<?xml version="1.0" encoding="utf-8"?>
<XML>
<JOURNAL>
<YEAR>2015</YEAR>
<VOL>19</VOL>
<NO>4</NO>
<MOSALSAL>59</MOSALSAL>
<PAGE_NO>284</PAGE_NO>


<ARTICLES>

	<ARTICLE> 
		<TitleF>Dissimilar mechanistic background of peripheral and orofacial hyperkinesia in patients with Parkinson’s disease and levodopa-induced dyskinesia</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: Long-term levodopa treatment of Parkinson&#8217;s disease (PD) is frequently complicated by spontaneously occurring involuntary muscle movements called dyskinesia. The exact pathological mechanism of this complication has not yet been elucidated. We have previously demonstrated that in PD patients the vulnerability to develop peripheral but not orofacial dyskinesia is associated with the presence of two variants of the GRIN2A gene. Moreover, we have shown that in tardive dyskinesia (TD) orofacial dyskinesia is associated with other polymorphisms as compared with peripheral dyskinesia. In the present study we investigate whether the peripheral versus orofacial nature of levodopa-induced dyskinesia (LID) in PD can be explained by considering polymorphisms for dopaminergic and serotonergic receptors.&#160;Materials and Methods: 101 Russian patients with PD (38M/63F) were examined. Genotyping was carried out on 19 SNPs for 3 neurotransmitter genes: 10 SNPs for DRD3 gene (rs11721264, rs167770, rs3773678, rs963468, rs7633291, rs2134655, rs9817063, rs324035, rs1800828, rs167771), 1 SNP for DRD4 gene (rs3758653), and 8 SNPs for HTR2C gene (rs6318, rs5946189, rs569959, rs17326429, rs4911871, rs3813929, rs1801412, rs12858300).&#160;Results: Genotyping patients with PD and LID revealed that only rs3773678 (DRD3, dominant, p = 0.042) was associated with orofacial dyskinesia.&#160;Conclusion: The findings of the current study are not related to LID in PD itself, but to other forms of orofacial dyskinesia in this patient group.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>216</FPAGE>
			<TPAGE>221</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2015/10/18
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1394/7/26
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2015/12/11
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1394/9/20
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Svetlana A</Name>
				<MidName></MidName>
				<Family>Ivanova</Family>
				<NameE>Svetlana A</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Ivanova</FamilyE>
				<Organizations>
				<Organization>Mental Health Research Institute, Tomsk, Russian Federation</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>svetlana@mail.tomsknet.ru</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Olga Yu</Name>
				<MidName></MidName>
				<Family>Fedorenko</Family>
				<NameE>Olga Yu</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Fedorenko</FamilyE>
				<Organizations>
				<Organization>Mental Health Research Institute, Tomsk, Russian Federation</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>f_o_y@mail.ru</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Maxim B</Name>
				<MidName></MidName>
				<Family>Freidin</Family>
				<NameE>Maxim B</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Freidin</FamilyE>
				<Organizations>
				<Organization>Research Institute for Medical Genetics, Tomsk, Russian Federation</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>mfreidin@medgenetics.ru</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Valentina M</Name>
				<MidName></MidName>
				<Family>Alifirova</Family>
				<NameE>Valentina M</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Alifirova</FamilyE>
				<Organizations>
				<Organization>Department of Neurology and Neurosurgery, Siberian State Medical University, Tomsk, Russian Federation</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>alifirova@mail2000.ru</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Natalia G</Name>
				<MidName></MidName>
				<Family>Zhukova</Family>
				<NameE>Natalia G</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Zhukova</FamilyE>
				<Organizations>
				<Organization>Department of Neurology and Neurosurgery, Siberian State Medical University, Tomsk, Russian Federation</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>znatali@yandex.ru</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Irina A</Name>
				<MidName></MidName>
				<Family>Zhukova</Family>
				<NameE>Irina A</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Zhukova</FamilyE>
				<Organizations>
				<Organization>Department of Neurology and Neurosurgery, Siberian State Medical University, Tomsk, Russian Federation</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>irzhukova@inbox.ru</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Asmar FY</Name>
				<MidName></MidName>
				<Family>Al Hadithy</Family>
				<NameE>Asmar FY</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Al Hadithy</FamilyE>
				<Organizations>
				<Organization>Department of Pharmacotherapy and Pharmaceutical Care, University of Groningen, Groningen, The Netherlands</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>a.alhadithy@parnassiabavogroep.nl</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Jacobus RBJ</Name>
				<MidName></MidName>
				<Family>Brouwers</Family>
				<NameE>Jacobus RBJ</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Brouwers</FamilyE>
				<Organizations>
				<Organization>Department of Pharmacotherapy and Pharmaceutical Care, University of Groningen, Groningen, The Netherlands</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>jrbjbrouwers@live.nl</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Nikolay A</Name>
				<MidName></MidName>
				<Family>Bokhan</Family>
				<NameE>Nikolay A</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Bokhan</FamilyE>
				<Organizations>
				<Organization>Mental Health Research Institute, Tomsk, Russian Federation</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>nikolay.bokhan.tomsk.russia@gmail.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Bob</Name>
				<MidName></MidName>
				<Family>Wilffert</Family>
				<NameE>Bob</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Wilffert</FamilyE>
				<Organizations>
				<Organization>Department of Pharmacotherapy and Pharmaceutical Care, University of Groningen, Groningen, The Netherlands</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>b.wilffert@rug.nl</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Anton JM</Name>
				<MidName></MidName>
				<Family>Loonen</Family>
				<NameE>Anton JM</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Loonen</FamilyE>
				<Organizations>
				<Organization>Department of Pharmacotherapy and Pharmaceutical Care, University of Groningen, Groningen, The Netherlands</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>a.j.m.loonen@rug.nl</Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Levodopa-induced dyskinesia</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Parkinson’s disease</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Dopaminergic receptors</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Serotonergic receptors</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Genetic variants</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>Al Hadithy AF, Ivanova SA, Pechlivanoglou P, Semke A, Fedorenko O, Kornetova E, Ryadovaya L, Brouwers JR, Wilffert B, Bruggeman R, Loonen AJ. Tardive dyskinesia and DRD3, HTR2A and HTR2C gene polymorphisms in Russian psychiatric inpatients from Siberia. Prog Neuropsychopharmacol Biol Psychiatry 33 (2009) 475-481.##Al Hadithy AF, Ivanova SA, Pechlivanoglou P, Wilffert B, Semke A, Fedorenko O, Kornetova E, Ryadovaya L, Brouwers JR, Loonen AJ. Missense polymorphisms in three oxidative-stress enzymes (GSTP1, SOD2, and GPX1) and dyskinesias in Russian psychiatric inpatients from Siberia. Hum Psychopharmacol 25 (2010) 84-91.##Arning L, Saft C, Wieczorek S, Andrich J, Kraus PH, Epplen JT. NR2A and NR2B receptor gene variations modify age at onset in Huntington disease in a sex-specific manner. Hum Genet 122 (2007) 175-182.##Bargiotas P, Konitsiotis S. Levodopa-induced dyskinesias in Parkinson\'s disease: emerging treatments. Neuropsychiatr Dis Treat 9 (2013) 1605-1617.##Cerasa A, Fasano A, Morgante F, Koch G, Quattrone A. Maladaptive plasticity in levodopa-induced dyskinesias and tardive dyskinesias: old and new insights on the effects of dopamine receptor pharmacology. Front Neurol 5 (2014) 1-5.##Del Sorbo F, Albanese A. Levodopa-induced dyskinesias and their management. J Neurol 2008; 255 (2008) 32-41.##Fahn S, Elton RL, UPDRS Development Committee. Unified Parkinson’s Disease Rating Scale. In: Fahn S, Marsden CD, Calne DB, Goldstein M, editors. Recent Developments in Parkinson’s Disease. Florham Park, NJ: Macmillan, 1987, pp. 153-163.##González JR, Armengol L, Solé X, Guinó E, Mercader JM, Estivill X, Moreno V. SNPassoc: an R package to perform whole genome association studies. Bioinformatics 23 (2007) 644-645.##Hoehn M, Jahr MD. Parkinsonism: onset, progression and mortality. Neurology 17 (1967) 427-442.##Hughes AJ, Daniel SE, Kilford L, Lees AJ. Accuracy of clinical diagnosis of idiopathic Parkinson’s disease. A clinico-pathological study of 100 cases.  J Neurol Neurosurg Psychiatry 55 (1992) 181-184.##Huot P, Johnston TH, Koprich JB, Fox SH, Brotchie JM. The pharmacology of L-DOPA-induced dyskinesia in Parkinson\'s disease.  