muscular dystrophies/triglyceride

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Applicability of the Protein-lipid Profile and Activity of Lactate Dehydrogenase Isoenzymes for Diagnosing Nutritional Muscular Dystrophy in Calves.

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In calves, hyposelenosis degenerates skeletal muscles in different parts of the body. The extent of damage to muscle cells can be diagnosed by determining the activity of creatine kinase (CK), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH). The aim of this study was

Utility of skinfold thickness measurement in non-ambulatory patients with Duchenne muscular dystrophy.

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Nutritional disorders in Duchenne muscular dystrophy (DMD) worsen the medical condition. In particular, obesity is a serious problem that increases the risk of cardiomyopathy and affects nursing care. However, it is often difficult to evaluate body fatness in the advanced stages of DMD. Skinfold

[Contiguous gene deletion syndrome in Xp21: the association between glycerol kinase deficiency, congenital suprarenal hypoplasia and Duchenne's muscular dystrophy].

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BACKGROUND Complex glycerol kinase (GK) deficiency is a contiguous deletion of genes in Xp21 with loss of the locus for GK, for congenital adrenal hypoplasia (AHC) and/or for Duchenne's muscular dystrophy (DMD). We report the case of a 7-year-old patient with this rare disease. METHODS Our patient

A specific decrease of the fluorescence depolarization of perylene in muscle membranes from mice with muscular dystrophy.

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The microviscosity of erythrocyte membranes and muscle microsomes from age matched 6-week old control mice REJ 129 Dy/Dy, and mice with muscular dystrophy REJ 129 DY/DY has been estimated by measuring the fluorescence depolarization of perylene. There was no difference between the erythrocyte

Alterations in lipid incorporation in Duchenne muscular dystrophy. Studies of fresh and cultured muscle.

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The incorporation of [3H] glycerol into lipids of fresh and cultured skeletal muscle obtained from patients with Duchenne muscular dystrophy (DMD), patients with myotonic dystrophy (My Dyst), controls, and aborted fetuses (10-12 weeks old) was studied. A significant increase of specific

Lipid imaging by gold cluster time-of-flight secondary ion mass spectrometry: application to Duchenne muscular dystrophy.

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Imaging with time-of-flight secondary ion mass spectrometry (TOF-SIMS) has expanded very rapidly with the development of gold cluster ion sources (Au(3+)). It is now possible to acquire ion density maps (ion images) on a tissue section without any treatment and with a lateral resolution of few

The fatty acid composition of various lipid fractions isolated from erythrocytes and blood plasma of patients with Duchenne and congenital myotonic muscular dystrophy.

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Ten lipid fractions, both neutral and phospholipids, were isolateed from erythrocytes of patients with Duchenne and congenital myotonic dystrophy. These fractions were: phosphatidylethanolamine, phosphatidylcholine, phosphatidylserine, sphingomyelin, lysophosphatidylcholine, phosphatidic acid,

Erythrocyte lipids in heterozygous carriers of duchenne muscular dystrophy.

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Erythrocyte membranes from heterozygous carriers of Duchenne muscular dystrophy exhibit a diminished amount of palmitoleic acid when compared to membranes from normal subjects. A similar, but more variable, diminution is observed in the case of patients with this disorder. The change in fatty acid

[Plasma lipids of patients with Duchenne's muscular dystrophy at different stages of the disease].

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Blood plasma lipids were studied in patients with Duchenne's myodystrophy. The authors examined 40 patients, aged 3-16 years suffering from different stages of Duchenne's muscular dystrophy. Lipids and fractional composition of plasma phospholipids were investigated by thin-layer chromatography on

Muscle lipids in Duchenne muscular dystrophy.

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The lipids of muscle and adipose tissue from normal males and of muscle from males with Duchenne muscular dystrophy were investigated. Triglyceride, the major neutral lipid, showed similar fatty acid compositions in all tissues examined. When the phospholipids of dystrophic muscle and of normal

Low intensity, high frequency vibration training to improve musculoskeletal function in a mouse model of Duchenne muscular dystrophy.

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The objective of the study was to determine if low intensity, high frequency vibration training impacted the musculoskeletal system in a mouse model of Duchenne muscular dystrophy, relative to healthy mice. Three-week old wildtype (n = 26) and mdx mice (n = 22) were randomized to non-vibrated or

High prevalence of plasma lipid abnormalities in human and canine Duchenne and Becker muscular dystrophies depicts a new type of primary genetic dyslipidemia

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Background: Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD) are allelic X-linked recessive muscle diseases caused by mutations in the DMD gene, with DMD being the more severe form. We have recently shown that

Increased plasma lipid levels exacerbate muscle pathology in the mdx mouse model of Duchenne muscular dystrophy.

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Duchenne muscular dystrophy (DMD) is caused by loss of dystrophin expression and leads to severe ambulatory and cardiac function decline. However, the dystrophin-deficient mdx murine model of DMD only develops a very mild form of the disease. Our group and others have shown vascular abnormalities in

High resolution NMR based analysis of serum lipids in Duchenne muscular dystrophy patients and its possible diagnostic significance.

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Proton NMR spectroscopic investigations on the lipid extract of the serum of 41 Duchenne muscular dystrophy (DMD) (age, mean +/- SD; 8.0 +/- 3.0 years) patients and 22 healthy subjects (age, mean +/- SD; 9.0 +/- 4.0 years) were performed in the northern Indian population. The concentration of

Angiotensin II receptor blocker losartan exacerbates muscle damage and exhibits weak blood pressure-lowering activity in a dysferlin-null model of Limb-Girdle muscular dystrophy type 2B.

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There is no cure or beneficial management option for Limb-Girdle muscular dystrophy (MD) type 2B (LGMD2B). Losartan, a blood pressure (BP) lowering angiotensin II (AngII) receptor type 1 (ATR1) blocker (ARB) with unique anti-transforming growth factor-β (TGF-β) properties, can protect muscles in

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