36 research outputs found
A contrastive study of metadiscourse in English and Arabic linguistics research articles
Get PDFThe present paper analyzes metadiscourse expressions to understand the cultural differences between English and Arabic-speaking researchers. It uses a contrastive corpus of seventy discussion sections of linguistics research articles written by native speakers of English and Arabic. Within metadiscourse there appear to be two types: interactive and interactional. Chi-square tests are carried out to clarify the probable differences between both groups.The present paper analyzes metadiscourse expressions to understand the cultural differences between English and Arabic-speaking researchers. It uses a contrastive corpus of seventy discussion sections of linguistics research articles written by native speakers of English and Arabic. Within metadiscourse there appear to be two types: interactive and interactional. Chi-square tests are carried out to clarify the probable differences between both groups
Annotation of conceptual co-reference and text Mining the Qur'an
Get PDFThis research contributes to the area of corpus annotation and text mining by developing novel domain specific language resources. Most practical text mining applications restrict their domain. This research restricts the domain to the Qur'anic Text.
In this thesis, a number of pre-processing steps were undertaken and annotation information were added to the Qur'an. The raw Arabic Qur'an was pre-processed into morphological units using the Qur'anic Arabic Corpus (QAC). Qur'anic terms were indexed and converted into a vector space model using techniques in Information Retrieval (IR). In parallel, nearly 24,000 Qur'anic personal pronouns were annotated with information on their referents. These referents are consolidated and organized into a total of over 1,000 ontological concepts. Moreover, a dataset of nearly 8,000 pairs of related Qur'anic verses are compiled from books of scholarly commentary on the Qur'an. This vector space model, the pronoun tagging, the verse relatedness dataset, and the part-of-speech tags available in QAC all together served for a number of Qur'anic text mining applications which were rendered online for public use. Among these applications: lemma concordance, collocation, POS search of the Qur'an, verse similarity measures, concept clouds of a given verse, pronominal anaphora and Qur'anic chapter similarity.
Furthermore, machine learning experiments were conducted on automatic detection of verse similarity/relatedness as well as categorization of Qur'anic chapters based on their chronology of revelation. Domain specific linguistic features were investigated to induct learning algorithms. Results show that deep linguistic and world knowledge is needed to reach the human upper bound in certain computational tasks such as detecting text relatedness, question answering and textual entailment. However, many useful queries can be addressed using text mining techniques and layers of annotations made available through this research. The works presented here can be extended to include other similar texts like Hadith (i.e., saying of Prophet Muhammad), or other scriptures like the Gospels
The Plight of Kurdish Natinonalism: Critical Analysis of the Kurds in Turkey, Iran, Iran, and Syria around First World War.
No full textDuring recent years the Kurdish question has reappeared, more intensely than before, on the international agenda. For years, this questino has been of fundamental concern to the countries of region,and it has led to intense internal controversies and economic and social crisis. The number of Kurds in fourt parts of Kurdistan and within the four borders of countries that have divided it up between themselves totals about 35 million.This makes the Kurds, after Arabs, the Turks, and Persians,the fourth largest nation in the middle east.
Kurds are, together with the Arabs,Persians and Armenians, one of the most ancient peoples of the near east. The country they inhabit is called Kurdistan. The Kurds have thier own language,Kurdish. Kurdish is a member of the Indo-European family of languages. Like Persian,Afghan and Bakuchi, it is one of the Iranian languages. Kurdish is unrelated to Arabic or Turkish languages.
Kurds have played a signoficant role in the history of this region since it's early epoches. A great deal of information can be found in numerous Greek, Arabs, Rokan , and Armenian.According to them, Kurds founded several important states druing early Islamic epoch between teenth and thirteenth centuries such as Salahadin, Merwandidis, and Ayubiat as well as in the distant past. Sultan Salahadin, the founder of the Ayubiad state, which included Egypt, Syria and Kurdistan, played a particularly significant role in history.
