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OBJECTIVE
Niacin is a B vitamin well-known for causing vasodilation and flushing. The purpose of this study was to investigate its effect on the retinal vasculature of patients with age-related macular degeneration (AMD).
METHODS
Twelve patients with AMD were enrolled in a double-blind, randomized,
OBJECTIVE
To investigate the effects of niacin on choroidal blood flow in age related macular degeneration (AMD).
METHODS
12 AMD patients with bilateral drusen and visual acuity of 20/40 or better in the study eye received a single oral dose of niacin (six subjects received 500 mg and six received
Neural degeneration is a very complicated process. In spite of all the advancements in the molecular chemistry, there are many unknown aspects of the phenomena of neurodegeneration which need to be put together. It is a common sequela of the conditions of niacin deficiency. Neural degeneration in
We report a case of 56-year-old man, chronic alcoholic, presented to us with progressive weakness in all the four limbs with stiffness and gait disturbance since 1-year associated with cognitive impairment. On examination he had mild confusion, spastic quadriparesis with brisk reflexes, extensor
Several phthalate esters (PhE), used as a plasticizer for numerous plastic devices, induce liver tumors and testicular atrophy, although the precise nature and mechanism for the action of PhE on these organs have remained unclear. We have previously reported that the administration of a large amount
Endothelial cells may play a potential role in cholesterol efflux from peripheral tissues to liver. Cholesterol efflux from cells is essential for activation of the reverse cholesterol transport pathway and cardiovascular health. One of the cholesterol transporters is steroidogenic acute regulatory
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
OBJECTIVE
This study examined whether the increase of adiponectin associated with extended-release (ER) niacin/laropiprant combination attenuates the adverse effect of niacin on glucose and insulin resistance in Hong Kong Chinese patients with dyslipidaemia.
METHODS
Patients (N = 121) were treated
AIM
To evaluate the protective effects of lipoic acid-
niacin (N2L) dimers against blue light (BL)-induced oxidative damage to human retinal pigment epithelium (hRPE) cells
in vitro.hRPE cells were divided into a control group (CG), a BL group, an N2L plus6-Aminonicotinamide (6-AN) is a niacin antagonist, which leads to degeneration of gray matter astrocytes. Metallothionein 1+2 (MT-1+2) are neuroprotective factors in the central nervous system (CNS), and to determine the roles for MT after 6-AN, we have examined transgenic mice overexpressing MT-1
Three experiments were carried out to determine the effects of feeding a niacin-free diet (NFD) to immature quail. The first two experiments demonstrated that the results were influenced by the age of the birds. Birds placed on test at 4 weeks of age (57 g) had reduced growth rates but did not
OBJECTIVE
This retrospective study was designed to assess the effects of the combination of pioglitazone and extended-release niacin on the lipid panel, particularly HDL-cholesterol, when used in patients with type 2 diabetes in an endocrinology specialty practice.
METHODS
The electronic medical
It is well known that niacin deficiency manifests with several psychiatric manifestations. Also historically evidence has accumulated that niacin augmentation can be used for treatment of schizophrenia. However, the etiopathological associations between niacin deficiency and schizophrenia as well as
OBJECTIVE
This review describes niacin's mechanism of action, efficacy in cardiovascular prevention, and safety.
RESULTS
A G-protein-coupled receptor [GPR109A/HM74A, mouse PUMA-G (protein upregulated in macrophages by interferon-gamma)] was found to mediate the antilipolytic effect of niacin via
6-Aminonicotinamide (6-AN), an antagonist of niacin and a potent CNS glio-toxin, selectively caused degeneration of glial cells in the central nervous system (CNS) of rodents. Suckling mice treated with 6-AN developed diarrhea clinically and displayed vacuolated degenerating glial cells in the