MATERIALISM AND UAE NATIONALS

Amongst examined populations, research has found materialistic values to be empirically associated with lower levels of life satisfaction. While the causes of materialistic values are plentiful, extant research suggests that a primary driver is the rapid urbanization and commercialization of a society, with youth being more susceptible. The dramatic transformation of the UAE over the past four decades, coupled with the relatively young population, increases the likelihood that materialistic values have been cultivated among the population. This study sheds light on the interesting but under researched case of materialism in the UAE. A self-report survey measured the materialism and life satisfaction levels of 210 UAE residents (80 nationals and 130 non-nationals). Materialistic values were found to be negatively correlated with life satisfaction amongst our sample. In addition, UAE nationals reported significantly higher levels of materialism than non-national residents. To uncover the causes and consequences of high levels of materialism amongst UAE nationals, four focus groups and 25 in-depth interviews were conducted. Five major consequences of materialistic values were revealed: 1) the development of an increasingly competitive and narcissistic society, 2) the development of a more judgmental and less accepting society, 3) the use of consumption as a tool to boost confidence and self-esteem, 4) an increase in family conflicts and the delaying of marriage, and 5) a lack of savings and an increase in debt. The primary causes of materialistic values were: 1) the rapid development and commercialization of the UAE, 2) the consequences of materialism propagating the values in a self-perpetuating cycle, 3) narcissism and competition on social media, 4) Emirati values of generosity, hospitality, perfection and pride, and 5) parenting and youths lack of financial responsibilities. To advance life satisfaction levels within the UAE population, we propose that policy makers implement awareness campaigns, educational programs, and legislation to reduce the current levels of materialism

Studying the Properties of Cationic Emulsified Asphalts Paving Mixture at Iraqi Environmental Conditions

Emulsified asphalt mixture is generally a mix made of emulsified asphalt with aggregate. Emulsified asphalt is manufactured from base asphalt, emulsifier agent and water. This study aims to study and improve the emulsified asphalt mixtures with using of ordinary Portland cement as filler materials for road construction and maintenance in Iraq as an alternative to the hot asphalt mixtures, due to its economical, practical and environmental advantages. Beside this study focused to test and evaluates the emulsified asphalt material properties to be used as paving mixture. The tested properties of emulsified asphalt mixture were bulk density, air voids, dry Marshall Stability, wet Marshall Stability, retained Marshall Stability, flow tests with different compaction efforts differ from standard Marshall Limitations and compared with the common used specification. The results indicate that the emulsified asphalt type cationic slow setting low viscosity (CSS-1) is very suitable with quartz type of aggregate from Al-Nibaay quarry. From many trial mixes it is found that the best percentages of initial residual bitumen content to produced adequate results for coating test ,mixing ,compaction ,curing and Marshall stability were ranged from (2.5%, 3%,3.5%,4% and 4.5%), and the optimum percentage is (3.5%).Finally it can be conducted that the emulsified asphalt mixture contained Portland cement filler material is a suitable alternative mixture to the hot asphalt mixture for road construction and specially maintenance of roadways in Iraq

Mutations in pericentrin cause Seckel syndrome with defective ATR-dependent DNA damage signaling

Large brain size is one of the defining characteristics of modern humans. Seckel syndrome (MIM 210600), a disorder of markedly reduced brain and body size, is associated with defective ATR-dependent DNA damage signaling. Only a single hypomorphic mutation of ATR has been identified in this genetically heterogeneous condition. We now report that mutations in the gene encoding pericentrin (PCNT)--resulting in the loss of pericentrin from the centrosome, where it has key functions anchoring both structural and regulatory proteins--also cause Seckel syndrome. Furthermore, we find that cells of individuals with Seckel syndrome due to mutations in PCNT (PCNT-Seckel) have defects in ATR-dependent checkpoint signaling, providing the first evidence linking a structural centrosomal protein with DNA damage signaling. These findings also suggest that other known microcephaly genes implicated in either DNA repair responses or centrosomal function may act in common developmental pathways determining human brain and body size

Characterization of novel isoforms and evaluation of SNF2L/SMARCA1 as a candidate gene for X-linked mental retardation in 12 families linked to Xq25-26