This thesis attempts to examine the main charecteristics of Kurdish natuionalism. In order to do that, the thesis analyses the social structure of Kurdish scoiety. The thesis thorougly explains the agitation of Kurds against the Ottoman Empire durng nineteenth century and beyond. This thesis examines Kurdish reactions in the course of the First World War against the Empires of Ottoman and Persia, which divided the Kurdish land between themselves. The thesis analyses the stunning obtacles in the face of the Kurds in formatinon of their national state in aftermath of the Ottoman Empire. This study can be a cornerstone to understand the inherent weakness of Kurdish nationalism in integrating all social and sectarian groups within the Kurdish society
Author Correction: The power of genetic diversity in genome-wide association studies of lipids (Nature, (2021), 600, 7890, (675-679), 10.1038/s41586-021-04064-3)
No full textCorrection to: Nature Published online 9 December 2021 In the version of this article initially published, Noha A. Yousri (Department of Genetic Medicine, Weill Cornell Medicine-Qatar, Doha, Qatar and Department of Computer and Systems Engineering, Alexandria University, Egypt) and Steven C. Hunt (Department of Internal Medicine, University of Utah, Salt Lake City, UT, USA and Department of Genetic Medicine, Weill Cornell Medicine-Qatar, Doha, Qatar) were not included in the author list. In addition, Hieab H. H. Adams (Department of Radiology and Nuclear Medicine, Erasmus MC, University Medical Center Rotterdam, Rotterdam, The Netherlands and Department of Clinical Genetics, Erasmus MC, University Medical Center Rotterdam, Rotterdam, The Netherlands) was shown with an incorrect second affiliation in the HTML and PDF versions of the article. Finally, in the HTML version, Cristen J. Willer was mistakenly listed with an extra affiliation (Princess Al-Jawhara Al-Brahim Centre of Excellence in Research of Hereditary Disorders (PACER-HD), King Abdulaziz University, Jeddah, Saudi Arabia). The authors and affiliations have been corrected in the HTML and PDF versions of the article. © 2023, The Author(s), under exclusive licence to Springer Nature Limited
FOG-1, a transcriptional regulator within the haematopoietic system
Get PDFFriend of GATA-1 (FOG-1) is a member of the friend of GATA (FOG)
family of proteins, which consists of large multitype zinc finger cofactors that
bind to the amino zinc finger of GATA transcription factors and modulate their
activity. FOG-1 also interacts with the C-terminal binding protein (CtBP),
mainly known as a corepressor and the nucleosome remodelling and histone
deacetylase repressive (NuRD) complex ; thus, integrating FOG-1 into the
transcription factor and chromatin modifier networks. Remarkably, the protein
activates or represses gene transcription by facilitating binding of GATA
factors to DNA, recruiting chromatin remodelling complexes, or by stabilizing
tissue-specific chromatin loops. Physical interaction between FOG and GATA
proteins in vivo is essential for the development of a broad array of tissues,
reflecting the overlapping expression patterns of these factors. Notably, within
the haematopoietic system, FOG-1 is absent in most of the myeloid lineages ;
it is expressed at high level in multipotent progenitors, erythroid and
megakaryocytic cells, low level in lymphoid and haematopoietic stem cells.
The cofactor is essential for differentiation of the erythroid and
megakaryocytic lineages, notably by interacting with GATA-1. FOG-1 also
plays a role in the T-lineage by repressing GATA-3 dependent induction of
Th2 development. Interestingly, overexpression of FOG-1 in avian
eosinophils, which do not normally express FOG-1, reprograms these
differentiated cells into multipotent cells. To study FOG-1 in mammals, we
used a novel transgenic mouse model strategy which we had designed to
generate mice with conditional overexpression of FOG-1. Our work with
enforced expression of FOG-1 in the whole murine haematopoietic system led
to a reduction in the number of circulating eosinophils, confirming and
extending to mammals the previously reported role of FOG-1 in repressing
this lineage development. Strikingly, we have identified the expression of
FOG-1 in early B lymphocytes, but not in late developmental stages such as
mature B cells and plasma cells. Moreover, FOG-1 function had never been
described in the B-lineage, where GATA factors are not expressed. Therefore,
we were intrigued by both the regulated expression of FOG-1 during B cell
development and its molecular mechanism of action in the absence of GATA
factors. Thus, we generated transgenic mice in which FOG-1 expression was
enforced at a physiologically relevant level in the B lymphoid system : in
mature B cells and from early B cell stages. We found that sustained FOG-1
expression in mature and late B cells did not affect their development or
function, contrary to our expected hypothesis. Although the mice
overexpressing FOG-1 from early B cell lineages showed only a weak
phenotype, we extensively studied FOG-1 partners in early B cell stages.
