No description available.

No description available.

No description available.

Diss. (sammanfattning) Stockholm : Karol. inst., 2005. / Härtill 4 uppsatser.

Thesis (Ph. D.)--Ohio State University, 2008. / Title from first page of PDF file. Includes bibliographical references (p. 117-129).

The early detection of acquired losses of colour vision can provide the ophthalmologist with a very sensitive indicator of visual dysfunction. As a result we have developed and tested an automated, CRT-based, chromatic discrimination system that allows us to measure acquired colour-vision deficits with great precision. This system, known as the Sussex Gratings Machine, can produce chromatic stimuli in any direction in equal luminance colour space. However, we have found that measurements made along a constant MIL-cone axis (Tritan) or a constant S-cone (Red/Green) confusion axis are most useful. Using this system we have investigated acquired colour vision deficits in diabetes ,. and thyroid eye disease. We have shown that tritan discrimination losses can be used to screen for severe diabetic retinopathy and also to predict those who are likely to develop it within 18 months. We have also confirmed that acquired tritan discrimination losses are a very useful indicator of optic-nerve compression in thyroid eye disease.

published_or_final_version / Molecular Biology / Doctoral / Doctor of Philosophy

Die Frühgeborenenretinopathie (Retinopathia praematurorum (RPM)) ist eine Erkrankung der Netzhaut, die vor allem sehr unreife Frühgeborene betrifft und in ihrem Endstadium zur Erblindung führen kann. Ein gesicherter Risikofaktor für die Entwicklung einer RPM ist die Gabe von hohen Konzentrationen an Sauerstoff nach der Geburt. Gegenstand dieser Arbeit war die Frage, ob nach der Einführung eines Sauerstoffprotokolls 2007 das Auftreten höherer Stadien der RPM reduziert werden konnte. Das Sauerstoffprotokoll hatte zum Ziel die Gabe von inspiratorischem Sauerstoff nach Möglichkeit zu senken und übermäßige Fluktuationen zu vermeiden. Hierfür wurden 268 Frühgeborene mit einem Gestationsalter < 32Wochen bei Geburt, welche in den Jahren von 2005 bis 2006 (pre-Gruppe) und 2008 bis 2009 (post-Gruppe) in der Universitätsklinik Leipzig geboren und einem RPM-Screening unterzogen wurden, verglichen. Es konnte gezeigt werden, dass die Inzidenz der RPM nach 2007 signifikant niedriger war. So erkrankten in der pre-Gruppe 12 von 102 Kinder an einer höhergradigen RPM (>Stadium 3), wohingegen diese Stadien in der post-Gruppe nicht mehr beobachtet wurden. Demzufolge reduzierte sich auch die Notwendigkeit einer Therapie von 7,4 % auf 0 % (jeweils p = 0.0005). In Hinblick auf die Kerndaten wie Gestationsalter, Geburtsgewicht, Körpergröße, sowie dem Auftreten schwerer Begleiterkrankungen wie u.a. der nekrotisierenden Enterokolitis oder der bronchopulmonalen Dysplasie fanden sich keine Unterschiede zwischen den Gruppen. Allerdings wies die post-Gruppe eine höheren Anteil an männlichen Frühgeborenen auf. Die Mortalität zeigte keine signifikante Veränderung nach der Intervention und lag bei 7.8 % in der pre- bzw. 6.6 % in der post-Gruppe (p = 0.81). Die Auswertung der pulsoximetrisch gemessenen Sauerstoffsättigung (SpO2) und der inspiratorischen Sauerstofffraktion (FiO2) zeigte, dass der SpO2 leicht und der FiO2 deutlich reduziert werden konnte. Ein signifikanter Unterschied ergab sich hier jedoch lediglich für den FiO2, insbesondere in den ersten 14 Lebenstagen. Die logistische Regressionsanalyse legt nahe, dass hohe SpO2- und FiO2-Werte sowie das Auftreten von intrakraniellen Blutungen mit schwerwiegenden ROP-Stadien korrelieren. Ein bedachter Umgang in der Sauerstofftherapie Frühgeborenen könnte in der Lage sein das Auftreten der Frühgeborenenretinopathie zu reduzieren ohne eine Erhöhung der Mortalitätsrate zu riskieren.

