Bjerknes-like Compensation in the Wintertime North Pacific

Observational and model evidence has been mounting that mesoscale eddies play an important role in air–sea interaction in the vicinity of western boundary currents and can affect the jet stream storm track. What is less clear is the interplay between oceanic and atmospheric meridional heat transport in the vicinity of western boundary currents. It is first shown that variability in the North Pacific, particularly in the Kuroshio Extension region, simulated by a high-resolution fully coupled version of the Community Earth System Model matches observations with similar mechanisms and phase relationships involved in the variability. The Pacific decadal oscillation (PDO) is correlated with sea surface height anomalies generated in the central Pacific that propagate west preceding Kuroshio Extension variability with a ~3–4-yr lag. It is then shown that there is a near compensation of O(0.1) PW (PW ≡ 10^(15) W) between wintertime atmospheric and oceanic meridional heat transport on decadal time scales in the North Pacific. This compensation has characteristics of Bjerknes compensation and is tied to the mesoscale eddy activity in the Kuroshio Extension region

What Maintains the SST Front North of the Eastern Pacific Equatorial Cold Tongue?

A coupled ocean–atmosphere regional model suggests a mechanism for formation of a sharp sea surface temperature (SST) front north of the equator in the eastern Pacific Ocean in boreal summer and fall. Meridional convergence of Ekman transport at 5°N is forced by eastward turning of the southeasterly cross-equatorial wind, but the SST front forms considerably south of the maximum Ekman convergence. Geostrophic equatorward flow at 3°N in the lower half of the isothermally mixed layer enhances mixed layer convergence. Cold water is upwelled on or south of the equator and is advected poleward by mean mixed layer flow and by eddies. The mixed layer current convergence in the north confines the cold advection, so the SST front stays close to the equator. Warm advection from the north and cold advection from the south strengthen the front. In the Southern Hemisphere, a continuous southwestward current advects cold water far from the upwelling core. The cold tongue is warmed by the net surface flux, which is dominated by solar radiation. Evaporation and net surface cooling are at a maximum just north of the SST front where relatively cool dry air is advected northward over warm SST. The surface heat flux is decomposed into a response to SST alone, and an atmospheric feedback. The atmospheric feedback enhances cooling on the north side of the front by 178 W m⁻², about half of which is due to enhanced evaporation from cold dry advection, while the other half is due to cloud radiative forcing.Keywords: Heat flux, Ekman pumping, Convergence, Fronts, Sea surface temperatur

A Regional Ocean–Atmosphere Model for Eastern Pacific Climate: Toward Reducing Tropical Biases

The tropical Pacific Ocean is a climatically important region, home to El Niño and the Southern Oscillation. The simulation of its climate remains a challenge for global coupled ocean–atmosphere models, which suffer large biases especially in reproducing the observed meridional asymmetry across the equator in sea surface temperature (SST) and rainfall. A basin ocean general circulation model is coupled with a full-physics regional atmospheric model to study eastern Pacific climate processes. The regional ocean–atmosphere model (ROAM) reproduces salient features of eastern Pacific climate, including a northward-displaced intertropical convergence zone (ITCZ) collocated with a zonal band of high SST, a low-cloud deck in the southeastern tropical Pacific, the equatorial cold tongue, and its annual cycle. The simulated low-cloud deck experiences significant seasonal variations in vertical structure and cloudiness; cloud becomes decoupled and separated from the surface mixed layer by a stable layer in March when the ocean warms up, leading to a reduction in cloudiness. The interaction of low cloud and SST is an important internal feedback for the climatic asymmetry between the Northern and Southern Hemispheres. In an experiment where the cloud radiative effect is turned off, this climatic asymmetry weakens substantially, with the ITCZ migrating back and forth across the equator following the sun. In another experiment where tropical North Atlantic SST is lowered by 2°C—say, in response to a slow-down of the Atlantic thermohaline circulation as during the Younger Dryas—the equatorial Pacific SST decreases by up to 3°C in January–April but changes much less in other seasons, resulting in a weakened equatorial annual cycle. The relatively high resolution (0.5°) of the ROAM enables it to capture mesoscale features, such as tropical instability waves, Central American gap winds, and a thermocline dome off Costa Rica. The implications for tropical biases and paleoclimate research are discussed.Keywords: Ocean models, Cloud radiative effects, Model evaluation, Pacific Ocean, Climate predictionKeywords: Ocean models, Cloud radiative effects, Model evaluation, Pacific Ocean, Climate predictio

Delayed mucosal anti-viral responses despite robust peripheral inflammation in fatal COVID-19

Background While inflammatory and immune responses to SARS-CoV-2 infection in peripheral blood are extensively described, responses at the upper respiratory mucosal site of initial infection are relatively poorly defined. We sought to identify mucosal cytokine/chemokine signatures that distinguished COVID-19 severity categories, and relate these to disease progression and peripheral inflammation. Methods We measured 35 cytokines and chemokines in nasal samples from 274 patients hospitalised with COVID-19. Analysis considered the timing of sampling during disease, as either the early (0-5 days post-symptom onset) or late (6-20 days post-symptom onset). Results Patients that survived severe COVID-19 showed IFN-dominated mucosal immune responses (IFN-γ, CXCL10 and CXCL13) early in infection. These early mucosal responses were absent in patients that would progress to fatal disease despite equivalent SARS-CoV-2 viral load. Mucosal inflammation in later disease was dominated by IL-2, IL-10, IFN-γ, and IL-12p70, which scaled with severity but did not differentiate patients who would survive or succumb to disease. Cytokines and chemokines in the mucosa showed distinctions from responses evident in the peripheral blood, particularly during fatal disease. Conclusions Defective early mucosal anti-viral responses anticipate fatal COVID-19 but are not associated with viral load. Early mucosal immune responses may define the trajectory of severe COVID-19