Pharmacol Rev 65 (2013) 171-222.##Ivanova SA, Loonen AJ, Pechlivanoglou P, Freidin MB, Al Hadithy AF, Rudikov EV, Zhukova IA, Govorin NV, Sorokina VA, Fedorenko OY, Alifirova VM, Semke AV, Brouwers JR, Wilffert B. NMDA receptor genotypes associated with the vulnerability to develop dyskinesia. Transl Psychiatry 2 (2012) e67.##Loonen AJ,  Ivanova SA. New insights into the mechanism of drug-induced dyskinesia. CNS Spectr 18 (2013) 15-20.##Loonen A, Van Praag HM. Measuring movement disorders in antipsychotic drug trials: the need to define a new standard. J Clin Psychopharmacol 27 (2007) 423-430.##Schooler NR, Kane JM. Research diagnoses for tardive dyskinesia. Arch Gen Psychiatry 39 (1982) 486-487.##Sturrock A, Leavitt BR. The clinical and genetic features of Huntington disease. J Geriatr Psychiatry Neurol 23 (2010) 243-259.##Thanvi BR, Lo TC. Long term motor complications of levodopa: clinical features, mechanisms, and management strategies. Postgrad Med J 80 (2004) 452-458.##Thanvi B, Lo N, Robinson T. Levodopa-induced dyskinesia in Parkinson\'s disease: clinical features, pathogenesis, prevention and treatment. Postgrad Med J 83 (2007) 384-388.##Woerner MG, Kane JM, Lieberman JA, Alvir J, Bergmann KJ, Borenstein M, Schooler NR, Mukherjee S, Rotrosen J, Rubinstein M, et al. The prevalence of tardive dyskinesia. J Clin Psychopharmacol 11 (1991) 34-42.## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>A study of variation in cardiocirculatory parameters with different body positions during isometric exercise in young adult males.</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: To study the effects of exercise, how important it is to choose a posture? We aimed to characterize the possible impact of different body positions on cardiovascular parameters during and after sustained isometric handgrip (IHG) exercise.&#160;Materials and Methods: Cross sectional study was carried out in 33 young adult males (mean age: 19.21&#177;1.083 years). We recorded Blood Pressure (BP), Heart Rate (HR) and SpO2 at rest, 1st minute of exercise, at 3rd minute of exercise or prior to failure and at 2 minutes after IHG exercise at 30% of Maximum voluntary contraction (MVC) in sitting, supine and standing positions. Mean arterial pressure (MAP), Pulse pressure (PP) and Rate pressure product (RPP) were calculated from BP and HR data.&#160;Results: SBP, DBP, MAP, HR and RPP increased significantly during 1st and 3rd min of exercise and returned to resting level at 2 min after exercise in all three postures. During resting period and at 2 min after IHG exercise SBP and PP were significantly higher in supine compared with sitting and standing position, while DBP, HR and RPP were significantly increased in standing position. DBP, PP, MAP and HR changed significantly in supine, sitting and standing posture with time of exercise (two-way repeated measure ANOVA).&#160;Conclusion: IHG exercise leads to an across the board increase of all the cardiovascular parameters. The effect of posture was more pronounced at rest and during initial duration of exercise. Thus, posture may be a factor to consider in testing initial response during IHG exercise, but not for studying effects of prolonged duration of exercise.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>222</FPAGE>
			<TPAGE>231</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2015/10/182015/09/27
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1394/7/5
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2015/12/112016/01/9
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1394/10/19
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Viral I</Name>
				<MidName></MidName>
				<Family>Champaneri</Family>
				<NameE>Viral I</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Champaneri</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, Pacific Institute of Medical Sciences, Udaipur-Rajasthan, India</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>drviralchampaneri@gmail.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Rajesh</Name>
				<MidName></MidName>
				<Family>Kathrotia</Family>
				<NameE>Rajesh</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Kathrotia</FamilyE>
				<Organizations>
				<Organization>Department of Physiology, All India Institute of Medical Sciences, Rishikesh, Uttarakhand, India</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>rajeshkathrotia@gmail.com</Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Isometric handgrip exercise</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Body positions</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Blood pressure</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Heart rate</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Rate pressure product</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>1.	Van Dongen, H.P. et al, The cumulative cost of additional wakefulness: dose-response effects on neurobehavioral functions and sleep physiology from chronic sleep restriction and total sleep deprivation. Sleep 26 (2003) 117–126.##2.	W P Laird, D E Fixler and F D Haffines, Cardiovascular response to isometric exercise in normal adolescent. Circulation 59 (1979) 651-654.##3.	Helfant RH, Devilla MA, Meister SG, Effect of sustained isometric handgrip exercise on left ventricular performance. Circulation 44 (1971) 982.##4.	Fisher ML, Nutter DO, Jacobs W, Schlant RC, Haemodynamic responses to isometric exercise (handgrip) in patients with heart disease. Br Heart J 35 (1973) 422.##5.	Veronica m. Quarry and David h. Spodick. Cardiac Responses to Isometric Exercise. Comparative Effects with Different Post and Levels of Exertions. Circulation 49 (1974) 905-920.##6.	LIND AR, mcnicol GW. Circulatory responses to sustained hand-grip contractions performed during other exercise, both rhythmic and static. J Physiol (Lond) 192 (1967) 595.##7.	TUTTLE WW, HORV\'ATH SM. Comparison of effects of static and dynamic work on blood pressure and heart rate. J Appl Physiol 10 (1957) 294.##8.	SPODICK DH, QUARRY-PIGOTT VM, Effects of posture on exercise performance: Measurement of systolic intervals. Circulation 48 (1973) 74.##9.	Sagive M et al. Effect of body position on the afterload response during sustained exercise. J Sport Med Phy Fitness 32 (1992 Jan) 170-4.##10.	Don Melrose. Gender differences in cardiovascular response to isometric exercise in the seated and supine positions. JEP online 8 (2005) 29-35.##11.	Kodzo K.K., Mohammed J.  Kodzo P. Gender and Postural Differences in Cardiovascular Response to Hand Grip Exercise among Elderly Normotensives. AJPARS 5 (1&#38;2) (June 2013) 45-49. ##12.	Martin EC, Shaver JA, Leon DF Mark E. Thompson, Pesara S. Reddy, Leonard JL. Autonomic Mechanisms in Hemodynamic Responses to Isometric Exercise. J Clin Invest 54 (1974) 104–115.##13.	Clausen JP, Klausen B, Rasmussen, Trapjensen J. Central and peripheral circulatory Changes after training of the arms or legs. Am. J. Physiol 225 (1973) 675-682.##14.	Hietanen E. Cardiovascular responses to static exercise. Scand J Work Environ Health 10 (1984) 397-402.##15.	Cramer D &#38; Howitt D. The sage dictionary of statistic, London SAGE (2004).##16.	Razali N.M. &#38; Wah Y.B. Power compressions of Shapiro-wilkKolmograv- Smorov,Lillefors and Anderson-Darling tests. Journal of statistical modelling and analysis 2 (2011) 21-33.##17.	Shapiro S.S. &#38;Wilk M.B. An analysis of variance Test for normality (complete samples). Biometrica 52 (1965) 91-611.##18.	Mehta V et al. Autonomic functions during different phases of menstrual cycle. Indian J Physiol Pharmacol 37(1) (1993 Jan) 56-8.##19.	Borg G. A. V. &#38; Noble B. J. (1974) Perceived exertion. In: Exercise and Sport Sciences Reviews, Vol 2 (ed. Wilmore, J.). New York: Academic Press, 1974, pp. 131±153.## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Melatonin and Alpha Lipoic Acid: Possible Mitigants for Lopinavir/Ritonavir- Induced Renal Toxicity in Male Albino Rats</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: This study evaluated the effects of pretreatments with melatonin (MT), and Alpha Lipoic acid (ALA) on lopinavir/ritonavir (LPV/r) -induced serum levels of creatinine (Cr), urea (U), uric acid (Ua) and kidney levels of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH) and catalase (CAT) in male albino rats. Effects of treatments with MT and ALA were also evaluated on baseline levels of the above parameters.&#160;Materials and Methods: Adult male albino rats orally received MT (10mg/kg), ALA (10mg/kg) and LPV/r (22.9/5.71, 45.6/11.4 and 91.4/22.9mg/kg) for 60 days. At the end of drug treatment animals were sacrificed, serum was extracted and evaluated for Cr, U, and Ua. Kidney was harvested and evaluated for MDA, SOD, CAT and GSH.&#160;Results: Treatment with MT and ALA significantly (p&#60;0.05) decreased baseline serum levels of Cr, U, Ua and kidney MDA level while kidney levels of SOD, CAT and GSH were decreased when compared to the control. On the contrary, treatment with LPV/r significantly (p&#60;0.05) and dose -dependently increased serum Cr, U, Ua levels and kidney MDA level while kidney levels of SOD, CAT and GSH were decreased when compared to the control. But pretreatments with MT and ALA mitigated LPV/r induced changes in all evaluated parameters. Pronounced mitigation was observed with pretreatment using a combination of MT and ALA.&#160;Conclusion: Observations in this study may be due to the oxidant effect of LPV/r and the antioxidant effects of MT and ALA. This study, therefore recommends MT and ALA as treatment or prevention for LPV/r induced renal toxicity.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>232</FPAGE>
