A mechanism of internal decadal atlantic ocean variability in a high-resolution coupled climate model

The North Atlantic Ocean subpolar gyre (NA SPG) is an important region for initialising decadal climate forecasts. Climate model simulations and palaeo climate reconstructions have indicated that this region could also exhibit large, internally generated variability on decadal timescales. Understanding these modes of variability, their consistency across models, and the conditions in which they exist, is clearly important for improving the skill of decadal predictions — particularly when these predictions are made with the same underlying climate models. Here we describe and analyse a mode of internal variability in the NA SPG in a state-of-the-art, high resolution, coupled climate model. This mode has a period of 17 years and explains 15–30% of the annual variance in related ocean indices. It arises due to the advection of heat content anomalies around the NA SPG. Anomalous circulation drives the variability in the southern half of the NA SPG, whilst mean circulation and anomalous temperatures are important in the northern half. A negative feedback between Labrador Sea temperatures/densities and those in the North Atlantic Current is identified, which allows for the phase reversal. The atmosphere is found to act as a positive feedback on to this mode via the North Atlantic Oscillation which itself exhibits a spectral peak at 17 years. Decadal ocean density changes associated with this mode are driven by variations in temperature, rather than salinity — a point which models often disagree on and which we suggest may affect the veracity of the underlying assumptions of anomaly-assimilating decadal prediction methodologies.

The Met Office Global Coupled model 2.0 (GC2) configuration

The latest coupled configuration of the Met Office Unified Model (Global Coupled configuration 2, GC2) is presented. This paper documents the model components which make up the configuration (although the scientific description of these components is detailed elsewhere) and provides a description of the coupling between the components. The performance of GC2 in terms of its systematic errors is assessed using a variety of diagnostic techniques. The configuration is intended to be used by the Met Office and collaborating institutes across a range of timescales, with the seasonal forecast system (GloSea5) and climate projection system (HadGEM) being the initial users. In this paper GC2 is compared against the model currently used operationally in those two systems. Overall GC2 is shown to be an improvement on the configurations used currently, particularly in terms of modes of variability (e.g. mid-latitude and tropical cyclone intensities, the Madden–Julian Oscillation and El Niño Southern Oscillation). A number of outstanding errors are identified with the most significant being a considerable warm bias over the Southern Ocean and a dry precipitation bias in the Indian and West African summer monsoons. Research to address these is ongoing.

Atmosphere-ocean coupled processes in the Madden-Julian oscillation

The Madden-Julian oscillation (MJO) is a convectively coupled 30-70 day (intraseasonal) tropical atmospheric mode that drives variations in global weather, but which is poorly simulated in most atmospheric general circulation models. Over the past two decades, field campaigns and modeling experiments have suggested that tropical atmosphere-ocean interactions may sustain or amplify the pattern of enhanced and suppressed atmospheric convection that defines the MJO, and encourage its eastward propagation through the Indian and Pacific Oceans. New observations collected during the past decade have advanced our understand of the ocean response to atmospheric MJO forcing and the resulting intraseasonal sea surface temperature (SST) fluctuations. Numerous modeling studies have revealed a considerable impact of the mean state on MJO ocean-atmosphere coupled processes, as well as the importance of resolving the diurnal cycle of atmosphere--upper-ocean interactions. New diagnostic methods provide insight to atmospheric variability and physical processes associated with the MJO, but offer limited insight on the role of ocean feedbacks. Consequently, uncertainty remains concerning the role of the ocean in MJO theory. Our understanding of how atmosphere-ocean coupled processes affect the MJO can be improved by collecting observations in poorly sampled regions of MJO activity, assessing oceanic and atmospheric drivers of surface fluxes, improving the representation of upper-ocean mixing in coupled-model simulations, designing model experiments that minimize mean-state differences, and developing diagnostic tools to evaluate the nature and role of coupled ocean-atmosphere processes over the MJO cycle.

