162,686 research outputs found
Accountability in Complex Organizations: World Bank Responses to Civil Society
No full textCivil society actors have been pushing for greater accountability of the World Bank for at least three decades. This paper outlines the range of accountability mechanisms currently in place at the World Bank along four basic levels: (1) staff, (2) project, (3) policy, and (4) board governance. We argue that civil society organizations have been influential in pushing for greater accountability at the project and policy levels, particularly through the establishment and enforcement of social and environmental safeguards and complaint and response mechanisms. But they have been much less successful in changing staff incentives for accountability to affected communities, or in improving board accountability through greater transparency in decision making, more representative vote allocation, or better parliamentary scrutiny. In other words, although civil society efforts have led to some gains in accountability with respect to Bank policies and projects, the deeper structural features of the institution - the incentives staff face and how the institution is governed- remain largely unchanged.
Equality of Google Scholar with Web of Science Citations: Case of Malaysian Engineering Highly Cited Papers
No full textThis study uses citation analysis from two citation tracking databases, Google Scholar (GS) and ISI Web of Science, in order to test the correlation between them and examine the effect of the number of paper versions on citations. The data were retrieved from the Essential Science Indicators and Google Scholar for 101 highly cited papers from Malaysia in the field of engineering. An equation for estimating the citation in ISI based on Google scholar is offered. The results show a significant and positive relationship between both citation in Google Scholar and ISI Web of Science with the number of versions. This relationship is higher between versions and ISI citations (r = 0.395, p<0.01) than between versions and Google Scholar citations (r = 0.315, p<0.01). Free access to data provided by Google Scholar and the correlation to get ISI citation which is costly, allow more transparency in tenure reviews, funding agency and other science policy, to count citations and analyze scholars’ performance more precisely.Ale Ebrahim, N., Salehi, H., Embi, M. A., Danaee, M., Mohammadjafari, M., Zavvari, A., . . . Shahbazi-Moghadam, M. (2014). Equality of Google Scholar with Web of Science Citations: Case of Malaysian Engineering Highly Cited Papers. Modern Applied Science, 8(5), 63-69. doi: 10.5539/mas.v8n5p6
Variations on the Author
No full text“Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship
Going Beyond Counting First Authors in Author Co-citation Analysis
No full textThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Larry O. Spencer, Conference Author Presentation
No full textGen. Larry O. Spencer, USAF (Ret.), author of Dark Horse: A Journey from the Horseshoe to the Pentago
Dispelling the Myths Behind First-author Citation Counts
No full textWe conducted a full-scale evaluative citation analysis study of scholars in the XML research field to explore just how different from each other author rankings resulting from different citation counting methods actually are, and to demonstrate the capability of emerging data and tools on the Web in supporting more realistic citation counting methods. Our results contest some common arguments for the continued
use of first-author citation counts in the evaluation of scholars, such as high correlations between author rankings by first-author citation counts and other citation
counting methods, and high costs of using more realistic citation counting methods that are not well-supported by the ISI databases. It is argued that increasingly available digital full text research papers make it possible for citation analysis studies to go beyond what the ISI databases have directly supported and to employ more
sophisticated methods
