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Mandarin Chinese does not grammaticalize tense, but makes abundant use of aspectual distinctions in the lexicon and grammar. The way it shapes reference to time and events is consequently very different from that in European languages. This dissertation studies the compositional interpretation of Mandarin aspect, grounded in empirical data from a parallel corpus. The corpus consists of French source texts and translations to a number of European languages and to Mandarin, allowing the author to use European tense-aspect distinctions as a probe into the Mandarin aspectual system. The corpus data provide empirical support for claims made in the literature about zhe (imperfective marker), zai (progressive marker), and guo (experiential perfect marker). They also provide support for the hypothesis that aspectually unmarked sentences have a stative interpretation by default, while eventive interpretations must use overt aspectual expressions. In the last part of the dissertation, the author builds a semantic analysis of so-called resultative verb compounds and their competitor, known as post-verbal le. Resultative verb compounds combine the verb with a resultative complement to produce a telic event plus a result state at the interface between lexicon and syntax. Post-verbal le is an aspectual marker that leads to a perfective or resultative perfect interpretation depending on the kind of eventuality description it combines with. The dissertation finds that Mandarin establishes more complex aspectual distinctions than the perfective/imperfective or progressive/non-progressive dichotomies in European languages, and that parallel corpus data can be fruitfully used to bring out the relevant differences.

This paper surveys the strategies that the Contrastive, Typological, and Translation Mining parallel corpus traditions rely on to deal with the issue of target language representativeness of translations. On the basis of a comparison of the corpus architectures and research designs of the three traditions, we argue that they have each developed their own representativeness strategies: (i) monolingual control corpora (Contrastive tradition), (ii) limits on the scope of research questions (Typological tradition), and (iii) parallel control corpora (Translation Mining tradition). We introduce normalized pointwise mutual information (NPMI) as a bi-directional measure of cross-linguistic association, allowing for an easy comparison of the outcomes of different traditions and the impact of the monolingual and parallel control corpus representativeness strategies. We further argue that corpus size has a major impact on the reliability of the monolingual control corpus strategy and that a sequential parallel control corpus strategy is preferable for smaller corpora.

The building industry is blamed for consuming enormous natural resources and creating massive solid waste worldwide. In response to this, the concept of circular economy (CE) has gained much attention in the sector in recent years. Many pilot building projects that implemented CE concepts started to appear around the world, including Taiwan. However, compared with the pilot projects in the Netherlands, which are regarded as the pioneer ones by international society, many CE-related practices are not implemented in pilot cases in Taiwan. To assist future project stakeholders to recognize what the key CE-related practices are and how they could be implemented in their building projects in Taiwan, this study has conducted a series of case studies of Dutch and Taiwanese pilot projects and semi-structured interviews with key project stakeholders of Taiwanese pilot projects. Thirty key CE-related practices are identified via case studies, along with their related 5R principles (Rethink, Reduce, Reuse, Repair, Recycle) and project phases. Suggestion on CE-related practices, their 5R principles, project items, and phases to implement in building projects in Taiwan is also proposed while discussion on differences between two countries&rsquo, pilot projects is presented.

In this paper, the all-optical spatial modulation of monolayer graphene-coated microfiber is proposed. Graphene is used as a saturable absorber wrapped on the microfiber produced by heating the carbon dioxide laser. When the signal light travels along the microfiber, part of the light will pass along the surface of the microfiber in the form of an evanescent field, and it will be absorbed by the graphene. Simultaneously we shoot the 808 nm pump light into the micro-nanofiber wrapped by the graphene vertically from the space. According to graphene characteristic of preferential absorption, the absorption of the signal light is controlled by the pump light, thus the broadband all-optical space modulation is realized. In a conventional graphene microfiber all-optical modulator, signal light and pump light are generally input into a microfiber via a coupler. However, the mode of operation of pump light and graphene in all-optical spatial modulation are different from those of the traditional modulation, the pump light works on the graphene outside the microfiber, which realizes the separation of the pump light and the signal light. The output signal does not need to be optically filtered for the pump light to obtain the modulated signal. The output signal light of the spatial all-optical modulator has the characteristics of “clean”. We also verify this in experiment. In addition, the pump light is vertically incident from space, the effect of the graphene length on the modulation is not considered and the modulation time is only related to the relaxation time of graphene, which is helpful in improving the response time. Modulation experiments include static spectral modulation and dynamic frequency modulation. In the static spectral modulation, the broad spectrum signal has a maximum modulation depth of 6 dB at 1095 nm when the pump power is 569 mW. The relationship among pump power, wavelength and modulation depth is also analyzed. The higher the pump power, the higher the modulation depth will be; with the same pump power, the modulation depth of long wave length is higher than that of short wave. In the dynamic modulation experiment with the modulation bandwidth~50 nm and the modulation rate~1.5 kHz, the influence of pump light and signal light on output dynamic signal are studied, the feasibility of all-optical space modulation based on graphene is verified experimentally. The composite waveguide of all-optical spatial modulator opens the door to micro-nano ultrafast signal, processing in a more flexible and efficient way.

