Influence of Preflaring on the Accuracy of Length Determination With Four Electronic Apex Locators

Introduction: The aim of this study was to compare the influence of preflaring on the accuracy of 4 electronic apex locators (EALs): Root ZX, Elements Diagnostic Unit and Apex Locator, Mini Apex Locator, and Apex DSP. Methods: Forty extracted teeth were preflared by using S1 and SX ProTaper instruments. The working length was established by reducing 1 mm from the total length (TL). The ability of the EALs to detect precise (-1 mm from TL) and acceptable (-1+/-0.5 mm from TL) measurements in unflared and preflared canals was determined. Results: The precise and acceptable (P/A) readings in unflared canals for Root ZX, Elements Diagnostic Unit and Apex Locator, Mini Apex and Apex DSP were 50%/97.5%, 47.5%/95%, 50%/97.5%, and 45%/67.5%, respectively. For preflared canals, the readings were 75%/97.5%, 55%/95%, 75%/97.5%, and 60%/87.5%, respectively. For precise criteria, the preflared procedure increased the percentage of accurate electronic readings for the Root ZX and the Mini Apex Locator (P < .05). For acceptable criteria, no differences were found among Root ZX, Elements Diagnostic Unit and Apex Locator, and Mini Apex Locator (P > .05). Fisher test indicated the lower accuracy for Apex DSP (P < .05). Conclusions: The Root ZX and the Mini Apex Locator devices increased significantly the precision to determine the real working length after the preflaring procedure. All the EALs showed an acceptable determination of the working length between the ranges of+/-0.5mm except for the Apex DSP device, which had the lowest accuracy. (J Endod 2009;35:1300-1302)

The metamorphosis of lambda-fold 4-wheel systems into lambda-fold 4-cycle systems

A 4-wheel is a simple graph on 5 vertices with 8 edges, formed by taking a 4-cycle and joining a fifth vertex (the centre of the 4-wheel) to each of the other four vertices. A lambda -fold 4-wheel system of order n is an edge-disjoint decomposition of the complete multigraph lambdaK(n) into 4-wheels. Here, with five isolated possible exceptions when lambda = 2, we give necessary and sufficient conditions for a lambda -fold 4-wheel system of order n to be transformed into a lambda -fold Ccyde system of order n by removing the centre vertex from each 4-wheel, and its four adjacent edges (retaining the 4-cycle wheel rim), and reassembling these edges adjacent to wheel centres into 4-cycles.

Twisted sl(3, C)(k)((2)) current algebra: free field representation and screening currents

Motivated by application of twisted current algebra in description of the entropy of Ads(3) black hole, we investigate the simplest twisted current algebra sl(3, c)(k)((2)). Free field representation of the twisted algebra, and the corresponding twisted Sugawara energy-momentum tensor are obtained by using three (beta, gamma) pairs and two scalar fields. Primary fields and two screening currents of the first kind are presented. (C) 2001 Published by Elsevier Science B.V.

Yarrol terrane of the northern New England Fold Belt: forearc or backarc?

The Upper Devonian to Lower Carboniferous volcanosedimentary rocks of the Yarrol terrane of the northern New England Fold Belt have previously been ascribed to a forearc basin setting. New data presented here, however, suggest that the Yarrol terrane developed as a backarc basin during the Middle to early Late Devonian. Based on field studies, we recognise four regionally applicable strati graphic units: (i) a basal, ?Middle to Upper Devonian submarine mafic volcanic suite (Monal volcanic facies association); (ii) the lower Frasnian Lochenbar beds that locally unconformably overlie the Monal volcanic facies association: (iii) the Three Moon Conglomerate (Upper Devonian - Lower Carboniferous): and (iv) the Lower Carboniferous Rockhampton Group characterised by the presence of oolitic limestone. Stratigraphic and compositional differences suggest the Monal volcanic facies association post-dates Middle Devonian silicic-dominated magmatism that was coeval with gold-copper mineralisation at Mt Morgan. The Lochenbar beds, Three Moon Conglomerate and Rockhampton Group represent a near-continuous sedimentary record of volcanism that changed in composition and style from mafic effusive (Late Devonian) to silicic explosive volcanism (Early Carboniferous). Palaeocurrent data from the Three Moon Conglomerate and Rockhampton Group indicate dispersal of sediment to the west and northwest, and are inconsistent with derivation from a volcanic-are source situated to the west (Connors-Auburn Arch). Geochemical data show that the Monal volcanic facies association ranges from tholeiitic subalkaline basalts to calc-alkaline basaltic andesite. Trace and rare-earth element abundances are distinctly MORE-like (e.g, light rare earth element depletion), with only moderate enrichment of the large-ion lithophile elements in some units, and negative Nb anomalies, suggesting a subduction-related signature. Basalts of the Monal volcanic facies association are best described as transitional between calc-alkali basalts and N-MORB. The elevated high field strength element contents (e.g. Zr, Y, Ti) are higher than modern island-are basalts, but comparable to basalts that floor modern backarc basins. This geochemical study, coupled with stratigraphic relationships, suggest that the eruption of backarc basin basalts followed widespread Middle Devonian, extension-related silicic magmatism (e.g. Retreat Batholith, Mt Morgan), and floored the Yarrol terrane. The Monal volcanic facies association thus shows similarities in its tectonic environment to the Lower Permian successions (e.g. Rookwood Volcanics) of the northern New England Fold Belt. These mafic volcanic sequences are interpreted to record two backarc basin-forming periods (Middle - Late Devonian and Late Carboniferous - Early Permian) during the Late Palaeozoic history of the New England Orogen. Silicic-dominated explosive volcanism, occurring extensively across the northern New England Fold Belt in the Early Carboniferous (Varrol terrane, Campwyn Volcanics, Drummond and Burdekin Basins), reflects another period of crustal melting and extension, most likely related to the opening of the Drummond Basin.

