می شود هدف این مطالعه بررسی رابطه ی بین موتاسیون های ITD (internal tandem duplication) FLT3 وFLT3 TKD(tyrosine kinase domain) و بیماری میلوم مالتیپل بود. مواد و روشها: این مطالعه ی مورد شاهدی روی60 بلاک پارافینی مغز استخوان (۳۰بیمارمبتلا به میلوم مالتیپل و ۳۰نمونه ی نرمال) در بخش های پاتولوژی بیمارستان های قائم و امام رضای شهر مشهد انجام شد. بعد از تهیه ی برشها ، DNA استخراج و دو آزمون PCR برای شناسایی موتاسیون های مذکور روی هر نمونه انجام شد. نتایج: متوسط سن بیماران۱۰± ۶۴ سال بود. هیچ نوع موتاسیون FLT3 در بیماران مبتلا به میلوم مالتیپل مشاهده نشد. نتیجه گیری: یافته های ما نشان داد که وقوع موتاسیون در ژن FLT3 در بیماران مبتلا به میلوم مالتیپل غیرمعمول به نظر می رسد. 2 Background and Aims: Multiple myeloma is a malignant proliferation of plasma cells derived from a single clone. The tumor, its products and the host response lead to organ damages. Some factors that are responsible in its pathogenesis are recognized. As FMS like Tyrosine Kinase 3 receptor (FLT3) mutation has been proved as a determining factor in leukemic patients the goal of this study was to find association of FLT3 internal tandem duplication (ITD) and FLT3 tyrosine kinase domain (TKD), mutations with multiple myeloma. Materials and Methods: This case-control study was conducted on 60 paraffin-embedded bone marrow biopsies (30 multiple myeloma and 30 normal bone marrow specimens) in the pathology departments of Ghaem and Imam Reza hospitals in Mashhad. After sections preparation, DNA was extracted and two PCR reactions were set up for detection of FLT3/ ITD and FLT3/TKD mutations. Results: The Mean age of samples was 64±10 years. No FLT3 mutations were detected in multiple myeloma patients. Conclusions: Our findings showed that FLT3 mutations occurrence seem unusual in multiple myeloma. 34 40 2015/05/112015/05/62015/05/112015/05/112015/05/11 1394/2/21 2015/05/112015/05/62015/05/112015/05/112015/05/11 1394/2/21 محمد مهدی کوشیار Mohammad Mehdi Kooshyar Department of Internal Medicine, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran Iran محمدهادی صادقیان Mohammad Hadi Sadeghian Department of Hematology and Blood Banking, Cancer Molecular Pathology Research Center, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Iran محمدرضا کرامتی Mohammad Reza Keramati Neonatal Research Center, Imam Reza Hospital, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Iran حسین رحیمی Hossein Rahimi Department of Internal Medicine, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran Iran سیده فاطمه شمس Seyyede Fatemeh Shams Department of Hematology and Blood Banking, Cancer Molecular Pathology Research Center, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Iran سپیده شاکری Sepideh Shakeri Department of Hematology and Blood Banking, Cancer Molecular Pathology Research Center, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Iran حسین ایت اللهی Hossein Ayatollahi Department of Hematology and Blood Banking, Cancer Molecular Pathology Research Center, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Iran Ayatollahih@mums.ac.ir FLT3 Multiple Myeloma Polymerase chain Reaction FLT3 میلوم ماتیپل PCR [1]. Small D. FLT3 mutations: biology and treatment. ASH Education Program Book 2006;2006(1):178-84.##[2]. Xu B, Chen G, Luo X, Tang J. Detection of FLT3/ITD gene mutations in patients with hematologic malignancy and their clinical significance. The Chinese-German Journal of Clinical Oncology 2009;8(2):100-3.##[3]. Meshinchi S, Appelbaum FR. Structural and functional alterations of FLT3 in acute myeloid leukemia. Clinical Cancer Research 2009;15(13):4263-69.##[4]. Chang P, Kang M, Xiao A, Chang J, Feusner J, Buffler P, et al. FLT3 mutation incidence and timing of origin in a population case series of pediatric leukemia. BMC cancer 2010;10(1):513.##[5]. Reilly JT. FLT3 and its role in the pathogenesis of acute myeloid leukaemia. Leukemia & lymphoma 2003;44(1):1-7.##[6]. Gilliland DG, Griffin JD. The roles of FLT3 in hematopoiesis and leukemia. Blood 2002;100(5):1532-42.##[7]. D Kottaridis P, Gale RE, Linch DC. Flt3 mutations and leukaemia. British journal of haematology 2003;122(4):523-38.##[8]. Lin P, Jones D, Medeiros LJ, Chen W, Vega-Vazquez F, Luthra R. Activating FLT3 mutations are detectable in chronic and blast phases of chronic myeloproliferative disorders other than chronic myeloid leukemia. American journal of clinical pathology 2006;126(4):530-533.##[9]. Keneth Kaushansky MAL, Ernest Bentler, Thomas J. Kipps, Uri Seligsohn, Josef T. Prechal. Plasma cell neoplasms, in: Williams hematology. 8 ed: MC Graw Hill Company 2010: 1627-35##[10]. Warren M, Luthra R, Yin CC, Ravandi F, Cortes JE, Kantarjian HM, et al. Clinical impact of change of FLT3 mutation status in acute myeloid leukemia patients. Modern Pathology 2012;25(10):1405-12.##[11]. Bacher U, Haferlach C, Kern W, Haferlach T, Schnittger S. Prognostic relevance of FLT3-TKD mutations in AML: the combination matters—an analysis of 3082 patients. Blood 2008;111(5):2527-37.##[12]. Bains A, Luthra R, Medeiros LJ, Zuo Z. FLT3 and NPM1 Mutations in Myelodysplastic Syndromes Frequency and Potential Value for Predicting Progression to Acute Myeloid Leukemia. American journal of clinical pathology 2011; 135(1):62-9.