<?xml version="1.0" encoding="utf-8"?>
<XML>
<JOURNAL>
<YEAR>2016</YEAR>
<VOL>3</VOL>
<NO>3</NO>
<MOSALSAL>0</MOSALSAL>
<PAGE_NO>204</PAGE_NO>


<ARTICLES>

	<ARTICLE> 
		<TitleF>Role of miR-146a in Immune System and Autoimmunity</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>MicroRNAs (miRNAs) are small preserved non-coding RNA molecules that regulate gene expression post-transcriptionally by targeting the 3&#39; UTR of mRNAs for translational repression or degradation. The rising evidence has established the significant role of miRNAs within the regulation of immune system and the prevention of autoimmunity. MiR-146a has obtained an importance as a modulator of differentiation and the function of cells of the adaptive, as well as innate immunity rapidly. In this paper, we summarize the recent understanding of the role of miR-146a in adaptive and innate immune responses, as well as in autoimmunity.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>150</FPAGE>
			<TPAGE>158</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2016/11/2
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1395/8/12
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2016/11/2
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1395/8/12
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Bahram</Name>
				<MidName></MidName>
				<Family>Moghimi</Family>
				<NameE>Bahram</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Moghimi</FamilyE>
				<Organizations>
				<Organization>Department of Genetics, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Saba</Name>
				<MidName></MidName>
				<Family>Gharibi</Family>
				<NameE>Saba</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Gharibi</FamilyE>
				<Organizations>
				<Organization>Department of Genetics, Faculty of Medicine, International Campus, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Ehsan</Name>
				<MidName></MidName>
				<Family>Farashahi Yazd</Family>
				<NameE>Ehsan</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Farashahi Yazd</FamilyE>
				<Organizations>
				<Organization>Department of Genetics, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Mohammad</Name>
				<MidName></MidName>
				<Family>Taher Tahoori</Family>
				<NameE>Mohammad</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Taher Tahoori</FamilyE>
				<Organizations>
				<Organization>Department of Immunology, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Seyed Mehdi</Name>
				<MidName></MidName>
				<Family>Kalantar</Family>
				<NameE>Seyed Mehdi</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Kalantar</FamilyE>
				<Organizations>
				<Organization>Department of Genetics, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Adaptive immunity</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Autoimmune disease</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Innate immunity</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>MicroRNA</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF> ##1]. Alexandrov PN, Dua P, Lukiw WJ. Upregulation of miRNA-146a in progressive, agerelated inflammatory neurodegenerative disorders of the human CNS. Frontiers in neurology 2014; 29(5): 181.  ##2]. Anglicheau D, Muthukumar T, Suthanthiran M. MicroRNAs: small RNAs with big effects. Transplantation 2010; 90(2): 105-12.  ##3]. Bartel DP. MicroRNAs:genomics, biogenesis, mechanism, and function. Cell 2004; 116(2): 281-97.  ##4]. Bartel DP. MicroRNAs:target recognition and regulatory functions. Cell 2009;136(2): 215-33.  ##5]. Bettelli E, Carrier Y, Gao W, Korn T, Strom TB, Oukka M, et al. Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells. Nature 2006; 441(7090): 235-38.  ##6]. Bhaumik D, Scott GK, Schokrpur S, Patil CK, Campisi J, Benz CC. Expression of microRNA- 146 suppresses NF-κB activity with reduction of metastatic potential in breast cancer cells. Oncogene 2008;27(42): 5643-647.  ##7]. Boldin MP, Taganov KD, Rao DS, Yang L, Zhao JL, Kalwani M, et al. miR-146a is a significant brake on autoimmunity, myeloproliferation, and cancer in mice. The Journal of experimental medicine 2011;208(6): 1189-201.  ##8]. Bresnihan B, Alvaro-Gracia JM, Cobby M, Doherty M, Domljan Z, Emery P, et al. Treatment of rheumatoid arthritis with recombinant human interleukin-1 receptor antagonist. Arthritis Rheum.1998;41(12): 2196-204.  ##9]. Buchanan MM, Hutchinson M, Watkins LR, Yin H. Toll like receptor 4 in CNS pathologies. Journal of neurochemistry 2010;114(1): 13-27.  ##10]. Cameron JE, Yin Q, Fewell C, Lacey M, McBride J, Wang X, et al. Epstein-Barr virus latent membrane protein 1 induces cellular MicroRNA miR-146a, a modulator of lymphocyte signaling pathways. Journal of virology 2008; 82(4): 1946-958.  ##11]. Ceribelli A, Nahid MA, Satoh M, Chan EK. MicroRNAs in rheumatoid arthritis. FEBS letters 2011; 585(23): 3667-674.  ##12]. Crow MK..Type I interferon in systemic lupus erythematosus, in Interferon: The 50th Anniversary. Springer 2007: 359-86.  ##13]. Cui JG, Li YY, Zhao Y, Bhattacharjee S, Lukiw WJ. Differential regulation of interleukin- 1 receptor-associated kinase-1 (IRAK-1) and IRAK-2 by microRNA-146a and NF-κB in stressed human astroglial cells and in Alzheimer disease. Journal of Biological Chemistry 2010; 285(50): 38951-8960.  ##14]. Curtale G, Citarella F, Carissimi C, Goldoni M, Carucci N, Fulci V, et al. An emerging player in the adaptive immune response: microRNA- 146a is a modulator of IL-2 expression and activation-induced cell death in T lymphocytes. Blood 2010; 115(2): 265-73.  ##15]. Denli AM, Tops BB, Plasterk RH, Ketting RF, Hannon GJ. Processing of primary microRNAs by the Microprocessor complex. Nature 2004; 432(7014): 231-35.  ##16]. Eriksson P, Andersson C, Ekerfelt C, Ernerudh J, Skogh T. Relationship between serum levels of IL_ 18 and IgG1 in patients with primary Sjögren's syndrome, rheumatoid arthritis and healthy controls. Clinical &amp; Experimental Immunology 2004;137(3): 617-20. B. Moghimi et al. 157 International Journal of Medical Laboratory 2016; 3(3): 150-158.  ##17]. Fernández M, Montalban X, Comabella. M. Orchestrating innate immune responses in multiple sclerosis: molecular players. Journal of neuroimmunology 2010; 225(1): 5-12.  ##18]. Fox RI. Sjögren's syndrome. The Lancet 2005;366(9482): 321-31.  ##19]. Gandhi R, Laroni A, Weiner HL. Role of the innate immune system in the pathogenesis of multiple sclerosis. Journal of neuroimmunology 2010; 221(1): 7-14.  ##20]. Guo Q, Zhang J, Li J, Zou L, Zhang J, Xie Z, et al. Forced miR-146a expression causes autoimmune lymphoproliferative syndrome in mice via downregulation of Fas in germinal center B cells. Blood 2013;121(24): 4875-883.  ##21]. Hill JM, Zhao Y, Clement C, Neumann DM, Lukiw WJ. HSV-1 infection of human brain cells induces miRNA-146a and Alzheimer-type inflammatory signaling. Neuroreport 2009; 20(16): 1500-1505.  ##22]. Hou J, Wang P, Lin L, Liu X, Ma F, An H, Wang Z, Cao X. MicroRNA-146a feedback inhibits RIG-I-dependent Type I IFN production in macrophages by targeting TRAF6, IRAK1, and IRAK2. The Journal of Immunology 2009; 183(3): 2150-158.  ##23]. Ingram G, Loveless S, Howell OW, Hakobyan S, Dancey B, Harris CL Complement activation in multiple sclerosis plaques: an immunohistochemical analysis. Acta neuropathologica communications 2014;9 (2):53.  ##24]. Junker A, Krumbholz M, Eisele S, Mohan H, Augstein F, Bittner R, et al. MicroRNA profiling of multiple sclerosis lesions identifies modulators of the regulatory protein CD47. Brain 2009;132(12): 3342-352.  ##25]. Jurkin J, Schichl YM, Koeffel R, Bauer T, Richter S, Konradi S, et al. miR-146a is differentially expressed by myeloid dendritic cell subsets and desensitizes cells to TLR2-dependent activation. The Journal of Immunology2010; 184(9): 4955-965.  ##26]. Kasper LH, Shoemaker J. Multiple sclerosis immunology The healthy immune system vs the MS immune system. Neurology 2010;74( Supp 1): S2-S8.  ##27]. Kawai T, Akira S. TLR signaling. Cell Death &amp; Differentiation 2006; 13(5): 816-25.  ##28]. Kroesen BJ, Teteloshvili N, Smigielska- Czepiel K, Brouwer E, Boots AM, van den Berg, et al. Immuno-miRs: critical regulators of T-cell development, function and ageing. Immunology 2015;144(1): 1-10.  ##29]. Kuchen S, Resch W, Yamane A, Kuo N, Li Z, Chakraborty T, et al. Regulation of microRNA expression and abundance during lymphopoiesis. Immunity 2010;32(6): 828-39.  ##30]. Li J, Wan Y, Guo Q, Zou L, Zhang J, et al. Research article Altered microRNA expression profile with miR-146a upregulation in CD4+ T cells from patients with rheumatoid arthritis. Arthritis research &amp; therapy 2010; 12: R81.  ##31]. Li YY, Cui JG, Dua P, Pogue AI, Bhattacharjee S, Lukiw WJ. Differential expression of miRNA- 146a-regulated inflammatory genes in human primary neural, astroglial and microglial cells. Neuroscience letters 2011; 499(2): 109-113.  ##32]. Lipsky PE, van der Heijde DM, St Clair EW, Furst DE, Breedveld FC, Kalden JR, et al. Infliximab and methotrexate in the treatment of rheumatoid arthritis. New England Journal of Medicine. 2000;343(22): p. 1594-602.  ##33]. Liston A, Linterman M, Lu.-lF. .MicroRNA in the adaptive immune system, in sickness and in health. Journal of clinical immunology 2010; 30(3): 339-46.  ##34]. Liston A, Linterman M, Lu LF. Lu.MicroRNA in the adaptive immune system, in sickness and in health. Journal of clinical immunology 2010; 30(3): 339-46.  ##35]. Monticelli S, Ansel KM, Xiao C, Socci ND, Krichevsky AM, Thai TH, et al.MicroRNA profiling of the murine hematopoietic system. Genome biology 2005; 6(8): R71.  ##36]. Motsch N, Pfuhl T, Mrazek J, Barth S, Grässer FA. Epstein-Barr virus-encoded latent membrane protein 1 (LMP1) induces the expression of the cellular microRNA miR-146a. RNA biolog 2007;4(3): 131-37.  ##37]. Nakasa T, Miyaki S, Okubo A, Hashimoto M, Nishida K, Ochi M, et al. Expression of microRNA-146 in rheumatoid arthritis synovial tissue. Arthritis &amp; Rheumatism 2008;58(5): 1284-292.  ##38]. Nahid MA, Pauley KM, Satoh M, Chan EK. miR-146a is critical for endotoxin-induced tolerance IMPLICATION IN INNATE IMMUNITY. Journal of Biological Chemistry 2009; 284(50): 34590-4599.  ##39]. Niimoto T, Nakasa T, Ishikawa M, Okuhara A, Izumi B, Deie M. MicroRNA-146a expresses in interleukin-17 producing T cells in rheumatoid arthritis patients. BMC musculoskeletal disorders 2010; 11(1): 209.  ##40]. O'Connell RM, Rao DS, Chaudhuri AA, Baltimore D. Physiological and pathological roles for microRNAs in the immune system. Nature Reviews Immunology 2010; 10(2): 111-22.  ##41]. O'Connell RM, Taganov KD, Boldin MP, Cheng G, Baltimore D. MicroRNA-155 is induced during the macrophage inflammatory response. Proceedings of the National Academy of Sciences 2007;104(5): 1604-1609.  ##42]. Pauley KM, Satoh M, Chan AL, Bubb MR, Reeves WH, Chan EK. Upregulated miR-146a expression in peripheral blood mononuclear cells from rheumatoid arthritis patients. Arthritis research &amp; therapy 2008; 10(4): R101.  ##43]. Pauley KM, Stewart CM, Gauna AE, Dupre LC, Kuklani R, Chan AL, et al. Altered miRROLE OF MIR-146a IN IMMUNE SYSTEM AND AUTOIMMUNITY International Journal of Medical Laboratory 2016; 3(3): 150-158. 158 146a expression in Sjögren's syndrome and its functional role in innate immunity. European journal of immunology 2011; 41(7):2029-2039.  ##44]. Perry MM, Moschos SA, Williams AE, Shepherd NJ, Larner-Svensson HM, Lindsay MA. Rapid changes in microRNA-146a expression negatively regulate the IL-1β-induced inflammatory response in human lung alveolar epithelial cells. The Journal of Immunology 2008;180(8): 5689-698.  ##45]. Pryce G, Ahmed Z, Hankey DJ, Jackson SJ, Croxford JL, Pocock JM, et al. Cannabinoids inhibit neurodegeneration in models of multiple sclerosis. Brain 2003, 126(10): 2191-2202.  ##46]. Rescigno M, Martino M, Sutherland CL, Gold MR, Ricciardi-Castagnoli P. Dendritic cell survival and maturation are regulated by different signaling pathways. The Journal of experimental medicine 1998;188(11):2175-180.  ##47]. Rom S, Rom I, Passiatore G, Pacifici M, Radhakrishnan S, Del Valle L, et al. CCL8/MCP-2 is a target for mir-146a in HIV-1- infected human microglial cells. The FASEB Journa 2010; 24(7): 2292-2300.  ##48]. Rönnblom L1, Eloranta ML, Alm GV. The type I interferon system in systemic lupus erythematosus. Arthritis &amp; Rheumatism. 2006; 54(2): 408-20.  ##49]. Smolen JS, Aletaha D, Koeller M, Weisman MH, Emery P. New therapies for treatment of rheumatoid arthritis. The Lancet 2007; 370(9602): 1861-874.  ##50]. Stürner KH, Verse N, Yousef S, Martin R, Sospedra M. Boswellic acids reduce Th17 differentiation via blockade of IL-1β-mediated IRAK1 signaling. European journal of immunology 2014;44(4): 1200-212.  ##51]. Szodoray P, Alex P, Brun JG, Centola M, Jonsson R. Circulating cytokines in primary Sjögren's syndrome determined by a multiplex cytokine array system. Scandinavian Journal of Immunolog 2004; 59(6): 592-99.  ##52]. Taganov KD, Boldin MP, Chang KJ, Baltimore D. NF-κB-dependent induction of microRNA miR-146, an inhibitor targeted to signaling proteins of innate immune responses. Proceedings of the National Academy of Sciences 2006;103(33): 12481-2486.  ##53]. Tang Y, Luo X, Cui H, Ni X, Yuan M, Guo Y, et al. MicroRNA-146a contributes to abnormal activation of the type I interferon pathway in human lupus by targeting the key signaling proteins. Arthritis &amp; Rheumatism 2009;60(4): 1065-1075.  ##54]. van de Laar L, van den Bosch A, van der Kooij SW, Janssen HL, Coffer PJ, van Kooten CV, et al. A nonredundant role for canonical NF-κB in human myeloid dendritic cell development and function. The Journal of Immunology 2010;185(12): 7252-261.  ##55]. Zhao JL, Rao DS, Boldin MP, Taganov KD, O'Connell RM, Baltimore D. NF-κB dysregulation in microRNA-146a–deficient mice drives the development of myeloid malignancies. Proceedings of the National Academy of Sciences 2010;108(22): 9184-189.  ##56]. Zhang J, Jia G, Liu Q, Hu J, Yan M, Yang B. Silencing miR-146a influences B cells and ameliorates experimental autoimmune myasthenia gravis. Immunology 2015;144(1): 56-67.  ##57]. Zilahi E, Tarr T, Papp G, Griger Z, Sipka S, Zeher M. Increased microRNA-146a/b, TRAF6 gene and decreased IRAK1 gene expressions in the peripheral mononuclear cells of patients with Sjögren's syndrome. Immunology letters 201;141(2): 165-68. ## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Prevalence of Seropositivity for Human T lymphocytes Virus in Patients with Hereditary Bleeding Diseases in Population of West Azerbaijan</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Background and Aims: Human T-lymphotropic virus (HTLV) is a human retrovirus which has been known to cause adult T-cell leukemia/lymphoma and some other inflammatory disorders. Patients with hereditary bleeding diseases are at high risk for these viruses. In this study, we evaluated serological HTLV-I/II infection among these patients in west Azerbaijan of Iran.

