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Sökning: WFRF:(Bergmanson Jan)

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1.
  • Galichanin, Konstantin, et al. (författare)
  • Evolution of damage in the lens after in vivo close to threshold exposure to UV-B radiation : cytomorphological study of apoptosis
  • 2010
  • Ingår i: Experimental Eye Research. - : Elsevier BV. - 0014-4835 .- 1096-0007. ; 91:3, s. 369-377
  • Tidskriftsartikel (refereegranskat)abstract
    • The purpose of the present study was to investigate cataractogenesis and recovery of lens damage after in vivo close to threshold ultraviolet (UV)-B radiation around 300nm. Eighty six-week-old albino Sprague-Dawley rats were familiarized to a rat restrainer five days prior to exposure. Groups of non-anesthetized rats were exposed unilaterally to 8kJ/m(2) UVR-300nm. The animals were sacrificed at 1, 7, 48 and 336h following exposure. The lenses were extracted for imaging of dark-field lens macro anatomy and measurement of intensity of forward lens light scattering to quantify lens opacities. Three exposed lenses and one non-exposed lens from each time interval were examined with light and transmission electron microscopy (TEM). Macro anatomy and lens light scattering revealed that all contralateral non-exposed lenses were clear. The degree of lens opacity (difference in lens light scattering between exposed and non-exposed lenses) increased during the 336h, reaching a plateau towards the end of the observation period. Light microscopy and TEM demonstrated that apoptotic features appeared in the epithelium already 1h after UVR exposure, and small vacuoles were seen in the outer cortex. Epithelial damage occurs during the first 48h after exposure and is followed by regenerative repair at 336h post-exposure. Apoptotic epithelial cells were phagocytized by adjacent epithelial cells. Cortical fiber cells exhibited increasing damage throughout the observation period without any clear repair after 336h. In conclusion, acute UVR-induced cataract is partly a reversible. Lens epithelium is a primary target for UVR exposure. Damage to cortical fiber cells remained irreversible.
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2.
  • Mathew, Jessica, et al. (författare)
  • Lamellar changes in the keratoconic cornea
  • 2015
  • Ingår i: Acta Ophthalmologica Scandinavica. - : Wiley. - 1395-3907 .- 1600-0420 .- 1755-375X. ; 93:8, s. 767-773
  • Tidskriftsartikel (refereegranskat)
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3.
  • Meyer, Linda, et al. (författare)
  • Ultrastructure of UVR-B-induced cataract and repair visualized with electron microscopy
  • 2014
  • Ingår i: Acta Ophthalmologica. - : Wiley. - 1755-375X .- 1755-3768. ; 92:7, s. 635-643
  • Tidskriftsartikel (refereegranskat)abstract
    • PurposeThe aim of the study is to investigate and visualize the ultrastructure of cataract morphology and repair, after in vivo exposure to double threshold dose UVR-B in the C57BL/6 mouse lens.MethodsTwenty-six-week-old C57BL/6 mice received in vivo double threshold dose (6.4 kJ/m2) UVR-B for 15 min. The radiation output of the UVR-source had λMAX at 302.6 nm. After a latency period of 1, 2, 4 and 8 days following UVR-B exposure, the induced cataract was visualized with electron microscopy techniques. Induced, cataract was quantified as forward lens light scattering. Damage to the lens epithelium and the anterior cortex was investigated with light microscopy in toluidine blue-stained semi-thin sections, transmission electron microscopy (TEM), scanning electron microscopy (SEM) and dark field illumination photography.ResultsUVR-B-exposed lenses developed anterior subcapsular and/or cortical and nuclear cataract after 1 day. Lens light scattering peaked 2 days after exposure. Lens epithelial cell damage was seen in TEM as apoptotic cells, apoptotic bodies, nuclear chromatin condensation, and swollen and disrupted anterior cortex fibres throughout the sections of the whole anterior lens surface. These morphologic changes were also visualized with SEM. Within 8 days, anterior subcapsular cataract was repaired towards the anterior sutures.ConclusionUVR-B exposure of double cataract threshold dose induces a subtotal loss of epithelial cells across the whole anterior surface of the lens. This damage to the epithelium is repaired by epithelial cell movement from the equator towards the lens sutures, thus in retrograde direction to regular epithelial cell differentiation.
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  • Resultat 1-3 av 3

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