Coupled Model Simulation of Wind Stress Effect on Far Wakes of Ships in SAR Images

A high-resolution 3-D hydrodynamic model capable of simulating far wakes of ships has been implemented using computational fluid dynamics software. We feed the surface velocity field produced by the hydrodynamic model into a numerical radar imaging model to simulate synthetic aperture radar (SAR) signatures of the wake. Potential capabilities of this modeling method are demonstrated for an example of wind stress effects on the centerline (turbulent) ship wake. The numerical simulations show that an interaction of the wind-induced surface current with circulations in the ship wake results in a convergence zone on the upwind side of the centerline wake and a divergence zone on the downwind side. In the simulated radar image, the convergence zone appears to be bright because of enhanced surface roughness and radar backscattering. The divergence zone looks dark due to an attenuation of short gravity capillary waves and a corresponding reduction of the backscattered power. This combined hydrodynamic and radar imaging model predicts an asymmetry of the centerline wake with respect to the wind direction, which is consistent with observed ship wake signatures in high-resolution satellite SAR images. The approach developed in this work could be also useful for simulations of other natural and artificial fine-scale features on the sea surface (sharp frontal interfaces, freshwater plumes, etc.) and their interpretation in high-resolution SAR imagery

Modification of Turbulence at the Air-Sea Interface Due to the Presence of Surfactants and Implications for Gas Exchange. Part II: Numerical Simulations

We conducted high-resolution non-hydrostatic numerical simulations to study the effect of surfactants on near-surface turbulence. Laboratory experiments at the UM RSMAS ASIST facility presented in a companion paper report a reduction of turbulence below the air-sea interface and an increase of the surface drift velocity in the presence of surfactants. We implement the effect of surfactants as a rheological, viscoelastic boundary condition at the surface. Our numerical experiments are consistent with the results of the laboratory experiments. We also simulated the effect of surfactants on the temperature difference across the thermal molecular sublayer (cool skin) and on gas transfer velocity. The numerical simulations demonstrate an increase in the temperature difference across the cool skin and reduction of the gas transfer velocity in the presence of surfactant. The results also reveal the effect of surfactants on the different types of molecular sublayers (viscous, thermal and diffusion), which is important for the development of proper parameterization of the interfacial component of air-sea gas exchange under low and moderate wind speed conditions.https://nsuworks.nova.edu/occ_facbooks/1052/thumbnail.jp

Rudder Gap Flow Control for Cavitation Suppression

For the suppression of rudder cavitation, especially within and around the gap between the stationary and movable parts, flow control devices were developed. In the present study, both experimental and computational analyses of the flow control devices were carried out. The new rudder system is equipped with cam devices, which effectively close the gap between the stationary horn/pintle and movable flaps. Model scale experiments of surface pressure measurements, flow field visualization near the gap using PIV, and cavitation behavior observation were conducted in a cavitation tunnel. The experiments were simulated using a computational fluid dynamics tool and the results are compared for validation. It is confirmed that the flow control devices effectively suppresses the rudder gap cavitation and, at the same time, augments lifthttp://deepblue.lib.umich.edu/bitstream/2027.42/84266/1/CAV2009-final70.pd

SPIN90 Knockdown Attenuates the Formation and Movement of Endosomal Vesicles in the Early Stages of Epidermal Growth Factor Receptor Endocytosis

The finding that SPIN90 colocalizes with epidermal growth factor (EGF) in EEA1-positive endosomes prompted us to investigate the role of SPIN90 in endocytosis of the EGF receptor (EGFR). In the present study, we demonstrated that SPIN90 participates in the early stages of endocytosis, including vesicle formation and trafficking. Stable HeLa cells with knockdown of SPIN90 displayed significantly higher levels of surface EGFR than control cells. Analysis of the abundance and cellular distribution of EGFR via electron microscopy revealed that SPIN90 knockdown cells contain residual EGFR at cell membranes and fewer EGFR-containing endosomes, both features that reflect reduced endosome formation. The delayed early endosomal targeting capacity of SPIN90 knockdown cells led to increased EGFR stability, consistent with the observed accumulation of EGFR at the membrane. Small endosome sizes and reduced endosome formation in SPIN90 knockdown cells, observed using fluorescent confocal microscopy, strongly supported the involvement of SPIN90 in endocytosis of EGFR. Overexpression of SPIN90 variants, particularly the SH3, PRD, and CC (positions 643 - 722) domains, resulted in aberrant morphology of Rab5-positive endosomes (detected as small spots located near the cell membrane) and defects in endosomal movement. These findings clearly suggest that SPIN90 participates in the formation and movement of endosomes. Consistent with this, SPIN90 knockdown enhanced cell proliferation. The delay in EGFR endocytosis effectively increased the levels of endosomal EGFR, which triggered activation of ERK1/2 and cell proliferation via upregulation of cyclin D1. Collectively, our findings suggest that SPIN90 contributes to the formation and movement of endosomal vesicles, and modulates the stability of EGFR protein, which affects cell cycle progression via regulation of the activities of downstream proteins, such as ERK1/2, after EGF stimulation