Material and Methods: We studied 50 hemophiliacs including 43 males and 7 females. Serum samples were screened for Anti-HTLV-I and II using enzyme-linked immunosorbent assay. Western blot method was applied on borderline results for confirmation.

Results and Conclusions: All studied patients were seronegative for HTLV-I/II and serologic evidence of HTLV I/II infection was not found in any of patients. Based on our results, blood donor population of Urmia must be increased to achieve more accurate results.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>159</FPAGE>
			<TPAGE>162</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2016/11/22016/11/9
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1395/8/19
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2016/11/22016/11/9
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1395/8/19
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Zakieh</Name>
				<MidName></MidName>
				<Family>Rostamzadeh</Family>
				<NameE>Zakieh</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Rostamzadeh</FamilyE>
				<Organizations>
				<Organization>Solid Tumor Research Center, Urmia University of Medical Sciences, Urmia, Iran.</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Nasim</Name>
				<MidName></MidName>
				<Family>Valizadeh</Family>
				<NameE>Nasim</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Valizadeh</FamilyE>
				<Organizations>
				<Organization>Hematology,Oncology and Stem Cell Transplantation Research Center, Tehran University of Medical Sciences, Tehran, Iran.</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Mahshid</Name>
				<MidName></MidName>
				<Family>Mohammadian</Family>
				<NameE>Mahshid</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Mohammadian</FamilyE>
				<Organizations>
				<Organization>Department of Biochemistry, School of Medicine, Urmia University of Medical Sciences, Urmia, Iran.</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Hereditary bleeding disease</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Human T-Lymphotropic virus</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Urmia</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>1]. Canavaggio M, Leckie G, Allain JP, Steaffens JW, Laurian Y, Brettler D, et al. The prevalence  of antibody to HTLV-1/2 in United States plasma donors and in United States and French hemophiliacs. Transfusion 1990; 30(9): 780-82.  ##2]. Casseb J. Is Human T Cell Lymphotropic Type  1 (HTLV-1)-Associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP) Syndrome a Neglected Disease? PLoS Negl Trop Dis.2009; 3(11): e487.   ##3]. Ramezani A, Aghakhani A, Banifazl M, Boland-Ghamat Z, Foroughi M, Gachkar L, et  al. Frequency of Human T-Cell Lymphotropic  Virus (HTLV) Type 1 and 2 Infection in HIV Infected Patients. Iranian journal of pathology. 2012;7(1): 9-13.   ##4]. Iga M, Okayama A, Stuver S, Matsuoka M, Mueller N, Aoki M, et al. 2002. Genetic  evidence of transmission of human T cell lymphotropic virus type 1 between spouses. J Infect Dis. 2002;185(5): 691-95.   ##5]. Carneiro-Proietti AB, Lima-Martins MV, Passos VM, Carmo RA, Pinheiro SR, Rocha  PR. Presence of human immunodeficiency virus (HIV) and T-lymphotropic virus type I and II (HTLV-I/II) in a hemophiliac’s population in  belohorizonte, Brazil, and correlation with additional serological results. Hemophilia1998; 4(1): 47-50.   ##6]. Rostamzadeh ZR, Baradaran M, Sepehrvand N. Survey of the Seroprovalence of HTLV 1/2 in  Hemodialysis Patients and Blood Donors in Urmia. Saudi J Kidney Dis Transpl. 2008;19(5): 838-41.   ##7]. Mahzounieh M, Ghorani M, Karimi A, Pourgheysari B, Nikoozad R. Prevalence of  Human T-Lymphotropic Virus Types I and II in Patients With Hematological Disorders in Isfahan, Iran. Jundishapur Journal of Microbiology 2015; 8(6): e17201.   ##8]. Moradi A, Mansurian AR, Ahmadi AR, Ghaemi, E, Kalavi KH, Marjani A, et al. Prevalence of  HTLV-1 antibody among major thalassemia patients in gorgan (South East of Caspian Sea). J Applied Sci. 2008; 8(1): 391-93.   ##9]. Tamura I, Koda T, Kobayashi Y, Ichimura H, Kurimura O, Kurimura T. Prevalence of four  blood-borne viruses (HBV, HC V, HTLV-I, HIV-1) among hemodialysis patients in Japan. J Med Virology 2005:.36(4): 271-73.   ##10]. Rezvan H, Nurkjuri S. Epidemiology of HTLV-1 among Thalassemia and hemophilic  patients in Tehran. Khoon (hematology) Res J. 1995;2: 1-5.   ##11]. Ziaee M, Namaei MH, Azarkar Gh. The prevalence of HTLV-1 and its Co-Infection  with HCV, HBV and HIV in Hemophilic patients. Pak J Med Sci. 2015;31(5): 1246-249. ## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Analysis of clbN and clbB genes in Isolated Klebsiella pneumonia of Biopsies from Patients with Colorectal Cancer</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Background and Aims: Recently it has been proved that some of Enterobacteriacea like Klebsiella pneumoniae, which carry PKS islands, damage dsDNA by encoding Colibactin genotoxin; and finally they induce some apoptosis in damaged mucosal cells. This study aimed to isolating the clbN and clbB genes, which are the markers of the PKS genomic island, from PKS cluster in these bacteria

Materials and Methods: In this study, 110 biopsies were obtained from colorectal cancer patients referred to the clinic of Imam Khomeini Hospital. Then, all samples were cultured in LB medium for bacterial isolation. In the next step, Klebsiella peunomoniae was detected by biochemical and microbiological tests. Finally, the genomes were extracted by boiling method and then were amplified by PCR with specific clbN and clbB gene primers.

Results: Our findings have showed 30 Klebsiella pneumonia isolated out of 110 biopsies (27.3%) from patients with colorectal cancer; in which all of biochemical and microbial experiments including Gram-negative staining confirmed this bacteria. Also, 23.23% frequency of clbN were positive, 20% frequency of clbB were positive genes in the isolated Klebsiella pneumonia, and 13.33% frequency were positive for both clbB and clbN genes as simultaneous.

