Effects of dietary supplementation of zinc oxide nanoparticles on some biochemical biomarkers in common carp (Cyprinus carpio)

If the dose and duration of zinc oxide nanoparticle (ZnO-NPs) supplementation optimize, low concentrations of Zn nanoparticles can replace conventional Zn sources in diets of different species of fish. Since evaluating the cytotoxicity of any nutritional supplement is one of the requirements for optimizing the dose for a specified time, we conducted this study to investigate the effects of oral administration of ZnO-NPs on oxidative stress and certain biochemical biomarkers in common carp, Cyprinus carpio, as an experimental model. For this purpose, ZnO-NPs were orally administered to fish for 21 days at 0 (control), 5, 10 and 15 mg kg-1 feed. Administration of ZnO-NPs (15 mg kg-1) significantly enhanced aspartate aminotransferase (AST), and lactate dehydro-genase (LDH) activities in liver, and alanine aminotransferase (ALT), alkaline phosphatase (ALP), and LDH activities in kidney. Dietary ZnO-NPs increased glucose-6-phosphate dehydrogenase (G6PDH) activity in liver of fish. The results indicated that administration of 10 mg kg-1 and 15 mg kg-1 ZnO-NPs caused a significant increase in ALT and catalase (CAT) activities and malondialdehyde (MDA) levels in liver, AST and CAT activities and MDA levels in kidney. ZnO-NPs decreased the liver ALP activity. Administration of 5 mg kg-1 ZnO-NPs significantly increased the cellular total antioxidant (TA) levels in various tissues. Therefore, we suggest that oral administration of 10 and 15 mg kg-1 ZnO NPs caused cytotoxicity and alterations in oxidative biomarkers, but 5 mg ZnO-NPs per kg feed had no side effects on oxidative stress and biochemical biomarkers in fish

