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

Biallelic loss-of-function variants in PLD1 cause congenital right-sided cardiac valve defects and neonatal cardiomyopathy

Congenital heart disease is the most common type of birth defect, accounting for one-third of all congenital anomalies. Using whole-exome sequencing of 2718 patients with congenital heart disease and a search in GeneMatcher, we identified 30 patients from 21 unrelated families of different ancestries with biallelic phospholipase D1 (PLD1) variants who presented predominantly with congenital cardiac valve defects. We also associated recessive PLD1 variants with isolated neonatal cardiomyopathy. Furthermore, we established that p.I668F is a founder variant among Ashkenazi Jews (allele frequency of ~2%) and describe the phenotypic spectrum of PLD1-associated congenital heart defects. PLD1 missense variants were overrepresented in regions of the protein critical for catalytic activity, and, correspondingly, we observed a strong reduction in enzymatic activity for most of the mutant proteins in an enzymatic assay. Finally, we demonstrate that PLD1 inhibition decreased endothelial-mesenchymal transition, an established pivotal early step in valvulogenesis. In conclusion, our study provides a more detailed understanding of disease mechanisms and phenotypic expression associated with PLD1 loss of function

Umbilical hypercoiling in 2nd- and 3rd-trimester intrauterine fetal death

Cases of unexplained intrauterine fetal death (IUFD) can be reduced by full placental examination, with or without autopsy. Determination of the umbilical coiling index (UCI) is considered to be a part of full placental examination. Umbilical hypercoiling (UCI above 0.30 coils/cm) is associated with IUFD. In a large retrospective study, we found an incidence of 18% umbilical hypercoiling in IUFD. We explored the association between umbilical hypercoiling and 2nd- and 3rd-trimester IUFD in 77 cases. There was a significant negative correlation between the UCI and gestational age of IUFD (P < 0.001). More severe cases of hypercoiling were observed in the categories of IUFD at a younger age and with a longer duration. Signs of fetal thrombosis were significantly more present in IUFDs with umbilical hypercoiling. An umbilical cord stricture and hypercoiling seem to be significantly more common in IUFD. The severity of hypercoiling was of no influence on the presence or absence of an umbilical cord stricture. Furthermore, there was no significant difference in signs of cardiac failure between the groups of IUFD with and without umbilical hypercoiling. Our findings may be explained by the theory that hypercoiling leads to a disturbed fetal-placental circulation. Therefore, determination of the UCI should be part of the routine placental examination of cases of IUFD

Physical activity and fat-free mass during growth and in later life

Background Physical activity may be a way to increase and maintain fat-free mass (FFM) in later life, similar to the prevention of fractures by increasing peak bone mass. Objectives A study is presented of the association between FFM and physical activity in relation to age. Methods In a cross-sectional study, FFM was analyzed in relation to physical activity in a large participant group as compiled in the International Atomic Energy Agency Doubly Labeled Water database. The database included 2000 participants, age 3–96 y, with measurements of total energy expenditure (TEE) and resting energy expenditure (REE) to allow calculation of physical activity level (PAL = TEE/REE), and calculation of FFM from isotope dilution. Results PAL was a main determinant of body composition at all ages. Models with age, fat mass (FM), and PAL explained 76% and 85% of the variation in FFM in females and males < 18 y old, and 32% and 47% of the variation in FFM in females and males ≥ 18 y old, respectively. In participants < 18 y old, mean FM-adjusted FFM was 1.7 kg (95% CI: 0.1, 3.2 kg) and 3.4 kg (95% CI: 1.0, 5.6 kg) higher in a very active participant with PAL = 2.0 than in a sedentary participant with PAL = 1.5, for females and males, respectively. At age 18 y, height and FM–adjusted FFM was 3.6 kg (95% CI: 2.8, 4.4 kg) and 4.4 kg (95% CI: 3.2, 5.7 kg) higher, and at age 80 y 0.7 kg (95% CI: −0.2, 1.7 kg) and 1.0 kg (95% CI: −0.1, 2.1 kg) higher, in a participant with PAL = 2.0 than in a participant with PAL = 1.5, for females and males, respectively. Conclusions If these associations are causal, they suggest physical activity is a major determinant of body composition as reflected in peak FFM, and that a physically active lifestyle can only partly protect against loss of FFM in aging adults