The present thesis aimed to identify and examine children with late-emerging dyslexia (LED) in Chinese. They were a group of children who only met the diagnostic criteria of dyslexia in their later stage of development after Grade 3. Their cognitive profile in word level and text level skills were compared with those who were diagnosed as dyslexia at their early grades (ED), i.e., before Grade 3. This thesis also aimed to identify early predictors which could discriminate the two groups, the LED and ED groups. Study 1 was a cross-sectional study which aimed to identify a group of LED children in Grade 4 and to examine their cognitive profile. Four groups of participants were recruited. Two groups of Grade 4 dyslexic children participated—36 dyslexic children diagnosed before Grade 3 (the ED group) and 41 dyslexic children diagnosed in Grade 4 (the LED group). There were two control groups, age-equivalent (CA) and reading level equivalent (RA) control groups. Totally 171 children were administered some word-level and text-level literacy and cognitive linguistic tasks. The LED group was found to be significantly higher than the ED group in word reading fluency and faster than the RA group in RAN, but poorer than the ED group in listening comprehension. Rapid naming, listening comprehension and age were able to predict correctly 73% membership of the LED group and 74.2% membership of the ED group. Subgroup analysis of both groups, with different word reading level, revealed the heterogeneity of the ED group which implied possible diversity in developmental changes prior Grade 4. As some children in the LED group of Study 1 might be unidentified but not late-emerging cases, a longitudinal study was necessary. Thus, Study 2 was a longitudinal study which followed 371 children from 4 local primary schools at Time 1 (Grade 2), Time 2 (Grade 3) and Time 3 (Grade 4). It aimed to identify early predictors which could discriminate the two groups, the ED and the LED who were diagnosed in Grade 3 and 4 respectively. The LED group was found to be similar to the CA group in text reading fluency and significantly better than the ED group in dictation at Time 1. Dictation and word reading fluency of Time 1 and text reading fluency of Time 2 were significant to predict 84.6% membership of the LED and the ED. Their late emerging difficulties were evident in word spelling and text reading fluency. The LED who were relatively superior in verbal memory and morphological awareness at Time 1, in orthographic skills and phonological retrieval at Time 2, are supposed to have acquired the basic skills necessary for word learning in the logographic, cipher and orthographic stage. But at Time 2 and 3, they were found to meet the criterion of dyslexia. Findings of the present study supported that Chinese word learning at the early stage, might only require few cognitive skills, such as phonological and semantic skills but at a later stage, it involved multiple cognitive skills of all three aspects, phonology, orthography and semantics. Overall speaking, a group of Chinese children with late-emerging dyslexia were identified in this study. The prevalence rate was estimated to be around 39% of the total number of dyslexic cases (including both with late-emerging and early diagnosed dyslexia). The LED groups in both studies were found to be better than the ED groups in reading fluency either of word only in Study 1 or both word and text in Study 2. In addition, the LED group of Study 2 was also found to have dictation better than the ED group in Grade 2 but not later. Despite the steady trend of deterioration in literacy skills, the cognitive linguistic skills of the LED group fluctuated. Thus, the present findings supported that younger Chinese learners, particularly in Hong Kong where pin-yin system was not adopted in most schools, could survive with strength in phonological memory and morphological awareness at the