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Figure 1: the LF representation of (10). (Huang & Liu 2001)
(10) Zhangsan shuo Lisi you zai piping ziji le. (Huang & Liu 2001) Zhangsan say Lisi again at criticisie self Prt ‘Zhangsan said that Lisi was again criticising him.’In an attempt to account for the syntax of logophoric zijiin the Logical Form (LF), Huang & Liu (2001)proposed that the logophor raises to the Spec of a CP-type functional category from its deep structure position within IP (Figure 1). This functional category attributes to the property of the logophor’s antecedent, being either the Source, Self or Pivot. Huang and Liu identified this functional category as ‘SourceP’. In his “split CP” hypothesis, Rizzi (1997)argued that a conventional CP could contain a number of functional categories, which play a critical part in “mediating between syntax and discourse”. The ‘SourceP’ is precisely one of such functional categories. According to Huang and Liu, zijiis co-indexed with the LD antecedent via “strong binding” (Chomsky & Keyser 1982, Chomsky 1986). As shown in the LF representation of (10) below, there are no further antecedents between the matrix constituent Zhangsan and the raised ziji. Thus, such binding is actually, “local”, albeit the trace appears to be long distance (Huang & Liu 2001). </div
VCC-LF dataset
This is readme for VCC-LF dataset.
This dataset provides light field mat files that capture by Lytro I.
The light field resolusion is [h,w,u,v,d].
If you use these data or our toolkit code, please cite our paper properly
@inproceedings{ lirsiggraphasia2019,
title={Hierarchical and View-invariant Light Field Segmentation by Maximizing Entropy Rate on 4D Ray Graphs},
author={Li, Rui and Heidrich, Wolfgang},
booktitle={ACM Transactions on Graphics (Proc. SIGGRAPH Asia)},
year={2019},
publisher={ACM}
DNA minor groove-binding ligands: A different class of mammalian DNA topoisomerase I inhibitors
A number of DNA minor groove-binding ligands (MGBLs) are known to exhibit antitumor and antimicrobial activities. We show that DNA topoisomerase (Topo) I may be a pharmacological target of MGBLs. In the presence of calf thymus Topo I, MGBLs induced limited but highly specific single-strand DNA breaks. The 3' ends of the broken DNA strands are covalently linked to Topo I polypeptides. Protein-linked DNA breaks are readily reversed by a brief heating to 65 degrees C or the addition of 0.5 M NaCl. These results suggest that MGBLs, like camptothecin, abort Topo I reactions by trapping reversible cleavable complexes. The sites of cleavage induced by MGBLs are distinctly different from those induced by camptothecin. Two of the major cleavage sites have been sequenced and shown to be highly A + T-rich, suggesting the possible involvement of a Topo I-drug-DNA ternary complex at the sites of cleavage. Different MGBLs also exhibit varying efficiency in inducing Topo I-cleavable complexes, and the order of efficiency is as follows: Hoechst 33342 and 33258 >> distamycin A > berenil > netropsin. The lack of correlation between DNA binding and cleavage efficiency suggest that, in addition to binding to the minor grooves of DNA, MGBLs must also interact with Topo I in trapping Topo I-cleavable complexes
LF-copying without LF
AbstractA copying approach to ellipsis is presented, whereby the locus of copying is not a level of derived syntactic structure (LF), but rather the derivation itself. The ban on preposition stranding in sprouting follows without further stipulation, and other, seemingly structure sensitive, empirical generalizations about elliptical constructions, including the preposition stranding generalization, follow naturally as well. Destructive operations which ‘repair’ non-identical antecedents are recast in terms of exact identity of derivations with parameters. In the context of a compositional semantic interpretation scheme, the derivational copying approach to ellipsis presented here is revealed to be a particular instance of a proform theory, thus showing that the distinctions between, and arguments about, syntactic and semantic theories of ellipsis need to be revisited
Differential poisoning of topoisomerases by menogaril and nogalamycin dictated by the minor groove-binding nogalose sugar
