The DRD2 TaqI polymorphism and symptoms of attention deficit hyperactivity disorder.

The relationship of the DRD2 TaqI-A1 allele to hyperactive/impulsive and inattentive symptoms of attention deficit hyperactivity disorder (ADHD) in children and adolescents was examined in a sample of clinic-referred children and their siblings, and control children and their siblings (n = 236). The contribution of genetic dominance and additivity to mean differences among the A2A2, A1A2, and A1A1 genotypes was estimated using structural equation modeling. The effect of genetic additivity was statistically significant for both traits in an analysis of all children.

Dopamine DRD4 receptor polymorphism and attention deficit hyperactivity disorder.

A polymorphism in the dopamine receptor 4 gene (DRD4) has been related to novelty seeking, Tourette's syndrome, and attention deficit hyperactivity disorder (ADHD). The variability is in a 48-bp repeat in exon 3 of the gene (a transmembrane region). This study examined the relation of the 7-repeat (i.

Depolarizing effects of catecholamines in quiescent sheep cardiac Purkinje fibers.

Isoproterenol reversibly depolarizes quiescent sheep cardiac Purkinje fibers, in contrast to its reported hyperpolarizing effect in many excitable tissues. The depolarization is inhibited by drugs that block beta 1-adrenergic receptors. Tetrodotoxin and verapamil have no effect on the isoproterenol-induced depolarization.

Effects of CI-914 in congestive heart failure due to coronary artery disease or idiopathic cardiomyopathy.

The hemodynamic effects of CI-914, a phosphodiesterase inhibitor, were studied in 12 patients with left ventricular (LV) dysfunction who were undergoing diagnostic cardiac catheterization. CI-914 was infused intravenously at a rate of 0.8 to 7.

Direct cardiac and peripheral vascular effects of intracoronary and intravenous nifedipine.

The hemodynamic effects of a new parenteral formulation of nifedipine administered by the intravenous (1 mg) and intracoronary (IC) (0.1 and 0.2 mg) routes were studied in 10 patients with symptomatic coronary artery disease undergoing diagnostic right- and left-sided cardiac catheterization.

Insulin-receptor turnover and down regulation in hepatocytes.

Receptor-mediated degradation of 125I-insulin by hepatocytes was studied to evaluate its role in down-regulation of insulin receptors in liver. The amount of 125I-insulin bound to the cell surface was found to remain relatively constant during times of active insulin degradation over a wide range of insulin concentrations, even in the presence of cycloheximide. This observation, as well as other considerations discussed in the text, suggest that down-regulation of insulin receptors is not an inevitable consequence of receptor-mediated degradation in insulin, but rather represents a distinct metabolic effect of the hormone.

Mode of uptake and degradation of 125I-labelled insulin by isolated hepatocytes and H4 hepatoma cells.

The effects of various agents on the binding and degradation of 125I-labelled insulin by isolated rat hepatocytes and cultured H4 hepatoma cells were studied. Various lysosomotropic agents, including chloroquine, ammonium chloride, and the topical anesthetics, lidocaine and procaine inhibited insulin degradation by H4 hepatoma cells but had little effect on the binding of the hormone. Similarly, tosyl-L-lysyl chloromethyl ketone selectively inhibited the degradation of 125I-labelled insulin by isolated hepatocytes, as did the sulfhydryl reagents, p-hydroxy- and p-chloromercuriphenyl sulfonic acid.

Insulin as a cellular growth regulator.

Previous studies from this laboratory have shown that insulin treatment greatly stimulates liver cell growth in chronically diabetic rats. The effect is striking, being preceded by massive glycogen deposition and water imbibition as well as enchanced RNA and protein synthesis. More recently we have directly confirmed the stimulatory effects of insulin on liver RNA and glycogen synthesis in intact hepatocytes isolated from normal and diabetic rats.

Retention and degradation of 125I-insulin by perfused livers from diabetic rats.

The retention of degradation of insulin by isolated perfused liver have been examined. Noncyclically perfused livers from streptozotocin-diabetic rats retained 25% and degraded 10% of 125I-insulin administered as a 1-min pulse. On gel filtration (Sephadex G50F), the degradation products released into the vascular effluent eluted in the salt peak.

Binding and degradation of 125I-insulin by rat hepatocytes.

The binding and the velocity of degradation of 125I-insulin in the absence or presence of varying concentrations of native procline insulin were studied using isolated rat hepatocytes. At insulin concentrations ranging from 5 X 10(-11) to 10(-6) M, insulin degradation velocity showed a first order dependence on the total concentration of insulin bound at steady state. The overall reaction had an apparent rate constant of 0.