Monahanburnham8024

Despite the rapid increase in electronic cigarette (e-cigarette) smoking, little is known about the factors associated with their use, particularly in adolescents with asthma. Our study investigated the prevalence of, and factors associated with asthma.

We analyzed data from the Korean Youth Risk Behavior Web-based Survey of 44,479 adolescents with physician-diagnosed asthma and 445,692 subjects without asthma. this website Sociodemographic factors, psychosocial factors, and e-cigarette smoking patterns were investigated by self-report questionnaires. Multiple logistic regression was used to investigate the factors associated with ever or current e-cigarette risks in adolescents with asthma, with adjustment for confounding factors.

Significantly more subjects had a smoking habit in the asthma group than in the non-asthma group. Among the adolescents with asthma, 4,420 (9.9%) smoked e-cigarettes (ever-users), and 1,962 (4.4%) smoked e-cigarettes within the last 30 days (current users). Multiple logistic regression shentify adolescents with asthma at high risk of e-cigarette smoking, to ultimately prevent and reduce this behavior.Hypereosinophilic syndrome is a rare entity and heterogeneous group of disorders characterized by hypereosinophilia and organ involvement. In this study, we presented a 49-year-old woman with cardiac tamponade in the context of Hypereosinophilic syndrome. Identifying hypereosinophilia as the underlying cause can have tremendous clinical implications for rapid initiation of appropriate treatment to minimize further end organ damage.

The aim of this study is to estimate a minimal clinically important difference (MCID) and a minimal detectable change (MDC) of the 12-item WHODAS 2.0 amongst patients with chronic musculoskeletal pain.

Cross-sectional cohort study.

Outpatient Physical and Rehabilitation Medicine clinic.

A total of 1988 consecutive patients with musculoskeletal pain.

A distribution-based approach was employed to estimate a minimal clinically important difference, a minimal detectable change, and a minimal detectable percent change (MDC%).

The mean age of the patients was 48 years, and 65% were women. The average intensity of pain was 6,3 (2.0) points (0-10 numeric rating scale) and the mean WHODAS 2.0 total score was 13 (9) points out of 48. The minimal clinically important difference ranged between 3.1 and 4.7 points. The minimal detectable change was 8.6 points and minimal detectable % change was unacceptably high 66%.

Amongst patients with chronic musculoskeletal pain, the 12-item WHODAS 2.0 demonstrated a high minimal detectable change of almost nine points. As the minimal detectable change exceeded the level of minimal clinically important difference, nine points were considered to be the amount of change perceived by a respondent as clinically significant.

Amongst patients with chronic musculoskeletal pain, the 12-item WHODAS 2.0 demonstrated a high minimal detectable change of almost nine points. As the minimal detectable change exceeded the level of minimal clinically important difference, nine points were considered to be the amount of change perceived by a respondent as clinically significant.

Peri-mitral atrial flutters frequently develop post-atrial fibrillation ablation or postcardiac surgery. The determinants of the flutter wave morphology on surface ECG have been less studied.

We retrospectively reviewed 24 patients with peri-mitral atrial flutters who underwent biatrial high-resolution mapping at 3 institutions with LUMIPOINT software. We analyzed the overlap between the right atrial (RA) activation time and flutter wave duration and compared the proportion of the endocardial area that was activated in both atria during the flutter wave duration. Biatrial activation patterns and interatrial conductions were also identified.

The mean tachycardia cycle length was 264±60 ms, with RA activation time 155±45 ms (60.8±20.6% of the tachycardia cycle length), and the flutter wave duration 107±31 ms (41.6±11.7% of the tachycardia cycle length). The overlap between the RA activation time and the flutter wave duration was 102±29 ms, which takes 68.5±17.2% of the RA activation time and 95.7±9.1% of the flutter wave duration, respectively. Quantitative analysis also showed that during the flutter wave duration, more percentage of the endocardial area was activated in the RA than in the left atrium (73.0±12.7% versus 45.2±13.0%,

<0.001). We consistently observed that the RA anterior wall rightward activation corresponded to the positive component in V1 in both flutter patterns, and the RA downward activation corresponded to the positive component in the counterclockwise group or the upward activation corresponded to the negative component in the clockwise group in the inferior leads. The passive RA activation patterns were varied with spontaneous atrial scarring or previous linear ablation.

ECG flutter wave morphology of peri-mitral atrial flutters is mainly dependent on RA activation patterns.

ECG flutter wave morphology of peri-mitral atrial flutters is mainly dependent on RA activation patterns.

In cardiac gene therapy to improve contractile function, achieving gene expression in the majority of cardiac myocytes is essential. In preventing cardiac arrhythmias, however, this goal may not be as important since transduction efficiencies as low as 40% suppressed ventricular arrhythmias in genetically modified mice with catecholaminergic polymorphic ventricular tachycardia.

Using computational modeling, we simulated 1-, 2-, and 3-dimensional tissue under a variety of conditions to test the ability of genetically engineered nonarrhythmogenic stabilizer cells to suppress triggered activity due to delayed or early afterdepolarizations.

Due to source-sink relationships in cardiac tissue, a minority (20%-50%) of randomly distributed stabilizer cells engineered to be nonarrhythmogenic can suppress the ability of arrhythmogenic cells to generate delayed and early afterdepolarizations-related arrhythmias. Stabilizer cell gene therapy strategy can be designed to correct a specific arrhythmogenic mutation, as in the catecholaminergic polymorphic ventricular tachycardia mice studies, or more generally to suppress delayed or early afterdepolarizations from any cause by overexpressing the inward rectifier K channel Kir2.