Zonisamide Efficacy as Adjunctive Therapy in Children With Refractory Epilepsy

How to Cite This Article: Karimzadeh P, Ashrafi MR, Bakhshandeh Bali MK, Nasehi MM, Taheri Otaghsara SM, Taghdiri MM, Ghofrani M. ZonisamideEfficacy as Adjunctive Therapy in Children With Refractory Epilepsy. Iran J Child Neurol. 2013 Spring; 7(2):37-42.ObjectiveApproximately one third of epileptic children do not achieve complete seizure improvement. Zonisamide is a new antiepileptic drug which is effective as adjunctive therapy in treatment of intractable partial seizures.The purpose of the current study was to evaluate the effectiveness, safety, and tolerability of Zonisamide in epileptic children.Materials & MethodsFrom November 2011 until October 2012, 68 children who referred to Children’s Medical Center and Mofid Children Hospital due to refractory epilepsy (failure of seizure control with the use of two or more anticonvulsant drugs) entered the study. The patients were treated with Zonisamide by dose of 2- 12 mg/kg daily in addition to the previous medication. We followed the children every three to four-weeks intervals based on daily frequency, severity and duration of seizures. During the follow-up equal and more than fifty percent reduction in seizurefrequency or severity known as response to the drug.ResultsIn this study 68 patients were examined that 61 children reached the last stage.35 (57.4%) were male and 26 (42.6%) patients were female.After first and six months of Zonisamide administration daily seizure frequency decreased to 2.95±3.54 and 3.73±3.5 respectively. There was significant difference between seizure frequency in first and six month after Zonisamide toward initial attacks. After six months ZNS therapy a little side effects were created in 10 patients (16.4%) including stuttering(4.9%), decreased appetite (4.9%), hallucination (1.6%), dizziness(1.6%), blurred vision(1.6%) and suspiring(1.6%) as all of them eliminated later dosage reduction.ConclusionThis study confirms the short term efficacy and safety of Zonisamide in children with refractory epilepsies. References1. Michal V. Johnston. Seizure in childhood. In: Robert M. Kliegman, Richad E. Behrman. Nelson Text book of pediatrics.18th edition; Philadelphia:Saunders,2010,p 2457-70.2. Icardi J.Epilepsy in children .3th Ed. Lippincott Williams &Wilkins .edition .2004:38.3. Barbara Olson.Treatment of refractory epilepsy.Adv stumed 2005:Vol 5;470-473.4. Berto P. Quality of life in patients with epilepsy and impactof treatments. Pharmacoeconomics 2002;20:1039-59.5. Lepikk IE. Zonisamide: chemistry, mechanism of action,and pharmacokinetics. Seizure 2004;13S: S5-9.6. Sobieszek G, Borowicz KK, Kimber-Trojnar Z, Małek R, Piskorska B, Czuczwar SJ. Zonisamide: a new antiepileptic drug. Pol J Pharmacol 2003 Sep- Oct; 55(5): 683-9.7. Ohtahara, S. Zonisamide in the management of epilepsyJapanese experience. Epilepsy Res 2006;68 (Suppl. 2):25-33.8. Baulac M. Introduction to zonisamide. Epilepsy Res 2006;68(Suppl. 2):S3-S9.9. Hwang H, Kim KJ. New antiepileptic drugs in pediatric epilepsy. Brain Dev 2008;30(9):549-55.10. Kyoung Heo, Byung In Lee, Sang Do Yi, Yong Won Cho, Dong Jin Shin, Hong Ki Song, et al. Shortterm efficacy and safety of zonisamide as adjunctive treatment for refractory partial seizures: A multicenter open-label single-arm trial in Korean patients. Seizure 2012;21:188-193.11. Schulze-Bonhage A. Zonisamide in the treatment of epilepsy. Expert Opin Pharmacother 2010;11(1):115-26.12. Lee YJ, Kang HC, Seo JH, Lee JS, Kim HD. Efficacy and tolerability of adjunctive therapy with zonisamide in childhood intractable epilepsy. Brain Dev 2010;32(3):208-12.13. Marmaroua A, Pellockb JM. Zonisamide: Physician and patient experiences. Epilepsy Res 2005 Mar-Apr;64(1-2):63-9.14. Fallah R, Divesalar S, Babaei A. The efficacy and safety of zonisamide as an add-on drug in the treatment of lennox–gastaut syndrome. Iran J Child Neurol 2010 Nov;l4(3):45-50.15. Shah J, Shellenberger K, Canafax DM. Zonisamide: chemistry, biotransformation, and pharmacokinetics. Healthcare, Philadelphia (2002), pp. 873-879.16. Baulac M. Introduction to zonisamide. Epilepsy Res2006 Feb;68 (Suppl 2):S3-9. 17. Baulac M, Ilo E. Leppik. Efficacy and safety of adjunctive zonisamide therapy for refractory partial seizures. Epilepsy Research 2007;75:75-83. 18. Coppola G, Grosso S, Verrotti A, Parisi P, Luchetti A,Franzoni E, et al. Zonisamide in children and young adults with refractory epilepsy: An open label, multicenter Italian study. Epilepsy Research 2009;83:112-116.19. Tan HJ, Martland TR, Appleton RE, Kneen R. Effectiveness and tolerability of zonisamide in children with epilepsy: A retrospective review. Seizure 2010;19:31-35.20. Stephen LJ, Kelly K, Wilson EA, Parker P, Brodie MJ. A prospective audit of adjunctive zonisamide in an everyday clinical setting. Epilepsy Behav 2010 Apr;17(4):455-60.21. Catarino CB, Bartolini E, Bell GS, Yuen AWC, Duncan JS, Sander JW.The long-term retention of zonisamide in a large cohort of people with epilepsy at a tertiary referral centre. Epilepsy Research 2011;96:39-44.22. Loscher W, Schmidt D. Experimental and clinical evidence for loss of effect(tolerance) during prolonged treatment with antiepileptic drugs. Epilepsia 2006;47(8):1253-84.23. Eun SH, Kim HD, Eun BL, Lee IK, Chung HJ, Kim JS, et al. Comparative trial of low- and high-dose zonisamide as monotherapy for childhood epilepsy.Seizure 2011;20(7):558-63