##[13]. Beitinjaneh A, Jang S, Roukoz H, Majhail NS. Prognostic significance of FLT3 internal tandem duplication and tyrosine kinase domain mutations in acute promyelocytic leukemia: a systematic review. Leukemia research 2010;34(7):831-36.##[14]. Levis M, Small D. FLT3: ITD does matter in leukemia. Leukemia 2003; 17(9):1738-52.##[15]. Wang L, Lin D, Zhang X, Chen S, Wang M, Wang J. Analysis of FLT3 internal tandem duplication and D835 mutations in Chinese acute leukemia patients. Leukemia research 2005;29(12):1393-98. ##[16]. Levis M. Who's dancing with FLT3? Blood 2008;111(5):2503-4.##[17]. Dombret H. Gene mutation and AML pathogenesis. Blood 2011;118(20):5366-7.##[18]. Yamamoto Y, Kiyoi H, Nakano Y, Suzuki R, Kodera Y, Miyawaki S, et al. Activating mutation of D835 within the activation loop of FLT3 in human hematologic malignancies. Blood 2001;97(8):2434-39.##[19]. Daver N, Strati P, Jabbour E, Kadia T, Luthra R, Wang S, et al. FLT3 mutations in myelodysplastic syndrome and chronic myelomonocytic leukemia. American journal of hematology 2013;88(1):56-9.##[20]. Sino-US SLCG. FLT3 gene mutation and its prognostic implication in patients with acute leukemia. Zhonghua xue ye xue za zhi=Zhonghua xueyexue zazhi 2010;31(1):1. ##[21]. Elyamany G, Awad M, Fadalla K, Albalawi M, Al Shahrani M, Al 3Abdulaaly A. Frequency and Prognostic Relevance of FLT3 Mutations in Saudi Acute Myeloid Leukemia Patients. Advances in hematology 2014;6:337-49.##[22]. Elyamany G, Awad M, Alsuhaibani O, Fadalla K, Al Sharif O, Al Shahrani M, et al. FLT3 Internal Tandem Duplication and D835 Mutations in Patients with Acute Lymphoblastic Leukemia and its Clinical Significance. Mediterranean journal of hematology and infectious diseases 2014;6(1): e2014038..##[23]. Annamaneni S, Kagita S, Gorre M, Digumarti RR, Satti V, Battini MR Incidence of internal tandem duplications and D835 mutations of FLT3 gene in chronic myeloid leukemia patients from Southern India. Hematology 2014;19(3):129-35.##[24]. Daver N, Strati P, Jabbour E, Kadia T, Luthra R, Wang S, et al. FLT3 mutations in myelodysplastic syndrome and chronic myelomonocytic leukemia. American journal of hematology 2013;88(1):56-9.##[25]. Zaremba CM, Oliver D, Cavalier M, Fuda F, Karandikar NJ, Chen W. Distinct immunophenotype of early T-cell progenitors in T lymphoblastic leukemia/lymphoma may predict FMS-like tyrosine kinase 3 mutations. Annals of diagnostic pathology 2012;16(1):16-20.##[26]. Liu H, Yu H, Jia HY, Zhang W, Guo CJ. Detection of FLT3 gene mutation in hematologic malignancies and its clinical significance. Hematology/Chinese Association of Pathophysiology 2007; 15(4):709-13. ##[27]. Yokota S, Kiyoi H, Nakao M, et al. Internal tandem duplication of the FLT3 gene is preferentially seen in acute myeloid leukemia and myelodysplastic Syndrome among various hematological malignancies: a study on a large series of patients and cell lines. Leukemia 1997; 11:1605-1609.## ##

Effect of Corn Oil, Olive Oil and Sheep’s and Cow’s Ghee on the Expression of apoB Protein in Syrian Mice’s Intestine and Liver اثر مصرف روغن های ذرت، زیتون، گوسفند و گاو بر بیان پروتئین apoB در روده و کبد موش سوری نر 2 1 مقدمه: نوع و درجه اشباع بودن اسیدهای چرب می تواند اثر متفاوتی بر روی مقدار سرمی تری گلیسیرید، کلسترول، لیپوپروتئین ها با تراکم کم یا بسیار کم داشته و از این رو اثر مهمی در بروز آترواسکلروز دارند. اسیدهای چرب اشباع اثر افزایشی بر روی کلسترول خون دارند در حالیکه برای اسیدهای چرب غیراشباع اثر کاهش دهندگی کلسترول خون گزارش شده است. بعلت اینکه روغنهای مورد استفاده انسان ها دارای محتوای اسید چرب متفاوتی است بنابراین اسیدهای چرب موجود در آنها میتوانند اثرات متفاوتی روی متابولیسم لیپوپروتئین ها و بیان آنها داشته باشند. یکی از مهمترین لیپوپروتئین ها، آپولیپوپروتئین (B (apoB است. هدف این مطالعه بررسی و مقایسه اثر چربی های غذایی مختلف بر روی بیان پروتئین apoB بود. مواد و روش ها: در این مطالعه تعداد ۴۸راس موش سوری نر انتخاب شده و بطور تصادفی به شش گروه هشت تایی تقسیم شدند: تغذیه معمولی ، تغذیه با ۱۰% روغن ذرت ، تغذیه با ۱۰% روغن زیتون ، تغذیه با ۱۰% روغن گاو ، تغذیه با ۱۰% روغن گوسفند و تغذیه با ۲% کلسترول. پس از دو ماه موش ها کشته شده و نمونه کبد و روده تهیه و در Cº ۷۰- نگهداری شد. از نمونه ها پروتئین استخراج شده و بیان apoB با استفاده از تکنینک وسترن بلاتینگ بررسی شد. یافته ها: بیان پروتئین apoB48 روده ای ، افزایش معنی داری در گروه های روغن زیتون و گاو نسبت به کنترل داشت. اختلاف معنی داری در بیان apoB100 کبدی در گروه کلسترول درمقایسه با گروه روغن ذرت دیده شد. نتیجه گیری: مطالعه ما نشان می دهد که مصرف روغن زیتون و گاو بیان apoB48 روده ای را افزایش میدهد. 