The Rao-Scott chi(2) test was performed to determine whether CT use was similar across subpopulations. Data were evaluated according to exponential and logistic growth models.
Results: From 1995 to 2007, the number of ED visits that included a CT examination increased from 2.7 million to 16.2 million, constituting a 5.9-fold increase and a compound annual growth rate of 16.0%.
The percentage of visits associated AZD1152 nmr with CT increased from 2.8% to 13.9%, constituting a 4.9-fold increase and a compound annual growth rate of 14.2%. The exponential growth model provided the best fit for the trend in CT use. CT use was greater in older patients, white patients, patients admitted to the hospital, and patients at facilities in metropolitan regions. By the end of the study period, the top chief complaints among those who underwent CT were abdominal pain, headache, and chest pain.
The percentage of patient visits associated with CT for all evaluated chief complaints increased-most substantially among those who underwent CT for flank, abdominal, or chest pain.
Conclusion: Use of CT has increased at a higher rate in the ED than in other settings. The overall use of CT had not begun to taper by 2007. (C) RSNA, 2010″
“Background: The protein DZNeP price MOG1 is a cofactor of the cardiac sodium channel, Nav1.5. Overexpression of MOG1 in Nav1.5-expressing cells increases sodium current markedly. Mutations in the genes encoding Nav1.5 and its accessory proteins have been associated with cardiac arrhythmias of significant clinical impact. We sought to investigate whether MOG1 is find more implicated in cardiac arrhythmias.
Methods: We performed a genetic screening of the MOG1-encoding gene (gene symbol RANGRF, alias MOG1) in 220 Danish patients with cardiac arrhythmia. Of the 220, 197 were young patients with lone atrial fibrillation and 23 were patients with Brugada syndrome. The effect of one variant was investigated functionally by patch-clamping CHO-K1 cells coexpressing Nav1.5 with MOG1.
Results: We uncovered a novel heterozygous nonsense variant,
c. 181G > T (p.E61X), that, however, was also present in control subjects, albeit at a lower frequency (1.8% vs 0.4%, P = 0.078). Electrophysiological investigation showed that the p.E61X variant completely eliminates the sodium current-increasing effect of MOG1 and thereby causes loss of function in the sodium current. When mimicking heterozygosity by coexpression of Nav1.5 with wild-type MOG1 and p.E61X-MOG1, no current decrease was seen.
Conclusions: Our screening of Nav1.5 cofactor MOG1 uncovered a novel nonsense variant that appeared to be present at a higher frequency among patients than control subjects. This variant causes MOG1 loss of function and therefore might be disease causing or modifying under certain conditions.”
“The growth kinetics of pathogenic and nonpathogenic rickettsiae were compared to elucidate the mechanism responsible for the pathogenicity of rickettsiae.