Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.73 (urokinase-type plasminogen activator)
10,685 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We treated 14 consecutive patients for acute central retinal artery occlusion. Eleven were treated with urokinase introduced through a microcatheter in the proximal segment of the ophthalmic artery. Fibrinolysis was succeeded by heparinization for two to three days. Instead of urokinase, we used tissue plasminogen activator in three patients. Vision improved markedly in four of the 14 patients. Five others had slight improvement of visual acuity, visual field, or both. In five patients, no change occurred. Such a recovery of visual acuity may be anticipated if treatment begins within the first few hours after the onset of central retinal artery occlusion. A control group of 41 consecutive patients treated conservatively showed almost no improvement in visual acuity. Eleven of these 41 patients were treated within the first six hours after the patient noticed the onset of blindness.
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PMID:Microcatheter urokinase infusion in central retinal artery occlusion. 155 18

We report a case of blindness due to occlusion of the ophthalmic artery following injection of autologous fat into the glabellar region for cosmetic surgery. A 30-year-old woman underwent aspiration of autologous fat from her gluteal region and injection of it into her breasts, nose, and glabellar area. At the time of injection into the glabellar area, she suffered nausea, pain, and visual loss in her right eye. She consulted an ophthalmologist. The first examination revealed that her right eye had loss of light perception, widespread retinal whitening, and obstruction of the retinal vessels of the fundus. It was suspected that she had occlusion of the central retinal artery, and drip infusion of urokinase and hyperbaric oxygen therapy were implemented. Since no improvement was seen, she was referred to Shinshu University hospital. Fundoscopy showed remarkable edema of the entire right retina and whitened retinal vessels. Fluorescein angiography showed no filling of the right retinal arterioles. Cerebral angiography showed complete obstruction of the right ophthalmic artery at its bifurcation. Subsequent administration of urokinase and corticosteroid had no effect. We considered that occlusion of the ophthalmic artery happened when autologous fat was injected into the glabellar area.
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PMID:[A case of ophthalmic artery obstruction following autologous fat injection in the glabellar area]. 1730 92

A 46-year-old man with a history of the left retinal central artery obstruction and old cerebral infarction in the right middle cerebral artery region presented with right total blindness due to the right retinal central artery occlusion accompanied by a cherry red spot. He had been found to have a giant, 17 mm-in-diameter aneurysm of the right internal carotid artery and a right vertebral arterial aneurysm. The intra-arterial thrombolysis was performed with urokinase injection for the right eye artery origin, and the right eyesight has improved. Cranial and pelvic angiography showed multiple stenosis and dilatation of external carotid and internal iliac arteries. The right superficial temporal artery biopsy revealed the arteritis with fibrinoid necrosis. He was diagnosed as having polyarteritis nodosa (PAN) by clinical course, angiography, and the superficial temporal artery biopsy. Several studies have reported that PAN had less intracranial aneurysm and the diameter of the aneurysm was less than 5 mm. Our case is the first report that PAN had giant aneurysm of 17 mm, diagnosed by temporal artery biopsy. The temporal artery biopsy should be considered to diagnose PAN.
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PMID:[A case of polyarteritis nodosa with giant intracranial aneurysm]. 2378 23

Age-related macular degeneration (AMD) is the leading cause of permanent, irreversible, central blindness (scotoma in the central visual field that makes reading and writing impossible, stereoscopic vision, recognition of colors and details) in patients over the age of 50 years in European and North America countries, and an important role is attributed to disorders in the regulation of the extracellular matrix (ECM). The main aim of this article is to present the crucial processes that occur on the level of Bruch's membrane, with special consideration of the metalloproteinase substrates, metalloproteinase, and tissue inhibitor of metalloproteinase (TIMP). A comprehensive review of the literature was performed through MEDLINE and PubMed searches, covering the years 2005-2012, using the following keywords: AMD, extracellular matrix, metalloproteinases, tissue inhibitors of metalloproteinases, Bruch's membrane, collagen, elastin. In the pathogenesis of AMD, a significant role is played by collagen type I and type IV; elastin; fibulin-3, -5, and -6; matrix metalloproteinase (MMP)-2, MMP-9, MMP-14, and MMP-1; and TIMP-3. Other important mechanisms include: ARMS2 and HTR1 proteins, the complement system, the urokinase plasminogen activator system, and pro-renin receptor activation. Continuous rebuilding of the extracellular matrix occurs in both early and advanced AMD, simultaneously with the dysfunction of retinal pigment epithelium (RPE) cells and endothelial cells. The pathological degradation or accumulation of ECM structural components are caused by impairment or hyperactivity of specific MMPs/TIMPs complexes, and is also endangered by the influence of other mechanisms connected with both genetic and environmental factors.
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PMID:Age-related macular degeneration and changes in the extracellular matrix. 2493 26