PURPOSE: Diabetic macular edema (DME) is the most common cause of vision loss in patients with diabetic retinopathy. This study aims to approach diabetic macular edema and diabetic retinopathy as ischemic conditions and explores a potential treatment through hyperoxia. The study measured changes in retinal thickness, visual acuity, and contrast sensitivity in subjects receiving normobaric oxygen. METHODS: Fifty-one patients with diabetic macular edema at Beth Israel Deaconess Medical Center Eye Clinic (Boston, MA) received oxygen via a face mask at 5 liters per minute for 3 hours. Retinal thickness at the central subfield and maximal retinal thickness were measured using optical coherence tomography. Contrast sensitivity, best corrected visual acuity, and intraocular pressure were measured before and after oxygen as well. RESULTS: Macular thickness from diabetic macular edema decreased by an average of 2.09% (p < .05) at the point of maximal thickness, and by 0.88% (p < .05) at the central subfield. Vision also improved by an average of 0.043 LogMAR units (p < .05). Changes in macular thickness and visual acuity were non-significant in healthy control eyes that received oxygen. The results of hyperoxia on contrast sensitivity were indeterminate. CONCLUSIONS: We found that normobaric hyperoxia for 3 hours reduces macular thickness from diabetic macular edema and improves visual acuity. This study offers additional evidence that diabetic macular edema is an ischemic disorder and suggests that oxygen therapy may serve as an alternate or complimentary treatment of DME. / 2020-06-17T00:00:00Z

Vascular complications, in microvessels resulting in nephropathy, retinopathy and neuropathy and in macrovessels resulting in atherosclerosis caused by hyperglycemia contribute greatly to the morbidity and mortality in diabetes mellitus. In the vasculature, the endothelial cells (ECs) are first to be damaged by hyperglycemia due to their unique location as the inner lining of all vessels. There are several mechanisms involved in endothelial injury or dysfunction, however, the degradation of heparan sulfate proteoglycan (HSPG) on the cell surface and in the extra cellular matrix (ECM) is considered to be of importance. Heparanase is believed to degrade heparan sulfate (HS). Our objectives were to determine if heparanase is responsible for endothelial injury and dysfunction in diabetes. <p>To determine if hyperglycemia and heparanase cause endothelial injury, high concentrations of glucose (30mM), mimicking hyperglycemia and optimal doses of heparinase I were used to treat cultured porcine aortic endothelial cells (PAECs). Cell injury was measured by determining live cell number and lactate dehydrogenase (LDH) release. To determine if heparanase is expressed in high glucose treated PAECs, reverse transcriptase polymerase chain reaction (RT-PCR) was used to amplify heparanase mRNA. In addition, heparanase activity was measured by incubating cell lysates with 35S-labelled ECM from cultured bovine corneal ECs, where released radioactive HS was analyzed by Sepharose gel filtration followed by â-scintillation counting. To help understand the mechanism of high glucose injury, heparanase mRNA and activity were also measured in PAECs treated with H2O2 or mannitol to determine if free radical injury or osmolarity caused effects similar to high glucose treatment. As well, high glucose or heparinase I treated PAECs were also treated with heparin (0.5 ìg/ml) and/or insulin (1 U/ml) and/or basic fibroblast growth factor (bFGF, 1 ng/ml) to determine if these compounds protected ECs from injury or inhibited heparanase expression induced by high glucose. p* PAECs injured by high glucose or heparinase I (0.3 U/ml in serum free medium) showed a significantly decreased live cell number and increased LDH release compared to control cells. High glucose or heparinase I treated ECs showed an increase in live cell number and decrease in LDH release when treated with heparin and/or insulin and bFGF. Heparanase mRNA and activity was expressed in PAECs treated with high glucose or H2O2. Heparin and/or insulin, but not bFGF prevented heparanase mRNA expression and activity in high glucose treated PAECs. Mannitol did not induce the upregulation of heparanase mRNA and activity. bFGF showed variable protection in cells treated with high glucose or heparinase I when combined with insulin or heparin. <p> From these results we conclude that hyperglycemia is a main cause of endothelial injury. Heparanase production induced by hyperglycemia is responsible for EC injury and vascular dysfunction likely through the degradation of HS, resulting in increased vascular permeability and detachment of cells from the basement membrane. The mechanism of heparanase upregulation may be related to the formation of reactive oxygen species, but not due to changes in osmolarity. Heparin and/or insulin and bFGF protect cells from injury caused by high glucose or heparinase I. Heparin and/or insulin but not bFGF inhibit heparanase mRNA upregulation induced by high glucose. This study provides new insight into the causes of vascular injury associated with diabetes and suggests possible treatments to reduce endothelial injury.