Lapsuusiällä alkavien epileptisten enkefalopatioiden ja liikehäiriöiden geneettiset syyt ja ilmiasun vaihtelu
No full textAbstractNovel genetic aetiologies for epileptic encephalopathies and movement disorders have been discovered by using next-generation sequencing methods. The phenotypic and genotypic variability in these conditions is very wide.The aim of this study was to discover novel genetic causes and phenotypes of childhood-onset drug-resistant epilepsy and epileptic or developmental encephalopathies that occur separately or together with movement disorders, and familial movement disorders. Furthermore, the use of whole-exome sequencing (WES) as a diagnostic tool in clinical practice was evaluated. Altogether, 12 children with undefined aetiology, who fulfilled the inclusion criteria, were included in the study.GABRG2 gene was identified as a genetic cause of epileptic encephalopathies. Novel GABRG2-associated phenotypes included progressive neurodegeneration, epilepsy in infancy with migrating focal seizures, and autism spectrum disorder. New pathogenic variants, GABRG2 p.P282T and p.S306F, were discovered.The pathogenic NACC1 variant caused focal epilepsy, developmental disability, bilateral cataracts, and dysautonomia. The novel phenotype associated with the NACC1 p.R298W variant included hyperkinetic movement disorder.SAMD9L was found to be the genetic cause for the familial movement disorder. The phenotype associated with the novel SAMD9L p.I891T variant was very variable. Neuroradiological findings included cerebellar atrophy and periventricular white matter changes. After publication of these results, SAMD9L was reported to be one of the most common genetic aetiologies of childhood bone marrow failure and myelodysplastic syndrome.The pathogenic homozygous MTR variant was found to cause early-onset epileptic encephalopathy that occurred together with movement disorder and haematological disturbances. Drug resistant seizures responded to cofactor and vitamin treatments.Whole-exome sequencing for 10 patients with drug-resistant epilepsy or epileptic or developmental encephalopathy provided a genetic diagnosis for two patients (20%).This study confirmed that, for epileptic encephalopathies and movement disorders in which the genetic causes and phenotypes are heterogeneous and sometimes treatable, WES is a useful tool for diagnostics and in the search for novel aetiologies, which might turn out to be more common than expected.Original papersOriginal papers are not included in the electronic version of the dissertation.Komulainen-Ebrahim, J., Schreiber, J. M., Kangas, S. M., Pylkäs, K., Suo-Palosaari, M., Rahikkala, E., … Uusimaa, J. (2019). Novel variants and phenotypes widen the phenotypic spectrum of GABRG2-related disorders. Seizure, 69, 99–104. https://doi.org/10.1016/j.seizure.2019.03.010Self-archived versionKomulainen-Ebrahim, J., Kuismin, O., Kangas, S. M., Kurian, M., Olsén P., & Uusimaa, J. (2019). Novel movement disorder caused by recurrent c.892C>T NACC1 variant. Manuscript in preparation.Tesi, B., Davidsson, J., Voss, M., Rahikkala, E., Holmes, T. D., Chiang, S. C. C., … Bryceson, Y. T. (2017). Gain-of-function SAMD9L mutations cause a syndrome of cytopenia, immunodeficiency, MDS, and neurological symptoms. Blood, 129(16), 2266–2279. https://doi.org/10.1182/blood-2016-10-743302Gorcenco, S., Komulainen-Ebrahim, J., Nordborg, K., Suo-Palosaari, M., Andréasson, S., Krüger, J., … Puschmann, A. (2017). Ataxia-pancytopenia syndrome with SAMD9L mutations. Neurology Genetics, 3(5), e183. https://doi.org/10.1212/nxg.0000000000000183Self-archived versionSaastamoinen, E., Rahikkala, E., Helander, H., Hinttala, R., Risteli, L., Rantala, H., … Komulainen-Ebrahim, J. (2017). Intractable Epilepsy due to MTR Deficiency: Importance of Homocysteine Analysis. Neuropediatrics, 48(6), 467–472. https://doi.org/10.1055/s-0037-1603976TiivistelmäUusien sekvensointimenetelmien käyttöönotto on mahdollistanut epileptisten enkefalopatioiden ja liikehäiriöiden uusien geneettisten