Biomedical subjects

Blanca Rojas

Publications and source records attributed to Blanca Rojas.

8 recordsLinked to original sources

PubMed2006

Alterations in the choroid in hypercholesterolemic rabbits: reversibility after normalization of cholesterol levels.

Endothelial damage in atherosclerosis is characterized by abnormal vascular functionality. Hyperlipidemic patients show alterations in ocular vascularization. However, it is not known whether these alterations are reversible after the lipid profile returns to normal. This study evaluates a rabbit model of hypercholesterolemia, examining the ultrastructural changes in the choroid, and the changes in it after a period of normal blood-cholesterol values induced by a standard diet. Rabbits were divided into three groups: G0, fed a standard diet; G1A, fed a 0.5% cholesterol-enriched diet for 8 months; and G1B, fed a 0.5% cholesterol-enriched diet for 8 months followed by a standard diet for a further 6 months. Eyes were processed for transmission electron microscopy. G1A had a buildup of lipids at the suprachoroidea that compressed the vascular layers, and hypertrophy of endothelial and vascular smooth muscle cells. In G1B there was less lipid accumulation than in G1A, but this was not followed by reversal of the choroidal damage. The suprachoroidea thickness of G1B was still greater than in G0 due to abundant collagen fibers. The intervascular spaces of the choroid had fewer lipids than G1A but more collagen fibers than G0. The large- and medium-sized vessel layers and choriocapillaris were less compressed than in G1A but exhibited basal membrane and endothelial changes similar to those in G1A. Normalization of serum cholesterol levels is not enough to reverse cholesterol-induced vascular damage to the choroid. These choroidal changes could be compatible with a chronic ischemia that could produce retinal degeneration.

Animals↗

PubMed2006

Macroglial and retinal changes in hypercholesterolemic rabbits after normalization of cholesterol levels.

This study evaluates hypercholesterolemic rabbits, examining the retinal changes in Müller cells and astrocytes as well as their variations after a period of normal blood-cholesterol values induced by a standard diet. New Zealand rabbits were divided into three groups: G0, fed a standard diet; G1A, fed a 0.5% cholesterol-enriched diet for 8 months; and G1B, fed as G1A followed by standard diet for 6 months. Eyes were processed for transmission electron microscopy and immunohistochemistry (GFAP). While G1B resembled G0 more than did G1A, they shared alterations with G1A: a) as in G1A, Müller cells were GFAP+, filled spaces left by axonal degeneration, formed glial scars and their nuclei were displaced to the nerve-fibre layer. The area occupied by the astrocytes associated with the nerve-fibre bundles (AANFB) and by perivascular astrocytes (PVA) in G1A and G1B was significantly lower than in controls. However, no significant differences in PVA were found between G1A and G1B. In G1B, type I PVA was absent and replaced by hypertrophic type II cells; b) Bruch's membrane (BM) was thinner in G1B than in G1A; c) the retinal pigment epithelium (RPE) cytoplasm contained fewer lipids in G1B than in G1A; d) in G1A and G1B choriocapillaris and retinal vessel showed alterations with respect to G0; e) cell death and axonal degeneration in the retina were similar in G1A and G1B. The substitution of a hyperlipemic diet by a standard one normalizes blood-lipid levels. However, the persistence of damage at retinal vessels and BM-RPE could trigger chronic ischemia.

Animals↗

PubMed2006

A cholesterol-enriched diet induces ultrastructural changes in retinal and macroglial rabbit cells.

