358 research outputs found

    Association of Family History of Epilepsy with Earlier Age Onset of Juvenile Myoclonic Epilepsy

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    How to Cite This Article: Najafi MR, Najafi MA, Safaei A. Association of Family History of Epilepsy with Earlier Age Onset of Juvenile Myoclonic Epilepsy. Iran J Child Neurol. Spring 2016; 10(2):10-15.AbstractObjectiveJuvenile myoclonic epilepsy (JME) is supposedly the most frequent subtype of idiopathic generalized epilepsies (IGE). The aim of this study was to determine the prevalence of JME and comparison of patients’ demographics as well as timeline of the disease between positive family history epileptic patients (PFHE) and negative family history epileptic patients (NFHE) among sample of Iranian epileptic patients.Materials & MethodsFrom Feb. 2006 to Oct. 2009, 1915 definite epileptic patients (873 females) referred to epilepsy clinics in Isfahan, central Iran, were surveyed and among them, 194 JME patients were diagnosed. JME was diagnosed by its specific clinical and EEG criteria. Patients were divided into two groups as PFHE and NFHE and data were compared between them.ResultsJME was responsible for 10% (194 patients) of all types of epilepsies. Of JME patients, 53% were female. In terms of family history of epilepsy, 40% were positive. No significant differences was found between PFHE and NFHE groups as for gender (P>0.05). Age of epilepsy onset was significantly earlier in PFHE patients (15 vs. 22 yr, P<0.001). Occurrence of JME before 18 yr old among PFHE patients was significantly higher (OR=2.356, P=0.007).ConclusionA family history of epilepsy might be associated with an earlier age of onset in patients with JME. References1. Banerjee PN, Filippi D, Allen Hauser W. The descriptive epidemiology of epilepsy—a review. Epilepsy Res 2009;85(1):31-45.2. Khedr EM, Shawky OA, Ahmed MA, Elfetoh NA, Al Attar G, Ali AM, et al. A community based epidemiological study of epilepsy in Assiut Governorate/Egypt. Epilepsy Res 2013;103(2):294-302.3. Rektor I, Schachter SC, Arzy S, Baloyannis SJ, Bazil C, Brázdil M, et al. Epilepsy, behavior, and art (Epilepsy, Brain, and Mind, part 1). Epilepsy Behav 2013;28(2):261-82.4. Steinlein OK. Genetics and epilepsy. Dialogues Clin Neurosci 2008;10(1):29-38.5. Engel Jr J. ILAE classification of epilepsy syndromes. Epilepsy Res 2006;70:5-10.6. Janz D. Epilepsy with impulsive petit mal (juvenile myoclonic epilepsy). Acta Neurol Scandinavica 1985;72(5):449-59.7. Alfradique I, Vasconcelos MM. Juvenile myoclonic epilepsy. Arquivos de Neuro-Psiquiatria 2007;65(4B):1266-71.8. Vijai J, Cherian P, Sylaja P, Anand A, Radhakrishnan K. Clinical characteristics of a South Indian cohort of juvenile myoclonic epilepsy probands. Seizure 2003;12(7):490-6.9. Babtain FA. Impact of a family history of epilepsy on the diagnosis of epilepsy in southern Saudi Arabia. Seizure 2013;22(7):542-7.10. Montenegro MA, Guerreiro MM, Lopes-Cendes I, Guerreiro CA, Li LM, Cendes F, editors. Association of family history of epilepsy with earlier age at seizure onset in patients with focal cortical dysplasia. Mayo Clinic Proceedings 2002;77(12): 1291–94.11. Berg AT, Berkovic SF, Brodie MJ, Buchhalter J, Cross JH, Van Emde Boas W, et al. Revised terminology and concepts for organization of seizures and epilepsies: report of the ILAE Commission on Classification and Terminology, 2005–2009. Epilepsia 2010;51(4):676-85.12. Janz D. Juvenile myoclonic epilepsy. Epilepsy with impulsive petit mal. Cleveland Clin J Med 1989;56 Suppl Pt 1:S23-33; discussion S40-2. Epub 1989/01/01.13. Najafi MR, Sonbolestan F, Sonbolestan SA, Zare M, Mehvari J, Meshkati SN. The course and outcome of pregnancy and neonatal situation in epileptic women. Adv Biomed Res 2012;1:4. Epub 2012/12/05. 14. Bittles AH. Consanguinity and its relevance to clinical genetics. Clin Genetics 2001;60(2):89-98.15. Johnston MV. Nelson’s Textbook of Pediatrics. 17th ed. Seizures in childhood. Vol. 2. Philadelphia: Saunders; 2004 p. 1993–2005.16. Sinha S, Pramod M, Dilipkumar S, Satishchandra P. Idiopathic generalized epilepsy: Phenotypic and electroencephalographic observations in a large cohort from South India. Ann Indian Academy Neurol 2013;16(2):163.17. Jallon P, Loiseau P, Loiseau J. Newly diagnosed unprovoked epileptic seizures: presentation at diagnosis in CAROLE study. Epilepsia 2001;42(4):464-75.18. Oka E, Ishida S, Ohtsuka Y, Ohtahara S. Neuroepidemiological study of childhood epilepsy by application of international classification of epilepsies and epileptic syndromes (ILAE, 1989). Epilepsia 1995;36(7):658-61.19. Murthy J, Yangala R, Srinivas M. The Syndromic Classification of the International League Against Epilepsy: A Hospital-Based Study from South India. Epilepsia 1998;39(1):48-54.20. Fittipaldi F, Curra A, Fusco L, Ruggieri S, Manfredi M. EEG discharges on awakening: a marker of idiopathic generalized epilepsy. Neurol 2001;56(1):123-6.21. Jallon P, Latour P. Epidemiology of idiopathic generalized epilepsies. Epilepsia 2005;46(s9):10-4.22. Classification Co, Epilepsy TotILA. Proposal for revised classification of epilepsies and epileptic syndromes. Epilepsia 1989;30:389-99.23. Berkovic, S. F. Genetics of epilepsy syndromes. In: Epilepsy: A Comprehensive Textbook (Eds J. Engel and T. A. Pedley). Lippincott-Raven Publ., 1997: pp. 217–224.24. Camfield CS, Striano P, Camfield PR. Epidemiology of juvenile myoclonic epilepsy. Epilepsy Behav 2013;28:S15-S7.25. Camfield CS, Camfield PR. Juvenile myoclonic epilepsy 25 years after seizure onset A population-based study. Neurol 2009;73(13):1041-5.26. Jayalakshmi SS, Mohandas S, Sailaja S, Borgohain R. Clinical and electroencephalographic study of first-degree relatives and probands with juvenile myoclonic epilepsy. Seizure 2006;15(3):177-83.27. Sozmen V, Baybas S, Dirican A, Koksal A, Ozturk M. Frequency of epilepsies in family members of patients with different epileptic syndromes. European Neurol 2010;65(1):4-9.28. Mullins G, O’sullivan S, Neligan A, McCarthy A, McNamara B, Galvin R, et al. A study of idiopathic generalised epilepsy in an Irish population. Seizure 2007;16(3):204-10.29. Shahnaz KS, Sattar RA. Clinical and EEG characteristics of Juvenile Myoclonic Epilepsy. Pak J Med Sci 2014;30(1):12.30. Liu A, Delgado-Escueta A, Gee M, Serratosa J, Zhang Q, Alonso M, et al. Juvenile myoclonic epilepsy in chromosome 6p12-p11: Locus heterogeneity and recombinations. Am J Medi Genetics 1996;63(3):438-46. 31. Figueredo R, Trevisol-Bittencourt PC, Ferro JBdM. Estudo clínico-epidemiológico de pacientes com epilepsia mioclônica juvenil em Santa Catarina. Arq Neuropsiquiatr 1999;57(2-B):401-4.32. Obeid T, Panayiotopoulos C. Juvenile myoclonic epilepsy: a study in Saudi Arabia. Epilepsia 1988;29(3):280-2.33. Nair RR, Thomas SV. Genetic liability to epilepsy in Kerala State, India. Epilepsy Res 2004;62(2):163-70. 34. Ottman R, Lee JH, Risch N, Hauser WA, Susser M. Clinical indicators of genetic susceptibility to epilepsy. Epilepsia 1996;37(4):353-61.35. Bianchi A, Viaggi S, Chiossi E. Family study of epilepsy in first degree relatives: data from the Italian Episcreen Study. Seizure 2003;12(4):203-10.36. Manganotti P, Bongiovanni LG, Fuggetta G, Zanette G, Fiaschi A. Effects of sleep deprivation on cortical excitability in patients affected by juvenile myoclonic epilepsy: a combined transcranial magnetic stimulation and EEG study. J Neurol Neurosurg Psychiatr 2006;77(1):56-60. Epub 2005/12/20.37. Roebling R, Scheerer N, Uttner I, Gruber O, Kraft E, Lerche H. Evaluation of cognition, structural, and functional MRI in juvenile myoclonic epilepsy. Epilepsia 2009;50(11):2456-65. Epub 2009/06/06.38. Edwards T, Scott AG, Munyoki G, Odera VMa, Chengo E, Bauni E, et al. Active convulsive epilepsy in a rural district of Kenya: a study of prevalence and possible risk factors. The Lancet Neurol 2008;7(1):50-6.

