42 resultados para mean pressure gradient.


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Arterial stiffness is an independent predictor of cardiovascular disease events and mortality, and like blood pressure, may be influenced by dairy food intake. Few studies have investigated the effects of consumption of these foods on prospective measures of arterial stiffness. The present analysis aimed to investigate the prospective relationship between milk, cheese, cream, and butter consumption and aortic pulse wave velocity, augmentation index, systolic and diastolic blood pressure, as well as cross-sectional relationships between these foods and systolic and diastolic blood pressure and metabolic markers using data from the Caerphilly Prospective Study. Included in this cohort were 2512 men, aged 45 to 59 years, who were followed up at 5-year intervals for a mean of 22.8 years (number follow-up 787). Augmentation index was 1.8% lower in subjects in the highest quartiles of dairy product intake compared with the lowest (P trend=0.021), whereas in the highest group of milk consumption systolic blood pressure was 10.4 mm Hg lower (P trend=0.033) than in nonmilk consumers after a 22.8-year follow-up. Cross-sectional analyses indicated that across increasing quartiles of butter intake, insulin (P trend=0.011), triacylglycerol (P trend=0.023), total cholesterol (P trend=0.002), and diastolic blood pressure (P trend=0.027) were higher. Across increasing groups of milk intake and quartiles of dairy product intake, glucose (P trend=0.032) and triglyceride concentrations (P trend=0.031) were lower, respectively. The present results confirm that consumption of milk predicts prospective blood pressure, whereas dairy product consumption, excluding butter, is not detrimental to arterial stiffness and metabolic markers. Further research is needed to better understand the mechanisms that underpin these relationships.

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Background and aims: Arterial stiffness is an independent predictor of cardiovascular disease (CVD) events and all-cause mortality and may be differentially affected by dietary fatty acid (FA) intake. The aim of this study was to investigate the relationship between FA consumption and arterial stiffness and blood pressure in a community-based population. Methods and results: The Caerphilly Prospective Study recruited 2398 men, aged 45-59 years, who were followed up at 5-year intervals for a mean of 17.8-years (n 787). A semi-quantitative food frequency questionnaire estimated intakes of total, saturated, mono- and poly-unsaturated fatty acids (SFA, MUFA, PUFA). Multiple regression models investigated associations between intakes of FA at baseline with aortic pulse wave velocity (aPWV), augmentation index (AIx), systolic and diastolic blood pressure (SBP, DBP) and pulse pressure after a 17.8-year follow-up - as well as cross-sectional relationships with metabolic markers. After adjustment, higher SFA consumption at baseline was associated with higher SBP (P = 0.043) and DBP (P = 0.002) and after a 17.8-year follow-up was associated with a 0.51 m/s higher aPWV (P = 0.006). After adjustment, higher PUFA consumption at baseline was associated with lower SBP (P = 0.022) and DBP (P = 0.036) and after a 17.8-year follow-up was associated with a 0.63 m/s lower aPWV (P = 0.007). Conclusion: This study suggests that consumption of SFA and PUFA have opposing effects on arterial stiffness and blood pressure. Importantly, this study suggests that consumption of FA is an important risk factor for arterial stiffness and CVD.

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he classical problem of the response of a balanced, axisymmetric vortex to thermal and mechanical forcing is re-examined, paying special attention to the lower boundary condition. The correct condition is DΦ/Dt = 0, where Φ is the geopotential and D/Dt the material derivative, which explicitly accounts for a mass redistribution as part of the mean-flow response. This redistribution is neglected when using the boundary condition Dp/Dt = 0, which has conventionally been applied in this problem. It is shown that applying the incorrect boundary condition, and thereby ignoring the surface pressure change, leads to a zonal wind acceleration δū/δt that is too strong, especially near the surface. The effect is significant for planetary-scale forcing even when applied at tropopause level. A comparison is made between the mean-flow evolution in a baroclinic life-cycle, as simulated in a fully nonlinear, primitive-equation model, and that predicted by using the simulated eddy fluxes in the zonally-symmetric response problem. Use of the correct lower boundary condition is shown to lead to improved agreement.

