88 research outputs found

    sj-pdf-1-mso-10.1177_20552173231208271 - Supplemental material for Identifying the white matter pathways involved in multiple sclerosis-related tremor using diffusion tensor imaging

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    Supplemental material, sj-pdf-1-mso-10.1177_20552173231208271 for Identifying the white matter pathways involved in multiple sclerosis-related tremor using diffusion tensor imaging by Ahmed Bayoumi, Khader M. Hasan, Jorge Patino, Zafer Keser, Joseph A. Thomas, Refaat E. Gabr, Claudia Pedroza, Arash Kamali, Mya C. Schiess, Jerry S. Wolinsky and John A. Lincoln in Multiple Sclerosis Journal – Experimental, Translational and Clinical</p

    sj-pdf-2-mso-10.1177_20552173231208271 - Supplemental material for Identifying the white matter pathways involved in multiple sclerosis-related tremor using diffusion tensor imaging

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    Supplemental material, sj-pdf-2-mso-10.1177_20552173231208271 for Identifying the white matter pathways involved in multiple sclerosis-related tremor using diffusion tensor imaging by Ahmed Bayoumi, Khader M. Hasan, Jorge Patino, Zafer Keser, Joseph A. Thomas, Refaat E. Gabr, Claudia Pedroza, Arash Kamali, Mya C. Schiess, Jerry S. Wolinsky and John A. Lincoln in Multiple Sclerosis Journal – Experimental, Translational and Clinical</p

    Refaat Alareer’s “If I Must Die”: The Death of the Author, the Afterlife of the Tale

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    This article traces the performative role of tales and storytelling in late Refaat Alareer’s life, career, (creative) writing, activism, and death. It ultimately examines this performativity’s intensification and culmination in Alareer’s Saidian late-style poem “If I Must Die.” The article combines close textual analysis and comparative literary criticism to investigate the intricate relationship between storytelling, mortality, and resistance in Alareer’s poem. Paying attention to nuance, the article examines the poem’s intertextual connections with Claude McKay’s “If We Must Die” (1919) to demonstrate how Alareer transforms storytelling into a powerful mode of cultural survival and a means of transcending physical destruction and preserving collective memory in the face of systematic oppression. Additionally, the research traces Alareer’s evolving conceptualization of storytelling from a personal imperative to a collective form of resistance, culminating in “If I Must Die” whose stylistic and thematic treatment of his impending death anchor his poem locally/nationally, namely in Gaza/Palestine

    3 MRI Basics

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    Cardiac electrophysiology in Lebanon

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    [No abstract available]10

    Utility of the exercise electrocardiogram testing in sudden cardiac death risk stratification