Indeed, describing FOG-1 molecular mechanism of action in the absence of
GATA factors is a question that warrant further investigation. We notably
found FOG-1 in complex with Ikaros, a transcription factor well described as
crucial for B cell development. The cofactor was also found associated to the
CtBP and NuRD epigenetic complexes in B cell lines
Estudo do efeito dos derivados de imidas cíclicas sobre os mecanismos de resistência tumoral e apoptose em células de linhagens tumorais
Get PDFTese (doutorado) - Universidade Federal de Santa Catarina, Centro de Ciências da Saúde, Programa de Pós-Graduação em Farmácia, Florianópolis, 2013.O câncer foi considerado uma das principais causas de morte no mundo, no ano de 2013, sendo responsável por 7,6 milhões de mortes (cerca de 13% de todas as causas de mortes). Para 2030 estima-se 27 milhões de novos casos. Embora a quimioterapia ainda seja a principal terapia utilizada para o tratamento da doença, a morbidade associada aos quimioterápicos ainda é um obstáculo a ser superado. Dessa forma, a busca por compostos antineoplásicos, que tenham maior eficiência em induzir apoptose nas células tumorais e com insignificantes efeitos colaterais, tornou-se alvo de investigação acadêmica e da indústria farmacêutica. Os compostos derivados de imidas cíclicas vêm sendo descritos como promissores agentes antitumorais. Assim, o objetivo deste estudo foi investigar o efeito dos derivados de imidas cíclicas sobre os mecanismos de resistência tumoral e apoptose sobre células de linhagem de melanoma murino (B16F10), de leucemia mieloide aguda humana (K562) e de leucemia linfoide aguda humana (Jurkat). Inicialmente, foi investigado o efeito citotóxico de nove derivados de imidas cíclicas sobre células de linhagem de melanoma murino (B16F10), e determinado suas CI50. O composto 2 foi o que apresentou melhor atividade citotóxica, com um valor de CI50 de 77,75 ?M (±1,3), por isso, foi selecionado para os demais experimentos. Os resultados mostram que esse composto apresenta atividade citotóxica concentração e tempo dependente, bloqueio das fases S e G2/M do ciclo celular, além do aumento de células na fase sub-G0G1, que sugere morte celular por apoptose. Como esses resultados foram considerados satisfatórios, o composto 2 e sete novos derivados de imidas cíclicas foram selecionados para uma nova triagem em células K562. Nessa nova etapa, o composto 15 demonstrou o melhor efeito citotóxico, por isso foi selecionado para modificações estruturais, que geraram cinco novos derivados (16, 17, 18, 19 e 20). O efeito citotóxico dos compostos (15, 16, 17, 18, 19 e 20) foi avaliado em células de leucemia aguda humana (K562 e Jurkat), e demonstram atividade citotóxica concentração e tempo dependente. Foi avaliado o efeito dos compostos (15, 16, 17, 18, 19 e 20) no ciclo celular, e estes demonstraram um bloqueio do ciclo celular na fase S para células Jurkat e na fase sub-G0/G1, para células K562 e Jurkat. A via de morte também foi avaliada por três diferentes metodologias, e os compostos demonstraram causar morte celular, via apoptose. Com esse conjunto de resultados os compostos 15, 17 e 19 foram selecionados para avaliar o seu efeito sobre o potencialmitocondrial, na expressão das proteínas AIF, Bcl-2, Bax, Fas, caspase-3 ativa, survivina, p53e Ki67. Os resultados demonstraram que os compostos (15, 17 e 19) causaram redução do potencial mitocondrial, aumento da expressão do AIF, diminuição da expressão da proteína antiapoptótica Bcl-2 e aumento da expressão da proteína pró-apoptótica Bax, sugerindo que o mecanismo de indução de apoptose desses compostos envolve a via intrínseca da apoptose. Ainda, nas células Jurkat, os compostos 15 e 17 também ativaram a apoptose pela via extrínseca, evidenciado pelo aumento da expressão do receptor Fas. Além disso, os compostos (15, 17 e 19) causaram aumento da atividade da proteína caspase-3 ativa, diminuição da expressão da proteína antiapoptótica survivina, aumento da expressão da proteína p53 e diminuição na expressão do marcador de proliferação celular Ki67. Também foi avaliado o efeito dos compostos (15, 17 e 19) sobre a expressão do gene abcc1, do fenótipo ABCC1 e do fenótipo LRP nas células K562 e Jurkat, e os resultados mostram que os compostos causaram diminuição da expressão constitutiva do gene abcc1 e da proteína LRP nas células K562 e Jurkat. Em conjunto, os resultados aqui expostos, sugerem que os compostos 15, 16, 17, 18, 19 e 20 causaram bloqueio do ciclo das células K562 e Jurkat, e, consequentemente, diminuição da proliferação celular, o que resulta na indução da apoptose via mecanismo intrínseco e/ou extrínseco, além de inibir os mecanismos de resistência à quimioterapia nessas células através da redução da transcrição do gene abcc1 e pela diminuição da expressão de LRP, Bcl-2 