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The authors study the role of ocean heat transport (OHT) in the maintenance of a warm, equable, ice-free climate. An ensemble of idealized aquaplanet GCM calculations is used to assess the equilibrium sensitivity of global mean surface temperature and its equator-to-pole gradient (ΔT) to variations in OHT, prescribed through a simple analytical formula representing export out of the tropics and poleward convergence. Low-latitude OHT warms the mid- to high latitudes without cooling the tropics; increases by 1°C and ΔT decreases by 2.6°C for every 0.5-PW increase in OHT across 30° latitude. This warming is relatively insensitive to the detailed meridional structure of OHT. It occurs in spite of near-perfect atmospheric compensation of large imposed variations in OHT: the total poleward heat transport is nearly fixed. The warming results from a convective adjustment of the extratropical troposphere. Increased OHT drives a shift from large-scale to convective precipitation in the midlatitude storm tracks. Warming arises primarily from enhanced greenhouse trapping associated with convective moistening of the upper troposphere. Warming extends to the poles by atmospheric processes even in the absence of high-latitude OHT. A new conceptual model for equable climates is proposed, in which OHT plays a key role by driving enhanced deep convection in the midlatitude storm tracks. In this view, the climatic impact of OHT depends on its effects on the greenhouse properties of the atmosphere, rather than its ability to increase the total poleward energy transport.

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In a series of papers, Killworth and Blundell have proposed to study the effects of a background mean flow and topography on Rossby wave propagation by means of a generalized eigenvalue problem formulated in terms of the vertical velocity, obtained from a linearization of the primitive equations of motion. However, it has been known for a number of years that this eigenvalue problem contains an error, which Killworth was prevented from correcting himself by his unfortunate passing and whose correction is therefore taken up in this note. Here, the author shows in the context of quasigeostrophic (QG) theory that the error can ulti- mately be traced to the fact that the eigenvalue problem for the vertical velocity is fundamentally a non- linear one (the eigenvalue appears both in the numerator and denominator), unlike that for the pressure. The reason that this nonlinear term is lacking in the Killworth and Blundell theory comes from neglecting the depth dependence of a depth-dependent term. This nonlinear term is shown on idealized examples to alter significantly the Rossby wave dispersion relation in the high-wavenumber regime but is otherwise irrelevant in the long-wave limit, in which case the eigenvalue problems for the vertical velocity and pressure are both linear. In the general dispersive case, however, one should first solve the generalized eigenvalue problem for the pressure vertical structure and, if needed, diagnose the vertical velocity vertical structure from the latter.

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The protein encoded by the PPARGC1A gene is expressed at high levels in metabolically active tissues and is involved in the control of oxidative stress via reactive oxygen species detoxification. Several recent reports suggest that the PPARGC1A Gly482Ser (rs8192678) missense polymorphism may relate inversely with blood pressure. We used conventional meta-analysis methods to assess the association between Gly482Ser and systolic (SBP) or diastolic blood pressures (DBP) or hypertension in 13,949 individuals from 17 studies, of which 6,042 were previously unpublished observations. The studies comprised cohorts of white European, Asian, and American Indian adults, and adolescents from South America. Stratified analyses were conducted to control for population stratification. Pooled genotype frequencies were 0.47 (Gly482Gly), 0.42 (Gly482Ser), and 0.11 (Ser482Ser). We found no evidence of association between Gly482Ser and SBP [Gly482Gly: mean = 131.0 mmHg, 95% confidence interval (CI) = 130.5-131.5 mmHg; Gly482Ser mean = 133.1 mmHg, 95% CI = 132.6-133.6 mmHg; Ser482Ser: mean = 133.5 mmHg, 95% CI = 132.5-134.5 mmHg; P = 0.409] or DBP (Gly482Gly: mean = 80.3 mmHg, 95% CI = 80.0-80.6 mmHg; Gly482Ser mean = 81.5 mmHg, 95% CI = 81.2-81.8 mmHg; Ser482Ser: mean = 82.1 mmHg, 95% CI = 81.5-82.7 mmHg; P = 0.651). Contrary to previous reports, we did not observe significant effect modification by sex (SBP, P = 0.966; DBP, P = 0.715). We were also unable to confirm the previously reported association between the Ser482 allele and hypertension [odds ratio: 0.97, 95% CI = 0.87-1.08, P = 0.585]. These results were materially unchanged when analyses were focused on whites only. However, statistical evidence of gene-age interaction was apparent for DBP [Gly482Gly: 73.5 (72.8, 74.2), Gly482Ser: 77.0 (76.2, 77.8), Ser482Ser: 79.1 (77.4, 80.9), P = 4.20 x 10(-12)] and SBP [Gly482Gly: 121.4 (120.4, 122.5), Gly482Ser: 125.9 (124.6, 127.1), Ser482Ser: 129.2 (126.5, 131.9), P = 7.20 x 10(-12)] in individuals <50 yr (n = 2,511); these genetic effects were absent in those older than 50 yr (n = 5,088) (SBP, P = 0.41; DBP, P = 0.51). Our findings suggest that the PPARGC1A Ser482 allele may be associated with higher blood pressure, but this is only apparent in younger adults.

