Effects of Two-Phase Treatment with the Herbst and Preadjusted Edgewise Appliances on the Upper Airway Dimensions

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A double-track greedy channel routing algorithm

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A New Optimization Cost Model for VLSI Standard Cell Placement

In this paper, we propose a new optimization cost model for VLSI placement. It distinguishes itself from the traditional wire-length cost model by having direct impact on the quality of the detailed routing phase. We also extend the well-known simulated annealing standard cell placement algorithm by applying our new cost model. Experimental results show that we got 13% layout area reduction compared to traditional wire length model, 11% reduction to commercial tool.published_or_final_versio

How ESP can we get in the new curriculum

postprintThe 2010 ELC Symposium on "The Challenges of the 4-year Curriculum for English Language Centres in Hong Kong", The Hong Kong Polytechnic University, Hong Kong, 2 June 2010

PMCA4 (ATP2B4) mutation in familial spastic paraplegia causes delay in intracellular calcium extrusion

Background: Familial spastic paraplegia (FSP) is a heterogeneous group of disorders characterized primarily by progressive lower limb spasticity and weakness. More than 50 disease loci have been described with different modes of inheritance. Recently, we described a novel missense mutation (c.803G>A, p.R268Q) in the plasma membrane calcium ATPase (PMCA4, or ATP2B4) gene in a Chinese family with autosomal dominant FSP. Further to this finding, here we describe the functional effect of this mutation. Methods: As PMCA4 removes cytosolic calcium, we measured transient changes and the time-dependent decay of cytosolic calcium level as visualized by using fura-2 fluorescent dye with confocal microscopy in human SH-SY5Y neuroblastoma cells overexpressing either wild-type or R268Q mutant PMCA4. Results: Overexpressing both wild-type and R268Q PMCA4 significantly reduced maximum calcium surge after KCl-induced depolarization as compared with vector control cells. However, cells overexpressing mutant PMCA4 protein demonstrated significantly higher level of calcium surge when compared with wild-type. Furthermore, the steady-state cytosolic calcium concentration in these mutant cells remained markedly higher than the wild-type after SERCA inhibition by thapsigargin. Conclusion: Our result showed that p.R268Q mutation in PMCA4 resulted in functional changes in calcium homeostasis in human neuronal cells. This suggests that calcium dysregulation may be associated with the pathogenesis of FSP. © 2015 The Authors. Brain and Behavior published by Wiley Periodicals, Inc.published_or_final_versio

Improvement of Myocardial Function Following Catheter-Based Renal Denervation in Heart Failure

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Assessment of Cellular Estrogenic Activity Based on Estrogen Receptor-Mediated Reduction of Soluble-Form Catechol-O-Methyltransferase (COMT) Expression in an ELISA-Based System

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Efficient attenuation of Friedreich's ataxia (FRDA) cardiomyopathy by modulation of iron homeostasis-human induced pluripotent stem cell (hiPSC) as a drug screening platform for FRDA

Friedreich’s ataxia (FRDA), a recessive neurodegenerative disorder commonly associated with hypertrophic cardiomyopathy, is caused by silencing of the frataxin (FXN) gene encoding the mitochondrial protein involved in iron-sulfur cluster biosynthesis. We aimed to utilize our previously established FRDA human induced pluripotent stem cell (hiPSC) derived cardiomyocytes model as a platform to assess the efficacy of treatment with either the antioxidant coenzyme Q10 analog, idebenone (IDE) or the iron chelator, deferiprone (DFP), which are both under clinical trial. In fact, DFP was able to more significantly suppress synthesis of reactive oxygen species (ROS) than IDE at the dosages of 10 nM and 25 μM respectively which agreed with the reduced rate of intracellular accumulation of iron by DFP treatment from 25 to 50 µM. With regard to cardiac electrical-contraction (EC) coupling function, decay velocity of calcium handling kinetics in FRDA-hiPSC-cardiomyocytes was significantly improved by DFP treatment but not by IDE. Further mechanistic studies revealed DFP also modulated iron induced mitochondrial stress as reflected by mitochondria network disorganization and decline in level of respiratory chain protein. In addition, iron-response protein (IRP-1) regulatory loop was overridden by DFP as reflected by the attenuated transferrin receptor (TSFR) suppression thereby reducing further iron uptake.published_or_final_versio

The effect of ex-vivo rotenone intoxication on dopamine re-uptake of LRRK2-R1441G mutant mouse

Poster presentationpublished_or_final_versio

To scale, or not to scale? : willingness-to-accept non-surgical periodontal treatment

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