Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetic maculopathy seen in the Philippines, specifically, the associated factors, the various lesions seen on fluorescein angiography, and the visual acuity associated with these lesions were characterized using 127 patients (254 eyes) with diabetic retinopathy based on the fluorescein angiography done at the Eye Referral Center in 1993. Results showed that 116 (91.34%) patients have maculopathy, the majority of which is bilateral (84.25%). Age (p=0.675), sex (p=0.357), hypertension (p=0.742), duration of diabetes (p=0.778) and myopia (p=0.742) were not significantly associated with maculopathy. However, severity of retinopathy (p=0.001) was significantly associated with it. Fluorescein angiographic findings are macular staining (83.86%), perifoveal capillary dropout or macular ischemia (10.76%), and preretinal traction and membrane (5.38%). Microaneurysm (72.65%) is the most common lesion associated with macular staining, followed by capillary leakage (4.04%), cystoid macular edema (3.59%), perifoveal capillary dropout with microaneurysm (2.24%), and capillary with microaneurysm leakage (1.34%). Exudates are associated with microaneurysm, perifoveal capillary dropout or a combination of the two. Vision was found to be marginally statistically different between the normal and maculopathy group (p=0.0505). The worst vision was seen in macular ischemia and preretinal traction and membrane, with mean visual acuity of 0.18 and 0.25, respectively. It is concluded that severity of retinopathy is the only variable significantly associated with maculopathy in this study. Good vision does not necessarily indicate a normal macula. Detailed examination and fluorescein angiography should be carried out, regardless of duration of diabetes.
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PMID:Fluorescein angiographically evident diabetic maculopathy. 1472 62

The authors report the case of a 25-year-old woman who presented unilateral Eales disease associated with biologically confirmed pulmonary tuberculosis. The patient, from a family with a history of tuberculosis, showed a painless and abrupt decrease in visual acuity of the right eye with venous and arterial vasculitis. Fluorescein angiography confirmed the existence of peripheral ischemia and vascular abnormalities. The biological exam showed a positive PPD and the BK was isolated. Antibiotic and corticosteroid drugs were used in the treatment. The clinical, immunopathological and therapeutic aspects of this disease are discussed.
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PMID:[Eales disease and tuberculous allergy]. 1554 76

There is a demand for studying the role of Toxoplasma gondii in cell death seeking aiding prevention of the disease. The neuro-pathological changes in the cerebellum cortex in case of acquired toxoplasmosis had been studied. Adult Balb C mice were infected by intra peritoneal injection of T. gondii RH strain. Immuno-histochemical expression of pro apoptotic marker Bax had been applied in parallel with Hematoxylin and Eosin stain to study the layers of cerebellum cortex. The focal necrosis in the cerebellum was expressed. Necrosis was explained on the basis of hypoxic ischemia resulting from existing vasculitis followed the infection. Purkinje cell layer was markedly affected in the form of disfiguring and focal loss of cells with apoptotic and necrotic changes. Thinning of both the molecular and internal granular layers was recorded morphometricly. Morphometric study reveals non significant change in the ratio between the viable to non viable cells in all cerebellum layers among experimental and control groups though the Purkinje cell layer was mostly affected. Statistical significant changes in depth proportion of molecular layer: Internal granular (ML: IGL) layers was noted in experimental and control group (p=0.05). Bax expression was not coexisting with the result of H & E stained cells. The hypothesis emphasizes that toxoplasmosis resist apoptosis seeking its benefit, and apoptosis followed toxoplasmosis may be due to another protein rather than Bax.
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PMID:Cell death pattern in cerebellum neurons infected with Toxoplasma gondii. 1633 90

An important mechanism underlying cochlear hair cell (HC) susceptibility to hypoxia/ischemia is the influx of Ca(2+). Two main ATP-dependent mechanisms contribute to maintaining low Ca(2+) levels: uptake of Ca(2+) into intracellular stores via smooth endoplasmic reticulum calcium ATPase (SERCA) and extrusion of Ca(2+) via plasma membrane calcium ATPase (PMCA). The effects of the SERCA inhibitors thapsigargin (10 nM-10 microM) and cyclopiazonic acid (CPA; 10-50 microM) and of the PMCA blockers eosin (1.5-10 microM) and o-vanadate (1-5 mM) on inner and outer hair cells (IHCs/OHCs) were examined in normoxia and ischemia using an in vitro model of the newborn rat cochlea. Exposure of the cultures to ischemia resulted in a significant loss of HCs. Thapsigargin and CPA had no effect. Eosin decreased the numbers of IHCs and OHCs by up to 25 % in normoxia and significantly aggravated the ischemia-induced damage to IHCs at 5 and 10 microM and to OHCs at 10 microM. o-Vanadate had no effect on IHC and OHC counts in normoxia, but aggravated the ischemia-induced HC loss in a dose-dependent manner. The effects of eosin and o-vanadate indicate that PMCA has an important role to play in protecting the HCs from ischemic cell death.
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PMID:Effects of SERCA and PMCA inhibitors on the survival of rat cochlear hair cells during ischemia in vitro. 1770 70