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The role of eddy fluxes in the general circulation is often approached by treating eddies as (macro)turbulence. In this approach, the eddies act to diffuse certain quasiconservative quantities, such as potential vorticity (PV), along isentropic surfaces in the free atmosphere. The eddy fluxes are determined primarily by the eddy diffusivities and are necessarily down-gradient of the basic state PV field. Support for the (macro)turbulence approach stems from the fact that the eddy fluxes of PV in the free atmosphere are generally down-gradient in the long-term mean. Here we call attention to a pronounced and significant region of upgradient eddy PV fluxes on the poleward flank of the jet core in both hemispheres. The region of up-gradient (i.e., notionally “antidiffusive”) eddy PV fluxes is most pronounced during the winter and spring seasons and partially contradicts the turbulence approach described above. Analyses of the PV variance (potential enstrophy) budget suggest that the up-gradient PV fluxes represent local wave decay and are maintained by poleward fluxes of PV variance. Finite-amplitude effects thus represent leading order contributions to the PV variance budget, whereas dissipation is only of secondary importance locally. The appearance of up-gradient PV fluxes in the long-term mean is associated with the poleward shift of the jet—and thus the region of wave decay relative to wave growth—following wave-breaking events.

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A parameterization of mesoscale eddies in coarse-resolution ocean general circulation models (GCM) is formulated and implemented using a residual-mean formalism. In that framework, mean buoyancy is advected by the residual velocity (the sum of the Eulerian and eddy-induced velocities) and modified by a residual flux which accounts for the diabatic effects of mesoscale eddies. The residual velocity is obtained by stepping forward a residual-mean momentum equation in which eddy stresses appear as forcing terms. Study of the spatial distribution of eddy stresses, derived by using them as control parameters to ‘‘fit’’ the residual-mean model to observations, supports the idea that eddy stresses can be likened to a vertical down-gradient flux of momentum with a coefficient which is constant in the vertical. The residual eddy flux is set to zero in the ocean interior, where mesoscale eddies are assumed to be quasi-adiabatic, but is parameterized by a horizontal down-gradient diffusivity near the surface where eddies develop a diabatic component as they stir properties horizontally across steep isopycnals. The residual-mean model is implemented and tested in the MIT general circulation model. It is shown that the resulting model (1) has a climatology that is superior to that obtained using the Gent and McWilliams parameterization scheme with a spatially uniform diffusivity and (2) allows one to significantly reduce the (spurious) horizontal viscosity used in coarse resolution GCMs.

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The generation of flow and current vortices in the dayside auroral ionosphere has been predicted for two processes ocurring at the dayside magnetopause. The first of these mechanisms is time-dependent magnetic reconnection, in “flux transfer events” (FTEs); the second is the action of solar wind dynamic pressure changes. The ionospheric flow signature of an FTE should be a twin vortex, with the mean flow velocity in the central region of the pattern equal to the velocity of the pattern as a whole. On the other hand, a pulse of enhanced or reduced dynamic pressure is also expected to produce a twin vortex, but with the central plasma flow being generally different in speed from, and almost orthogonal to, the motion of the whole pattern. In this paper, we make use of this distinction to discuss recent observations of vortical flow patterns in the dayside auroral ionosphere in terms of one or other of the proposed mechanisms. We conclude that some of the observations reported are consistent only with the predicted signature of FTEs. We then evaluate the dimensions of the open flux tubes required to explain some recent simultaneous radar and auroral observations and infer that they are typically 300 km in north–south extent but up to 2000 km in longitudinal extent (i.e., roughly 5 hours of MLT). Hence these observations suggest that recent theories of FTEs which invoke time-varying reconnection at an elongated neutral line may be correct. We also present some simultaneous observations of the interplanetary magnetic field (IMF) and solar wind dynamic pressure (observed using the IMP8 satellite) and the ionospheric flow (observed using the EISCAT radar) which are also only consistent with the FTE model. We estimate that for continuously southward IMF ( ≈ 5 nT) these FTEs contribute about 30 kV to the mean total transpolar voltage (∼30%).

