dihydroxyacetone/atrophy

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Dihydroxyacetone-induced death is accompanied by advanced glycation endproduct formation in selected proteins of Saccharomyces cerevisiae and Caenorhabditis elegans.

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Advanced glycation endproduct (AGE) formation is an important mechanism for protein deterioration during diabetic complications and ageing. The effects on AGE formation following dihydroxyacetone (DHA) stress were studied in two model organisms, the yeast Saccharomyces cerevisiae and the nematode

Contact dermatitis caused by sunless tanning treatment with dihydroxyacetone in hairless descendants of Mexican hairless dogs.

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Dihydroxyacetone (DHAT) is a color additive that is added to sunless tanning products to produce an artificial tan. Although this agent has been used extensively as safe sunless tanning, no published data are available to judge whether the abuse of DHAT causes a potential hazard to the human skin.

Plasmalogen deficiency in cerebral adrenoleukodystrophy and its modulation by lovastatin.

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In cerebral adrenoleukodystrophy (cALD), an accumulation of very long chain fatty acids stems from a defect of the peroxisomal ALD protein (ALDP) and results in the loss of myelin/oligodendrocytes, induction of inflammatory disease and mental deterioration. In brain white matter of cALD patients, we

Degradation of functional triose phosphate isomerase protein underlies sugarkill pathology.

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Triose phosphate isomerase (TPI) deficiency glycolytic enzymopathy is a progressive neurodegenerative condition that remains poorly understood. The disease is caused exclusively by specific missense mutations affecting the TPI protein and clinically features hemolytic anemia, adult-onset

Neuronal death in cultured murine cortical cells is induced by inhibition of GAPDH and triosephosphate isomerase.

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Polyglutamine-containing proteins expressed in the CAG repeat diseases Huntington's disease and dentatorubralpallidoluyisian atrophy have recently been suggested to inhibit the key glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH). To examine the consequences of GAPDH inhibition

Zellweger syndrome in Saudi Arabia and its distinct features.

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Clinical and laboratory findings of Zellweger syndrome (ZS) patients diagnosed at King Faisal Specialist Hospital and Research Center (KFSH & RC), Riyadh, Saudi Arabia over a period of 10 years are presented in this report. Eleven patients (nine females and two males) from 2 to 4 months old were

Late-onset generalized disorder of peroxisomes.

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We diagnosed a unique peroxisomal disorder in a 32-year-old man with profound mental retardation, mild facial dysmorphism, retinal pigmentary degeneration, seizures, and sensorineural deafness. Although plasma very-long-chain fatty acid profile suggested X-linked adrenoleukodystrophy, marked

A new peroxisomal disease with impaired phytanic and pipecolic acid oxidation.

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Phytanic acid (PA) accumulates in patients with adult Refsum disease (ARD) and with peroxisomal disorders. In three related patients with ARD, PA levels were moderately increased in plasma, whereas phytanic oxidation was severely deficient in the fibroblasts. Two of these patients had a significant

Pemafibrate, a selective PPARα modulator, prevents non-alcoholic steatohepatitis development without reducing the hepatic triglyceride content.

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Non-alcoholic steatohepatitis (NASH) is characterized by macrovesicular steatosis with ballooning degeneration of hepatocytes, diffused lobular inflammation, and fibrosis. PPAR ligands are promising therapeutic agents in NASH; accordingly, we evaluated the effects of the first clinically available

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