Stiffly accurate Runge-Kutta methods for stiff stochastic differential equations

In this paper we discuss implicit methods based on stiffly accurate Runge-Kutta methods and splitting techniques for solving Stratonovich stochastic differential equations (SDEs). Two splitting techniques: the balanced splitting technique and the deterministic splitting technique, are used in this paper. We construct a two-stage implicit Runge-Kutta method with strong order 1.0 which is corrected twice and no update is needed. The stability properties and numerical results show that this approach is suitable for solving stiff SDEs. (C) 2001 Elsevier Science B.V. All rights reserved.

On the intersection problem for 1-factorizations and near 1-factorizations of K-v

The number of 1-factors (near 1-factors) that mu 1-factorizations (near 1-factorizations) of the complete graph K-v, v even (v odd), can have in common, is studied. The problem is completely settled for mu = 2 and mu = 3.

Binding and functional studies with the growth hormone receptor antagonist, B2036-PEG (pegvisomant), reveal effects of pegylation and evidence that it binds to a receptor dimers

GH actions are dependent on receptor dimerization. The GH receptor antagonist, B2036-PEG, has been developed for treating acromegaly. B2036 has mutations in site 1 to enhance receptor binding and in site 2 to block receptor dimerization. Pegylation (B2036-PEG) increases half-life and lowers immunogenicity, but high concentrations are required to control insulin-like growth factor-I levels. We examined antagonist structure and function and the impact of pegylation on biological efficacy. Unpegylated B2036 had a 4.5-fold greater affinity for GH binding protein (GHBP) than GH but similar affinity for membrane receptor. Pegylation substantially reduced membrane binding affinity and receptor antagonism, as assessed by a transcription assay, by 39- and 20-fold, respectively. GHBP reduced antagonist activity of unpegylated B2036 but did not effect antagonism by B2036-PEG. B2036 down-regulated receptors, and membrane binding sites doubled in the presence of dimerization-blocking antibodies, suggesting that B2036 binds to a receptor dimer. It is concluded that the high concentration requirement of B2036-PEG for clinical efficacy relates to pegylation, which decreases binding to membrane receptor but has the advantages of reduced clearance, immunogenicity, and interactions with GHBP. Our studies suggest that B2036 binds to a receptor dimer and induces internalization but not signaling.

Properties and function of KCNQ1 K+ channels isolated from the rectal gland of Squalus acanthias

KCNQ1 (K(V)LQT1) K+ channels play an important role during electrolyte secretion in airways and colon. KCNQ1 was cloned recently from NaCl-secreting shark rectal glands. Here we study. the properties and regulation of the cloned sK(V)LQT1 expressed in Xenopus oocytes and Chinese hamster ovary (CHO) cells and compare the results with those obtained from in vitro perfused rectal gland tubules (RGT). The expression of sKCNQ1 induced voltage-dependent, delayed activated K+ currents, which were augmented by an increase in intracellular cAMP and Ca2+. The chromanol derivatives 293B and 526B potently inhibited sKCNQ1 expressed in oocytes and CHO cells, but had little effect on RGT electrolyte transport. Short-circuit currents in RGT were activated by alkalinization and were decreased by acidification. In CHO cells an alkaline pH activated and an acidic pH inhibited 293B-sensitive KCNQ1 currents. Noise analysis of the cell-attached basolateral membrane of RGT indicated the presence of low-conductance (

Regulation and properties of KCNQ1 (K(v)LQT1) and impact of the cystic fibrosis transmembrane conductance regulator

