Investigative ophthalmology & visual science
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Invest. Ophthalmol. Vis. Sci. · Jul 2007
Downregulation of endotoxin-induced uveitis by intravitreal injection of vasoactive intestinal Peptide encapsulated in liposomes.
To reestablish the immunosuppressive microenvironment of the eye, disrupted by ocular inflammation during endotoxin-induced uveitis (EIU), by means of intravitreal injection of vasoactive intestinal peptide (VIP) in saline or encapsulated in liposomes, to increase its bioavailability and efficiency. ⋯ VIP was efficient at reducing EIU only when formulated in liposomes, which enhanced its immunosuppressive effect and controlled its delivery to all tissues affected by or involved in ocular inflammation.
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Invest. Ophthalmol. Vis. Sci. · Jun 2007
Expression of Th-1 chemokines and chemokine receptors on the ocular surface of C57BL/6 mice: effects of desiccating stress.
To evaluate the effects of desiccating ocular surface stress on the expression of chemokines and their receptors by the corneal epithelium and conjunctiva of C57BL/6 and BALB/c mice. ⋯ Specific patterns of Th-1 and -2 chemokines and their receptors are induced in the mouse ocular surface by desiccating stress in a strain-related fashion. Desiccating stress potently stimulates the expression of Th-1 cell-attracting chemokines and chemokine receptors on the ocular surface of C57BL/6 mice.
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Invest. Ophthalmol. Vis. Sci. · Jun 2007
Oculomotor control in children who were born very prematurely.
Preterm infants are at increased risk of a variety of cerebral lesions, involving the white matter, cortex, cerebellum, thalamus, and caudate nucleus, many of which could compromise the control of eye movement. Visual problems and disorders of binocularity and alignment have been reported, but little if any quantitative assessment of oculomotor control has been undertaken. The purpose of this study was to extend the initial pilot study and quantitatively examine the control of saccades, smooth pursuit, and antisaccades in children who were born very prematurely. ⋯ Despite the increased risk of cerebral lesions, the control of saccades and pursuit was largely normal in the preterm children, suggesting that pathways at the level of the brain stem were principally intact. However, the preterm children had difficulties with the voluntary control of saccades, particularly in the area of inhibition, which may be indicative of a deficit in the region of the dorsolateral prefrontal cortex. This finding is consistent with other reports in preterm children in whom executive function has been found to be compromised, and both these aspects of behavior are likely to share similar areas of cortical control.
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Invest. Ophthalmol. Vis. Sci. · Jun 2007
A cholinergic agonist attenuates endotoxin-induced uveitis in rats.
Investigation of physiological anti-inflammatory mechanisms can contribute to the treatment of inflammatory disorders. The purpose of the present study was to investigate the effect of nicotine, a selective cholinergic agonist, on endotoxin-induced uveitis (EIU) in rats and the underlying molecular mechanism. ⋯ Nicotine attenuated endotoxin-induced uveitis through directly decreasing the levels of multiple cytokines and chemokines in the aqueous humor, but did not affect the mRNA levels of these factors. The findings suggest that the nicotinic anti-inflammatory pathway may be involved in the pathogenesis of EIU.
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Invest. Ophthalmol. Vis. Sci. · May 2007
Increased sensitivity to light-induced damage in a mouse model of autosomal dominant retinal disease.
To describe a sensitivity to light-induced damage associated with expression of a T17M mutant human rhodopsin (hT17M) transgene in mice, with the goal of minimizing retinal injury during the subretinal delivery of rAAV-mediated gene therapy. ⋯ Expression of a human hT17M mutant rhodopsin transgene in mice is associated with photoreceptor apoptosis in response to moderate exposure to light. This phenotype was not observed in nontransgenic littermates or in mice expressing an hP23H mutant human rhodopsin transgene. The results suggest that elimination of the glycosylation site at N15 is associated with increased sensitivity to light-induced damage.