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1572 citation(s) found for "Wu, Samuel".

P3‐271: Association of candidate gene susceptibility alleles on chromosome 10 with Alzheimer's disease risk and endophenotypes
Walker, Louise, Allen, Mariet , Cox, Claire , Younkin, Samuel , Younkin, Linda H., Carrasquillo, Minerva M. , Zou, Fanggeng, Petersen, Ronald C. , Graff‐Radford, Neill R. , Younkin, Steven G. , Ertekin‐Taner, Nilüfer , Carrasquillo, Minerva M. , Ma, Li , Kouri, Naomi , Pankratz, V. Shane , Dickson, Dennis W. , Boeve, Bradley F.

Alzheimer's & Dementia | July 24, 2008 | Volume: 4 | Issue: 4S_Part_18 | Pages: No page available

10.1016/j.jalz.2008.05.1839 Get It

P3‐216: Identification of CIS variants associating with expression levels of 12 late‐onset Alzheimer's disease (LOAD) candidate genes in a Genome‐Wide Association Study (GWAS)
Ertekin‐Taner, Nilüfer , Zou, Fanggeng, Carrasquillo, Minerva M. , Walker, Louise P., Wilcox, Samantha L., Bisceglio, Gina, Cunningham, Julie M. , Petersen, Ronald C. , Graff‐Radford, Neill R. , Younkin, Steven G., Carrasquillo, Minerva M. , Younkin, Samuel , Ma, Li , Kouri, Naomi , Pankratz, V. Shane , Dickson, Dennis W.

Alzheimer's & Dementia | July 24, 2008 | Volume: 4 | Issue: 4S_Part_18 | Pages: No page available

10.1016/j.jalz.2008.05.1783 Get It

P3‐208: Genetic variation in PCDH11X associates with Alzheimer's disease in a two‐stage GWAS study
Carrasquillo, Minerva M. , Zou, Fanggeng, Wilcox, Samantha L., Walker, Louise P., Bisceglio, Gina, Ertekin‐Taner, Nilüfer , Cunningham, Julie M. , Petersen, Ronald C. , Graff‐Radford, Neill R. , Younkin, Steven G., Carrasquillo, Minerva M. , Younkin, Samuel , Ma, Li , Pankratz, V. Shane , Dickson, Dennis W.

Alzheimer's & Dementia | July 24, 2008 | Volume: 4 | Issue: 4S_Part_18 | Pages: No page available

10.1016/j.jalz.2008.05.1775 Get It

O2‐06–04: Identification of late‐onset Alzheimer's disease (LOAD) susceptibility alleles in the PAI‐1 gene
Wilcox, Samantha L., Carrasquillo, Minerva M. , Younkin, Samuel , Li, Ma, Bisceglio, Gina, Zou, Fanggeng, Walker, Louise, Allen, Mariet , Younkin, Linda H., Graff‐Radford, Neill R. , Petersen, Ronald C. , Younkin, Steven G., Carrasquillo, Minerva M. , Dickson, Dennis W.

Alzheimer's & Dementia | July 24, 2008 | Volume: 4 | Issue: 4S_Part_4 | Pages: No page available

10.1016/j.jalz.2008.05.352 Get It

Ambulatory Electroencephalography (EEG) in Children: Diagnostic Yield and Tolerability
Kozlik, Silvia, Tellez, Jose, Wiebe, Samuel , Hamiwka, Lorie, Wirrell, Elaine , Tellez, Jose, Wiebe, Samuel

Journal of Child Neurology | June 6, 2008 | Volume: 23 | Issue: 6 | Pages: 655-662

10.1177/0883073808314158 | PMID 18539990 Get It

Sixty-four children, aged 0-17 years, undergoing ambulatory electroencephalography (EEG) were prospectively recruited during a 12-month period. The diagnostic yield of ambulatory electroencephalography was determined for each of the following groups: group 1: differentiation of seizures from nonepileptic events; group 2: determination of seizure/interictal discharge frequency; and group 3: classification of seizure type or localization. The ambulatory electroencephalography answered the clinical question in 61% of group 1 (27/44) and 100% of groups 2 (16/16) and 3 (4/4). Of 44 cases in Group 1, clinical events were recorded in 61%; the ambulatory electroencephalography result changed the diagnosis from epileptic to nonepileptic or vice versa in 27%. When clinicians suspected that events were epileptic, ambulatory electroencephalography changed the clinical impression in 50%, whereas when events were suspected to be nonepileptic, ambulatory electroencephalography confirmed that impression in 83%.
Mechanisms and Utility of Discrete Great Arterial Potentials in the Ablation of Outflow Tract Ventricular Arrhythmias
Bunch, T. Jared , Asirvatham, Samuel J. , Edwards, William D. , Friedman, Paul A. , Munger, Thomas M. , Hammill, Stephen C., Cha, Yong‐Mei , Brady, Peter A. , Rea, Robert F., Packer, Douglas L. , Shen, Win-Kuang, Srivathsan, Komandoor , Jahangir, Arshad , Bradley, David J. , Asirvatham, Samuel J

Circulation: Arrhythmia and Electrophysiology | June 5, 2008 | Volume: 1 | Issue: 1 | Pages: 30-38