early stage. But mature Chinese learners have to acquire multiple cognitive skills of all three aspects phonology, orthography and semantics, in order to maintain adequacy in literacy skills. This was consistent with the multiple deficit model in previous Chinese studies (Ho et al, 2002 & 2004) in contrast with the double deficit model of English (Bowers & Wolf, 1993; Wolf, 1997; Wolf & Bowers, 1999). Such findings also suggested that the development of phonological pathway followed by the semantic pathway in English, proposed by Seidenberg, and McChelland (1989), was not found in Chinese. Instead, the connection between phonology and semantics was first developed followed by the triangular model of phonology, semantics and orthography. Besides, present findings have some implications for practice in assessment and intervention. Educational practitioners should be aware that the performance in dictation, among some children, could be deviated from their reading and that their performance fluctuated developmentally. Also, identification has to be done universally and timely with sensitive screening tools. Assessment tools may include word level such as dictation and word reading fluency and text level such as text level fluency and intervention has to be linked with assessment so as to strengthen the aspect which the children might be weak at a particular stage. / published_or_final_version / Educational Psychology / Doctoral / Doctor of Psychology

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讀寫障礙是最普遍的一種學習障礙（80%)，影響全球大約一成的學童。讀寫障礙患者於閱讀及書寫能力方面出現困難，而這並非因為患者本身的智力、學習動機或學習機會引致。對於引至讀寫障礙的理仍未清楚，但在西方人士的遺傳研究方面已發現多個與讀寫障礙相聯的基因位點及基因。本研究針對其中4個基因位點（DYX1 ’ DYX2 ’ DYX3 ’ DKX8)及其覆蓋的11基因測試了 131讀寫障礙的中國人家庭與讀寫障礙的關聯性。是項研究從國際人類基因組單體型圖(HapMap)中選擇標籤單核苷酸多型性(Tag-SNPs)及選擇以往報告與讀寫障礙有關的單核苷酸多型性進行測試。並在DYXZa基因（rs3743205 ’ padjusted =0.0072' OR = 0.08 ( 95% CI: 0.01 - 0.64 ))私MRPL19 (風險單体型rs2422229-rs7570229,風險單体型T-G, Padjusted=0.0020, OR = 2.345 (95% CI: 1.402 - 3.923))發現與讀寫障礙有正關聯性。單核苷酸多態性亦與閱讀的幾個特徵相關：DYX1C1 ( rs3743205 )與快速命名（Digit Rapid Naming ) ’語音記憶（Non-word repetition)，字型結構的左右逆轉（Left-Right Reversal )相關；KIAA0319 ( rs2760157 rs807507 )與語音意識（Onset Detection )相關；MRPL19 ( rs2422229-rs7570229 ) 與字型結構的部首位置(Radical Position)相關；SFPQand ZMYM4 ( rs3738697 - rs12093076 )與詞彙決策（Lexical Decision )相關。本研究是首個對於讀寫障礙的中國人族群進行的的基因研究（Lim et al. 2011) ’結果有助提供我們了解讀寫障礙在使用不同語言的族群的情況。 / 在過往歐洲的研究樣本中’位於KAA0319基因5'-上游的基因變異重複地被找出與讀寫障礙有關的閱讀特徵有關。過往研究亦指出位於KIAA0319的假定調控區上的單核苷酸多態性(SNP)顯示與KIAA0315的基因表達有關。唯本項研究於這區域並無發現陽性結果。為了找出這區域中與讀寫障礙有關聯但未被本研究策略選擇使用基因組單體型圖的標籤-單核苷酸多態性(Hapmap Tag-SNPs)的基因變異，本研究對KAM0319基因的5'-上游進行了基因组重测序。其中發現的3個短序變異（-121的rs6456625，-128到- 1 5 4 的r s 7 1 8 1 5 1 4 3 及- 1 5 7 的6 > A )出現了不同的榮光素酶報告基因活動，當中單体型A-DEL-A的活動訊號最高，而G-INS-G則最低。然而，它們的等位基因和單体型基因出現率於讀寫障礙樣本與對照組沒有顯著不同。 / 至今有關對KIAA0319基因抑制的行為研究仍然不足。本研究亦對位於果繩的CG7565基因，即KIAA0319的同源基因’進行特性分析。CG7565在果繩的發展階段出現了不同的表達水平及基因剪接形式。本研究使用了UAS-RNAi糸統和飛行模擬器對CG7565基因抑制的果繩的行為變化作出了分析，結果顯示於泛神經基因抑制晰/+; e/aV-Gal4/+; 3707/+及晰/+; e/av-Gal4/+; 8396/+的果蠅視覺模式記憶出現了缺陷。當CG7565在果繩大腦中央複合區的神經元F5(扇形體)和R2/R4m(摘球体)被基因抑制時，果繩視覺模式記憶亦出現了缺陷。是次有關M/PL119的遺傳關聯研究跟以往MRPL19中5'-上游與讀寫障礙的關聯報導的一致’顯示這可能是真正的致病序列變異的位置。在M/PL119上的假定調控區進行基因突變分析顯示，在其中一個讀寫障礙的樣本中發現一個新的序列變化(-647 T>G)，而在對照組則沒有發現此變化。計算機預測模型分析估計這個序列變化會取消了熱休克轉錄因子1的結合位點。攜帶了 G等位基因的調控區會增加榮光素酶的活動。這種變異的作用必須得到進一步的證實。我們亦觀察到在其中兩個讀寫障礙樣本中出現了非孟德爾遺傳，在一個個体身上帶有3或4種單倍型的基因。基因拷貝數目變異或基因轉換可能是一個引至這種現象的因素。 / Developmental dyslexia is a learning disability characterized by difficulties in acquisition of reading and writing skills not due to intelligence, motivation or schooling. Being the most common form of learning disability (80%), it affects 10% of schoolchildren worldwide. Research delineating genetic factors in developmental dyslexia identified loci and candidate genes in Caucasian populations, although disease mechanisms are still unknown. Four loci covering eleven genes (DYX1, DYX2, DYX3, DYXS) were tested for association in 131 Chinese families with dyslexic children in our study. Tagged-SNPs