glycolipid/i̇nme

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[Blood glycolipids of patients with cerebral circulatory disorders].

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The paper is concerned with a study of the glycolipid content in the blood of 70 patients with acute disorders of brain circulation and in 14 patients with the initial signs of insufficiency of circulation. It was established that in the plasma and blood cells in patients with ischemic and

Orally administered glycolipid derivative LIGA20 reduces infarct volume and behavioral impairment after focal cerebral ischemia.

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The efficacy of p.o. semisynthetic glycolipid LIGA20 (II3Neu5-AcGgOse4-2-d-erythro-1,3-dihydroxy-2-dichloro-aceta mide-4-trans- octadecene) treatment in stroke was studied in a permanent left middle cerebral artery occlusion model in the rat. A dose-dependent increase of plasma LIGA20 and its

Can we use statins to prevent stroke in Fabry disease?

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Fabry disease is a rare, X-linked lysosomal storage disease caused by an inborn deficiency of alpha-galactosidase A, which results in the progressive accumulation of globotriaosylceramide and other neutral glycolipids in a range of cells and tissues. In association with the renal and cardiac

Effect of diabetes on levels of lipid peroxides and glycolipids in rat brain.

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The effects of diabetes on levels of lipid peroxides and glycolipids in brain were studied in alloxan (18 mg/100 g body weight) diabetic rats. Free fatty acid (FFA) and malondialdehyde (MDA) levels were increased in the brains of diabetic animals. On the other hand, activities of the antioxidative

Infiltration of invariant natural killer T cells occur and accelerate brain infarction in permanent ischemic stroke in mice.

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Invariant natural killer T (iNKT) cells are a unique subset of T cells that have been implicated in inflammation, atopy, autoimmunity, infections, and cancer. Although iNKT cells have been extensively studied over the past decade, its role in the pathogenesis of ischemic brain injury is still

Retraction to: Increased Bone Resorption During the First Year After Stroke

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A novel Gram-stain-positive, aerobic, non-spore-forming, irregular short rod-shaped actinobacterial strain, designated YIM 102482-1^T, was isolated from the faeces of Macaca mulatta. Strain YIM 102482-1^T grew optimally at 30-37 °C, at pH 8.0 and in the presence of

Anderson-Fabry disease: a multiorgan disease.

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Fabry disease (FD) is a rare X-linked lysosomal storage disorder caused by a deficiency of the enzyme α-galactosidase A. FD causes glycolipids, such as globotriaosylceramide (Gb3), to accumulate in the vascular endothelium of several organs (Fig. 2), including the skin, kidneys, nervous system, and

Brain embolic phenomena associated with cardiopulmonary bypass.

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Various biologic and non-biologic materials may be embolized to the brain after the use of cardiopulmonary bypass (CPB) pumps during open heart surgery but their relative frequency and importance are uncertain. Among the nonbiologic materials, Antifoam A, which contains organosilicates and silicon,

[A boy with Fabry disease with the onset at the age of four].

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Fabry disease is an X-linked recessive lysosomal storage disorder caused by a deficiency of α-galactosidase A (GLA). Intracellular accumulation of globotriaosylceramide, the glycolipid substrate of this enzyme, leads to severe painful neuropathy with progressive renal, cardiovascular, and

[Fabry disease: clinic and enzymatic diagnosis of homozygous and heterozygous. New therapeutic prospects].

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Fabry disease is an X-linked recessive lysosomal storage disorder caused by a partial or complete deficiency of alpha-galactosidase A. Intracellular accumulation of globotriaosylceramide, the glycolipid substrate of this enzyme, leads to severe painful neuropathy with progressive renal,

Antibodies to glycosphingolipids in patients with multiple sclerosis and SLE.

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We used a liposome lysis assay to measure antibodies against a panel of glycolipids. Antibodies to one or more compounds were detected in 34 of 46 patients with multiple sclerosis, 19 of 31 patients with systemic lupus erythematosus (SLE), and in the majority of patients with cranial trauma or

Neurological manifestation of Fabry disease--a case report.

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Fabry disease is an X-linked recessive glycolipid storage disease. It is caused by deficiency of the lysosomal enzyme alpha-galactosidase A and leads to the accumulation of the enzyme substrate, globotriasylceramide (Gb3) in many tissues including endothelial cells, pericytes and smooth muscle cells

Fabry disease: raising awareness of the disease among physicians.

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Fabry disease is an X-linked inherited lysosomal disorder due to dysfunctions of the lysosomal enzyme alpha-galactosidase A, causing insufficient breakdown of glycolipids, which are stored in the eyes, kidneys, autonomic nervous system, skin, vessels and cardiovascular system. Manifestations of

Antibodies to glycosphingolipids in patients with multiple sclerosis.

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Antibodies to one or more glycosphingolipids were detected by means of a liposome lysis assay in the sera of 60/81 patients with multiple sclerosis, 24/42 patients with systemic lupus erythematosus and in the majority of patients with cranial trauma or cerebrovascular accidents. Antibodies against

Misdiagnosis of multiple sclerosis in a female heterozygote with Fabry's disease.

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Fabry's disease is an X-linked disorder of enzyme alpha-galactosidase A which leads to an accumulation of the glycolipids in lysosomes in vessels and organs. The disorder is rare with an estimated incidence of 1 in 40,000 and disease occurs more rarely in women than men. Paresthesias, hearing loss,

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