ABSTRACT
The aim of this study was to examine the expression of the cytokines and chemokines receptor-3 (CCR3) molecule in endothelial cells and vascular structures in a murine model of corneal neovascularization and in samples of neovascularized human corneas. An immunofluorescence assay using the murine model showed a greater proportion and intensity of CCR3 in the epithelium and corneal subepithelial regions in corneas with neovascularization. In the absence of vascularization, no CCR3 was found. Of the 32 studied tissues, eight were vascularized and 24 were avascular. In the human corneas, vascularized corneas showed positive labeling for CD31 in all the analzedtissues, as well as positive labeling for CCR3. Therefore, all vascularized tissues showed positive coexpression of CCR3 and CD31, whereas none of the avascular corneas showed immunolabeling for either of these receptors. These results suggest that CCR3 could be a possible marker for corneal neovascularization with potential to be a therapeutic target.
Subject(s)
Cornea/metabolism , Corneal Neovascularization/genetics , Gene Expression Regulation , RNA/genetics , Receptors, CCR3/genetics , Animals , Cornea/pathology , Corneal Neovascularization/metabolism , Corneal Neovascularization/pathology , Disease Models, Animal , Humans , Immunohistochemistry , Mice , Mice, Inbred BALB C , Receptors, CCR3/biosynthesisABSTRACT
Resumen Tras la colocación de un filtro de vena cava inferior, hasta un 30% de los pacientes puede desarrollar trombosis, una complicación severa con alta morbimortalidad. Presentamos el caso de una paciente de 84 años con trombosis masiva en la vena cava inferior y sistema venoso de miembros inferiores tras la colocación de un filtro de vena cava inferior.
Abstract After lower vena cava filter placement, up to 30% of patients can develop thrombosis, a severe complication with high morbidity and mortality. We present the case of an 84-year-old patient with massive thrombosis in the inferior vena cava and venous system of the lower limbs after a lower vena cava filter placement.
ABSTRACT
Purpose: Breakdown of the inner blood-retinal barrier (iBRB) occurs in many retinal disorders and may cause retinal edema often responsible for vision loss. Dexamethasone is used in clinical practice to restore iBRB. The aim of this study was to characterize the impact of a surgically induced iBRB breakdown on retinal homeostatic changes due to dystrophin Dp71, aquaporin-4 (AQP4), and Kir4.1 alterations in Müller glial cells (MGC) in a mouse model. The protective effect of dexamethasone was assessed in this model. Moreover, retinal explants were used to control MGC exposure to a hypoosmotic solution containing barium. Methods: Partial lens surgery was performed in C57BL6/J mice. Dystrophin Dp71, AQP4, and Kir4.1 expression was analyzed by quantitative RT-PCR, Western blot, and immunohistochemistry. Twenty-four hours after surgery, mice received a single intravitreal injection of dexamethasone or of vehicle. Results: After partial lens surgery, iBRB permeability increased while Dp71 and AQP4 were downregulated and Kir4.1 was delocalized. These effects were partially prevented by dexamethasone injection. In the retinal explant model, MGC were swollen and Dp71, AQP4, and Kir4.1 were downregulated after exposure to a hypoosmotic solution containing barium, but not in the presence of dexamethasone. Heat shock factor protein 1 (HSF1) was overexpressed in dexamethasone-treated retinas. Conclusions: Partial lens surgery induces iBRB breakdown and molecular changes in MGC, including a downregulation of Dp71 and AQP4 and the delocalization of Kir4.1. Dexamethasone seems to protect retina from these molecular changes by upregulating HSF1.
Subject(s)
Anti-Inflammatory Agents/pharmacology , Blood-Retinal Barrier/drug effects , Dexamethasone/pharmacology , Ependymoglial Cells/drug effects , Retinal Degeneration/drug therapy , Animals , Aquaporin 4/metabolism , Blood-Retinal Barrier/metabolism , Blotting, Western , DNA-Binding Proteins/metabolism , Disease Models, Animal , Dystrophin/metabolism , Ependymoglial Cells/metabolism , Heat Shock Transcription Factors , Immunohistochemistry , Intravitreal Injections , Mice , Mice, Inbred C57BL , Potassium Channels, Inwardly Rectifying/metabolism , Retina/drug effects , Retina/metabolism , Retinal Degeneration/metabolism , Transcription Factors/metabolismSubject(s)
Dark Adaptation , Retinal Cone Photoreceptor Cells , Adaptation, Ocular , Light , Photoreceptor Cells , RetinaABSTRACT
Sight is one of the most important senses that human beings possess. The ocular system is a complex structure equipped with mechanisms that prevent or limit damage caused by physical, chemical, infectious and environmental factors. These mechanisms include a series of anatomical, cellular and humoral factors that have been a matter of study. The cornea is not only the most powerful and important lens of the optical system, but also, it has been involved in many other physiological and pathological processes apart from its refractive nature; the morphological and histological properties of the cornea have been thoroughly studied for the last fifty years; drawing attention in its molecular characteristics of immune response. This paper will review the anatomical and physiological aspects of the cornea, conjunctiva and lacrimal apparatus, as well as the innate immunity at the ocular surface.
ABSTRACT
In 1970, Kindier described the morning glory syndrome. This syndrome is a congenital abnormality of the optic nerve with unilateral presence and very low incidence. It is characterized by an enlarged optical disc, deep excavation, presence of traces of radial glia, and arrangement of retinal vascularization. This report describes the fundoscopic image in a patient with morning glory syndrome.
