Ekman decay of a dipolar vortex in a rotating fluid

The evolution of quasi-two-dimensional (2D) dipolar vortices over a flat bottom in a rotating fluid system is studied numerically, and the main results are experimentally verified. Our aim is to examine the dipole decay due to bottom friction effects. The numerical simulations are based on the 2D physical model derived by Zavala Sansón and van Heijst [J. Fluid Mech. 412, 75 (2000)], which contains nonlinear Ekman terms, associated with bottom friction, in the vorticity equation. In contrast, the conventional 2D model with bottom friction only retains a linear stretching term in the same equation. It is shown that the dipole trajectory is deflected towards the right (i.e., in the anticyclonic direction) when nonlinear Ekman terms are included. This effect is not observed in simulations based on the conventional model, where the dipole trajectory is a straight line. The basic reason for this behavior is the slower decay of the anticyclonic part of the dipole, with respect to the cyclonic one, due to nonlinear Ekman effects. Another important result is the exchange of fluid between the cyclonic part and the ambient, leaving a tail behind the dipole. By means of laboratory experiments in a rotating tank, these results are qualitatively verified

Ekman decay of a dipolar vortex in a rotating fluid

The evolution of quasi-two-dimensional (2D) dipolar vortices over a flat bottom in a rotating fluid system is studied numerically, and the main results are experimentally verified. Our aim is to examine the dipole decay due to bottom friction effects. The numerical simulations are based on the 2D physical model derived by Zavala Sansón and van Heijst [J. Fluid Mech. 412, 75 (2000)], which contains nonlinear Ekman terms, associated with bottom friction, in the vorticity equation. In contrast, the conventional 2D model with bottom friction only retains a linear stretching term in the same equation. It is shown that the dipole trajectory is deflected towards the right (i.e., in the anticyclonic direction) when nonlinear Ekman terms are included. This effect is not observed in simulations based on the conventional model, where the dipole trajectory is a straight line. The basic reason for this behavior is the slower decay of the anticyclonic part of the dipole, with respect to the cyclonic one, due to nonlinear Ekman effects. Another important result is the exchange of fluid between the cyclonic part and the ambient, leaving a tail behind the dipole. By means of laboratory experiments in a rotating tank, these results are qualitatively verified

Molecular cytogenetic characterisation of a mosaic add(12)(p13.3) with an inv dup(3)(q26.31 --> qter) detected in an autistic boy

BACKGROUND: Inverted duplications (inv dup) of a terminal chromosome region are a particular subset of rearrangements that often results in partial tetrasomy or partial trisomy when accompanied by a deleted chromosome. Associated mosaicism could be the consequence of a post-zygotic event or could result from the correction of a trisomic conception. Tetrasomies of distal segments of the chromosome 3q are rare genetic events and their phenotypic manifestations are diverse. To our knowledge, there are only 12 cases reported with partial 3q tetrasomy. Generally, individuals with this genomic imbalance present mild to severe developmental delay, facial dysmorphisms and skin pigmentary disorders. RESULTS: We present the results of the molecular cytogenetic characterization of an unbalanced mosaic karyotype consisting of mos 46,XY,add(12)(p13.3) [56]/46,XY [44] in a previously described 11 years old autistic boy, re-evaluated at adult age. The employment of fluorescence in situ hybridization (FISH) and multicolor banding (MCB) techniques identified the extra material on 12p to be derived from chromosome 3, defining the additional material on 12p as an inv dup(3)(qter --> q26.3::q26.3 --> qter). Subsequently, array-based comparative genomic hybridization (aCGH) confirmed the breakpoint at 3q26.31, defining the extra material with a length of 24.92 Mb to be between 174.37 and 199.29 Mb. CONCLUSION: This is the thirteenth reported case of inversion-duplication 3q, being the first one described as an inv dup translocated onto a non-homologous chromosome. The mosaic terminal inv dup(3q) observed could be the result of two proposed alternative mechanisms. The most striking feature of this case is the autistic behavior of the proband, a characteristic not shared by any other patient with tetrasomy for 3q26.31 --> 3qter. The present work further illustrates the advantages of the use of an integrative cytogenetic strategy, composed both by conventional and molecular techniques, on providing powerful information for an accurate diagnosis. This report also highlights a chromosome region potentially involved in autistic disorders