10.1161/circep.107.750315 | PMID 19808391 Get It

Background— Outflow tract ventricular tachycardia originating above the semilunar valves has been reported in a small number of studies. Discrete potentials in the great arteries (above the semilunar valves) have been rarely described in patients undergoing electrophysiology evaluation and radiofrequency ablation for ventricular arrhythmias. The mechanisms of these discrete potentials in the great arteries and the utility of such potentials in guiding radiofrequency ablation are unknown. Methods and Results— Twelve patients with outflow tract ventricular arrhythmia originating above the semilunar valves with discrete arterial potentials were studied. The clinical characteristics, properties of the arterial potentials, electrophysiological evaluation and ablation, and short- and long-term outcomes were reviewed. Of the twelve patients, 8 (67%) were women. The patients’ average age was 41�14 years. The average ejection fraction was 0.52�0.16 (range: 0.16 to 0.75). Contact mapping in the great artery demonstrated discrete near-field electrograms that were separate from far-field ventricular electrograms in all patients (8 above the pulmonary valve and in 4 the aortic valve). One or more of the following electrophysiological characteristics, supportive of an arrhythmogenic substrate, were observed in 10 of 12 patients: (1) A fixed or reproducibly variable pattern of discrete potential–ventricular arrhythmia relationship was present at baseline or during pacing; (2) the discrete potential–ventricular electrogram relationship during sinus rhythm was the reverse of that during the ventricular arrhythmia; (3) during sustained ventricular tachycardia, spontaneous variation of the ventricular (V-V) cycle length was preceded by a similar variation of arterial spike potential–spike potential cycle length; and (4) ablation guided by the discrete arterial potential successfully eliminated the clinical arrhythmia. Ablation was successful in these patients. In the remaining 2 patients, the potentials were believed to be bystanders. Over 10�4 months (range: 5 to 32 months) of follow-up, there have been no recurrences of the premature ventricular complex or ventricular arrhythmia. Conclusions— Discrete potentials are present in the great arteries of a select group of patients with outflow tract ventricular tachycardia originating above the semilunar valves. When an arrhythmogenic relationship can be demonstrated, discrete potentials are useful in guiding ablation within the great vessels, despite significant anatomic complexity.
Catheter Ablation for Atrial Fibrillation in Patients With Obesity
Cha, Yong‐Mei , Friedman, Paul A. , Asirvatham, Samuel J. , Shen, Win-Kuang, Munger, Thomas M. , Rea, Robert F., Brady, Peter A. , Monahan, Kristi H. , Hodge, David O. , Meverden, Ryan A., Hammill, Stephen C., Packer, Douglas L. , Jahangir, Arshad , Gersh, Bernard J. , Asirvatham, Samuel J

Circulation | May 13, 2008 | Volume: 117 | Issue: 20 | Pages: 2583-2590

10.1161/circulationaha.107.716712 | PMID 18474813 Get It

Background— Obesity is a risk factor for atrial fibrillation and other cardiovascular conditions. Our objective was to determine whether catheter-based ablation effectively treated atrial fibrillation in obese patients. Methods and Results— Five hundred twenty-three consecutive patients with symptomatic, medication-refractory atrial fibrillation underwent catheter ablation. Patients were grouped by body mass index (lean, <25 kg/m 2 ; overweight, 25 to 29.9 kg/m 2 ; obese, ≥30 kg/m 2 ). Outcome and quality of life were measured with a general health survey (Medical Outcomes Study 36-item Short-Form General Health Survey [SF-36]); patients were assessed before ablation and at 3 and 12 months after the procedure. Two hundred twenty-eight study patients (44%) were overweight, and 201 (38%) were obese. Twelve months after curative ablation, 72% of patients were free of atrial fibrillation without the use of antiarrhythmic agents; 84% were arrhythmia free when those receiving medication were included. Atrial fibrillation was eliminated in 75%, 72%, and 70% of the lean, overweight, and obese patients, respectively, at 12 months ( P =0.41, trend test). SF-36 scores were lower for patients with higher body mass index ( P <0.05) at baseline. SF-36 scores improved in every functional domain for all body mass index groups after ablation. The mean SF-36 total physical score increased from 59±20 at baseline to 77±19 in 12 months ( P <0.001). The total mental health score improved from 66±18 to 79±16 in 12 months ( P <0.001). Conclusions— Catheter ablation of atrial fibrillation was effective in obese patients. Coexistence of atrial fibrillation and obesity indicated lower SF-36 scores, but the improvement in quality of life was consistent across all body mass index categories.
Supplementation of ascorbic acid and α-tocopherol prevents arsenic-induced protein oxidation and DNA damage induced by arsenic in rats
Kadirvel, Ramanathan , Sundaram, K., Mani, Santhosh K. , Samuel, Shila , Elango, N., Panneerselvam, C.

Human & Experimental Toxicology | March 28, 2008 | Volume: 26 | Issue: 12 | Pages: 939-946

10.1177/0960327107087909 | PMID 18375637 Get It

Contamination of arsenic in drinking water is associated with several human diseases including cancer. It has been reported that oxidative stress plays a vital role in arsenic-induced biochemical and molecular alterations. The aim of the present study was to improve the understanding of arsenic-induced oxidative damage to proteins and to DNA and the role of antioxidants such as ascorbic acid and α-tocopherol in alleviating arsenic-induced damages in experimental rats. A significant increase in the levels of protein oxidation, DNA strand breaks, and DNA–protein cross-links was observed in blood, liver, and kidney of rats exposed to arsenic (100 ppm in drinking water) for 30 days. Co-administration of ascorbic acid and α-tocopherol to arsenic-exposed rats showed a substantial reduction in the levels of arsenic-induced oxidative products of protein and DNA. The results of this study support that free radical–mediated toxic manifestations of arsenic and also suggest that ascorbic acid and α-tocopherol supplementation can improve the arsenic-induced molecular alterations.
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Lakhani, Vipul T. , Wells, Samuel A., You, Y. Nancy

World Journal of Surgery | February 22, 2008 | Volume: 32 | Issue: 6 | Pages: 1221-1222

10.1007/s00268-007-9426-3 Get It