    Diagnosis and Management of Multiple Sclerosis in Children

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    How to Cite This Article: Najafi MR, Najafi MA, Nasr Z. Diagnosis and Management of Multiple Sclerosis in Children. Iran J Child Neurol. Summer 2016; 10(3): 13-23.AbstractGrowing evidence indicates the safety and well toleration of treatment by Disease-modifying in children suffering multiple sclerosis (MS). The treatment is not straight forward in a great number of patients, thus patients with pediatric MS must be managed by experienced specialized centers. Common treatments of multiple sclerosis for adults are first-line therapies. These therapies (firstline) are safe for children. Failure in treatment that leads to therapy alteration is almost prevalent in pediatric MS. Toleration against current second-line therapies has been shown in multiple sclerosis children. Oral agents have not been assessed in children MS patients. Although clinical trials in children are insufficient, immunomodulating managed children, experience a side effect similar to the adult MS patients. However, further prospective clinical studies, with large sample size and long follow-up are needed to distinguish the benefits and probable side effects of pediatric MS therapies. ReferencesJulian L, Serafin D, Charvet L, Ackerson J, Benedict R, Braaten E, et al. Cognitive Impairment Occurs in Children and Adolescents With Multiple Sclerosis Results From a United States Network.J Child Neurol 2013;28(1):102-7.Inaloo S, Haghbin S. Multiple sclerosis in children. Iran J Child Neurol 2013;7(2):1-10. Epub 2014/03/26.Patel Y, Bhise V, Krupp L. Pediatric multiple sclerosis. Ann Indian Acad Neurol 2009;12(4):238.Saadatnia M, Najafi MR, Najafi F, Davoudi V, Keyhanian K, Maghzi AH. CD24 gene allele variation is not associated with oligoclonal IgG bands and IgG index of multiple sclerosis patients. Neuroimmunomodulation 2012;19(3):195-9.Inaloo S, Haghbin S. Multiple Sclerosis in Children. Iran J Child Neurol 2013 Spring; 7(2): 1–10.Jutta Gartner PH. MS disease-modifying therapies in children: ECTRIMS 2010;8:21-4.Kornek B A-EF, Rostasy K, Milos RI. Natalizumab therapy for highly active pediatric multiple sclerosis. JAMA Neurol 2013;Apr;70(4):469-75.Yeh E, Weinstock-Guttman B, Ramanathan M, Ramasamy D, Willis L, Cox J, et al. Magnetic resonance imaging characteristics of children and adults with paediatric-onset multiple sclerosis. Brain 2009;132(12):3392-400.Chabas D, Green AJ, Waubant E. Pediatric multiple sclerosis. NeuroRx 2006;3(2):264-75.McDonald WI, Compston A, Edan G, Goodkin D, Hartung HP, Lublin FD, et al. Recommended diagnostic criteria for multiple sclerosis: guidelines from the International Panel on the diagnosis of multiple sclerosis. Ann Neurol 2001;50(1):121-7.Polman CH, Reingold SC, Banwell B, Clanet M, Cohen JA, Filippi M, et al. Diagnostic criteria for multiple sclerosis: 2010 revisions to the McDonald criteria. Ann Neurol 2011;69(2):292-302.Polman CH, Reingold SC, Edan G, Filippi M, Hartung HP, Kappos L, et al. Diagnostic criteria for multiple sclerosis: 2005 revisions to the “McDonald Criteria”. Ann Neurol 2005;58(6):840-6.Krupp LB, Tardieu M, Amato MP, Banwell B, Chitnis T, Dale RC, et al. International Pediatric Multiple Sclerosis Study Group criteria for pediatric multiple sclerosis and immune-mediated central nervous system demyelinating disorders: revisions to the 2007 definitions. Mult Scler2013 Sep;19(10):1261-7. doi: 10.1177/1352458513484547.Krupp LB, Banwell B, Tenembaum S. Consensus definitions proposed for pediatric multiple sclerosis and related disorders. Neurology 2007;68(16 suppl 2):S7-S12.Amato M, Goretti B, Ghezzi A, Lori S, Zipoli V, Portaccio E, et al. Cognitive and psychosocial features of childhood and juvenile MS. Neurology 2008;70(20):1891-7.Ghezzi A, Amato M, Capobianco M, Gallo P, Marrosu G, Martinelli V, et al. Disease-modifying drugs in childhood-juvenile multiple sclerosis: results of an Italian co-operative study. Mult Scler 2005;11(4):420-4.Mikaeloff Y, Caridade G, Tardieu M, Suissa S. Effectiveness of early beta interferon on the first attack after confirmed multiple sclerosis: a comparative cohort study. Eur J Paediatr Neurol 2008;12(3):205-9.Callen D, Shroff