17 research outputs found

    Occult alpha globin gene mutations are the commonest causes of red cell microcytosis unexplained by phenotypic testing

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    HAA: Haematology Society of Australia and New Zealand, The Australian & New Zealand Society of Blood Transfusion and The Australasian Society of Thrombosis and HaemostasisAIM: Hypochromic microcytic anaemia is the hallmark phenotype of thalassaemia. Current phenotypic tests do not provide a diagnosis in a small proportion of patients with red cell microcytosis. We investigated the genetic basis of microcytosis in a cohort of such subjects. METHOD: We identified from a large cohort of 1684 unselected requests for thalassaemia testing 25 Chinese subjects who had unexplained microcytosis after phenotypic haemoglobin studies. Extensive genotypic analysis of the α and β globin gene cluster was performed in 20 of these subjects who had adequate DNA. Techniques employed included gap-polymerase chain reaction, amplification-refractory mutation system, Sanger sequencing and multiplex ligation-dependent …postprin

    To what extent does Hong Kong primary school students’ Chinese reading comprehension benefit from after-school private tuition?

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    The reading attainment of the 3,875 primary 4 Hong Kong primary school students participating in the 2011 Progress in International Reading Literacy Study ranked first among 49 countries and regions surveyed worldwide. Analysis of the association between (a) participating students’ reading attainment and (b) responses to questionnaires completed by the students and their parents revealed that classroom teaching, the school curriculum, the reader’s social and economic background and support from home had all helped shape reading performance. It is not unusual for school students in many Asian countries to receive after-school tuition in various areas of the curriculum to boost performance in impending examinations. The study reported here focussed (1) on the Chinese language reading attainment of students who had attended private tutoring classes after school in this subject against the scores of fellow students who had not and (2) asking whether such after-school tutoring had been of any notable benefit to their reading. Although a majority of the parents questioned said they paid for extra tuition for their children after school, analyses of the data found there was a statistically significant difference between the scores of students who received extra tuition and those who did not, the score of the latter group being superior. It is suggested that the Hong Kong education authorities reassure parents about the quality of teaching in primary schools and publicly pronounce on the potential value of after-school private tutoring

    Protein arginine-methyltransferase-dependent oncogenesis

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    Enzymes that mediate reversible epigenetic modifications have not only been recognized as key in regulating gene expression and oncogenesis, but also provide potential targets for molecular therapy. Although the methylation of arginine 3 of histone 4 (H4R3) by protein arginine methyltransferase 1 (PRMT1) is a critical modification for active chromatin and prevention of heterochromatin spread, there has been no direct evidence of any role of PRMTs in cancer. Here, we show that PRMT1 is an essential component of a novel Mixed Lineage Leukaemia (MLL) oncogenic transcriptional complex with both histone acetylation and H4R3 methylation activities, which also correlate with the expression of critical MLL downstream targets. Direct fusion of MLL with PRMT1 or Sam68, a bridging molecule in the complex for PRMT1 interaction, could enhance self-renewal of primary haematopoietic cells. Conversely, specific knockdown of PRMT1 or Sam68 expression suppressed MLL-mediated transformation. This study not only functionally dissects the oncogenic transcriptional machinery associated with an MLL fusion complex, but also uncovers - for the first time - an essential function of PRMTs in oncogenesis and reveals their potential as novel therapeutic targets in human cancer.link_to_subscribed_fulltex
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