The purpose of this study was to ascertain whether the excess of cholesterol in rabbits induces ultrastructural retinal changes similar to those observed in human age-related macular degeneration (AMD). New Zealand rabbits were divided into two groups: Control (GO; n=10), fed standard diet for 8 months; hypercholesterolemic (G1; n=10), fed with 0.5% cholesterol-enriched diet for 8 months. Eyes were processed for transmission electron microscopy (TEM) and immunohistochemistry (anti-glial fibrillary acidic protein, GPAP). In comparison with GO, G1 exhibited alterations in all the retinal layers that were more intense in areas overlying altered retinal pigment epithelium (RPE). RPE changes showed no preferential location. In G1, Bruch's membrane was thicker as a result particle build-up in the collagen layers; the cytoplasm of RPE showed dense bodies, debris from cell membranes, vacuoles and numerous clumps of lipids; necrosis and apoptosis were detected in different retinal layers; Müller cells and astrocytes were reactive with instances of apoptosis and necrosis; some Müller cells filled up the empty spaces left by degenerated neurons in all retinal layers; some Müller cell nuclei were displaced to the nerve-fiber layer (NFL); epiretinal perivascular astrocytes contained drops of lipids; the NFL had very few astrocytes and the basal membranes of capillaries in the NFL was thicker. Excess cholesterol induces ultrastructural changes in the rabbit retina similar to those in human AMD. Given that lipid intake is most dependent on food composition, dietary regimen could help induce or prevent retinal disease.

Animals↗

PubMed2006

Mooren ulcer: an immunopathologic study.

PURPOSE: To determine the pattern and distribution of mononuclear cells, adhesion, and co-stimulatory molecules in the conjunctiva of patients with Mooren ulcer. METHODS: Conjunctival biopsy specimens were obtained from 6 patients with Mooren ulcer and 6 healthy individuals. Immunohistochemistry was performed on frozen sections of the cryopreserved human conjunctivas using monoclonal antibodies directed against CD1alpha, CD3, CD4, CD8, CD20, CD25, CD57, and CD68 cells; the adhesion molecules E-selectin, vascular cell adhesion molecule-1 (VCAM-1), very late activation-4 (VLA-4), ICAM-1, and LFA-1; and the co-stimulatory molecules CD28, B7-1, B7-2, and CTLA-4. RESULTS: Differences in expression on the conjunctival epithelium from patients with Mooren ulcer and normal subjects were noted only for VCAM-1, VLA-4, ICAM-1, and LFA-1. The ratio of CD4+/CD8+ cells in Mooren ulcer specimens was significantly higher (3.5-fold). However, in the substantia propria, Mooren ulcer specimens revealed significantly increased numbers of CD1alpha+, CD3+, CD4+, CD20+, CD28+, B7-1+, B7-2+, and CD68+ cells. The ratios of CD4+/CD8+ cells and B7-2+/antigen-presenting cells in Mooren ulcer specimens were significantly higher (5-fold). All tested adhesion molecules showed significant up-regulation in the patients' conjunctivas. Mooren ulcer vascular endothelial cells prominently expressed E-selectin, VCAM-1, VLA-4, and ICAM-1 compared with normal conjunctiva. CONCLUSION: The simultaneous presence of multiple types of inflammatory cells, adhesion, and co-stimulatory molecules in Mooren ulcer conjunctiva suggests that their interaction may contribute to a sustained immune activation as at least part of the pathogenic mechanism of this disorder.

Antibodies, Monoclonal↗

PubMed2005

Eosinophil activation in Wegener's granulomatosis: a harbinger of disease progression?

PURPOSE: To investigate the relation between eosinophil activation in tissue from patients with an active, limited form of Wegener's granulomatosis (WG) affecting the eye and subsequent systemic disease activity. METHODS: Analysis of ocular specimens obtained from 10 patients was performed. Sections were probed with antibodies to assess the presence of major basic protein (MBP) and eosinophil cationic protein (ECP). RESULTS: Four of the 10 specimens demonstrated the presence of MBP and ECP. WG progressed to the complete form in two of these patients, who received no or inadequate treatment. The other two, treated with cyclophosphamide for one year, did not progress to the complete form of WG during observation after therapy. CONCLUSIONS: Activated eosinophils in sclera or conjunctiva of patients with ocular limited WG may predict progression to complete WG.

Adult↗

PubMed2004

Schlemm's canal and the collector channels at different developmental stages in the human eye.

