The frequency and dynamics of stratospheric sudden warmings in the 21st century

Changes to stratospheric sudden warmings (SSWs) over the coming century, as predicted by the Geophysical Fluid Dynamics Laboratory (GFDL) chemistry climate model [Atmospheric Model With Transport and Chemistry (AMTRAC)], are investigated in detail. Two sets of integrations, each a three-member ensemble, are analyzed. The first set is driven with observed climate forcings between 1960 and 2004; the second is driven with climate forcings from a coupled model run, including trace gas concentrations representing a midrange estimate of future anthropogenic emissions between 1990 and 2099. A small positive trend in the frequency of SSWs is found. This trend, amounting to 1 event/decade over a century, is statistically significant at the 90% confidence level and is consistent over the two sets of model integrations. Comparison of the model SSW climatology between the late 20th and 21st centuries shows that the increase is largest toward the end of the winter season. In contrast, the dynamical properties are not significantly altered in the coming century, despite the increase in SSW frequency. Owing to the intrinsic complexity of our model, the direct cause of the predicted trend in SSW frequency remains an open question.

A new look at stratospheric sudden warmings. Part III. Polar vortex evolution and vertical structure

The evolution of the Arctic polar vortex during observed major mid-winter stratospheric sudden warmings (SSWs) is investigated for the period 1957-2002, using European Centre for Medium-Range Weather Forecasts (ECMWF) ERA-40 Ertel’s potential vorticity (PV) and temperature fields. Time-lag composites of vertically weighted PV, calculated relative to the SSW onset time, are derived for both vortex displacement SSWs and vortex splitting SSWs, by averaging over the 15 recorded displacement and 13 splitting events. The evolving vertical structure of the polar vortex during a typical SSW of each type is clearly illustrated by plotting an isosurface of the composite PV field, and is shown to be very close to that observed during representative individual events. Results are verified by comparison with an elliptical diagnostic vortex moment technique. For both types of SSW, little variation is found between individual events in the orientation of the developing vortex relative to the underlying topography, i.e. the location of the vortex during SSWs of each type is largely fixed in relation to the Earth’s surface. During each type of SSW, the vortex is found to have a distinctive vertical structure. Vortex splitting events are typically barotropic, with the vortex split occurring near-simultaneously over a large altitude range (20-40 km). In the majority of cases, of the two daughter vortices formed, it is the ‘Siberian’ vortex that dominates over its ‘Canadian’ counterpart. In contrast, displacement events are characterized by a very clear baroclinic structure; the vortex tilts significantly westward with height, so that the top and bottom of the vortex are separated by nearly 180◦ longitude before the upper vortex is sheared away and destroyed.

Sudden stratospheric warmings as noise-induced transitions

Sudden stratospheric warmings (SSWs) are usually considered to be initiated by planetary wave activity. Here it is asked whether small-scale variability (e.g., related to gravity waves) can lead to SSWs given a certain amount of planetary wave activity that is by itself not sufficient to cause a SSW. A highly vertically truncated version of the Holton–Mass model of stratospheric wave–mean flow interaction, recently proposed by Ruzmaikin et al., is extended to include stochastic forcing. In the deterministic setting, this low-order model exhibits multiple stable equilibria corresponding to the undisturbed vortex and SSW state, respectively. Momentum forcing due to quasi-random gravity wave activity is introduced as an additive noise term in the zonal momentum equation. Two distinct approaches are pursued to study the stochastic system. First, the system, initialized at the undisturbed state, is numerically integrated many times to derive statistics of first passage times of the system undergoing a transition to the SSW state. Second, the Fokker–Planck equation corresponding to the stochastic system is solved numerically to derive the stationary probability density function of the system. Both approaches show that even small to moderate strengths of the stochastic gravity wave forcing can be sufficient to cause a SSW for cases for which the deterministic system would not have predicted a SSW.

A Possible Influence of Equatorial Winds on the September 2002 Southern Hemisphere Sudden Warming Event

The stratospheric sudden warming in the Southern Hemisphere (SH) in September 2002 was unexpected for two reasons. First, planetary wave activity in the Southern Hemisphere is very weak, and midwinter warmings have never been observed, at least not since observations of the upper stratosphere became regularly available. Second, the warming occurred in a west phase of the quasi-biennial oscillation (QBO) in the lower stratosphere. This is unexpected because warmings are usually considered to be more likely in the east phase of the QBO, when a zero wind line is present in the winter subtropics and hence confines planetary wave propagation to higher latitudes closer to the polar vortex. At first, this evidence suggests that the sudden warming must therefore be simply a result of anomalously strong planetary wave forcing from the troposphere. However, recent model studies have suggested that the midwinter polar vortex may also be sensitive to the equatorial winds in the upper stratosphere, the region dominated by the semiannual oscillation. In this paper, the time series of equatorial zonal winds from two different data sources, the 40-yr ECMWF Re-Analysis (ERA) and the Met Office assimilated dataset, are reviewed. Both suggest that the equatorial winds in the upper stratosphere above 10 hPa were anomalously easterly in 2002. Idealized model experiments are described in which the modeled equatorial winds were relaxed toward these observations for various years to examine whether the anomalous easterlies in 2002 could influence the timing of a warming event. It is found that the 2002 equatorial winds speed up the evolution of a warming event in the model. Therefore, this study suggests that the anomalous easterlies in the 1–10-hPa region may have been a contributory factor in the development of the observed SH warming. However, it is concluded that it is unlikely that the anomalous equatorial winds alone can explain the 2002 warming event.