selected from International HapMap Consortium and reported SNPs were used as markers for this study. Positive associations with dyslexia were found in two genes, DYX1C1 (rs3743205, padjusted=0.0072, OR =0.08 (95% CI: 0.01 - 0.64)) and MRPL19(rs2422229-rs7570229, risk haplotype T-G,Padjusted=0.0020, OR = 2.345 (95% CI: 1.402 一 3.923)), in our study. SNPs associated with several reading-related traits were also identified: DYX1C1(rs3743205) associated with Rapid Naming (Digit Rapid Naming), Phonological Memory (Non-word repetition),Orthographic skill (Left-Right Reversal); KIAA0319 (rs2760157-rs807507) with honological awareness (Onset Detection); MRPL19 (rs2422229-rs7570229) with Orthographic knowledge (Radical Position); SFPQ and ZMYM4 (rs3738697 - rs12093076) with Orthographic knowledge (Lexical Decision). This is the first genetic study in Chinese dyslexia (Lim et al.2011), and results provide knowledge into dyslexia in populations using different languages. / Variants located 5' upstream of KIAA0319 were consistently reported for association with DD reading-related traits in European samples. A SNP in the putative promoter of KIAA0319 showed functional significance in KIAA0319 expression. However, no positive result of this region is found in this study. Resequencing of the 5' upstream of KIAA0319 was done to reveal potentially associated variants not selected using current strategies in genetic association (Hapmap Tagged-SNPs). A short sequence fragment of 3 variants (-121 rs6456625, -128 to -154 rs71815143 and -157 G>A) show differential luciferase activities, haplotype A-del-A have highest signal, G-Ins-G the lowest. However, allele and haplotype frequencies in dyslexia samples were not significantly different from controls. / Direct behavioral study of KIAA0319-knockdown is still inadequate. A homolog of KIAA0319, CG7565 in Drosophila, was characterized. Differential gene expression and splicing forms were observed during Drosophila development stages. Using UAS-RNAi system and flight simulator to study behavioral change in CG7565-knockdown Drosophila showed pan-neural knockdown lines w/+; elav-Gal4/+; 3707/+ and w/+; elav-Gal4/+; 8396/+ are defective in visual pattern memory. The study of neuronal specific knockdown showed this memory was impaired when CG7565 was selectively knocked down in F5 neuron (fan-shaped body) and R2/R4m (ellipsoid body) of the central complex in Drosophila brain. / Our genetic association study of MRPL19 agrees with reports of the association of 5' upstream of MRPL19 with DD, showing that true causative sequence variants may lie here. Mutational analyses of the putative promoter of MRPL19 revealed a novel sequence change T>G at -647 in a dyslexic sample not found in controls. In-silico analysis indicates a binding site of heat shock factor-1 that is predicted to be abolished by this variant. Luciferase activity increased in the promoter carrying the G allele. The role of this variant must be confirmed. Non-Mendelian Inheritance was observed in 2 individual dyslexic samples with 3 and 4 types of haplotypes. Copy number variation or gene conversion may be a factor. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Lim, King Poo. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2012. / Includes bibliographical references (leaves 201-225). / Abstracts also in Chinese. / Dedication --- p.I / Abstract --- p.II / 摘要 --- p.IV / Acknowledgements --- p.V / Table of contents --- p.VI / List of Figures --- p..XI / List of Tables --- p.XIV / List of Abbreviations --- p.XVII / Chapter 1. --- Chapter 1 --- p.1 / Genetic Association of dyslexia-candidate genes in Chinese children with dyslexia --- p.1 / Chapter 1.1. --- Introduction --- p.2 / Chapter 1.2. --- Prevalence --- p.4 / Chapter 1.3. --- Definition --- p.7 / Chapter 1.4. --- Theories of developmental dyslexia --- p.9 / Chapter 1.4.1. --- Phonological deficit theory --- p.9 / Chapter 1.4.2. --- Double deficit