We examined the cross-lagged relations between word reading fluency in the two orthographic systems of Japanese: phonetic (syllabic) Hiragana and morphographic Kanji. One hundred forty-two Japanese-speaking children were assessed on word reading fluency twice in Grade 1 (Times 1 and 2) and twice in Grade 2 (Times 3 and 4). Nonverbal IQ, vocabulary, phonological awareness, morphological awareness, and rapid automatized naming were also assessed in Time 1. Results of path analysis revealed that Time 1 Hiragana fluency predicted Time 2 Kanji fluency after controlling for the cognitive skills. Time 2 Hiragana fluency did not predict Time 3 Kanji fluency or vice versa after the autoregressor was controlled, but Hiragana and Kanji fluency were reciprocally related between Times 3 and 4. These findings provide evidence for a cross-script transfer of word reading fluency across the two contrastive orthographic systems, and the first evidence of fluency in a morphographic script predicting fluency development in a phonetic script within the same language.
Surface phenotypic characterization of megakaryoblasts, identified by platelet peroxidase activity, was investigated in four patients who showed increased proliferation of megakaryoblasts: one patient with typical features of acute leukemia, one presenting with acute myelofibrosis, and two with Down's syndrome in whom blasts disappeared spontaneously (transient abnormal myelopoiesis, TAM). MY10 and/or MY9 antigens were expressed on the surface of some megakaryoblasts, but MY7, and MY4, antigens specific to granulocytic or monocytic cells, were not. Some megakaryoblasts were positive for only anti-HLA-DR antibodies. It was speculated that, during the differentiation of the megakaryocytic lineage, MY9 antigen appears transiently on the surface of megakaryoblasts that have lost HLA-DR antigens and have gained the glycoprotein IIb/IIIa antigen. This study also demonstrated that the proliferating blasts in some patients with TAM were mainly megakaryoblasts and suggested that the target cells in TAM are CFU-GEMM.
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