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    Background Sudden cardiac death (SCD) remains a major public health problem. Current established criteria identifying those at risk of sudden arrhythmic death, and likely to benefit from implantable cardioverter defibrillators (ICDs), are neither sensitive nor specific. Exercise electrocardiogram (ECG) testing was traditionally used for information concerning patients' symptoms, exercise capacity, cardiovascular function, myocardial ischemia detection, and hemodynamic responses during activity in patients with hypertrophic cardiomyopathy. Methods We conducted a systematic review of MEDLINE on the utility of exercise ECG testing in SCD risk stratification. Results Exercise testing can unmask suspected primary electrical diseases in certain patients (catecholaminergic polymorphic ventricular tachycardia or concealed long QT syndrome) and can be effectively utilized to risk stratify patients at an increased (such as early repolarization syndrome and Brugada syndrome) or decreased risk of SCD, such as the loss of preexcitation on exercise testing in asymptomatic Wolff-Parkinson-White syndrome. Conclusions Exercise ECG testing helps in SCD risk stratification in patients with and without arrhythmogenic hereditary syndromes. © 2014 Wiley Periodicals, Inc.Adler A, 2012, HEART RHYTHM, V9, P901, DOI 10.1016-j.hrthm.2012.01.026; Atta S, 2012, J CLIN EXP CARDIOLOG, V3, P223; Bastiaenen R, 2013, HEART RHYTHM, V10, P247, DOI 10.1016-j.hrthm.2012.10.032; Bershader RS BC, 2007, HEART RHYTHM, V4, pS138; Calloe K, 2013, CIRC-ARRHYTHMIA ELEC, V6, P177, DOI 10.1161-CIRCEP.112.974220; Chattha IS, 2010, HEART RHYTHM, V7, P906, DOI 10.1016-j.hrthm.2010.03.006; Cohen MI, 2012, HEART RHYTHM, V9, P1006, DOI 10.1016-j.hrthm.2012.03.050; Elhendy A, 2002, AM J CARDIOL, V90, P95, DOI 10.1016-S0002-9149(02)02428-1; Engel G, 2004, CURR PROB CARDIOLOGY, V29, P365, DOI 10.1016-j.cpcardiol.2004.02.007; Frolkis JP, 2003, NEW ENGL J MED, V348, P781, DOI 10.1056-NEJMoa022353; Gimeno JR, 2009, EUR HEART J, V30, P2599, DOI 10.1093-eurheartj-ehp327; Goldberger Jeffrey J, 2008, Heart Rhythm, V5, pe1, DOI 10.1016-j.hrthm.2008.05.031; Haissaguerre M, 2008, NEW ENGL J MED, V358, P2016, DOI 10.1056-NEJMoa071968; HINDMAN MC, 1973, ANN INTERN MED, V79, P654; Horner JM, 2011, HEART RHYTHM, V8, P1698, DOI 10.1016-j.hrthm.2011.05.018; Josephson ME, 2000, ANN INTERN MED, V133, P901; Kentta T, 2012, HEART RHYTHM, V9, P1083, DOI 10.1016-j.hrthm.2012.02.030; Lahat H, 2001, AM J HUM GENET, V69, P1378, DOI 10.1086-324565; Laitinen PJ, 2001, CIRCULATION, V103, P485; Makimoto H, 2010, J AM COLL CARDIOL, V56, P1576, DOI 10.1016-j.jacc.2010.06.033; MARIEB MA, 1990, AM J CARDIOL, V66, P172, DOI 10.1016-0002-9149(90)90583-M; Meli AC, 2011, CIRC RES, V109, P281, DOI 10.1161-CIRCRESAHA.111.244970; Morshedi-Meibodi A, 2004, CIRCULATION, V109, P2417, DOI 10.1161-01.CIR.0000129762.41889.41; O'Neill JO, 2004, J AM COLL CARDIOL, V44, P820, DOI 10.1016-j.jacc.2004.02.063; Priori SG, 2002, CIRCULATION, V106, P69, DOI 10.1161-01.CIR.0000020013.73106.D8; Priori SG, 2013, EUROPACE, V15, P1389, DOI 10.1093-europace-eut272; Raju H, 2011, HEART RHYTHM, V8, pS41; Roux-Buisson N, 2012, HUM MOL GENET, V21, P2759, DOI 10.1093-hmg-dds104; Steinhaus DA, 2012, AM HEART J, V163, P125, DOI 10.1016-j.ahj.2011.09.016; Sy RW, 2011, CIRCULATION, V124, P2187, DOI 10.1161-CIRCULATIONAHA.111.028258; Tseng ZH, 2009, HEART RHYTHM, V6, P1315, DOI 10.1016-j.hrthm.2009.06.034; van der Werf C, 2010, CIRC-ARRHYTHMIA ELEC, V3, P96, DOI 10.1161-CIRCEP.109.877142; Watanabe J, 2001, CIRCULATION, V104, P1911; Zheng ZJ, 2001, CIRCULATION, V104, P2158, DOI 10.1161-hc4301.098254; Zipes DP, 2006, J AM COLL CARDIOL, V48, pe247, DOI DOI 10.1016-J.JACC.2006.07.0100

    Pilot study for early prognosis of Azoospermia in relation to Y-STR Profiling

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    AbstractBackgroundAzoospermia constitutes 20% of male infertility situations and affects 1% of the total male population (Jarvi et al., 2010). This condition is classified into three major types; pre-testicular, testicular and post-testicular Azoospermia (Sermondade et al., 2012). Genetic defects causing Azoospermia are due to chromosomal or non-chromosomal alterations on the Y-Chromosome (Lee et al., 2011). Initial diagnosis of Azoospermia is established when no spermatozoa are detected on microscopic examination of semen (World Health Organisation, 1999).ObjectiveTo evaluate the correlation of Y-STR Profiling results and the prevalence of Azoospermia, to help for early prognosis of Azoospermia before puberty.MethodsBuccal swab samples were taken from two groups of individuals (50 fertile and 50 Azoospermic patients), then DNA was isolated using QIAamp DNA Micro kit. DNA quantification was done using a Real-time PCR utilizing Quantifiler Kit. PCR was done using PowerPlex® Y PCR Amplification Kit, then amplified products were typed using a 3130 Genetic Analyzer.ResultsFive haplotypes in four different Y-STR loci were found to possess significantly higher occurrence percentages in Azoospermic than in fertile Saudi individuals, which can serve as a group of pre-diagnostic markers for early prognosis of Azoospermia in Saudi population.ConclusionThere was a significant correlation of Y-STR Profiling results and the prevalence of Azoospermia condition, which supports the idea of using Y-STR Profiling in early prognosis of Azoospermia
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