Atmospheric Circulation Response to Anomalous Siberian Forcing in October 2016 and its Long‐Range Predictability

Abstract: The warm Arctic-cold continent pattern was of record strength in October 2016, providing the opportunity to test its proposed influence on large-scale atmospheric circulation. We find a record weak polar stratospheric vortex and negative North Atlantic Oscillation in November-December 2016 and link them to increased planetary wave generation associated with cold Siberian anomalies followed by troposphere-stratosphere dynamical coupling. At the same time the warm Arctic anomalies, in particular those over the Barents-Kara Seas, do not appear to play an important role in forcing the atmospheric circulation. Long-range forecasts initialized on 1 October 2016 reproduced both the weak polar vortex and negative North Atlantic Oscillation, as well as their link with the Siberian temperatures. Our results support the stratospheric pathway for atmospheric circulation forcing associated with Siberian surface anomalies and uncover a source of skill for subseasonal forecasts from October to December. Plain Language Summary: The warm Arctic-cold continent pattern is an observed, large-scale pattern of near-surface temperatures where the Arctic is warmer than average and Siberia is colder than average. This pattern was of record strength in October 2016, providing the opportunity to test its influence on the Northern Hemisphere atmospheric circulation and the possibility of skillful long-range forecasts. It has been proposed that the warm Arctic-cold continent pattern can drive large atmospheric waves, which are able to travel from the troposphere into the stratosphere, where they weaken the strong wintertime winds that make up the stratospheric polar vortex. A weakened polar vortex can then lead to changes in the surface pressure that can affect weather patterns. We find a record weak polar stratospheric vortex in late autumn 2016 and link that to cold Siberian anomalies. At the same time the warm Arctic anomalies do not appear to play an important role in forcing the atmospheric circulation. Long-range forecasts initialized in October 2016 reproduced both the weak polar vortex and resulting surface pressure patterns. Our results support the stratospheric pathway for atmospheric circulation forcing by Siberian surface anomalies and uncover a source of skill for subseasonal forecasts in the Northern Hemisphere autumn.Peer reviewe

Quantifying stratospheric biases and identifying their potential sources in subseasonal forecast systems

The stratosphere can be a source of predictability for surface weather on timescales of several weeks to months. However, the potential predictive skill gained from stratospheric variability can be limited by biases in the representation of stratospheric processes and the coupling of the stratosphere with surface climate in forecast systems. This study provides a first systematic identification of model biases in the stratosphere across a wide range of subseasonal forecast systems. It is found that many of the forecast systems considered exhibit warm global-mean temperature biases from the lower to middle stratosphere, too strong/cold wintertime polar vortices, and too cold extratropical upper-troposphere/lower-stratosphere regions. Furthermore, tropical stratospheric anomalies associated with the Quasi-Biennial Oscillation tend to decay toward each system\u27s climatology with lead time. In the Northern Hemisphere (NH), most systems do not capture the seasonal cycle of extreme-vortex-event probabilities, with an underestimation of sudden stratospheric warming events and an overestimation of strong vortex events in January. In the Southern Hemisphere (SH), springtime interannual variability in the polar vortex is generally underestimated, but the timing of the final breakdown of the polar vortex often happens too early in many of the prediction systems. These stratospheric biases tend to be considerably worse in systems with lower model lid heights. In both hemispheres, most systems with low-top atmospheric models also consistently underestimate the upward wave driving that affects the strength of the stratospheric polar vortex. We expect that the biases identified here will help guide model development for subseasonal-to-seasonal forecast systems and further our understanding of the role of the stratosphere in predictive skill in the troposphere

A novel pancoronavirus RT-PCR assay: frequent detection of human coronavirus NL63 in children hospitalized with respiratory tract infections in Belgium