hypothesis --- p.10 / Chapter 1.4.3. --- Cerebellar deficit theory --- p.11 / Chapter 1.4.4. --- Magnocellular deficit theory --- p.12 / Chapter 1.4.5. --- Deficits in Chinese people with dyslexia --- p.12 / Chapter 1.5. --- Neurobiological aspects of Dyslexia --- p.15 / Chapter 1.5.1. --- Postmortem studies --- p.15 / Chapter 1.5.2. --- Structural Neuroimaging studies of dyslexia --- p.16 / Chapter 1.5.3. --- Functional Neuroimaging studies --- p.17 / Chapter 1.5.4. --- fMRI results in Chinese --- p.18 / Chapter 1.6. --- Genetics of Dyslexia --- p.19 / Chapter 1.6.1. --- Familial studies --- p.19 / Chapter 1.6.2. --- Twin studies --- p.21 / Chapter 1.6.3. --- Mode of Inheritance --- p.24 / Chapter 1.6.4. --- Genetic mapping of disease gene --- p.26 / Linkage analysis --- p.26 / Association study --- p.29 / Molecular genetic findings in dyslexia --- p.33 / Chapter 1.6.5. --- Statement of Research Rationale --- p.47 / Chapter 1.6.6. --- Objectives --- p.48 / Chapter 1. --- Chapter 2 --- p.49 / Genetic association of dyslexia-candidate genes in Chinese children with dyslexia --- p.49 / Chapter 2.1. --- Introduction --- p.50 / Chapter 2.2. --- Materials and methods --- p.51 / Chapter 2.2.1. --- Subjects --- p.51 / Chapter 2.2.2. --- DNA extraction and genotyping --- p.54 / Chapter 2.2.3. --- SNP marker selection --- p.55 / Chapter 2.2.4. --- Statistical analyses --- p.57 / Chapter 2.3. --- Results --- p.59 / Chapter 2.3.1. --- DYX1C1 --- p.59 / Single marker analysis --- p.59 / Haplotype analyses --- p.62 / Chapter 2.3.2. --- KIAA0319 --- p.67 / Association of KIAA0319 with Chinese dyslexic children --- p.67 / Association of KIAA0319 with reading related traits --- p.67 / Chapter 2.3.3. --- DCDC2 --- p.74 / Association of DCDC2 with Chinese dyslexic children --- p.74 / Chapter 2.3.4. --- MRPL19 and C2orf3 --- p.78 / Haplotypes located within 5' upstream of MRPL19 are significantly associated with DD --- p.78 / Association of the 5' upstream variants with reading related traits --- p.79 / Chapter 2.3.5. --- KIAA0319L and its surrounding genes --- p.85 / Association of KIAA03190L and its surrounding genes with Chinese dyslexic children --- p.85 / Chapter 2.3.6. --- Gene-Gene interaction analyses --- p.88 / Chapter 2.3.7. --- Parent-of-origin analysis --- p.92 / Chapter 2.4. --- Discussion --- p.94 / Chapter 2.4.1. --- DYX1C1 variant associated with DD and reading skills --- p.94 / Chapter 2.4.2. --- KIAA0319 associated with phonological awareness in Chinese --- p.99 / Chapter 2.4.3. --- DCDC2 is not associated with DD in Chinese children --- p.108 / Chapter 2.4.4. --- Association of MRPL19 and C2ORF3 in a Chinese sample --- p.111 / Chapter 2.4.5. --- Association of KIAA03190L and its surrounding genes with Chinese children with dyslexia --- p.115 / Chapter 2.4.6. --- Gene-Gene interaction --- p.118 / Chapter 2.4.7. --- Parent-of-origin --- p.119 / Chapter 2.5. --- Summary --- p.122 / Chapter 3. --- Chapter 3 --- p.126 / Resequencing analyses and characterization of 5' upstream of KIAA0319 --- p.126 / Chapter 3.1. --- Introduction --- p.127 / Chapter 3.2. --- Materials and Methods --- p.129 / Chapter 3.2.1. --- DNA samples --- p.129 / Chapter 3.2.2. --- DNA re-sequencing --- p.129 / Chapter 3.2.3. --- KIAA0319 Promoter constructs --- p.131 / Chapter 3.2.4. --- Luciferase Reporter Assays --- p.133 / Chapter 3.2.5. --- In-silico sequence analyses --- p.133 / Chapter 3.3. --- Results --- p.134 / Chapter 3.4. --- Discussion --- p.143 / Chapter 4. --- Chapter 4 --- p.148 / Characterization of CG7565, a homolog of KIAA0319, in a Drosophila model --- p.148 / Chapter 4.1. --- Introduction --- p.149 / Chapter 4.2. --- Methods and Materials --- p.152 / Chapter 4.2.1. --- Drosophila stock --- p.152 / Chapter 4.2.2. --- Sequence analyses --- p.153 / Chapter 4.2.3. --- RNA extraction and quantitative reverse-transcription PCR (RT-PCR) --- p.153 / Chapter 4.2.4. --- Behavioral Assays --- p.156 / Visual