			<TPAGE>240</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2015/10/182015/09/272015/09/16
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1394/6/25
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2015/12/112016/01/92015/12/28
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1394/10/7
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Elias</Name>
				<MidName></MidName>
				<Family>Adikwu</Family>
				<NameE>Elias</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Adikwu</FamilyE>
				<Organizations>
				<Organization>Department of Pharmacology, Faculty of Basic Medical Sciences, University of Port Harcourt, Choba, Rivers State, Nigeria</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>adikwuelias@gmail.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Nelson</Name>
				<MidName></MidName>
				<Family>Braimbaifa</Family>
				<NameE>Nelson</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Braimbaifa</FamilyE>
				<Organizations>
				<Organization>Department of Pharmacology, Faculty of Basic Medical Sciences, University of Port Harcourt, Choba, Rivers State, Nigeria</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>brambaifan@gmail.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Atuboyedia Wolfe</Name>
				<MidName></MidName>
				<Family>Obianime</Family>
				<NameE>Atuboyedia Wolfe</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Obianime</FamilyE>
				<Organizations>
				<Organization>Department of Pharmacology, Faculty of Basic Medical Sciences, University of Port Harcourt, Choba, Rivers State, Nigeria</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>adikwuelias@yahoo.com</Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Kidney</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Toxicity</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Lopinavir/Ritonavir</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Melatonin</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Alpha Lipoic Acid</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Rats</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>Abd EL Salam S, Elnady, K , Zahran WM, and Ayobe  MH. Protective effects of alpha lipoic acid on gamma irradiation hazards in male rats.  Isotope &#38; Rad. Res., 2011, 43(1), 223-232.##Adewole O S,  Salako AA,  Doherty O W,  and Naicker T. Effect of Melatonin on Carbon Tetrachloride-Induced Kidney Injury in Wistar Rats, African Journal of Biomedical Research,  2007 ; 10 :153 – 164##Adaramoye OA, Adewumi OM, Adesanoye  OA, Faokule OO, Farombi EO . Effect of tenofovir, an antiretroviral drug, on hepatic and renal functional indices of Wistar rats: protective role of vitamin E. Journal of Basic and Clinical Physiology and Pharmacology 2012; 23 ( 2):  69–75, ##Antolin I, Rodriguez C, Sainz RM, et al. Neurohormone melatonin prevents cell damage: effect on gene expression for antioxidant enzymes. FASEB J 1996; 10: 882-890 ##Adikwu E, Oputiri D, and Oru-Bo P. G. Effect of Coadministered Lopinavir/Ritonavir and Sulfamethoxazole/Trimethoprim on Liver Function and Achitecture of Albino Rats.&#34; American Journal of Pharmacological Sciences, 2014 2; 4 : 65-71##Ahmed AM and Hassanein  KMA. Cardioprotective effects of Nigella sativa oil on lead induced cardio toxicity anti-inflammatory and antioxidant mechanism.  Jour Physio and Patho. 2013; 24 (5); 72-80 ##Annino  JS and Giese RW.  1979. Clinical Chemistry, 4th ed. Little Brown, Boston, pp 170-177,  ## Avery   SV. Molecular targets of oxidative stress. Biochemical Journal, 2011 ; 434 ( 2)  201–210, ##Anderson. M E  Glutathione: an overview of biosynthesis and modulation. Chemico- Biological Interactions. 1998; 111; (2)1–14##Abdel-Zaher, A.O.; Abdel-Hady, R.H.; Mahmoud, M.M.; Farrag, M.M.Y. The potential protective role of α-lipoic acid against acetaminophen-induced hepatic and renal damage. Toxicology 2008, 243, 261–270 ##Ali W. S. Comparative study betweem marjoram and alpha lipoic acid on potassium bromide induced oxidatives stress in rats Word Jour of Dairy and food Sciences , 2013; 8 (1),94-99## Babiak, EMV,  Campello AP, Carnieri ES, Oliveira MB. Methotrexate, pentose cycle and oxidative stress Cell Biochemistry and Function. 1998:  283:  93 ##Bowler C,  Montagu MV and Irize D, Superoxide Dismutase and stress tolerance  Annual Review of Plant Physiology and Plant Molecular Biology. 1992; 43, 83-11##Bilginoğlu A,  D. Aydın,  S. Özsoy ,  H. Aygün Protective effect of melatonin on adriamycin-induced cardiotoxicity in ratsArch Turk Soc Cardiol 2014;  42(3):265-273##Busse E, Zimmer G, Schopohl B, Kornhuber B. Influence of alpha-lipoic acid on intracellular glutathione in vitro and in vivo. Arzneimittelforschung . 1992;42 (6):829-831.##Cihlar T, Birkus G, Greenwalt DE, Hitchcock MJ. Tenofovir exhibits low cytotoxicity in various human cell types: comparison with other nucleoside reverse transcriptase inhibitors. Antiviral Res. 2002;54 (1):37-45.##Chander V, Singh D, Tirkey N, Chander H, Chopra K. Amelioration of cyclosporine nephrotoxicity by irbesartan, a selective AT1 receptor antagonist. Ren Fail 2004; 26: 467-77##Chughlay M F, Njuguna C,  Cohen K, Maartens G. Acute interstitial nephritis caused by lopinavir/ritonavir in a surgeon receiving antiretroviral postexposure prophylaxis AIDS:  2005, 29 ;4 : 503–504## Deavall DG, Martin EA, Horner JM, and Roberts R. Drug-Induced Oxidative Stress and Toxicity.  Journal of Toxicology Volume 2012 (2012), Article ID 645460, 13 page##Durak I, Ozbek H, Elgun S. Cyclosporine reduces hepatic antioxidant capacity: protective roles of antioxidants. Int Immunopharmacol 2004; 4: 469-73.##Doco-Lecompte T, Garrec A, Thomas L, Trechot P, May T, Rabaud C  Lopinavir-ritonavir (Kaletra) and lithiasis: seven cases. AIDS 2004, 18, 705–706##Elens L, Tyteca D, Panin N, Courtoy P, Lison D, Demoulin JB, et al. Functional defect caused by the 4544G&#62;A SNP in ABCC2: potential impact for drug cellular disposition. Pharmacogenet Genomics 2011; 21:884–893##Ferguson M A, Vaidya, SV Bonventre JV Biomarkers of nephrotoxic acute kidney injury. Toxicology. 2008 , 245:182–193, ## Fridovich I. Superoxide radical and superoxide dismutases. Annual Review of Biochemistry, 1995 : 64; 97-112##Galle J Oxidative stress in chronic renal failure Nephrology Dialysis Transplantation  2001 , 16, : 11 : 2135-2137##Hu S, Yin S, Jiang X, Huang D, Shen G. Melatonin protects against alcoholic liver injury by attenuating oxidative stress, inflammatory response, and apoptosis. Eur J Pharmacol. 2009;616(1–3):287–92.##Hull M. W, M. Harris, V. Lima, et al. Lopinavir/ritonavir pharmacokinetics in a substitution of high-dose soft-gelatin capsule to tablet formulation. J Clin Pharmacol. 2009: 49: 155-61 ##Huang HS, M. C. Ma, J. Chen, and C. F. Chen, “Changes in the oxidant-antioxidant balance in the kidney of rats with nephrolithiasis induced by ethylene glycol,” Journal of Urology, 2002; 167; 6; 2584–2593, ##Hussein AS,  Abd el-hamid OM  and  Fayed AS. 	Protective effects of alpha-lipoic acid and melatonin against cadmium-induced oxidative stress in erythrocytes##of rats  Benha Veterinary Medical Journal, 2014; 26; 1:19-33, ##Hagar   H. H, El Etter E, Arafa M. Taurine attenuates hypertension and renal dysfunction induced by cyclosporine in rats. Clin Exp. Pharmacol and Pharmacol and Physiol, 2006 :33; 189, ##Ho ES, Lin DC, Mendel DB, Cihlar T. Cytotoxicity of antiviral nucleotides adefovir and cidofovir is induced by the expression of human renal organic anion transporter . J Am Soc Nephrol. 2000;11(3):383-93.##Johnson, F and Giulivi, C Superoxide dismutases and their impact upon human health, Molecular Aspects Medicine. 2005 : 26 ;340–352, ##Kagan VE, Shvedova A, Serbinova E, Khan S, Swanson C, Powell R, et al.,. Dihydrolipoic acid–a universal antioxidant both in the membrane and in the aqueous phase. Reduction of peroxyl, ascorbyl, and chromanoxyl radicals. Biochemistry and Pharmacology, 1992, 44(8): 1637–1649.##Kilic F, Handelman GJ, Traber K, Tsang K, Packer L, Trevithick JR. Modelling cortical cataractogenesis XX. In vitro effect of alpha lipoic acid on glutathione concentrations in lens in model diabetic cataractogenesis. Biochemistry and Molecular Biology International, 1998 ; 46(3): 585–595.##Kang KP.  Kim DH,  Jung YJ.,  Lee AS,  Lee S,  Lee  SY.  Alpha-lipoic acid attenuates cisplatin-induced acute kidney injury in mice by suppressing renal inflammation, Nephrol. Dial. Transplant. 2009 24 (10): 3012-3020.##Kaplan M, Atakan HI, Aydoğdu N,   Aktoz T,  Puyan, FO, et al. The effect of melatonin on cadmium-induced renal injury in chronically exposed rats Turkish Journal of Urology 2009; 35(2):139-147##Kim YO, Ahn YK, Kim JH. Influence of melatonin on immunotoxicity of cadmium. Int J Immunopharmacol 2000;22:275-84##Kozirog M, Poliwczak AR, Duchnowicz P, Koter-Michalak M, Sikora J, Broncel M. Melatonin treatment improves blood pressure, lipid profile, and parameters of oxidative stress in patients with metabolic syndrome. J Pineal Res. 2011;50(3):261–6.##Lilling CH, Holmgren A. Thioredoxin and related molecules from biology to health and disease. Antioxid. Redox. Sign., 2007;  9: 25-47.