BACKGROUND: Four human coronaviruses are currently known to infect the respiratory tract: human coronaviruses OC43 (HCoV-OC43) and 229E (HCoV-229E), SARS associated coronavirus (SARS-CoV) and the recently identified human coronavirus NL63 (HCoV-NL63). In this study we explored the incidence of HCoV-NL63 infection in children diagnosed with respiratory tract infections in Belgium. METHODS: Samples from children hospitalized with respiratory diseases during the winter seasons of 2003 and 2004 were evaluated for the presence of HCoV-NL63 using a optimized pancoronavirus RT-PCR assay. RESULTS: Seven HCoV-NL63 positive samples were identified, six were collected during January/February 2003 and one at the end of February 2004. CONCLUSIONS: Our results support the notation that HCoV-NL63 can cause serious respiratory symptoms in children. Sequence analysis of the S gene showed that our isolates could be classified into two subtypes corresponding to the two prototype HCoV-NL63 sequences isolated in The Netherlands in 1988 and 2003, indicating that these two subtypes may currently be cocirculating

Changing atmospheric CO2 concentration was the primary driver of early Cenozoic climate

The Early Eocene Climate Optimum (EECO, which occurred about 51 to 53 million years ago)1, was the warmest interval of the past 65 million years, with mean annual surface air temperature over ten degrees Celsius warmer than during the pre-industrial period2–4. Subsequent global cooling in the middle and late Eocene epoch, especially at high latitudes, eventually led to continental ice sheet development in Antarctica in the early Oligocene epoch (about 33.6 million years ago). However, existing estimates place atmospheric carbon dioxide (CO2) levels during the Eocene at 500–3,000 parts per million5–7, and in the absence of tighter constraints carbon–climate interactions over this interval remain uncertain. Here we use recent analytical and methodological developments8–11 to generate a new high-fidelity record of CO2 concentrations using the boron isotope (δ11Β) composition of well preserved planktonic foraminifera from the Tanzania Drilling Project, revising previous estimates6. Although species-level uncertainties make absolute values difficult to constrain, CO2 concentrations during the EECO were around 1,400 parts per million. The relative decline in CO2 concentration through the Eocene is more robustly constrained at about fifty per cent, with a further decline into the Oligocene12. Provided the latitudinal dependency of sea surface temperature change for a given climate forcing in the Eocene was similar to that of the late Quaternary period13, this CO2 decline was sufficient to drive the well documented high- and low-latitude cooling that occurred through the Eocene14. Once the change in global temperature between the pre-industrial period and the Eocene caused by the action of all known slow feedbacks (apart from those associated with the carbon cycle) is removed2–4, both the EECO and the late Eocene exhibit an equilibrium climate sensitivity relative to the pre-industrial period of 2.1 to 4.6 degrees Celsius per CO2 doubling (66 per cent confidence), which is similar to the canonical range (1.5 to 4.5 degrees Celsius15), indicating that a large fraction of the warmth of the early Eocene greenhouse was driven by increased CO2 concentrations, and that climate sensitivity was relatively constant throughout this period

Genome-wide associations for birth weight and correlations with adult disease

Birth weight (BW) has been shown to be influenced by both fetal and maternal factors and in observational studies is reproducibly associated with future risk of adult metabolic diseases including type 2 diabetes (T2D) and cardiovascular disease. These life-course associations have often been attributed to the impact of an adverse early life environment. Here, we performed a multi-ancestry genome-wide association study (GWAS) meta-analysis of BW in 153,781 individuals, identifying 60 loci where fetal genotype was associated with BW ($\textit{P}$  < 5 × 10$^{-8}$). Overall, approximately 15% of variance in BW was captured by assays of fetal genetic variation. Using genetic association alone, we found strong inverse genetic correlations between BW and systolic blood pressure ($\textit{R}$ $_{g}$ = -0.22, $\textit{P}$  = 5.5 × 10$^{-13}$), T2D ($\textit{R}$ $_{g}$ = -0.27, $\textit{P}$  = 1.1 × 10$^{-6}$) and coronary artery disease ($\textit{R}$ $_{g}$ = -0.30, $\textit{P}$  = 6.5 × 10$^{-9}$). In addition, using large -cohort datasets, we demonstrated that genetic factors were the major contributor to the negative covariance between BW and future cardiometabolic risk. Pathway analyses indicated that the protein products of genes within BW-associated regions were enriched for diverse processes including insulin signalling, glucose homeostasis, glycogen biosynthesis and chromatin remodelling. There was also enrichment of associations with BW in known imprinted regions ($\textit{P}$ = 1.9 × 10$^{-4}$). We demonstrate that life-course associations between early growth phenotypes and adult cardiometabolic disease are in part the result of shared genetic effects and identify some of the pathways through which these causal genetic effects are mediated.For a full list of the funders pelase visit the publisher's website and look at the supplemetary material provided. Some of the funders are: British Heart Foundation, Cancer Research UK, Medical Research Council, National Institutes of Health, Royal Society and Wellcome Trust

