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Studies were performed on two types of infection of teleost fish where viruses have been observed by electron microscopy: erythrocytic infections in the Atlantic Cod (Gadus morhua) and the Common Blenny (Blennius hpo lis) and lymphcystis disease., Searches were made for new, isolations of these infections Ja British coastal waters and on shores chiefly in the vicinity of Plymouth and Aberystwyth. In the absence of disease symptoms, the blood of fish was, screened for the presence of viral inclusion bodies by standard haematological methods. PEN in cod was found in the North Sea-. and in the Celtic Sea off southern Eire, thus extending the previous distribution data from the Atlantic-coastal waters. of North America. The blenny infection was also found in new sites on shores in the vicinity of Plymouth. Moreover, the cytology of these infectionswas as had been previously described. Collection data for the PEN infections showed an inverses; - relationship of infection incidence-with age for cod sample populations but no correlation was found for blenny sample populations. In addition, no external disease symptoms were observed in either type of infection. Concerning the recognition of the blenny infection, observations from maintaining blennies suggested the length of the natural infection might be inversely related to temperature; non-experimental longevities are quoted in this connection. The degree of infection in individual fish was estimated by light microscopy and the estimates for both erythrocytic infections cover the range 1-60% infection. Attempts were made to propagate the viruses in vitro using fish cell and organ cultures. Primary cell cultures were originated from tissues of the Blenny, Flounder, Plaice and Dab using the protocol in the literature for marine fish cell culture. Vigorous cell outgrowth was observed in the flounder cultures and in these the time to confluence was only 3-5 days. However, established secondary cultures could not be derived from tissues of either species. Plaice and dab cultures were used for virus inoculation but the virus from the blenny infection and lymphocystis virus could not be propagated. , Organ cultures were set up using skin blocks from the Flounder. With tris-buffered maintenance medium such cultures maintained histological integrity for 15 days. However, one - trial inoculation with lymphocystis virus showed no-integration or multiplication of the virus in the tissue. In connection with attempts to induce the blenny infection, the. effect of high temperature-in the Blenny was investigated. The infection was not induced over a9 day holding period but lytic effects on the erythrocyte nuclei were observed. The effect of the drug acetylphenylhydrazine (APH) in the Blenny was also investigated with the aim of reproducing its reported action of anaemia induction and ensuing erythropoiesis. Marked anaemia was produced but not erythropoiesis. However, this result could not nesessarily be interpreted as the effect of APH alone. The viruses were identified and characterized with emphasis on their mophology, using ultrathin sectioning, negative staining and shadowing methods. It was concluded that the virus from the Blenny and lymphocystis virus conform to the structural measurements in the literature but negative staining indicated that both viruses display unique core structures. These are discussed in the light of the knowledge of other DNA virus cores. The position of these viruses is further considered with respect to their classification in the virus family Iridoviridae.

M.Dent., Faculty of Health Sciences, University of the Witwatersrand, 2008. / Objective: To determine the aetiology, biomechanics and demographics of patients with fractures of the midface. Materials and Methods: Patients with midface fractures (who consented to participate in the study) who presented to the Division of Maxillofacial and Oral Surgery over a 12 month period from December 2005 to December 2006 were included in the study. Data was recorded on age, race, gender, date and cause of injury, associated injuries and use of alcohol at the time of injury. The fractures were grouped into Le Fort, zygomatico‐maxillary, dentoalveolar and panfacial fractures. Results: The sample comprised 94 patients; 78 (82.98%) males and 16 (17.02%) females with an age range of 3 to 67 years. Blacks accounted for 77.66% of the total sample, followed by Whites (12.77%), Coloureds (6.38%) and Asians (3.19%). Blunt trauma due to interpersonal violence, motor vehicle accidents, gun shot wounds and falls contributed to 40.5%, 26.6%, 13.8% and 5.3% of the fractures respectively. Le Fort fractures were less commonly observed than zygomaticomaxillary complex midface fractures. Conclusion: A relationship exists between facial trauma, poverty and alcohol consumption. Blunt trauma due to interpersonal violence is the most common cause of midface injuries. Majority of injuries are sustained during weekends. Zygomaticomaxillary complex fractures are the most common midface fractures.