##Leon, J, Acuna-Castroviejo D, Sainz R.M, Mayo JC, Tan DX. and Reiter RJ. Melatonin and mitochondrial function. Life Sci, 2004, 75: 765-790##Miller WG, Myers GL, Ashwood ER, Killeen AA, Wang E, Thienpont LM, et al. Creatinine measurement: state of the art in accuracy and interlaboratory harmonization. Arch Pathol Lab Med. 2005;129 (3):297-304.## Mullineaux,P  and G. Creissen  Glutathione reductase: regulation and role in oxidative stress, Oxidative stress and the molecular biology of antioxidant defenses. Cold Spring Harbor Laboratory Press; 1997.##Montilla P, Tunez I, Munoz MC, et al. Antioxidative effect of melatonin in rat brain oxidative stress induced by Adriamycin. Rev Esp Fisiol 1997; 53:301-305##Mocroft A, Kirk O, Reiss P, De Wit S, Sedlacek D, Beniowski M, et al. Estimated glomerular filtration rate, chronic kidney disease and antiretroviral drug use in HIV-positive patients. AIDS 2010; 24:1667–1678.##Mao L,  Yuan L, Slakey LM,  Jones EF, Burow ME,   Hil SM,  Inhibition of breast cancer cell invasion by melatonin is mediated through regulation of the p38 mitogen-activated protein kinase signaling pathway, Breast Cancer Research 2010, 12, :R107##Moini H, Tirosh O, Park YC, Cho KJ, Packer L, R-alpha lipoic acid action on cell redox status, the insulin receptor and glucose uptake in 3T3-L1 adipocytes. Archives of Biochemistry and Biophysics, 2002, 397(2): 384–391.##Nistico G, Ciriolo MR, Fiskin K, Iannone M, De Martino A, Rotilio G: NGF restores decrease in catalase activity and increases superoxide dismutase and glutathione peroxidase activity in the brain of aged rats. Free Radic Biol Med 12: 177-181, 1992##Orkin C, DeJesus E, Khanlou H, Stoehr A, Supparatpinyo K, Lathouwers E, et al. Final 192-week efficacy and safety of once-daily darunavir/ritonavir compared with lopinavir/ritonavir in HIV-1-infected treatment-naive patients in the ARTEMIS trial. HIV Med 2013; 14:49–59.##Parker,.Alpha Lipoic Acid Regeneration .LE Magazine The pathways of the antioxidants., Mol. Nutr. Food Res.1996; 57: 114–125##Packer L, Witt EH, Tritschler HJ.  Alpha-lipoic acid as a biological antioxidant. Free Radic Biol Med 1995.;19(2):227-250. ##Packer, L. α-lipoic acid: A metabolic antioxidant which regulates NF-kappa B signal transduction and protects against oxidative injury. Drug Metab. Rev. 1998; 30: 245-275.##PaulisL. And Simko F. Blood pressure modulation and cardiovascular protection by melatonin: Potential mechanism behind. Physiol Res. 2007; 56: 671-687.##Richardson BA, Studier EH and Kennedy C.M, Effects of melatonin on water metabolism and renal function in male Syrian hamsters (Mesocricetus auratus). Journal of Pineal Research, 1992; 13: 49-59.##Reiter R J, Paredes SD, Manchester LC and Tan DX.  Reducing oxidative/nitrosative stress: a newly-discovered gene for melatonin. Critical Reviews in Biochemistry and Molecular Biology, 2009: 44: 175-200.##Reiter R J. Pineal melatonin: Cell biology of its synthesis and of its physiological interactions. Endocr Rev. 1991, 12:151–80##Reiter R J, Melchiorri D, Sewerynek E, Poeggeler B, Barlow-Walden, L et al. review of the evidence supporting melatonin\'s role as an antioxidant. Journal of Pineal Research, 1995; 18: 1–11.##Rezzani R, Rodella L, Buffoli B. Change in renal heme oxygenase expression in cyclosporine A- induced injury J. Histochem Cytochem 2005: 53:105,.##Raju   DSSK, Lalitha DL, Kiranmayi P  A Study of Lipid Profile and Lipid Peroxidation in Chronic Kidney Disease with Special Reference to Hemodialysis. J Clinic Res Bioeth 4: 143, 2013##Ryom L, Mocroft A, Kirk O, Worm SW, Kamara DA, Reiss P, et al. Association between antiretroviral exposure and renal impairment among HIV-positive persons with normal baseline renal function: the D:A:D study. J Infect Dis. 2013 ; 207:1359–1369. ##Sola, S.; Mir, M.Q.; Cheema, F.A.; Khan-Merchant, N.; Menon, R.G.; Parthasarathy, S.; Khan, B.V. Irbesartan and lipoic acid improve endothelial function and reduce markers of inflammation in the metabolic syndrome results of the irbesartan and lipoic acid in endothelial dysfunction (island) study. Circulation 2005, 111, 343–348 ##Sun J, Zhang H, Guan L, Zhou H, Sun M. Alpha-lipoic acid attenuates trinitrobenzene sulfonic acid-induced ulcerative colitis in mice, Int J Clin Exp Med 2015;8(1):358-367 ##Saravanan R, Rajendra N,  Prasad RN, and Pugalendi KV, Effect of Piper betle leaf extract on alcohol toxicity in the rat brain. Journal of Medicinal Food, 2003; 6 (3) 261-265, 2003##Shokrzadeh M, Ahmad A,  Naghshva F, Chabra,A  and  Jafarinejhad M.  Prophylactic Efficacy of Melatonin on Cyclophosphamide-Induced Liver Toxicity in Mice, BioMed Research International Volume 2014, Article ID 470425, 6 pages##Tan DX, Manchester LC, Burkhardt S, Sainz RM, Mayo JC, Kohen R, Shohami E, Huo YS, Hardeland R, Reiter RJ. N1-acetyl-N2-formyl-5-methoxykynuramine, a biogenic amine and melatonin metabolite, functions as a potent antioxidant. FASEB J 2001; 15: 2294-2296##Tan DX, Manchester LC, Terron MP, Flores LJ, Reiter RJ. One molecule, many derivatives: a never-ending interaction of melatonin with reactive oxygen and nitrogen species? J Pineal Res 2007; 42: 28-42##Toro, G and Ackermann, P.G.  . Practical clinical chemistry. Little Brown, Boston, 1975; pp 148-156.##Trujillo, M. and Radi R. Peroxynitrite reaction with the reduced and the oxidized forms of lipoic acid: New insights into the reaction of peroxynitrite with thiols. Arch. Biochem. Biophysc. 2002; 397: 91-98.##Wang LI , Chen-Guang W, Fang C Q,   Gao J, Liu Y,  Chen Y, Chen Y,  and  Xu Z The protective effect of α-Lipoic acid on mitochondria in the kidney of diabetic rats  Int J Clin Exp Med. 2013; 6(2): 90–97. ##Wong, A.,  Dukic-Stefanovic, S,  Gasic-Milenkovic, J, Schinzel, R,  Wiesinger, H,  Riederer, P, Münch, G. Anti-inflammatory antioxidants attenuate the expression of inducible nitric oxide synthase mediated by advanced glycation endproducts in murine microglia. Eur. J. Neurosci. 2001, 14, 1961–1967. ##Wolf A, Clemann N, Frieauff W, Ryffel B, Cordier A. Role of reactive oxygen formation in the cyclosporine A mediated impairment of renal functions. Transplants Proc 1994; 26: 2902-07.##Young J, Schafer J, Fux CA, Furrer H, Bernasconi E, Vernazza P, et al. Renal function in patients with HIV starting therapy with tenofovir and either efavirenz, lopinavir or atazanavir. AIDS; 2012, 26:567–575.## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Acute application of cholecystokinin and its effect on long-term potentiation induction at CA1 area of hippocampal formation in rat</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: It has been demonstrated that cholecystokinin sulfated octapeptide (CCK-8s) can affect synaptic transmission in the hippocampus. Because one of the major experimental models to understand the events happening in synaptic plasticity is To Study the long-term potentiation (LTP), we decided to investigate the effect of concomitant administration of CCK-8s and tetanic stimulation of Schaffer collateral path-CA1 synapses on LTP induction and maintenance.&#160;Materials and Methods: Experimental groups were control, CCK-5min and CCK-30min. CCK-8s was injected 5 or 30 min (1.6 &#956;g/kg; i.p.) prior to induction of LTP. The stimulating and the recording electrodes were placed in the Schaffer collateral pathway and hippocampal CA1, respectively. LTP was induced by 100 Hz tetanization and field excitatory postsynaptic potentials (fEPSP) slope, area and amplitude were measured and compared during 30 minutes Interval before, and 90 minutes Interval after LTP induction in each group.&#160;Results: The results showed that maintenance of the induced LTP was significantly improved in the CCK-30min group comparing to the control group. This improvement was particularly visible in the fEPSP slope (p&#60;0.001) and the fEPSP area (p&#60;0.001). Seventy minutes after the LTP induction, fEPSP was similar in both the CCK-5min and the CCK-30min groups and there was Also a significant difference between the treated groups comparing to the control group (p&#60;0.05).&#160;Conclusion: These results indicated that LTP induction and maintenance is carried out effectively, at higher levels of CCK in the brain. The data suggest that CCK-8s has pronounced effects on synaptic plasticity in the hippocampus and the consequent cognitive functions.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>241</FPAGE>
			<TPAGE>246</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2015/10/182015/09/272015/09/162015/09/14
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1394/6/23
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2015/12/112016/01/92015/12/282015/11/28
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1394/9/7
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Farzane</Name>
				<MidName></MidName>
				<Family>Dehghani</Family>
				<NameE>Farzane</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Dehghani</FamilyE>
				<Organizations>
				<Organization>Applied Physiology Research Center, Isfahan University of Medical Sciences, Isfahan, Iran.</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>dehghani.med@gmail.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Parham</Name>
				<MidName></MidName>
				<Family>Reisi</Family>
				<NameE>Parham</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Reisi</FamilyE>
				<Organizations>
