en
jalali
1394
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gregorian
2015
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Dissimilar mechanistic background of peripheral and orofacial hyperkinesia in patients with Parkinson’s disease and levodopa-induced dyskinesia
Introduction: Long-term levodopa treatment of Parkinson’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. 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). Results: Genotyping patients with PD and LID revealed that only rs3773678 (DRD3, dominant, p = 0.042) was associated with orofacial dyskinesia. 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.
Levodopa-induced dyskinesia, Parkinson’s disease, Dopaminergic receptors, Serotonergic receptors, Genetic variants
216
221
http://ppj.phypha.ir/browse.php?a_code=A-10-891-1&slc_lang=en&sid=1
2015/10/18
1394/7/26
2015/12/11
1394/9/20
Svetlana A
Ivanova
Mental Health Research Institute, Tomsk, Russian Federation
svetlana@mail.tomsknet.ru
00319475328460015821
00319475328460015821
No
Olga Yu
Fedorenko
Mental Health Research Institute, Tomsk, Russian Federation
f_o_y@mail.ru
00319475328460015822
00319475328460015822
No
Maxim B
Freidin
Research Institute for Medical Genetics, Tomsk, Russian Federation
mfreidin@medgenetics.ru
00319475328460015823
00319475328460015823
No
Valentina M
Alifirova
Department of Neurology and Neurosurgery, Siberian State Medical University, Tomsk, Russian Federation
alifirova@mail2000.ru
00319475328460015824
00319475328460015824
No
Natalia G
Zhukova
Department of Neurology and Neurosurgery, Siberian State Medical University, Tomsk, Russian Federation
znatali@yandex.ru
00319475328460015825
00319475328460015825
No
Irina A
Zhukova
Department of Neurology and Neurosurgery, Siberian State Medical University, Tomsk, Russian Federation
irzhukova@inbox.ru
00319475328460015826
00319475328460015826
No
Asmar FY
Al Hadithy
Department of Pharmacotherapy and Pharmaceutical Care, University of Groningen, Groningen, The Netherlands
a.alhadithy@parnassiabavogroep.nl
00319475328460015827
00319475328460015827
No
Jacobus RBJ
Brouwers
Department of Pharmacotherapy and Pharmaceutical Care, University of Groningen, Groningen, The Netherlands
jrbjbrouwers@live.nl
00319475328460015828
00319475328460015828
No
Nikolay A
Bokhan
Mental Health Research Institute, Tomsk, Russian Federation
nikolay.bokhan.tomsk.russia@gmail.com
00319475328460015829
00319475328460015829
No
Bob
Wilffert
Department of Pharmacotherapy and Pharmaceutical Care, University of Groningen, Groningen, The Netherlands
b.wilffert@rug.nl
00319475328460015830
00319475328460015830
No
Anton JM
Loonen
Department of Pharmacotherapy and Pharmaceutical Care, University of Groningen, Groningen, The Netherlands
a.j.m.loonen@rug.nl
00319475328460015831
00319475328460015831
Yes
en
A study of variation in cardiocirculatory parameters with different body positions during isometric exercise in young adult males.
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. Materials and Methods: Cross sectional study was carried out in 33 young adult males (mean age: 19.21±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. 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). 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.
Isometric handgrip exercise, Body positions, Blood pressure, Heart rate, Rate pressure product
222
231
http://ppj.phypha.ir/browse.php?a_code=A-10-888-1&slc_lang=en&sid=1
2015/10/182015/09/27
1394/7/5
2015/12/112016/01/9
1394/10/19
Viral I
Champaneri
Department of Physiology, Pacific Institute of Medical Sciences, Udaipur-Rajasthan, India
drviralchampaneri@gmail.com
00319475328460015832
00319475328460015832
Yes
Rajesh
Kathrotia
Department of Physiology, All India Institute of Medical Sciences, Rishikesh, Uttarakhand, India
rajeshkathrotia@gmail.com
00319475328460015833
00319475328460015833
No
en
Melatonin and Alpha Lipoic Acid: Possible Mitigants for Lopinavir/Ritonavir- Induced Renal Toxicity in Male Albino Rats
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. 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. Results: Treatment with MT and ALA significantly (p<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<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. 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.
Kidney, Toxicity, Lopinavir/Ritonavir, Melatonin, Alpha Lipoic Acid, Rats
232
240
http://ppj.phypha.ir/browse.php?a_code=A-10-861-2&slc_lang=en&sid=1
2015/10/182015/09/272015/09/16
1394/6/25
2015/12/112016/01/92015/12/28
1394/10/7
Elias
Adikwu
Department of Pharmacology, Faculty of Basic Medical Sciences, University of Port Harcourt, Choba, Rivers State, Nigeria
adikwuelias@gmail.com
00319475328460015886
00319475328460015886
Yes
Nelson
Braimbaifa
Department of Pharmacology, Faculty of Basic Medical Sciences, University of Port Harcourt, Choba, Rivers State, Nigeria
brambaifan@gmail.com
00319475328460015887
00319475328460015887
No
Atuboyedia Wolfe
Obianime
Department of Pharmacology, Faculty of Basic Medical Sciences, University of Port Harcourt, Choba, Rivers State, Nigeria
adikwuelias@yahoo.com
00319475328460015888
00319475328460015888
No
en
Acute application of cholecystokinin and its effect on long-term potentiation induction at CA1 area of hippocampal formation in rat
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. Materials and Methods: Experimental groups were control, CCK-5min and CCK-30min. CCK-8s was injected 5 or 30 min (1.6 μg/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. 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<0.001) and the fEPSP area (p<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<0.05). 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.
