No description available.

Prompting methods are common amongst animal trainers, both novice and experts. However, there is little empirical evidence to demonstrate the strengths or weaknesses of common prompting procedures. The current study assessed the strengths and weaknesses during behavior acquisition of two prompting methods, luring and targeting. Luring placed an edible directly in front of the animal which guided the animal through the desired behavior. Targeting, however used a target, an arbitrary object the animal has been trained to touch, guide behavior. A cat was trained, using each method, to walk around a flower. Walking around the right flower pot was trained using luring and walking around the left flower pot was trained using targeting. After both behaviors were acquired, a delay cue method was designed to transfer stimulus control. Later a combination of a delay cue and prompt fading was used. During acquisition the luring method acquired the behavior of walking around a pot more quickly with consistently fewer errors. During stimulus transfer the cat began independently initiating the behavior earlier with the target trained behavior and produced more correct behaviors after the verbal cue. Luring appeared to produce the faster behavior, but after stimulus transfer it could be concluded that the cat did not learn the desired behavior, but rather following the lure. Both methods could be beneficial in different circumstance, however, given the desired behavior was to walk around a flower pot on cue, targeting would be considered best practice.

No description available.

<p>Television (TV) is the predominant advertising medium, and recent technological advances such as digital video recorders (DVRs) and set-top boxes (STBs) have the potential to transform this industry by enabling household-specific advertising. Since exposure to TV represents a substantial share of consumer time and attention, this potential to micro-target communications represents an enormous opportunity for the TV advertising market. </p><p>This paper outlines an approach to facilitate the micro-targeting of TV advertising. We employ a unique dataset, integrating TV program and advertisement viewing at the household level with purchase data, to address the question of how advertisers can achieve better advertising targeting in the digital context. Based on this dataset, we first develop a model of household TV viewing behavior. The viewing model comprises three integrated components: TV show sampling and watching, TV show recording, and advertising viewing. All three components are motivated by the theoretical concept of flow utility, that is, the moment-by-moment enjoyment a household derives from different activities: watching a TV show, watching a TV advertisement, and other non-TV activities. This model has decent out-of-sample prediction power on show choices and time spent on each selected show. We then link household advertising exposure with purchase. Finally, the viewing model and identified advertising-sales relationship are utilized to conduct counterfactual policy experiments on advertising targeting. We consider several household-level targeting scenarios by manipulating: 1) whether the advertising purchase is made in advance; and 2) whether the objective function is to minimize costs for a given set of exposures or to maximize revenues from advertising. Results indicate micro-targeting can lower advertising costs and raise incremental revenue.</p><p>The key contributions of this paper are as follows. Theoretically, we develop an integrated model on TV show viewing, TV advertising viewing, purchasing and advertising targeting. Methodologically, we propose a new modeling framework on media consumption by explicitly accounting for the role of uncertainty, and propose targeting strategies leveraging household-level data. Substantively, we offer policy recommendations to advertisers on micro-targeting which can be of great potential.</p> / Dissertation

Mospd3, a gene located on mouse chromosome 5, was identified in a gene trap screen in ES cells. The gene trap vector integration in multiple copies into the putative promoter of the gene, resulted in a loss of expression of Mospd3 at the trapped allele. In mice generated from ES cells carrying the vector integration it was found that the lack of Mospd3 expression resulted in the death of a proportion of the homozygote mutants within the first day after birth. Homozygote neonates exhibited a thinning of the right ventricular free heart wall which resembles other mouse mutant phenotypes as well as human congenital heart defects caused by a loss of desmosome and adherens junction mediated cell adhesion between cardiomyocytes. The protein encoded by Mospd3, contains an N-terminal Major Sperm Protein (MSP) domain implicated as a mediator of protein- protein interactions, as well as a two C-terminal transmembrane domains. Both, protein structure and phenotypic similarities with defects in desmosomal and adherens junction proteins suggests that Mospd proteins might play a role in cell adhesion and maintaining the structural integrity of the heart. The phenotype of Mospd3 mutants was highly dependent on genetic background, which led us to speculate that there might be genetic redundancy between Mospd3 and its closest family member the X-linked Mospd1. The aims of this thesis were to generate tools to better understand the function of the Mospd gene family in cardiac development as well as assessing genetic redundancy between Mospd1 and Mospd3. A conditional gene targeting strategy was designed for both Mospd genes. Large genomic regions of the Mospd1 and Mospd3 loci were subcloned from bacterial artificial chromosomes (BACs) and using a recombineering approach, loxP sites and a drug selection cassette (neomycin) were placed in precise locations surrounding the MSP domain of both genes. The conditional targeting vectors were electroporated into both CGR8 and E14 ES cells and homologous recombinant clones were identified at a frequency of 2% and 1.3% for Mospd1 and Mospd3 respectively. Five euploid targeted clones for both Mospd1 and Mospd3 have been generated. Transient expression of Cre recombinase in ES cells carrying the conditional Mospd1 allele was used to delete the one copy of this X-linked gene. Phenotypic characterisation of this null ES cell line revealed that Mospd1 is neither essential for ES cell viability and self-renewal, nor for the early differentiation of these cells towards a cardiac fate. In order to investigate the mechanism of action of Mospd proteins, specific polyclonal antibodies were generated to detect either Mospd1 or Mospd3. These antibodies were purified and tested by western blotting using COS7 cells overexpressing either Mospd protein as well as mouse tissue lysates. Whilst the antibodies were found to detect the proteins and differentiate between Mospd1 and Mospd3, they showed insufficient purification to be used in co-localisation and co-immunoprecipitation experiments to identify interacting proteins and determine whether Mospd proteins are involved in cell adhesion complexes. Monoclonal antibodies were subsequently generated and initial western blotting experiments showed promising results, indicating that these antibodies may be better suited for immunohistochemical analysis of Mospd proteins.

published_or_final_version / Biochemistry / Doctoral / Doctor of Philosophy

published_or_final_version / Paediatrics / Master / Master of Philosophy

published_or_final_version / abstract / Biochemistry / Doctoral / Doctor of Philosophy

published_or_final_version / Biochemistry / Doctoral / Doctor of Philosophy

No description available.