				<Organization>Applied Physiology Research Center, Isfahan University of Medical Sciences, Isfahan, Iran.</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>p_reisi@med.mui.ac.ir</Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Cholecystokinin sulfated octapeptide</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>CA1</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Hippocampus</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>LTP.</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>Acosta GB. Administration of cholecystokinin sulphated octapeptide (cck-8s) induces changes on rat amino acid tissue levels and on a behavioral test for anxiety. Gen Pharmacol 1998; 31: 637-41.##Altar CA, Boyar WC. Brain cck-b receptors mediate the suppression of dopamine release by cholecystokinin. Brain Res 1989; 483: 321-6.##Baptista V, Browning KN, Travagli RA. Effects of cholecystokinin-8s in the nucleus tractus solitarius of vagally deafferented rats. Am J Physiol Regul Integr Comp Physiol 2007; 292: R1092-100.##Blandizzi C, Natale G, Carignani D, Colucci R, Lazzeri G, Del Tacca M. Central administration of cholecystokinin stimulates gastric pepsinogen secretion from anaesthetized rats. Neurosci Lett 1995; 193: 13-6.##Bohme GA, Stutzmann JM, Blanchard JC. Excitatory effects of cholecystokinin in rat hippocampus: Pharmacological response compatible with \'central\'- or b-type cck receptors. Brain Res 1988; 451: 309-18.##Deng PY, Lei S. Bidirectional modulation of gabaergic transmission by cholecystokinin in hippocampal dentate gyrus granule cells of juvenile rats. J Physiol 2006; 572: 425-42.##Deng PY, Xiao Z, Jha A, Ramonet D, Matsui T, Leitges M, et al. Cholecystokinin facilitates glutamate release by increasing the number of readily releasable vesicles and releasing probability. J Neurosci 2010; 30: 5136-48.##Dolatabadi LK, Reisi P. Acute effect of cholecystokinin on short-term synaptic plasticity in the rat hippocampus. Res Pharm Sci 2014; 9: 331-6.##Gronier B, Debonnel G. Electrophysiological evidence for the implication of cholecystokinin in the modulation of the n-methyl-d-aspartate response by sigma ligands in the rat ca3 dorsal hippocampus. Naunyn Schmiedebergs Arch Pharmacol 1996; 353: 382-90.##Kohler C, Chan-Palay V. Cholecystokinin-octapeptide (cck-8) receptors in the hippocampal region: A comparative in vitro autoradiographic study in the rat, monkey and the postmortem human brain. Neurosci Lett 1988; 90: 51-6.##Liu XJ, Huang FS, Huang C, Yang ZM, Feng XZ. Analysis of high-frequency stimulation-evoked synaptic plasticity in mouse hippocampal ca1 region. Sheng Li Xue Bao 2008; 60: 284-91.##MacVicar BA, Kerrin JP, Davison JS. Inhibition of synaptic transmission in the hippocampus by cholecystokinin (cck) and its antagonism by a cck analog (cck27-33). Brain Res 1987; 406: 130-5.##Miller KK, Hoffer A, Svoboda KR, Lupica CR. Cholecystokinin increases gaba release by inhibiting a resting k+ conductance in hippocampal interneurons. J Neurosci 1997; 17: 4994-5003.##Paxinos G, Watson C. The rat brain in stereotaxic coordinates-the new coronal set: Academic press, 2004.##Rezayat M, Roohbakhsh A, Zarrindast MR, Massoudi R, Djahanguiri B. Cholecystokinin and gaba interaction in the dorsal hippocampus of rats in the elevated plus-maze test of anxiety. Physiol Behav 2005; 84: 775-82.##Sadeghi M, Radahmadi M, Reisi P. Effects of repeated treatment with cholecystokinin sulfated octapeptide on passive avoidance memory under chronic restraint stress in male rats. Adv Biomed Res 2015; 4: 150.##Tirassa P, Costa N. Cck-8 induces ngf and bdnf synthesis and modulates trka and trkb expression in the rat hippocampus and septum: Effects on kindling development. Neurochem Int 2007; 50: 130-8.##Voits M, Hasenohrl RU, Huston JP, Fink H. Repeated treatment with cholecystokinin octapeptide improves maze performance in aged fischer 344 rats. Peptides 2001; 22: 1325-30.##Whissell PD, Cajanding JD, Fogel N, Kim JC. Comparative density of cck- and pv-gaba cells within the cortex and hippocampus. Front Neuroanat 2015; 9: 124.## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Antibacterial and Immunomodulatory Effects of Hexamethylenetetramine (Methenamine) Silver Nitrate </TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: Currently, developing new antibacterial drugs as alternative antibiotics is a very active area of research, due to widspreading widespread prevalence of resistant strains of microorganisms. This work intends to investigate of antibacterial properties and influence on immune blood cells of the silver-based compound hexamethylenetetramine (methenamine) silver nitrate with general formula [Ag(CH2)6 N4]NO3.&#160;Materials and Methods: The antibacterial effect of the silver complex was investigated by agar diffusion and serial dilution methods. Silver complex have been investigated for its impact on the phagocytic activity of neutrophils and on immune cells during the reaction of blast transformation of lymphocytes (RBTL).&#160;Results: Studies have shown that hexamethylenetetramine silver nitrate possesses both bactericidal and bacteriostatic dose-dependent effect on tested bacterial strains, including Staphylococcus aureus, Proteus vulgaris, Pseudomonas aeruginosa, Streptococcus pneumoniae. Escherichia coli were shown to be the most susceptible bacteria. Cytotoxic effect of silver salt on lymphocytes was detected in high dosage in RBTL. No significant immunosuppressive impact on neutrophils phagocytic activity of tested complex was shown.&#160;Conclusion: Agents of nosocomial infections were highly susceptible to the drug. Complex has proved to be promising as a prospective antibacterial drug with wide range of activity.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>247</FPAGE>
			<TPAGE>252</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2015/10/182015/09/272015/09/162015/09/142015/09/20
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1394/6/29
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2015/12/112016/01/92015/12/282015/11/282015/12/28
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1394/10/7
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Evgenii</Name>
				<MidName></MidName>
				<Family>Plotnikov</Family>
				<NameE>Evgenii</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Plotnikov</FamilyE>
				<Organizations>
				<Organization>Tomsk Polytechnic University, Tomsk, Russia</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>plotnikov.e@mail.ru</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Vladimir</Name>
				<MidName></MidName>
				<Family>Pehenko</Family>
				<NameE>Vladimir</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Pehenko</FamilyE>
				<Organizations>
				<Organization>Siberian State Medical University, Tomsk, Russia</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>vovapekhenko@sibmail.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Vladimir</Name>
				<MidName></MidName>
				<Family>Plotnikov</Family>
				<NameE>Vladimir</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Plotnikov</FamilyE>
				<Organizations>
				<Organization>“Polytech” ltd, Tomsk, Russia</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>plotnikov.vm@mail.ru</Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Silver-based complex</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Methenamine</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Antibacterial drug</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Nosocomial infections</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Staphylococcus</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Streptococcus</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Silver hexamethylenetetramine</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Phagocytosis</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Lymphocytes blast transformation</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>Cavassin ED, Poli de Figueiredo LF, Otoch JP, Seckler MM, Oliveira RA, Franco FF, Marangoni VS, Zucolotto V, Shafferman Levin AS, Costa SF.	Comparison of methods to detect the in vitro activity of silver nanoparticles (AgNP) against multidrug resistant bacteria. Journal of Nanobiotechnology 2015, 13:64##Dawson PA, Filipe MI. An ultrastructural application of silver methenamine to the study of mucin changes in the colonic mucosa adjacent to and remote from carcinoma. Histochemical Journal. 1976; 8(2):143-158##Greulich C, Diendor J, Zeßmann J, Simon T, Habijan T, Eggeler G, Schildhauer TA, Epple M, Köller M. Cell type-specific responses of peripheral blood mononuclear cells to silver nanoparticles.  Acta Biomaterialia. 2011; 7(9):3505-3514##Haase H, Fahmi A, Mahltig B. Impact of silver nanoparticles and silver ions on innate immune cells. J Biomed Nanotechnol. 2014;10(6):1146-56.##Jung WK, Koo HC, Kim KW, Shin S, Kim SH, Park YO. Antibacterial Activity and Mechanism of Action of the Silver Ion in Staphylococcus aureus and Escherichia coli. Appl Environ Microbiol, 2008; 74(7):2171-2178.##Kvitek L, Panacek A, Prucek R, Soukupova J, Vanickova M, Zboril R. Antibacterial activity and toxicity of silver - nanosilver versus ionic silver. Journal of Physics: Conference Series  2011; 304: 1-8.##Maillard JY,  Hartemann P. Silver as an antimicrobial: Facts and gaps in knowledge Critical Reviews in Microbiology. 