نتایج جستجو برای: romano ward syndrome

تعداد نتایج: 645734  

2002
Shigemi Ohta

The domain wall fermion (DWF) method, with its almost perfectly preserved chiral symmetry on the lattice, makes the calculation of the nucleon axial charge particularly easy. By maintaining chiral symmetry and using the Ward-Takahashi (WT) identity, one has ZA = ZV and the bare lattice calculation yields the physical value without explicit renormalization. The DBW2 improved gauge action provide...

Journal: :Clinical science 1999
D A Skelton S K Phillips S A Bruce C H Naylor R C Woledge

A randomized open trial of hormone replacement therapy was used to assess changes in adductor pollicis muscle strength during 6-12 months of treatment with Prempak C 0.625(R) in comparison with an untreated control group. Muscle strength (maximal voluntary force; MVF), muscle cross-sectional area and bone mineral density were measured. Women entering the trial had oestrogen levels below 150 pmo...

2003
Bing An Li

It is found that in the SM the Ward-Takahashi(WT) identities of the axial-vector currents and the charged vector currents of fermions are invalid after spontaneous symmetry breaking. The spin-0 components of Z and W fields are revealed from the invalidity of these WT identities. The masses of these spin-0 components are at 10 14 GeV. They are ghosts. Therefore, unitarity of the SM after spontan...

Journal: :Journal of the American College of Cardiology 2001
Y Tanabe M Inagaki T Kurita N Nagaya A Taguchi K Suyama N Aihara S Kamakura K Sunagawa K Nakamura T Ohe J A Towbin S G Priori W Shimizu

OBJECTIVES The study compared the influence of sympathetic stimulation on transmural and spatial dispersion of repolarization between LQT1 and LQT2 forms of congenital long QT sYndrome (LQTS). BACKGROUND Cardiac events are more associated with sympathetic stimulation in LQT1 than in LQT2 or LQT3 syndrome. Experimental studies have suggested that the interval between Tpeak and Tend (Tp-e) in t...

Journal: :Circulation 1999
Q Chen D Zhang R L Gingell A J Moss C Napolitano S G Priori P J Schwartz E Kehoe J L Robinson E Schulze-Bahr Q Wang J A Towbin

BACKGROUND Long-QT (LQT) syndrome is a cardiac disorder that causes syncope, seizures, and sudden death from ventricular arrhythmias, specifically torsade de pointes. Both autosomal dominant LQT (Romano-Ward syndrome) and autosomal recessive LQT (Jervell and Lange-Nielsen syndrome, JLNS) have been reported. Heterozygous mutations in 3 potassium channel genes, KVLQT1, KCNE1 (minK), and HERG, and...

Journal: :Circulation 2002
Matti Viitasalo Lasse Oikarinen Heikki Swan Heikki Väänänen Kathy Glatter Päivi J Laitinen Kimmo Kontula Hal V Barron Lauri Toivonen Melvin M Scheinman

BACKGROUND Transmural dispersion of repolarization (TDR) may be related to the genesis of torsade de pointes (TdP) in patients with the long-QT (LQT) syndrome. Experimentally, LQT2 models show increased TDR compared with LQT1, and beta-adrenergic stimulation increases TDR in both models. Clinically, LQT1 patients experience symptoms at elevated heart rates, but LQT2 patients do so at lower rate...

Journal: :Circulation 2000
I Splawski J Shen K W Timothy M H Lehmann S Priori J L Robinson A J Moss P J Schwartz J A Towbin G M Vincent M T Keating

BACKGROUND Long-QT Syndrome (LQTS) is a cardiovascular disorder characterized by prolongation of the QT interval on ECG and presence of syncope, seizures, and sudden death. Five genes have been implicated in Romano-Ward syndrome, the autosomal dominant form of LQTS: KVLQT1, HERG, SCN5A, KCNE1, and KCNE2. Mutations in KVLQT1 and KCNE1 also cause the Jervell and Lange-Nielsen syndrome, a form of ...

Journal: :American journal of medical genetics 1999
D Wattanasirichaigoon M R Vesely P Duggal J C Levine E D Blume G S Wolff S B Edwards A H Beggs

Long QT syndrome (LQTS) is a heterogeneous disorder caused by mutations of at least five different loci. Three of these, LQT1, LQT2, and LQT5, encode potassium channel subunits. LQT3 encodes the cardiac-specific sodium channel, SCN5A. Previously reported LQTS-associated mutations of SCN5A include a recurring three amino acid deletion (DeltaKPQ1505-1507) in four different families, and four diff...

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