2 Background and Aims: Type and saturation of fatty acids can have an important impact on the level of triglyceride, cholesterol, very low and low-density lipoproteins in the blood and thus affect the development of atherosclerosis. Saturated fatty acids have an additive effect on blood cholesterol while for unsaturated fatty acids, a lowering effect has been reported. Fatty acids can have different effects on lipoproteins metabolism and apolipoproteins expression because oils used by human have different compositions. One of the important apolipoprotein is apolipoproteinB ( apoB) .This study was conducted to compare the effect of different nutritious fats on expression of apoB protein. Materials and Methods: For this purpose, 48 Syrian male mice were selected and randomly divided into six groups of eight: chow, diet with10%corn oil, diet with10% olive oil, diet with10% cow ghee), diet with10% sheep ghee, and diet with 2% cholesterol. After two months, liver and intestine were removed and transferred into liquid nitrogen and were frozen at -70ºC. Protein was extracted and the expression of apoB was studied by western blotting. Results: An increase in the expression of intestinal apoB48 was identified in olive oil and cow ghee groups. Hepatic apoB100 expression increased in the cholesterol group compared with the corn oil group. Conclusions: This study indicates that olive oil and cow ghee consumption increase intestinal apoB48 expression. 41 49 2015/05/112015/05/62015/05/112015/05/112015/05/112015/05/11 1394/2/21 2015/05/112015/05/62015/05/112015/05/112015/05/112015/05/11 1394/2/21 غلامعباس محمدی Gholamabbas Mohammadi Department of Biochemistry, Physiology Research Center, Kerman University of Medical Sciences, Kerman, Iran. Iran حسن عزیزی Hasan Azizi Department of Biochemistry, Kerman University of Medical Sciences, Kerman, Iran. Iran hazizimellelu@yahoo.com ApoB Cholesterol Corn oil Cow ghee Olive oil Sheep ghee آپولیپوپروتئین B روغن گیاهی روغن جانوری کلسترول [1]. Hackam D.G and Anand S.S. Emerging risk factors for atherosclerotic vascular disease. JAMA: the journal of the American Medical Association 2003. 290(7): 932-940.##[2]. Hatmi ZN. Tahvildari, S.Motlag, A.G. Kashani, A.S, Prevalence of coronary artery disease risk factors in Iran: a population based survey. BMC Cardiovascular Disorders 2007. 7(1): 32.##[3]. Lucas A.D and Greaves D.R. Atherosclerosis: role of chemokines and macrophages. Expert reviews in molecular medicine 2001; 2(1): 1-18.##[4]. Glass C.K and Witztum J.L. Atherosclerosis: The Road Ahead Review. Cell 2001; 104: 503-516.##[5]. Blasi C. The autoimmune origin of atherosclerosis. Atherosclerosis 2008; 201(1): 17-32.##[6]. Contois JH, McConnell JP, Sethi AA, Csako G, Devaraj S, Hoefner DM, et al. Apolipoprotein B and cardiovascular disease risk: position statement from the AACC Lipoproteins and Vascular Diseases Division Working Group on Best Practices. (1530-8561 (Electronic)##[7]. Olofsson S.O, Boren J. Apolipoprotein B: a clinically important apolipoprotein which assembles atherogenic lipoproteins and promotes the development of atherosclerosis. (0954-6820 (Print).##[8]. Yang Zhi-Hong. Miyahara, Hiroko.Takeo, Jiro. Hatanaka, Akimasa. Katayama, Masashi##[9]. Pollock oil supplementation modulates hyperlipidemia and ameliorates hepatic steatosis in mice fed a high-fat diet. Lipids in health and disease 2011; 10(1):189.##[10]. Mohammadifard N, Nazem M, Naderi Gh, Saghafian F, Sajjadi F, Maghroon M, et al. Effect of hydrogenated, liquid and ghee oils on serum lipids profile. ARYA atherosclerosis 2010; 6(1): 16.##[11]. Tadin-Strapps, Marija. Peterson, Laurence B. Cumiskey, Anne-Marie. Rosa, Raymond L. Mendoza, Vivienne Halili. Castro-Perez, Jose et al., siRNA-induced liver ApoB knockdown lowers serum LDL-cholesterol in a mouse model with human-like serum lipids. Journal of lipid research 2011; 52(6): 1084-1097.##[12]. Ko C, O'Rourke S.M, Huang L.-S. A fish oil diet produces different degrees of suppression of apoB and triglyceride secretion in human apoB transgenic mouse strains. Journal of lipid research 2003; 44(10):1946-1955.##[13]. Hu F.B, Manson J.E, Willett W.C. Types of dietary fat and risk of coronary heart disease: a critical review. Journal of the American College of Nutrition 2001; 20(1): 5-19.##[14]. Kris-Etherton P.M, Yu S. Individual fatty acid effects on plasma lipids and lipoproteins: human studies. The American journal of clinical nutrition 1997; 65(5): 1628S-1644S.##[15]. dalfardi f, mohammadi G. A. comparing the effect of clarified butter fat (ghee) and vegetable oil on serum lipid profile and athrosclerotic plaque formation in male hamsters aorta Clin Chem. 2009;55(3):407-19.##[16]. Van Greevenbroek M.M, Voorhout Wim F, Erkelens D, Willem G, De Bruin T.W. Palmitic acid and linoleic acid metabolism in Caco-2 cells: different triglyceride synthesis and lipoprotein secretion. Journal of lipid research 1995; 36(1):13-24.##[17]. Ackson Kim G, Robertson M, Denise Fielding, Barbara A, Frayn Keith, Williams N, Christine M. Olive oil increases the number of triacylglycerol-rich chylomicron particles compared with other oils: an effect retained when a second standard meal is fed. The American journal of clinical nutrition 2002; 76(5):942-949.##[18]. Dashti N, Smith E.A, Alaupovic P. Increased production of apolipoprotein B and its lipoproteins by oleic acid in Caco-2 cells. Journal of lipid research 1990; 31(1): 113-123.##[19]. Field F, Albright E, Mathur S. Regulation of triglyceride-rich lipoprotein secretion by fatty acids in CaCo-2 cells. Journal of lipid research 1988; 29(11): 1427-1437.##[20]. Magun A.M, Mish B, Glickman R.M. Intracellular apoA-I and apoB distribution in rat intestine is altered by lipid feeding. Journal of lipid research 1988; 29(9):1107-1116.##[21]. López-Soldado I, Avella M, Botham KM. Differential influence of different dietary fatty acids on very low-density lipoprotein secretion when delivered to hepatocytes in chylomicron remnants. Metabolism 2009; 58(2):186.##[22]. Dashti N. The effect of low density lipoproteins, cholesterol, and 25-hydroxycholesterol on apolipoprotein B gene expression in HepG2 cells. Journal of biological chemistry 1992; 267(10): 7160-7169.## ##