syiden löytymisen. Näissä sairausryhmissä geenien ja ilmiasujen vaihtelevuus on suurta.Tutkimuksen tarkoituksena oli löytää uusia geneettisiä syitä ja ilmiasuja lapsuusiällä alkavissa vaikeahoitoisissa epilepsioissa ja epileptisissä tai kehityksellisissä joko itsenäisesti tai yhdessä liikehäiriön kanssa esiintyvissä enkefalopatioissa sekä perheittäin esiintyvissä liikehäiriöissä. Lisäksi selvitettiin eksomisekvensoinnin käyttökelpoisuutta kliinisessä diagnostiikassa näiden potilasryhmien kohdalla. Tutkimukseen osallistui yhteensä 12 sisäänottokriteerit täyttävää lasta, joiden sairauden syy oli jäänyt tuntemattomaksi.GABRG2-geenin mutaatiot aiheuttivat epileptisiä enkefalopatioita, joiden uutena ilmiasuna oli etenevä taudinkuva, johon liittyivät aivojen rappeutuminen, migroiva imeväisiän paikallisalkuinen epilepsia sekä autismikirjon häiriö. Tutkimuksessa löydettiin uusia GABRG2-mutaatioita: p.P282T ja p.S306F.NACC1-geenin mutaatio aiheutti epilepsian, kehitysvammaisuuden, molemminpuolisen kaihin ja autonomisen hermoston toiminnan häiriön. Hyperkineettinen liikehäiriö oli uusi NACC1 p.R298W -mutaatioon liittyvä ilmiasu.SAMD9L-geenin mutaatio aiheutti perheessä esiintyvän liikehäiriön. Neurologinen ja hematologinen ilmiasu olivat hyvin vaihtelevia. Aivojen kuvantamislöydöksiin sisältyi pikkuaivojen rappeutumista ja valkoisen aivoaineen muutoksia aivokammioiden ympärillä. Näiden tutkimustulosten julkaisemisen jälkeen SAMD9L-geenin mutaatioiden on todettu olevan yksi yleisimmistä perinnöllisistä luuytimen vajaatoiminnan ja myelodysplasian syistä.Homotsygoottinen MTR-geenin mutaatio aiheutti varhain alkaneen epileptisen enkefalopatian, liikehäiriön ja hematologisen häiriön. Kofaktori- ja vitamiini hoidot vähensivät epileptisiä kohtauksia, joihin tavanomainen lääkitys ei tehonnut.Geneettiset syyt ja ilmiasut ovat epileptisissä enkefalopatioissa ja liikehäiriöissä hyvin vaihtelevia, ja osaan on olemassa spesifi hoito. Eksomisekvensointi on käyttökelpoinen diagnostiikan ja uusien geneettisten syiden etsimisen apuna. Tässä tutkimuksessa eksomisekvensoinnin avulla kymmenestä potilaasta kahdelle (20 %) saatiin varmistettua geneettinen diagnoosi.OsajulkaisutOsajulkaisut eivät sisälly väitöskirjan elektroniseen versioon.Komulainen-Ebrahim, J., Schreiber, J. M., Kangas, S. M., Pylkäs, K., Suo-Palosaari, M., Rahikkala, E., … Uusimaa, J. (2019). Novel variants and phenotypes widen the phenotypic spectrum of GABRG2-related disorders. Seizure, 69, 99–104. https://doi.org/10.1016/j.seizure.2019.03.010Rinnakkaistallennettu versioKomulainen-Ebrahim, J., Kuismin, O., Kangas, S. M., Kurian, M., Olsén P., & Uusimaa, J. (2019). Novel movement disorder caused by recurrent c.892C>T NACC1 variant. Manuscript in preparation.Tesi, B., Davidsson, J., Voss, M., Rahikkala, E., Holmes, T. D., Chiang, S. C. C., … Bryceson, Y. T. (2017). Gain-of-function SAMD9L mutations cause a syndrome of cytopenia, immunodeficiency, MDS, and neurological symptoms. Blood, 129(16), 2266–2279. https://doi.org/10.1182/blood-2016-10-743302Gorcenco, S., Komulainen-Ebrahim, J., Nordborg, K., Suo-Palosaari, M., Andréasson, S., Krüger, J., … Puschmann, A. (2017). Ataxia-pancytopenia syndrome with SAMD9L mutations. Neurology Genetics, 3(5), e183. https://doi.org/10.1212/nxg.0000000000000183Rinnakkaistallennettu versioSaastamoinen, E., Rahikkala, E., Helander, H., Hinttala, R., Risteli, L., Rantala, H., … Komulainen-Ebrahim, J. (2017). Intractable Epilepsy due to MTR Deficiency: Importance of Homocysteine Analysis. Neuropediatrics, 48(6), 467–472. https://doi.org/10.1055/s-0037-1603976Academic dissertation to be presented with the assent of the Doctoral Training Committee of Health and Biosciences of the University of Oulu for public defence in Auditorium 12 of the Department of Paediatrics, on 10 May 2019, at 12 noonAbstract
Novel genetic aetiologies for epileptic encephalopathies and movement disorders have been discovered by using next-generation sequencing methods. The phenotypic and genotypic variability in these conditions is very wide.