Left ventricular mechanics in late second trimester of healthy pregnancy

Objective: To evaluate left ventricular (LV) mechanics in the second trimester of healthy pregnancy and to determine the influence of underpinning hemodynamics (heart rate (HR), preload and afterload) on LV mechanics during gestation. Methods: This was a cross‐sectional study of 18 non‐pregnant, 14 nulliparous pregnant (22–26 weeks' gestation) and 13 primiparous postpartum (12–16 weeks after delivery) women. All pregnant and postpartum women had uncomplicated, singleton gestations. Cardiac structure and function were assessed using echocardiography. LV mechanics, specifically longitudinal strain, circumferential strain and twist/untwist, were measured using speckle‐tracking echocardiography. Differences between groups were identified using ANCOVA, with age, HR, end‐diastolic volume (EDV) and systolic blood pressure (SBP) as covariates. Relationships between LV mechanics and hemodynamics were examined using Pearson's correlation. Results: There were no significant differences in LV structure and traditional measurements of systolic and diastolic function between the three groups. Pregnant women, compared with non‐pregnant ones, had significantly higher resting longitudinal strain (–22 ± 2% vs –17 ± 3%; P = 0.002) and basal circumferential strain (–23 ± 4% vs –16 ± 2%; P = 0.001). Apical circumferential strain and LV twist and untwist mechanics were similar between the three groups. No statistically significant relationships were observed between LV mechanics and HR, EDV or SBP within the groups. Conclusions: Compared to the non‐pregnant state, pregnant women in the second trimester of a healthy pregnancy have significantly greater resting systolic function, as assessed by LV longitudinal and circumferential strain. Contrary to previous work, these data show that healthy pregnant women should not exhibit reductions in resting systolic function between 22 and 26 weeks' gestation. The enhanced myocardial contractile function during gestation does not appear to be related to hemodynamic load and could be the result of other physiological adaptations to pregnancy

Comparison between Modelflow® and echocardiography in the determination of cardiac output during and following pregnancy at rest and during exercise

During pregnancy, assessment of cardiac output (Q ̇), a fundamental measure of cardiovascular function, provides important insight into maternal adaptation. However, methods for dynamic Q ̇ measurement require validation. The purpose of this study was to estimate the agreement of Q ̇ measured by echocardiography and Modelflow® at rest and during submaximal exercise in non-pregnant (n = 18), pregnant (n = 15, 22-26 weeks gestation) and postpartum women (n = 12, 12-16 weeks post-delivery). Simultaneous measurements of Q ̇ derived from echocardiography [criterion] and Modelflow® were obtained at rest and during low-moderate intensity (25% and 50% peak power output) cycling exercise and compared using Bland-Altman analysis and limits of agreement. Agreement between echocardiography and Modelflow® was poor in non-pregnant, pregnant and postpartum women at rest (mean difference ± SD: -1.1 ± 3.4; -1.2 ± 2.9; -1.9 ± 3.2 L.min-1), and this remained evident during exercise. The Modelflow® method is not recommended for Q ̇ determination in research involving young, healthy non-pregnant and pregnant women at rest or during dynamic challenge. Previously published Q ̇ data from studies utilising this method should be interpreted with caution

