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Query: UMLS:C0086543 (cataract)
 29,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anterior segment ischemia changes can occur without detachment of any muscles. The most common cause of such ischemic changes of the anterior segment is the removal of too many rectus muscles in one operation. Twenty dog eyes and eight monkey eyes were subjected to the disinsertion and detachment of various combinations of extraocular muscles. They were sacrificed at intervals from 30 to 90 days. During the observation period, they were observed for gross and slit lamp changes. The enucleated eyes were studied microscopically for signs of ischemic and necrotic changes. Two patients who were studied, observed, and treated for anterior segment ischemia following muscle surgery are described. The changes which occur after muscle surgery are extensive and include corneal edema, cataract, chemosis, corneal changes, decreases in intraocular pressure, decreases in outflow or glaucoma and frank necrosis. The variables which lead to this reaction is described in detail. Also, some unanswered queries, such as the duration of the reaction and the time interval of the reaction after multiple muscle surgeries, are discussed.
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PMID:Production of anterior segment ischemia. 10 21

Anterior segment ischemic changes can occur without detachment of any muscles. The most common cause of such ischemic changes of the anterior segment is the removal of too many rectus muscles in one operation. Twenty dog eyes and eight monkey eyes were subjected to the disinsertion and detachment of various combinations of extraocular muscles. The dogs were sacrificed at intervals from 30 to 90 days. During the observation period, they were observed for gross and slit-lamp changes. The enucleated eyes were studied microscopically for signs of ischemic and necrotic changes. Two patients who were studied, observed, and treated for anterior segment ischemia following muscle surgery are described. The changes which occur after extraocular muscle surgery are extensive and include corneal edema, cataract, chemosis, corneal changes, decreases in intraocular pressure, decreases in outflow or glaucoma, and frank necrosis. The variables which lead to this reaction are described in detail. Also, some unanswered queries, such as the duration of the reaction and the time interval of the reaction after multiple muscle operations are discussed.
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PMID:Production of anterior segment ischemia. 41 49

The frequency of complications after surgical iridectomy in angle-closure glaucoma is normally considered low. In order to estimate the influence of the surgical intervention independent from other factors (such as ischemia caused by angle-closure, progression of glaucomatous disease, medical treatment), 35 eyes that had undergone a prophylactic iridectomy because of acute angle closure of the contralateral eye were investigated retrospectively. The mean follow-up time of the 35 eyes was 6.1 years. None of the prophylactically iridectomized eyes developed angle-closure during follow-up. No significant change in visual acuity was present in the group of patients less than 65 years of age (n = 12). This group had a preoperative visual acuity of 0.85 +/- 0.18 and a visual acuity of 0.81 +/- 0.20 at the last visit. A considerable decrease in visual acuity, however, was found in the group of patients more than 65 years of age (n = 23). This group had a preoperative visual acuity of 0.64 +/- 0.24 and a visual acuity of 0.36 +/- 0.23 at the last visit. Biomicroscopically, one eye (8%) in the age group less than 65 years developed further lens opacity, whereas 15 eyes (65%) in the age group more than 65 years developed further lens opacity. In 2 eyes in the older group a cataract operation was performed. Five eyes developed posterior synechiae; in all of these eyes cataract formation increased. The results indicate that cataract progresses more rapidly after iridectomy if the patients are older.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Long-term results following preventive iridectomy. A retrospective study]. 237 74

Iris neovascularization and neovascular glaucoma were diagnosed in three diabetic patients following neodymium-YAG laser posterior capsulotomy. Each of the patients had previously undergone an uncomplicated extracapsular cataract extraction with insertion of a posterior chamber lens implant. These occurrences are consistent with the hypothesis that the posterior lens capsule may serve as a protective barrier to a diffusible vasoproliferative factor from the vitreous or retina. Both the beneficial optical effects and the potential adverse effects should be carefully considered prior to performing neodymium-YAG laser posterior capsulotomy in diabetic patients or other patients with ischemia in the fundus. Following neodymium-YAG laser posterior capsulotomy, these eyes should be closely followed up for signs of neovascularization and possible panretinal photocoagulation.
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PMID:Neovascular glaucoma following neodymium-YAG laser posterior capsulotomy. 242 63