The effect of DNA binding on poisoning of human DNA TOP1 has been studied using a pair of related anthracyclines which differ only by a nogalose sugar ring. We show that the nogalose sugar ring of nogalamycin, which binds to the minor groove of DNA, plays an important role in affecting topoisomerase-specific poisoning. Using purified mammalian topoisomerases, menogaril is shown to poison topoisomerase II but not topoisomerase I. By contrast, nogalamycin poisons topoisomerase I but not topoisomerase II. Consistent with the biochemical studies, CEM/VM-1 cells which express drug-resistant TOP2alpha are cross-resistant to menogaril but not nogalamycin. The mechanism by which nogalamycin poisons topoisomerase I has been studied by analyzing a major topoisomerase I-mediated DNA cleavage site induced by nogalamycin. This site is mapped to a sequence embedded in an AT-rich region with four scattered GC base pairs (bps) (at -10, -6, +2, and +12 positions). GC bps embedded in AT-rich regions are known to be essential for nogalamycin binding. Surprisingly, DNase I footprinting analysis of nogalamycin-DNA complexes has revealed a drug-free region from -2 to +9 encompassing the major cleavage site. Our results suggest that nogalamycin, in contrast to camptothecin, may stimulate TOP1 cleavage by binding to a site(s) distal to the site of cleavage
Structure-activity relationships of benzimidazoles and related heterocycles as topoisomerase I poisons
A series of substituted 2-(4-methoxyphenyl)-1H-benzimidazoles were synthesized and evaluated as inhibitors of topoisomerase I. The presence of a 5-formyl-, 5-(aminocarbonyl)-, or 5-nitro group (i.e., substituents capable of acting as hydrogen bond acceptors) correlated with the potential of select derivatives to inhibit topoisomerase I. In contrast to bi- and terbenzimidazoles, the substituted benzimidazoles that were active as topoisomerase I poisons exhibited minimum or no DNA binding affinity. 5-Nitro-2-(4-methoxyphenyl)-1H-benzimidazole exhibited the highest activity and was significantly more active than the 4-nitro positional isomer. The 5- and 6-nitro derivatives of 2-(4-methoxyphenyl) benzoxazole, 2-(4-methoxyphenyl)benzothiazole, and 2-(4-methoxyphenyl)indole were synthesized and their relative activity as topoisomerase I inhibitors determined. None of these heterocyclic analogues were effective in significantly inhibiting cleavable-complex formation in the presence of DNA and topoisomerase I, suggesting a high degree of structural specificity associated with the interaction of these substituted benzimidazoles with the enzyme or the enzyme-DNA complex. In evaluating their cytotoxicity, these new topoisomerase I poisons also exhibited no significant cross-resistance against cell lines that express camptothecin-resistant topoisomerase I
Coralyne and related compounds as mammalian topoisomerase I and topoisomerase II poisons
DNA topoisomerases are nuclear enzymes responsible for modifying the topological state of DNA. The development of agents capable of poisoning topoisomerases has proved to be an attractive approach in the search for novel cancer chemotherapeutics. Coralyne, an antileukemic alkaloid, has appreciable structural similarity to the potent topoisomerase I and II poison, nitidine. Analogues of coralyne were synthesized and evaluated for their activity as topoisomerase I and topoisomerase II poisons. These analogues were also evaluated for cytotoxicity in the human lymphoblast cell line, RPMI 8402, and its camptothecin-resistant variant, CPT-K5. The pharmacological activity of these analogues exhibited a strong dependence on the substitution pattern and the nature of substituents. Several 1-benzylisoquinolines and 3-phenylisoquinolines were also synthesized. These compounds, which incorporate only a portion of the ring structure of coralyne, were evaluated as topoisomerase poisons and for cytotoxicity. These structure-activity studies indicate that the structural rigidity associated with the coralyne ring system may be critical for pharmacological activity. The presence of a 3,4-methylenedioxy substituent on these coralyne analogues was generally associated with enhanced activity as a topoisomerase poison. 5,6-Dihydro-3,4-methylenedioxy-10,11-dimethoxydibenzo[a,g]quinoliz inium chloride was the most potent topoisomerase I poison among the coralyne analogues evaluated, having similar activity to camptothecin. This analogue also possessed exceptional potency as a topoisomerase II poison. Despite the pronounced activity of several of these coralyne derivatives as topoisomerase I poisons, none of these compounds had cytotoxic activity similar to camptothecin. Possible differences in cellular absorption between these coralyne analogs, which possess a quaternary ammonium group, and camptothecin may be responsible for the differences observed in their relative cytotoxicity
Synthesis and evaluation of terbenzimidazoles as topoisomerase I inhibitors
The synthesis and pharmacological activity of a series of terbenzimidazoles are described. The ability of these derivatives to induce DNA cleavage in the presence of topoisomerase I was evaluated in vitro. These analogs were also assayed for their cytotoxicity in RPMI 8402 cells and the camptothecin-resistant CPT-K5 cells. In addition the potential for these compounds to serve as substrates for MDR1 was also determined. Several terbenzimidazoles exhibited similar cytotoxicity against variants of human tumor cells that either overexpress MDR1 or are camptothecin-resistant
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