Investigation of high-efficiency Wireless Power Transfer criteria of resonantly-coupled loops and dipoles through analysis of the figure of merit

The efficiency of a Wireless Power Transfer (WPT) system is greatly dependent on both the geometry and operating frequency of the transmitting and receiving structures. By using Coupled Mode Theory (CMT), the figure of merit is calculated for resonantly-coupled loop and dipole systems. An in-depth analysis of the figure of merit is performed with respect to the key geometric parameters of the loops and dipoles, along with the resonant frequency, in order to identify the key relationships leading to high-efficiency WPT. For systems consisting of two identical single-turn loops, it is shown that the choice of both the loop radius and resonant frequency are essential in achieving high-efficiency WPT. For the dipole geometries studied, it is shown that the choice of length is largely irrelevant and that as a result of their capacitive nature, low-MHz frequency dipoles are able to produce significantly higher figures of merit than those of the loops considered. The results of the figure of merit analysis are used to propose and subsequently compare two mid-range loop and dipole WPT systems of equal size and operating frequency, where it is shown that the dipole system is able to achieve higher efficiencies than the loop system of the distance range examined.

Regionally coupled atmosphere-ocean-sea ice-marine biogeochemistry model ROM: 1. Description and validation

The general circulation models used to simulate global climate typically feature resolution too coarse to reproduce many smaller-scale processes, which are crucial to determining the regional responses to climate change. A novel approach to downscale climate change scenarios is presented which includes the interactions between the North Atlantic Ocean and the European shelves as well as their impact on the North Atlantic and European climate. The goal of this paper is to introduce the global ocean-regional atmosphere coupling concept and to show the potential benefits of this model system to simulate present-day climate. A global ocean-sea ice-marine biogeochemistry model (MPIOM/HAMOCC) with regionally high horizontal resolution is coupled to an atmospheric regional model (REMO) and global terrestrial hydrology model (HD) via the OASIS coupler. Moreover, results obtained with ROM using NCEP/NCAR reanalysis and ECHAM5/MPIOM CMIP3 historical simulations as boundary conditions are presented and discussed for the North Atlantic and North European region. The validation of all the model components, i.e., ocean, atmosphere, terrestrial hydrology, and ocean biogeochemistry is performed and discussed. The careful and detailed validation of ROM provides evidence that the proposed model system improves the simulation of many aspects of the regional climate, remarkably the ocean, even though some biases persist in other model components, thus leaving potential for future improvement. We conclude that ROM is a powerful tool to estimate possible impacts of climate change on the regional scale.

Regulation of the ERK subgroup of MAP kinase cascades through G protein-coupled receptors.

The extracellularly-responsive kinase (ERK) subfamily of mitogen-activated protein kinases (MAPKs) has been implicated in the regulation of cell growth and differentiation. Activation of ERKs involves a two-step protein kinase cascade lying upstream from ERK, in which the Raf family are the MAPK kinase kinases and the MEK1/MEK2 isoforms are the MAPK kinases. The linear sequence of Raf --> MEK --> ERK constitutes the ERK cascade. Although the ERK cascade is activated through growth factor-regulated receptor protein tyrosine kinases, they are also modulated through G protein-coupled receptors (GPCRs). All four G protein subfamilies (Gq/11 Gi/o, Gs and G12/13) influence the activation state of ERKs. In this review, we describe the ERK cascade and characteristics of its activation through GPCRs. We also discuss the identity of the intervening steps that may couple agonist binding at GPCRs to activation of the ERK cascade.

Stimulation of the p38 mitogen-activated protein kinase pathway in neonatal rat ventricular myocytes by the G protein-coupled receptor agonists, endothelin-1 and phenylephrine: a role in cardiac myocyte hypertrophy?

We examined the activation of the p38 mitogen-activated protein kinase (p38-MAPK) pathway by the G protein-coupled receptor agonists, endothelin-1 and phenylephrine in primary cultures of cardiac myocytes from neonatal rat hearts. Both agonists increased the phosphorylation (activation) of p38-MAPK by approximately 12-fold. A p38-MAPK substrate, MAPK-activated protein kinase 2 (MAPKAPK2), was activated approximately fourfold and 10 microM SB203580, a p38-MAPK inhibitor, abolished this activation. Phosphorylation of the MAPKAPK2 substrate, heat shock protein 25/27, was also increased. Using selective inhibitors, activation of the p38-MAPK pathway by endothelin-1 was shown to involve protein kinase C but not Gi/Go nor the extracellularly responsive kinase (ERK) pathway. SB203580 failed to inhibit the morphological changes associated with cardiac myocyte hypertrophy induced by endothelin-1 or phenylephrine between 4 and 24 h. However, it decreased the myofibrillar organization and cell profile at 48 h. In contrast, inhibition of the ERK cascade with PD98059 prevented the increase in myofibrillar organization but not cell profile. These data are not consistent with a role for the p38-MAPK pathway in the immediate induction of the morphological changes of hypertrophy but suggest that it may be necessary over a longer period to maintain the response.