M, Branson H, Lotze T, Li D, Stephens D, et al. MRI in the diagnosis of pediatric multiple sclerosis. Neurology 2009;72(11):961-7.Jacobs LD, Cookfair DL, Rudick RA, Herndon RM, Richert JR, Salazar AM, et al. Intramuscular interferon beta-1a for disease progression in relapsing multiple sclerosis. Ann Neurol 1996;39(3):285-94.Pohl D, Rostasy K, Gärtner J, Hanefeld F. Treatment of early onset multiple sclerosis with subcutaneous interferon beta-1a. Neurology 2005;64(5):888-90.Banwell B, Reder A, Krupp L, Tenembaum S, Eraksoy M, Alexey B, et al. Safety and tolerability of interferon beta-1b in pediatric multiple sclerosis. Neurology 2006;66(4):472-6.Tenembaum SN, Segura MJ. Interferon beta-1a treatment in childhood and juvenile-onset multiple sclerosis. Neurology 2006;67(3):511-3.Pohl D, Waubant E, Banwell B, Chabas D, Chitnis T, Weinstock-Guttman B, et al. Treatment of pediatric multiple sclerosis and variants. Neurology 2007;68(16 suppl 2):S54-S65.Kornek B, Bernert G, Balassy C, Geldner J, Prayer D, Feucht M. Glatiramer acetate treatment in patients with childhood and juvenile onset multiple sclerosis. Neuropediatrics 2003;34(03):120-6.Ghezzi A. Immunomodulatory treatment of early onset multiple sclerosis: results of an Italian Co-operative Study. Neurol Sci 2005;26(4):s183-s6.Tenembaum SN, Banwell B, Pohl D, Krupp LB, Boyko A, Meinel M, et al. Subcutaneous Interferon Beta-1a in Pediatric Multiple Sclerosis A Retrospective Study.J Child Neurol 2013:0883073813488828.Sloka JS, Stefanelli M. The mechanism of action of methylprednisolone in the treatment of multiple sclerosis. Mult Scler (Houndmills, Basingstoke, England) 2005;11(4):425-32. Epub 2005/07/27.Gorman MP, Healy BC, Polgar-Turcsanyi M, Chitnis T. Increased relapse rate in pediatric-onset compared with  adult-onset multiple sclerosis. Arch Neurol 2009;66(1):54.Shahar E, Andraus J, Savitzki D, Pilar G, Zelnik N. Outcome of Severe Encephalomyelitis in Children Effect of High-Dose Methylprednisolone and Immunoglobulins. J Child Neurol 2002;17(11):810-4.Spalice A, Properzi E, Faro VL, Acampora B, Iannetti P. Intravenous immunoglobulin and interferon: successful treatment of optic neuritis in pediatric multiple sclerosis. J Child Neurol 2004;19(8):623-6.Koziolek M, Mühlhausen J, Friede T, Ellenberger D, Sigler M, Huppke B, et al. Therapeutic Apheresis in Pediatric Patients with Acute CNS Inflammatory Demyelinating Disease. Blood Purification 2013;36(2):92-7.Najafi F, Ghaffarpour M, Najafi M, Aghamohammadi A, Saadatnia M. Prognostic value of intrathecal IgG synthesis in multiple sclerosis: a study in 54 patients. Tehran University Medical Journal 2008;66(1):1-6.Yeh E KL, Ness J, Chabas D, et al. Breakthrough disease in pediatric MS patients: a pediatric network experience: Annual Meeting of the American Academy of Neurology. Seattle WA: 2009.Yeh EA. Diagnosis and treatment of multiple sclerosis in pediatric and adolescent patients: current status and future therapies. Adolesc Health Med Ther 2010;1:61-71.Borriello G, Prosperini L, Luchetti A, Pozzilli C. Natalizumab treatment in pediatric multiple sclerosis: a case report. Eur J Paediatr Neurol 2009;13(1):67-71.Huppke P, Stark W, Zurcher C, Huppke B, Bruck W, Gartner J. Natalizumab use in pediatric multiple sclerosis. Arch Neurol 2008;65(12):1655.Makhani N, Gorman M, Branson H, Stazzone L, Banwell B, Chitnis T. Cyclophosphamide therapy in pediatric multiple sclerosis. Neurology 2009;72(24):2076-82.Rice GP, Hartung H-P, Calabresi PA. Anti-α4 integrin therapy for multiple sclerosis Mechanisms and rationale. Neurology 2005;64(8):1336-42.Polman CH, O’Connor PW, Havrdova E, Hutchinson M, Kappos L, Miller DH, et al. A randomized, placebo-controlled trial of natalizumab for relapsing multiple sclerosis. N Engl J Med 2006;354(9):899-910.Ghezzi A, Pozzilli C, Grimaldi L, Morra VB, Bortolon F, Capra R, et al. Safety and efficacy of natalizumab in children with multiple sclerosis. Neurology   2010;75(10):912-7.Sousa L, de Sa J, Sa MJ, Cerqueira JJ, Martins-Silva A, En Nombre Del Portugal Experience With Natalizumab Study Group Snapshot EN. The efficacy and safety of natalizumab for the treatment of multiple sclerosis in Portugal.: a retrospective study. Revista de Neurologia 2014;59(9):399-406. Epub 