| 1. |
- Frisén, Lars, 1939
(author)
-
High-pass resolution perimetry: central-field neuroretinal correlates.
- 1995
-
In: Vision research. - 0042-6989. ; 35:2, s. 293-301
-
Journal article (peer-reviewed)abstract
- Minimum angles of resolution (MAR) were measured at 0-10 deg horizontal eccentricity in three normal subjects, using high-pass spatial frequency filtered targets, at four different contrast levels. Results were correlated with recent data on human cone and ganglion cell separations in corresponding retinal locations. MARs and cone separations showed a close proportionality through the origin for all contrast levels. Ganglion cell correlates were more difficult to elucidate as the cell bodies are displaced from their input cones. Taking a functional estimate of the displacement into account, the number of ganglion cells appeared to be large enough to uphold an "effective" distribution that obeys the same proportional relationship to MAR that previously has been demonstrated outside 10 deg. Analysis of the nature of age effects provided support for this model.
|
|
| 2. |
|
|
| 3. |
- Ponjavic, Vesna, et al.
(author)
-
Phenotype variation within a choroideremia family lacking the entire CHM gene
- 1995
-
In: Ophthalmic Genetics. - : Informa UK Limited. - 1744-5094 .- 1381-6810. ; 16:4, s. 143-150
-
Journal article (peer-reviewed)abstract
- A Swedish family with choroideremia and a deletion of the CHM gene has been studied with ophthalmological examination, full-field electro-retinography, and DNA analysis in order to characterize the phenotype of the disease. Although all four patients studied had a complete deletion of the gene, they showed a considerable variability regarding the phenotype, including the electroretinogram tracings. Two of the affected males demonstrated a severe form of choroideremia with low or nondetectable ERG recordings, while the other two affected males showed a less severe phenotype with only a slight reduction of the ERG amplitudes. The variation of the clinical phenotype among family members carrying the same mutation indicates that the severity of choroideremia is not solely a function of the CHM gene.
|
|
| 4. |
|
|
| 5. |
- Thaung, Jörgen, 1965, et al.
(author)
-
The 'light scattering factor'. Importance of stimulus geometry, contrast definition, and adaptation.
- 1995
-
In: Investigative ophthalmology & visual science. - 0146-0404 .- 1552-5783. ; 36:11, s. 2313-7
-
Journal article (peer-reviewed)abstract
- PURPOSE. Paulsson and Sjöstrand have suggested that the light scattering factor (LSF) can be estimated by using the equation: LSF = L/E (M2/M1-1). Here L is the space average luminance of the target, E is the illuminance of the glare source, and M2 and M1 are modulation contrast thresholds in the presence and absence of the glare source. To compensate for change of adaptation. Abrahamsson and Sjöstrand later modified the above equation by introducing a correction factor (CF): LSF = L/E ((CF) (M2/M1-1). The purpose of this study is to analyze the validity of the above equations. METHODS. The importance of stimulus geometry, contrast definition, background luminance, and glare illumination is studied through theoretical analysis and comparison with earlier studies. Stimulus geometry and contrast definition are studied through optical modeling. Adaptation is modeled according to the laws of Weber and DeVries-Rose. RESULTS. The choice of contrast definition may corrupt the result by a factor of 2. At background luminance levels above approximately 10 cd/m2, the Paulsson-Sjöstrand equation agrees well with theory. At lower background levels, the Abrahamsson-Sjöstrand equation is used with correction factors derived from adaptation measurements. Using this equation and earlier published data from glare testing performed at 2 cd/m2, the results are found to be in fair agreement with the light scattering theory. CONCLUSIONS. Glare testing using the Paulsson-Sjöstrand equation is found to be valid as long as the measurements are performed at high luminance levels (above 10 cd/m2), with targets of low spatiotemporal frequencies (e.g., 2 cpd and 1 Hz) and with the use of a properly chosen definition of contrast. At lower luminance levels, the Abrahamsson-Sjöstrand equation may be used with well-derived correction factors.
|
|
| 6. |
- Zhang, Hui, et al.
(author)
-
Increased catalase levels and hypoxanthine-enhanced nitro-blue tetrazolium staining in rat retina after ischemia followed by recirculation
- 1995
-
In: Current Eye Research. - : Informa UK Limited. - 0271-3683 .- 1460-2202. ; 14:1, s. 47-54
-
Journal article (peer-reviewed)abstract
- In the present study, using retinal ischemia as a model, we examined if different periods of ischemia and recirculation influenced the generation of reactive oxygen species, i.e. in hydrogen peroxide generation and nitroblue tetrazolium (NBT) reduction. Ischemia was induced for 30 and 90 min by ligation of the optic nerve with the vessels and recirculation was established by removing the ligature. The rats were sacrificed after 15 min or 3 days of recirculation. The retinas were separated from the pigment epithelium for measurements of catalase activity and examination of NBT staining. Compared to controls, the catalase activity was increased after 30 and 90 min of ischemia followed by 15 min of recirculation, and after 90 min of ischemia followed by 3 days of recirculation. As in controls, NBT staining was observed, both after 30 and 90 min of ischemia followed by 15 min of recirculation, in photoreceptors, in both plexiform layers, in some ganglion and glial cells, and, occasionally, in cells in the inner nuclear layer. Opposite to controls, addition of hypoxanthine to the NBT solution resulted in an increased staining in vessels in the inner nuclear layer in retinas subjected to 30 min of ischemia followed by 3 days of recirculation. The increased catalase activity suggests an increased amount of this free radical scavenger after ischemia followed by short-term and long-term recirculation. The hypoxanthine-enhanced NBT staining of blood vessel walls after ischemia followed by long-term recirculation indicates an activation of xanthine oxidase and an increased production of NBT reductants, some of which may represent oxygen free radicals.
|
|