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Introduction A literature review of the evidence regarding aetiology, classification, epidemiology and treatment of depressive disorders was conducted. All of the domains that constitute the biopychosocial model were investigated as a basis for testing the hypothesis that a biomedical approach, or any domain in isolation, is inadequate for fully understanding depression. An integrative, explanatory, conceptual model was developed, based on supportive evidence that can better inform the clinical encounter. Methods A combination of manual and electronic searches were conducted. Medline, Psychlit, Sociofile and the Social Science index databases were accessed with multiple key words. The University of Queensland library catalogue was also searched. Part A - Historical and Philosophical Basis The limitations and challenges of the biomedical model are followed by suggested responses, in particular a biopsychosocial model applied within a patient-centred consultation style. Various methods of scientific enquiry are needed to develop a more complete understanding of depression. Part B - Assessing the Evidence Evidence from epidemiological, biological and psychosocial research is reviewed. Depressive illness tends to be a chronic or recurrent condition with multifactorial causation, and occurs on a complex spectrum of severity. There is emerging evidence for a chronic stress response being the initial biological dysfunction, This is consistent with the frequency of stressful life events that precipitate depressive episodes. There is convincing evidence for predisposing factors such as low self-esteem, poor interpersonal skills and deficiency of social support. A range of treatment modalities, for example pharmacotherapy and various psychotherapies, appear to have similar effectiveness, which suggests that recovery occurs when the perpetuating cycle is broken at different sites. Part C - Integrative Models. Available schematic integrative models are reviewed and most fall short of integrating the three domains of the biopsychosocial, or fail to illustrate the circular nature of causation. A model is proposed, based on the evidence reviewed in Part B, that addresses both considerations. Conclusion Some causal factors for depression are supported by evidence. Models that integrate these findings are necessary to more fully explain depression. When applied in conjunction with patient-centred consultation styles, improved clinical outcomes could be expected. There is the potential for further research to test out the benefit of such a biopsychosocial approach, and to better elucidate component causes and reversible risk factors. There is a need for narrative approaches to receive considerably greater attention.

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The Irritable Bowel Syndrome (IBS) is one of the most common conditions referred to a gastroenterologist, but there is no consensus of opinion regarding either its aetiology or its treatment. This is partly due to an absence of any physiological marker, and to the variability of presenting symptoms. It has been suggested that it is due to a fibre depleted diet, although this has never been shown. The diets of 187 patients with the IBS and 61 control subjects were investigated using a validated dietary diary method. The patients were subdivided according to presenting complaint. It was found that patients had a lower intake of dietary fibre than controls,and in particular those with diarrhoea had a low intake of fruit fibre. Patients with constipation had a lower food intake. To help in the dietary assessment of patients a computer programme based on a simple prospective dietary questionnaire was written. It proved to be an effective and rapid guide to fibre intakes. Gut transit times were measured using the breath hydrogen technique for mouth to caecum transit times and the continuous marker technique for whole gut transit times. The possible effect of abnormal transit through the gut on food handling was investigated. It was found that patients presenting with diarrhoea had significantly shorter mouth to caecum transit times (with implications for the absorption of food) and that patients with constipation had lengthened transit times, both mouth to caecum and whole gut. Malabsorption of simple sugar solutions leading to gut symptoms was demonstrated both in patients and controls. Finally, 11 patients with food intolerance were investigated, as it has been suggested that food intolerance is a major factor in the aetiology of the IBS. The results suggest that low fibre intakes are probably important in the aetiology of IBS and that, at least in some individuals, carbohydrate malabsorption may also be a significant factor.

HLA genotypes were determined and prospective investigations performed on members of 166 families, each including a Type 1 diabetic proband. A computer-based system (Genobase) was created for data storage and analysis. Newly-diagnosed cases ascertained in East Berkshire (incidence rate: 17.8 x 10^-5/year) and additional data from two other studies contribute to some analyses. Major findings include non-random assortment of HLA-B8 within families and a tendency for HLA-identical siblings of diabetic probands to be younger than expected. Discrete multivariate analysis and other methods show no major genetic heterogeneity within Type 1 diabetes. However, there is minor heterogeneity affecting the interaction of age and seasonal variation in incidence of the diabetes. Furthermore, the HLA genotype B8,15 is here shown to be significantly more frequent in Type 1 diabetic probands than expected assuming Hardy-Weinberg equilibrium. With support from other internal and published data, it is concluded that susceptibility to Type 1 diabetes is genetically multifactorial. Increased prevalence of organ-specific autoimmunity is confirmed in the families, and differences in distribution of islet-cell antibodies (ICA) and thyroid/gastric antibodies demonstrated. Five subjects, ICA-positive from the first test, developed diabetes after up to 30 months, demonstrating prolonged latency. Quantitative risk of diabetes is estimated (separately) in terms of ICA results and of HLA genotypes. Non-diabetic siblings of affected probands are investigated for evidence that an HLA-linked immune response gene might contribute to susceptibility. Response patterns to previous polio vaccination give some support, but the excess of thyroid/gastric antibodies in the siblings is not due to such a gene. The dissertation concludes with discussion of aetiological hypotheses and indications for further work.