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Numerical simulations are performed to assess the influence of the large-scale circulation on the transition from suppressed to active convection. As a model tool, we used a coupled-column model. It consists of two cloud-resolving models which are fully coupled via a large-scale circulation which is derived from the requirement that the instantaneous domain-mean potential temperature profiles of the two columns remain close to each other. This is known as the weak-temperature gradient approach. The simulations of the transition are initialized from coupled-column simulations over non-uniform surface forcing and the transition is forced within the dry column by changing the local and/or remote surface forcings to uniform surface forcing across the columns. As the strength of the circulation is reduced to zero, moisture is recharged into the dry column and a transition to active convection occurs once the column is sufficiently moistened to sustain deep convection. Direct effects of changing surface forcing occur over the first few days only. Afterward, it is the evolution of the large-scale circulation which systematically modulates the transition. Its contributions are approximately equally divided between the heating and moistening effects. A transition time is defined to summarize the evolution from suppressed to active convection. It is the time when the rain rate within the dry column is halfway to the mean value obtained at equilibrium over uniform surface forcing. The transition time is around twice as long for a transition that is forced remotely compared to a transition that is forced locally. Simulations in which both local and remote surface forcings are changed produce intermediate transition times.

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Background: Public health strategies to lower cardiovascular disease (CVD) risk involve reducing dietary saturated fatty acid (SFA) intake to ≤10% of total energy (%TE). However, the optimal type of replacement fat is unclear. Objective: We investigated the substitution of 9.5-9.6%TE dietary SFA with either monounsaturated (MUFA) or n-6 polyunsaturated fatty acids (PUFA) on vascular function and other CVD risk factors. Design: Using a randomized, controlled, single-blind, parallel group dietary intervention, 195 men and women aged 21-60 y with moderate CVD risk (≥50% above the population mean) from the United Kingdom followed one of three 16-wk isoenergetic diets (%TE target compositions, total fat:SFA:MUFA:n-6 PUFA): SFA-rich (36:17:11:4, n = 65), MUFA-rich (36:9:19:4, n = 64) or n-6 PUFA-rich (36:9:13:10, n = 66). The primary outcome measure was flow-mediated dilatation (%FMD); secondary outcome measures included fasting serum lipids, microvascular reactivity, arterial stiffness, ambulatory blood pressure, and markers of insulin resistance, inflammation and endothelial activation. Results: Replacing SFA with MUFA or n-6 PUFA did not significantly impact on %FMD (primary endpoint) or other measures of vascular reactivity. Of the secondary outcome measures, substitution of SFA with MUFA attenuated the increase in night systolic blood pressure (-4.9 mm Hg, P = 0.019) and reduced E-selectin (-7.8%, P = 0.012). Replacement with MUFA or n-6 PUFA lowered fasting serum total cholesterol (TC; -8.4% and -9.2%, respectively), low-density lipoprotein cholesterol (-11.3% and -13.6%) and TC to high-density lipoprotein cholesterol ratio (-5.6% and -8.5%) (P ≤ 0.001). These changes in low-density lipoprotein cholesterol equate to an estimated 17-20% reduction in CVD mortality. Conclusions: Substitution of 9.5-9.6%TE dietary SFA with either MUFA or n-6 PUFA did not impact significantly on %FMD or other measures of vascular function. However, the beneficial effects on serum lipid biomarkers, blood pressure and E-selectin offer a potential public health strategy for CVD risk reduction.

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Background: Although a large number of randomized controlled trials (RCTs) have examined the impact of the n-3 (ω-3) fatty acids EPA (20:5n-3) and DHA (22:6n-3) on blood pressure and vascular function, the majority have used doses of EPA+DHA of > 3 g per d,which are unlikely to be achieved by diet manipulation. Objective: The objective was to examine, using a retrospective analysis from a multi-center RCT, the impact of recommended, dietary achievable EPA+DHA intakes on systolic and diastolic blood pressure and microvascular function in UK adults. Design: Healthy men and women (n = 312) completed a double-blind, placebo-controlled RCT consuming control oil, or fish oil providing 0.7 g or 1.8 g EPA+DHA per d in random order each for 8 wk. Fasting blood pressure and microvascular function (using Laser Doppler Iontophoresis) were assessed and plasma collected for the quantification of markers of vascular function. Participants were retrospectively genotyped for the eNOS rs1799983 variant. Results: No impact of n-3 fatty acid treatment or any treatment * eNOS genotype interactions were evident in the group as a whole for any of the clinical or biochemical outcomes. Assessment of response according to hypertension status at baseline indicated a significant (P=0.046) fish oil-induced reduction (mean 5 mmHg) in systolic blood pressure specifically in those with isolated systolic hypertension (n=31). No dose response was observed. Conclusions: These findings indicate that, in those with isolated systolic hypertension, daily doses of EPA+DHA as low as 0.7 g bring about clinically meaningful blood pressure reductions which, at a population level, would be associated with lower cardiovascular disease risk. Confirmation of findings in an RCT where participants are prospectively recruited on the basis of blood pressure status is required to draw definite conclusions. The Journal of Nutrition NUTRITION/2015/220475 Version 4