The minibrain kinase (Mnbk)/dual specificity Yak 1-related kinase 1A (Dyrk1A) gene is implicated in the mental retardation associated with Down's syndrome. It encodes a proline-directed serine/threonine kinase whose function has yet to be defined. We have used a solid-phase Mnbk/Dyrk1A kinase assay to aid in the search for the cellular Mnbk/Dyrk1A substrates. The assay revealed that rat brain contains two cytosolic proteins, one with a molecular mass of 100 kDa and one with a molecular mass of 140 kDa, that were prominently phosphorylated by Mnbk/Dyrk1A. The 100-kDa protein was purified and identified as dynamin 1. The conclusion was further supported by evidence that a recombinant glutathione S-transferase fusion protein containing dynamin isoform 1aa was phosphorylated by Mnbk/Dyrk1A. In addition to isoform 1aa, Mnbk/Dyrk1A also phosphorylated isoforms 1ab and 2aa but not human MxA protein when analyzed by the solid-phase kinase assay. Upon Mnbk/Dyrk1A phosphorylation, the interaction of dynamin 1 with the Src homology 3 domain of amphiphysin 1 was reduced. However, when Mnbk/Dyrk1A phosphorylation was allowed to proceed more extensively, the phosphorylation enhanced rather than reduced the binding of dynamin 1 to amphiphysin 1. The result suggests that Mnbk/Dyrk1A can play a dual role in regulating the interaction of dynamin 1 with amphiphysin 1. Mnbk/Dyrk1A phosphorylation also reduced the interaction of dynamin with endophilin 1, whereas the same phosphorylation enhanced the binding of dynamin 1 to Grb2. Nevertheless, the dual function of Mnbk/Dyrk1A phosphorylation was not observed for the interaction of dynamin 1 with endophilin 1 or Grb2. The interactions of dynamin with amphiphysin and endophilin are essential for the formation of endocytic complexes; our results suggest that Mnbk/Dyrk1A may function as a regulator controlling the assembly of endocytic apparatus.

In a search for Alzheimer beta-amyloid peptide precursor ligands, Potempska et al. (Arch. Biochem. Biophys. (1993) 304, 448) found that histones bind with high affinity and specificity to the secreted precursor. Because exogenous histones can be cytotoxic, we compared the effects of histones on the viability of cells which produce little beta-amyloid peptide precursor (U-937) to those on cells that produce twenty times as much precursor (COS-7). Addition of purified histones caused necrosis of U-937 cells (histone H4, LD50 = 1.5 microM). Extracellular A beta precursor in the submicromolar range prevented histone-induced U-937 cell necrosis. Cell-surface precursor also reduced histone toxicity: COS-7 cells were less sensitive to the toxic effects of histone H4 (LD50 = 5.4 microM). COS-7 cells in which the expression of an APP mRNA-directed ribozyme reduced the synthesis of the protein by up to 80% were more sensitive to histone H4 (LD50 = 3.2 microM) than cells that expressed the vector alone. Histone H4 binds to cell-associated A beta precursor. Cells expressing the A beta precursor-directed ribozyme bound less 125I-labeled histone H4 than those expressing the vector alone. In the limited extracellular space of tissues in vivo, both secreted and cell-surface A beta precursor protein may play significant roles in trapping chromatin or histones and removing them from the extracellular milieu.

We examined the effects of the Gly-60 to Ala mutation on the interaction of H-Ras with Ras GTPase activating protein (GAP), neurofibromin 1 (NF1), Raf-1, and ral guanine nucleotide dissociation stimulator (ralGDS), factors that interact with GTP-bound form of H-Ras. Previous study has shown that the G60A mutation perturbs GTP-induced conformational changes of H-Ras. We found that the G60A mutation decreases GTPase activity of H-Ras without significantly affecting GTP/GDP binding. The reduction in GTPase activity is most dramatic in the presence of GAP or NF1. Interestingly, the G60A mutation does not appear to alter the affinity of H-Ras for GAP or NF1. The G60A mutation moderately reduces the binding of H-Ras to Raf-1 Ras binding domain; however, the binding of H-Ras to ralGDS Ras binding domain was more significantly affected by the same mutation. These results indicate that although GAP, NF1, Raf-1, and ralGDS all interact with H-Ras in a GTP-dependent manner and they are able to compete against each other for binding to H-Ras, these factors share overlapping but not identical binding domains on H-Ras. The significance of our findings is discussed in the light of the GTP-induced conformational change model.

