Oceanic submesoscale currents (SMCs) occur on an scale of 0.1-10 km horizontally and have a large influence on the oceanic variability and on ecosystems. At the mesoscale (10-250 km), oceanic thermal and current feedbacks are known to have a significant influence on the atmosphere and on oceanic dynamics. However, air-sea interactions at the submesoscale are not well known because the small size of SMCs presents observational and simulation barriers. Using high-resolution coupled oceanic and atmospheric models for the Central California region during the upwelling season, we show that the current feedback acting through the surface stress dominates the thermal feedback effect on the ocean and dampens the SMC variability by ≈17% ± 4%. As for the mesoscale, the current feedback induces an ocean sink of energy at the SMCs and a source of atmospheric energy that is related to induced Ekman pumping velocities. However, those additional vertical velocities also cause an increase of the injection of energy by baroclinic conversion into the SMCs, partially counteracting the sink of energy by the stress coupling. These stress coupling effects have important implications in understanding SMC variability and its links with the atmosphere and should be tested in other regions.

Most of the ocean kinetic energy is contained in the large scale currents and the vigorous geostrophic eddy field, at horizontal scales of order 100 km. To achieve equilibrium the geostrophic currents must viscously dissipate their kinetic energy at much smaller scale. However, geostrophic turbulence is characterized by an inverse cascade of energy towards larger scale, and the pathways of energy toward dissipation are still in question. Here, we present a mechanism, in the context of the Gulf Stream, where energy is transferred from the geostrophic flow to submesoscale wakes through anticyclonic vertical vorticity generation in the bottom boundary layer. The submesoscale turbulence leads to elevated local dissipation and mixing outside the oceanic boundary layers. This process is generic for boundary slope currents that flow in the direction of Kelvin wave propagation. Topographic generation of submesoscale flows potentially provides a new and significant route to energy dissipation for geostrophic flows.

The southward-flowing deep limb of the Atlantic meridional overturning circulation is composed of both the deep western boundary current (DWBC) and interior pathways. The latter are fed by ‘‘leakiness’’ from the DWBC in the Newfoundland Basin. However, the cause of this leakiness has not yet been explored mechanistically. Here the statistics and dynamics of the DWBC leakiness in the Newfoundland Basin are explored using two float datasets and a high-resolution numerical model. The float leakiness around Flemish Cap is found to be concentrated in several areas (hot spots) that are collocated with bathymetric curvature and steepening. Numerical particle advection experiments reveal that the Lagrangian mean velocity is offshore at these hot spots, while Lagrangian variability is minimal locally. Furthermore, model Eulerian mean streamlines separate from the DWBC to the interior at the leakiness hot spots. This suggests that the leakiness of Lagrangian particles is primarily accomplished by an Eulerian mean flow across isobaths, though eddies serve to transfer around 50% of the Lagrangian particles to the leakiness hot spots via chaotic advection, and rectified eddy transport accounts for around 50% of the offshore flow along the southern face of Flemish Cap. Analysis of the model’s energy and potential vorticity budgets suggests that the flow is baroclinically unstable after separation, but that the resulting eddies induce modest modifications of the mean potential vorticity along streamlines. These results suggest that mean uncompensated leakiness occurs mostly through inertial separation, for which a scaling analysis is presented. Implications for leakiness of other major boundary current systems are discussed.

Tidal currents and large-scale oceanic currents are known to modify ocean wave properties, causing extreme sea states that are a hazard to navigation. Recent advances in the understanding and modeling capability of open ocean currents have revealed the ubiquitous presence of eddies, fronts, and filaments at scales 10–100 km. Based on realistic numerical models, we show that these structures can be the main source of variability in significant wave heights at scales less than 200 km, including important variations down to 10 km. Model results are consistent with wave height variations along satellite altimeter tracks, resolved at scales larger than 50 km. The spectrum of significant wave heights is found to be of the order of 70‹Hs›2/(g2‹Tm0,-1›) times the current spectrum, where ‹Hs› is the spatially averaged significant wave height, ‹Tm0, -1› is the energy-averaged period, and g is the gravity acceleration. This variability induced by currents has been largely overlooked in spite of its relevance for extreme wave heights and remote sensing.

Monte Carlo simulations are widely used in nuclear physics to model experimental systems. In cases where there are significant unknown quantities, such as energies of states, an iterative process of simulating and fitting is often required to describe experimental data. We describe a Bayesian approach to fitting experimental data, designed for data from a 12Be(d,p) reaction measurement, using simulations made with GEANT4. Q-values from the 12C(d,p) reaction to well-known states in 13C are compared with simulations using BayesOpt. The energies of the states were not included in the simulation to reproduce the situation for 13Be where the states are poorly known. Both cases had low statistics and significant resolution broadening owing to large proton energy losses in the solid deuterium target. Excitation energies of the lowest three excited states in 13C were extracted to better than 90 keV, paving a way for extracting information on 13Be.

Background

Insight into type 5 long QT syndrome (LQT5) has been limited to case reports and small family series. Improved understanding of the clinical phenotype and genetic features associated with rare KCNE1 variants implicated in LQT5 was sought through an international multicenter collaboration.

Methods

Patients with either presumed autosomal dominant LQT5 (N = 229) or the recessive Type 2 Jervell and Lange-Nielsen syndrome (N = 19) were enrolled from 22 genetic arrhythmia clinics and 4 registries from 9 countries. KCNE1 variants were evaluated for ECG penetrance (defined as QTc >460 ms on presenting ECG) and genotype-phenotype segregation. Multivariable Cox regression was used to compare the associations between clinical and genetic variables with a composite primary outcome of definite arrhythmic events, including appropriate implantable cardioverter-defibrillator shocks, aborted cardiac arrest, and sudden cardiac death.

Results

A total of 32 distinct KCNE1 rare variants were identified in 89 probands and 140 genotype positive family members with presumed LQT5 and an additional 19 Type 2 Jervell and Lange-Nielsen syndrome patients. Among presumed LQT5 patients, the mean QTc on presenting ECG was significantly longer in probands (476.9±38.6 ms) compared with genotype positive family members (441.8±30.9 ms, P<0.001). ECG penetrance for heterozygous genotype positive family members was 20.7% (29/140). A definite arrhythmic event was experienced in 16.9% (15/89) of heterozygous probands in comparison with 1.4% (2/140) of family members (adjusted hazard ratio [HR] 11.6 [95% CI, 2.6-52.2]; P=0.001). Event incidence did not differ significantly for Type 2 Jervell and Lange-Nielsen syndrome patients relative to the overall heterozygous cohort (10.5% [2/19]; HR 1.7 [95% CI, 0.3-10.8], P=0.590). The cumulative prevalence of the 32 KCNE1 variants in the Genome Aggregation Database, which is a human database of exome and genome sequencing data from now over 140 000 individuals, was 238-fold greater than the anticipated prevalence of all LQT5 combined (0.238% vs 0.001%).

Conclusions

The present study suggests that putative/confirmed loss-of-function KCNE1 variants predispose to QT prolongation, however, the low ECG penetrance observed suggests they do not manifest clinically in the majority of individuals, aligning with the mild phenotype observed for Type 2 Jervell and Lange-Nielsen syndrome patients.