e survivina. Abstract : In 2008, cancer was considered a major cause of death in the world, accounting for 7.6 million deaths (around 13% of all causes of death). For 2030, 27 million new cases of cancer are estimated. Although chemotherapy is still the main therapy used for the treatment of this disease, the morbidity associated with chemotherapeutic drugs is still an obstacle to be overcome. Thus, the search for new anticancer compounds, with higher efficiency in inducing apoptosis in tumor cells with negligible side effects, has become an important target of the pharmaceutical industry. The compounds derived from cyclic imides have been described as promising with antitumor agents. The aim of this study was to investigate the effects of derivatives of cyclic imides on the mechanisms of tumor resistance and apoptosis in murine melanoma cells (B16F10), human acute myeloid leukemia cells (K562) and human acute lymphoblastic leukemia cells (Jurkat). First we have investigated the cytotoxic effect of nine derivatives of cyclic imides in murine melanoma cells (B16F10), and their IC50 have been calculated. Compound 2 has shown the best cytotoxic activity with an IC50 value of 77.75 ?M (±1.3), therefore, it was selected for further studies. The results have shown that this compound reduced the cell viability in a concentration and time-dependent manner, caused cell cycle arrest in S and G2/M phases and increased the number of cells in the sub-G0G1 phase, suggesting cell death by apoptosis. For these promising results, compound 2 and seven new derivatives of cyclic imides have been selected for a new screening in K562 cells. In this new stage, compound 15 has shown the best cytotoxic effect, so it was selected for structural modifications, which has generated five new compounds (16, 17, 18, 19 and 20). The cytotoxic effects of these compounds (15, 16, 17, 18, 19 and 20) have been evaluated in K562 and Jurkat cells, and they have demonstrated a cytotoxic concentration-and-time-dependent activity. The effects of these compounds (15, 16, 17, 18, 19 and 20) on cell cycle have demonstrated a blockage in S phase for Jurkat cells and in sub-G0/G1 phase in K562 and Jurkat cells. Apoptosis has been evaluated and confirmed by three different methodologies. Based on these results, compounds 15, 17 and 19 have been selected to evaluate their effects on the mitochondrial potential and on the expression of AIF, Bcl-2, Bax, Fas, caspase-3 active, survivin, Ki67 and p53 proteins. These compounds (15, 17, 19) have reduced the mitochondrial potential and have caused increased expression of AIF, decreased expression ofantiapoptotic protein Bcl-2 and increased expression of pro-apoptotic protein Bax, which suggests that the apoptosis caused by the compounds involves the intrinsic pathway. In Jurkat cells, apoptosis caused by compounds 15 and 17 also involves the extrinsic pathway, as it has been evidenced by the increased expression of Fas receptor. Furthermore, the compounds (15, 17, 19) have increased the activity of caspase-3 active and the expression of p53 protein, and they have decreased the expression of antiapoptotic survivin and the cell proliferation marker Ki67 proteins. The effect of these compounds (15, 17, 19) have also been evaluated on abcc1 gene expression, on ABCC1 phenotype and on LRP phenotype in Jurkat and K562 cells. The results have shown that the compounds reduced the constitutive expression of abcc1 gene and the expression of LRP protein in Jurkat and K562 cells. Together, these results suggest that compounds 15, 16, 17, 18, 19 and 20 cause cell cycle blockage in Jurkat and K562 cells and, therefore, decrease cell proliferation, which result in the induction of apoptosis by intrinsic and/or extrinsic pathways and in the inhibition of the resistance mechanisms to chemotherapy in these cells by reducing the transcription of abcc1 gene and by decreasing the expression of LRP, survivin and Bcl-2 proteins
Characterisation of T cell defects in acute myeloid leukaemia
No full textPhDUnderstanding the immune system in patients with cancer and how it interacts with malignant cells is critical for the development of successful immunotherapeutic strategies at a time when novel cancer treatment approaches are required. Acute myeloid leukaemia (AML) results in widespread interaction between the malignant cells and T cells and as such, offers an opportunity to study these interactions. A flow cytometric analysis of T cells in the peripheral blood of patients presenting with AML illustrated that the absolute number of T cells is increased in AML compared with healthy controls. Furthermore, a large population of CD3+56+ cells was identified. These cells are not natural killer T cells but effector T cells that may represent a failing immunosurveillance mechanism. Two