The Relationship Between Ambulatory Arterial Stiffness Index and Blood Pressure Variability in Hypertensive Patients

Background and Objectives: Ambulatory arterial stiffness index (AASI) is well known as a predictor of cardiovascular mortality in hypertensive patients. Mathematically, AASI reflect the standard deviation (SD) of blood pressure (BP) variation. AASI is measured higher levels in non-dipper than dipper. Thus, AASI has a possibility of not only reflecting arterial stiffness but also BP variability and/or autonomic nervous dysfunction. Subjects and Methods: Consecutive data from 418 untreated hypertensive patients were analyzed retrospectively. We examined the association between the 24-hour ambulatory BP monitoring (ABPM) parameters and AASI. Results: AASI had a simple correlation with age (R=0.189, p<0.001), relative wall thickness (RWT) (R=0.115, p=0.019), left ventricular mass index (LVMI) (R=0.192, p<0.001), average systolic BP (SBP) (R=0.232, p<0.001), average pulse pressure (PP) (R=0.363, p<0.001), SD of diastolic BP (DBP) (R=-0.352,p<0.001), SD of PP (R=0.330, p<0.001), SD of heart rate (HR) (R=-0.268, p<0.001), and nocturnal dipping (R=-0.137, p=0.005). In multiple linear regression analysis model including clinical parameters and 24 hour-ABPM parameters, independent predictors of AASI were SD of PP (beta=1.246, p<0.001), SD of DBP (beta=-1.067, p<0.001), SD of SBP (beta=-0.197, p<0.001), and non-dipper (beta=0.054, p=0.033). Conclusion: AASI is closely correlated with BP variability. The result of this study shows that AASI is not only a parameter for arterial stiffness, but also a parameter for BP variability

Obesity and the Metabolic Syndrome in Korean Adolescents

This study evaluated the prevalence of metabolic syndrome and investigated its association with being overweight in Korean adolescents. Data were obtained from 1,393 students between 12 and 13 yr of age in a cross-sectional survey. We defined the metabolic syndrome using criteria analogous to the Third Report of the Adult Treatment Panel (ATP III) as having at least three of the following: fasting triglycerides ≥100 mg/dL; HDL <50 mg/dL; fasting glucose ≥110 mg/dL; waist circumference >75th percentile for age and gender; and systolic blood pressure >90th percentile for age, gender, and height. Weight status was assessed using the age- and gender-specific body mass index (BMI), and a BMI ≥85th percentile was classified as overweight. Of the adolescents, 5.5% met the criteria for the metabolic syndrome, and the prevalence increased with weight status; it was 1.6% for normal weight and 22.3% in overweight (p<0.001). In multivariate logistic regression analyses among adolescents, overweight status was independently associated with the metabolic syndrome (odds ratio, 17.7; 95% confidence interval, 10.0-31.2). Since childhood metabolic syndrome and obesity likely persist into adulthood, early identification helps target interventions to improve future cardiovascular health

Implicating genes, pleiotropy, and sexual dimorphism at blood lipid loci through multi-ancestry meta-analysis