2012; 39(4): 1-11##Mase D. Alterations of glomerular basement membrane and electron dense deposits in various renal diseases--an electron microscopic study using periodic acid methenamine silver stain and immunohistochemical technique. Nippon Jinzo Gakkai shi. 1988; 30(6):671-8##Novikov DK, Novikova VA. Immune Status Assessment. Moscow: Medicine, 1996.##Plotnikov E, Gapeyev A, Plotnikov V. Investigation genotoxicity of new silver-based complex with antimicrobial activity. Int J Pharm Pharm Sci,  2015; 7(7): 1-2.##Reller LB. Antimicrobial Susceptibility Testing: A Review of General Principles and Contemporary Practices. Clin Infect Dis, 2009; 49 (11): 1749-1755.##Silnikov V, Plotnikov E, Plotnikov V. Pharmacokinetic studies of new silver-based complex. Int J Pharm Pharm Sci,  2015; 6:1-6.##Sondi I, Salopek-Sondi B. Silver nanoparticles as antimicrobial agent: a case study on E. coli as a model for Gram-negative bacteria. J Colloid Interface Sci. 2004; 275(1):177-182.##Sukdeb P, Tak YK, Song JM. Does the Antibacterial Activity of Silver Nanoparticles Depend on the Shape of the Nanoparticle? A Study of the Gram-Negative Bacterium Escherichia coli. Appl. Environ. Microbiol. 2007; 73: 1712-1720.##Thurman RB, Gerba CP. The molecular mechanisms of copper and silver ion disinfection of bacteria and viruses. CRC Crit. Rev. Environ. Control, 1989; 18:295-315.##Zapata-Sirvent RL, Hansbrough JF. Cytotoxicity to human leukocytes by topical antimicrobial agents used for burn care.  Journal of Burn Care and Rehabilitation. 1993; 14(2):132-140.##Zhao G, Stevens SE. Multiple parameters for the comprehensive evaluation of the susceptibility of Escherichia coli to the silver ion. BioMetals 1998; 11: 27–32.## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Gemfibrozil protect PC12 cells through modulation of Estradiol receptors against oxidative stress</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: Neurodegenerative diseases are progressive disorders that could impair neuronal functions and structures. Oxidative stress and mitochondrial dysfunction are involved in the etiology of neurodegenerative diseases such as Alzheimer&#8217;s disease, Parkinson&#8217;s disease and etc. Gemfibrozil is used as a therapeutic drug for hyperlipidemia. It has been shown that gemfibrozil is neuroprotective via modulation of mitochondrial biogenesis pathway under oxidative stress condition and in a sex-dependent manner.&#160;Materials and Methods: In this study, neuronal-like PC12 cells with were pretreated with different concentrations of gemfibrozil and H2O2, concomitantly.&#160;Results: In gemfibrozil pretreated groups, reduced level of caspase-3 and raised mitochondrial transcription factor A (TFAM) levels were detected. In contrast, adding fulvestrant, an Estradiol receptor antagonist, prevents the impact of gemfibrozil on oxidative stress condition, reducing its efficacy to protect the neurons against stress.&#160;Conclusion: Our results indicated the involvement of estradiol receptors in gemfibrozil neuroprotective mechanism, in diminishing oxidative stress-induced damage via reducing caspase-3 and inducing the level of TFAM that plays a crucial role in the mitochondrial biogenesis.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>253</FPAGE>
			<TPAGE>262</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2015/10/182015/09/272015/09/162015/09/142015/09/202015/09/7
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1394/6/16
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2015/12/112016/01/92015/12/282015/11/282015/12/282015/11/28
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1394/9/7
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Ghorbangol</Name>
				<MidName></MidName>
				<Family>Ashabi</Family>
				<NameE>Ghorbangol</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Ashabi</FamilyE>
				<Organizations>
				<Organization>Physiology Research Center and Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>as_habi@yahoo.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Leila</Name>
				<MidName></MidName>
				<Family>Khalaj</Family>
				<NameE>Leila</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Khalaj</FamilyE>
				<Organizations>
				<Organization>Medical School, Alborz University of Medical Sciences, Alborz, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>lkhalaj@yahoo.com</Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Gemfibrozil</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Mitochondrial transcription factor A</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Fulvestrant</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Caspase 3</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>H2O2</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>Amer J, Ghoti H, Rachmilewitz E, Koren A, Levin C, Fibach E. Red blood cells, platelets and polymorphonuclear neutrophils of patients with sickle cell disease exhibit oxidative stress that can be ameliorated by antioxidants. Br J Haematol 132(2006) 108-13.##Bain DL, Heneghan AF, Connaghan-Jones KD, Miura MT. Nuclear receptor structure: Implications for function. Annu Rev Physiol 69(2007) 201-20.##Boitier E, Gautier JC, Roberts R. Advances in understanding the regulation of apoptosis and mitosis by peroxisome-proliferator activated receptors in pre-clinical models: Relevance for human health and disease. Comp Hepatol 2(2003) 3.##Bordet R, Ouk T, Petrault O, Gele P, Gautier S, Laprais M, et al. Ppar: A new pharmacological target for neuroprotection in stroke and neurodegenerative diseases. Biochem Soc Trans 34(2006) 1341-6.##Bradford MM. A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. Anal Biochem 72(1976) 248-54.##Calkin AC, Cooper ME, Jandeleit-Dahm KA, Allen TJ. Gemfibrozil decreases atherosclerosis in experimental diabetes in association with a reduction in oxidative stress and inflammation. Diabetologia 49(2006) 766-74.##Camara-Lemarroy CR, Guzman DELAGFJ, Cordero-Perez P, Ibarra-Hernandez JM, Munoz-Espinosa LE, Fernandez-Garza NE. Gemfibrozil attenuates the inflammatory response and protects rats from abdominal sepsis. Exp Ther Med 9(2015) 1018-22.##Canu N, Ciotti MT, Pollegioni L. Serine racemase: A key player in apoptosis and necrosis. Front Synaptic Neurosci 6(2014) 9.##Carre JE, Orban JC, Re L, Felsmann K, Iffert W, Bauer M, et al. Survival in critical illness is associated with early activation of mitochondrial biogenesis. Am J Respir Crit Care Med 182(2010) 745-51.##Chen H, Hu CJ, He YY, Yang DI, Xu J, Hsu CY. Reduction and restoration of mitochondrial dna content after focal cerebral ischemia/reperfusion. Stroke 32(2001) 2382-7.##Chen SD, Lin TK, Lin JW, Yang DI, Lee SY, Shaw FZ, et al. Activation of calcium/calmodulin-dependent protein kinase iv and peroxisome proliferator-activated receptor gamma coactivator-1alpha signaling pathway protects against neuronal injury and promotes mitochondrial biogenesis in the hippocampal ca1 subfield after transient global ischemia. J Neurosci Res 88(2010) 3144-54.##Corbett GT, Roy A, Pahan K. Gemfibrozil, a lipid-lowering drug, upregulates il-1 receptor antagonist in mouse cortical neurons: Implications for neuronal self-defense. J Immunol 189(2012) 1002-13.##Corton JC, Bocos C, Moreno ES, Merritt A, Cattley RC, Gustafsson JA. Peroxisome proliferators alter the expression of estrogen-metabolizing enzymes. Biochimie 79(1997) 151-62.##Deplanque D, Gele P, Petrault O, Six I, Furman C, Bouly M, et al. Peroxisome proliferator-activated receptor-alpha activation as a mechanism of preventive neuroprotection induced by chronic fenofibrate treatment. J Neurosci 23(2003) 6264-71.##Dong W, Gao D, Zhang X. Mitochondria biogenesis induced by resveratrol against brain ischemic stroke. Med Hypotheses 69(2007) 700-1.##Emerit J, Edeas M, Bricaire F. Neurodegenerative diseases and oxidative stress. Biomed Pharmacother 58(2004) 39-46.##Fan LQ, You L, Brown-Borg H, Brown S, Edwards RJ, Corton JC. Regulation of phase i and phase ii steroid metabolism enzymes by ppar alpha activators. Toxicology 204(2004) 109-21.##Fernandez-Silva P, Enriquez JA, Montoya J. Replication and transcription of mammalian mitochondrial DNA. Exp Physiol 88(2003) 41-56.##Finck BN, Kelly DP. Pgc-1 coactivators: Inducible regulators of energy metabolism in health and disease. J Clin Invest 116(2006) 615-22.##Finck BN, Kelly DP. Peroxisome proliferator-activated receptor gamma coactivator-1 (pgc-1) regulatory cascade in cardiac physiology and disease. Circulation 115(2007) 2540-8.##Ghosh A, Pahan K. Gemfibrozil, a lipid-lowering drug, induces suppressor of cytokine signaling 3 in glial cells: Implications for neurodegenerative disorders. J Biol Chem 287(2012) 27189-203.##Goldenberg NM, Wang P, Glueck CJ. An observational study of severe hypertriglyceridemia, hypertriglyceridemic acute pancreatitis, and failure of triglyceride-lowering therapy when estrogens are given to women with and without familial hypertriglyceridemia. Clin Chim Acta 332(2003) 11-9.##Gonzalez FJ. The peroxisome proliferator-activated receptor alpha (pparalpha): Role in hepatocarcinogenesis. Mol Cell Endocrinol 193(2002) 71-9.##Greene LA, Tischler AS. Establishment of a noradrenergic clonal line of rat adrenal pheochromocytoma cells which respond to nerve growth factor. Proc Natl Acad Sci U S A 73(1976) 2424-8.##Gust M, Fortier M, Garric J, Fournier M, Gagne F. Effects of short-term exposure to environmentally relevant concentrations of different pharmaceutical mixtures on the immune response of the pond snail lymnaea stagnalis. Sci Total Environ 445-446(2013) 210-8.