The Effect of an Intense Anaerobic Exercise Session on Serum Levels of IgG, IgM and IgA in Handball, Volleyball and Climbing Sports اثر یک جلسه تمرین شدید بی هوازی برمیزان سطح سرمی IgG , IgM, IgA در ورزشکاران هندبال، والیبال و کوهنوردی 2 1 مقدمه: سیستم ایمنی ما را در مقابل عوامل مهاجم بیگانه محافظت می کند. هدف از انجام این مطالعه بررسی اثر یک تمرین شدید بی هوازی بر روی سطح سرمی ایمونوگلوبولینهای G, A و M ورزشکاران هندبالیست، والیبالیست و کوهنوردان بود. مواد و روش ها: در این مطالعه تعداد ۴۵ ورزشکار حرفه ای رشته های کوهنوردی، والیبال و هندبال با دامنه سنی ۲۰تا ۳۰سال که در لیگ برتر و دسته یک کشورشرکت داشتند به صورت هدفمند دعوت به همکاری شدند. در این تحقیق از آزمون وینگیت ۳۰ ثانیه برای ارزیابی توان بی هوازی استفاده شد. نمونه های خونی قبل، بلافاصله بعد و دو ساعت بعد از تمرین جمع آوری شد و سطح سرمی ایمونوگلوبولین های IgM,IgG,IgAبه روش نفلومتری تعیین گردید. یافته ها: نتایج حاصل از تحقیق نشان داد که سطح سرمی IgG , IgM وIgA قبل، بعد و دو ساعت پس از تمرین در سه رشته ورزشی تغییر معناداری نداشت (P>۰/۰۵ ). نتیجه گیری: یافته های ما نشان داد که تمرین کوتاه مدت بی هوازی تاثیر معناداری بر سطح سرمی ایمونوگلوبولین های ورزشکاران ندارد. 2 Background and Aims: The immune system protects the body against many invasive foreign materials. The aim of this study was to investigate the effect of an intense anaerobic exercise session on serum IgG, IgM and IgA levels in handballists, volleybalists and climbers. Materials and Methods: In this study, 45 professional athletes with the average age of 20-30 years who had participated in the major leagues and the first batch of Zahedan city were enrolled. To assess anaerobic power the 30 second Wingate test was used. Blood samples before, immediately after, and 2h after exercises were collected, and serum levels of immunoglobulins IgG, IgM and IgA were measured by nephelometry method. Results: The results of this study indicated that the level of serum immunoglobulins IgG, IgM ˛ IgA concentration in all three study groups before and after and two hours past exercise did not show significant change (P>0.05). Conclusions: Our findings showed that short anaerobic exercise does not have any effect on the level of immunoglobulins in athletes. 50 57 2015/05/112015/05/62015/05/112015/05/112015/05/112015/05/112015/05/11 1394/2/21 2015/05/112015/05/62015/05/112015/05/112015/05/112015/05/112015/05/11 1394/2/21 آرمان جلیلی Arman Jalili Physiology Department, School of Medicine, Zahedan University of Medical Science, Zahedan, Iran Iran حسینعلی خزاعی Hossein Ali Khazae Immunology and hematology Department, School of Medicine, Zahedan University of Medical Science, Zahedan, Iran Iran زری سنچولی Zari anchuli Physiology Department, University of Ferdosi, Mashhad, Iran Iran Anaerobic exercise Climbing Handball Immunoglobulin Volleyball تمرین بی هوازی ایمونوگلوبولین هندبال والیبال کوهنوردی [1]. Hejazi K and Attarzadeh Hosseini R. Influence of Selected Exercise on Serum Immunoglobulin, Testosterone and Cortisol in Semi-Endurance Elite Runners. Asian Journal of Sports Medicine 2012; 3(3):185-192. ##[2]. Hoff P, Belavý D.L, Huscher D, Lang A, Hahne M, Kuhlmey A.K, et al. Effects of 60-day bed rest with and without exercise on cellular and humoral immunological parameters. Cell Mol Immunol 2014 Nov 10.##[3]. Jeng KC1, Yang CS, Siu WY, Tsai YS, Liao WJ, Kuo JS. Supplementation with vitamins c and e enhances cytokine production by peripheral blood mononucler cells in healthy adults. Am.jclin. Nutr 1996; 64:960-5##[4]. Laing S.J, Gwynne D, Blackwell J, Williams M, Walters R, Walsh N.P. Salivary IgAresponse to prolonged exercise in a hot environment in trained cyclists, Eur. J. Appl. Physiol 2005; 93: 665- 671.##[5]. Alexander J Koch. Immune Response to Resistance Exercise, American Journal of Lifestyle medicine 2010;4: 244-252.##[6]. Koch A.J. Immune Response to Exercise, Brazilian Journal of Biomotricity 2010; 2: 92-103.##[7]. Moreira A, Delgado L, Moreira P, Haahtela T. Does exercise increase the risk of upper respiratory tract infections? British Medical Bulletin 2009; 90: 111-131.##[8]. Mackinnon L.T, Hooper S. Mucosal (secretory) immune system responses to exercise of varying intensity and during overtraining, Int. J. Sports. Med 1994; 3:179-183.##[9]. Fahlman M.M, Engels H.J. Mucosal IgA and URTI in American college football players: a year longitudinal study, Med. Sci. Sports Exerc 2005; 37: 374-380.