A prenylated dsRNA sensor protects against severe COVID-19

Inherited genetic factors can influence the severity of COVID-19, but the molecular explanation underpinning a genetic association is often unclear. Intracellular antiviral defenses can inhibit the replication of viruses and reduce disease severity. To better understand the antiviral defenses relevant to COVID-19, we used interferon-stimulated gene (ISG) expression screening to reveal that OAS1, through RNase L, potently inhibits SARS-CoV-2. We show that a common splice-acceptor SNP (Rs10774671) governs whether people express prenylated OAS1 isoforms that are membrane-associated and sense specific regions of SARS-CoV-2 RNAs, or only express cytosolic, nonprenylated OAS1 that does not efficiently detect SARS-CoV-2. Importantly, in hospitalized patients, expression of prenylated OAS1 was associated with protection from severe COVID-19, suggesting this antiviral defense is a major component of a protective antiviral response

Effect of angiotensin-converting enzyme inhibitor and angiotensin receptor blocker initiation on organ support-free days in patients hospitalized with COVID-19

IMPORTANCE Overactivation of the renin-angiotensin system (RAS) may contribute to poor clinical outcomes in patients with COVID-19. Objective To determine whether angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) initiation improves outcomes in patients hospitalized for COVID-19. DESIGN, SETTING, AND PARTICIPANTS In an ongoing, adaptive platform randomized clinical trial, 721 critically ill and 58 non–critically ill hospitalized adults were randomized to receive an RAS inhibitor or control between March 16, 2021, and February 25, 2022, at 69 sites in 7 countries (final follow-up on June 1, 2022). INTERVENTIONS Patients were randomized to receive open-label initiation of an ACE inhibitor (n = 257), ARB (n = 248), ARB in combination with DMX-200 (a chemokine receptor-2 inhibitor; n = 10), or no RAS inhibitor (control; n = 264) for up to 10 days. MAIN OUTCOMES AND MEASURES The primary outcome was organ support–free days, a composite of hospital survival and days alive without cardiovascular or respiratory organ support through 21 days. The primary analysis was a bayesian cumulative logistic model. Odds ratios (ORs) greater than 1 represent improved outcomes. RESULTS On February 25, 2022, enrollment was discontinued due to safety concerns. Among 679 critically ill patients with available primary outcome data, the median age was 56 years and 239 participants (35.2%) were women. Median (IQR) organ support–free days among critically ill patients was 10 (–1 to 16) in the ACE inhibitor group (n = 231), 8 (–1 to 17) in the ARB group (n = 217), and 12 (0 to 17) in the control group (n = 231) (median adjusted odds ratios of 0.77 [95% bayesian credible interval, 0.58-1.06] for improvement for ACE inhibitor and 0.76 [95% credible interval, 0.56-1.05] for ARB compared with control). The posterior probabilities that ACE inhibitors and ARBs worsened organ support–free days compared with control were 94.9% and 95.4%, respectively. Hospital survival occurred in 166 of 231 critically ill participants (71.9%) in the ACE inhibitor group, 152 of 217 (70.0%) in the ARB group, and 182 of 231 (78.8%) in the control group (posterior probabilities that ACE inhibitor and ARB worsened hospital survival compared with control were 95.3% and 98.1%, respectively). CONCLUSIONS AND RELEVANCE In this trial, among critically ill adults with COVID-19, initiation of an ACE inhibitor or ARB did not improve, and likely worsened, clinical outcomes. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT0273570

The Global Sink of Available Potential Energy by Mesoscale Air‐Sea Interaction

Abstract The thermal component of oceanic eddy available potential energy (EPE) generation due to air‐sea interaction is proportional to the product of anomalous sea surface temperature (SST) and net air‐sea heat flux (SHF). In this study we assess EPE generation and its timescale and space‐scale dependence from observations and a high‐resolution coupled climate model. A dichotomy exists in the literature with respect to the sign of this term, that is, whether it is a source or a sink of EPE. We resolve this dichotomy by partitioning the SST and net heat flux into climatological mean, climatological seasonal cycle, and remaining transient contributions, thereby separating the mesoscale eddy variability from the forced seasonal cycle. In this decomposition the mesoscale air‐sea SST‐SHF feedbacks act as a 0.1 TW global sink of EPE. In regions of the ocean with a large seasonal cycle, for example, midlatitudes of the Northern Hemisphere, the EPE generation by the forced seasonal cycle exceeds the mesoscale variability sink, such that the global generation by seasonal plus eddy variability acts as a 0.8 TW source. EPE destruction is largest in the midlatitude western boundary currents due to mesoscale air‐sea interaction and in the tropical Pacific where SST variability is due mainly to the El Niño–Southern Oscillation. The EPE sink in western boundary currents is spatially aligned with SST gradients and offset to the poleward side of currents, while the mean and seasonal generation are aligned with the warm core of the current. By successively smoothing the data in space and time we find that half of the EPE sink is confined to timescales less than annual and length scales less than 2°, within the oceanic mesoscale band