Using a dataset from TAIFEX, Taiwan Futures Exchange, we conduct an account-level analysis of the relation between prior loss consequences and subsequent trading behaviors. We apply two proxy variables of trading activities into our analysis, which are trade size and number of trades. We find that the degree of prior losses has a great effect upon trade size and trading number on the next trading day. This finding proves to the evidence that hedonic editing hypothesis sometimes fails and there are some limitations for it. We further examine for different trader types and the empirical results show that individual investors exhibit the strongest bias while other trader types do uncertainly. We also find the behavioral bias is a persistent phenomenon for individual investors. Overall, our study suggests that prior loss degree has a significant influence on investors’ following trading behaviors.

Thesis (M.A.) -- Central Connecticut State University, 2008. / Thesis advisor: Barry Hoopengardner. "... in partial fulfillment of the requirements for the degree of Master of Arts in Biomolecular Sciences." Includes bibliographical references (leaves 34-36). Also available via the World Wide Web.

Editing is an important aspect of film. This thesis tests the effects of specific edits and how they influence the opinion of the audience.

Post-transcriptional regulation of gene expression involves a diverse set of mechanisms such as RNA splicing, RNA localization, and RNA turn-over. Adenosine to Inosine (A-to-I) RNA editing is an additional post-transcriptional regulatory mechanism. Temporally, it occurs after transcription and before RNA splicing and has been shown in some instances to possibly modulate alternative splicing events. This is the case for example, with the pre-mRNA encoding the GluR- 2 subunit of AMPA receptor, a glutamate-activated ion channel. ADAR (Adenosine deaminase acting on RNA) proteins bind to double-stranded regions in pre-messenger RNAs. They deaminate specific adenosines, generating inosines; if the editing event occurs within the coding region, inosine is then interpreted as guanosine by the ribosomal translational machinery, changing codon meaning. These editing events can increase the repertoire of translated proteins, generating molecular diversity and modifying protein function. In mammals there are four ADAR genes: ADAR1, ADAR2, ADAR3 and TENR. ADAR3 and TENR are enzymatically inactive. All the proteins have two types of functional domains: (i) the catalytic deaminase domain at the carboxyl-terminus and (ii) the double stranded RNA binding domains, dsRBDs, at the amino terminus. ADAR1 and ADAR2 differ significantly at the amino terminus, by the number of the dsRNA binding domains (three and two dsRBDs for ADAR1 and ADAR2 protein, respectively). The differences observed between ADAR1 and ADAR2 are likely to reflect the different repertoires of substrates edited by these two enzymes. Data concerning the conservation of Adar genes throughout evolution suggest that Drosophila melanogaster has a unique Adar gene which is a true ortholog of human ADAR2 rather than an invertebrate gene ancestral for both vertebrate genes. Flies that are null mutants for Adar (Adar5G1 mutants) display profound behavioral and locomotive deficits. Impairment in motor activity of the mutants is succeeded by age-dependent neurodegeneration, characterized by swelling within the Adar-null mutant fly brain. The initial focus of my thesis was to elucidate what causes Adar mutant phenotypes or, whether it is possible, to suppress them. I took advantage of Drosophila genetics to establish a forward genetic screen for suppressors of reduced Adar5G1 viability which is approximately 20-30% in comparison to control flies at eclosion. The results from an interaction screen on Chromosome 2L were further confirmed using Exelixis P-element insertion lines. The screen revealed that decreasing Tor (Target of rapamycin) expression suppresses Adar mutant phenotypes. TOR plays a role in maintaining cellular homeostasis by balancing the metabolic processes. It controls anabolic events by phosphorylating eukaryotic translation initiation factor 4E-binding protein (4E-BP) and p70 S6 kinase (S6K) and inducing cap-mediated translation. However, different types of stress, signals or increased demand in catabolic processes, converge to reduce TOR enzymatic activity. This results in long-lived proteins and organelles being engulfed in double-membrane vesicles and degraded; this bulk degradation process is called (macro)autophagy. The second aim of my thesis was to clarify which pathway, downstream to TOR, was responsible for the suppression of Adar-null phenotypes. I mimicked the effect of reduced Tor expression by manipulating genetically the cap-dependent translation and the autophagy pathways. Interestingly, boosting the expression of Atg (autophagy specific genes) genes, such as, Atg1 and Atg5, thereby increasing the activation rate of the autophagy pathway, suppresses Adar5G1 phenotypes. Finally, I found that Adar5G1 mutant flies have an increased level of autophagy that is observable from the larval stage. I investigated possible stresses affecting our mutants; Adar-mutant larval fat cells show ER stress triggering an unfolded protein response as indicated by expression of XbpI-eGFP reporter. Thus, ER stress might induce increased autophagy and it can lead to locomotive impairments and neurodegeneration in Adar-null mutants. These results suggest a function for the Adar gene in regulating cellular stress.

