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ABSTRACT: Retinal ischemia arises from circulatory failure. As the retinal blood vessels are key organs in circulatory failure, our aim was to study the retinal vasculature separately from the neuroretina to elucidate the role of hypoxia-inducible factor (HIF) 1α and 1β and vascular endothelial growth factor (VEGF) in retinal ischemia. Retinal ischemia was induced in porcine eyes by applying an intraocular pressure, followed by 12 h of reperfusion. HIF-1α mRNA expression was not affected by ischemia, while immunofluorescence staining was higher after ischemia in the neuroretina. HIF-1β immunoreactivity and mRNA expression were unaffected. VEGF protein levels in the vitreous humor and VEGF staining in the neuroretina were more pronounced in eyes subjected to ischemia than in the sham eyes. VEGF may be activated downstream of HIF-1 and is known to stimulate retinal neovascularization, which causes sight-threatening complications. These results emphasize the need for pharmacological treatment to block the HIF and VEGF signaling pathways in retinal ischemia.
Journal of Ocular Biology Diseases and Informatics 01/2010; 3(1):20-9.
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ABSTRACT: Numerous studies have been performed aimed at limiting the extent of retinal injury after ischemia, but there is still no effective pharmacological treatment available. The aim of the present study was to examine the role of tumor necrosis factor (TNF)α and its receptors (TNF-R1 and TNF-R2), especially considering the neuroretina and the retinal vasculature since the retinal blood vessels are key organs in circulatory failure.
Retinal ischemia was induced in pigs by elevating the intraocular pressure to 80 mmHg in one eye, while the other eye served as a control (sham-operated). One hour of ischemia was followed by 5 or 12 h of reperfusion. Retinal circulation was examined in vivo by fundus imaging and fluorescein angiography. TNF-α levels were measured in the vitreous using an angiogenesis antibody array test. The presence and amounts of TNF-α, TNF-R1, and TNF-R2 were investigated in the neuroretina and in the retinal blood vessels, using immunofluorescence staining and real-time PCR techniques.
Fundus imaging showed obstructed blood flow when ischemia was induced, and reperfusion was clearly visualized using fluorescein angiography. Ischemia resulted in elevated levels of TNF-α protein in the vitreous and TNF-α mRNA in the neuroretina. TNF-α immunofluorescence staining was localized to the Müller cells and the outer plexiform layer of the neuroretina. The expression of TNF-R1 and TNF-R2 mRNA was increased in both the neuroretina and retinal arteries following ischemia-reperfusion. Immunofluorescence double staining for TNF-R1 and either smooth muscle actin or 4',6-diamidino-2-phenylindole (DAPI) indicated expression in the cell membranes of the vascular smooth muscle cells. Double staining with TNF-R1 and calbindin showed localization to the horizontal cells in the outer plexiform layer of the neuroretina.
Retinal ischemia results in increased expression of TNF-α and its receptors (TNF-R1 and TNF-R2). Cellular signaling pathways involving TNF may be important in the development of retinal injury following ischemia and thus an interesting target for future development of pharmacological therapeutics.
Molecular vision 01/2010; 16:2317-27. · 2.20 Impact Factor
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ABSTRACT: The aim of the present study was to examine changes in the expression of intracellular signal-transduction pathways, specifically mitogen-activated protein kinases, following retinal ischemia-reperfusion.
Retinal ischemia was induced by elevating the intraocular pressure in porcine eyes, followed by 5, 12, or 20 h of reperfusion. The results were compared to those of the sham- operated fellow eye. The retinal arteries and neuroretina were isolated separately and examined. Tissue morphology and DNA fragmentation were studied using histology. Extracellular signal-regulated kinase 1 and 2 (ERK1/2), p38, c-junNH(2)-terminal kinases (JNK), and c-jun protein and mRNA expression were examined using immunofluorescence staining, western blot, and real-time PCR techniques.
Pyknotic cell nuclei, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive cells, and glial fibrillary acidic protein mRNA expression were increased in ischemia, suggesting injury. Phosphorylated ERK1/2 protein levels were increased in the neuroretina following ischemia, while mRNA levels were unaltered. p38 protein and mRNA levels were not affected by ischemia. Immunofluorescence staining for phosphorylated p38 was especially intense in the retinal blood vessels, while only weak in the neuroretina. Phosphorylated JNK protein and mRNA were slightly decreased in ischemia. Phosphorylated c-jun protein and mRNA levels were higher in the neuroretina after ischemia-reperfusion.
Retinal ischemia-reperfusion alters expression of mitogen-activated protein kinases, particularly ERK1/2, in the neuroretina and retinal arteries. The development of pharmacological treatment targeting these intracellular transduction pathways may prevent injury to the eye following retinal circulatory failure.
Molecular vision 01/2010; 16:392-407. · 2.20 Impact Factor
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ABSTRACT: This article presents data from an on-going project comparing L1 and L2 acquisition of Swedish syntax. Within the L1 group, normal as well as specifically language impaired (SLI) children are included; the L2 group consists of pre-school immigrant children. The analyses of the data are made within a second language acquisition perspective with a focus on word order. One basic issue within second language acquisition research is the question of natural developmental sequences, i.e. do all learners follow the same development? Another important issue is whether the development in L2 acquisition is the same as or different from L1 acquisition. Both issues are addressed in the study. The results show interesting similarities between the SLI group and the L2 group. The L1 group differed from the other two groups in important ways. The findings suggest that there is no fundamental difference between L1 and L2 acquisition of syntax, as has been claimed.
International Journal of Applied Linguistics 04/2007; 3(2):131 - 155.
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ABSTRACT: There is a need for studies on bilingual language acquisition in combination with language impairment (LI). The speech and language clinician must have tools to differentiate between problems depending on inadequate exposure to a language and problems depending on a LI. Another important issue is the pace of bilingual language acquisition relative to the severity of LI.
To investigate grammatical development over 12 months in both languages in 10 Swedish-Arabic pre-school children with severe LI and 10 Swedish-Arabic pre-school children without LI.
The children were matched for age, gender, exposure to Swedish dialect, and exposure to Arabic dialect. The developmental hierarchy predicted by Processability Theory was used in tests in both Swedish and Arabic. Processability Theory was used as a yardstick to measure grammatical development in both languages.
Bilingual children, both with and without LI, developed grammatical structures in Swedish and Arabic in the same implicational way. Children with severe LI could develop two languages, although the pace of development was much slower in both languages. Bilingual children with severe LI were also more vulnerable to limited exposure of both their languages.
A developmental perspective is important to understand the nature of LI in bilingual children. The results also have implications for the assessment of language development in bilingual children with severe LI, since a hardly perceptible development over time is observed.
International Journal of Language & Communication Disorders 39(1):65-90. · 1.95 Impact Factor
