Неустойчивость двухслойных течений в проливах Черного моря

Рассмотрена плоская задача о прогрессивных гравитационных внутренних волнах в горизонтальном двухслойном течении Кельвина-Гельмгольца. Найдено аналитическое решение задачи и условия существования внутренних волн. Для течений с параметрами, типичными для пролива Босфор и Керченского пролива, рассчитаны характеристики бароклинных волн. В пространстве волновых чисел определены диапазоны устойчивости и неустойчивости двухслойных течений с характерными для этих проливов параметрами относительно малых возмущений в форме прогрессивных волн.Розглянуто плоску задачу про прогресивні гравітаційні внутрішні хвилі у горизонтальній двошаровій течії Кельвіна-Гельмгольца. Знайдено аналітичне рішення задачі та умови існування внутрішніх хвиль. Для течій з параметрами, типовими для протоки Босфор і Керченської протоки, розраховані характеристики бароклінних хвиль. У просторі хвильових чисел визначені діапазони стійкості і нестійкості двошарових течій з характерними для цих проток параметрами відносно малих збурень у формі прогресивних хвиль.The plane problem of the progressive internal gravity waves in a horizontal two-layer Kelvin-Helmholtz flow is considered. The analytical solution of the problem and the conditions of existence of internal waves are found. For the flows with the typical parameters for the Bosphorus Strait and the Strait of Kerch, characteristics of baroclinic waves are calculated. The stability and instability regimes of two-layer currents with characteristic parameters of these straits with respect to small wave disturbances are found in the space of wave numbers

P62-positive aggregates are homogenously distributed in the myocardium and associated with the type of mutation in genetic cardiomyopathy

Genetic cardiomyopathy is caused by mutations in various genes. The accumulation of potentially proteotoxic mutant protein aggregates due to insufficient autophagy is a possible mechanism of disease development. The objective of this study was to investigate the distribution in the myocardium of such aggregates in relation to specific pathogenic genetic mutations in cardiomyopathy hearts. Hearts from 32 genetic cardiomyopathy patients, 4 non-genetic cardiomyopathy patients and 5 controls were studied. Microscopic slices from an entire midventricular heart slice were stained for p62 (sequestosome-1, marker for aggregated proteins destined for autophagy). The percentage of cardiomyocytes with p62 accumulation was higher in cardiomyopathy hearts (median 3.3%) than in healthy controls (0.3%; P <.0001). p62 accumulation was highest in the desmin (15.6%) and phospholamban (7.2%) groups. P62 accumulation was homogeneously distributed in the myocardium. Fibrosis was not associated with p62 accumulation in subgroup analysis of phospholamban hearts. In conclusion, accumulation of p62-positive protein aggregates is homogeneously distributed in the myocardium independently of fibrosis distribution and associated with desmin and phospholamban cardiomyopathy. Proteotoxic protein accumulation is a diffuse process in the myocardium while a more localized second hit, such as local strain during exercise, might determine whether this leads to regional myocyte decay