The K+ channel KCNQ1 (K(V)LQT1) is a voltage-gated K+ channel, coexpressed with regulatory subunits such as KCNE1 (IsK, mink) or KCNE3, depending on the tissue examined. Here, we investigate regulation and properties of human and rat KCNQ1 and the impact of regulators such as KCNE1 and KCNE3. Because the cystic fibrosis transmembrane conductance regulator (CFTR) has also been suggested to regulate KCNQ1 channels we studied the effects of CFTR on KCNQ1 in Xenopus oocytes, Expression of both human and rat KCNQ1 induced time dependent K+ currents that were sensitive to Ba2+ and 293B. Coexpression with KCNE1 delayed voltage activation, while coexpression with KCNE3 accelerated current activation. KCNQ1 currents were activated by an increase in intracellular cAMP, independent of coexpression with KCNE1 or KCNE3. cAMP dependent activation was abolished in N-terminal truncated hKCNQ1 but was still detectable after deletion of a single PKA phosphorylation motif. In the presence but not in the absence of KCNE1 or KCNE3, K+ currents were activated by the Ca2+ ionophore ionomycin. Coexpression of CFTR with either human or rat KCNQ1 had no impact on regulation of KCNQ1 K+ currents by cAMP but slightly shifted the concentration response curve for 293B. Thus, KCNQ1 expressed in Xenopus oocytes is regulated by cAMP and Ca2+ but is not affected by CFTR.

Cloning and function of the rat colonic epithelial K+ channel K(V)LQT1

K(V)LQT1 (K(V)LQ1) is a voltage-gated K+ channel essential for repolarization of the heart action potential that is defective in cardiac arrhythmia. The channel is inhibited by the chromanol 293B, a compound that blocks cAMP-dependent electrolyte secretion in rat and human colon, therefore suggesting expression of a similar type of K+ channel in the colonic epithelium. We now report cloning and expression of K(V)LQT1 from rat colon. Overlapping clones identified by cDNA-library screening were combined to a full length cDNA that shares high sequence homology to K(V)LQT1 cloned from other species. RT-PCR analysis of rat colonic musoca demonstrated expression of K(V)LQT1 in crypt cells and surface epithelium. Expression of rK(V)LQT1 in Xenopus oocytes induced a typical delayed activated K+ current. that was further activated by increase of intracellular cAMP but not Ca2+ and that was blocked by the chromanol 293B. The same compound blocked a basolateral cAMP-activated K+ conductance in the colonic mucosal epithelium and inhibited whole cell K+ currents in patch-clamp experiments on isolated colonic crypts. We conclude that K(V)QT1 is forming an important component of the basolateral cAMP-activated K+ conductance in the colonic epithelium and plays a crucial role in diseases like secretory diarrhea and cystic fibrosis.

Expression and function of colonic epithelial K(v)LQT1 K+ channels

1. K(V)LQT1 (KCNQ1) is a voltage-gated K+ channel essential for repolarization of the heart action potential Defects in ion channels have been demonstrated in cardiac arrhythmia. This channel is inhibited potently by the chromanol 293B, The same compound has been shown to block cAMP-dependent electrolyte secretion in rat and human colon, Therefore, it was suggested that a K+ channel similar to K(V)LQT1 is expressed in the colonic epithelium. 2, In the present paper, expression of K(V)LQT1 and its function in colonic epithelial cells is described. Reverse transcription-polymerase chain reaction analysis of rat colonic mucosa demonstrated expression of K(V)LQT1 in both crypt cells and surface epithelium. When expressed in Xenopus oocytes, K(V)LQT1 induced a typical delayed activated K+ current. 3, As demonstrated, the channel activity could be further activated by increases in intracellular cAMP. These and other data support the concept that K(V)LQT1 is forming a component of the basolateral cAMP-activated Kf conductance in the colonic epithelium.

Heritability and gene-environment interactions for melanocytic nevus density examined in a U.K. adolescent twin study

Risk factors for melanoma include environmental (particularly ultraviolet exposure) and genetic factors. In rare families, susceptibility to melanoma is determined by high penetrance mutations in the genes CDKN2A or CDK4, with more common, less penetrant genes also postulated. A further, potent risk factor for melanoma is the presence of large numbers of melanocytic nevi so that genes controlling nevus phenotype could be such melanoma susceptibility genes. A large Australian study involving twins aged 12 y of predominantly U.K. ancestry showed strong evidence for genetic influence on nevus number and density. We carried out essentially the same study in the U.K. to gain insight into gene-environment interactions for nevi. One hundred and three monozygous (MZ) and 118 dizygous (DZ) twin pairs aged 10-18 y were examined in Yorkshire and Surrey, U.K. Nevus counts were, on average, higher in boys (mean = 98.6) than girls (83.8) (p = 0.009) and higher in Australia (110.4) than in the U.K. (79.2, adjusted to age 12 y, p < 0.0001), and nevus densities were higher on sun-exposed sites (92 per m(2)) than sun-protected sites (58 per m(2)) (p < 0.0001). Correlations in sex and age adjusted nevus density were higher in MZ pairs (0.94, 95% CI 0.92-0.96) than in DZ pairs (0.61, 95%CI 0.49-0.72), were notably similar to those of the Australian study (MZ = 0.94, DZ = 0.60), and were consistent with high heritability (65% in the U.K., 68% in Australia). We conclude that emergence of nevi in adolescents is under strong genetic control, whereas environmental exposures affect the mean number of nevi.