The aim of this study was to characterize the molecular and histological changes that occur in the retina following central retinal artery occlusion (CRAO) in a mouse model. CRAO was induced in 60 mice by laser photoactivation of intravenously injected rose bengal. Mice were sacrificed at 3, 6, 12, and 24h and 7 and 21 days after CRAO induction for molecular analysis (5-13 mice/time point) and histological and apoptosis studies (3-4 mice/time point). Fundus examination and fluorescein angiography were also performed at various points. Retinal mRNA was analyzed for expression of T-cell antigen 1 (Thy-1), vascular endothelial growth factor (VEGF), heme oxygenase-1 (HO-1), and hypoxia-induced factor 1 alpha (HIF-1 alpha) using real-time polymerase chain reaction. The results showed that at 6-24h following CRAO induction, the retina was edematous, with interrupted blood perfusion. Fluorescein angiography showed reperfusion at 6h, and TdT-mediated dUTP nick end-labeling (TUNEL) assay revealed an increase in apoptotic cells in the first 24h. On histological sections, nuclear loss in the inner retinal layers was maximal on day 21. Thy-1 expression decreased to 30% of baseline (P<or=0.002). VEGF expression increased in the first 3h and gradually decreased thereafter, reaching 75% of baseline on day 21 (P<or=0.005). HO-1 was upregulated at all time points, with a peak at 12h. No change was noted in HIF-1 alpha expression at any time. In conclusion, CRAO in mice causes cell apoptosis in the inner layers of the retina, with a significant cell loss and a decrease in Thy-1 expression by 21 days. These changes are accompanied by a rise in expression of the ischemia-related protein HO-1 to a peak at 12h, with levels remaining above control values at day 21. Given the similarity of the mouse model to human CRAO, these findings may have implications for the future clinical management of CRAO.
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PMID:Molecular and histological changes following central retinal artery occlusion in a mouse model. 1863 47

A 58-year-old woman with non-proliferative diabetic retinopathy presented with decreased visual acuity from chronic macular edema. She had undergone multiple treatments previously, including focal laser treatment and intravitreal triamcinolone acetonide. Within 2 days of treatment with intravitreal bevacizumab, the patient noted a significant decrease in visual acuity. Fluorescein angiogram demonstrated an enlargement of the foveal avascular zone and persistent late leakage following intravitreal bevacizumab; optical coherence tomography performed before and after treatment revealed persistent cystoid macular edema. The use of intravitreal bevacizumab in chronic, refractory diabetic macular edema may cause acute visual acuity loss by disrupting an already fragile vascular perfusion status, leading to macular ischemia.
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PMID:Acute visual acuity loss following intravitreal bevacizumab for diabetic macular edema. 1920 2

Takayasu disease was first reported in 1908 by Mikito Takayasu as "a case of peculiar changes in the central retinal vessels." Because in these patients the pulse of the radial artery is impalpable, investigations focusing on the ischemic symptoms of the upper body were conducted. In 1948, Shimizu and Sano named this pathological condition "pulseless disease." Since then, the lesions of Takayasu disease have been detected not only in the aortic arch and its main branches but also in various vessels, including the abdominal aorta and renal arteries. The ocular symptoms of Takayasu disease are considered to be due to ischemia in the retina and choroid. The typical wreath-like arteriovenous anastomosis around the disc reported by Takayasu is observed at a relatively late stage of the disease. The characteristic fundus findings of Takayasu disease include tortuosity and dilatation of the central retinal artery and vein, retinal arteriovenous anastomosis, prominent retinal vasculature, microaneurysms in the capillaries, occlusion of retinal arterioles, soft exudate, choked disc, and optic atrophy. Fluorescein angiography reveals retinal microaneurysms, sludging, slower blood flow, dilatation of retinal vessels, leakage of fluorescence dye due to increased vascular permeability, and arteriovenous anastomosis. Arteriovenous anastomosis initially appears in the periphery at the early stage, and in the arteriovenous crossing at the advanced stage. Systemic administration of corticosteroids is required to prevent vascular stenosis during the early stages of Takayasu disease. Reconstruction of the carotid artery may improve subjective symptoms and fundus findings.
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PMID:Takayasu disease on the centenary of its discovery. 1933 90