<p>Abstract</p> <p>Background</p> <p>Mutations in genes whose products modify chromatin structure have been recognized as a cause of X-linked mental retardation (XLMR). These genes encode proteins that regulate DNA methylation (<it>MeCP2</it>), modify histones (<it>RSK2 </it>and <it>JARID1C</it>), and remodel nucleosomes through ATP hydrolysis (<it>ATRX</it>). Thus, genes encoding other chromatin modifying proteins should also be considered as disease candidate genes. In this work, we have characterized the <it>SNF2L </it>gene, encoding an ATP-dependent chromatin remodeling protein of the ISWI family, and sequenced the gene in patients from 12 XLMR families linked to Xq25-26.</p> <p>Methods</p> <p>We used an <it>in silico </it>and RT-PCR approach to fully characterize specific SNF2L isoforms. Mutation screening was performed in 12 patients from individual families with syndromic or non-syndromic XLMR. We sequenced each of the 25 exons encompassing the entire coding region, complete 5' and 3' untranslated regions, and consensus splice-sites.</p> <p>Results</p> <p>The <it>SNF2L </it>gene spans 77 kb and is encoded by 25 exons that undergo alternate splicing to generate several distinct transcripts. Specific isoforms are generated through the alternate use of exons 1 and 13, and by the use of alternate donor splice sites within exon 24. Alternate splicing within exon 24 removes a NLS sequence and alters the subcellular distribution of the SNF2L protein. We identified 3 single nucleotide polymorphisms but no mutations in our 12 patients.</p> <p>Conclusion</p> <p>Our results demonstrate that there are numerous splice variants of SNF2L that are expressed in multiple cell types and which alter subcellular localization and function. <it>SNF2L </it>mutations are not a cause of XLMR in our cohort of patients, although we cannot exclude the possibility that regulatory mutations might exist. Nonetheless, <it>SNF2L </it>remains a candidate for XLMR localized to Xq25-26, including the Shashi XLMR syndrome.</p

Characterization of novel isoforms and evaluation of SNF2L/SMARCA1 as a candidate gene for X-linked mental retardation in 12 families linked to Xq25-26

<p>Abstract</p> <p>Background</p> <p>Mutations in genes whose products modify chromatin structure have been recognized as a cause of X-linked mental retardation (XLMR). These genes encode proteins that regulate DNA methylation (<it>MeCP2</it>), modify histones (<it>RSK2 </it>and <it>JARID1C</it>), and remodel nucleosomes through ATP hydrolysis (<it>ATRX</it>). Thus, genes encoding other chromatin modifying proteins should also be considered as disease candidate genes. In this work, we have characterized the <it>SNF2L </it>gene, encoding an ATP-dependent chromatin remodeling protein of the ISWI family, and sequenced the gene in patients from 12 XLMR families linked to Xq25-26.</p> <p>Methods</p> <p>We used an <it>in silico </it>and RT-PCR approach to fully characterize specific SNF2L isoforms. Mutation screening was performed in 12 patients from individual families with syndromic or non-syndromic XLMR. We sequenced each of the 25 exons encompassing the entire coding region, complete 5' and 3' untranslated regions, and consensus splice-sites.</p> <p>Results</p> <p>The <it>SNF2L </it>gene spans 77 kb and is encoded by 25 exons that undergo alternate splicing to generate several distinct transcripts. Specific isoforms are generated through the alternate use of exons 1 and 13, and by the use of alternate donor splice sites within exon 24. Alternate splicing within exon 24 removes a NLS sequence and alters the subcellular distribution of the SNF2L protein. We identified 3 single nucleotide polymorphisms but no mutations in our 12 patients.</p> <p>Conclusion</p> <p>Our results demonstrate that there are numerous splice variants of SNF2L that are expressed in multiple cell types and which alter subcellular localization and function. <it>SNF2L </it>mutations are not a cause of XLMR in our cohort of patients, although we cannot exclude the possibility that regulatory mutations might exist. Nonetheless, <it>SNF2L </it>remains a candidate for XLMR localized to Xq25-26, including the Shashi XLMR syndrome.</p