technical issues were explored: how to separate T cells from the peripheral blood of newly diagnosed AML patients and the impact of the method of immunomagnetic cell separation on the gene expression profile of healthy T cells. Gene expression profiling was subsequently performed on T cells from AML patients compared with healthy controls. Global differences in transcription were observed suggesting aberrant T cell activation patterns in AML. As differentially regulated genes involved in actin cytoskeletal formation were noted, a functional assessment of the ability of T cells from AML patients to form immunological synapses was performed. This illustrated that although T cells from AML patients can form conjugates with autologous blasts, their ability to form immune synapses and recruit phosphotyrosine signalling molecules to that signalling interface is impaired. Taken together, these findings demonstrate that numerically T cells are plentiful in AML however they are abnormal in terms of the genes they are transcribing and in their interactions with tumour cells. Targeting immunological synapse formation may represent an important means of improving T cell recognition of tumour cells across a range of cancers
Global age-sex-specific fertility, mortality, healthy life expectancy (HALE), and population estimates in 204 countries and territories, 1950–2019: a comprehensive demographic analysis for the Global Burden of Disease Study 2019
No full text© 2020 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 licenseBackground: Accurate and up-to-date assessment of demographic metrics is crucial for understanding a wide range of social, economic, and public health issues that affect populations worldwide. The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019 produced updated and comprehensive demographic assessments of the key indicators of fertility, mortality, migration, and population for 204 countries and territories and selected subnational locations from 1950 to 2019. Methods: 8078 country-years of vital registration and sample registration data, 938 surveys, 349 censuses, and 238 other sources were identified and used to estimate age-specific fertility. Spatiotemporal Gaussian process regression (ST-GPR) was used to generate age-specific fertility rates for 5-year age groups between ages 15 and 49 years. With extensions to age groups 10–14 and 50–54 years, the total fertility rate (TFR) was then aggregated using the estimated age-specific fertility between ages 10 and 54 years. 7417 sources were used for under-5 mortality estimation and 7355 for adult mortality. ST-GPR was used to synthesise data sources after correction for known biases. Adult mortality was measured as the probability of death between ages 15 and 60 years based on vital registration, sample registration, and sibling histories, and was also estimated using ST-GPR. HIV-free life tables were then estimated using estimates of under-5 and adult mortality rates using a relational model life table system created for GBD, which closely tracks observed age-specific mortality rates from complete vital registration when available. Independent estimates of HIV-specific mortality generated by an epidemiological analysis of HIV prevalence surveys and antenatal clinic serosurveillance and other sources were incorporated into the estimates in countries with large epidemics. Annual and single-year age estimates of net migration and population for each country and territory were generated using a Bayesian hierarchical cohort component model that analysed estimated age-specific fertility and mortality rates along with 1250 censuses and 747 population registry years. We classified location-years into seven categories on the basis of the natural rate of increase in population (calculated by subtracting the crude death rate from the crude birth rate) and the net migration rate. We computed healthy life expectancy (HALE) using years lived with disability (YLDs) per capita, life tables, and standard demographic methods. Uncertainty was propagated throughout the demographic estimation process, including fertility, mortality, and population, with 1000 draw-level estimates produced for each metric. Findings: The global TFR decreased from 2·72 (95% uncertainty interval [UI] 2·66–2·79) in 2000 to 2·31 (2·17–2·46) in 2019. Global annual livebirths increased from 134·5 million (131·5–137·8) in 2000 to a peak of 139·6 million (133·0–146·9) in 2016. Global livebirths then declined to 135·3 million (127·2–144·1) in 2019. Of the 204 countries and territories included in this study, in 2019, 102 had a TFR lower than 2·1, which is considered a good approximation of replacement-level fertility. All countries in sub-Saharan Africa had TFRs above replacement level in 2019 and accounted for 27·1% (95% UI 