Conclusions: It is expected to find a significant correlation between Klebsiella bacteria which carries PKS genes and colorectal cancer by increased number of samples. The lower frequencies for Klebsiella with clbB and clbN positive strain in patients with colorectal cancer were shown in European countries based on the results of this study rather than the similar studies.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>163</FPAGE>
			<TPAGE>169</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2016/11/22016/11/92016/11/9
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1395/8/19
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2016/11/22016/11/92016/11/9
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1395/8/19
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Amir</Name>
				<MidName></MidName>
				<Family>Cheraghi</Family>
				<NameE>Amir</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Cheraghi</FamilyE>
				<Organizations>
				<Organization>Islamic Azad Univercity, Farahan Branch, Farahan, Iran.</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Shahla</Name>
				<MidName></MidName>
				<Family>Mohammad Ganji</Family>
				<NameE>Shahla</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Mohammad Ganji</FamilyE>
				<Organizations>
				<Organization>National Institute Genetic Engineering and Biotechnology, Tehran, Iran.</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Bita</Name>
				<MidName></MidName>
				<Family>Najmi</Family>
				<NameE>Bita</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Najmi</FamilyE>
				<Organizations>
				<Organization>Islamic Azad University, Qom Branch, Qom, Iran.</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>clbB</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>clbN</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Colorectal cancer</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Klebsiella pneumoniae</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>PCR</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF> 1]. Boleij A, Tjalsma H, Gut bacteria in health and disease: a survey on the interface between intestinal microbiology and colorectal cancer. Biol Rev Camb Philos Soc. 2012;87(3): 701-30.  ##2]. Martin HM, Campbell BJ, Hart CA, Mpofu C, Nayar M, Singh R, et al. Enhanced Escherichia coli adherence and invasion in Crohn's disease and colon cancer. Gastroenterology 2004;127(1): 80-93.  ##3]. Mohandas Km. Colorectal cancer in India: controversies, enigmas and primary prevention Indian Journal of Gastroenterology.2011; 30(1): 3-6.  ##4]. Parkin DM. International variation. Oncogene 2004;23(38): 6329-340.  ##5]. Kefalas CH. Gastroduodenal Crohn's disease. Proc (Bayl Univ Med Cent).2003;16(2): 147- 51.  ##6]. Parray FQ, Wani M, Bijli AH, Thakur N, Irshad I, Nayeem-ul-Hassan. Crohn's disease: a surgeon's perspective. Saudi J Gastroenterol. 2011; 17(1): 6-15.  ##7]. Hawker PC, Gyde SN, Thompson H, Allan RN. Adenocarcinoma of the small intestine complicating Crohn's disease. Gut. 1982;23(3): 188-93.  ##8]. Jawetz, Jawetz, Melnick &amp; Adelbergs's medical microbiology, ed. 26th ed 2013.  ##9]. Putze J, Hennequin C, Nougayrède JP, Zhang W, Homburg S, Karch H, et al. Genetic structure and distribution of the colibactin genomic island among members of the family Enterobacteriaceaeaeaeae. Infect Immun. 2009,77(11): 4696-703.  ##10]. Guerra L, Guid R, Frisan T. Do bacterial genotoxins contribute to chronic inflammation, genomic instability and tumor progression? FEBS J. 2012;278(23): 4577-588.  ##11]. Homburg S, Oswald E, Hacker J, Dobrindt U. Expression analysis of the colibactin gene cluster coding for a novel polyketide in Escherichia coli. FEMS Microbiol Lett.2007;. 275(2): 255-62.  ##12]. Brotherton CA, Balskus EP. A prodrug resistance mechanism is involved in colibactin biosynthesis and cytotoxicity. J Am Chem Soc. 2013;135(9): 3359-362  ##13]. Kurokawa K, Itoh T, Kuwahara T, Oshima K, Toh H, Toyoda A, et al.. Comparative metagenomics revealed commonly enriched gene sets in human gut microbiomes. DNA Res. 2007;14(4): 169-81.  ##14]. Chichlowski M, Hale LP. Bacterial-mucosal interaction in inflamatory bowel disease: an alliance gone bad. Am J Physiol Gastrointest Liver Physiol. 2008;295(6): G1139-149.  ##15]. Cuevas-Ramos G, Petit CR, Marcq I, Boury M, Oswald E, Nougayrède JP. Escherichia coli induces DNA damage in vivo and triggers genomic instability in mammalian cells. Proc Natl Acad Sci U S A.2010;107(25):11537-1542  ##16]. Johnson JR, Johnston B, Kuskowski MA, Nougayrede JP, Oswald E. Molecular epidemiology and phylogenetic distribution of the Escherichia coli pks genomic island. J Clin Microbiol. 2008;46(12): 3906-911. ## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Molecular Characterization and SCCmec in Methicillin Resistant Staphylococcus aureus from Healthy Worker Nasal Swab in Larestan Hospital</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Background and Aims: The aim of present study was to investigate the molecular characteristic of Staphylococcus aureus to detect mec A gene and to type SCCmec in strain isolated from healthy worker at Larestan Hospital.

Material and Methods: This study was carried out from the 250 nasal swab healthy worker&#160; at Larestan hospital. Multiplex polymerase chain reaction for mecA gene was performed in all samples. Also, agar screen plate with oxacillin was carried out using CLSI guidelines. The two methods were then compared.

Results: Of 250 samples, 37 (14.8%) samples are Staphylococcus aureus, 28 (75.7%) of samples were confirmed at Methicillin-resistant Staphylococcus aureus (MRSA) harboring mec A gene detected by Multiplex polymerase chain reaction (PCR) and 9 (24.3%) negative mec A. Sixteen of 28 (57.1%) were HA-MRSA and the remaining 12 (42.8%) were CA-MRSA. The Multiplex PCR assay for SCCmec complex of MRSA strains showed that 9 (32.1%) samples were SCCmec type I, 8 (28.6%) SCCmec type IVb, 5 (17.9%) SCCmec type II, 4 (14.3%) SCCmec type V and 2 (7.1%) SCCmec type III. Agar screen plate with oxacillin was found in all the 28 MRSA samples to harbor mecA gene and all was resistant.

Conclusion: Our results illustrated that more than 70% of staph aureus strains were positive for mec A gene and more than 50% of them were HA-MRSA. In comparison to other methods, PCR and Agar screen method more sensitivity determines MRSA isolates. However, PCR was identified as the ideal method for detecting MRSA strains.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>170</FPAGE>
			<TPAGE>175</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2016/11/22016/11/92016/11/92016/11/9
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1395/8/19
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2016/11/22016/11/92016/11/92016/11/9
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1395/8/19
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Mehdi</Name>
				<MidName></MidName>
				<Family>Ebadi</Family>
				<NameE>Mehdi</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Ebadi</FamilyE>
				<Organizations>
				<Organization>Department of Microbiology, Islamic Azad University, Larestan branch, Larestan, Iran.</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Hossein</Name>
				<MidName></MidName>
				<Family>Faramarzi</Family>
				<NameE>Hossein</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Faramarzi</FamilyE>
				<Organizations>
				<Organization>Department of Community Medicine, Medical school, Shiraz University of Medical Sciences, Shiraz, Iran.</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Healthy worker</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Methicillin-resistant</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Staphylococcus aureus</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>1]. Shittu AO, Okon K, Adesida S, Oyedara O, Witte W, Strommenger B, et al. Antibiotic resistance and molecular epidemiology of staphylococcus aureus in Nigera. BMC Microbial. 2011;5(11): 92. ##2]. Takano T, Higuchi W, Otsuka T, Baranovich T,Enany S, Saito K, et al. Novel characteristics of community acquired methicillin-resistant Staphy lococcusaureus belonging to multilocus sequence type 59 in Taiwan. Ntimicrob Agents Chemother 2008;52(3): 837-45. ##3]. Makgotlho PE, Kock MM, Hoosen A, Lekalakala R, Omar S, Dove M, et al. Molecular identification and genotyping of MRSA isolates. FEMS Imanol Med Microbial.2009;57(2): 104– 15. ##4]. Novick RP, Christie GE, Penades JR. The phage-related chromosomal islands of Grampositive bacteria. Nat Rev Microbial. 2010;8(8):541-51. ##5]. Tsubakishita S, Kuwahara-Arai K, Sasaki T, Hiramatsu K.. Origin and molecular evolution of the determinant of methicillin resistance in staphylococci. Antimicrobial agents and chemotherapy. 2010;54(10):4352-359. ##6]. Kluytmans-Vandenbergh MF, Kluytmans JA. Community-acquired methicillin-resistant Staphylococcus ureus: current perspectives. Clin Microbiol Infect. 2006;12(Suppl 1): 9- 15. ##7]. Van Duijkeren E, Wolfhagen MJ, Box AT, Heck ME, Wannet WJ, Fluit AC. Human-to-dog transmission of methicillin-resistant Staphylococcus aureus. Emerge Infect Dis. 2004;1 0(12): 2235-237. ##8]. Perez LR, Dias C, Azevedo PA. Agar dilution and agar screen with oxacillin: what is known and what is unknown in detection of MRSA. Journal of Medical Microbiology 2008;57(8): 954-956. ##9]. Gunawardena ND, Thevanesam V, Kanakaratne N, Abeysekera D, Ekanayake A, Perera N. Molecular identification of methicillin resistance and virulence marker in staphylococcus aureus. Sri Lankan J infect Dis.2012;2(2): 18-29. ##10]. Vandenesch F, Naimi T, Enright MC, Lina G, Nimmo GR, Heffernan H, et al. Community acquired methicillin-resistant Staphylococcus aureus carrying Panton-Valentine leukocidin genes: worldwide emergence. Emerge Infect Dis. 2003;9(8): 978-84. ##11]. De Carvalho MJ, Pimenta FC, Hayashida M, Gir E, da Silva AM, Barbosa CP, et al. Prevalence of methicillin-resistant and methicillin susceptible S. aureus in the saliva of health professionals. Clinics (Sao Paulo). 2009;64(4): 295-302. ##12]. Baba-Moussa L, Sina H, Scheftel JM, Moreau B, Sainte-Marie D. Staphylococcal Panton- Valentine Leucocidin as a Major Virulence Factor Associated to Furuncles. PLOS ONE. 2011;6(10); 25716. ##13]. Ito T, Katayama Y, Asada K, Mori N, Tsutsumimoto K, Tiensasitorn C, et al. Structural comparison of three types of staphylococcal cassette chromosome mec integrated in the chromosome in methicillinresistant Staphylococcus aureus. Antimicrob Agents Chemother.2001;45 (12): 1323 -326. ##14]. Deurenberg R, Vink C, Kalenic S, Friedrich A, Bruggeman C, Stobberingh E. The molecular evolution of methicillin-resistant Staphylococcus aureus. Clinical Microbiology and Infection. 2007;13(3): 222-35. ## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>The Relationship between Thyroid Hormone Levels and Body Iron Status in Iranian Hypothyroidism Patients</TitleF>
		<TitleE>-</TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>1</Language_ID>
			<CONTENT>-</CONTENT>
			</ABSTRACT>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Backgrounds and Aims: Thyroid hormones have a crucial physiological role to maintain balance of metabolism of body. Thyroid hormones have an important role in metabolism and proliferation of blood cells. Thyroid gland also has a vital influence on erythropoiesis by induction of erythropoietin secretion and proliferation of erythroid progenitors. In the present study, it was tried to evaluate the effect of hypothyroidism on hematological parameters and also body iron store.