Atypical Findings of Guillain-Barré Syndrome in Children

How to cite this article: Karimzadeh P, Bakhshandeh Bali MK, Nasehi MM, Taheri Otaghsara SM, Ghofrani M. Atypical Findings of Guillain-Barré Syndrome in Children. Iran J Child Neurol Autumn 2012;6(4):17-22. AbstractObjectiveGuillain-Barre syndrome (GBS) is an immune-mediated polyneuropathy that occurs mostly after  prior infection. The diagnosis of this syndrome is dependent heavily on the history and examination, although cerebrospinal fluid analysis and electrodiagnostic testing usually confirm the diagnosis. This is a retrospective study which was performed to investigate the atypical features of GBS.Materials & MethodsThirty three patients (21/63.6% males and 12/36.4% females) with GBS were retrospectively studied and prospectively evaluated at the Child Neurology institute of Mofid Children Hospital of Shahid Beheshti University of Medical Sciences between May 2011 and September 2012.ResultsThe mean age was 5.4 years (range, 1.5-10.5).Twenty one patients (87.9 %) had previous history of infections. Eight patients (24.2%) admitted with atypical symptoms like upper limb weakness (3%), ptosis (3%), neck stiffness (3%), inability to stand (proximal weakness) (9.1%), headache (3%) and dysphagia (3%).According to disease process, weakness was ascending in 26 (78.8%), descending in 5 (15.2%) and static in 2 (6.1%) patients. Cranial nerve involvement was found in 8(24.3%) children, most commonly as facial palsy in 3 (9.1%).ConclusionIn this study, 24.3% of our patients presented with atypical symptoms of GBS as upper limb weakness, ptosis, neck stiffness, inability to stand (proximal weakness), headache and dysphagia References:Hughes RA, Cornblath DR. Guillain-Barré syndrome. Lancet. 2005 Nov 5;366(9497):1653-66.McGillicuddy DC, Walker O, Shapiro NI, Edlow JA. Guillain-Barré syndrome in the emergency department. Ann Emerg Med. 2006 Apr;47(4):390-3.Cosi V, Versino M. Guillain-Barré syndrome. Neurol Sci. 2006;27(Suppl 1):S47-51.Hughes RA, Cornblath DR. Guillain-Barré syndrome. Lancet. 2005 Nov;366(9497):1653-66.Barzegar M, Dastgiri S, Karegarmaher MH, Varshochiani A. Epidemiology of childhood Guillan Barre syndrome in the north west of Iran. BMC Neurol. 2007 Aug 5;7:22.Vriesendorp FJ, Mishu B, Blaser MJ, Koski CL. Serum antibodies to GM1, GD1b, peripheral nerve myelin, and Campylobacter jejuni in patients with Guillain-Barre syndrome and controls: correlation and prognosis. Ann Neurol. 1993 Aug;34(2):130-5.Asbury AK, Cornblath DR. Assessment of current diagnostic criteria for Guillain-Barre syndrome. Ann Neurol. 1990;27 Suppl:S21-4.Hughes RA, Cornblath DR. Guillain-Barre syndrome. Lancet. 2005 Nov;366(9497):1653-66.Govoni V, Granieri E. Epidemiology of the Guillain-Barre syndrome. Curr Opin Neurol. 2001 Oct;14(5):605-13.Gordon PH, Wilbourn AJ. Early electrodiagnostic findings in Guillain-Barré syndrome. Arch Neurol. 2001 Jun;58(6):913-7.Darabi K, Abdel-Wahab O, Dzik WH. Current usage of intravenous immune globulin and the rationale behind it: the Massachusetts General Hospital data and a review of the literature. Transfusion. 2006 May;46(5):741-53.Hughes RA, Raphaël JC, Swan AV, van Doorn PA. Intravenous immunoglobulin for Guillain-Barré syndrome. Cochrane Database Syst Rev. 2006 Jan 25;(1):CD002063.Hughes RA, Swan AV, van Koningsveld R, van Doorn PA. Corticosteroids for Guillain-Barré syndrome. Cochrane Database Syst Rev. 2006 Apr 19;(2):CD001446.Asbury AK, Cornblath DR. Assessment of Current Diagnostic Criteria for Guillain-Barre syndrome. Ann Neurol. 1990; 27 Suppl:S21-4.van Doorn PA, Ruts L, Jacobs BC. Clinical features, pathogenesis, and treatment of Guillain-Barré syndrome. Lancet Neurol. 2008 Oct;7(10):939-50.Levin KH. Variants and mimics of Guillain-Barré Syndrome. Neurologist. 2004 Mar;10(2):61-74.Winer JB. Guillain-Barré syndrome: clinical variants and their pathogenesis. J Neuroimmunol. 2011 Feb;231(1-2):70-2.Susuki K, Koga M, Hirata K, Isogai E, Yuki N. A Guillain-Barré syndrome variant with prominent facial diplegia. J Neurol. 2009 Nov;256(11):1899-905.Jin Park H, Hyang Lee K. Atypical Miller-Fisher Syndrome Presenting as an Isolated Internal Ophthalmoplegia Following Epstein-Barr Virus Infection. J Pediatr Care for review 2012 Mar; 20(1):39-42.Etem Pişkin I, Calık M, Yarımay G, Adresi Y. Neck stiffness in Guillaine-Barre syndrome subsequent to cytomegalovirus Infection. Dicle Med J. 2011;38(1):104-6.Koul R, Chacko A, Ahmed R, Varghese T, Javed H, Al-Lamki Z. Ten year prospective study (clinical spectrum) of childhood Guillain Barré syndrome in the Arabian peninsula: comparison of  outcome in patients in the pre and post intravenous immunoglobulin eras. J Child Neurol. 2003;18(11):767-71.Linden V, da Paz JA, Casella EB, Marques-Dias MJ. Guillain-Barré syndrome in children: clinic, laboratorial and epidemiologic study of 61 patients. Arq Neuropsiquiatr. 2010 Feb;68(1):12-7.Winer JB, Hughes RA, Anderson MJ, Jones DM, Kangro H, Watkins RP. A prospective study of acute idiopathic neuropathy: II antecedent events. J Neurol Neurosurg Psychiatry. 1988 May;51(5):613-18.Ho TW, Mishu B, Li CY, Gao CY, Cornblath DR, Griffin JW et al. Guillain-Barre syndrome in northern China. Relationship to Campylobacter jejuni infection and anti-glycolipid antibodies. Brain. 1995 Jun;118(Pt 3):597-605.Bahou YG, Biary N, al Deeb S. Guillain-Barre syndrome: a series observed at Riyadh Armed Forces Hospital. J Neurol. 1996 Feb;243(2):147-52.Cosi V, Versino M. Guillain-Barré syndrome. J Neurol Sci. 2006;27 (Suppl 1):S47-S51.Winer JB. Guillain Barré syndrome. Mol Pathol. 2001 Dec;54(6):381-5.The prognosis and main prognostic indicators of Guillain-Barré syndrome: A multicentre prospective study of 297 patients. The Italian Guillan-Barre Study Group. Brain. 1996 Dec;119(Pt 6):2053-61

