Засади та історія становлення соціального вчення Українського католицизму

In equine medicine the use of Botox® is experimental. Dosages are determined from human treatment-protocols and limited numbers of equine studies. Determination of target-muscle volume can be helpful to extrapolate human dosages. The aim of the study was to calculate a formula enabling the estimation of the deep digital flexor muscle (DDFM) volume based on distances between anatomical landmarks. Nineteen cadaveric limbs were collected and distance A (top of olecranon to Os carpi accessorium) and B (circumference of limb) were measured. Converting mathematical formulas, C was calculated: π × (((0.5B)/π)(2)) × A. DDFM volume was determined by water displacement. Linear Regression Analysis was used to analyse data. The line best fitting the observed points was: Ln(volume[ml]) = -1.89 + 0.98 × Ln(value C[cm(3)]). Correlation was highest when natural logarithm was applied to both variables and was 0.97. The calculated formula enables estimating DDFM volume of a living horse. This estimated volume can be useful to apply human Botox® treatment-protocols

Three method factors explaining the low correlations between assessment center dimension ratings and scores on personality inventories

In general, correlations between assessment centre (AC) ratings and personality inventories are low. In this paper, we examine three method factors that may be responsible for these low correlations: differences in (i) rating source (other versus self), (ii) rating domain (general versus specific), and (iii) rating format (multi- versus single item). This study tests whether these three factors diminish correlations between AC exercise ratings and external indicators of similar dimensions. Ratings of personality and performance were combined in an analytical framework following a 2 × 2 × 2 (source, domain, format) completely crossed, within subjects design. Results showed partial support for the influence of each of the three method factors. Implications for future research are discussed. Copyright © 2004 John Wiley & Sons, Ltd

The phospholamban p.(Arg14del) pathogenic variant leads to cardiomyopathy with heart failure and is unreponsive to standard heart failure therapy

Phospholamban (PLN) plays a role in cardiomyocyte calcium handling as primary inhibitor of sarco/endoplasmic reticulum Ca2+-ATPase (SERCA). The p.(Arg14del) pathogenic variant in the PLN gene results in a high risk of developing dilated or arrhythmogenic cardiomyopathy with heart failure. There is no established treatment other than standard heart failure therapy or heart transplantation. In this study, we generated a novel mouse model with the PLN-R14del pathogenic variant, performed detailed phenotyping, and tested the efficacy of established heart failure therapies eplerenone or metoprolol. Heterozygous PLN-R14del mice demonstrated increased susceptibility to ex vivo induced arrhythmias, and cardiomyopathy at 18 months of age, which was not accelerated by isoproterenol infusion. Homozygous PLN-R14del mice exhibited an accelerated phenotype including cardiac dilatation, contractile dysfunction, decreased ECG potentials, high susceptibility to ex vivo induced arrhythmias, myocardial fibrosis, PLN protein aggregation, and early mortality. Neither eplerenone nor metoprolol administration improved cardiac function or survival. In conclusion, our novel PLN-R14del mouse model exhibits most features of human disease. Administration of standard heart failure therapy did not rescue the phenotype, underscoring the need for better understanding of the pathophysiology of PLN-R14del-associated cardiomyopathy. This model provides a great opportunity to study the pathophysiology, and to screen for potential therapeutic treatments

Author Correction:The phospholamban p.(Arg14del) pathogenic variant leads to cardiomyopathy with heart failure and is unresponsive to standard heart failure therapy (Scientific Reports, (2020), 10, 1, (9819), 10.1038/s41598-020-66656-9)

The title in the original version of this Article contained a typographical error of ‘unresponsive’. The error has now been corrected in the PDF and HTML versions of the Article