Activation of mitogen-activated protein kinases (p38-MAPKs, SAPKs/JNKs and ERKs) by the G-protein-coupled receptor agonist phenylephrine in the perfused rat heart.

We investigated the ability of phenylephrine (PE), an alpha-adrenergic agonist and promoter of hypertrophic growth in the ventricular myocyte, to activate the three best-characterized mitogen-activated protein kinase (MAPK) subfamilies, namely p38-MAPKs, SAPKs/JNKs (i.e. stress-activated protein kinases/c-Jun N-terminal kinases) and ERKs (extracellularly responsive kinases), in perfused contracting rat hearts. Perfusion of hearts with 100 microM PE caused a rapid (maximal at 10 min) 12-fold activation of two p38-MAPK isoforms, as measured by subsequent phosphorylation of a p38-MAPK substrate, recombinant MAPK-activated protein kinase 2 (MAPKAPK2). This activation coincided with phosphorylation of p38-MAPK. Endogenous MAPKAPK2 was activated 4-5-fold in these perfusions and this was inhibited completely by the p38-MAPK inhibitor, SB203580 (10 microM). Activation of p38-MAPK and MAPKAPK2 was also detected in non-contracting hearts perfused with PE, indicating that the effects were not dependent on the positive inotropic/chronotropic properties of the agonist. Although SAPKs/JNKs were also rapidly activated, the activation (2-3-fold) was less than that of p38-MAPK. The ERKs were activated by perfusion with PE and the activation was at least 50% of that seen with 1 microM PMA, the most powerful activator of the ERKs yet identified in cardiac myocytes. These results indicate that, in addition to the ERKs, two MAPK subfamilies, whose activation is more usually associated with cellular stresses, are activated by the Gq/11-protein-coupled receptor (Gq/11PCR) agonist, PE, in whole hearts. These data indicate that Gq/11PCR agonists activate multiple MAPK signalling pathways in the heart, all of which may contribute to the overall response (e.g. the development of the hypertrophic phenotype).

Regulation of Ras.GTP loading and Ras-Raf association in neonatal rat ventricular myocytes by G protein-coupled receptor agonists and phorbol ester. Activation of the extracellular signal-regulated kinase cascade by phorbol ester is mediated by Ras.

The small G protein Ras has been implicated in hypertrophy of cardiac myocytes. We therefore examined the activation (GTP loading) of Ras by the following hypertrophic agonists: phorbol 12-myristate 13-acetate (PMA), endothelin-1 (ET-1), and phenylephrine (PE). All three increased Ras.GTP loading by 10-15-fold (maximal in 1-2 min), as did bradykinin. Other G protein-coupled receptor agonists (e.g. angiotensin II, carbachol, isoproterenol) were less effective. Activation of Ras by PMA, ET-1, or PE was reduced by inhibition of protein kinase C (PKC), and that induced by ET-1 or PE was partly sensitive to pertussis toxin. 8-(4-Chlorophenylthio)-cAMP (CPT-cAMP) did not inhibit Ras.GTP loading by PMA, ET-1, or PE. The association of Ras with c-Raf protein was increased by PMA, ET-1, or PE, and this was inhibited by CPT-cAMP. However, only PMA and ET-1 increased Ras-associated mitogen-activated protein kinase kinase 1-activating activity, and this was decreased by PKC inhibition, pertussis toxin, and CPT-cAMP. PMA caused the rapid appearance of phosphorylated (activated) extracellular signal-regulated kinase in the nucleus, which was inhibited by a microinjected neutralizing anti-Ras antibody. We conclude that PKC- and Gi-dependent mechanisms mediate the activation of Ras in myocytes and that Ras activation is required for stimulation of extracellular signal-regulated kinase by PMA.

