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nicotinic acid/atrofia
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Inflammatory degeneration of joint tissue in adjuvant arthritis after intraarticular treatment with the mixture of silver drug and nicotinic acid.
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Combination intraarticular administration of Poviargol (0.5 mg/kg) and nicotinic acid (1.0 mg/kg) reduced symptoms of local and general inflammation in rats with adjuvant arthritis. We revealed a decrease in morphological signs of inflammatory degeneration of joint tissue and reduction of metabolic
[Injections of nicotinic acid in the treatment of atrophy of the optic nerve and of certain diseases of the fundus oculi].
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[Variations in the hemato-ophthalmic fluid permeability after retrobulbar injection of nicotinic acid in chronic retrobulbar neuritis and in subclinical atrophy of the optic nerves; research with fluorescein test].
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[Latent hyperbilirubinemias elicited by nicotinic acid test among the family of a case of Gilbert's syndrome with a kind of muscle atrophy which is similar to Charcot-Marie-Tooth disease (author's transl)].
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Nicotinic acid in optic atrophy complicating tuberculous meningitis.
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Value of priscol nicotinic acid in optic atrophy following tuberculous meningitis.
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Nicotinic acid impairs assembly of leading edge in glioma cells.
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Malignant glioma is a clinically formidable disease. It commonly leads to death within 5 years after diagnosis. Physicians are often baffled since the inevitable diffuse invasion deteriorates clinical outcomes rapidly. Therefore, cancerous infiltration presents a foremost challenge to all
Nicotinic acid in the management of dyslipidaemia associated with diabetes and metabolic syndrome: a position paper developed by a European Consensus Panel.
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Individuals with type 2 diabetes and metabolic syndrome are at markedly increased risk of cardiovascular morbidity and mortality. The increasing prevalence of both conditions poses a major challenge for clinicians in the 21st century. Both diabetes and metabolic syndrome are associated with a
Niaspan, the prolonged release preparation of nicotinic acid (niacin), the broad-spectrum lipid drug.
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Niacin (nicotinic acid) is the broad-spectrum lipid drug, which lowers the concentration of all atherogenic plasma lipids/lipoproteins and at the same time raises the levels of the protective HDL (high-density lipoprotein). Niaspan is a prolonged release (PR) formulation of niacin, which has
[Nicotinic acid: an unjustly neglected remedy].
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In human organism, the administration of nicotinic acid (niacin) leads to two types of effects. Within the physiological range (approximately = 20 mg/day), niacin has a vitamin-like role as pellagra preventing factor. The pharmacological dosage (approximately 0,5-4,5 g/day) substantially influences
The effects of glyceryl trinitrate and nicotinic acid ointments during cold exposure.
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The aim of the present experimental study was to examine the effects of local application of glyceryl trinitrate and nicotinic acid on the cold-provoked haemodynamic responses, pain and hand dexterity. Ten young healthy volunteers participated in this randomized, cross-over study with three phases
Nicotinic acid: clinical considerations.
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BACKGROUND
Nicotinic acid (NA), the oldest hypolipidemic drug, possesses unique broad-spectrum beneficial effects on lipid profiles. Specifically, NA reduces both triglycerides and low-density lipoprotein cholesterol levels, while significantly increasing high-density lipoprotein cholesterol levels.
Degeneration of an intracellular ion channel in the primate lineage by relaxation of selective constraints.
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Ion channel genes are highly conserved and are rarely degenerated in the primate lineage leading to humans. So far, the only well-characterized ion channel known to be degenerated in primates is the plasma membrane transient receptor potential channel TRPC2, possibly due to changes in the pheromone
Nicotinic acid as therapy for dyslipidemia in non-insulin-dependent diabetes mellitus.
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Recently, nicotinic acid has been recommended as a first-line hypolipidemic drug. To determine the effectiveness of nicotinic acid in dyslipidemic patients with non-insulin-dependent diabetes mellitus, 13 patients were treated in a randomized crossover trial. Patients received either nicotinic acid
Stimulation of nicotinamide adenine dinucleotide biosynthetic pathways delays axonal degeneration after axotomy.
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Axonal degeneration occurs in many neurodegenerative diseases and after traumatic injury and is a self-destructive program independent from programmed cell death. Previous studies demonstrated that overexpression of nicotinamide mononucleotide adenylyltransferase 1 (Nmnat1) or exogenous application
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