##[10]. Hanns C.G, Andreas M, Wolfgang S, Markus M, Karl K, Eberhard K, Lothar R. IgG, IgA, IgM, and Plasma Volume Changes During Long-distance Running 2002; 13:15-20.##[11]. Vahid I, Valiollah S, Mehdi A. The Effects of Physical Activity OnHomoral Immune System (IgA, IgG, IgM), Procedia Social And Behavioral Sciences 2009; 1: 2718–2721.##[12]. Mckune A.J, Semple S.J, Smith L.L, Wadee A.A. Complement, immunoglobulin and creatine kinase response in black and white males after muscle-damaging exercise. 2009; SAJSM 2: 47-52.##[13]. David C, Nieman. Marathon Training and Immune Function, Sports Med 2007; 37: 412-415.##[14]. Dimitriou L, Sharp N.C, Doherty M. Circadian effects on the acute responses of salivary cortisol and IgA in well trained swimmers. Br J Sports Med 2002; 36(4): 260-64.##[15]. Daly R.M, Rich P.A, Klein R. Hormonal responses to physical training in high-level peripubertal male gymnasts. Eur J ApplPhysiolOccupPhysiol 1998; 79(1): 74-81.##[16]. Gleeson M, Hall S.T, McDonald W.A, Flanagan A.J, Clancy R.L. Salivary IgA subclasses and infection risk in elite swimmers. Immunol Cell Biol 1999; 77(4): 351-55.##[17]. Gleeson M, McDonald W.A. The effect on immunity of long term intensive training in elite swimmers". Clinical and Experimental Immunology 1995; 102: 210-216.##[18]. A Crdova A, Sureda A, TurJ.A, Pons A. Immune Response To Exercise In Elite Sportsmen During The Competitive Season, J. Physiol. Biochem. 2010; 66: 1-6.##[19]. Mashiko T, Umed T, Nakaji S, Sugawara K. Effect of exercise on the physical condition of college rugby players during summer training camp. Sports Med 2004; 38:186-190.##[20]. Shoelson, Jongsoon Lee and Allison B, Goldfine. “Inflammation and insulin resistance”. J Clin Invest 2006; 116:1793-801.##[21]. Thomas N.E, Leyshon A, Hughes M.G, Davies B, Graham M, Baker J.S, The efect of anaerobic exercise on salivary cortisol, testosterone and immunoglobulin (A) in boys aged 15–16 years, Eur J ApplPhysiol 2009; 107: 455–461.##[22]. David C. Marathon Training and Immune Function. Sports Med 2007; 37: 412-415.##[23]. McKune A.J, Smith L, Semple S.J, Wadee A. Influence of ultra-endurance exerciseon immunoglobulin isotypes and subclasses, Br. J. Sports Med 2005; 39: 665-670##[24]. Walsh N.P, Blannin A.K, Clark A.M, Cook L, Robson P.J, Glesson M. The Effect of High intensity Intermittent Exercise on Saliva IgA, Total Protein and a- Amilase. J Sports Sei 1999; 17: 129-1374.##[25]. Leonard joseph H, Roslizaeati N, Safrusahar M.Y, Efri N.M, Das S, et al. Effect of pubertal developmental stages and lower limb kinetics during vertical jump task in sepak takraw sport. Clin ter 2009;160(5):403-407.##[26]. Verde T.J, Thomas S.G, Moore R.W, Shek P, Shephard R.J. Immune responses and increased training of the elite athlete, Immune function in sport and exercise J. Appl. Physiol 2007; 103: 693-699.##[27]. Byum A, Wiik B.P, Gustavsson E, Veiby O.P, Reseland J, Haugen A.H, Opstad P.K. The Effect Of Strenuous Exercise, Calorie Deficiency And Sleep Deprivation On White Blood Cells, Plasma Immunoglobulin And Cytokines. Scandinavian Journal Of Immunology 1996; 43(2): 228-235##[28]. Fry A.C, Kraemer W.J, Ramsey L.T. Pituitary-adrenalgonadal responses to high-intensity resistance exercise overtraining. J ApplPhysiol 1998; 85: 2352-9.##[29]. Mackinnon L.T. Immunity in athletes. Int J SportMed 1997; 98: 562–568.##[30]. Armstrong R. "Initial events in exercise-induced muscular injury". Med Sci Sports Exert 1990; 22.(4): 429-35.##[31]. Poortmans J.R. 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Evaluation of HIV Indeterminate Confirmatory Tests' Results in Blood Donors in Northeast of Iran ارزیابی نتایج تست های تائیدی نامشخص HIV در اهداء کنند گان خون در شمال شرق ایران 2 1 مقدمه: شیوع ویروس نقص ایمنی انسانی (HIV)به سرعت در دنیا در حال گسترش است. آلودگی با این ویروس منجر به مهار سیستم ایمنی و نهایتا سیندرم نقص ایمنی اکتسابی می شود. تشخیص اولیه ی بیماری با شناسایی آنتی بادی علیه ویروس به روش الایزا (ELISA)انجام می شود. برخی تست های تکمیلی بعنوان مثال وسترن بلات و آزمون ایمنوبلاتینگ نوترکیب (RIBA) برای تایید عفونت ویروسی مورد استفاده قرار می گیرد. بسیاری از نتایج تست های تاییدی نامشخص است. هدف این مطالعه مقایسه ی فراوانی و الگوهای تست های تاییدی نامشخص در دو گروه، اهداکنندگان خون و افراد با رفتارهای پرخطر در شمال شرق ایران بود. مواد و روش ها : دراین مطالعه ی توصیفی مقطعی ۱۰۵۵نمونه سرم از اکتبر ۲۰۰۹تا مارس ۲۰۱۴با سابقه ی الایزای مثبت برای HIV در آزمایشگاه سازمان انتقال خون مشهد مورد ارزیابی قرار گرفت. بعضی از نمونه ها با روش وسترن بلات وبرخی با تکنیکRIBA مورد ارزیابی قرار گرفتند. نتایج: بیشتر نتایج نامشخص مربوط به گروه افراد با رفتارهای پرخطر و روش وسترن بلات بود. بیشترین باند آشکار شده در هر دو روش متعلق به باندP24 بود. نتیجه گیری: روشRIBA حساس تر و قابل اعتمادتراز وسترن بلات می باشد اما استفاده از سایر تست های مکمل با نتایج نامشخص کمتر ضروری به نظر می رسد. توجه به گلیکوپروتئین های واکنش داده در بعضی روش ها نیز ضروری است. 2 Background and Aims: Human Immunodeficiency virus (HIV) is spreading rapidly among the people worldwide. Infection with this virus leads to immune suppression and finally acquired immune deficiency syndrome. Early HIV