Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of (n-3) fatty acids on the postprandial state were investigated by monitoring the alimentary responses to identical test meals fed to adults [n = 11; fasting triacylglycerol (TG) 2.55 +/- 0.24 mmol/L; mean +/- SEM] after a self-selected diet baseline period (BLP) and then after a 6-wk (n-3) fatty acid period (FOP) [ approximately 5.2 g (n-3) fatty acids] and a 6-wk control oil period (COP) administered in random order. Samples were drawn immediately prior to the test meal (time 0) and then hourly from 2 to 6 h postmeal. Postprandial plasma triacylglycerol (TG) and TG-rich lipoprotein (TRL) TG apo B48, and B100 absolute concentrations were significantly lower after FOP than after COP or BLP, while plasma cholesterol was unchanged. Normalizing the results as increments over time 0 eliminated the diet effect on all but plasma TG. Time remained a significant effect for plasma TG, TRL TG, and TRL TC. Finally, only absolute TRL B48 and absolute and incremental plasma TG concentrations displayed significant time-diet interactions. These results suggest that postprandial TRL apo B reductions are likely caused by (n-3) fatty acid suppression of both hepatic and intestinal apoB secretion/synthesis. Altered TRL metabolism, i.e. changes in postprandial TG, cholesterol, apo B48, and increase in LDL particle size, may represent an additional mechanism for the reduced heart disease risk associated with fish [(n-3) fatty acid] consumption.
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PMID:(n-3) fatty acid supplementation in moderately hypertriglyceridemic adults changes postprandial lipid and apolipoprotein B responses to a standardized test meal. 1035 76

The aim of our study was evaluate the clinical outcome of PFO without associated congenital heart disease, in the 1st year of life, in a consecutive series of preterm vs term infants. Out of 178 infants, 83 F/94 M, 49% born preterm, with echo diagnosis of PFO (< 5 mm) by 1 month of age, 122 were controlled at 3 mo, 67 at 6 mo and 30 at 12 mo distance. 23 (12%) had an associated PDA, 11 preterm (6 G.A. <32 w). Closure at f-u GA > 38 > 32 < 38 < 32 3mo 38/122 31% 24/66 35% 11/42 26% 3/14 22% 6mo 38/67 57% 20/35 57% 13/25 52% 5/7 71% 12 m 11/30 37% 5/13 38% 5/15 33% 1/2 50% PFO diameter slightly increased in 2 out of 122 (ga. > 38 w), remained so in 6, and decreased in 108. Only 3/33 children whose PFO was closed at 3rd month control were. <32 wGA. No one was hemodynamically significant. In all right ventricular prevalence both at ECG and Echo normalized by 3 mo of age: 21/23 PDA spontaneously closed by the following control before PFO closure. Our data show that: (1) PFO has no clinical relevance even in the WLGA newborn; (2) Inverse correlation between GA and early closure; (3) PDA was'nt predictive for early closure; (4) Spontaneous closure of ductus was always earlier the the FOP's one. Our data support that even in preterm infants PFO is benign and there is no need for an emotionally expensive and time losing follow-up.
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PMID:[Patency of foramen ovale in fullterm and preterm neonates. A follow-up study]. 1921 2

Fibrodysplasia ossificans progressiva (FOP) is a genetic disorder characterized by progressive heterotopic ossification in soft tissues, such as the skeletal muscles. FOP has been shown to be caused by gain-of-function mutations in activin receptor-like kinase (ALK)-2, which is a type I receptor for bone morphogenetic proteins (BMPs). In the present study, we examined the molecular mechanisms that underlie the activation of intracellular signaling by mutant ALK2. Mutant ALK2 from FOP patients enhanced the activation of intracellular signaling by type II BMP receptors, such as BMPR-II and activin receptor, type II B, whereas that from heart disease patients did not. This enhancement was dependent on the kinase activity of the type II receptors. Substitution mutations at all nine serine and threonine residues in the ALK2 glycine- and serine-rich domain simultaneously inhibited this enhancement by the type II receptors. Of the nine serine and threonine residues in ALK2, T203 was found to be critical for the enhancement by type II receptors. The T203 residue was conserved in all of the BMP type I receptors, and these residues were essential for intracellular signal transduction in response to ligand stimulation. The phosphorylation levels of the mutant ALK2 related to FOP were higher than those of wild-type ALK2 and were further increased by the presence of type II receptors. The phosphorylation levels of ALK2 were greatly reduced in mutants carrying a mutation at T203, even in the presence of type II receptors. These findings suggest that the mutant ALK2 related to FOP is enhanced by BMP type II receptors via the T203-regulated phosphorylation of ALK2.
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PMID:Mutant activin-like kinase 2 in fibrodysplasia ossificans progressiva are activated via T203 by BMP type II receptors. 2535 96