MNB/DYRK1A is a proline-directed serine/threonine kinase implicated in Down syndrome (DS). In an earlier screening, two proteins from adult rat brain, one 100 kDa and the other 140 kDa, were found to be prominently phosphorylated by the kinase. The 100-kDa protein was previously characterized as an isoform of dynamin 1. In this study, we identified the 140-kDa protein as synaptojanin 1 (SJ1). MNB/DYRK1A phosphorylates SJ1 at multiple sites and produces complex behaviors in binding to amphiphysin 1 and intersectin 1 (ITSN1). However, the phosphorylation has little effect on the phosphatidylinositol phosphatase activity of SJ1. These results suggest that MNB/DYRK1A is involved in regulating the recruitment activity but not the phosphatase activity of SJ1. Our findings may be especially important in the etiology of DS because MNB/DYRK1A, SJ1, and ITSN1 are all located at or near the region of human chromosome 21, which is postulated to be involved in the disease.

Minibrain kinase/dual-specificity tyrosine phosphorylation-regulated kinase (Mnb/Dyrk1A) is a proline-directed serine/threonine kinase encoded in the Down syndrome critical region of human chromosome 21. This kinase has been shown to phosphorylate dynamin 1 and synaptojanin 1. Here we report that amphiphysin I (Amph I) is also a Mnb/Dyrk1A substrate. This kinase phosphorylated native Amph I in rodent brains and recombinant human Amph I expressed in Escherichia coli. Serine 293 (Ser-293) was identified as the major site, whereas serine 295 and threonine 310 were found as minor kinase sites. In cultured cells, recombinant Amph I was phosphorylated at Ser-293 by endogenous kinase(s). Because mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) has been suggested to phosphorylate Amph I at Ser-293, our efforts addressed whether Ser-293 is phosphorylated in vivo by MAPK/ERK or by Mnb/Dyrk1A. Overnight serum-withdrawal inactivated MAPK/ERK; nonetheless, Ser-293 was phosphorylated in Chinese hamster ovary and SY5Y cells. Epigallocatechin-3-gallate, a potent Mnb/Dyrk1A inhibitor in vitro, apparently reduced the phosphorylation at Ser-293, whereas PD98059, a potent MAPK/ERK inhibitor, did not. High frequency stimulation of mouse hippocampal slices reduced the phosphorylation at Ser-293, albeit in the midst of MAPK/ERK activation. The endophilin binding in vitro was inhibited by phosphorylating Amph I with Mnb/Dyrk1A. However, phosphorylation at Ser-293 did not appear to alter cellular distribution patterns of the protein. Our results suggest that Mnb/Dyrk1A, not MAPK/ERK, is responsible for in vivo phosphorylation of Amph I at Ser-293 and that phosphorylation changes the recruitment of endophilin at the endocytic sites.

v-H-Ras harboring the Gly-60 to Ala mutation (G60A) lacks the ability to induce germinal vesicle breakdown in Xenopus oocytes. Moreover, this mutant is capable of inhibiting the activity of v-H-Ras to induce oocyte germinal vesicle breakdown when co-injected. The duration and the extent of inhibition depends on the molar ratio of v-H-Ras(G60A) to v-H-Ras. The inhibition is not due to a general toxicity of v-H-Ras(G60A) to oocytes because oocytes injected with v-H-Ras(G60A) can be readily induced to mature by other mitogenic agents, such as insulin, insulin-like growth factor 1, insulin-like growth factor 2, and phosphatidylcholine-specific phospholipase C. The dominant negative effect of v-H-Ras(G60A) requires proper membrane attachment of v-H-Ras(G60A). By using a competition assay, it was concluded that the dominant negative phenotype of v-H-Ras(G60A) resulted from sequestering H-Ras downstream effector(s). Raf-1 was identified as one of the sequestered targets.

We examined c-Ha-Ras harboring an aspartate to asparagine substitution at position 119 (mutation D119N). The Asp-119 is part of the conserved NK XD motif shared by members of the regulatory GTPase family. This asparagine residue has been proposed to participate in direct bonding to the guanine ring and to determine the guanine-nucleotide binding specificity. The D119N mutation was found to alter nucleotide specificity of Ha-Ras from guanine to xanthine, an observation that directly supports the essential role of hydrogen bonding between the side chain of the aspartic acid residue and the guanine ring in nucleotide binding specificity. Besides nucleotide binding specificity, the D119N mutation has little or no effect on the interaction of Ha-Ras with SDC25C, SOS1, GAP, or Raf. Neither does it affect the hydrolysis of nucleotide triphosphate. Like xanthine-nucleotide-specific EF-Tu, xanthine-nucleotide-specific Ras and related proteins will be useful tools for elucidating cellular systems containing multiple regulatory GTPases.