Study of Translating Semantic Oppositions of Hafez's Poems in Translation of Ali Abbas Zoleikhe

The language of Hafez's poetry is very delicate and mysterious. In his sonnets (Qazals), the words have been accurately selected with great aesthetic taste. In such a way, all the words are somehow connected and intertwined with each other. One of the linguistic features of Hafez is the collocation of oppositions together. Oppositions used in Hafez's poems not only have explicit and implicit semantic connections but also are related to other words. Therefore, understanding the conceptual relationship of words, and in particular, oppositions, plays a great role in discovering the meaning and the elegance of Hafez's poetry. Hence, in this study, an attempt has been made to select examples of "gradable, complementary, symmetrical, directional, lexical, and implicit” oppositions in Hafez's sonnets. Also, the conceptual relationship with other words of the verse will be analyzed and its semantic and aesthetic function will be explained. Subsequently, Ali Abbas Zoleikhe's translation of semantic oppositions and their functions will be discussed and criticized. The results of the research indicate that the oppositions in question, especially implicit oppositions, have created many clear and hidden rhetorical meanings in poetry and the slightest change in the oppositions and balance of words leads to the reduction of coherence and meaning of the verse

Sodium Channel Gene Mutations in Children with GEFS+ and Dravet Syndrome: A Cross Sectional Study