Lens repair and calcification have been studied in an experimental rabbit model of anterior segment necrosis. Findings were compared with those in a human senile cataractous lens with subcapsular calcification. Rabbit lenses subjected to anterior segment ischemia underwent a repair process similar to that observed in perforating lens injuries. Cellular response included the formation of fibroblast-like cells that covered epithelial defects of the anterior pole. These observations suggest that the lens epithelium can transform into fibroblast-like cells. The calcification process was a non-cell-induced, and the observed mineral was probably nucleating on organic molecules. Elemental analysis demonstrated that crystals contained calcium and phosphorus with a ratio of 2:1. The mineral was probably hydroxyapatite. Since morphological findings in rabbit lenses closely resemble those of the studied cataractous human lens, the rabbit model appears to simulate one type of lens calcification in senile cataract.
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PMID:Human and experimental lens repair and calcification. 302 47

A new digestion chamber was developed which made it possible to isolate 500 islets from the pancreas of one adult rat. The mesh chamber enabled us to remove islets out of the collagenase solution as soon as they are separated from pancreatic tissue. The islet injury due to collagenase was diminished, and the time of warm ischemia during digestion was considerably reduced. With this method it was possible to treat the diabetes successfully in eight of 14 rats. The condition of the remaining six rats was considerably improved, and no animal died due to diabetes during 90 days of surveillance as compared to a 50% death rate in the diabetic control group. A cataract did not occur in any transplanted rat, whereas it was observed in all surviving animals of the diabetic control group. If the complete separation of endocrine and exocrine tissue in a density gradient was abandoned the transplantation results improved significantly.
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PMID:Successful treatment of streptozotocin diabetes of the rat by transplantation of the islets from a single donor pancreas. 621 27

When radial cortical opacities occurred in the lenses of glaucomatous eyes, ocular hypertension soon became normal. Glaucoma operations were not performed on patients over 50 years of age, and medical control or simple lens extraction was adopted. In 86% of the lenses extracted from glaucomatous eyes no medication was necessary to keep normal ocular tension for two years postoperatively. The water content of extracted lens from glaucomatous eyes was always in the lower half compared to water content of nonglaucomatous cataractous lenses. Thus the absence of radial cortical opacities is a cause of senile glaucoma. Three laws of aging in the human body and eye are advocated and hypothesized. Simple glaucoma is caused by an ischemia of Schlemm's canal through bending of the scleral branch of anterior ciliary artery caused by continuous zonular traction. From the cation material assortment of extracted dried lenses, it was found that human senile cataracts including glaucomatous nuclear cataracts had normal membranes except in the final stage. Glaucomatous diffuse cortical opacities also had normal membrane, contrary to the damaged membrane in the swollen lens in the final stage of cortical senile cataract.
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PMID:Nuclear cataract as a cause of senile glaucoma. 725 55

Release of angiogenic factors in response to the ischaemic retina is currently the most favoured hypothesis for the pathogenesis of proliferative diabetic retinopathy. Reducing the stimulus for angiogenesis by destroying the ischaemic retina also forms the basis of the most effective treatment of diabetic retinopathy by photocoagulation. Though ischaemia is undoubtedly important for neovascularization, there is recent evidence which cast doubts on ischemia being the sole mechanism for diabetic retinopathy. Many clinical observations viz. the protective effects of glaucoma, myopia, unilateral carotid stenosis on diabetic retinopathy; and its worsening after cataract extraction are not adequately explained by the present hypothesis. Moreover, the recent in vitro culture studies on retinal pigment epithelial cells have suggested an alternative explanation for the effectiveness of photocoagulation in proliferative diabetic retinopathy. Furthermore, hyperglycemia has been strongly correlated with the incidence and progression of diabetic retinopathy, but has only been indirectly indicted in its pathogenesis. These facts can be integrated into a more plausible hypothesis for the pathogenesis of diabetic retinopathy. It is hypothesized that a relative reduction in intra-ocular pressure caused by persistent or intermittent hyperglycemia may be the missing link that induces certain morphological changes in the retinal pigment epithelium. These changes, in addition to the ischaemic retina, may be important for the pathogenesis of diabetic retinopathy. Such a hypothesis also explains most of the hitherto unexplained features of diabetic retinopathy.
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PMID:Pathogenesis of diabetic retinopathy--the missing link? 750 46

