Quantum Liouville Theory from a Diffeomorphism Chern-Simons Action

A Chern-Simons action written with Christoffel Symbols has a natural gauge symmetry of diffeomorphisms. This Chern-Simons action will induce a Wess-Zumio-Witten model on the boundary of the manifold. If we restrict the diffeomorphisms to chiral diffeomorphism, the Wess-Zumio-Witten model is equivalent to a quantum Liouville action.Comment: Minor typo correcte

Coherent State Approach to Quantum Clocks

The ``problem of time'' has been a pressing issue in quantum gravity for some time. To help understand this problem, Rovelli proposed a model of a two harmonic oscillators system where one of the oscillators can be thought of as a ``clock'' for the other oscillator thus giving a natural time reference frame for the system. Recently, the author has constructed an explicit form for the coherent states on the reduced phase space of this system in terms of Klauder's projection operator approach. In this paper, by using coherent state representations and other tools from coherent state quantization, I investigate the construction of gauge invariant operators on this reduced phase space, and the ability to use a quantum oscillator as a ``clock.''Comment: 13 pages, Late

The Effects of Deception and Manipulation of Motivation to Deceive on Event Related Potentials

The Correct Response Negativity (CRN) is an event-related potential component that is affected by the act of deception. However, there have been inconsistent findings on the effect of deception on the CRN. Suchotzki, et al. (2015) suggested that the design of the paradigm used to elicit the deceptive response is what controls the size of the CRN. Specifically, motivation to deceive changes the size of deception relative to telling the truth. This study attempted to follow up on suggestions made by Suchotzki et al. (2015) to investigate if extraneous motivation to lie does indeed invert the ratio of CRN in lie compared to truth responses in a deception experiment by manipulating the motivation to lie. This study used a modification of the image-based guilty knowledge test (GKT) paradigm used in Langleben et al. (2002). The first hypothesis of this experiments was that a larger CRN during deception relative to truth-telling will be observed when participants are not motivated to lie, while a larger CRN during truth-telling relative to deception will be observed when participants are motivated to lie. The hypothesis was not supported. The second hypothesis of this experiment was that the P300 component would be larger when participants were motivated to lie, as compared to when they were instructed to lie. Results indicated that P300 was significantly higher in the lie conditions than in the truth conditions; however, there was no difference in amplitude as a function of whether they were in the informed or motivated lie condition

Brca2 and Trp53 deficiency cooperate in the progression of mouse prostate tumourigenesis.

Epidemiological studies have shown that one of the strongest risk factors for prostate cancer is a family history of the disease, suggesting that inherited factors play a major role in prostate cancer susceptibility. Germline mutations in BRCA2 predispose to breast and ovarian cancer with its predominant tumour suppressor function thought to be the repair of DNA double-strand breaks. BRCA2 has also been implicated in prostate cancer etiology, but it is unclear the impact that mutations in this gene have on prostate tumourigenesis. Here we have undertaken a genetic analysis in the mouse to determine the role of Brca2 in the adult prostate. We show that deletion of Brca2 specifically in prostate epithelia results in focal hyperplasia and low-grade prostate intraepithelial neoplasia (PIN) in animals over 12 months of age. Simultaneous deletion of Brca2 and the tumour suppressor Trp53 in prostate epithelia gave rise to focal hyperplasia and atypical cells at 6 months, leading to high-grade PIN in animals from 12 months. Epithelial cells in these lesions show an increase in DNA damage and have higher levels of proliferation, but also elevated apoptosis. Castration of Brca2;Trp53 mutant animals led to regression of PIN lesions, but atypical cells persisted that continued to proliferate and express nuclear androgen receptor. This study provides evidence that Brca2 can act as a tumour suppressor in the prostate, and the model we describe should prove useful in the development of new therapeutic approaches