 How to Cite This Article: Tonekaboni SH, Ebrahimi A, Bakhshandeh Bali MK, Houshmand M, Moghaddasi M, Taghdiri MM, Nasehi MM. Sodium Channel Gene Mutations in Children with GEFS+ and Dravet Syndrome: A Cross Sectional Study. Iran J Child Neurol. 2013 Winter; 7 (1):25-29. Objective Dravet syndrome or severe myoclonic epilepsy of infancy (SMEI) is a baleful epileptic encephalopathy that begins in the first year of life. This syndrome specified by febrile seizures followed by intractable epilepsy, disturbed psychomotor development, and ataxia. Clinical similarities between Dravet syndrome and generalized epilepsy with febrile seizure plus (GEFS+) includes occurrence of febrile seizures and joint molecular genetic etiology. Shared features of these two diseases support the idea that these two disorders represent a severity spectrum of the same illness. Nowadays, more than 60 heterozygous pattern SCN1A mutations, which many are de novo mutations, have been detected in Dravet syndrome. Materials & Methods From May 2008 to August 2012, 35 patients who referred to Pediatric Neurology Clinic of Mofid Children Hospital in Tehran were enrolled in this study. Entrance criterion of this study was having equal or more than four criteria for Dravet syndrome. We compared clinical features and genetic findings of the patients diagnosed as Dravet syndrome or GEFS+. Results 35 patients (15 girls and 20 boys) underwent genetic testing. Mean age of them was 7.7 years (a range of 13 months to 15 years). Three criteria that were best evident in SCN1A mutation positive patients are as follows: Normal development before the onset of seizures, onset of seizure before age of one year, and psychomotor retardation after onset of seizures. Our genetic testing showed that 1 of 3 (33.3%) patients with clinical Dravet syndrome and 3 of 20 (15%) patients that diagnosed as GEFS+, had SCN1A mutation. Conclusion In this study, normal development before seizure onset, seizures beginning before age of one year and psychomotor retardation after age of two years are the most significant criteria in SCN1A mutation positive patients.References Dravet C, Bureau M, Oguni H, Fukuyama Y, Cokar O.Severe myoclonic epilepsy in infancy (Dravet syndrome). In: Roger J, Bureau M, Dravet C, Genton P, Tassinari CA, Wolf P, eds. Epileptic Syndromes in Infancy, Childhood and Adolescence, 4th  ed. London: John Libbey Eurotext Publishers; 2005. p. 89-113.Dalla Bernardina B, Colamaria V, Capovilla G, Bondavalli S. Nosological classification of epilepsies in the first three years years of life. Prog Clin Biol Res 1983;124:165-83.Commission on Classification and Terminology of the International League against Epilepsy. Proposal for revised classification of epilepsies and epileptic syndromes. Epilepsia 1989;30:389-99.Scheffer IE, Zhang. YH, Jansen FE, Dibbens L. Dravet syndrome or genetic (generalized) epilepsy with febrile seizures plus? Brain Dev 2009;31(5):394-400.Singh R, Andermann E, Whitehouse WP, Harvey AS, Keene DL, Seni MH, et al. severe myoclonic epilepsy of infancy: extended spectrum of GEFS+? Epilepsia 2001;42(7):837-44.Scheffer IE, Harkin LA, Dibbens LM, Mulley JC, Berkovic SF. Neonatal epilepsy syndromes and generalized epilepsy with febrile seizures plus (GEFS+). Epilepsia 2005;46 Suppl 10:41-7.Harkin LA, McMahon JM, Iona X, Dibbens L, Pelekanos JT, Zuberi SM, et al. The spectrum of SCN1A-related infantile enceptic encephalopathies. Brain 2007;130(Pt 3):843-52.Sun H, Zhang Y, Liang J, Liu X, Ma X, Qin, et al. Seven novel SCN1A mutations in Chinese patients with severe myoclonic epilepsy of infancy. Epilepsia 2008;49:1104-7.Miller SA, Dykes DD, polesky HF. A simple salting out procedure  for  extracting  DNA from  human  cucleated Nucleated cells. Nucleic Acids Res 1988;16(3):2115.Marini C, Scheffer IE, Nabbout R, Mei D, Cox K, Dibbens LM, et al. SCN1A duplications and deletions detected in dravet syndrome: implications for molecular diagnosis. Epilepsia 2009; 50(7):1670-8.Striano P, Mancardi MM, Biancheri R, Madia F, Gennaro E, Paravidino R, et al. Brain MRI findings in severe myoclonic epilepsy in infancy and genotype- correlations. Epilepsia 2007;48(6):1092-6.Wang JW, Kurahashi H, Ishii A, Kojima T, Ohfu M, Inoue T, et al. Micro chromosomal deletions involving SCN1A and adjacent genes in severe myoclonic epilepsy in infancy. Epilepsia 2008;49(9):1528-34.Lossin C. A catalog  of  SCN1A variants.  Brain  Dev 2009;31:114-30.Fountain-Capal JK, Holland KD, Gilbert DL, Hallinan BE When should clinicians order genetic testing for Dravet syndrome? Pediatr Neurol 2011;45(5): 319-23. Hattori J, Ouchida M, Ono J, Miyake S, Maniwa S, Mimaki  N,  et  al. A screening  test  for  the  prediction of Dravet syndrome before one year of age. Epilepsia 2008;49(4):626–33.Nabbout R, Gennaro E, Dalla Bernardina B, Dulac O, Madia F, Bertini E, et al. spectrum of SCN1A mutations severe myoclonic epilepsy of infancy. Neurology 2003;60(12):1961-7.Ohmori I, Ouchida M, Ohtsuka, Y oka E, Shimizu K. Significant correlation  of  The  SCN1A mutations  and severe myoclonic epilepsy in infancy. Biochem Biophys Res Commun 2002;295:17-23.Cales. L, Del-favero J, Ceulemans B, Lagae L, Van Broeckhoven C, De jonghe P. De novo mutations in the sodium- chnnel gene SCN1A cause severe myoclonic epilepsy of infancy. Am J Hum Genet 2001; 68(8):1327-32.Brunklaus A, Ellis R, Reavey E, Forbes GH, Zuberi SM.Prognostic, clinical and demographic features in SCN1A mutation-positive Dravet syndrome. Brain 2012;135(Pt 8):2329-36.Engel J Jr; International League Against Epilepsy (ILAE).A proposed diagnostic scheme for people with epileptic seizures  and  with  epilepsy:  report  of  the  ILAE Task force  on  Classifications  and  Terminology.  Epilepsia 2001;42(6):796-803.Fujiwara T, Sugawara T, Mazaki-Miyazaki E, Takahashi Y, Fukushima K, Watanabe M, et al. Mutations of sodium channel alpha subunit type 1 (SCN1A) in intractable childhood epilepsies with frequent generalized tonic- clonic seizures. Brain 2003;126:(Pt 3):531-46.Claes L, Ceulemans B, Audenaert D, Smets K, Löfgren A, Del-Favero J. De novo SCN1A mutations are a major cause of severe myoclonic epilepsy of infancy. Hum Mutat 2003;21(6):615-21.Lakhan R, Kumari R, Misra UK, Kalita J, Pradhan S, Mittal B. Differential role of sodium channels SCN1A and SCN2A gene polymorphisms with epilepsy and multiple drug resistance in the north Indian population. Br J Clin Pharmacol 2009;68(2):214-20