Materials and Methods: The research population consisted of 90 subjects divided into two groups: 45 people with hypothyroidism and 45 age-matched healthy individuals. This study checked the amounts of total triiodothyronine (T3), total thyroxine (T4), thyroid stimulating hormone (TSH), and some iron status and hematological parameters.

Results: The mean TSH levels were significantly increased in hypothyroid patients compared to control group. On the other hand, the levels of T4 and total iron binding capacity, serum iron, ferritin, Hemoglobin, and Hematocrit were significantly lower in hypothyroid patients compared to control group (p&#60;0.05). However, there was no significant difference in the mean of T3 between hypothyroidism and control.

Conclusion: Our data suggest that alterations in thyroid status change serum iron metabolism and hematological index. Hypothyroidism is often associated with anemia,depleted body iron store. As there is no significant clinical manifestation of hypothyroidism at earlier stages with anemia, it is advisable to routinely investigate it for early detection allowing its early management.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>176</FPAGE>
			<TPAGE>184</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2016/11/22016/11/92016/11/92016/11/92016/11/13
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1395/8/23
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2016/11/22016/11/92016/11/92016/11/92016/11/13
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1395/8/23
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Niko</Name>
				<MidName></MidName>
				<Family>Rostaei Rad</Family>
				<NameE>Niko</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Rostaei Rad</FamilyE>
				<Organizations>
				<Organization>Department of Clinical Biochemistry, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Mahmood</Name>
				<MidName></MidName>
				<Family>Vakili</Family>
				<NameE>Mahmood</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Vakili</FamilyE>
				<Organizations>
				<Organization>Department of Community Medicine, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran. 3Department</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Javad</Name>
				<MidName></MidName>
				<Family>Zavar-reza</Family>
				<NameE>Javad</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Zavar-reza</FamilyE>
				<Organizations>
				<Organization>Department of Clinical Biochemistry, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Sona</Name>
				<MidName></MidName>
				<Family>Rezaie</Family>
				<NameE>Sona</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Rezaie</FamilyE>
				<Organizations>
				<Organization>Department of Clinical Biochemistry, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Ahmad Reza</Name>
				<MidName></MidName>
				<Family>Shirvani</Family>
				<NameE>Ahmad Reza</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Shirvani</FamilyE>
				<Organizations>
				<Organization>Department of Clinical Laboratory Sciences, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Ferritin</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Hyperthyroidism</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Serum iron</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>TIBC</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF> ##1]. Guerrero A, Pamplona R, Postero-Otin M, López-Torres M. Effect of thyroid status on lipid composition and peroxidation in the mouse liver. Free Rad Biol Med. 1999; 26(1-2): 73-80.  ##2]. Chu JY, Monteleone JA, Peden VH, Graviss ER, Vernava AM. Anemia in children and adolescents with hypothyroidism. Clin Pediatr  ##Phila]. 1981; 20 (11): 696-99.  ##3]. Franzese A, Salemo M, Argenziano A, Buongiovanni C, Limauro R, Tenore A. Anemia in infants with congenital hypothyroidism diagnosed by neonatal screening. J Endocrinol Invest. 1996;19(9): 613-19.  ##4]. Lippi G, Montagnana M, Salvagno GL, Guidi GC. Should women with abnormal serum thyroid stimu-lating hormone undergo screening for Anaemia? Arch Pathol Lab Med. 2008; 132(3): 321- 22.  ##5]. Leedman JP, Stein AR, Chin WW, Rogers JT. Thyroid Hormone Modulates the Interaction between Iron Regulatory Proteins and the Ferritin mRNA Iron-responsive Element. the journal of biological chemistry 1996;271(20): 12017–2023.  ##6]. Levenson CW, Fitch CA. Affect of altered thyroid hormon status on rat brain ferritin H and ferritin L mRNA during postnatal development, Develop .Brain Res. 2000; 119(1): 105-109.  ##7]. Bothwell TH, Charlton RW, Cook JB, Finch CA. Iron metabolism in man. Oxford: Blackwell Scientific, 1979;20-39.  ##8]. Dallman PR, Beutler E, Finch CA. Effects of iron deficiency exclusive of anaemia. Br J Haematol. 1978; 40(2): 179-184.  ##9]. Zwirska-Korczala K, Buntner B, Sobieraj H, Ostrowska Z, Kniazewski B, Swietochowska E. Serum ferritin, iron and transferrin in women with thyrotoxicgraves' disease before and after methimazole treatment Acta Physiol. 1990; 41(7): 163-168.  ##10]. Sakata S, Nagai K, Maekawa H, Kimata Y, Komaki T, Nakamura S, et al. Serum ferritin concentration in subacute thyroiditis Metabolism 1991; 40(7): 683-88.  ##11]. Lingidi JL, Mohapatra E, Zephy D, Kumari S. Serum Lipids and Oxidative Stress in Hyporthyrodism. Journal of Advance Researches in Biological Sciences 2013; 5 (1): 63-66.  ##12]. Mackenzie GM. Anemia in hypothyroidism. JAMA. 1926; 86(7): 462-64.  ##13]. Fein HG, Rivlin RS. Anemia in thyroid diseases. Med Clin North Am.1975;59(5): 1133- 145.  ##14]. Lima CS, ZantutWittmann DE, Castro V, Tambascia MA, Lorand-Metze I, Saad ST, et al. Pancytopenia in untreated patients with Graves' disease. Thyroid 2006; 16 (4): 403-409.  ##15]. Kawa MP, Grymuła K, Paczkowska E, Baśkiewicz-Masiuk M, Dąbkowska E, Koziołek M, et al. Clinical relevance of thyroid dysfunction in human haematopoiesis: biochemical and molecular studies. Eur J Endocrinol. 2010; 162(2): 295-305.  ##16]. Golde DW, Bersch N, Chopra IJ, Cline MJ. Thyroid hormones stimulate erythropoiesis in vitro. Br J Haematol. 1977; 37(2): 173-77.  ##17]. Das KC, Mukherjee M, Sarkar TK, Dash RJ, Rastogi GK. Erythropoiesis and erythropoietin in hypo-and hyperthyroidism. J Clin Endocrinol Metab. 1975; 40(2): 211-20.  ##18]. Dorgalaleh A, Mahmoodi M, Varmaghani B, Kiani node F, Saeeidi Kia O, Alizadeh Sh, et al. Effect of Thyroid Dysfunctions on Blood Cell Count and Red Blood Cell Indice, Iranian Journal of Pediatric Hematology Oncology, 2012; 3(2): 73-77.  ##19]. Geetha J, Srikrishna R. Role of red blood cell distribution width (rdw) in thyroid dysfunction. Int J Biol Med Res.2012;3(2): 1476-478.  ##20]. Kubota K., Kurabayashi H., Tamura J, Kawada E, Tamura K, Nagashima K, et al. Change in the thyroid function by use of deferoxamine in a patient with hemochromatosis complicated by hyperthyroidism. J Med. 1992;23(1):75-7.  ##21]. Seven A, Toktamis N, Hacibekiroglu M, Candan G, Yigit G, Hatemi S. et al. Fe parameters and erythrocytic parameters in experimental hypothyroidism Biocem Soc Transact. 1993;21: 224-35.  ##22]. Winkleman JC, Mariash CN, Towle HC, Oppenheimer JH. Thyroidectomy increases rat hepatic ferritin iron. Science 1981;213(4507): 569- 71.  ##23]. Jump DB, Mariash CN, Oppenheimer JH. Evidence for post-transcriptional effects of T3 on hepatic ferritin synthesis. Biochem Biophys Res Commun. 1982;104(2): 701-707.  ##24]. Deshpande UR, Nadkarni GD. Relation between thyroid status and ferritin metabolism in rats. Thyroidology 1992;4(3): 93-7.  ##25]. Iwasa Y, Aida K, Yokomori N, Inoue M, Onaya T. Transcriptional regulation of ferritin heavy chain messenger RNA expression by thyroid hormone. Biochem Biophys Res Commun. 1990;167(3): 1279-285.  ##26]. Macaron CI, Macaron ZG. Increased serum ferritin levels of hyperthyroidism. Ann Int Med. 1982;96(5): 617-18.  ##27]. Van de Vyver FL, Blockx PP, Van den Bogaert WG, Bekaert JL. Serum ferritin levels in hyperthyroidism. Ann Int Med. 1982;97(6): 930- 31.  ##28]. Takamatsu J, Majima M, Miki K, Kuma K, Mozai T. Serum ferritin as a marker of thyroid hormone action on peripheral tissues. J Clin Endocrinol Metab. 1985;61(4): 672-76.  ##29]. Hashimoto T, Matsubara F. Changes in the tumor marker concentration in female patients with hyper-, eu-, and hypothyroidism. Endocrinol Jpn. 1989;36(6): 873–79.  ##30]. Kubota K, Tamura J, Kurabayashi, Shirakura T, Kobayashi. Evaluation of increased serum ferritin levels in patients with hyperthyroidism. Clin Invest. 1993;72(1): 26-9.  ##31]. Perrin MC, Blanchet JP, Mouchiroud G. Modulation of human and mouse erythropoiesis by thyroid hormone and retinoic acid: evidence for specific effects at different steps of the erythroid pathway. Hematol Cell Ther.1997;39(1): 19-26.  ##32]. Cinemre H, Bilir C, Gokosmanoglu F, Bahcebasi T. Effects of Levothyroxine in Iron- Deficient Subclinical Hypothyroid Patients:A Randomized, Double-Blind, Controlled Study. J Clin Endocrinol Metab.2009;94(1):151-56.  ##33]. Duntas LH, Papanastasiou L, Mantzou E, Koutras DA. Incidence of sideropenia and effects of iron repletion treatment in women with subclinical hypothyroidism. Exp Clin Endocrinol Diabetes. 1999;107(6): 356–60.  ##34]. Christ-Crain M, Meier C, Huber P, Zulewski H, Staub JJ, Müller B. Effect of restoration of euthyroidism on peripheral blood cells and erythropoietin in women with subclinical hypothyroidism. Hormones (Athens) 2003; 2(4):237-42.  ##35]. Touam M, Gue´ry B, Goupy C, Menoyo V, Drüeke T. Hypothyroidism and resistance to human recombinant erythropoietin. Nephrol Dial Transplant 2004; 19(4): 1020-1021. ## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Frequency of Polymorphism Alu Insertion in Progesterone Receptor Gene in Endometriosis</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Background and Aims: This research aimed to study a possible link between endometriosis and polymorphism of the progesterone receptor gene.

