Thesis (doctoral)--Lund University, 1997. / Added t.p. with thesis statement inserted.

Thesis (doctoral)--Lund University, 1997. / Added t.p. with thesis statement inserted.

No description available.

No description available.

No description available.

Xu Ge-Zhi. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1995. / Includes bibliographical references (leaves 56-69). / List of figures --- p.IV / Abstract --- p.V / Chapter Chapter1 --- Introduction --- p.1 / Literature review --- p.2 / Chapter 1. --- Necrosis --- p.2 / Chapter 2. --- Apoptosis --- p.3 / Chapter 2.1. --- Morphologic features of apoptosis --- p.4 / Chapter 2.2. --- Biochemical mechanism of apoptosis --- p.5 / Chapter 2.3. --- Genetic regulation of apoptosis --- p.7 / Chapter 2.4. --- Techniques for identifying apoptosis --- p.7 / Chapter 3. --- Retinal degeneration --- p.9 / Chapter 3.1. --- Pathologic myopia --- p.9 / Chapter 3.2. --- Age-related macular degeneration (ARM) --- p.11 / Chapter 3.3. --- Retinal detachment --- p.12 / Chapter 4. --- Apoptosis and retinal degeneration --- p.14 / Chapter 5. --- Scope and definition of the thesis problem --- p.15 / Chapter Chapter2 --- Materials and methods --- p.16 / Chapter 1. --- Cases selection and tissue preparation --- p.16 / Chapter 2. --- TdT-mediated dUTP-biotin nick-end Labelling (TUNEL) --- p.17 / Chapter Chapter3 --- Results --- p.20 / Chapter 1. --- Pathologic myopia group --- p.20 / Chapter 2. --- Age-related macular degeneration group --- p.22 / Chapter 3. --- Retinal detachment group --- p.23 / Chapter 4. --- Peripheral retinal degeneration group --- p.26 / Chapter Chapter4 --- Discussion --- p.44 / References --- p.56

OBJECTIVE To determine whether grading for AMD during a diabetic retinopathy (DR) screening program would be cost-effective in Hong Kong. METHODS A cost-effectiveness analysis based on a Markov model with six mutually exclusive health states was undertaken. It included grading for AMD and treatment with vitamin therapy for those with intermediate AMD. The outcome of the model was cost per quality-adjusted life year (QALY) gained. A public provider perspective was used. The measures of effectiveness were mostly taken from a local DR screening project except the transition probabilities and the utility values which were taken from overseas data. Costs were mainly taken from the Hospital Authority and salary scale 2009. The main assumptions and estimates were tested in sensitivity analyses. In this model, only subjects with non-sight threatening diabetic retinopathy were included and the possibility of disease regression and treatment benefit for those with advanced AMD were not considered. Both costs and benefits were discounted at 3%. RESULTS The cost per QALY gained through grading for AMD at the time of DR screening and treatment with vitamins of appropriate cases was HK$47,397 after discounting. This would be considered highly cost-effective based on the World Health Organization’s threshold of willingness-to-pay (WTP) for a QALY, e.g. less than the annual per capita GDP HK$300,000. One way sensitivity analyses revealed that the cost per QALY was most sensitive to utility value, discount rate, progression rate from intermediate to advanced AMD, and compliance rate for the treatment. The cost-effectiveness acceptability curve showed that at a WTP for a QALY of $100,000 or more, this AMD screening programme has over 90% of probability of being cost-effective compared with no screening. CONCLUSION Our cost-effectiveness analysis demonstrated that grading for AMD at the time of DR screening among diabetic patients would probably be cost-effective in a Hong Kong public hospital setting. / published_or_final_version / Public Health / Master / Master of Public Health