Parkinson’s Disease Is Associated With Dysregulation of Circulatory Levels of lncRNAs

Long non-coding RNAs (lncRNAs) have been recently reported to be involved in the pathoetiology of Parkinson’s disease (PD). Circulatory levels of lncRNAs might be used as markers for PD. In the present work, we measured expression levels of HULC , PVT1 , MEG3 , SPRY4-IT1 , LINC-ROR and DSCAM-AS1 lncRNAs in the circulation of patients with PD versus healthy controls. Expression of HULC was lower in total patients compared with total controls (Expression ratio (ER)=0.19, adjusted P value<0.0001) as well as in female patients compared with female controls (ER=0.071, adjusted P value=0.0004). Expression of PVT1 was lower in total patients compared with total controls (ER=0.55, adjusted P value=0.0124). Expression of DSCAM-AS1 was higher in total patients compared with total controls (ER=5.67, P value=0.0029) and in male patients compared with male controls (ER=9.526, adjusted P value=0.0024). Expression of SPRY4-IT was higher in total patients compared with total controls (ER=2.64, adjusted P value<0.02) and in male patients compared with male controls (ER=3.43, P value<0.03). Expression of LINC-ROR was higher in total patients compared with total controls (ER=10.36, adjusted P value<0.0001) and in both male and female patients compared with sex-matched controls (ER=4.57, adjusted P value=0.03 and ER=23.47, adjusted P value=0.0019, respectively). Finally, expression of MEG3 was higher in total patients compared with total controls (ER=13.94, adjusted P value<0.0001) and in both male and female patients compared with sex-matched controls (ER=8.60, adjusted P value<0.004 and ER=22.58, adjusted P value<0.0085, respectively). ROC curve analysis revealed that MEG3 and LINC-ROR have diagnostic power of 0.77 and 0.73, respectively. Other lncRNAs had AUC values less than 0.7. Expression of none of lncRNAs was correlated with age of patients, disease duration, disease stage, MMSE or UPDRS. The current study provides further evidence for dysregulation of lncRNAs in the circulation of PD patients