##Hodges RM. Gemfibrozil--a new lipid lowering agent. Proc R Soc Med 69 Suppl 2(1976) 1-2.##Isidori M, Bellotta M, Cangiano M, Parrella A. Estrogenic activity of pharmaceuticals in the aquatic environment. Environ Int 35(2009) 826-9.##James SJ, Cutler P, Melnyk S, Jernigan S, Janak L, Gaylor DW, et al. Metabolic biomarkers of increased oxidative stress and impaired methylation capacity in children with autism. Am J Clin Nutr 80(2004) 1611-7.##Jana M, Pahan K. Gemfibrozil, a lipid lowering drug, inhibits the activation of primary human microglia via peroxisome proliferator-activated receptor beta. Neurochem Res 37(2012) 1718-29.##Khalaj L, Nejad SC, Mohammadi M, Zadeh SS, Pour MH, Ahmadiani A, et al. Gemfibrozil pretreatment proved protection against acute restraint stress-induced changes in the male rats\' hippocampus. Brain Res 1527(2013) 117-30.##Knutti D, Kralli A. Pgc-1, a versatile coactivator. Trends Endocrinol Metab 12(2001) 360-5.##Lennon SV, Martin SJ, Cotter TG. Dose-dependent induction of apoptosis in human tumour cell lines by widely diverging stimuli. Cell Prolif 24(1991) 203-14.##Lin MT, Beal MF. Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases. Nature 443(2006) 787-95.##Madamanchi NR, Vendrov A, Runge MS. Oxidative stress and vascular disease. Arterioscler Thromb Vasc Biol 25(2005) 29-38.##Maritim AC, Sanders RA, Watkins JB, 3rd. Diabetes, oxidative stress, and antioxidants: A review. J Biochem Mol Toxicol 17(2003) 24-38.##Miglio G, Rosa AC, Rattazzi L, Grange C, Camussi G, Fantozzi R. Protective effects of peroxisome proliferator-activated receptor agonists on human podocytes: Proposed mechanisms of action. Br J Pharmacol 167(2012) 641-53.##Miranda S, Foncea R, Guerrero J, Leighton F. Oxidative stress and upregulation of mitochondrial biogenesis genes in mitochondrial DNA-depleted hela cells. Biochem Biophys Res Commun 258(1999) 44-9.##Mohagheghi F, Ahmadiani A, Rahmani B, Moradi F, Romond N, Khalaj L. Gemfibrozil pretreatment resulted in a sexually dimorphic outcome in the rat models of global cerebral ischemia-reperfusion via modulation of mitochondrial pro-survival and apoptotic cell death factors as well as mapks. J Mol Neurosci 50(2013a) 379-93.##Mohagheghi F, Khalaj L, Ahmadiani A, Rahmani B. Gemfibrozil pretreatment affecting antioxidant defense system and inflammatory, but not nrf-2 signaling pathways resulted in female neuroprotection and male neurotoxicity in the rat models of global cerebral ischemia-reperfusion. Neurotox Res 23(2013b) 225-37.##Mosmann T. Rapid colorimetric assay for cellular growth and survival: Application to proliferation and cytotoxicity assays. J Immunol Methods 65(1983) 55-63.##Mutez E, Duhamel A, Defebvre L, Bordet R, Destee A, Kreisler A. Lipid-lowering drugs are associated with delayed onset and slower course of parkinson\'s disease. Pharmacol Res 60(2009) 41-5.##Nagai Y, Nishio Y, Nakamura T, Maegawa H, Kikkawa R, Kashiwagi A. Amelioration of high fructose-induced metabolic derangements by activation of pparalpha. Am J Physiol Endocrinol Metab 282(2002) E1180-90.##Nakajima T, Tanaka N, Li G, Hu R, Kamijo Y, Hara A, et al. Effect of bezafibrate on hepatic oxidative stress: Comparison between conventional experimental doses and clinically-relevant doses in mice. Redox Rep 15(2010) 123-30.##Onyango IG, Lu J, Rodova M, Lezi E, Crafter AB, Swerdlow RH. Regulation of neuron mitochondrial biogenesis and relevance to brain health. Biochim Biophys Acta 1802(2010) 228-34.##Osborne CK, Wakeling A, Nicholson RI. Fulvestrant: An oestrogen receptor antagonist with a novel mechanism of action. Br J Cancer 90 Suppl 1(2004) S2-6.##Ostronoff LK, Izquierdo JM, Enriquez JA, Montoya J, Cuezva JM. Transient activation of mitochondrial translation regulates the expression of the mitochondrial genome during mammalian mitochondrial differentiation. Biochem J 316 ( Pt 1)(1996) 183-91.##Paterson PY, Day ED. Neuroimmunologic disease: Experimental and clinical aspects. Hosp Pract 14(1979) 49-58.##Prossnitz ER, Arterburn JB, Sklar LA. Gpr30: A g protein-coupled receptor for estrogen. Mol Cell Endocrinol 265-266(2007) 138-42.##Ramond A, Godin-Ribuot D, Ribuot C, Totoson P, Koritchneva I, Cachot S, et al. Oxidative stress mediates cardiac infarction aggravation induced by intermittent hypoxia. Fundam Clin Pharmacol 27(2013) 252-61.##Rasbach KA, Schnellmann RG. Signaling of mitochondrial biogenesis following oxidant injury. J Biol Chem 282(2007) 2355-62.##Rubinsztein DC. The roles of intracellular protein-degradation pathways in neurodegeneration. Nature 443(2006) 780-6.##Sanoudou D, Duka A, Drosatos K, Hayes KC, Zannis VI. Role of esrrg in the fibrate-mediated regulation of lipid metabolism genes in human apoa-i transgenic mice. Pharmacogenomics J 10(2010) 165-79.##Scatena R, Nocca G, De Sole P, Fresu R, Zuppi C, Giardina B. The priming effect of gemfibrozil on reactive oxygen metabolism of phagocytic leucocytes. An intriguing side effect. Clin Chim Acta 266(1997) 173-83.##Seaver LC, Imlay JA. Are respiratory enzymes the primary sources of intracellular hydrogen peroxide? J Biol Chem 279(2004) 48742-50.##Tang XQ, Feng JQ, Chen J, Chen PX, Zhi JL, Cui Y, et al. Protection of oxidative preconditioning against apoptosis induced by h2o2 in pc12 cells: Mechanisms via mmp, ros, and bcl-2. Brain Res 1057(2005) 57-64.##Villena JA, Hock MB, Chang WY, Barcas JE, Giguere V, Kralli A. Orphan nuclear receptor estrogen-related receptor alpha is essential for adaptive thermogenesis. Proc Natl Acad Sci U S A 104(2007) 1418-23.##Wei YH, Lee CF, Lee HC, Ma YS, Wang CW, Lu CY, et al. Increases of mitochondrial mass and mitochondrial genome in association with enhanced oxidative stress in human cells harboring 4,977 bp-deleted mitochondrial DNA. Ann N Y Acad Sci 928(2001) 97-112.##Wenz T. Pgc-1alpha activation as a therapeutic approach in mitochondrial disease. IUBMB Life 61(2009) 1051-62.##Xu J, Racke MK, Drew PD. Peroxisome proliferator-activated receptor-alpha agonist fenofibrate regulates il-12 family cytokine expression in the cns: Relevance to multiple sclerosis. J Neurochem 103(2007) 1801-10.##Xu S, Zhu BT, Cai MX, Conney AH. Stimulatory effect of clofibrate on the action of estradiol in the mammary gland but not in the uterus of rats. J Pharmacol Exp Ther 297(2001a) 50-6.##Xu S, Zhu BT, Conney AH. Stimulatory effect of clofibrate and gemfibrozil administration on the formation of fatty acid esters of estradiol by rat liver microsomes. J Pharmacol Exp Ther 296(2001b) 188-97.##Xu S, Zhu BT, Turan V, Rusyn I, Thurman R, Peters JM, et al. Pparalpha-dependent induction of liver microsomal esterification of estradiol and testosterone by a prototypical peroxisome proliferator. Endocrinology 142(2001c) 3554-7.##Zenobio JE, Sanchez BC, Archuleta LC, Sepulveda MS. Effects of triclocarban, n,n-diethyl-meta-toluamide, and a mixture of pharmaceuticals and personal care products on fathead minnows (pimephales promelas). Environ Toxicol Chem 33(2014) 910-9.#### ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Activation of Inward Rectifier Potassium Channels in High Salt Impairment of Hydrogen Sulfide-Induced Aortic Relaxation in Rats</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: Hydrogen sulfide (H2S) plays a key role in the regulation of vascular tone and protection of blood vessels against endothelial dysfunction. Since the mechanism of salt impairing H2S-induced vascular relaxation is not fully clear, therefore this study was designed to investigate the role of potassium (K+) channels in the vasodilatory effects of exogenous H2S in rat aortic rings.&#160;Materials and Methods: Isolated thoracic aortic rings of adult male albino rats fed 8% NaCl diet for six weeks were used for isometric tension recording using PowerLab tissue bath system.&#160;Results: The relaxation response to sodium disulfide (Na2S, an H2S donor) was reduced in aortic rings of rats that were either fed high salt (HS) or incubated in a medium containing 1,3 or 5mM/L of extra NaCl compared with control rings. Na2S-induced relaxation was lower in rings precontracted by high K+ than phenylephrine (PE, a selective &#945;1adrenergic receptor agonist). In addition, incubation of aortic rings of HS loaded rats with inward-rectifier K+ (KIR) channels blocker individually or simultaneously with either ATP-dependent (KATP) or voltage-sensitive K+ (KV) channels blockers inhibited Na2S-induced relaxation in PE-precontracted rings; however it had no effects on rings pretreated with KATP channels blocker. In contrast, incubation of aortic rings of HS loaded rats with Ca+2 activated K+ (KCa) channels blocker individually or in combination with KIR channels blocker significantly enhanced Na2S-induced relaxation.&#160;Conclusion: These results revealed that HS partially impairs aortic relaxation caused by H2S, and that the mechanism of relaxation is mainly mediated by the stimulation of KIR channels and inhibition of KCa channels.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>263</FPAGE>
			<TPAGE>273</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2015/10/182015/09/272015/09/162015/09/142015/09/202015/09/72015/10/1
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1394/7/9
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2015/12/112016/01/92015/12/282015/11/282015/12/282015/11/282016/01/19