pattern memory assays --- p.156 / Optomotor Response Assays --- p.158 / Visual Discrimination Analyses --- p.159 / Chapter 4.3. --- Results --- p.160 / Chapter 4.4. --- Discussion --- p.174 / Chapter 5. --- Chapter 5 --- p.181 / Mutational analyses of 5' region of MRPL19 in children with dyslexia --- p.181 / Chapter 5.1. --- Introduction --- p.182 / Chapter 5.2. --- Materials and Methods --- p.183 / Chapter 5.2.1. --- DNA samples --- p.183 / Chapter 5.2.2. --- High resolution melting analyses (HRM) --- p.183 / Chapter 5.2.3. --- MRPL19 promoter constructs --- p.185 / Chapter 5.2.4. --- In-silico sequence analyses --- p.186

Tsang, Wan Hong. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 156-165). / Abstracts in English and Chinese. / Abstract --- p.iii / Abstract in Chinese (摘要） --- p.V / Acknowledgement --- p.vi / Table of Content --- p.vii / List of Figures and Tables --- p.xiv / List of Abbreviations --- p.xvii / Chapter Chapter 1 --- Introduction --- p.Page / Chapter 1.1 --- Developmental Dyslexia --- p.1 / Chapter 1.1.1 --- Study of Developmental Dyslexia --- p.1 / Chapter 1.1.2 --- Genetic Basis of Developmental Dyslexia --- p.2 / Chapter 1.1.3 --- Susceptibility Gene for Developmental Dyslexia --- p.3 / Chapter 1.2 --- Dyslexia-Susceptibility Gene KIAA0319-Like --- p.5 / Chapter 1.2.1 --- Association Studies of KIAA0319-Like --- p.5 / Chapter 1.2.2 --- KIAA0319-Like Gene and Protein --- p.6 / Chapter 1.2.3 --- Functional prediction of KIAA0319-Like Protein --- p.10 / Chapter 1.3 --- Potential Interacting Partners of KIAA0319-Like Protein --- p.12 / Chapter 1.3.1 --- Nogo Receptor 1 (NgR) --- p.12 / Chapter 1.3.2 --- SH2B Adaptor Protein 1 (SH2) --- p.13 / Chapter 1.3.3 --- FEM-1-like death receptor binding protein (FEM) --- p.14 / Chapter 1.3.4 --- Adaptor-related protein complex 2，mu 1 subunit (AP2) --- p.14 / Chapter 1.4 --- Notch Signaling Pathway and KIAA0319-Like --- p.16 / Chapter 1.5 --- Previous Research on KIAA0319-Like --- p.18 / Chapter 1.6 --- Research Objectives --- p.20 / Chapter Chapter 2 --- Materials and Methods --- p.Page / Chapter 2.1 --- Gene Cloning --- p.21 / Chapter 2.1.1 --- Cloning of Human KIAA0319-Like into expression vectors --- p.21 / Chapter 2.1.2 --- Gel Extraction of PCR Product --- p.22 / Chapter 2.1.3 --- Restriction enzyme digestion --- p.22 / Chapter 2.1.4 --- Ligation of gene products with vector --- p.23 / Chapter 2.1.5 --- "Cloning of Human SH2, FEM, AP2 and NgR gene" --- p.23 / Chapter 2.1.7 --- Preparation of chemically competent E.coli strain DH5a --- p.26 / Chapter 2.1.8 --- Transformation of the ligation product into competent cells --- p.26 / Chapter 2.1.9 --- Diagnostic PCR for confirmation of successful ligation --- p.27 / Chapter 2.1.10 --- Small scale preparation of bacterial plasmid DNA --- p.27 / Chapter 2.1.11 --- DNA sequencing of the cloned plasmid DNA --- p.28 / Chapter 2.1.12 --- Large scale preparation of target recombinant plasmid DNA --- p.28 / Chapter 2.2 --- Cell Culture --- p.30 / Chapter 2.2.1 --- Culture medium --- p.30 / Chapter 2.2.2 --- Cell lines --- p.30 / Chapter 2.2.3 --- Freezing and thawing cells --- p.31 / Chapter 2.3 --- DNATransfection --- p.32 / Chapter 2.3.1 --- Transfection of HEK293 Cells with LipofectaminéёØ Reagent --- p.32 / Chapter 2.3.2 --- Transfection of Neuronal Cells with Tranfas´tёØ Reagent --- p.32 / Chapter 2.4 --- Immunocytochemical Staining --- p.33 / Chapter 2.5 --- Immunohistochemical Staining --- p.34 / Chapter 2.6 --- Western Blotting --- p.36 / Chapter 2.6.1 --- Collection of Cell Lysate --- p.36 / Chapter 2.6.2 --- Collection of Mouse Tissue Lysate --- p.36 / Chapter 2.6.3 --- Protein concentration determination by Bradford Protein Assay --- p.36 / Chapter 2.6.4 --- Sodium Dodecyl Sulfate Polyacrylamide Gel Electrophoresis --- p.37 / Chapter 2.6.5 --- Semidry Transfer to PVDF Membrane --- p.37 / Chapter 2.6.6 --- Blocking and Antibody Probing --- p.38 / Chapter 2.6.7 --- Enhanced