We studied Schlemm's canal (SC) and other posttrabecular structures of aqueous humor outflow in eyes from human fetuses (at 24, 26, 33 and 36 weeks of gestation), eyes from normal children (2 months and 8 years old) and normal adult eyes, using mesoscopy/diaphanization and light microscopy. This study points to the presence of a collector canal parallel to the outer wall of SC (the outer collector). At 24 weeks of gestation, the SC was observable throughout the entire circumference (360 degrees) and the anlage of the outer collector was present. At 26 weeks of gestation, the outer collector was still growing. At 33 weeks of gestation, the outer collector was parallel to the SC and had become visible in some sectors. At 36 weeks, the SC and the outer collector were clearly defined and connected by intercanal links. The intrascleral plexus was growing. At 2 months, the deep intrascleral plexus and the episcleral plexus continued to grow, developing by sectors. At 8 years of age, the same structures corresponded to those in adults. The outer collector and the intrascleral plexuses were divided into sectors not greater than 120 degrees.

Adult↗

PubMed2002

Distribution and organization of the nerve fiber and ganglion cells of the human choroid.

Antibodies to the 68, 160 and 200 kD of the neurofilament triplets were used to study the distribution and organization of neuronal structures in the human choroid. Choroidal axons were observed in the suprachoroid and vascular laminae but absent from the choriocapillary layer. Most axons were situated in the suprachoroid. In this layer, there were band-like bundles. The two thickest band-like bundles could constitute the long ciliary nerve, while the rest could constitute short ciliary nerves. These bundles ran through the suprachoroid, branching out on the suprachoroid and the vascular laminae until they reached the ciliary body. In the submacular area of the suprachoroid, the branches of the band-like bundles were so intermingled that they looked like a meshwork. In the vascular layer, the large vessels and their primary branches were accompanied by paravascular axons. Some paravascular axons penetrated the medium-caliber vessel layer and in the submacular area interwove to form a network parallel to the arteriole walls. In addition, perivascular axons were revealed by antibodies to neuropeptides. Choroidal ganglion cells were more numerous in the central choroid, specifically in a circumferential area corresponding to the entrance of the short posterior ciliary arteries and their primary branches, and in the vicinity of the submacular area. These cells presented bipolar and multipolar morphology. The high concentration of innervation in the central human choroid could be necessary to maintain strict blood flow in this zone; thus if required, these neuron structures could induce early vasodilation reflexes at the entrance of the choroidal blood vessels to increase the blood flow.

Adolescent↗

PubMedDate not supplied

Calcium dobesilate attenuates vascular injury and the progression of diabetic retinopathy in streptozotocin-induced diabetic rats.

BACKGROUND: Diabetic retinopathy (DR) is a highly specific vascular complication of type 1 and type 2 diabetes mellitus. Calcium dobesilate (DOBE) has been tested in the treatment of diabetic retinopathy showing a slowdown of the progression of the disease after long-term oral treatment. The aim of this study was to determine the effects of DOBE on vascular and diabetic retinopathy in streptozotocin (STZ) diabetic rats. METHODS: Diabetes was induced in wistar rats by the administration of STZ (60 mg/kg, i.p.). Rats were divided into three groups (n = 30). Group 0 (GO): nondiabetic rats. Group 1 (G1): 14 months of insulin treatment after diabetes development. Group 2 (G2): 14 months of insulin treatment after diabetes development plus DOBE (500 mg/kg/day). At the end of the treatment, vascular reactivity was tested. The study of the vascularization of the retina was performed on wholemounts of trypsin retinal digest preparations and retinal sections. RESULTS: Relaxation induced by acetylcholine decreased in the aorta arteries from diabetic rats but it was restored to control values in the DOBE-treated group (71.8 +/- 4.5%, 53.3 +/- 0.5%, 67.4 +/- 4.6% in group 0, 1 and 2 respectively). DOBE treatment also restored noradrenaline (1.08 +/- 0.05 g, 1.70 +/- 0.08 g, 1.13 +/- 0.05 g in group 0, 1 and 2 respectively) and caffeine-induced contractions. Diabetic state did not cause any alteration in mesenteric arteries. The analysis of the retinal digests showed vascular tortuosity, acellular capillaries, focal accumulations of capillaries and reduction of the number of pericytes in G1. The vascular changes observed in G2 seem to be intermediate between the control and the diabetic rats. CONCLUSIONS: We showed that long-term treatment with DOBE attenuated the progression of diabetic retinopathy and the alterations in vascular reactivity in streptozotocin-induced diabetic rats.

Animals↗