Activation of protein kinase cascades in the heart by hypertrophic G protein-coupled receptor agonists.

Cardiac myocyte hypertrophy involves changes in cell structure and alterations in protein expression regulated at both the transcriptional and translational levels. Hypertrophic G protein-coupled receptor (GPCR) agonists such as endothelin-(ET-1) and phenylephrine stimulate a number of protein kinase cascades in the heart. Mitogen-activated protein kinase (MAPK) cascades stimulated include the extracellularly regulated kinase cascade, the stress-activated protein kinase/c-Jun N-terminal kinase cascade, and the p38 MAPK cascade. All 3 pathways have been implicated in hypertrophy, but recent ex vivo evidence also suggests that there may be additional effects on cell survival. ET-1 and phenylephrine also stimulate the protein kinase B pathway, and this may be involved in the regulation of protein synthesis by these agonists. Thus, protein kinase-mediated signaling may be important in the regulation of the development of myocyte hypertrophy.

Atmospheric impact of Arctic Sea ice loss in a coupled ocean–atmosphere simulation

The atmospheric response to an idealized decline in Arctic sea ice is investigated in a novel fully coupled climate model experiment. In this experiment two ensembles of single-year model integrations are performed starting on 1 April, the approximate start of the ice melt season. By perturbing the initial conditions of sea ice thickness (SIT), declines in both sea ice concentration and SIT, which result in sea ice distributions that are similar to the recent sea ice minima of 2007 and 2012, are induced. In the ice loss regions there are strong (~3 K) local increases in sea surface temperature (SST); additionally, there are remote increases in SST in the central North Pacific and subpolar gyre in the North Atlantic. Over the central Arctic there are increases in surface air temperature (SAT) of ~8 K due to increases in ocean–atmosphere heat fluxes. There are increases in SAT over continental North America that are in good agreement with recent changes as seen by reanalysis data. It is estimated that up to two-thirds of the observed increase in SAT in this region could be related to Arctic sea ice loss. In early summer there is a significant but weak atmospheric circulation response that projects onto the summer North Atlantic Oscillation (NAO). In early summer and early autumn there is an equatorward shift of the eddy-driven jet over the North Atlantic as a result of a reduction in the meridional temperature gradients. In winter there is no projection onto a particular phase of the NAO.

An assessment of air-sea heat fluxes from ocean and coupled reanalyses

Sixteen monthly air–sea heat flux products from global ocean/coupled reanalyses are compared over 1993–2009 as part of the Ocean Reanalysis Intercomparison Project (ORA-IP). Objectives include assessing the global heat closure, the consistency of temporal variability, comparison with other flux products, and documenting errors against in situ flux measurements at a number of OceanSITES moorings. The ensemble of 16 ORA-IP flux estimates has a global positive bias over 1993–2009 of 4.2 ± 1.1 W m−2. Residual heat gain (i.e., surface flux + assimilation increments) is reduced to a small positive imbalance (typically, +1–2 W m−2). This compensation between surface fluxes and assimilation increments is concentrated in the upper 100 m. Implied steady meridional heat transports also improve by including assimilation sources, except near the equator. The ensemble spread in surface heat fluxes is dominated by turbulent fluxes (>40 W m−2 over the western boundary currents). The mean seasonal cycle is highly consistent, with variability between products mostly <10 W m−2. The interannual variability has consistent signal-to-noise ratio (~2) throughout the equatorial Pacific, reflecting ENSO variability. Comparisons at tropical buoy sites (10°S–15°N) over 2007–2009 showed too little ocean heat gain (i.e., flux into the ocean) in ORA-IP (up to 1/3 smaller than buoy measurements) primarily due to latent heat flux errors in ORA-IP. Comparisons with the Stratus buoy (20°S, 85°W) over a longer period, 2001–2009, also show the ORA-IP ensemble has 16 W m−2 smaller net heat gain, nearly all of which is due to too much latent cooling caused by differences in surface winds imposed in ORA-IP.