detection is dependent on antibody screening against virus by Enzyme Linked Immunosorbent Assay (ELISA). Some confirmatory tests such as Western Blot and Recombinant Immunobloting Assay (RIBA) are used to verify viral infection. Many of the confirmatory test results are indeterminate. The aim of this study was to compare the frequency and patterns of indeterminate results of confirmatory tests in two groups blood donors and patients with high risk behaviors in the northeast of Iran. Materials and methods: It is a cross-sectional study from October 2009 to March 2014, a total number of 1055 serum samples with previous positive HIV ElISA test history were tested in our laboratory, Some by RIBA and some by western blot method. Results: Most of the indeterminate results belonged to blood donors and Western Blot analysis. The most reacting band was P24 in both methods and groups. Conclusions: RIBA assay is more sensitive and reliable than western Blot but it’s necessary to use other supplementary tests with less indistinctive results. It’s necessary to pay attention to HIV glycoprotein reactivity in some methods too. 58 64 2015/05/112015/05/62015/05/112015/05/112015/05/112015/05/112015/05/112015/05/17 1394/2/27 2015/05/112015/05/62015/05/112015/05/112015/05/112015/05/112015/05/112015/05/17 1394/2/27 سیده فاطمه شمس Seyyede Fatemeh Shams Hematology and Blood Banking Department, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran Iran Shams8869@yahoo.com زهرا اریان پور Zahra Arian pour Blood Transfusion Organization Research Center, Mashhad, Iran. Iran فرزاد ملاحسینی فومنی Farzad Molahosseini Foomani Blood Transfusion Organization Research Center, Mashhad, Iran. Iran حسین قلی نوری Hossein Gholi Noori Blood Transfusion Organization Research Center, Mashhad, Iran. Iran HIV Indeterminate RIBA Western blot وسترن بلات RIBA HIV اهدا کنندگان خون [1]. Cremonezi D, Mesquita P.E.D, Romão M.M, Prestes-Carneiro L.E. Prevalence of indeterminate human immunodeficiency virus western blot results in pregnant Cliams. ABC of HIV and AIDS: black well; 2012.##[2]. Huang L, Liu C, Chu S, Wong W, Lin Y, Liu W, et al. Predictive value of two commercial human immunodeficiency virus serological tests in cases with indeterminate Western blot results. J Microbiol Immunol Infect 2006;39(3):219-24.##[3]. Erickson C.P, McNiff T, Klausner J.D. Influenza vaccination and false positive HIV results. New England Journal of Medicine 2006;354(13):1422-3.##[4]. Owen S.M, Yang C, Spira T, Ou C, Pau C, Parekh B, et al. Alternative algorithms for human immunodeficiency virus infection diagnosis using tests that are licensed in the United States. Journal of clinical microbiology 2008;46(5):1588-95.##[5]. Mas A, Soriano V, Gutierrez M, Fumanal F, Alonso A, González-Lahoz J. Reliability of a new recombinant immunoblot assay (RIBA HIV-1/HIV-2 SIA) as a supplemental (confirmatory) test for HIV-1 and HIV-2 infections. Transfusion science 1997;18(1):63-9.##[6]. Guan M. Frequency, causes, and new challenges of indeterminate results in Western blot confirmatory testing for antibodies to human immunodeficiency virus. Clinical and vaccine immunology 2007;14(6):649-59.##[7]. Fearon M. The laboratory diagnosis of HIV infections. The Canadian Journal of Infectious Diseases & Medical Microbiology 2005;16(1):26.##[8]. Mylonakis E, Paliou M, Lally M, Flanigan T.P, Rich J.D. Laboratory testing for infection with the human immunodeficiency virus: established and novel approaches. The American journal of medicine 2000;109(7):568-76.##[9]. Syed I.H, Balakrishnan P, Solomon S.S, Murugavel K, Kumarasamy N, Vidya S, et al. HIV-1 western blot assay: What determines an indeterminate status? Indian journal of medical sciences 2005;59(10):443.##[10]. Dodd R.Y, Stramer S.L. Indeterminate results in blood donor testing: what you don't know can hurt you. Transfusion medicine reviews 2000;14(2):151-60.##[11]. Hart D.J, Heath R.G, Sautter Jr F.J, Schwartz B.D, Garry R.F, Choi B, et al. Antiretroviral antibodies: implications for schizophrenia, schizophrenia spectrum disorders, and bipolar disorder. Biological psychiatry 1999;45(6):704-14.##[12]. Talal N, Dauphinee M.J, Dang H, Alexander S.S, Hart D.J, Garry R.F. Detection of serum antibodies to retroviral proteins in patients with primary Sjogren's syndrome (autoimmune exocrinopathy). Arthritis and rheumatism 1990;33(6):774-81. ##[13]. Talal N, Flescher E, Dang H. Are endogenous retroviruses involved in human autoimmune disease? J Autoimmun. 1992;5:61-6.##[14]. Tesoro-Cruz E, Hernández-González R, Kretschmer-Schmid R, Aguilar-Setién A. Cross-reactivity between caprine arthritis-encephalitis virus and type 1 human immunodeficiency virus. Archives of medical research 2003;34(5):362-6.##[15]. Constantine N.T, Zink H. HIV testing technologies after two decades of evolution. The Indian journal of medical research 2005;121(4):519-38. ##[16]. Roy S, Fitz-Gibbon L, Spira B, Portnoy J, Wainberg M.A. False-positive results of confirmatory testing for antibody to HIV-I. CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne 1987 Mar 15;136(6):612-614. ##[17]. Salinas A, Górgolas M, Fernández-Guerrero M. Refrain from telling bad news: patients with leishmaniasis can have false-positive HIV test results. Clinical infectious diseases 2007;45(1):139-40.