Quantifying stratospheric biases and identifying their potential sources in subseasonal forecast systems

The stratosphere can be a source of predictability for surface weather on timescales of several weeks to months. However, the potential predictive skill gained from stratospheric variability can be limited by biases in the representation of stratospheric processes and the coupling of the stratosphere with surface climate in forecast systems. This study provides a first systematic identification of model biases in the stratosphere across a wide range of subseasonal forecast systems. It is found that many of the forecast systems considered exhibit warm global-mean temperature biases from the lower to middle stratosphere, too strong/cold wintertime polar vortices, and too cold extratropical upper-troposphere/lower-stratosphere regions. Furthermore, tropical stratospheric anomalies associated with the Quasi-Biennial Oscillation tend to decay toward each system's climatology with lead time. In the Northern Hemisphere (NH), most systems do not capture the seasonal cycle of extreme-vortex-event probabilities, with an underestimation of sudden stratospheric warming events and an overestimation of strong vortex events in January. In the Southern Hemisphere (SH), springtime interannual variability in the polar vortex is generally underestimated, but the timing of the final breakdown of the polar vortex often happens too early in many of the prediction systems. These stratospheric biases tend to be considerably worse in systems with lower model lid heights. In both hemispheres, most systems with low-top atmospheric models also consistently underestimate the upward wave driving that affects the strength of the stratospheric polar vortex. We expect that the biases identified here will help guide model development for subseasonal-to-seasonal forecast systems and further our understanding of the role of the stratosphere in predictive skill in the troposphere

Genome-wide meta-analysis of 241,258 adults accounting for smoking behaviour identifies novel loci for obesity traits

Few genome-wide association studies (GWAS) account for environmental exposures, like smoking, potentially impacting the overall trait variance when investigating the genetic contribution to obesity-related traits. Here, we use GWAS data from 51,080 current smokers and 190,178 nonsmokers (87% European descent) to identify loci influencing BMI and central adiposity, measured as waist circumference and waist-to-hip ratio both adjusted for BMI. We identify 23 novel genetic loci, and 9 loci with convincing evidence of gene-smoking interaction (GxSMK) on obesity-related traits. We show consistent direction of effect for all identified loci and significance for 18 novel and for 5 interaction loci in an independent study sample. These loci highlight novel biological functions, including response to oxidative stress, addictive behaviour, and regulatory functions emphasizing the importance of accounting for environment in genetic analyses. Our results suggest that tobacco smoking may alter the genetic susceptibility to overall adiposity and body fat distribution.Peer reviewe

Maternal and fetal genetic effects on birth weight and their relevance to cardio-metabolic risk factors.

Birth weight variation is influenced by fetal and maternal genetic and non-genetic factors, and has been reproducibly associated with future cardio-metabolic health outcomes. In expanded genome-wide association analyses of own birth weight (n = 321,223) and offspring birth weight (n = 230,069 mothers), we identified 190 independent association signals (129 of which are novel). We used structural equation modeling to decompose the contributions of direct fetal and indirect maternal genetic effects, then applied Mendelian randomization to illuminate causal pathways. For example, both indirect maternal and direct fetal genetic effects drive the observational relationship between lower birth weight and higher later blood pressure: maternal blood pressure-raising alleles reduce offspring birth weight, but only direct fetal effects of these alleles, once inherited, increase later offspring blood pressure. Using maternal birth weight-lowering genotypes to proxy for an adverse intrauterine environment provided no evidence that it causally raises offspring blood pressure, indicating that the inverse birth weight-blood pressure association is attributable to genetic effects, and not to intrauterine programming.The Fenland Study is funded by the Medical Research Council (MC_U106179471) and Wellcome Trust