2014/10/25. Estudio retrospectivo de la eficacia y seguridad del natalizumab en el tratamiento de la esclerosis multiple en Portugal.Huppke P, Stark W, Zürcher C, Huppke B, Brück W, Gärtner J. Natalizumab use in pediatric multiple sclerosis. Arch Neurol 2008;65(12):1655-8.Hauser SL, Dawson DM, Lehrich JR, Beal MF, Kevy SV, Propper RD, et al. Intensive immunosuppression in progressive multiple sclerosis. A randomized, three-arm study of high-dose intravenous cyclophosphamide, plasma exchange, and ACTH. N Engl J Med 1983;308(4):173-80. Epub 1983/01/27.Weiner HL, Mackin GA, Orav EJ, Hafler DA, Dawson DM, LaPierre Y, et al. Intermittent cyclophosphamide pulse therapy in progressive multiple sclerosis: final report of the Northeast Cooperative Multiple SclerosisTreatment Group. Neurology 1993;43(5):910-8. Epub 1993/05/01.Hauser SL, Waubant E, Arnold DL, Vollmer T, Antel J, Fox RJ, et al. B-cell depletion with rituximab in relapsing–remitting multiple sclerosis. N Engl J Med 2008;358(7):676-88.Tzaribachev N, Koetter I, Kuemmerle-Deschner JB, Schedel J. Rituximab for the treatment of refractory pediatric autoimmune diseases: a case series. Cases J 2009;2:6609.Carson KR, Focosi D, Major EO, Petrini M, Richey EA, West DP, et al. Monoclonal antibody-associated progressive multifocal leucoencephalopathy in patientstreated with rituximab, natalizumab, and efalizumab: a Review from the Research on Adverse Drug Events and Reports (RADAR) Project. Lancet Oncology 2009;10(8):816-24.Beres SJ, Graves J, Waubant E. Rituximab Use in Pediatric Central Demyelinating Disease. Pediatr Neurol 2014 Jul;51(1):114-8.Wynn D, Kaufman M, Montalban X, Vollmer T, Simon J, Elkins J, et al. Daclizumab in active relapsing multiple  sclerosis (CHOICE study): a phase 2, randomised, double-blind, placebo-controlled, add-on trial with interferon beta. Lancet Neurol 2010;9(4):381-90.Bielekova B, Howard T, Packer AN, Richert N, Blevins G, Ohayon J, et al. Effect of anti-CD25 antibody daclizumab in the inhibition of inflammation and stabilization of disease progression in multiple sclerosis. Arch Neurol 2009;66(4):483-9.Rose JW, Watt HE, White AT, Carlson NG. Treatment of multiple sclerosis with an anti–interleukin-2 receptor monoclonal antibody. Ann Neurol 2004;56(6):864-7.Ali E, Healy B, Stazzone L, Brown B, Weiner H, Khoury S. Daclizumab in treatment of multiple sclerosis patients. Mult Scler 2009;15(2):272-4.Gorman MP, Tillema J-M, Ciliax AM, Guttmann CR, Chitnis T. Daclizumab use in patients with pediatric multiple sclerosis. Arch Neurol 2012;69(1):78-81.Gorelik L, Lerner M, Bixler S, Crossman M, Schlain B, Simon K, et al. Anti-JC virus antibodies: implications for PML risk stratification. Ann Neurol 2010;68(3):295-303.Bloomgren G, Richman S, Hotermans C, Subramanyam M, Goelz S, Natarajan A, et al. Risk of natalizumab-associated progressive multifocal leukoencephalopathy. N Engl J Med 2012;366(20):1870-80.Sørensen PS, Bertolotto A, Edan G, Giovannoni G, Gold R, Havrdova E, et al. Risk stratification for progressive multifocal leukoencephalopathy in patients treated with natalizumab. Mult Scler 2012;18(2):143-52.Yildirim-Toruner C, Diamond B. Current and novel therapeutics in the treatment of systemic lupus erythematosus. J Allergy Clin Immunol 2011;127(2):303-12.Zappitelli M, Duffy CM, Bernard C, Gupta IR. Evaluation of activity, chronicity and tubulointerstitial indices for childhood lupus nephritis. Pediatr Nephrol 2008;23(1):83-91.Di Filippo S. Anti-IL-2 receptor antibody vs. polyclonal anti-lymphocyte antibody as induction therapy in Pediatr Transplant. Pediatr Transplant 2005;9(3):373-80.Gallagher M, Quinones K, Cervantes-Castaneda RA, Yilmaz T, Foster CS. Biological response modifier therapy for refractory childhood uveitis. Br J Ophthalmol 2007;91(10):1341-4.Giovannoni G, Comi G, Cook S, Rammohan K, Rieckmann P, Sørensen PS, et al. A placebo-controlled trial of oral cladribine for relapsing multiple sclerosis. N Engl J Med 2010;362(5):416-26.Kappos L, Radue E-W, O’Connor P, Polman C, Hohlfeld R, Calabresi P, et al. 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    Impact of computer game and computer assisted type instruction on inattention and impulsivity of children suffering from attention deficit hyperactivity disorder