No description available.

Deamination or the hydrolytic removal of one hydroxyl group from a base in DNA or RNA can lead to changes in the transcript and protein produced. Examples of this are the deamination of cytosine residues in DNA by activation induced deaminase (AID) during antibody diversification, or deamination of adenosine at the Q/R site in the GluR-B transcript by adenosine deaminase acting on RNA 2 (ADAR2), which regulates calcium permeability in neurons. The initial focus of my thesis was to characterise a putative novel deaminase APOBEC4. APOBEC4 was identified in a bioinformatic search for proteins containing the core catalytic residues common to the whole family of Cytidine Deaminase enzymes. The aim of the project was to express and purify recombinant APOBEC4 for in vitro characterization, however despite using different expression systems and purification conditions the majority of the recombinant protein was inherently insoluble and I could not isolate sufficient amounts of protein for further studies. Recombinant protein with a GST-tag was used to generate polyclonal antibodies which recognised recombinant protein but were unable to detect endogenous APOBEC4. The focus of my thesis then changed to the process of adenosine to inosine editing in RNA, which is a post-transcriptional mechanism for generating protein diversity. The enzyme family responsible for catalysing this reaction is known as ADAR, and Drosophila melanogaster has only one Adar gene. Flies lacking the Adar gene show locomotion defects and age-dependent neurodegeneration, however little is known about the molecular mechanism underlying these defects. To investigate this phenotype I performed microarray analysis on RNA isolated from heads of 5 day old flies lacking the Adar gene to characterize gene expression changes in the fly heads before neurodegeneration caused secondary effects. Analysis was also performed on Adar-null flies expressing either an active Adar gene or a catalytically-inactive Adar gene in cholinergic neurons to determine which transcripts could be directly regulated by Adar. I confirmed the microarray results by real-time PCR, and demonstrated that the changes in transcript level could be reversed by expression of either active or catalytically-inactive Adar. Expression of edited transcripts did not change dramatically. Filter-binding analysis and electrophoretic mobility shift assay revealed that recombinant ADAR could bind to all RNA transcripts analysed with similar affinity; both known substrates and potential new substrates for Adar, as well as transcripts that were chosen as negative controls due to their expression not altering in the expression microarray. Recombinant ADAR bound to dsRNA with a very high affinity; other transcripts investigated bound with considerably lower affinity, yet all transcripts investigated were bound by ADAR. Further analysis of transcript changes in Adar-null flies was investigated by performing microarray analysis with a custom-made splicing-sensitive microarray. Analysis revealed that a subset of transcripts were differentially spliced in Adar-null flies; however this group of transcripts was distinct from the group identified as being altered on the expression microarray, indicating that the splicing changes are independent of changes in expression. Analysis of exon-specific probes on the splicing array confirmed the transcript changes identified in the expression array. Real-time PCR confirmed the changes in splicing, and these transcripts were further examined by sequence analysis. This revealed several transcripts identified as altered by the AS array showed use of alternative polyadenylation sites indicating ADAR may have a role in detemining polyadenylation site selection.

No description available.