chemiluminescence (ECL) --- p.38 / Chapter 2.6.8 --- Synthetic peptide based neutralization --- p.39 / Chapter 2.7 --- Quantitative Real-Time PCR --- p.40 / Chapter 2.7.1 --- RNA extraction from Cell culture --- p.40 / Chapter 2.7.2 --- Genomic DNA Elimination and Reverse Transcription --- p.40 / Chapter 2.7.3 --- Quantitative Real-Time PCR --- p.41 / Chapter 2.8 --- Coimmunoprecipitation --- p.42 / Chapter 2.9 --- Luciferase Reporter Assay --- p.43 / Chapter 2.10 --- Wound-Healing Assay --- p.44 / Chapter Chapter 3 --- Distribution of KIAA0319-Like Protein --- p.Page / Chapter 3.1 --- Study of the Distribution of KIAA0319-Like Protein --- p.45 / Chapter 3.1.1 --- Anti-KIAA0319-Like Antisera H635 --- p.45 / Chapter 3.1.2 --- Affinity Purification of Anti-KIAA0319-Like Antisera H635 --- p.45 / Chapter 3.2 --- C57/BL6 Mouse Tissue Expression Pattern of KIAA0319-Like --- p.48 / Chapter 3.3 --- C57/BL6 Mouse Brain Regional Expression Pattern of KIAA0319-Like --- p.50 / Chapter 3.4 --- Immunostaining of Sagittal Section of C57/BL6 Mouse Brain --- p.52 / Chapter 3.5 --- Mouse Brain Co-staining with KIAA0319-Like Protein and Markers --- p.54 / Chapter 3.6 --- Subcelluar Localization of KIAA0319-Like Protein in Human Neurons --- p.57 / Chapter 3.7 --- Discussion --- p.59 / Chapter 3.7.1 --- Affinity Purification of Anti-KIAA0319-Like Antisera --- p.59 / Chapter 3.7.2 --- Mouse Tissue Expression Pattern of KIAA0319-Like --- p.59 / Chapter 3.7.3 --- Mouse Brain Regional Expression Pattern of KIAA0319-Like --- p.59 / Chapter 3.7.4 --- Brain Cell Types expressing KIAA0319-Like Protein --- p.61 / Chapter 3.7.5 --- Subcellular Localization of KIAA0319-Like Protein --- p.62 / Chapter 3.7.6 --- Future Perspectives --- p.63 / Chapter Chapter 4 --- KIAA0319-Like Modulates Neuronal Migration --- p.Page / Chapter 4.1 --- Study of the effect of KIAA0319-Like on Neuronal Migration --- p.64 / Chapter 4.2 --- Establish Stable Cell Lines with Altered KIAA0319-Like Expression --- p.65 / Chapter 4.2.1 --- Cloning of siRNA into Lentiviral Vector pLVTHM --- p.65 / Chapter 4.2.2 --- Lentivirus packaging in HEK293 Cells --- p.67 / Chapter 4.2.3 --- Checking of Lentivirus by HEK293 Cells Transduction --- p.70 j / Chapter 4.2.4 --- Lentiviral Transductions to Neuronal Cells --- p.70 / Chapter 4.2.5 --- Fluorescent-Activated Cell Sorting of Transduced Cells --- p.70 / Chapter 4.2.6 --- KIAA0319-Like Expression Changes in Stable Cell Lines --- p.71 / Chapter 4.3 --- Effects of KIAA0319-Like Overexpression on Neuronal Migration --- p.75 / Chapter 4.4 --- Effects of KIAA0319-Like Knockdown on Neuronal Migration --- p.77 / Chapter 4.5 --- Effect of Anti-KIAA0319-Like Antibody on Neuronal Migration --- p.79 / Chapter 4.6 --- Discussion --- p.81 / Chapter 4.6.1 --- Stable Cell line with altered KIAA0319-Like Level --- p.81 / Chapter 4.6.2 --- Disruption of KIAA0319-Like expression affects Cell Migration --- p.81 / Chapter 4.6.3 --- Antibody Blockade of KIAA0319-Like Inhibits Cell Migration --- p.81 / Chapter 4.6.4 --- Possible existence of Multiple Regulatory Pathways --- p.82 / Chapter 4.6.5 --- Possible Limitations of Expression alternations by Transduction --- p.83 / Chapter 4.6.6 --- Possible Susceptibility Polymorphism of KIAA0319-Like --- p.83 / Chapter 4.6.7 --- Future Perspectives X --- p.84 / Chapter Chapter 5 --- Interacting Partners of KIAA0319-Like Protein --- p.Page / Chapter 5.1 --- Study of Interacting Partners of KIAA0319-Like Protein --- p.85 / Chapter 5.1.1 --- Identification of Potential Interacting Partners of KIAA0319-Like --- p.85 / Chapter 5.1.2 --- Identification of Domains involved in Interactions --- p.86 / Chapter 5.1.3 --- Subcloning of KIAA0319-Like Protein Domain Deletion Mutant --- p.86 / Chapter 5.2 --- Interaction between NgR and KIAA0319-Like Protein --- p.92 / Chapter 5.2.1 --- Reciprocal Coimmunoprecipitation of NgR for KIAA0319-Like --- p.92 / Chapter 5.2.2 --- Colocalization of NgR and