##[18]. Tinguely C, Schild-Spycher T, Bahador Z, Gowland P, Stolz M, Niederhauser C. Comparison of a conventional HIV 1/2 line immunoassay with a rapid confirmatory HIV 1/2 assay Journal of Virological Methods 2014; 206 : 1–4.##[19]. Carneiro-Proietti A.B, Cunha I.W, Souza M.M, Oliveira D.R, Mesquita N.M, Andrade C.A, et al. HIV-(1/2) indeterminate western blot results: follow-up of asymptomatic blood donors in belo horizonte, minas gerais, brazil. Revista do Instituto de Medicina Tropical de Sao Paulo 1999 May;41(3):155-8. ##[20]. Sudha T, Lakshmi V, Teja V. Western blot profile in HIV infection. Indian Journal of Dermatology, Venereology & Leprology 2006;72(5):357-360.## ##

Effects of Ecstasy on Mouse Cardiac Histopathology, Electrocardiogram and Blood Cell Counts اثراکستازی بر هیستو پاتولوژی بافت قلب ، الکتروکاردیوگرام و شمارش سلولهای خونی موش 2 1 مقدمه: اکستازی یا ۳-۴- متیلن دی اکسید متامفتامین ماده ای محرک مغز و توهم زاست که از تغییر فرمول شیمیایی آمفتامین بدست می آید. هدف از انجام این مطالعه ارزیابی تغییرات القائئ توسط این دارو بر هیستوپاتولوژی قلب، الکتروکاردیوگرام و نیز سلولهای خون موش بود. مواد و روشها: در این مطالعه از ۳۰موش در سه گروه ده تایی استفاده شد. گروه اول گروه کنترل که پلاسبو دریافت می کردند، گروه دوم دوز کم (۲۰mg/kg) دارو اکستازی و گروه سوم دوز بالای (۴۰mg/kg) داروی اکستازی بصورت داخل صفاقی و روزانه به مدت ۲۸روز دریافت می کردند. سپس از تمامی نمونه ها الکتروکاردیوگرام(ECG) وAVF تهیه و نمونه خون برای شمارش سلولهای خونی گرفته شد. نمونه های قلب موش ها نیز برش زده شد و با رنگ آمیزی روتین تحت بررسی میکروسکوپی قرار گرفت. نتایج: درگروه سه، کاهش در اریتروسیت ها، میوکاردیت در ۷ نمونه و اینفیلتراسیون منوسیت ها در اطراف میوسیت ها در ۶ نمونه مشاهده شد. در گروه دو، درجات کمتری از تخریب میوکارد با افزایش معنی دار در QT و QTeدر ECG وجود داشت. در گروه دریافت کننده دوز بالای دارو، گلبولهای قرمز، هماتوکریت، میانگین حجم گلبول و میانگین میزان هموگلوبولین گلبول در مقایسه با گروه کنترل بطور معنی داری کاهش نشان می داد. بحث و نتیجه گیری: اکستازی با اثر بر شاخص های گلبول قرمز ممکن است در ایجاد کم خونی نقش داشته باشد. اینفیلتراسیون منوسیت ها در اطراف سلولهای قلب و افزایش دپولاریزاسیون و رپولاریزاسیون بطنی منجر به افزایش QRS –QT میگردد که همراه بودن دو مورد فوق با افزایش تاکیکاردی سینوسی و میوکاردیت نشان دهنده تغییرات ساختمانی و عملکرد در میو کارد و صدمات ناشی از کمبود اکسیژن است که ایسکمی و انفارکتوس قلبی را به دنبال خواهد داشت. 2 Background and Aims: Ecstasy or 3, 4-methylenedioxymethamphetamine (MDMA) is a brain stimulant and a hallucinogenic material prepared by chemical changes in amphetamine. The aim of this study was to evaluate the changes induced by this drug in mouse cardiac histopathology, electrocardiogram (ECG) and blood cell counts. Materials and Methods: In this experiment, 3 groups (n=10) of mice were enrolled. Group 1, as control, received placebo. Group 2 mice were given single daily low dose (20 mg/kg/d for 28 days) of intraperitoneal MDMA, and group 3 were given single daily high dose (40 mg/kg/d for 28 days) of intraperitoneal MDMA. An ECG, aVF lead record was obtained, and then a blood sample was taken for complete blood counts and the heart was removed for microscopic study of tissue sections with routine staining. Results: The group 3 showed significant decrease in erythrocyte indices, myocarditis in 7 cases and monocyte infiltration around cardiac myocytes in 6 cases. In group 2, lower degree of myocardial injury was observed, displaying significant increase in QT and QTc durations in ECG. In high dose group, red blood count, hematocrit, mean cell volume and mean corpuscular hemoglobin concentration showed significant changes with comparison control group. Conclusions: Ecstasy can effect on red blood cell index and can lead to anemia. Many monocytes see around of cardiac cell with increase of ventricular depolarization and repolarization can lead to increase of QRS-QT interval. Combination myocarditis with arythmia and increase of sinus tachycardia show change in cardiac function and myocardial structure, cardiac injury due to hypoxia and ischemic can cause of myocardial infarction. 65 72 2015/05/112015/05/62015/05/112015/05/112015/05/112015/05/112015/05/112015/05/172015/05/17 1394/2/27 2015/05/112015/05/62015/05/112015/05/112015/05/112015/05/112015/05/112015/05/172015/05/17 1394/2/27 محمد حسینی شریف آباد Mohammad Hosseini-Sharifabad Department of Anatomical Sciences, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran. Iran فاطمه حاجی مقصودی Fatheme Hajimaghsoodi Department of Anatomical Sciences, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran. Iran علی کریم زاده Ali Karimzade Department of Internal Medicine, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran. Iran سیدحسین حکمتی مقدم Seyedhossein Hekmatimoghaddam Department of Laboratory Sciences, School of Paramedicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran. Iran shhekmati2002@yahoo.com منصور اسماعیلی دهج Mansour Esmailidehaj Department of Physiology, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran. Iran فریبا بینش Fariba Binesh Department of Pathology, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran. Iran Blood Count Ecstasy Electrocardiography Methamphetamine اکستازی الکتروکاردیوگرافی سلولهای خونی متامفتامین [1]. Sprague JE, Banks ML, Cook VJ, Mills EM. Hypothalamic-pituitary-thyroid axis and sympathetic nervous system involvement in hyperthermia induced by 3, 4-methylenedioxymethamphetamine (Ecstasy). J Pharmacol Exp Ther 2003; 305(1): 159-66.