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    زمینه و هدف: بهبود کاهش توجه و تکانشگری مبتلایان به اختلال نقص توجه- بیش فعالی یکی از مهمترین اهداف درمان این بیماران و از دشوارترین مسائل بالینی در آنها محسوب می شود. مطالعه حاضر با هدف مقایسه تأثیر بازی های کامپیوتری و آموزش تایپ کامپیوتری بر توجه و تکانشگری در کودکان مبتلا با اختلال نقص توجه- بیش فعالی انجام گرفت. روش بررسی: در این تحقیق که به صورت کارآزمایی بالینی یک سوکور انجام شد، 37 کودک دبستانی مبتلا به اختلال نقص توجه- بیش فعالی به دو گروه وارد شدند. گروه 1 (17 نفر) 8 جلسه یک ساعته به مدت یک ماه بازی کامپیوتری انجام دادند، گروه 2 (20 نفر) طی یک ماه تحت هشت جلسه یک ساعته آموزش تایپ کامپیوتری قرار گرفتند و با استفاده از تست عملکرد مداوم شامل بی توجهی (خطای حذف)، تکانشگری (خطای ارتکاب و زمان واکنش) و زمان واکنش قبل و پس از مداخله مقایسه شدند و نتایج با استفاده از آزمون های آماری مجذور کا، t مستقل و t جفت تجزیه و تحلیل گردید. یافته ها: دو گروه از نظر سن، مقطع تحصیلی، جنس، بهره هوشی، داروهای مصرفی، نمرات پرسشنامه کانرز والدین و معلمین، دارا بودن کامپیوتر در منزل و سابقه کار با کامپیوتر همسان بودند. تفاوت تعداد خطای ارتکاب قبل و پس از مداخله در گروه اول معنی دار نبود، اما در گروه دوم، پس از مداخله (44/20±64/11) در مقایسه با قبل از مداخله (18/10±10/14) کاهش معنی داری را نشان داد (05/0