KIAA0319-Like Protein --- p.94 / Chapter 5.2.3 --- Interaction between NgR and KIAA0319-Like Deletion Mutants --- p.97 / Chapter 5.3 --- Interaction between SH2 and KIAA0319-Like Protein --- p.99 / Chapter 5.3.1 --- Coimmunoprecipitation between SH2 and KIAA0319-Like --- p.» 99 / Chapter 5.3.2 --- Colocalization of SH2 and KIAA0319-Like Protein --- p.101 / Chapter 5.3.3 --- Interaction between SH2 and KIAA0319-Like Deletion Mutants --- p.103 / Chapter 5.4 --- Interaction between FEM and KIAA0319-Like Protein --- p.105 / Chapter 5.4.1 --- Coimmunoprecipitation between FEM and KIAA0319-Like --- p.105 / Chapter 5.4.2 --- Colocalization of FEM and KIAA0319-Like Protein --- p.107 / Chapter 5.4.3 --- Interaction between FEM and KIAA0319-Like Deletion Mutants --- p.109 / Chapter 5.5 --- Interaction between AP2 and KIAA0319-Like Protein --- p.111 / Chapter 5.5.1 --- Coimmunoprecipitation between AP2 and KIAA0319-Like --- p.111 / Chapter 5.5.2 --- Colocalization of AP2 and KIAA0319-Like Protein --- p.113 / Chapter 5.5.3 --- Interaction between AP2 and KIAA0319-Like Deletion Mutants --- p.115 / Chapter 5.6 --- Discussion --- p.117 / Chapter 5.6.1 --- The Interaction of KIAA0319-Like with NgR and SH2 Protein --- p.118 / Chapter 5.6.2 --- Interaction between FEM and KIAA0319-Like Protein --- p.121 / Chapter 5.6.3 --- Interaction between AP2 and KIAA0319-Like Protein --- p.121 / Chapter 5.6.4 --- Future Perspectives --- p.122 / Chapter Chapter 6 --- KIAA0319-Like Association with Notch Pathway --- p.Page / Chapter 6.1 --- Study of KIAA0319-Like association with Notch Pathway --- p.123 / Chapter 6.1.1 --- Luciferase Reporter System for quantifying y-Secretase Activity --- p.123 / Chapter 6.2 --- Effects of KIAA0319-Like Expression Alternations on y-Secretase Activity in HEK293 Cells --- p.126 / Chapter 6.3 --- Effects of Increasing KIAA0319-Like Protein Level in Culture Medium on y-Secretase Activity in HEK293 Cells --- p.128 / Chapter 6.4 --- Effects of KIAA0319-Like Expression Alternations on y-Secretase Activity in SH-SY5Y Cells --- p.130 i / Chapter 6.5 --- Effects of KIAA0319-Like Expression Alternations on y-Secretase Activity in Neuro-2a Cells --- p.132 / Chapter 6.6 --- Effect of Notch Blockade on SH-SY5Y Cells Migration Rate --- p.134 / Chapter 6.7 --- Effect of KIAA0319-Like Expression changes on Notch Inhibited SH-SY5Y Cells Migration Rate --- p.136 / Chapter 6.8 --- Discussion --- p.139 / Chapter 6.8.1 --- Luciferase Reporter System for quantifying y-Secretase Activity --- p.139 / Chapter 6.8.2 --- Cell-Type Specific association of KIAA0319-Like expression level and y-Secretase activity --- p.139 / Chapter 6.8.3 --- Entry Point of KIAA0319-Like to the Notch Signaling Pathway --- p.140 / Chapter 6.8.4 --- Functional relationship between KIAA0319-Like and Notch --- p.141 / Chapter 6.8.5 --- Future Perspectives --- p.142 / Chapter Chapter 7 --- Discussions and Conclusions --- p.Page / Chapter 7.1 --- Discussions --- p.143 / Chapter 7.1.1 --- Further Evidence for KIAA0319-Like Association with Dyslexia --- p.143 / Chapter 7.1.2 --- Possible Pathways connecting KIAA0319-Like with Cell Motility --- p.145 / Chapter 7.1.3 --- Nogo Receptor Pathway association with Cell Motility --- p.146 / Chapter 7.1.4 --- Notch Signaling Pathway association with Cell Motility --- p.146 / Chapter 7.1.5 --- Combined Effects of NgR and Notch Pathway on Cell Migration --- p.149 / Chapter 7.1.6 --- Cellular Compartment for Interactions of KIAA0319-Like --- p.151 / Chapter 7.2 --- Conclusions --- p.153 / Chapter Chapter 8 --- References --- p.156 / Chapter Chapter 9 --- Appendix --- p.166