Materials and Methods: The control group consisted of 86 women without endometriosis and the case group comprised 86 patients with a diagnosis of endometriosis by laparoscopy. Genotypes for Alu insertion polymorphisms (A1/A1, A1/A2 and A2/A2) were described by polymerase chain reaction and determined on a 2% agarousegel.

Results: The genotype frequencies of A1/A2 and A2/A2 were not significantly higher in patients than in the control group without endometriosis. On the other hand differences in the Alu insertion polymorphism frequencies were not significant.

Conclusion: According to our investigations, we conclude that there is not a significant correlation between Alu insertion polymorphism and endometriosis. ;line-height:115%&#39;&#62; According to our investigations, we conclude that there is not a significant correlation between Alu insertion polymorphism and endometriosis.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>185</FPAGE>
			<TPAGE>190</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2016/11/22016/11/92016/11/92016/11/92016/11/132016/11/13
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1395/8/23
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2016/11/22016/11/92016/11/92016/11/92016/11/132016/11/13
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1395/8/23
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Mohammad</Name>
				<MidName></MidName>
				<Family>Ataei</Family>
				<NameE>Mohammad</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Ataei</FamilyE>
				<Organizations>
				<Organization>Department of Medical Genetics, International Campus, Shahid Sadoughi University of Medical Science, Yazd, Iran.</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Ehsan</Name>
				<MidName></MidName>
				<Family>Farashahi</Family>
				<NameE>Ehsan</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Farashahi</FamilyE>
				<Organizations>
				<Organization>Department of Medical Genetics, Faculty of Medicine, Shahid Sadoughi University of Medical Science,Yazd, Iran.</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Morteza</Name>
				<MidName></MidName>
				<Family>Seifati</Family>
				<NameE>Morteza</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Seifati</FamilyE>
				<Organizations>
				<Organization>Department of Genetics, Islamic Azad University, Ashkezar Branch,Yazd, Iran.</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Nasrin</Name>
				<MidName></MidName>
				<Family>Ghasemi</Family>
				<NameE>Nasrin</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Ghasemi</FamilyE>
				<Organizations>
				<Organization>Recurrent Abortion Research Centre, Reproductive Sciences Institute, Shahid Sadoughi University of Medicinal Sciences, Yazd, Iran.</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Endometriosis</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Polymerase chain reaction</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Progesterone receptor gene</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF> 1]. Smarr MM, Kannan K, Buck Louis GM. Endocrine disrupting chemicals and endometriosis. Fertil Steril. 2016;106(4): 959-66.  ##2]. Rahmioglu N, Fassbender A, Vitonis AF, Tworoger SS, Hummelshoj L, D'Hooghe TM, et al. World Endometriosis Research Foundation Endometriosis Phoneme and Bio banking Harmonization Project: III. Fluid bio specimen collection, processing, and storage in endometriosis research. Fertil Steril. 2014; 102(5): 1233-243.  ##3]. Allaire C. Endometriosis and infertility:a review. J Reprod Med.2006;51(3): 164-68.  ##4]. Kvaskoff M, Mu F, Terry KL., Harris HR, Poole EM, Farland L, et al.Endometriosis: a high-risk population for major chronic diseases? Hum Reprod Update. 2015;21(4): 500-16.  ##5]. Olson JE, Cerhan JR, Janney CA, Anderson KE, Vachon CM, Sellers TA. Postmenopausal cancer risk after self-reported endometriosis diagnosis in the Iowa Women's Health Study. Cancer 2002; 94(5): 1612-618.  ##6]. Palep-Singh M, Gupta S. Endometriosis: associations with menopause, hormone replacement therapy and cancer. Menopause Int. 2009;15 (4): 169-74.  ##7]. Gupta S, Goldberg JM, Aziz N, Goldberg E, Krajcir N, Agarwal A. Pathogenic mechanisms in endometriosis –associated infertility. Fertile Steril. 2008; 90(2): 247-57.  ##8]. ASRM. Endometriosis and infertility. Fertil Steril. 81: 1441-446.  ##9]. Sains de la Cuesta R, Eichhorn JH, Rice LW, Fuller AF Jr. Histologic Transformation of benign endometriosis to early epithelial ovarian Cancer. Gynecol oncol. 1966;60(2): 238-44.  ##10]. Sanchez AM, Somigliana E, Vercellini P, Pagliardini L, Candiani M, Vigano P. Endometriosis as a detrimental condition for granulose cell steroid genesis and development: From molecular alterations to clinical impact. J Steroid Biochem Mol Biol. 2016;155(Pt A): 35- 46.  ##11]. Silva KS, Moura KK. Genetic polymorphisms in patients with endometriosis: an analytical study in Goiania (Central West of Brazil). Genet Mol Res. 2016;15(2).  ##12]. Romano A, Delvoux B, Fischer DC, Groothuis P. The PROGINS polymorphism of the human progesterone receptor diminishes the response to progesterone. J Mol Endocrinol. 2007;38(1-2): 331-50.  ##13]. Bischoff F, Simpson JL. Genetics of endometriosis: heritability and candidate genes. Best Pract Res Clin Obstet Gynaecol.2004; 18(2): 219-32.  ##14]. Donaldson CJ, Crapanzano JP, Watson JC, Levine EA, Batzer MA. PROGINS Alu insertion and human genomic diversity. Mutat Res. 2002;501(1-2): 137-41.  ##15]. Rowe SM, Coughlan SJ, McKenna NJ, Garrett E, Kieback DG, Carney DN, et al. Ovarian carcinoma-associated Taqi restriction fragment length polymorphism in intron G of the progesterone receptor gene is due to an Alu sequence insertion. Cancer Res.1995; 55(13): 2743-745.  ##16]. Agoulnik IU, Tong XW, Fischer DC, Körner K, Atkinson NE, Edwards DP, et al. A germ line variation in the progesterone receptor gene increases transcriptional activity and may modify ovarian cancer risk. J Clin Endocrinal Metab. 