The aim of this study was to discover novel genetic causes and phenotypes of childhood-onset drug-resistant epilepsy and epileptic or developmental encephalopathies that occur separately or together with movement disorders, and familial movement disorders. Furthermore, the use of whole-exome sequencing (WES) as a diagnostic tool in clinical practice was evaluated. Altogether, 12 children with undefined aetiology, who fulfilled the inclusion criteria, were included in the study.
GABRG2 gene was identified as a genetic cause of epileptic encephalopathies. Novel GABRG2-associated phenotypes included progressive neurodegeneration, epilepsy in infancy with migrating focal seizures, and autism spectrum disorder. New pathogenic variants, GABRG2 p.P282T and p.S306F, were discovered.
The pathogenic NACC1 variant caused focal epilepsy, developmental disability, bilateral cataracts, and dysautonomia. The novel phenotype associated with the NACC1 p.R298W variant included hyperkinetic movement disorder.
SAMD9L was found to be the genetic cause for the familial movement disorder. The phenotype associated with the novel SAMD9L p.I891T variant was very variable. Neuroradiological findings included cerebellar atrophy and periventricular white matter changes. After publication of these results, SAMD9L was reported to be one of the most common genetic aetiologies of childhood bone marrow failure and myelodysplastic syndrome.
The pathogenic homozygous MTR variant was found to cause early-onset epileptic encephalopathy that occurred together with movement disorder and haematological disturbances. Drug resistant seizures responded to cofactor and vitamin treatments.
Whole-exome sequencing for 10 patients with drug-resistant epilepsy or epileptic or developmental encephalopathy provided a genetic diagnosis for two patients (20%).
This study confirmed that, for epileptic encephalopathies and movement disorders in which the genetic causes and phenotypes are heterogeneous and sometimes treatable, WES is a useful tool for diagnostics and in the search for novel aetiologies, which might turn out to be more common than expected.Tiivistelmä
Uusien sekvensointimenetelmien käyttöönotto on mahdollistanut epileptisten enkefalopatioiden ja liikehäiriöiden uusien geneettisten syiden löytymisen. Näissä sairausryhmissä geenien ja ilmiasujen vaihtelevuus on suurta.
Tutkimuksen tarkoituksena oli löytää uusia geneettisiä syitä ja ilmiasuja lapsuusiällä alkavissa vaikeahoitoisissa epilepsioissa ja epileptisissä tai kehityksellisissä joko itsenäisesti tai yhdessä liikehäiriön kanssa esiintyvissä enkefalopatioissa sekä perheittäin esiintyvissä liikehäiriöissä. Lisäksi selvitettiin eksomisekvensoinnin käyttökelpoisuutta kliinisessä diagnostiikassa näiden potilasryhmien kohdalla. Tutkimukseen osallistui yhteensä 12 sisäänottokriteerit täyttävää lasta, joiden sairauden syy oli jäänyt tuntemattomaksi.