When animating characters, a key goal is the creation of a believable, expressive performance that gives a character a unique personality with a distinct style of movement. While animators are skilled at creating expressive, personalized performances, it remains challenging to change performance-related aspects of movement in existing motion data. In recent years, motion data reuse has become increasingly important as recorded motion capture data has come into widespread use. This thesis investigates the use of a sparse set of pose-centric editing controls for editing existing motion data using techniques similar to those used by keyframe animators when they create new motion. To do this, this thesis proposes the use of motion extrema--the poses a character passes through when there is a significant change in movement--as a means for choosing effective pose-centric editing controls. First, I present algorithms for identifying motion extrema. Motion extrema can be associated with individual joints or the full body of the character. I introduce a set of approaches for identifying motion extrema; these include the use of extrema of differential measures and the explicit search for times at which the body or a joint is in a spatially extreme configuration. I then present three motion editing applications that use motion extrema as a foundation for applying motion edits. The first application, pose-centric editing, allows users to interactively change poses in a motion, and the system modifies the motion to respect existing ground contact. The second application--staggered poses, introduces a model of character pose that explicitly encodes how timing varies among motion extrema on different parts of the body. This timing variation is commonly used by animators to model overlapping action. By introducing an algorithm for finding timing variation on motion extrema in existing motion, this system enables users to make high-level changes to timing patterns to change overlap effects in existing motion. Finally, I present a procedural motion editing application that targets a specific aspect of motion style; this technique is called spatial exaggeration. Spatial exaggeration changes the geometric relationships among extreme poses. Such edits cause movement to appear more or less energetic. Overall, these applications demonstrate that performance-related aspects of existing motion can be edited using a sparse set of controls in the form of motion extrema.

When animating characters, a key goal is the creation of a believable, expressive performance that gives a character a unique personality with a distinct style of movement. While animators are skilled at creating expressive, personalized performances, it remains challenging to change performance-related aspects of movement in existing motion data. In recent years, motion data reuse has become increasingly important as recorded motion capture data has come into widespread use. This thesis investigates the use of a sparse set of pose-centric editing controls for editing existing motion data using techniques similar to those used by keyframe animators when they create new motion. To do this, this thesis proposes the use of motion extrema--the poses a character passes through when there is a significant change in movement--as a means for choosing effective pose-centric editing controls. First, I present algorithms for identifying motion extrema. Motion extrema can be associated with individual joints or the full body of the character. I introduce a set of approaches for identifying motion extrema; these include the use of extrema of differential measures and the explicit search for times at which the body or a joint is in a spatially extreme configuration. I then present three motion editing applications that use motion extrema as a foundation for applying motion edits. The first application, pose-centric editing, allows users to interactively change poses in a motion, and the system modifies the motion to respect existing ground contact. The second application--staggered poses, introduces a model of character pose that explicitly encodes how timing varies among motion extrema on different parts of the body. This timing variation is commonly used by animators to model overlapping action. By introducing an algorithm for finding timing variation on motion extrema in existing motion, this system enables users to make high-level changes to timing patterns to change overlap effects in existing motion. Finally, I present a procedural motion editing application that targets a specific aspect of motion style; this technique is called spatial exaggeration. Spatial exaggeration changes the geometric relationships among extreme poses. Such edits cause movement to appear more or less energetic. Overall, these applications demonstrate that performance-related aspects of existing motion can be edited using a sparse set of controls in the form of motion extrema.

A new approach is proposed to transparently share familiar single-user editors without modifying their source code. This approach tweaks a classic diff algorithm to derive edit scripts between document states. Concurrent edit scripts are merged to synchronize states of coauthoring sites. Our concept-proving prototype currently works with familiar, heterogeneous text editors such as GVim and WinEdt that can be adapted to support two basic interfaces, GetState and SetState. The adaption is less expensive and more robust than recent approaches such as ICT and CoWord, which must understand and translate editing operations at the operating system level. Experimental data show that our approach is able to provide sufficient performance for near-realtime group editing.