Disease relevance of Fblim1

• These single-cell oils produced no adverse effects in rats when administered in utero and for 90 days at dietary levels resulting in exposures up to 22 or 66 times higher than those expected in infant formulas when extrapolated on the basis of diet composition (g/100 Cal) or intake (g/kg body weight), respectively [1].
• The animals were maintained on a synthetic diet (4.2 Cal/g) and tap water ad lib, and body weight, Lee (obesity) Index, tail length and food and water intake were recorded weekly for 6 weeks [2].
• These results indicate that administration of EAA alone for treatment of renal failure needs high-calorie and low-nitrogen conditions such as Cal/N 600 for avoiding complications [3].
• The BUN was lower and the nutritional index was better in rats infused with EAA compared with those administrated SAA, while severe distortion of plasma amino acid concentration, hyperammonemia, and fatty liver were observed at the Cal/N 300 condition [3].
• Rats with established uremia, by 5/6 nephrectomy, were treated with various isocaloric solutions containing different amount of essential amino acids and histidine (EAA) or standard amino acids (SAA) which were formulated to provide Cal/N ratios of 300, 600, and 900 [3].

High impact information on Fblim1

• A plasmid containing psi Cal cDNA sequences has been constructed, and calcitonin genomic clones have been isolated [4].
• AM were obtained by lung lavage, cultured, and exposed to one or more of the following: PAF, zileuton (5-lipoxygenase inhibitor), Ro 25-4331 (dual PLA2 inhibitor), and either A23187 (Cal) or zymosan [5].
• DESIGN: Eighty-four bilaterally ovariectomized retired breeder female rats were randomized into 12 groups to examine the effects of chronic treatment (10 months) with oral micronized estradiol (0, 0.5, 1, and 2 mg/1,800 Cal), SPEs (0, 72, and 144 mg/1,800 Cal), and all combinations of these doses of estradiol and SPEs on working memory [6].
• In neurons pretreated with Cal plus omegaAgTx, cilnidipine induced a potent inhibition of the N-type current, but was unable to block the residual Ba++ current [7].
• Accordingly, rats were fed for 8 weeks our standard liquid diet containing ethanol (36% of energy) or isocaloric carbohydrates, with either PPC (3 g/1000 Cal) or equivalent amounts of linoleate (as safflower oil) [8].

Anatomical context of Fblim1

• Synaptically evoked extracellular field potentials were obtained from the pyramidal cell layer of the Cal field of rat hippocampus slices [9].
• We also showed that TPA and Cal C treatment had an influence on the subcellular distribution of syndecan-4, but there was no influence on myoblast differentiation [10].

Associations of Fblim1 with chemical compounds

• With ethanol (36% of energy) replacing carbohydrates, 2E1 content increased 10-fold, with a corresponding increase in PNP and MEOS activities, but when carbonyl iron (5 g/1000 Cal) was added, the induction was significantly reduced [8].
• The activation energies for dissociation of cholesterol from this phospholipid were three Cal/mole smaller than those for cholesterol-phosphatidylcholine dissociation, at both concentrations of cholesterol [11].
• We used the PKC activator TPA (12-O-tetradecanoyl phorbol 13-acetate) and the PKC inhibitor Calphostin C (Cal C) [10].
• At all Cal/N, the MRX-III groups showed low levels of blood urea nitrogen and urinary excretion of ammonia and urea nitrogen as compared with the MPR-F groups at the same Cal/N [12].

Analytical, diagnostic and therapeutic context of Fblim1

• Rats with CRF, induced by 7/8 renal ablation, were divided into 6 groups of 8 rats each receiving total parenteral nutrition (TPN) containing MRX-III or MPR-F at a non-protein calorie/nitrogen ratio (Cal/N) of 300, 600 or 900 for 7 d [12].

References