No abstract

It has been widely assumed since Kitagawa and Ross (Linguist Anal 9: 19-53, 1982) that noun phrases in Chinese and Japanese are quite similar in structure. They are N-final in surface word order, they employ ''modifying markers'' (de in Chinese and no in Japanese) extensively, and they require classifiers for numeral expressions. In this paper, we argue that, contrary to appearance, they have quite distinct structures. We examine N¢-ellipsis in the two languages and present supporting evidence for the hypothesis argued for by Simpson (in: Tang and Liu (eds.) On the formal way to Chinese languages, 2003), among others, that Chinese noun phrases are head-initial. According to this hypothesis, de is D, and a classifier heads another projection within DP. Japanese noun phrases, on the other hand, are headfinal. No is a contextual Case marker, as proposed by Kitagawa and Ross (Linguist Anal 9: 19-53, 1982), and classifier phrases are adjuncts modifying nominal projections. Our discussion shows that Kayne's (The antisymmetry of syntax, 1994) analysis of N-final relatives applies elegantly to Chinese but not to Japanese. It thus suggests that Japanese relative clauses are head-final throughout the derivation.

No abstract

Kawasaki disease (KD) is a type of acute febrile vasculitis syndrome and is the most frequent cause of cardiac illness in children under the age of five years old. Although the etiology of KD remains largely unknown, some recent genome-wide studies have indicated that epigenetic factors may be important in its pathogenesis.We enrolled 24 KD patients and 24 non-KD controls in this study to access their DNA methylation status using HumanMethylation450 BeadChips. Another 34 KD patients and 62 control subjects were enrolled for expression validation. Of the 3193 CpG methylation regions with a methylation difference ≥ 20% between KD and controls, 3096 CpG loci revealed hypomehtylation, with only 3% being hypermethylated. Pathway buildup identified 11 networked genes among the hypermethylated regions, including four transcription factors: nuclear factor of activated T-cells 1, v-ets avian erythroblastosis virus E26 oncogene homolog 1, runt related transcription factor 3, and retinoic acid receptor gamma, as well as the activator β-catenin. Ten of these network-selected genes demonstrated a significant decrease in mRNA in KD patients, whereas only CTNNB1 significantly decreased in correlation with coronary artery lesions in KD patients. Furthermore, CTNNB1-silenced THP-1 monocytic cells drastically increased the expression of CD40 and significantly increased the expression of both CD40 and CD40L in cocultured human coronary artery endothelial cells.This study is the first to identify network-based susceptible genes of hypermethylated CpG loci, their expression levels, and the functional impact of β-catenin, which may be involved in both the cause and the development of KD.