Static and Dynamic Properties of Dissipative Particle Dynamics

The algorithm for the DPD fluid, the dynamics of which is conceptually a combination of molecular dynamics, Brownian dynamics and lattice gas automata, is designed for simulating rheological properties of complex fluids on hydrodynamic time scales. This paper calculates the equilibrium and transport properties (viscosity, self-diffusion) of the thermostated DPD fluid explicitly in terms of the system parameters. It is demonstrated that temperature gradients cannot exist, and that there is therefore no heat conductivity. Starting from the N-particle Fokker-Planck, or Kramers' equation, we prove an H-theorem for the free energy, obtain hydrodynamic equations, and derive a non-linear kinetic equation (the Fokker-Planck-Boltzmann equation) for the single particle distribution function. This kinetic equation is solved by the Chapman-Enskog method. The analytic results are compared with numerical simulations.Comment: 22 pages, LaTeX, 3 Postscript figure

Altered Calcium Homeostasis Does Not Explain the Contractile Deficit of Diabetic Cardiomyopathy

OBJECTIVE—This study examines the extent to which the contractile deficit of diabetic cardiomyopathy is due to altered Ca2+ homeostasis

Prospective Evaluation of Sleep Apnea as Manifestation of Heart Failure in Children

In adults with heart failure, central sleep apnea (CSA), often manifested as Cheyne–Stokes respiration, is common, and has been associated with adverse outcome. Heart failure in children is commonly caused by dilated cardiomyopathy (DCM). It is unknown whether children with heart failure secondary to DCM have CSA, and whether CSA is related to the severity of heart failure. In this prospective observational study, 37 patients (<18 year) with heart failure secondary to DCM were included. They underwent polysomnography, clinical and laboratory evaluation and echocardiographic assessment. After a median follow-up time of 2 years, eight patients underwent heart transplantation. CSA (apnea–hypopnea index [AHI] ≥1) was found in 19 % of the patients. AHI ranged from 1.2 to 4.5/h. The occurrence of CSA was not related to the severity of heart failure. Three older patients showed a breathing pattern mimicking Cheyne–Stokes respiration, two of whom required heart transplantation. CSA was found in 19 % of the children with heart failure secondary to DCM. No relation was found with the severity of heart failure. In a small subset of children with severe DCM, a pattern mimicking Cheyne–Stokes respiration was registered

Congenital Heart Block Maternal Sera Autoantibodies Target an Extracellular Epitope on the α1G T-Type Calcium Channel in Human Fetal Hearts

Background:Congenital heart block (CHB) is a transplacentally acquired autoimmune disease associated with anti-Ro/SSA and anti-La/SSB maternal autoantibodies and is characterized primarily by atrioventricular (AV) block of the fetal heart. This study aims to investigate whether the T-type calcium channel subunit α1G may be a fetal target of maternal sera autoantibodies in CHB.Methodology/Principal Findings:We demonstrate differential mRNA expression of the T-type calcium channel CACNA1G (α1G gene) in the AV junction of human fetal hearts compared to the apex (18-22.6 weeks gestation). Using human fetal hearts (20-22 wks gestation), our immunoprecipitation (IP), Western blot analysis and immunofluorescence (IF) staining results, taken together, demonstrate accessibility of the α1G epitope on the surfaces of cardiomyocytes as well as reactivity of maternal serum from CHB affected pregnancies to the α1G protein. By ELISA we demonstrated maternal sera reactivity to α1G was significantly higher in CHB maternal sera compared to controls, and reactivity was epitope mapped to a peptide designated as p305 (corresponding to aa305-319 of the extracellular loop linking transmembrane segments S5-S6 in α1G repeat I). Maternal sera from CHB affected pregnancies also reacted more weakly to the homologous region (7/15 amino acids conserved) of the α1H channel. Electrophysiology experiments with single-cell patch-clamp also demonstrated effects of CHB maternal sera on T-type current in mouse sinoatrial node (SAN) cells.Conclusions/Significance:Taken together, these results indicate that CHB maternal sera antibodies readily target an extracellular epitope of α1G T-type calcium channels in human fetal cardiomyocytes. CHB maternal sera also show reactivity for α1H suggesting that autoantibodies can target multiple fetal targets. © 2013 Strandberg et al