Funding GMP, PN, and CW are supported by NHLBI R01HL127564. GMP and PN are supported by R01HL142711. AG acknowledge support from the Wellcome Trust (201543/B/16/Z), European Union Seventh Framework Programme FP7/2007–2013 under grant agreement no. HEALTH-F2-2013–601456 (CVGenes@Target) & the TriPartite Immunometabolism Consortium [TrIC]-Novo Nordisk Foundation’s Grant number NNF15CC0018486. JMM is supported by American Diabetes Association Innovative and Clinical Translational Award 1–19-ICTS-068. SR was supported by the Academy of Finland Center of Excellence in Complex Disease Genetics (Grant No 312062), the Finnish Foundation for Cardiovascular Research, the Sigrid Juselius Foundation, and University of Helsinki HiLIFE Fellow and Grand Challenge grants. EW was supported by the Finnish innovation fund Sitra (EW) and Finska Läkaresällskapet. CNS was supported by American Heart Association Postdoctoral Fellowships 15POST24470131 and 17POST33650016. Charles N Rotimi is supported by Z01HG200362. Zhe Wang, Michael H Preuss, and Ruth JF Loos are supported by R01HL142302. NJT is a Wellcome Trust Investigator (202802/Z/16/Z), is the PI of the Avon Longitudinal Study of Parents and Children (MRC & WT 217065/Z/19/Z), is supported by the University of Bristol NIHR Biomedical Research Centre (BRC-1215–2001) and the MRC Integrative Epidemiology Unit (MC_UU_00011), and works within the CRUK Integrative Cancer Epidemiology Programme (C18281/A19169). Ruth E Mitchell is a member of the MRC Integrative Epidemiology Unit at the University of Bristol funded by the MRC (MC_UU_00011/1). Simon Haworth is supported by the UK National Institute for Health Research Academic Clinical Fellowship. Paul S. de Vries was supported by American Heart Association grant number 18CDA34110116. Julia Ramierz acknowledges support by the People Programme of the European Union’s Seventh Framework Programme grant n° 608765 and Marie Sklodowska-Curie grant n° 786833. Maria Sabater-Lleal is supported by a Miguel Servet contract from the ISCIII Spanish Health Institute (CP17/00142) and co-financed by the European Social Fund. Jian Yang is funded by the Westlake Education Foundation. Olga Giannakopoulou has received funding from the British Heart Foundation (BHF) (FS/14/66/3129). CHARGE Consortium cohorts were supported by R01HL105756. Study-specific acknowledgements are available in the Additional file 32: Supplementary Note. The views expressed in this manuscript are those of the authors and do not necessarily represent the views of the National Heart, Lung, and Blood Institute; the National Institutes of Health; or the U.S. Department of Health and Human Services.Peer reviewedPublisher PD

Implicating genes, pleiotropy, and sexual dimorphism at blood lipid loci through multi-ancestry meta-analysis

Publisher Copyright: © 2022, The Author(s).Background: Genetic variants within nearly 1000 loci are known to contribute to modulation of blood lipid levels. However, the biological pathways underlying these associations are frequently unknown, limiting understanding of these findings and hindering downstream translational efforts such as drug target discovery. Results: To expand our understanding of the underlying biological pathways and mechanisms controlling blood lipid levels, we leverage a large multi-ancestry meta-analysis (N = 1,654,960) of blood lipids to prioritize putative causal genes for 2286 lipid associations using six gene prediction approaches. Using phenome-wide association (PheWAS) scans, we identify relationships of genetically predicted lipid levels to other diseases and conditions. We confirm known pleiotropic associations with cardiovascular phenotypes and determine novel associations, notably with cholelithiasis risk. We perform sex-stratified GWAS meta-analysis of lipid levels and show that 3–5% of autosomal lipid-associated loci demonstrate sex-biased effects. Finally, we report 21 novel lipid loci identified on the X chromosome. Many of the sex-biased autosomal and X chromosome lipid loci show pleiotropic associations with sex hormones, emphasizing the role of hormone regulation in lipid metabolism. Conclusions: Taken together, our findings provide insights into the biological mechanisms through which associated variants lead to altered lipid levels and potentially cardiovascular disease risk.Peer reviewe

Implicating genes, pleiotropy, and sexual dimorphism at blood lipid loci through multi-ancestry meta-analysis

Abstract Background Genetic variants within nearly 1000 loci are known to contribute to modulation of blood lipid levels. However, the biological pathways underlying these associations are frequently unknown, limiting understanding of these findings and hindering downstream translational efforts such as drug target discovery. Results To expand our understanding of the underlying biological pathways and mechanisms controlling blood lipid levels, we leverage a large multi-ancestry meta-analysis (N = 1,654,960) of blood lipids to prioritize putative causal genes for 2286 lipid associations using six gene prediction approaches. Using phenome-wide association (PheWAS) scans, we identify relationships of genetically predicted lipid levels to other diseases and conditions. We confirm known pleiotropic associations with cardiovascular phenotypes and determine novel associations, notably with cholelithiasis risk. We perform sex-stratified GWAS meta-analysis of lipid levels and show that 3–5% of autosomal lipid-associated loci demonstrate sex-biased effects. Finally, we report 21 novel lipid loci identified on the X chromosome. Many of the sex-biased autosomal and X chromosome lipid loci show pleiotropic associations with sex hormones, emphasizing the role of hormone regulation in lipid metabolism. Conclusions Taken together, our findings provide insights into the biological mechanisms through which associated variants lead to altered lipid levels and potentially cardiovascular disease risk