Modulation of equatorial Pacific westerly/easterly wind events by the Madden-Julian oscillation and convectively-coupled Rossby waves

Synoptic wind events in the equatorial Pacific strongly influence the El Niño/Southern Oscillation (ENSO) evolution. This paper characterizes the spatio-temporal distribution of Easterly (EWEs) and Westerly Wind Events (WWEs) and quantifies their relationship with intraseasonal and interannual large-scale climate variability. We unambiguously demonstrate that the Madden–Julian Oscillation (MJO) and Convectively-coupled Rossby Waves (CRW) modulate both WWEs and EWEs occurrence probability. 86 % of WWEs occur within convective MJO and/or CRW phases and 83 % of EWEs occur within the suppressed phase of MJO and/or CRW. 41 % of WWEs and 26 % of EWEs are in particular associated with the combined occurrence of a CRW/MJO, far more than what would be expected from a random distribution (3 %). Wind events embedded within MJO phases also have a stronger impact on the ocean, due to a tendency to have a larger amplitude, zonal extent and longer duration. These findings are robust irrespective of the wind events and MJO/CRW detection methods. While WWEs and EWEs behave rather symmetrically with respect to MJO/CRW activity, the impact of ENSO on wind events is asymmetrical. The WWEs occurrence probability indeed increases when the warm pool is displaced eastward during El Niño events, an increase that can partly be related to interannual modulation of the MJO/CRW activity in the western Pacific. On the other hand, the EWEs modulation by ENSO is less robust, and strongly depends on the wind event detection method. The consequences of these results for ENSO predictability are discussed.

The role of local atmospheric forcing on the modulation of the ocean mixed layer depth in reanalysis and a coupled single column ocean model

The role of the local atmospheric forcing on the ocean mixed layer depth (MLD) over the global oceans is studied using ocean reanalysis data products and a single-column ocean model coupled to an atmospheric general circulation model. The focus of this study is on how the annual mean and the seasonal cycle of the MLD relate to various forcing characteristics in different parts of the world's ocean, and how anomalous variations in the monthly mean MLD relate to anomalous atmospheric forcings. By analysing both ocean reanalysis data and the single-column ocean model, regions with different dominant forcings and different mean and variability characteristics of the MLD can be identified. Many of the global oceans' MLD characteristics appear to be directly linked to different atmospheric forcing characteristics at different locations. Here, heating and wind-stress are identified as the main drivers; in some, mostly coastal, regions the atmospheric salinity forcing also contributes. The annual mean MLD is more closely related to the annual mean wind-stress and the MLD seasonality is more closely to the seasonality in heating. The single-column ocean model, however, also points out that the MLD characteristics over most global ocean regions, and in particular the tropics and subtropics, cannot be maintained by local atmospheric forcings only, but are also a result of ocean dynamics that are not simulated in a single-column ocean model. Thus, lateral ocean dynamics are essentially in correctly simulating observed MLD.

Interactions between wind-blown snow redistribution and melt ponds in a coupled ocean–sea ice model

Introducing a parameterization of the interactions between wind-driven snow depth changes and melt pond evolution allows us to improve large scale models. In this paper we have implemented an explicit melt pond scheme and, for the first time, a wind dependant snow redistribution model and new snow thermophysics into a coupled ocean–sea ice model. The comparison of long-term mean statistics of melt pond fractions against observations demonstrates realistic melt pond cover on average over Arctic sea ice, but a clear underestimation of the pond coverage on the multi-year ice (MYI) of the western Arctic Ocean. The latter shortcoming originates from the concealing effect of persistent snow on forming ponds, impeding their growth. Analyzing a second simulation with intensified snow drift enables the identification of two distinct modes of sensitivity in the melt pond formation process. First, the larger proportion of wind-transported snow that is lost in leads directly curtails the late spring snow volume on sea ice and facilitates the early development of melt ponds on MYI. In contrast, a combination of higher air temperatures and thinner snow prior to the onset of melting sometimes make the snow cover switch to a regime where it melts entirely and rapidly. In the latter situation, seemingly more frequent on first-year ice (FYI), a smaller snow volume directly relates to a reduced melt pond cover. Notwithstanding, changes in snow and water accumulation on seasonal sea ice is naturally limited, which lessens the impacts of wind-blown snow redistribution on FYI, as compared to those on MYI. At the basin scale, the overall increased melt pond cover results in decreased ice volume via the ice-albedo feedback in summer, which is experienced almost exclusively by MYI.