Cholecystokinin sulfated octapeptide, CA1, Hippocampus, LTP.
241
246
http://ppj.phypha.ir/browse.php?a_code=A-10-886-2&slc_lang=en&sid=1
2015/10/182015/09/272015/09/162015/09/14
1394/6/23
2015/12/112016/01/92015/12/282015/11/28
1394/9/7
Farzane
Dehghani
Applied Physiology Research Center, Isfahan University of Medical Sciences, Isfahan, Iran.
dehghani.med@gmail.com
00319475328460015837
00319475328460015837
No
Parham
Reisi
Applied Physiology Research Center, Isfahan University of Medical Sciences, Isfahan, Iran.
p_reisi@med.mui.ac.ir
00319475328460015838
00319475328460015838
Yes
en
Antibacterial and Immunomodulatory Effects of Hexamethylenetetramine (Methenamine) Silver Nitrate
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. 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). 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. 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.
Silver-based complex, Methenamine, Antibacterial drug, Nosocomial infections, Staphylococcus, Streptococcus, Silver hexamethylenetetramine, Phagocytosis, Lymphocytes blast transformation
247
252
http://ppj.phypha.ir/browse.php?a_code=A-10-846-2&slc_lang=en&sid=1
2015/10/182015/09/272015/09/162015/09/142015/09/20
1394/6/29
2015/12/112016/01/92015/12/282015/11/282015/12/28
1394/10/7
Evgenii
Plotnikov
Tomsk Polytechnic University, Tomsk, Russia
plotnikov.e@mail.ru
00319475328460015839
00319475328460015839
Yes
Vladimir
Pehenko
Siberian State Medical University, Tomsk, Russia
vovapekhenko@sibmail.com
00319475328460015840
00319475328460015840
No
Vladimir
Plotnikov
“Polytech” ltd, Tomsk, Russia
plotnikov.vm@mail.ru
00319475328460015841
00319475328460015841
No
en
Gemfibrozil protect PC12 cells through modulation of Estradiol receptors against oxidative stress
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’s disease, Parkinson’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. Materials and Methods: In this study, neuronal-like PC12 cells with were pretreated with different concentrations of gemfibrozil and H2O2, concomitantly. 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. 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.
Gemfibrozil, Mitochondrial transcription factor A, Fulvestrant, Caspase 3, H2O2
253
262
http://ppj.phypha.ir/browse.php?a_code=A-10-881-2&slc_lang=en&sid=1
2015/10/182015/09/272015/09/162015/09/142015/09/202015/09/7
1394/6/16
2015/12/112016/01/92015/12/282015/11/282015/12/282015/11/28
1394/9/7
Ghorbangol
Ashabi
Physiology Research Center and Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
as_habi@yahoo.com
00319475328460015845
00319475328460015845
No
Leila
Khalaj
Medical School, Alborz University of Medical Sciences, Alborz, Iran
lkhalaj@yahoo.com
00319475328460015846
00319475328460015846
Yes
en
Activation of Inward Rectifier Potassium Channels in High Salt Impairment of Hydrogen Sulfide-Induced Aortic Relaxation in Rats
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. 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. 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 α1adrenergic 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. 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.
Hydrogen sulfide, KIR channels, Relaxation, Aorta, High-salt diet
263
273
http://ppj.phypha.ir/browse.php?a_code=A-10-883-1&slc_lang=en&sid=1
2015/10/182015/09/272015/09/162015/09/142015/09/202015/09/72015/10/1
1394/7/9
2015/12/112016/01/92015/12/282015/11/282015/12/282015/11/282016/01/19
1394/10/29
Abbas BQ
Salihi
Biology Department, College of Science, Salahaddin University-Erbil, Kurdistan Region, Iraq
abbas.salihi@uni-sci.org
00319475328460015844
00319475328460015844
Yes
en
Asymmetric Involvement of Central and the Peripheral NMDA Glutamate Receptors in the Expression of Withdrawal Syndrome in Morphine-Dependent Mice
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. 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 μg/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. 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<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<0.05), pretreatment within memantine in LNAcc, RNAcc and BNAcc had no effect on defecation (P>0.05). Conclusion: These findings indicated asymmetric involvement of central and peripheral NMDA glutamate receptors in withdrawal syndrome development in morphine-dependent mice.
Memantine, NMDA glutamate receptors, Morphine withdrawal syndrome, Mice
274
284
http://ppj.phypha.ir/browse.php?a_code=A-10-887-1&slc_lang=en&sid=1
2015/10/182015/09/272015/09/162015/09/142015/09/202015/09/72015/10/12015/09/17
1394/6/26
2015/12/112016/01/92015/12/282015/11/282015/12/282015/11/282016/01/192016/01/16
1394/10/26
Mahboubeh
Kamali
Department of Biology, Islamic Azad University, North Tehran Branch, Tehran, Iran
habib.yari@yahoo.com
00319475328460015847
00319475328460015847
No
Hedayat
Sahraei
Neurosciences Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran
sahraei1343@gmail.com
00319475328460015848
00319475328460015848
No
Maryam
Khosravi
Department of Biology, Islamic Azad University, North Tehran Branch, Tehran, Iran
habib.yari@gmail.com
00319475328460015849
00319475328460015849
No
Shahin
Hassanpour
Section of Physiology, Department of Basic Sciences, Faculty of Veterinary Medicine, Science and Research Branch, Islamic Azad University, Tehran, Iran
habib.yari@gmail.com
00319475328460015850
00319475328460015850
No
Habib
Yaribeygi
Neurosciences Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran
habib.yari@gmail.com
00319475328460015851
00319475328460015851
Yes