The association between choroidal neovascularization (CNV) and retinal vein occlusive disease is uncommon. Before the introduction of anti-vascular endothelial growth factor (VEGF) drugs, photodynamic therapy (PDT) was used, with conflicting functional results. We report a case of a 69-year-old male patient who came to our attention for macular edema in hemiretinal vein occlusion. Fluorescein angiogram showed presence of venous collaterals, but the pattern of the edema was atypical; optical coherence tomography (OCT) and indocyanine green angiography (ICG) were used to confirm the diagnosis of CNV. A chorio-retinal shunt was demonstrated. The autofluorescence technique was used to predict the risk of CNV in the fellow eye. PDT was performed twice, but after the second cycle, patient developed choroidal ischemia and the visual outcomes were poor. The temporal course of CNV, the presence of a chorio-retinal shunt, and the autofluorescence pattern in the fellow eye let us to speculate that the CNV was related to the vascular occlusive process. We can speculate that the overexpression of VEGF induced by local ischemia and inflammation can make these patients more likely to have CNV. However, to our knowledge, there are no accurate estimates of the incidence of CNV in other retinal vascular diseases, such as diabetic retinopathy.
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PMID:Subfoveal choroidal neovascularization in a patient with hemicentral vein occlusion. 1943 Jul 31

Monosialotetrahexosy-1 ganglioside (GM1) has been shown to reduce brain damage induced by cerebral ischemia. The objective of this study is to determine whether GM1 is able to ameliorate hyperglycemia-exacerbated ischemic brain damage in hyperglycemia-recruited areas such as the hippocampal CA3 sub regions and the cingulated cortex. Histologic stainings of Haematoxylin and Eosin, Nissl body, the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) and phospho-ERK1/2 were performed on brain sections that have been subjected to 15 min of forebrain ischemia with reperfusion of 0, 1, 3, and 6h in normoglycemic, hyperglycemic and GM1-pretreated hyperglycemic groups. The results showed that GM1 ameliorated ischemic neuronal injuries in the CA3 area and cingulated cortex of the hyperglycemic animals after ischemia and reperfusion. Immunohistochemistry of phospho-ERK1/2 revealed that the neuroprotective effects of GM1 were associated with suppression of phospho-ERK1/2. The results suggest that GM1 attenuates diabetic-augmented ischemic neuronal injuries probably through suppression of ERK1/2 phosphorylation.
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PMID:Monosialotetrahexosy-1 ganglioside attenuates diabetes-enhanced brain damage after transient forebrain ischemia and suppresses phosphorylation of ERK1/2 in the rat brain. 2054 7

Retinal vein occlusions (RVOs) have been defined as retinal vascular disorders characterized by dilatation of the retinal veins with retinal and subretinal hemorrhages and macular edema, and/or retinal ischemia. Fluorescein angiography (FA) remains essential for the diagnosis and prognosis of RVO, allowing recognition of the diverse types of RVO, such as perfused or nonperfused, as well as detection of the different modalities in natural history. F A is the most effective method to determine the presence (or absence) of macular cystoid edema, its extension, persistence, regression, or the degree of ischemia. Spectral domain optical coherence tomography (SD-OCT) helps to quantify the changes in retinal thickness, the amount of cystoid macular edema, and supplies additional information, such as whether the accumulated fluid is located mostly within the retinal layers or additionally in the sub retinal space. SD-OCT can display the presence and integrity of the outer limiting membrane and of the inner and outer segments of the photoreceptors, useful information for prognosis and a guide for treatment in the management of RVO. Laser photocoagulation in a 'grid' pattern over the area, demonstrated as leaking by FA, remains the 'reference treatment for macular edema due to branch retinal vein occlusion', according to the recent results of the SCORE Trial. Recent case series studies and prospective randomized trials strongly suggest an antiedematous effect of intravitreal steroids and an associated improvement in vision. These studies have suggested that intravitreal steroids (triamcinolone, fluocinolone, dexamethasone in a slow-release device) and intravitreal anti-VEGF drugs (bevacizumab, ranibizumab, pegabtanib) may at least temporarily reduce foveal edema and correspondingly improve visual function. Surgical treatment modalities have been reported for RVOs. The positive action of vitrectomy seems durable; the combination of surgery and intravitreal injection of steroids and/or an injection of tissue plasminogen activator could permit a more rapid and lasting action. However, strong data from randomized trials are warranted.
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PMID:Retinal vein occlusions. 2070 46


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