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1.
PLoS One ; 15(1): e0227483, 2020.
Article in English | MEDLINE | ID: mdl-31935233

ABSTRACT

BACKGROUND: Little is known about depressive symptoms among adolescents in the United Arab Emirates (UAE). This study aimed to identify the prevalence of depression and its association with self-esteem, individual, parental and family factors among adolescents aged 12 to 18 in UAE. METHODS: Six hundred adolescents, aged 12 to 18 years were recruited from 4 of 111 schools in a cross-sectional study. We administered Beck Depression Inventory Scale and Rosenberg Self-esteem Scale to measure self-report symptoms of depression and self-esteem. We used multiple linear regression to identify significant predictors of depression. RESULTS: Over 86% of the identified sample participated to the survey. The mean age of the sample was 14.3 (±1.3) with an excess of girls (61%). Depressive symptoms were detected in 17.2% (95% CI 14.2-20.7). There was an inverse relationship between self-esteem scores and depressive symptoms. Positive predictors of depressive symptoms, having controlled for age, gender, and ethnicity included experiencing neglect, being verbally abused in school, having no monthly allowance to spend in school, a history of physical morbidities requiring treatment, being a current or past smoker and a low family income. CONCLUSION: The high prevalence of depressive symptoms measured in this survey suggests a significant public health problem among adolescents in the UAE. Public health interventions aimed at facilitating education and early detection and potential treatment of depressive symptoms are a priority in the region.


Subject(s)
Depressive Disorder/psychology , Self Concept , Adolescent , Child , Cross-Sectional Studies , Depressive Disorder/epidemiology , Depressive Disorder/pathology , Female , Humans , Male , Prevalence , Risk Factors , Self Report , Surveys and Questionnaires , United Arab Emirates/epidemiology
2.
PLoS One ; 6(10): e26206, 2011.
Article in English | MEDLINE | ID: mdl-22022569

ABSTRACT

Hereditary haemorrhagic telangiectasia (HHT) is an autosomal dominant genetic condition affecting the vascular system and is characterised by epistaxis, arteriovenous malformations and mucocutaneous and gastrointestinal telangiectases. This disorder affects approximately 1 in 8,000 people worldwide. Significant morbidity is associated with this condition in affected individuals, and anaemia can be a consequence of repeated haemorrhages from telangiectasia in the gut and nose. In the majority of the cases reported, the condition is caused by mutations in either ACVRL1 or endoglin genes, which encode components of the TGF-beta signalling pathway. Numerous missense mutations in endoglin have been reported as causative defects for HHT but the exact underlying cellular mechanisms caused by these mutations have not been fully established despite data supporting a role for the endoplasmic reticulum (ER) quality control machinery. For this reason, we examined the subcellular trafficking of twenty-five endoglin disease-causing missense mutations. The mutant proteins were expressed in HeLa and HEK293 cell lines, and their subcellular localizations were established by confocal fluorescence microscopy alongside the analysis of their N-glycosylation profiles. ER quality control was found to be responsible in eight (L32R, V49F, C53R, V125D, A160D, P165L, I271N and A308D) out of eleven mutants located on the orphan extracellular domain in addition to two (C363Y and C382W) out of thirteen mutants in the Zona Pellucida (ZP) domain. In addition, a single intracellular domain missense mutant was examined and found to traffic predominantly to the plasma membrane. These findings support the notion of the involvement of the ER's quality control in the mechanism of a significant number, but not all, missense endoglin mutants found in HHT type 1 patients. Other mechanisms including loss of interactions with signalling partners as well as adverse effects on functional residues are likely to be the cause of the mutant proteins' loss of function.


Subject(s)
Antigens, CD/metabolism , Endoplasmic Reticulum/metabolism , Receptors, Cell Surface/metabolism , Telangiectasia, Hereditary Hemorrhagic/metabolism , Antigens, CD/chemistry , Antigens, CD/genetics , Cell Membrane/metabolism , Endoglin , Glycoside Hydrolases/metabolism , HeLa Cells , Humans , Models, Molecular , Mutant Proteins/chemistry , Mutant Proteins/metabolism , Mutation, Missense/genetics , Protein Structure, Tertiary , Protein Transport , Receptors, Cell Surface/chemistry , Receptors, Cell Surface/genetics , Subcellular Fractions/metabolism , Telangiectasia, Hereditary Hemorrhagic/genetics
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