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1394/10/29
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Abbas BQ</Name>
				<MidName></MidName>
				<Family>Salihi</Family>
				<NameE>Abbas BQ</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Salihi</FamilyE>
				<Organizations>
				<Organization>Biology Department, College of Science, Salahaddin University-Erbil, Kurdistan Region, Iraq</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>abbas.salihi@uni-sci.org</Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Hydrogen sulfide</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>KIR channels</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Relaxation</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Aorta</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>High-salt diet</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>Adegunloye B, Sofola O. Relaxation responses of aortic rings from salt-loaded high calcium fed rats to potassium chloride, calcium chloride and magnesium sulphate. Pathophysio. 1998; 4: 275–280.##Al-Habib O, Salihi A. Endothelium derived relaxation factors reduce sulfur dioxide-induced aortic relaxation. OJMIP. 2013; 03: 181-185.##Altaany Z, Moccia F, Munaron L, Mancardi D, Wang R. Hydrogen sulfide and endothelial dysfunction: Relationship with nitric oxide. Curr Med Chem. 2014; 21: 3646-61.##Amberg GC, Bonev AD, Rossow CF, Nelson MT, Santana LF. Modulation of the molecular composition of large conductance, ca2+ activated k+ channels in vascular smooth muscle during hypertension. JCI. 2003; 112: 717-724.##Beltowski J, Jamroz-Wisniewska A. Hydrogen sulfide and endothelium-dependent vasorelaxation. Mol. 2014; 19: 21183-21199.##Bernatova I. Endothelial dysfunction in experimental models of arterial hypertension: Cause or consequence? Biomed Res Int. 2014; 2014: 598271.##Blanco-Rivero J, Gamallo C, Aras-López R, Cobeño L, Cogolludo A, Pérez-Vizcaino F, et al. Decreased expression of aortic kir6.1 and sur2b in hypertension does not correlate with changes in the functional role of katp channels. Eur J Pharmacol. 2008; 587: 204-208.##Callera G, Yogi A, Tostes R, Rossoni L, Bendhack L. Ca2+-activated k+ channels underlying the impaired acetylcholine-induced vasodilation in 2k-1c hypertensive rats. J Pharmacol Exp Ther. 2004; 309: 1036-42.##Cheng Y, Ndisang JF, Tang G, Cao K, Wang R. Hydrogen sulfide-induced relaxation of resistance mesenteric artery beds of rats. Am J Physiol Heart Circ Physiol. 2004; 287: 10.##Cordaillat M, Fort A, Virsolvy A, Elghozi JL, Richard S, Jover B. Nitric oxide pathway counteracts enhanced contraction to membrane depolarization in aortic rings of rats on high-sodium diet. Am J Physiol Regul Integr Comp Physiol. 2007; 292: R1557-62.##de Wardener HE, He FJ, MacGregor GA. Plasma sodium and hypertension. Kidney Int. 2004; 66: 2454-66.##Dombkowski R, Russell M, Olson K. Hydrogen sulfide as an endogenous regulator of vascular smooth muscle tone in trout. Am J Physiol Regul Integr Comp Physiol. 2004; 286: R678–R685.##Edwards D, Farquhar W. Vascular effects of dietary salt. Curr Opin Nephrol Hypertens. 2015; 24: 8-13.##Edwards FR, Hirst GD. Inward rectification in submucosal arterioles of guinea-pig ileum. J Physiol. 1988; 404: 437-54.##Elliot P, Stamler J, Nichols R, Dyer AR, Stamler R, Kesteloot H, et al. Intersalt revisited: Further analyses of 24 hour sodium excretion and blood pressure within and across populations. Br. Med. J. 1996; 312: 1249-1253.##Faber ES, Sah P. Calcium-activated potassium channels: Multiple contributions to neuronal function. Neurosci. 2003; 9: 181-94.##Giardina J, Green G, Rinewalt A, Granger J, Khalil R. Role of endothelin b receptors in enhancing endothelium-dependent nitric oxide–mediated vascular relaxation during high salt diet. Hypertens. 2001; 37: 516-523.##Haddy F, Vanhoutte P, Feletou M. Role of potassium in regulating blood flow and blood pressure. Am J Physiol Regul Integr Comp Physiol. 2006; 290: R546–R552.##Izzard A, Heagerty A. Impaired flow dependent dilation in distal mesenteric arteries from the spontaneously hypertensive rat. J Physiol. 1999; 518: 239–245.##Jackson W. Ion channels and vascular tone. Hypertension. 2000; 35: 173-178.##Joseph BK, Thakali KM, Moore CL, Rhee SW. Ion channel remodeling in vascular smooth muscle during hypertension: Implications for novel therapeutic approaches. Pharmacol Res. 2013; 70: 126-38.##Kagota S, Tamashiro A, Yamaguchi Y, Nakamura K, Kunitomo M. High salt intake impairs vascular nitric oxide/cyclic guanosine monophosphate system in spontaneously hypertensive rats. 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			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Asymmetric Involvement of Central and the Peripheral NMDA Glutamate Receptors in the Expression of Withdrawal Syndrome in Morphine-Dependent Mice</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: Morphine withdrawal syndrome is mediated via several central and peripheral neurological pathways. In the present study we investigated the role of N-methyl-D aspartic acid (NMDA) glutamate receptor on naloxone-induced withdrawal syndrome in morphine-conditioned mice.&#160;Materials and Methods: We designed two separate experiments. In experiment one, 30 male NMRI mice were divided into 5 groups, pretreated with memantine (0.1, 1 and 5 mg/kg; I.P.) followed by morphine-dependence period for 3 days. In the other experiment, 48 male NMRI mice distributed into 8 groups, pretreated with intra-accumbens (IAc) memantine (1 and 5 &#956;g/animal) within the right, left and both side of nucleus accumbens (RNAcc, LNAcc and BNAcc) followed by I.P. morphine-dependence (3 days). On day 4, in both experiments, morphine was injected into mice, followed by naloxone. Then naloxone-induced total jumping count, jump height and defecation in morphine-conditioned mice were recorded for 30 min.&#160;Results: Pre-treatment by I.P. injection of memantine significantly attenuated naloxone precipitated jumping count/30 min, jumping height (mm) and fecal material output in morphine dependent mice (P&#60;0.05). Also, IAC pretreatment with memantine in LNAcc, RNAcc and BNAcc significantly declined the effect of I.P. injection of naloxone on total jumping count and jumping height (P&#60;0.05), pretreatment within memantine in LNAcc, RNAcc and BNAcc had no effect on defecation (P&#62;0.05).&#160;Conclusion: These findings indicated asymmetric involvement of central and peripheral NMDA glutamate receptors in withdrawal syndrome development in morphine-dependent mice.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>274</FPAGE>
			<TPAGE>284</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2015/10/182015/09/272015/09/162015/09/142015/09/202015/09/72015/10/12015/09/17
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1394/6/26
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2015/12/112016/01/92015/12/282015/11/282015/12/282015/11/282016/01/192016/01/16
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1394/10/26
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Mahboubeh</Name>
				<MidName></MidName>
				<Family>Kamali</Family>
				<NameE>Mahboubeh</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Kamali</FamilyE>
				<Organizations>
				<Organization>Department of Biology, Islamic Azad University, North Tehran Branch, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>habib.yari@yahoo.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Hedayat</Name>
				<MidName></MidName>
				<Family>Sahraei</Family>
				<NameE>Hedayat</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Sahraei</FamilyE>
				<Organizations>
				<Organization>Neurosciences Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>sahraei1343@gmail.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Maryam</Name>
				<MidName></MidName>
				<Family>Khosravi</Family>
				<NameE>Maryam</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Khosravi</FamilyE>
				<Organizations>
				<Organization>Department of Biology, Islamic Azad University, North Tehran Branch, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>habib.yari@gmail.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Shahin</Name>
				<MidName></MidName>
				<Family>Hassanpour</Family>
				<NameE>Shahin</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Hassanpour</FamilyE>
				<Organizations>
				<Organization>Section of Physiology, Department of Basic Sciences, Faculty of Veterinary Medicine, Science and Research Branch, Islamic Azad University, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>habib.yari@gmail.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Habib</Name>
				<MidName></MidName>
				<Family>Yaribeygi</Family>
				<NameE>Habib</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Yaribeygi</FamilyE>
				<Organizations>
				<Organization>Neurosciences Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>habib.yari@gmail.com</Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Memantine</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>NMDA glutamate receptors</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Morphine withdrawal syndrome</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Mice</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
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			</REFRENCE>
		</REFRENCES>

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