Peripherin, a membrane protein with an apparent molecular weight of 34 kDa, has been previously localized to the rim region of the vertebrate rod photoreceptor disk membrane using monoclonal antibodies and immunocytochemical labelling techniques. As an initial step in determining the structure and function of this protein, cDNA containing its coding sequence has been cloned and sequenced. A bovine retinal ʎgtll expression library was screened with antiperipherin monoclonal antibodies, and a 583 base pair clone was initially isolated. The remaining part of the coding sequence was obtained from subsequent rescreenings of the same library and an independent ʎgt10 library. A C-terminal CNBr fragment of peripherin was purified by immunoaffinity chromatography and reverse phase high-performance liquid chromatography. The amino acid sequence of the isolated C-terminal peptide and the N-terminal sequence analysis of immunoaffinity purified peripherin are in agreement with the cDNA sequence. At the amino acid level, the sequence of peripherin has 92.5% sequence identity to the gene proposed to be responsible for the retinal degeneration slow defect in mice (Travis et al.(1989) Nature 338, 70-73) The differences between the two sequences can be attributed to species differences. The identity of the retinal degeneration slow gene product and its intracellular localization were previously unknown. The cDNA sequence of peripherin predicts that there are possibly four transmembrane domains. On the basis of immunocytochemical studies and sequence analysis, the hydrophilic C-terminal segment containing the antigenic sites for the antiperipherin monoclonal antibodies has been localized on the cytoplasmic side of the disk membrane. There are three consensus sequences for asparagine linked glycosylation. Deglycosylation studies have indicated that at least one of these sites is utilized. The complete coding sequence of peripherin was expressed in COS-1 cells. Western blot analysis of the expressed peripherin suggest that it exists as a homodimer in the absence of a reducing agent. The possible function of peripherin in relation to its primary structure is discussed. / Medicine, Faculty of / Biochemistry and Molecular Biology, Department of / Graduate

Thesis (M.A.)--Boston University / PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you. / Retinitis pigmentosa (RP) is a collection of inherited retinal degenerations that afflicts 50,000- 100,000 people in the United States. The hallmark pathology of RP is apoptosis of photoreceptor cells. Currently there is no treatment for this disease. The equivalent light hypothesis states that some RP mutations cause retinal degeneration by mimicking a continuous phototransduction signal. We tested this hypothesis in transducin knockout (TKO-/-) mice, deficient for the a - subunit of transducin, the heterotrimeric G-protein which mediates light signaling in photoreceptors. Methods: We used light microscopy to compare the retinal morphology of TKO-/- and wild-type (TKO+/+) mice: 1) exposed to continuous bright light, or 2) crossed with mice carrying three different rhodopsin mutations leading to retinal degeneration: A) Proline347Serine (P347S), B) Valine20Giycine, Proline23Histidine, Proline27Leucine (VPP), and C) Lysine296Giutamic acid (K296E). Results: We predicted two types of photoreceptor cell apoptosis: 1) signal-dependent mutants in which degeneration was blocked in the absence of transducin, and 2) signal-independent mutants, not affected by the presence or absence of transducin signaling. To our surprise,we found three classes of retinal degeneration: 1) the VPP triple mutant caused photoreceptor apoptosis, at the same rate, regardless of the presence or absence of a-transducin, 2) the P347S and K296E opsin mutants caused an accelerated rate of degeneration on the TKO -/- background as compared to on the TKO+/+ background, and 3) the damaging effects of continuous light were retarded on the null transducin background. These data support the equivalent light hypothesis as a mechanism for some, but not all forms of retinal degeneration. Thus, the cellular signal that triggers photoreceptor apoptosis can occur either upstream or downstream of transducin signaling. Classifying different types of mutations that lead to photoreceptor cell death will be important for determining effective therapies for different classes of human retinal degeneration. / 2999-01-01

Thesis (Ph. D.)--University of Sydney, 2008. / Title from title screen (viewed 18 June 2008). Submitted in fulfilment of the requirements for the degree of Doctor of Philosophy to the Department of Clinical Ophthalmology and Eye Health, Faculty of Medicine. Degree awarded 2008; thesis submitted 2007. Includes bibliographical references. Also available in print form.