The aims of this research were to explore the perceptions of the impact of dyslexia on nursing and midwifery students in practice, and of the coping strategies they develop and/or use to help them cope. To achieve the above aims, the following questions were set and addressed: 1. What is the perceived impact of dyslexia on the nursing and midwifery student in clinical practice? 2. How are any difficulties associated with dyslexia managed by the nursing or midwifery student? 3i. What strategies can help and support nursing and midwifery students with dyslexia? 3ii. What are students’ and mentors’ perceptions of the poster guidelines (developed following a previous study), which are designed to help and support nursing and midwifery students with dyslexia in clinical practice? A qualitative study underpinned by a constructivist, interpretive ontological perspective was undertaken, based on a grounded theory case study approach. After seeking and gaining research ethics approval and informed written consent from potential participants, a purposive sample of 12 nursing and midwifery students with dyslexia, and 22 mentors was recruited and used for the study. Varied methods including tape recorded semi-structured interviews and content analysis of students’ practice portfolios (n=8) and files (n=12) were used to collect data from the students. Evaluative comments from the mentors were also collected. The data were then analysed using Glasarian grounded theory method. Findings suggest that dyslexia impacts on the student negatively as well as positively. There was expression of strong support with reference to demonstration of empathy and acceptance of students with dyslexia in both academic and practice settings, however, disclosure remained an issue for some students. Apart from already available strategies, the students managed to develop and used simple and effective coping strategies in a non-stressful environment. In a busy environment however, they became stressed and frustrated with cascading effects. Many of the strategies used including the poster guidelines were identified as very useful and or helpful and suggestions made by both students and mentors led to the development of a tool kit to be use used interactively by the students and their mentors in practice.

Ng, Kwun Kei. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2007. / Includes bibliographical references (leaves 74-85). / Abstracts in English and Chinese. / Abstract (English) --- p.i / Abstract (Chinese) --- p.iii / Acknowledgement --- p.iv / Table of Contents --- p.vi / List of Tables --- p.viii / List of Figures --- p.ix / Chapter Chapter 1: --- Introduction --- p.1 / Rapid Naming in Chinese Dyslexic Children: A Glimpse --- p.1 / What is Rapid Naming --- p.2 / Processing Speed Deficit and RAN Deficit in Chinese Dyslexia --- p.5 / Consequence of Processing Speed Deficit: Automaticity --- p.12 / Automaticity and Attention --- p.16 / Discriminative Power of RAN Tasks --- p.19 / Object Rapid Naming --- p.19 / Letter Rapid Naming --- p.21 / Digit Rapid --- p.23 / Adopting ERP and Oddball Task to Investigate RAN Tasks --- p.25 / High-temporal-resolution Electrophysiological Signals --- p.25 / The Oddball Task --- p.26 / The ERPs --- p.28 / Current Study --- p.39 / Chapter Chapter 2: --- Method --- p.41 / Participants --- p.41 / Procedure --- p.41 / Oddball Stimulus Classification Tasks --- p.42 / The RAN Tasks --- p.44 / The Hong Kong Test of Specific Learning Difficulties in Reading and Writing --- p.44 / Chinese Phonology Segmental Test --- p.44 / Raven's Standard Progressive Matrices --- p.45 / Chapter Chapter 3: --- Results --- p.47 / Behavioural Results --- p.47 / ERP Results --- p.55 / Chapter Chapter 4: --- Discussion --- p.59 / Digit Naming and Digit Oddball in Chinese Dyslexia --- p.59 / Letter RAN --- p.63 / Oddball RTs and Response Execution --- p.65 / Limitations and Future Directions: The Issue of Task Demands and the Multiple Deficits Hypothesis --- p.66 / References --- p.74 / Appendix A: ERP Grand Average for the Object Oddball Task --- p.86 / Appendix B: ERP Grand Average for the Letter Oddball Task --- p.87 / Appendix C: ERP Grand Average for the Digit Oddball Task --- p.88

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