    Production of Bioactive Peptides in Milk Using Two Native Strains of Levilactobacillus brevis

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    Background and Objective: Milk proteins are precursors of several biologically active peptides. One of the methods of producing these peptides is fermentation using lactic acid bacteria. The aim of this study was to investigate production of antioxidant and angiotensin-I converting enzyme inhibitory bioactive peptides in cow milk fermented by two strains of Levilactobacillus brevis. Material and Methods: Two strains of Levilactobacillus brevis KX572376 (M2) and Levilactobacillus brevis KX572382 (M8) were used in fermentation of low-fat cow milk. Moreover, pH changes, proteolytic activity, water-soluble extract biological activity (antioxidant activity and angiotensin-I converting enzyme inhibition) of the samples and peptide fraction less than 3 kDa were investigated at 24 and 48 h of fermentation (30 °C). Peptide profile of the superior sample was analyzed as well. Statistical analysis was carried out using one-way of variance, Tukey test and SPSS software v.25. Results and Conclusion: The two strains decreased milk pH to a similar level in the first 24 h. Quantities of free amine groups in the samples treated with M2 and M8 strains within 24 and 48 h of fermentation were significantly different (p≤0.05), compared to the control sample. In the first 24 h of fermentation, no difference was observed in the quantity of free amines of M2 and M8 samples. In the second 24 h, further free amine groups were produced due to the activity of M8 strain in milk. Antioxidant activity of the water-soluble extracts of M2 and M8 samples was significantly (p≤0.05) higher than that of the control sample during fermentation. Antioxidant activity in fractions less than 3 kDa did not show significant differences in M2 and M8 samples at 24 and 48 h of fermentation. In the control sample, no antioxidant activity was observed in fractions less than 3 kDa. The highest ACE inhibitory activity in fractions less than 3 kDa of M8 was observed after 48 h. No angiotensin-I converting enzyme inhibition was seen in fractions less than 3 kDa of M2 and control sample. The RP-HPLC peptide patterns of the fraction less than 3 kDa of M8 and control sample were different, which was a justification for the biological activity in this sample. Conflict of interest: The authors declare no conflict of interest

    Lateral Growth of Three-Dimensional Turbidity Current for Supercritical Initial Conditions

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    The aim of this paper is to investigate the lateral growth of an unsteady turbulent inclined turbidity current. To do so, the Buckingham Π theorem together with a dimensional analysis are implemented to derive two appropriate relations, one of which relates the current width to the current length and the other one expresses the current width in terms of time. The coefficients of the two relations are determined experimentally. Based on the results obtained, three different regimes namely, inertia-viscous as the first regime, buoyancy-viscous, and gravity-viscous as the second and third regimes are distinguished within the current. The experimental results indicate that the lateral growth rate in the first regime is less than that in the second one. Based on the results obtained, the lateral growth in some particular regions is independent of slope, concentration, and volumetric flow rate variations

    COMPARING THE MOTOR SKILLS OF 4 AND 5-YEAR-OLD EDUCABLE MENTALLY RETARDED GIRLS WITH THEIR PEER GROUPS USING PEABODY DEVELOPMENTAL MOTOR SCALES

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    Abstract. Objective: The development of motor skills in preschool children plays a fundamental role insubsequent learning, with some researchers believing that motor skill learning determines future learning, and superior mental processes result from the proper development of the perceptual-motor systems. Motor performance in children affects their learning skills, so the lack of proper motor activity is a hurdle involved in a child’s explorative, playing and learning experiences. Method This descriptive, analytical study is cross-sectional in nature. The researcher described and analyzed the motor skill of two subject groups, one consisting of normal girls and the other consisting of educable mentally retarded girls, aged 4 to 5, across Tehran’s kindergartens. Multistage randomization was performed to select a statistical population totaling 60 subjects. The test consisted of two parts; one assessed the gross motor skills and the other assessed the fine motor skills. Results: Data were analyzed by the analysis of variance and t-test. The results indicated that there was a statistically significant deference between 4 and 5-year old normal and educable mentally retarded girls. There was not a significant difference between 5-year old normal and educable mentally retarded girls in terms of the mean value of the fine and gross motor skills and their sub-categories. There was not a significant difference between 4 and 5-year old normal girlsin the fine and gross skills based on the Peabody test. Conclusion: Mentally retarded girls had lower ability at gross and soft motor skills than normal girls, and the Peabody test was a proper method to examine this property.Keywords: Motor skills, mentally retarded children, Peabody tes