GABRG2-geenin mutaatiot aiheuttivat epileptisiä enkefalopatioita, joiden uutena ilmiasuna oli etenevä taudinkuva, johon liittyivät aivojen rappeutuminen, migroiva imeväisiän paikallisalkuinen epilepsia sekä autismikirjon häiriö. Tutkimuksessa löydettiin uusia GABRG2-mutaatioita: p.P282T ja p.S306F.
NACC1-geenin mutaatio aiheutti epilepsian, kehitysvammaisuuden, molemminpuolisen kaihin ja autonomisen hermoston toiminnan häiriön. Hyperkineettinen liikehäiriö oli uusi NACC1 p.R298W -mutaatioon liittyvä ilmiasu.
SAMD9L-geenin mutaatio aiheutti perheessä esiintyvän liikehäiriön. Neurologinen ja hematologinen ilmiasu olivat hyvin vaihtelevia. Aivojen kuvantamislöydöksiin sisältyi pikkuaivojen rappeutumista ja valkoisen aivoaineen muutoksia aivokammioiden ympärillä. Näiden tutkimustulosten julkaisemisen jälkeen SAMD9L-geenin mutaatioiden on todettu olevan yksi yleisimmistä perinnöllisistä luuytimen vajaatoiminnan ja myelodysplasian syistä.
Homotsygoottinen MTR-geenin mutaatio aiheutti varhain alkaneen epileptisen enkefalopatian, liikehäiriön ja hematologisen häiriön. Kofaktori- ja vitamiini hoidot vähensivät epileptisiä kohtauksia, joihin tavanomainen lääkitys ei tehonnut.
Geneettiset syyt ja ilmiasut ovat epileptisissä enkefalopatioissa ja liikehäiriöissä hyvin vaihtelevia, ja osaan on olemassa spesifi hoito. Eksomisekvensointi on käyttökelpoinen diagnostiikan ja uusien geneettisten syiden etsimisen apuna. Tässä tutkimuksessa eksomisekvensoinnin avulla kymmenestä potilaasta kahdelle (20 %) saatiin varmistettua geneettinen diagnoosi
A Comparative Study of Reflections of Resistance in the Poetry of Malek-o-Shoara Bahar and Amal Donqol
No full textResistance literature is usually created in the conditions of oppression, inner despotism, lack of social and individual freedom, defiance of law, and foreign aggression. Since the old times to the period of Constitutionalism in Iran, and the contemporary Arab Movement, Iran and Egypt have produced valuable works in resistance literature due to their outstanding resistance to indoor injustice, foreign aggression and cultural attacks. In Iran, resistance literature has a flourishing in Constitutionalism era, and poets like Mirzadeh Eshghi, Seyed Ashrafodin Gilani, Aref Ghazvini, Farokhi Yazdi, and Bahar are the most active in this field; as for the contemporary Egyptian-Arabic Movement, poets like Hafez Ebrahim, Marouf Al-Rassafi, Mohammad Mahdi Al-Javaheri, Mahmoud Darvish, Ebrahim Toqan, and Amal Donqol are among the celebrated ones. Malek-o-Shoara Bahar and Amal Donqol are political and liberal elite poets of Iran and Egypt who fought culturally against autarchy and colonizers. Based on the American school of comparative criticism, this study tries to illustrate resistance literature during Constitutionalism era in Iran, and the era of the Arab Movement
Home, This Way
No full textHome, This Way is a novel I began working on during my time as an MFA student at Creighton University. It is a fictional account of my childhood and upbringing in a small house in Bloomington, Minnesota. The story follows Sara, who is learning how to navigate the world as a young, Sudanese immigrant, how to cope with Mama's depression, and where her relationship stands with each of her six siblings. While writing this story, I was inspired greatly by Justin Torres, Sandra Cisneros and Ocean Vuong. As part of my thesis, I have also included a short collection of poems titled "O Father,." These poems helped me process a lot of what I wanted to write about in Home, This Way.Do NOT submit to ProQuest (MFA thesis
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