The impact of the stratosphere on the troposphere during the southern hemisphere stratospheric sudden warming, September 2002

Recent research has established that a small but statistically significant link exists between the stratosphere and the troposphere in the northern hemisphere extratropics. In this paper it is shown that a similar link exists between the stratosphere and troposphere during the unprecedented September 2002 sudden warming in the southern hemisphere. Two ensemble forecasts of the stratospheric sudden warming are run which have different stratospheric initial conditions and identical tropospheric initial conditions. Stratospheric initial conditions have an impact on the tropospheric flow at the peak of the major warming (5 days into the run) and on longer time-scales (18 days into the run). The character of this influence is a localized, equatorward shift of the tropospheric storm track. The averaged impact of the change in the position of the storm-track maps strongly onto the Southern Annular Mode structure, but does not have an annular character.

Over expression of Plk1 does not induce cell division in rat cardiac myocytes in vitro

BACKGROUND: Mammalian cardiac myocytes withdraw from the cell cycle during post-natal development, resulting in a non-proliferating, fully differentiated adult phenotype that is unable to repair damage to the myocardium, such as occurs following a myocardial infarction. We and others previously have shown that forced expression of certain cell cycle molecules in adult cardiac myocytes can promote cell cycle progression and division in these cells. The mitotic serine/threonine kinase, Polo-like kinase-1 (Plk1), is known to phosphorylate and activate a number of mitotic targets, including Cdc2/Cyclin B1, and to promote cell division. PRINCIPAL FINDINGS: The mammalian Plk family are all differentially regulated during the development of rat cardiac myocytes, with Plk1 showing the most dramatic decrease in both mRNA, protein and activity in the adult. We determined the potential of Plk1 to induce cell cycle progression and division in cultured rat cardiac myocytes. A persistent and progressive loss of Plk1 expression was observed during myocyte development that correlated with the withdrawal of adult rat cardiac myocytes from the cell cycle. Interestingly, when Plk1 was over-expressed in cardiac myocytes by adenovirus infection, it was not able to promote cell cycle progression, as determined by cell number and percent binucleation. CONCLUSIONS: We conclude that, in contrast to Cdc2/Cyclin B1 over-expression, the forced expression of Plk1 in adult cardiac myocytes is not sufficient to induce cell division and myocardial repair.

A continuum of sudden stratospheric warmings

The k-means cluster technique is used to examine 43 yr of daily winter Northern Hemisphere (NH) polar stratospheric data from the 40-yr ECMWF Re-Analysis (ERA-40). The results show that the NH winter stratosphere exists in two natural well-separated states. In total, 10% of the analyzed days exhibit a warm disturbed state that is typical of sudden stratospheric warming events. The remaining 90% of the days are in a state typical of a colder undisturbed vortex. These states are determined objectively, with no preconceived notion of the groups. The two stratospheric states are described and compared with alternative indicators of the polar winter flow, such as the northern annular mode. It is shown that the zonally averaged zonal winds in the polar upper stratosphere at 7 hPa can best distinguish between the two states, using a threshold value of 4 m s−1, which is remarkably close to the standard WMO criterion for major warming events. The analysis also determines that there are no further divisions within the warm state, indicating that there is no well-designated threshold between major and minor warmings, nor between split and displaced vortex events. These different manifestations are simply members of a continuum of warming events.

Modelling seasonally varying data: A case study for sudden infant death syndrome (SIDS)

Many time series are measured monthly, either as averages or totals, and such data often exhibit seasonal variability-the values of the series are consistently larger for some months of the year than for others. A typical series of this type is the number of deaths each month attributed to SIDS (Sudden Infant Death Syndrome). Seasonality can be modelled in a number of ways. This paper describes and discusses various methods for modelling seasonality in SIDS data, though much of the discussion is relevant to other seasonally varying data. There are two main approaches, either fitting a circular probability distribution to the data, or using regression-based techniques to model the mean seasonal behaviour. Both are discussed in this paper.

