The effects of accumulated experience on radiofrequency ablation of accessory pathways

Increasing experience in radiofrequency ablation for accessory pathways appears to reduce the procedure time, radiation time and radiofrequency pulse number, and results in a higher success rate. However, the effect of a learning curve on this procedure from the perspective of location and conduction direction of accessory pathways has not been reported before. The purpose of this study was to determine the effect of accumulated experience on the outcomes of radiofrequency ablation for accessory pathways and on the duration of the procedure parameters by analyzing the results of a dedicated ablation team. The first 512 patients with a single accessory pathway treated in this laboratory were included for analysis of the procedure parameters with respect to locations and conduction directions of accessory pathways. The results showed that the average procedure time, radiation time, and radiofrequency pulse number differed significantly among the different subgroups (left free wall, right free wall, posteroseptal and anteromidseptal location; manifest or concealed conduction). All subgroups except the anteromidseptal pathways showed a significant improvement of the procedure parameters with increased ablation experience. Although the initial rate of improvement was similar among the different subgroups, the rate of improvement in left free wall pathways nearly reached a plateau after 120 ablation procedures. Thus it was concluded that a certain number of ablation procedures was necessary before achievement of a high success rate with shorter procedure and radiation times and a lower radiofrequency pulse number.     

Polypropylene composites. III: Chemical modification of the interphase and its influence on the properties of PP/mica composites

A surface treatment technology was developed for PP/mica composites that produces a diffuse interlayer with excellent adhesion between the components. The interlayer is created by the silane treatment of the filler and the chemical modification of the polymer components, and its polarity gradually decreases from the surface of the filler to the matrix. Properties of the composites depend on the characteristics of the interphase. With changing chemical composition, the characteristics of the interphase change from a thin, rigid layer to a more diffuse, elastic one. Properties of the composites change accordingly, optimum properties are achieved with a thick interlayer ensuring good stress transfer, strength, hardness, acceptable impact properties, and low mold shrinkage.     

An iterative coordinate setup algorithm for airfoil blades inspection

The six-point principle was widely used in blade design to provide a reference coordinate for dimensioning. The coordinate setup for CMM inspection was conventionally done manually. It was not only time-consuming, but also inaccurate. We proposed an algorithm for the coordinate setup of airfoil blades inspection. The datum points were divided into five types based on their locations. A specific algorithm was applied to measure each type of the datum points. A procedure based on 3-2-1 method was developed to establish the coordinate system. The coordinate setup process was formulated as an iterative procedure where an error function was derived to evaluate the convergence of the iteration. Experimental results and practical applications were also provided to demonstrate the feasibility of the proposed algorithm.     

Effect of high intensity drive train stimulation on dispersion of atrial refractoriness: role of autonomic nervous system

OBJECTIVES: This study evaluated the effect of high intensity drive train (S1) stimulation on the atrial effective refractory period (ERP) and its relation to the autonomic nervous system. BACKGROUND: High intensity S1 stimulation was demonstrated to shorten the ventricular ERP and to increase dispersion of refractoriness. These effects may be due to local release of neurotransmitters. The response of the atrium and ventricle to neurotransmitters was different. The effects of high intensity S1 stimulation at the atrial tissue were evaluated. METHODS: Forty patients without structural heart disease were studied. In group 1, 20 patients, the atrial ERP was measured at 0, 7, 14, 21 and 28 mm away from the S1 site under both twice diastolic threshold and high intensity (10 mA) S1 stimulation. The same protocol was repeated after sequential administration of propranolol (0.2 mg/kg body weight) and atropine (0.04 mg/kg). In group 2, the other 20 patients, the atrial ERP was studied at three atrial sites (high lateral right atrium [HLRA], right posterior interatrial septum [RPS] and distal coronary sinus [DCS] with twice diastolic threshold and high intensity S1 stimulation at baseline and after sequential autonomic blockade. The three atrial sites were randomly assigned as the S1 location. RESULTS: In group 1, high intensity S1 stimulation shortened the atrial effective refractory period most prominently at the site of S1: (mean +/- SD) 13.3 +/- 6.4% (p < 0.001), 8.1 +/- 3.8% (p < 0.001), 4.8 +/- 4.3% (p < 0.001), 3.7 +/- 4.7% (p < 0.001) and 0.5 +/- 2.6% at 0, 7, 14, 21 and 28 mm from the S1 site, respectively. The effect of high intensity S1 stimulation was blunted with propranolol and autonomic blockade but persisted after atropine alone. High intensity S1 stimulation also increased dispersion of refractoriness (from 23 +/- 11 ms to 31 +/- 12 ms, p = 0.01), which was eliminated with autonomic blockade. In group 2, high intensity S1 stimulation had similar effects at different locations (ERP shortening of 10.8 +/- 2.7%, 10.8 +/- 2.2% and 12.2 +/- 4.6% at the HLRA, RPS and DCS, respectively). The responses to sequential autonomic blockade were similar to those in group 1. However, high intensity S1 stimulation at HLRA increased dispersion of refractoriness, but at DCS it reduced dispersion of refractoriness. CONCLUSIONS: High intensity S1 stimulation led to local shortening of the atrial ERP and increased dispersion of refractoriness. These effects were blunted with propranolol and autonomic blockade. High intensity S1 stimulation at the HLRA increased dispersion of atrial refractoriness, whereas the same stimulation at the DCS decreased dispersion of atrial refractoriness.     

