riboflavin/hâlsizlik

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[Use of riboflavin with the purpose of reducing eye fatigue under industrial conditions].

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The Effect of Riboflavin on Corneal Vascularization and Symptoms of Eye Fatigue in R.C.A.F. Personnel.

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Sweet potato acid phosphatase immobilized on glutaraldehyde-activated aminopropyl controlled-pore glass: activation, repeated use and enzyme fatigue.

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Sweet potato acid phosphatase was covalently coupled with glutaraldehyde to aminopropyl controlled-pore glass, and used as a pre-column enzyme reactor. The immobilized enzyme reactor (IMER) was continuously operated using an automated chromatographic detection system we developed. Functional

Riboflavin responsive multiple acyl-CoA dehydrogenation deficiency. Assessment of 3 years of riboflavin treatment.

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A boy with riboflavin-responsive beta-oxidation deficiency (multiple acyl-CoA dehydrogenation deficiency) was assessed clinically and biochemically after 3 years of continuous riboflavin medication. He was diagnosed at the age of three years after an attack of a Reye's syndrome-like disease. During

Established and novel measures of upper limb impairment in children with Charcot-Marie-Tooth disease type 1A and Riboflavin Transporter Deficiency type 2.

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Hand function is a problem in patients with Charcot-Marie-Tooth disease type 1A (CMT1A) and Riboflavin Transporter Deficiency type 2 (RTD2). However, a detailed understanding of upper limb involvement in these conditions is lacking. The aim of this pilot study was to compare hand and upper limb

Determinants of Riboflavin Responsiveness in Multiple Acyl-CoA Dehydrogenase Deficiency.

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Multiple acyl-CoA dehydrogenase (MADD) deficiency, which is a rare metabolic disorder involving electron transport flavoproteins, has a wide array of clinical phenotypes. In this article, we describe 25 patients with MADD deficiency and present the clinical and laboratory

Mitochondrial myopathy with tRNA(Leu(UUR)) mutation and complex I deficiency responsive to riboflavin.

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Deficiency of complex I (reduced nicotinamide adenine dinucleotide dehydrogenase-ubiquinone oxidoreductase) of the mitochondrial respiratory chain may be seen as a pure myopathy or as a neuromuscular disorder at presentation. Efficacy of long- term therapy for these disorders is yet to be

Mitochondrial Myopathy in Follow-up of a Patient With Chronic Fatigue Syndrome.

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Introduction. Symptoms of mitochondrial diseases and chronic fatigue syndrome (CFS) frequently overlap and can easily be mistaken. Methods. We report the case of a patient diagnosed with CFS and during follow-up was finally diagnosed with mitochondrial myopathy by histochemical study of muscle

Vitamin B status in patients with chronic fatigue syndrome.

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Some patients with chronic fatigue syndrome say they benefit from taking vitamin supplements. We assessed functional status for the B vitamins pyridoxine, riboflavin and thiamine in 12 vitamin-untreated CFS patients and in 18 healthy controls matched for age and sex. Vitamin-dependent

Riboflavin responsive mitochondrial myopathy is a new phenotype of dihydrolipoamide dehydrogenase deficiency. The chaperon-like effect of vitamin B2.

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Dihydrolipoamide dehydrogenase (DLD, E3) is a flavoprotein common to pyruvate, α-ketoglutarate and branched-chain α-keto acid dehydrogenases. We found two novel DLD mutations (p.I40Lfs*4; p.G461E) in a 19 year-old patient with lactic acidosis and a complex amino- and organic aciduria consistent with

Metabolic features of chronic fatigue syndrome.

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More than 2 million people in the United States have myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). We performed targeted, broad-spectrum metabolomics to gain insights into the biology of CFS. We studied a total of 84 subjects using these methods. Forty-five subjects (n = 22 men and 23

Recurrent myoglobinuria and deranged acylcarnitines due to a mutation in the mtDNA MT-CO2 gene.

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Mitochondrial myopathies commonly present with exercise intolerance typified by breathlessness and fatigue on exercise. In contrast, exercise-induced rhabdomyolysis and myoglobinuria occur rarely. We present a 43-year-old man with a lifelong history of exercise intolerance associated with myalgia

Lipid Storage Myopathy with Ketonuria: A Case of Fatty Acid Oxidation-Related Myopathy and Encephalopathy due to Multiple Acyl-CoA Dehydrogenase Deficiency.

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Encephalopathy and Myopathy in children of varying ages can be due to variety of causes including Mitochondrial diseases, metabolic diseases like renal tubular acidosis, storage diseases as well as fatty acid oxidation (FAO) disorders. FAO related disorders have variable clinical presentation and

Celecoxib-induced methemoglobinemia.

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OBJECTIVE To report a case of acute methemoglobinemia in a patient treated with celecoxib for osteoarthritis. METHODS A 72-year-old African American man developed an acute confusional state (ACS) one month after receiving celecoxib for osteoarthritis of his knee joints. There was no other

FDG PET/CT of Metabolic Myopathy With Posttreatment Follow-up.

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A 38-year-old woman presented with extreme fatigue and multiple lung nodules. She was referred for a PET/CT, which demonstrated multiple FDG-avid pulmonary nodules and lymph nodes with intense uptake within multiple muscle groups predominantly involving the paraspinal muscles and muscles of

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