Comprehensive phylogenetic, similarity and allergenicity analysis of Boophilus genus tick Tropomyosin protein

     Boophilus genus ticks are responsible for transferring some pathogens and reducing production factors in cattle. Tropomysin (TPM) protein has actin regulator activity and playing important role in immune and allergic reactions. The main goal is to determine different aspects of phylogenetic, similarity, homology, structure and allergenicity of TPM protein. In prior study, we identified TPM by using Mass-spectrometry in Boophilus anulatus larva proteins extraction. Analysis by NCBI and Mascot software showed complete similarity of this protein with Boophilus microplus. TPM Blasting, invertebrates TPM sequences retrieval, aligning and analyzing of conserved and variable regions along sequences were next steps. Also, construction the phylogenetic tree, overall mean distances estimation, homology protein secondary structure, allergencity analysis was achieved. The most similar sequences to Boophilus genus TPM are Haemaphysalis sp., Scolopendra sp. and etc., respectively. The multiple sequence alignment showed that conserved and variable regions stretched in different part of TPM. The close relationships in Phylogenetic tree between Ticks and Mites were seen, although the TPM sequences in ticks are more similar to each other than to mites and assume as the nearest relatives. Insects TPM like worms, located in two separated clades, and Trichinella spiralis in worm clades are more related taxa to members of ticks and mites groups. Furthermore, overall mean distances over sequence pairs reflects TPM conservation during speciation. TPM has high homology in different species and has two domain of α-helix that cannot form disulfide bonds. Finally, allergenicity analysis by separated and hybrid approach showed it undoubted is allergen and candidates some peptides as responsible for allergenicity of TPM. The comprehensive analysis of TPM has never been easy, especially when we attempt to make statements from different aspects about this protein.  Our study revealed the some unique and valuable aspects of TPM protein of Boophilus genus, and will help to further studies on mentioned protein

Effect of Squill Oxymel on Knee Osteoarthritis: A Triple-Blind, Randomized, Controlled Clinical Trial

Osteoarthritis (OA) of the knee is a major health problem in the society. Iranian Traditional Medicine (ITM) or Persian Medicine (PM) as a branch of complementary medicine has been practiced in Iran for many centuries. An herbal medication known as squill oxymel has been used by PM physicians for OA. Our aim is to investigate the effect of squill oxymel on OA of the knee joint. Eighty eight patients were assigned to receive a placebo or squill oxymel syrup (10 ml each morning on empty stomach) for 8 consecutive weeks. Acetaminophen tablets were considered as the rescue medicine. Ultimately, 43 patients in the placebo group and 40 patients in the treatment group completed the trial and were included in the statistical analysis. Patients were followed for 4 weeks after cessation of treatment. The Knee injury and Osteoarthritis Outcome Score (KOOS) questionnaire and Visual Analog Scale (VAS) were considered as the main outcome measures. Laboratory tests including AST, ALT, BUN, Cr plus inflammatory tests including WBC, ESR, and CRP with specific tests i.e. IL6 and SOD at the beginning and the end of intervention were measured. The results showed the positive effect of treatment on the outcome of knee pain (p=0.04) and daily activity (p=0.01) of KOOS after Cessation of treatment. On the other hand, VAS decreased in both treatment and placebo groups while it showed significance intra-group and showed no significance between the two groups. After 4 weeks of cessation of treatment, the positive effect of the squill oxymel on the treatment group continued in some of the subscales of KOOS, including symptoms, knee pain and daily activities, but stopped in the placebo group. In general, both clinically and statistically significant improvement was observed after cessation of treatment. Squill oxymel syrup showed promising results in management of knee OA but future researches with larger sample size and longer duration are necessary