Induction of cytochrome P450 1A in hamster liver and lung by 6-nitrochrysene

The present study has determined the effect of 6-nitrochrysene (6-NC) on hepatic and pulmonary cytochrome P450 (P450)-dependent monooxygenases using hamsters pretreated with the nitrated polycyclic aromatic hydrocarbon (nitro-PAH) at 5 mg/kg per day for 3 days. Pretreatment with 6-NC elevated serum gamma-glutamyltranspeptidase, lactate dehydrogenase, and bilirubin levels. Liver S9 fractions prepared from controls and hamsters pretreated with 6-NC markedly increased mutagenicity of the nitro-PAH in Salmonella typhimurium tester strains TA98, TA100, and TA102. The pretreatment selectively increased 1-nitropyrene reductase activities of lung cytosol and liver and lung microsomes. Pretreatment with 6-NC resulted in increases of microsomal 7-ethoxyresorufin and methoxyresorufin O-dealkylases activities in liver and lung without affecting the monooxygenase activities in kidney. Immunoblot analysis of microsomal proteins using mouse monoclonal antibody 1-12-3 to rat P450 1A1 revealed that 6-NC induced P450 1A-immunorelated proteins in liver and lung. RNA blot analysis using mouse P450 1A1 cDNA showed that 6-NC increased liver and lung P450 1A mRNA. 6-NC had no effect on the kidney P450 protein and mRNA. The present study demonstrates that the hamster enzymes can support 6-NC metabolic activation and the nitro-PAH induces liver and lung P4501A via a pretranslational mechanism.     

Oxidation of benzo[a]pyrene by recombinant human cytochrome P450 enzymes

The oxidation of benzo[a]pyrene (B[a]P) was examined using reconstituted systems prepared with recombinant human cytochrome P450 (P450) enzymes 1A1, 1A2, 2C8, 2C10, 2E1, and 3A4 and with microsomes prepared from Saccharomyces cerevisiae expressing recombinant human P450s 2C8, 2C9, and 2C18. Products measured by HPLC included the 3- and 9-phenols, the 4,5-, 7,8-, and 9,10-dihydrodiols (detected in the presence of epoxide hydrolase), and products in the polar fraction eluting immediately after the void volume. The most active enzyme in all reactions was P450 1A1. P450 3A4 and P450 1A2 formed appreciable amounts of several of the products, including the 3-phenol. P450 2C enzymes and P450 2E1 formed relatively low amounts of all B[a]P products. Consideration of these patterns along with knowledge of levels of expression of the P450s in human tissues and previous results with microsomes leads to the conclusion that P450 1A1 should dominate the oxidation of B[a]P in tissues where it is present and inducible. In human liver the level of P450 1A1 is low and P450 3A4, P450 2C subfamily enzymes, and P450 1A2 probably all contribute. Of the human P450s considered here, P450 1A2 was the most active hepatic enzyme forming the 7,8-dihydrodiol. 7,8-Benzoflavone stimulated the oxidation of B[a]P by P450 3A4 and inhibited the oxidations catalyzed by P450 1A2. The extent of inhibition of P450 1A1 was less (than with P450 1A2), probably due to the rapid oxidation of 7,8-benzoflavone by P450 1A1. The major 7,8-benzoflavone product appears to be the 5,6-oxide.     

Inhibition of Drug-Metabolizing Enzymes in Mouse Liver by a Water Soluble Fullerene C60

The microsomal cytochrome P450-dependent monooxygenase system is responsible for the metabolism a variety of xenobiotics including drugs and carcinogens. Fullerenol-1 is a water soluble polyhydroxylated C₆₀ derivative synthesized by a sequence of reactions involving the electrophilic attack of nitronium tetrafluoroborate on fullerenes in the presence of organocarboxylic acids. The present study has evaluated the acute toxicity of fullerenol-1 and determined the effects of the C₆₀ compound on the P450-dependent drug-metabolzing activities. Pretreatments with 0.5 and 1.0g/kg fullerenol-1 decreased P450 and cytochrome b₅ contents, and NADPH-cytochrome P450 reductase, as well as drug metabolizing activities toward test substrates benzo[a]pyrene, 7-ethoxycoumarin, aniline, and erythromycin in liver microsomes. Pretreatments with 0.01 and 0.1 g/kg fullerenol-1 had no effect on these monooxygenases. Immunoblotting anlysis of the microsomal proteins revealed that pretreatments with fullerenol-1 did not alter the protein levels of P450s 1A, 2E and 3A. Additions of fullerenol-1 to mouse liver microsomes suppressed monooxygenases activities toward benzo[a]pyrene, 7-ethoxycoumarin, aniline, and erythromycin with IC₅₀ values of 42, 94, 102 and 349 μM, respectively. These results demonstrate that fullerenol-1 can decrease the activities of microsomal drug-metabolizing enzymes in vivo and in vitro. Proper adjustment of the functionalized fullerene compound may facilitate the biomedical application of the new material.