##[2]. Gerra G, Bassignana S, Zaimovic A, Moi G, Bussandri M, Caccavari R, et al. Hypothalamic-pituitary-adrenal axis responses to stress in subjects with 3,4 - methylenedioxy-methamphetamine ('ecstasy') use history: correlation with dopamine receptor sensitivity. Psychiatry Res 2003 Sep 30; 120(2): 115-24.##[3]. Faria R, Magalhães A, Monteiro PR, Gomes-Da-Silva J, Amélia Tavares M, Summavielle T. MDMA in adolescent male rats: decreased serotonin in the amygdala and behavioral effects in the elevated plus-maze test. Ann N Y Acad Sci 2006; 1074: 643-9.##[4]. Mas M, Farre M, de la Torre R, Roset PN, Ortuno J, Segura J, et al. Cardiovascular and neuroendocrine effects and pharmacokinetics of 3, 4-methylenedioxymethamphetamine in humans. J Pharmacol Exp Ther 1999; 290(1): 136-45.##[5]. Koesters SC, Rogers PD, Rajasingham CR. MDMA ('ecstasy') and other 'club drugs'. The new epidemic. Pediatr Clin North Am 2002 Apr; 49(2): 415-33.##[6]. Beebe DK, Walley E. Smokable methamphetamine (ice): an old drug in a different form. Am Fam Phys 1995; 51: 449-53.##[7]. Mizia-Stec K, Gasior Z, Wojnicz R, Haberka M, Mielczarek M, Wierzbicki A, et al. Severe dilated cardiomyopathy as a consequence of Ecstasy intake. Cardiovasc pathol 2008; 17(4): 250-3.##[8]. Hysek CM, Vollen Weider Fx, Liechti ME. Effects of a beta-blocker on the cardiovascular response to MDMA (Exstasy). Emerg med J 2010; 27(8): 586 -9. Epub 2010 April 8.##[9]. Patel MM. Belson MG, Wright D, Lu H, Heninger M, Miller MA. Methylenedioxymethamphetamine (ecstasy)-related myocardial hypertrophy: an autopsy study. Resuscitation 2005; 66(2): 197-202.##[10]. Shenouda Sk, Carvalho F, Varner KJ. The cardiovascular and cardiac actions of MDMA ecstasy and its metabolites. Curr Pharm Biotechnol 2010: 11(5): 470-5.##[11]. Gesi M, Lenzi P, Soldani P, Ferrucci M, Giusiani A, Fornai F, et al. Morphological effects in the mouse myocardium after methylenedioxymethamphetamine administration combined with loud noise exposure. Anat Rec 2002; 267(1): 37-46.##[12]. Yi SH, Ren L, Yang TT, Liu L. Myocardial lesions after long term administration of methamphetamine in rats. Chin Med Sci J 2008; 23(4): 239-43.##[13]. Sano R, Hasuike T, Nakano M, Kominato Y, Itoh H. A fatal case of myocardial damage due to misuse of the "designer drug" MDMA. Leg Med (Tokyo) 2009 Nov; 11(6): 294-7.##[14]. Pilgrim JL, Gerostamoulos D, Drummer OH. Involvement of amphetamines in sudden and unexpected death. J Forensic 2009; 54(2): 478-85.##[15]. Suriyaprom K, Tanateerabunjong R, Tungtrongchitr. Alterations in malondialdehyde levels and laboratory parameters among methamphetamine abusers. J Med Assoc Thai 2011; 94 (12): 1533-9.##[16]. Shenouda SK, Lord KC, Mcllwain E. Ecstasy produces left ventricular dysfunction and oxidative stress in rats. Cardiovasc Res 2008; 79(4): 662-70.##[17]. Yu Q, Montes S, Larson DF, Watson RR. Effects of chronic methamphetamine exposure on heart function in uninfected and retrovirus-infected mice. Life Sciences 2002: 71: 953–65.##[18]. Cerretani D, Riezzo I, Fiaschi Al, Centini F, Giorgi G, DErrico S, et al. Cardiac oxidative stress determination and myocardial morphology after a single ecstasy (MDMA) administration in a rat model. Int J Legal Med 2008; 122(6): 461-9.##[19]. Neri M, Bello S, Bonsignore A, Centini F, Fiore C, Földes-Papp Z, et al. Myocardial expression of TNF-alpha, IL-1beta, IL-6, IL-8, IL-10 and MCP-1 after a single MDMA dose administered in a rat model. Curr pharm biotechnol 2010; 11(5): 413-20.##[20]. Sadeghian S, Darvish S, Shahbazi S. Two ecstasy induced myocardial infarctions during a three month period in a young man. Arch Iran Med 2007; 10(3): 409-12.##[21]. Baumann MH, Rothman RB. Neural and cardiac toxicities associated with 3,4 methylendioxymethamphetamine (MDMA). Int Rev Neurobiol 2009; 88: 257-96.##[22]. Setola V, Hufeisen SJ, Grande-Allen KJ, Vesely I, Glennon RA, Blough B, et al. 3-4 methylenedioxymethamphetamine (MDMA, Ecstasy) induces fenfluramine-like proliferative actions on human cardiac valvular interstitial cells in vitro. Mol pharmacol 2003; 63(6): 1223-9.##[23]. Tiangco DA, Halcomb S, Lattanzio FA, HargraveBY.3,4-Methylenedioxymethamphetamine alters left ventricular function and activates nuclear factor-kappa B (NF-κB) in a time and dose dependent manner. Int J Mol Sci 2010; 11(12): 4843-63.##[24]. Qianli Yu, Sergiomontes, Douglas F. Effects of chronic methamphetamine exposure on heart function in uninfected and retrovirus-infected mice. Health promotion science division 2002; 953-65.## ##