A GCM study of the influence of equatorial winds on the timing of sudden stratospheric warmings

A full troposphere-stratosphere-mesosphere global circulation model is used in a set of idealised experiments to investigate the sensitivity of the Northern Hemisphere winter stratospheric flow to improvements in the equatorial zonal winds. The model shows significant sensitivity to variability in the upper equatorial stratosphere, the imposition of SAO and QBO like variability in this region advances the timing of midwinter sudden warmings by about one month. Perturbations to the lower equatorial stratosphere are mainly found to influence early winter polar variability. These results suggest that it is important to pay attention to the capability of models to simulate realistic variability in the upper equatorial stratosphere.

Omega-3 fatty acids, cardiovascular disease and stability of atherosclerotic plaques

Long-chain n-3 polyunsaturated fatty acids are found in oily fish and in fish oils and similar preparations. Substantial evidence from epidemiological and case-control studies indicates that consumption of fish, oily fish and long-chain n-3 fatty acids reduces risk of cardiovascular mortality. Secondary prevention studies using long-chain n-3 fatty acids in patients post-myocardial infarction have shown a reduction in total and cardiovascular mortality with an especially potent effect on sudden death. Long-chain n-3 fatty acids have been shown to beneficially modify a range of cardiovascular risk factors, which may result in primary cardiovascular prevention. However, reduced non-fatal and fatal events and a reduction in sudden death probably involve other mechanisms. Reduced thrombosis following long-chain n-3 fatty acids may play a role. A decrease in arrhythmias is a favoured mechanism of action of long-chain n-3 fatty acids and is supported by cell culture and animal studies. However human trials using implantable cardiac defibrillators have produced inconsistent findings and a recent meta-analysis does not support this mechanism of action. An alternative mechanism of action may be stabilisation of atherosclerotic plaques by long-chain n-3 fatty acids. This is suggested by one published human study which showed that incorporation of long-chain n-3 fatty acids into plaques collected at carotid endarterectomy resulted in fewer macrophages in the plaque and a morphology indicative of increased stability. These findings are supported from observations in an animal model and suggest that the primary effect of long-chain n-3 fatty acids might be on macrophages within the plaque.

Understanding post-operative temperature drop in cardiac surgery: a mathematical model

A mathematical model is presented to understand heat transfer processes during the cooling and re-warming of patients during cardiac surgery. Our compartmental model is able to account for many of the qualitative features observed in the cooling of various regions of the body including the central core containing the majority of organs, the rectal region containing the intestines and the outer peripheral region of skin and muscle. In particular, we focus on the issue of afterdrop: a drop in core temperature following patient re-warming, which can lead to serious post-operative complications. Model results for a typical cooling and re-warming procedure during surgery are in qualitative agreement with experimental data in producing the afterdrop effect and the observed dynamical variation in temperature between the core, rectal and peripheral regions. The influence of heat transfer processes and the volume of each compartmental region on the afterdrop effect is discussed. We find that excess fat on the peripheral and rectal regions leads to an increase in the afterdrop effect. Our model predicts that, by allowing constant re-warming after the core temperature has been raised, the afterdrop effect will be reduced.

Inhibition of E2F abrogates the development of cardiac myocyte hypertrophy

Growth of the post- natal mammalian heart occurs primarily by cardiac myocyte hypertrophy. Previously, we and others have shown that a partial re- activation of the cell cycle machinery occurs in myocytes undergoing hypertrophy such that cells progress through the G(1)/ S transition. In this study, we have examined the regulation of the E2F family of transcription factors that are crucial for the G(1)/ S phase transition during normal cardiac development and the development of myocyte hypertrophy in the rat. Thus, mRNA and protein levels of E2F- 1, 3, and 4 and DP- 1 and DP- 2 were down- regulated during development to undetectable levels in adult myocytes. Interestingly, E2F- 5 protein levels were substantially up- regulated during development. In contrast, an induction of E2F- 1, 3, and 4 and the DP- 1 protein was observed during the development of myocyte hypertrophy in neonatal myocytes treated with serum or phenylephrine, whereas the protein levels of E2F- 5 were decreased with serum stimulation. E2F activity, as measured by a cyclin E promoter luciferase assay and E2F- DNA binding activity, increased significantly during the development of hypertrophy with serum and phenylephrine compared with non- stimulated cells. Inhibiting E2F activity with a specific peptide that blocks E2F- DP heterodimerization prevented the induction of hypertrophic markers ( atrial natriuretic factor and brain natriuretic peptide) in response to serum and phenylephrine, reduced the increase in myocyte size, and inhibited protein synthesis in stimulated cells. Thus, we have shown that the inhibition of E2F function prevents the development of hypertrophy. Targeting E2F function might be a useful approach for treating diseases that cause pathophysiological hypertrophic growth.