2004;89(12): 6340-347.  ##17]. Romano A, Delvoux B, Fischer DC, Groothuis P. The PROGINS polymorphism of the human progesterone receptor diminishes the response to progesterone. J Mol Endocrinal. 2007;38(1-2): 331-50.  ##18]. Pijnenborg JM, Romano A, Dam-de Veen GC, Dun Selman GA, Fischer DC, Groothuis PG, et al. Aberrations in the progesterone receptor gene and the risk of recurrent endometrial carcinoma. Journal of Pathology 2005;205(5): 597-605.  ##19]. Romano A, Lindsey PJ, Fischer DC, Delvoux B, Paulussen AD, Janssen RG, et al. Two functionally relevant polymorphisms in the human progesterone receptor gene (+331 G/A and progins) and the predisposition for breast and/or ovarian cancer. Gynecologic Oncology 2006;101(2): 287-95.  ##20]. Pearce CL, Hirschhorn JN, Wu AH, Burtt NP, Stram DO, Young S, et al. Clarifying the PROGINS allele association in ovarian and breast cancer risk: a haplotype-based analysis. J. Natl. Cancer Inst. 2005;97(1): 51-59.  ##21]. Costa IR, Silva RC, Frare AB, Silva CT, Bordin BM, Souza SR, et al.Polymorphism of the progesterone receptor gene associated with endometriosis in patients from Goiás, Brazil. Genet Mol Res. 2011;10(3): 1364-370.  ##22]. Osti C., Biscione A., Morgante G., Bifulco G., Luisi S., and Petraglia F. 2016. Hormonal therapy for endometriosis: from molecular research to bedside. Eur J Obstet Gynecol Reprod Biol. 2016; pii: S0301-2115(16)30250-0.  ##23]. Teng SW, Horng HC, Ho CH, Yen MS, Chao HT,Wang PH. Taiwan Association of Gynecology Systematic Review Group. Women with endometriosis have higher comorbidities: Analysis of domestic data in Taiwan. J Chin Med Assoc. 2016;79(11): 577-82. M. Ataei et al. International Journal of Medical Laboratory 2016; 3(3): 185-190. 190  ##24]. Berlanda N, Somigliana E, Frattaruolo MP, Buggio L, Dridi D, Vercellini P. Surgery versus hormonal therapy for deep endometriosis: is it a choice of the physician? Eur J Obstet Gynecol Reprod Biol. 2016: pii: S0301-2115(16)30845- 4.  ##25]. Abrao MS, Gonçalves MO, Dias JA Jr, Podgaec S, Chamie LP, Blasbalg R.Comparison between clinical examination, transvaginal solography and magnetic resonance imaging for the diagnosis of deep endometriosis. Hum Reprod.2007;22(12): 3092-97.  ##26]. Vahdat M, Sariri E, Kashanian M, Najmi Z, Mobasseri A, Marashi M, et al.Can combination of hysterosalpingography and ultrasound replace hysteroscopy in diagnosis of uterine malformations in infertile women? Med J Islam Repub Iran. 2016;30: 352.  ##27]. Ejzenberg D, Podgaec S, Dias JA Jr, de Oliveira RM, Baracat EC, Abrão MS. Measurement of serum and peritoneal levels of amyloid protein A and their importance in the diagnosis of pelvic endometriosis. J Reprod Med. 2013;58(9-10): 411-16.  ##28]. Zondervan KT, Rahmioglu N, Morris AP, Nyholt DR, Montgomery GW, Becker CM, et al. Beyond Endometriosis Genome-Wide Association Study: From Genomics to Phonemics to the Patient. Semin Reprod Med. 2016;34(4): 242-54.  ##29]. Ricci MS, Toscano DG, Toscano WA Jr. ECC-1 human endometrial cells as a model system to study dioxin disruption of steroid hormone function. In Vitro Cell Dev Biol Anim. 1999;35(4): 183-89.  ##30]. Lattuada D, Somigliana E, Viganò P, Candiani M, Pardi G, Di Blasio AM.Genetics of endometriosis: a role for the progesterone receptor gene polymorphism PROGINS? Clin Endocrinol (Oxf). 2004;61(2): 190-94.  ##31]. Wieser F, Schneeberger C, Tong D, Tempfer C, Huber JC, Wenzl R. PROGINS receptor gene polymorphism is associated with endometriosis. Fertil Steril. 2002;77(2):309-12.  ##32]. Carvalho CV, D'Amota P, Sato H, Girao MJBC, Lima GRd, Silva ICDG, et al. Polimorfismo de gene do receptor de progester. One (PROGINS) emmulheres Com endometrioses pe’lvica.R B G O. 2004;26(8): 613-17.  ##33]. Govindan S, Ahmad SN, Vedicherla B, Kodati V, Jahan P, Rao KP, et al. Association of progesterone receptor gene polymorphism (PROGINS) with endometriosis, uterine fibroids and breast cancer. Cancer Bio mark. 2007;3(2): 73-78  ##34]. Treloar SA, Zhao ZZ, Armitage T, Duffy DL, Wicks J, O'Connor DT, et al. Association between polymorphisms in the progesterone receptor gene and endometriosis. Mol Hum Reprod.2005; 11(9): 641-47.  ##35]. Van Kaam KJ, Romano A, Schouten JP, Dun Selman GA, Groothuis PG. Progesterone receptor polymorphism +331G/A is associated with a decreased risk of deep infiltrating endometriosis.Hum Reprod. 2007;22(1): 129- 35.  ##36]. Gimenes C1, Bianco B, Mafra FA, Rosset V, Christofolini DM, Barbosa CP.The progins progesterone receptor gene polymorphism is not related to endometriosis-associated infertility or to idiopathic infertility. Clinics (Sao Paulo). 2010;65(11): 1073-76. ## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Prevalence of Brucella Species in Raw Milk Produced in the Industrial and Traditional Production Units in Yazd</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Backgrounds and Aims: Healthy milk and dairy products are important in human nutrition&#160; because of the high value of the food. Contaminated raw milk is the mainly way of transmition of brucellosis to humans.Unpasteurized milk and dairy products can contagion to human and cause mallta fever. So brucellosis is an important zoonotic disease in human and animals especially domestic animals. The aim of this study is determining the contamination of traditional and industrial cow and sheep milk to brucella spp in Yazd.

Materials and Methods: Totally 198 raw milk samples were randomly cultured in three months period from the units of distribution supply of the milk centers at diffrenet regions in yazd, examined by special brucella agar,species identification was performed&#160; by Gram stain, and growth in the presence of aniline dyes, hydrogen sulfide production, and urease test.

