On the V-DE Construction in Mandarin Chinese

The paper proposes a novel classification and analysis of the V-DE construction in Mandarin Chinese. On this proposal, the V-DE construction is divided into two types, predicative and non-predicative. The predicative type can be further divided into entity-predicative V-DE constructions and eventuality-predicative V-DE constructions. With respect to the analysis of the V-DE construction, the paper identifies four different structures. It points out that the de-part (i.e. the part after and marked by 得-de) in most V-DE constructions is a clause with or without an overt subject. Moreover, with respect to the cases where the de-part has an overt NP that can be interpreted as the Patient argument of the verb before -de and at the same time is semantically compatible with the VP or AP in the de-part, the paper proposes that the overt NP in such cases is syntactically the subject of the de-clause and syntactically is not the direct object of V-DE or the verb before -de. Finally, when the de-part of an entity-predicative V-DE construction has an overt NP between -de and the predicate of the de-clause, the AP or VP of the de-part generally needs to be predicated of the overt NP in the de-part. This constraint, however, can be occasionally relaxed to allow for a pragmatically-inducted interpretation when both of the following conditions are met: (i) the de-part is a well-formed clause in both form and meaning and (ii) the pragmatically-induced interpretation is pragmatically plausible

Cancer Genomics Identifies Regulatory Gene Networks Associated with the Transition from Dysplasia to Advanced Lung Adenocarcinomas Induced by c-Raf-1

Background: Lung cancer is a leading cause of cancer morbidity. To improve an understanding of molecular causes of disease a transgenic mouse model was investigated where targeted expression of the serine threonine kinase c-Raf to respiratory epithelium induced initialy dysplasia and subsequently adenocarcinomas. This enables dissection of genetic events associated with precancerous and cancerous lesions. Methodology/Principal Findings: By laser microdissection cancer cell populations were harvested and subjected to whole genome expression analyses. Overall 473 and 541 genes were significantly regulated, when cancer versus transgenic and non-transgenic cells were compared, giving rise to three distinct and one common regulatory gene network. At advanced stages of tumor growth predominately repression of gene expression was observed, but genes previously shown to be upregulated in dysplasia were also up-regulated in solid tumors. Regulation of developmental programs as well as epithelial mesenchymal and mesenchymal endothelial transition was a hall mark of adenocarcinomas. Additionaly, genes coding for cell adhesion, i.e. the integrins and the tight and gap junction proteins were repressed, whereas ligands for receptor tyrosine kinase such as epi- and amphiregulin were up-regulated. Notably, Vegfr- 2 and its ligand Vegfd, as well as Notch and Wnt signalling cascades were regulated as were glycosylases that influence cellular recognition. Other regulated signalling molecules included guanine exchange factors that play a role in an activation of the MAP kinases while several tumor suppressors i.e. Mcc, Hey1, Fat3, Armcx1 and Reck were significantly repressed. Finally, probable molecular switches forcing dysplastic cells into malignantly transformed cells could be identified. Conclusions/Significance: This study provides insight into molecular pertubations allowing dysplasia to progress further to adenocarcinoma induced by exaggerted c-Raf kinase activity