alpha-Lipoic acid, which plays an essential role in mitochondrial dehydrogenase reactions, has recently gained considerable attention as an antioxidant. Lipoate, or its reduced form, dihydrolipoate, reacts with reactive oxygen species such as superoxide radicals, hydroxyl radicals, hypochlorous acid, peroxyl radicals, and singlet oxygen. It also protects membranes by interacting with vitamin C and glutathione, which may in turn recycle vitamin E. In addition to its antioxidant activities, dihydrolipoate may exert prooxidant actions through reduction of iron. alpha-Lipoic acid administration has been shown to be beneficial in a number of oxidative stress models such as ischemia-reperfusion injury, diabetes (both alpha-lipoic acid and dihydrolipoic acid exhibit hydrophobic binding to proteins such as albumin, which can prevent glycation reactions), cataract formation, HIV activation, neurodegeneration, and radiation injury. Furthermore, lipoate can function as a redox regulator of proteins such as myoglobin, prolactin, thioredoxin and NF-kappa B transcription factor. We review the properties of lipoate in terms of (1) reactions with reactive oxygen species; (2) interactions with other antioxidants; (3) beneficial effects in oxidative stress models or clinical conditions.
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PMID:alpha-Lipoic acid as a biological antioxidant. 764 94

Experimental work in our laboratory has confirmed the protective activity of vanadium compounds on hyperglycemia and glycosuria in streptozotocin (STZ) diabetes. Furthermore, diabetic cataract has also been partially prevented. Nevertheless, the combination of a natural antioxidant, vitamin E, with Na3 VO4 has not further enhanced this ameliorating effect. Our experimental approach has been an attempt to block the prooxidant activity of both STZ and vanadate, with the purpose of eliciting the best possible antidiabetic protection. More recently, a lipid soluble synthetic antioxidant U-78517F, a 2-methylaminochroman, has been reported to have a significant protective effect against brain injury and ischemia. This compound inhibits the iron-dependent lipid peroxidation 100 times more effectively than vitamin E. This investigation has introduced a combination of the vanadium compound plus the aforesaid lazaroid, as its (-) enantiomer, U-83836E, in order to improve the insufficient protection when vitamin E was used. For twelve weeks, male Wistar rats, rendered diabetic with STZ, were administered Na3VO4 in drinking water along with the lazaroid carried by the food. Four, eight and twelve weeks after the beginning of the protective treatment, fluid and food intake, diuresis and excreted feces, glycosuria and proteinuria were determined on biological samples obtained in metabolic cages; body weight and glycemia were also recorded. At weeks 6 and 12 of the treatment, the opaqueness of the eye lenses was controlled and registered. At the end of the experiment, circulating glycosylated hemoglobin (HbA1c), fructosamine, N-acetyl-beta-D-glucosaminidase (NAG), and fluorescent peroxides were evaluated. Within the first month of treatment, protection by the combination paralleled that elicited by vanadate alone. At subsequent steps, U-83836E significantly improved the protective effect of vanadate alone on polydipsia and polyuria, but especially on hyperglycemia and glycosuria. The further ameliorating effect of the lazaroid was also observed on HbA1c and NAG, and, most important, on the cataract. In conclusion, these findings demonstrate that the lazaroid U-83836E succeeds in further protecting the most important symptoms of diabetes treated with vanadate, and that this antioxidant acts effectively even when it is administered orally in food, in a non invasive manner.
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PMID:Amelioration of diabetes and cataract by Na3VO4 plus U-83836E in streptozotocin treated rats. 782 6


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