Dickens's comic art: a study of the comic element in Dombey and .son, little Dorrit, and great expectations

The new Clarendon Dickens Edition (General Editors: John Butt and Kathleen Tillotson), was not available at the time' of writing for all of the novels which are studied in this thesis. Considerations of consistency and availability, therefore, dictated my use of the New Oxford Illustrated Edition of Dickens's novels. Details of the three main works referred to in this thesis are as follows: Dealings with the Firm of Dombey and Son (1848; rpt. Oxford: O.U.P., 1950) Little Dorrit (1857; rpt. Oxford: O.U.P., 1953) Great Expectations (1861; rpt. Oxford: O.U.P., 1953) All other quotations and references to Dickens's. works also refer to the New Oxford Illustrated Edition, unless otherwise noted. I have consulted the Clarendon Dickens (Variorum) Edition where applicable, and the few pertinent textual variations have been duly footnoted. All word-divisions at line endings are sanctioned by the Collins Ge~ Dictionary of Spelling and Word Division, compiled by S.8. Marshall (London: Collins, 1968)

Dickens's comic art: a study of the comic element in Dombey and Son, Little Dorrit, and Great Expectations

It is my contention in this thesis that the comic nature of Dickens's mature fiction has not received the degree of attention that its importance warrants. In particular, the questions left unanswered, or to my mind not satisfactorily answered, by modern critics of Dickens are: why does Dickens consistently adopt modes of comedy in his mature works; what are the modes that he adopts; and what are the implications of these modes in terms of his later achievement? Finally, in what way can his vision be judged to be a comic vision

Impacts of the Mission Continues Fellowship Program on Post-9/11 Disabled Military Veterans, Their Families, and Their Communities

Impacts of the Mission Continues Fellowship Program on Post-9/11 Disabled Military Veterans, Their Families, and Their Communitie

The Mission Continues: Engaging Post-9/11 Disabled Military Veterans in Civic Service

The Mission Continues: Engaging Post-9/11 Disabled Military Veterans in Civic Servic

The chicken type III GnRH receptor homologue is predominantly expressed in the pituitary, and exhibits similar ligand selectivity to the type I receptor

Two GnRH isoforms (cGnRH-I and GnRH-II) and two GnRH receptor subtypes (cGnRH-R-I and cGnRH-R-III) occur in chickens. Differential roles for these molecules in regulating gonadotrophin secretion or other functions are unclear. To investigate this we cloned cGnRH-R-III from a broiler chicken and compared its structure, expression and pharmacological properties with cGnRH-R-I. The broiler cGnRH-R-III cDNA was 100% identical to the sequence reported in the red jungle fowl and white leghorn breed. Pituitary cGnRH-R-III mRNA was ∼1400-fold more abundant than cGnRH-R-I mRNA. Northern analysis indicated a single cGnRH-R-III transcript. A pronounced sex and age difference existed, with higher pituitary transcript levels in sexually mature females versus juvenile females. In contrast, higher expression levels occurred in juvenile males versus sexually mature males. Functional studies in COS-7 cells indicated that cGnRH-R-III has a higher binding affinity for GnRH-II than cGnRH-I (Kd: 0·57 vs 19·8 nM) with more potent stimulation of inositol phosphate production (ED50: 0·8 vs 4·38 nM). Similar results were found for cGnRH-R-I, (Kd: 0·51 vs 10·8 nM) and (ED50: 0·7 vs 2·8 nM). The initial rate of internalisation was faster for cGnRH-R-III than cGnRH-R-I (26 vs 15·8%/min). Effects of GnRH antagonists were compared at the two receptors. Antagonist #27 distinguished between cGnRH-R-I and cGnRH-R-III (IC50: 2·3 vs 351 nM). These results suggest that cGnRH-R-III is probably the major mediator of pituitary gonadotroph function, that antagonist #27 may allow delineation of receptor subtype function in vitro and in vivo and that tissue-specific recruitment of cGnRH-R isoforms has occurred during evolution

Incidence, Mechanisms of Injury and Mortality of Severe Traumatic Brain Injury: An Observational Population-Based Cohort Study from New Zealand and Norway

Background Comparing trauma registry data from different countries can help to identify possible differences in epidemiology, which may help to improve the care of trauma patients. Methods This study directly compares the incidence, mechanisms of injuries and mortality of severe TBI based on population-based data from the two national trauma registries from New Zealand and Norway. All patients prospectively registered with severe TBI in either of the national registries for the 4-year study period were included. Patient and injury variables were described and age-adjusted incidence and mortality rates were calculated. Results A total of 1378 trauma patients were identified of whom 751 (54.5%) from New Zealand and 627 (45.5%) from Norway. The patient cohort from New Zealand was significantly younger (median 32 versus 53 years; p < 0.001) and more patients from New Zealand were injured in road traffic crashes (37% versus 13%; p < 0.001). The age-adjusted incidence rate of severe TBI was 3.8 per 100,000 in New Zealand and 2.9 per 100,000 in Norway. The age-adjusted mortality rates were 1.5 per 100,000 in New Zealand and 1.2 per 100,000 in Norway. The fatality rates were 38.5% in New Zealand and 34.2% in Norway (p = 0.112). Conclusions Road traffic crashes in younger patients were more common in New Zealand whereas falls in elderly patients were the main cause for severe TBI in Norway. The age-adjusted incidence and mortality rates of severe TBI among trauma patients are similar in New Zealand and Norway. The fatality rates of severe TBI are still considerable with more than one third of patients dying.publishedVersio

An evaluation of section 1 of the Offensive Behaviour at Football and Threatening Communications (Scotland) Act 2012

A mixed methods evaluation of a legislation introduced by the Scottish Government to tackle sectarian and other offensive behaviours at regulated fotoball matche

A transgenic zebrafish model expressing KIT-D816V recapitulates features of aggressive systemic mastocytosis

Summary: Systemic mastocytosis (SM) is a rare myeloproliferative disease without curative therapy. Despite clinical variability, the majority of patients harbour a KIT-D816V mutation, but efforts to inhibit mutant KIT with tyrosine kinase inhibitors have been unsatisfactory, indicating a need for new preclinical approaches to identify alternative targets and novel therapies in this disease. Murine models to date have been limited and do not fully recapitulate the most aggressive forms of SM. We describe the generation of a transgenic zebrafish model expressing the human KIT-D816V mutation. Adult fish demonstrate a myeloproliferative disease phenotype, including features of aggressive SM in haematopoeitic tissues and high expression levels of endopeptidases, consistent with SM patients. Transgenic embryos demonstrate a cell-cycle phenotype with corresponding expression changes in genes associated with DNA maintenance and repair, such as reduced dnmt1. In addition, epcam was consistently downregulated in both transgenic adults and embryos. Decreased embryonic epcam expression was associated with reduced neuromast numbers, providing a robust in vivo phenotypic readout for chemical screening in KIT-D816V-induced disease. This study represents the first zebrafish model of a mast cell disease with an aggressive adult phenotype and embryonic markers that could be exploited to screen for novel agents in SM