    Factores que afectan la ubicación de los centros médicos en la ciudad de Teherán Estudio de caso: Distrito 1 del municipio de Teherán

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    The historical growth of cities due to the rapid increase of population led to the increased land price in cities and caused problems to theappropriate distribution system as well as the allocation of suitable spaces to some fundamental services like medical centers. Supplyinghealth for all people in every society is one of the basic human rights which should be regarded by governments. The imbalancein fundamental services such as medical care and its imbalanced distribution system cause major challenges expressing themselvesin different economic and skeletal dimensions. In this study which aimed at determining the factors affecting the location of medicalcenters, first the main variables and indicators affecting the location of such centers were extracted and then ranked using the hierarchicalquestionnaire by some relevant experts. After ranking the obtained indicators using the hierarchical method to examine the medicalcenters at district 1 of Tehran and investigating the balance and proportion of medical centers, the location of medical centersin district 1 were examined using the geographical information system by hierarchical model. The obtained results indicated thatthe northeast and east areas of district 1 in Tehran had faced major challenges in terms of the access to medical centers and a specifiedarea in the geographical information system indicated this challenge in the north and northeast areas. The selected point by geographicalinformation system were the areas in this district

    Porównanie wpływu leczenia metforminą i insuliną na kontrolę glikemii u krytycznie chorych pacjentów

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    Introduction: It is accepted that preventing hyperglycaemia during critical illness while assuring adequate caloric intake can reduce mortality and morbidity. The aim of this study was to compare the metabolic effects of metformin and insulin on hyperglycaemia in ICU patients. Methods: This double-blind randomised clinical trial was performed on 24 patients who were admitted to the intensive care unit (ICU) from 20 March to 20 September 2007. All patients with serious injuries or with major non-abdominal surgeries were included if they met the inclusion criteria, and were assigned randomly to one of the study groups. Patients in Group 1 received intensive insulin therapy, and patients in Group 2 were treated with metformin. Moreover, the Acute Physiology And Chronic Health Evaluation (APACHE) II scoring system was used to grade disease severity. Results: Both glycaemic management protocols led to significantly improved glucose levels without any report of hypoglycaemia. The mean initial glucose levels for the insulin group decreased significantly after the intravenous infusion of insulin (p < 0.001). Additionally, the blood glucose concentration was significantly lower after two weeks of metformin administration compared to baseline measurements (p < 0.001). Moreover, the blood glucose concentration decrease during these two weeks was significantly higher in the insulin group (p = 0.01). Besides, APACHE II score was lower than baseline at the end of the study for both therapeutic groups (score of 10 vs. 15 [insulin] and 16 [metformin]). Finally, new renal dysfunction (maximum serum creatinine level at least double the initial value) was observed in three of the patients (two patients from the metformin group and one from the insulin group) in the last days of the protocol, although none of the patients showed lactic acidosis after ICU admission. Conclusions: Both metformin and intensive insulin therapy significantly decreased hyperglycaemia in ICU patients. Insulin caused a greater reduction in blood glucose concentration but required more attention and trained personnel.Wstęp: Dowody naukowe wskazują, że zapobieganie hiperglikemii u osób w stanie krytycznym przy zapewnieniu odpowiedniego poboru kalorii może zmniejszyć śmiertelność i chorobowość. Celem niniejszego badania było porównanie wpływu metforminy i insuliny na występowanie hiperglikemii u pacjentów leczonych na oddziale intensywnej opieki medycznej (OIOM). Materiał i metody: Badanie z randomizacją przeprowadzone metodą podwójnie ślepej próby obejmowało 24 chorych przyjętych na OIOM w okresie od 20 marca do 20 października 2007 roku. Wszystkich pacjentów z ciężkimi obrażeniami lub po poważnych zabiegach chirurgicznych niedotyczących jamy brzusznej, którzy spełniali kryteria włączenia, przydzielono losowo do jednej z grup terapeutycznych. U chorych przydzielonych do grupy 1. stosowano intensywną insulinoterapię, natomiast chorym z grupy 2. podawano metforminę. Do oceny ciężkości stanu chorych wykorzystano skalę APACHE (Acute Physiologic Assessment and Chronic Health Evaluation) II. Wyniki: Oba protokoły leczenia hipoglikemizującego spowodowały istotną poprawę wyrównania glikemii, przy czym nie odnotowano żadnego przypadku hipoglikemii. W grupie stosującej insulinoterapię średnie stężenie glukozy obniżyło się istotnie w stosunku do wartości wyjściowych po dożylnym wlewie insuliny (p < 0, 001). U osób leczonych metforminą po 2 tygodniach przyjmowania leku stężenie glukozy we krwi było istotnie niższe od poziomu wyjściowego (p < 0,001). Redukcja stężenia glukozy w ciągu tych 2 tygodni była istotnie większa w grupie przyjmującej insulinę (p = 0,01). W obu grupach terapeutycznych punktacja w skali APACHE II w momencie zakończenia badania była niższa od wartości wyjściowych (10 punktów v. 15 [insulina] i 16 [metformina]). U 3 chorych (2 osoby przydzielone do leczenia metforminą i 1 osoba przydzielona do insulinoterapii) zaobserwowano rozwój niewydolności nerek de novo (maksymalne stężenie kreatyniny w surowicy co najmniej 2-krotnie większe od wartości wyjściowych) w ostatnich dniach stosowania protokołu leczenia hipoglikemizującego, chociaż u żadnego z pacjentów nie stwierdzono kwasicy mleczanowej po przyjęciu na OIOM. Wnioski: Zarówno leczenie metforminą, jak i intensywna insulinoterapia istotne zmniejszają hiperglikemię u pacjentów na OIOM. Insulina powoduje większą redukcję stężenia glukozy, jednak jej stosowanie wymaga większej uwagi, a personel medyczny musi być odpowiednio przeszkolony