26·4–27·8) of global livebirths. Global life expectancy at birth increased from 67·2 years (95% UI 66·8–67·6) in 2000 to 73·5 years (72·8–74·3) in 2019. The total number of deaths increased from 50·7 million (49·5–51·9) in 2000 to 56·5 million (53·7–59·2) in 2019. Under-5 deaths declined from 9·6 million (9·1–10·3) in 2000 to 5·0 million (4·3–6·0) in 2019. Global population increased by 25·7%, from 6·2 billion (6·0–6·3) in 2000 to 7·7 billion (7·5–8·0) in 2019. In 2019, 34 countries had negative natural rates of increase; in 17 of these, the population declined because immigration was not sufficient to counteract the negative rate of decline. Globally, HALE increased from 58·6 years (56·1–60·8) in 2000 to 63·5 years (60·8–66·1) in 2019. HALE increased in 202 of 204 countries and territories between 2000 and 2019. Interpretation: Over the past 20 years, fertility rates have been dropping steadily and life expectancy has been increasing, with few exceptions. Much of this change follows historical patterns linking social and economic determinants, such as those captured by the GBD Socio-demographic Index, with demographic outcomes. More recently, several countries have experienced a combination of low fertility and stagnating improvement in mortality rates, pushing more populations into the late stages of the demographic transition. Tracking demographic change and the emergence of new patterns will be essential for global health monitoring. Funding: Bill & Melinda Gates Foundation.American Journal of Public HealthAperfei?oamento de Pessoal de N?vel SuperiorBausch & LombCNDS-UEFISCDICentro de Investigaci?n en Red de Enfermedades RespiratoriasCentro de Investigación en Red de Enfermedades RespiratoriasCi?ncia e TecnologiaConselho Nacional de Desenvolvimento Cient?fico e Tecnol?gicoEgyptian Fulbright Mission ProgramFRIATFondazione Istituto NeurologicoFundação para a Ciência e TecnologiaGerman National Cohort StudyHealth Data Research UKISCIII?FEDERInstitute of SociologyManipal Academy of Higher EducationMedical Research Council, and Scottish Government Chief Scientist OfficeMinistry of the Environment JapanNorwegian Institute of Public HealthPanjab University, ChandigarhPopulation and Development departmentResearch Management OfficeRussia Academy of SciencesScottish Government Chief Scientist OfficeSistema Nacional de Investigaci?nSpanish Ministry of Science, Innovation and Universities Miguel ServetUAB Cochrane Musculoskeletal Group Satellite Center on Network Meta-analysisUS Food and Drug Administration Arthritis Advisory CommitteeVeterans Affairs Rheumatology Field Advisory CommitteeWellcome Trust DBTXiamen University MalaysiaNational Institutes of HealthNational Institute of Mental HealthNational Institute of AgingFogarty International CentreUS Environmental Protection AgencyBill & Melinda Gates FoundationDamon Runyon Cancer Research FoundationNRSAlexander von Humboldt FoundationDuke UniversityEdwards LifesciencesUniversity of TennesseeUniversity of MichiganArizona State UniversityOhio UniversityJohns Hopkins Bloomberg School of Public HealthBoston ScientificQueensland Department of HealthWellcome TrustUniversity of IllinoisComunidad de MadridNIHR Biomedical Research CentreSouth African Department of Science and InnovationMedical Research CouncilNational Institute for Health ResearchDepartment of HealthRoyal SocietyEUNational Health and Medical Research CouncilSouth African Medical Research CouncilMinistry of Education, Culture, Sports, Science, and Technology of JapanEuropean & Developing Countries Clinical Trials PartnershipDanish National Research FoundationUniversity of MelbourneUniversity of Western AustraliaFCTPublic Health EnglandCoordenação de Aperfeiçoamento de Pessoal de Nível SuperiorGerman Federal Ministry of Education and ResearchSeoul National UniversityItalian Ministry of HealthCNPqNational Research FoundationSwedish Research CouncilHong Kong Polytechnic UniversityNational University of MalaysiaMinistry of Education, Science and Technological Development of the Republic of SerbiaInstituto de Salud Carlos IIIESFBiotronikBHF Centre of Research Excellence, OxfordNational Authority for Scientific Research and InnovationMCTESSENACYTEuropean Regional Development FundCOMPETENIHR Oxford Biomedical Research CentreSistema Nacional de Investigació
Defending the “Satanic Verses” : constructive engagement: British-Iranian relations and the right to freedom of expression (1989-2004)