Results: Five samples (2.52%) were positive, 4 samples (2.02%) of Brucella.abortus and 1 sample (0.5%) of Brucella.melitensis were confirmed out of 198 cultured milk samples.

Conclusions: The results show the seriousness of the brucllosis transmission to human (Malta fever) through raw and unpasteurized milk.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>191</FPAGE>
			<TPAGE>197</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2016/11/22016/11/92016/11/92016/11/92016/11/132016/11/132016/11/21
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1395/9/1
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2016/11/22016/11/92016/11/92016/11/92016/11/132016/11/132016/11/21
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1395/9/1
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Farideh</Name>
				<MidName></MidName>
				<Family>Jamali</Family>
				<NameE>Farideh</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Jamali</FamilyE>
				<Organizations>
				<Organization>Department of Biology, Islamic Azad University, Ashkezar Branch, Iran.</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Sahar-sadat</Name>
				<MidName></MidName>
				<Family>Emadi</Family>
				<NameE>Sahar-sadat</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Emadi</FamilyE>
				<Organizations>
				<Organization>Department of Microbiology, Faculty of Medicine,Shahid Sadoughi University of Medical Sciences,Yazd, Iran.</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Ahmad</Name>
				<MidName></MidName>
				<Family>Mosadegh</Family>
				<NameE>Ahmad</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Mosadegh</FamilyE>
				<Organizations>
				<Organization>Department of Microbiology, Faculty of Medicine,Shahid Sadoughi University of Medical Sciences,Yazd, Iran.</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Brucella</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Malta fever</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Yazd</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>1]. Najwa GhR, Mullah Shirmohammadi H, Hashemi M.Brucellosis epidemiological pattern and found disease in the Shahrood city, Fourth National Conference brucellosis.2011.   ##2]. Ragona G, Corrias F, Benedetti M, Paladini M, Salari F, Altomonte L, et al. Amiata donkey milk chain: Animal health evaluation and milk quality. Ital J Food Saf. 2016; 5(3): 5951.  ##3]. Azar D, Khosrav ,A, Abassi E, Alavi SM. Isolation of Brucella Melitensis and Brucella Abortus from Brucelosis Patients by Conventional Culture Method and Polymerase Chain Reaction Technique. Pakistan Journal of Medicine Science 2006;22(4):396-400.  ##4]. Doosti A, Ghasemidehkordi P. Application of real-time PCR for identification and differentiation of Brucella abortus and Brucella melitensisin cattle. Bulgarian Journal of Veterinary Mmedicine 2011;14(2):109-115.  ##5]. Izadi A, Moslemi A. Study and Molecular identification brucella spp in dairy products by Nested per techniques. New Cellular and Molecular Biotechnology Journal 2011; 3(11): 91-8.  ##6]. Franco MP, Mulder M, Gilman RH, Smits HL.Human brucellosis. Lancet Infect Dis. 2007;7(12):775-86.  ##7]. Cloeckaert A, Verger JM, Garyon M, Grépinet O. Restriction site polymorphism of the genes encoding the major 25 and 36kDa outermembrane proteins of Brucella. Microbiology 1995;141: 2111-121.  ##8]. Ilhan Z , Keskin O, sareyyupoglu B, Kokcu L, Akan M.Bir sigircilik isletmesinde Brucella salgini. Ankara universitesi Vetteriner Fakultesi Dergisi.1999;46(2-3): 257-262.  ##9]. Khamiri M, Ghasemianfard M. Compare the microbial quality of raw milk produced in the traditional and industrial livestock farming in gorgan. 16th National Congress of Food Industries. 2007.  ##10]. Alavi SM, Motlagh ME. A Review of Epidemiology, Diagnosis and Management of Brucellosis for General Physicians Working in the Iranian Health Network. Jundishapour J Microbial. 2012;5(2):384-87.  ##11]. Gul ST, Khan A. Epidemiology and epizoology of brucellosis: A Review. Pakistan Vet. J. 2007; 27(3): 145-51.  ##12]. Kazemi B, Yousefi Nmin SA, Dowlatshahi M, Bandepour M, Kafilzade F, Gachkar L, et al. Detection Of Brusella by Peripheral Blood PCR and Comparison With Culture and Serological Methods in Suspected Cases. Iranian J Publ Health 2008; 37(4):96-102.  ##13]. Esmaeli H, Khanjari A, Mohammadian MR .Frequency of brucella in milk samples of sheep and goat with history of abortion in some provinces of Iran. Iranian Journal of Veterinary Clinical Sciences 2012;6(2):65-70.  ##14]. Mohsenzade M, Ghazvini K, Noorani H. Prevalence of Brucella in raw milk supply and its effect on public health in mashhad. Horizon Science, Journal of faculty Medical Sciences, Gonabad. 2004;l9(2): 80-84.  ##15]. Mert A. Ankara yöresinde pazarlanan taze beyaz peynirlerde Brucella'ların varlığı üzerinde araştırmalar. Doktora Tezi. A.U. Sağ Bilim Enst. Ankara 1984. ## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Effect of Lactobacillus delbrueckii on Blood Sugar in Diabetic Mice</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Background and Aims: Probiotics are defined as live microorganisms that are beneficial to human health. Probiotics are commonly found in some foods such as dairy products or complementary tablets. A recent research shows that probiotics have a significant role in diabetes type 1 and 2 treatment. Among the variety of lactic acid bacteria, Lactobacillus strains are well known in probiotics for their different properties. The aim of this study is to investigate the effect of Lactobacillus delbrueckii PTCC1057 on diabetic mice blood sugar.

Materials and Methods: sample mice were selected from the age range of 6 to 8 weeks. Then for converting the normal mouse to diabetic type, 180 mg/kg streptozotocin was injected intraperitoneally. 10 days later, the blood sugar of the mice was measured and the mice with higher than 200 mg/dl of blood sugar were considered as diabetic mice. Finally, the diabetic mice were divided into two groups of experimental and control for next investigation. For a survey of probiotics effect on blood sugar, an amount of 3&#215;106 CFU of L. delbrueckii was fed by gavage feeding approach daily during 4 weeks and the blood sugar level was determined at the end of the week after streptozotocin injection.

Results: the result showed that the diabetic mice blood sugar level significantly decreased conspicuously by feeding L. delbrueckii in comparison to diabetic control group.

Conclusion: The result of this study suggests that L. delbrueckii can be impressive in diabetes treatment. However, another clinical study is needed for proving the exact effect of this probiotic on diabetes.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>198</FPAGE>
			<TPAGE>204</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2016/11/22016/11/92016/11/92016/11/92016/11/132016/11/132016/11/212016/11/21
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1395/9/1
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2016/11/22016/11/92016/11/92016/11/92016/11/132016/11/132016/11/212016/11/21
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1395/9/1
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Reza Dolatyari</Name>
				<MidName></MidName>
				<Family>Eslami</Family>
				<NameE>Reza Dolatyari</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Eslami</FamilyE>
				<Organizations>
				<Organization>Department of Microbiology, Higher Education Institute of Rabe Rashid, Tabriz, Iran.</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Asghar</Name>
				<MidName></MidName>
				<Family>Tanomand</Family>
				<NameE>Asghar</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Tanomand</FamilyE>
				<Organizations>
				<Organization>Department of Microbiology, Maragheh University of Medical Sciences, Maragheh,Iran.</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Jamal</Name>
				<MidName></MidName>
				<Family>Hallajzadeh</Family>
				<NameE>Jamal</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Hallajzadeh</FamilyE>
				<Organizations>
				<Organization>Department of Microbiology, Maragheh University of Medical Sciences, Maragheh,Iran.</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Mehdi</Name>
				<MidName></MidName>
				<Family>Ariana</Family>
				<NameE>Mehdi</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Ariana</FamilyE>
				<Organizations>
				<Organization>Department of Microbiology, University of Tehran, Tehran, Iran.</Organization>
				</Organizations>
				<Countries>
				<Country>Iran</Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Diabetic mice</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Lactobacillus delbrueckii</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Probiotic</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
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