    Drug withdrawal in patients with epilepsy: Prognostic value of the EEG

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    توصیه شده است که در کودکان واجد شرایط، هرچه سریعتر نسبت به قطع داروهای ضد صرع کودکان اقدام شود. به نظر می رسد که در هنگام تصمیم گیری نسبت به قطع داروهای ضد صرع می توان باتوجه به خصوصیات EEG بیماران، وقوع مجدد حملات را پیش بینی کرد. لذا با انجام یک مطالعه آینده نگر، کودکان در فواصل سه ماهه به مدت دو سال به منظور بررسی امکان پیش بینی حملات صرع قبل از قطع مصرف دارو با استفاده از EEG پیگیری شدند. هرکدام از الکتروانسفالوگرام ها برحسب وجود یا عدم وجود متغیرهای 1) فعالیت زمینه ای نوار (Background) و 2) فعالیت آهسته موضعی (Focal slowing) و 3) امواج سوزنی موضعی (Focal spike) و 4) امواج سوزنی نوک تیز منتشر (Generaliz sharp & spike wave) در دو حالت بیداری و اکتیواسیون (مثل هیپرونتیلاسیون) توسط یک نفر از متخصصین اعصاب مورد ارزیابی قرار می گرفتند. در صورت عود حملات، داروهای قبلی آنها مجددا تجویز می گردید. در این تحقیق، میانگین مدت زمان پیگیری بیماران از زمان شروع به قطع داروها 19 ماه بود. احتمال عود حملات پس از یکسال پیگیری 24.8 (26.5 و 22.5 :CI با احتمال 95) بدست آمد. در مورد وضعیت زمینه نوار مغز و وجود امواج نوک تیز سوزنی منتشر و موضعی و همچنین امواج آهسته موضعی (قبل از اقدام به قطع) در EEG بیماران با عود حملات ارتباط معنی داری یافت نشد. رابطه معنی داری در مورد مقایسه وضعیت فعلی EEG با نوارهای قبلی کودکان و عود حملات یافت گردید (

    Species Composition and Some Biological Features of Scorpions in Kazerun District, Southern Iran

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    Background: Scorpions have medical importance in the studied area with 2377 cases of envenoming during past six years. This study was the first to explore the scorpion species and dispersion in the Kazerun District during 2014–2015. Methods: The studied sites were selected based on different topographic conditions such as plain, foothill and mountainous which formed four geographical zones with three villages in each zone. The sampling was carried out twice each month throughout the year. Daytime collections were carried out using hand digging tools for moving stones and excavate the borrows, as well as night sampling, is done with the black light device. The co­ordinate of locations was recorded with a GPS. The collected specimens were maintained in 70% ethanol and identified using authorized keys. Results: Overall, 800 scorpions were sampled from different parts of Kazerun District, bringing the species rich­ness to 9 belonged to 3 families of Buthidae, Scorpionidae, and Hemiscorpionidae. The Mesobuthus eupeus (84.6%) was prominent vice versa M. caucasicus (0.1%) had lowest abundance. Other species comprised Comp­sobuthus matthiesseni (5.3%), Androctonus crassicauda (5.0%), Razianus zarudnyi (2.0%), Hemiscorpius lep­turus (1.5%), Orthochirus sp (0.9%), Hottentotta zagrosensis (0.4%), and Scorpio maurus (0.3%). The sea­sonal activity of the scorpions showed a lower peak in Mar, with the main peaks in Aug for the dominant spe­cies. Mesobuthus caucasicus is recorded for the first time in the Fars Province, southern Iran. Conclusion: All the known dangerous scorpions, including H. lepturus, M. eupeus and A. crassicauda were re­vealed in the studied area
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