No full textThis thesis aims to conceptualize what is often referred to in diplomacy, as a policy of “constructive engagement”, by employing neoliberal-institutionalist theories and conflict resolution approaches. The adopted “model for constructive engagement” serves as the theoretical framework and centres on the basic assumption that non-coercive diplomacy coupled with the offer of incentives is best suited at resolving conflict as well as promoting human rights in international relations. Rather than looking at determinants of foreign policy making, the thesis focuses, therefore, on the actual exercise of power and influence in international relations. As such, power, both in terms of a state’s available assets as well as seen as a form causation, is considered the crucial variable in determining diplomatic manoeuvring and negotiation behaviour. The empirical context for the research project is provided by the case of British-Iranian relations during the period from 1989 to 2004. The narrative is divided into two parts: the first one deals with the impact of the fatwa against Salman Rushdie by Ayatollah Khomeini on bilateral relations and investigates British diplomacy towards Tehran, which followed the European Union’s policy of “Critical Dialogue” with Iran. Whilst the promotion of human rights was on the agenda of the “Critical Dialogue”, findings indicate that contrary to other EU member states, most notably Germany, Whitehall was able to genuinely pursuing a policy of “constructive engagement”, demanding meaningful changes in Iranian behaviour. However, findings also show that Britain’s priority was at resolving the “Rushdie affair” and not necessarily at promoting and protecting human rights in Iran. The second part of the narrative looks at the “Comprehensive Dialogue” which was implemented by the European Union in 2000 and established a direct linkage between economic rewards and the improvements of human rights in Iran. Whilst the Iranian government and parliament met EU demands, the country’s maze of power centres, most notably those dominated by hardliners and conservatives, worked against any meaningful improvements in the protection and respect of human rights. Both narratives indicate to what extent diplomacy and negotiations were influenced by domestic constituents, referred to as the Two-Level Game, as well as by asymmetries of interdependence between the EU and Iran. Overall, the data implies that constructive engagement, whilst subject to political and economic interdependence, constitutes an effective form of human rights diplomacy
The global burden of cancer attributable to risk factors, 2010-19: a systematic analysis for the Global Burden of Disease Study 2019
Get PDFBackground Understanding the magnitude of cancer burden attributable to potentially modifiable risk factors is crucial for development of effective prevention and mitigation strategies. We analysed results from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019 to inform cancer control planning efforts globally.Methods The GBD 2019 comparative risk assessment framework was used to estimate cancer burden attributable to behavioural, environmental and occupational, and metabolic risk factors. A total of 82 risk-outcome pairs were included on the basis of the World Cancer Research Fund criteria. Estimated cancer deaths and disability-adjusted life-years (DALYs) in 2019 and change in these measures between 2010 and 2019 are presented.Findings Globally, in 2019, the risk factors included in this analysis accounted for 4.45 million (95% uncertainty interval 4.01-4.94) deaths and 105 million (95.0-116) DALYs for both sexes combined, representing 44.4% (41.3-48.4) of all cancer deaths and 42.0% (39.1-45.6) of all DALYs. There were 2.88 million (2.60-3.18) risk-attributable cancer deaths in males (50.6% [47.8-54.1] of all male cancer deaths) and 1.58 million (1.36-1.84) risk-attributable cancer deaths in females (36.3% [32.5-41.3] of all female cancer deaths). The leading risk factors at the most detailed level globally for risk-attributable cancer deaths and DALYs in 2019 for both sexes combined were smoking, followed by alcohol use and high BMI. Risk-attributable cancer burden varied by world region and Socio-demographic Index (SDI), with smoking, unsafe sex, and alcohol use being the three leading risk factors for risk-attributable cancer DALYs in low SDI locations in 2019, whereas DALYs in high SDI locations mirrored the top three global risk factor rankings. From 2010 to 2019, global risk-attributable cancer deaths increased by 20.4% (12.6-28.4) and DALYs by 16.8% (8.8-25.0), with the greatest percentage increase in metabolic risks (34.7% [27.9-42.8] and 33.3% [25.8-42.0]).Interpretation The leading risk factors contributing to global cancer burden in 2019 were behavioural, whereas metabolic risk factors saw the largest increases between 2010 and 2019. Reducing exposure to these modifiable risk factors would decrease cancer mortality and DALY rates worldwide, and policies should be tailored appropriately to local cancer risk factor burden. Copyright (C) 2022 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license
