The Response of the Tropospheric Circulation to Water Vapor–Like Forcings in the Stratosphere

An idealized, dry general circulation model is used to examine the response of the tropospheric circulation to thermal forcings that mimic changes in stratospheric water vapor (SWV). It is found that SWV-like cooling in the stratosphere produces a poleward-shifted, strengthened jet and an expanded, weakened Hadley cell. This response is shown to be almost entirely driven by cooling located in the extratropical lower stratosphere; when cooling is limited to the tropical stratosphere, it generates a much weaker and qualitatively opposite response. It is demonstrated that these circulation changes arise independently of any changes in tropopause height, are insensitive to the detailed structure of the forcing function, and are robust to model resolution. The responses are quantitatively of the same order as those due to well-mixed greenhouse gases, suggesting a potentially significant contribution of SWV to past and future changes in the tropospheric circulation

Understanding Hadley Cell Expansion versus Contraction: Insights from Simplified Models and Implications for Recent Observations

This study seeks a deeper understanding of the causes of Hadley Cell (HC) expansion, as projected under global warming, and HC contraction, as observed under El Niño. Using an idealized general circulation model, the authors show that a thermal forcing applied to a narrow region around the equator produces “El Niño–like” HC contraction, while a forcing with wider meridional extent produces “global warming–like” HC expansion. These circulation responses are sensitive primarily to the thermal forcing’s meridional structure and are less sensitive to its vertical structure. If the thermal forcing is confined to the midlatitudes, the amount of HC expansion is more than three times that of a forcing of comparable amplitude that is spread over the tropics. This finding may be relevant to recently observed trends of rapid tropical widening. The shift of the HC edge is explained using a very simple model in which the transformed Eulerian mean (TEM) circulation acts to diffuse heat meridionally. In this context, the HC edge is defined as the downward maximum of residual vertical velocity in the upper troposphere ϖmax *; this corresponds well with the conventional Eulerian definition of the HC edge. In response to a positive thermal forcing, there is anomalous diabatic cooling, and hence anomalous TEM descent, on the poleward flank of the thermal forcing. This causes the HC edge (ϖmax *) to shift toward the descending anomaly, so that a narrow forcing causes HC contraction and a wide forcing causes HC expansion

Ozone hole and Southern Hemisphere climate change

Climate change in the Southern Hemisphere (SH) has been robustly documented in the last several years. It has altered the atmospheric circulation in a surprising number of ways: a rising global tropopause, a poleward intensification of the westerly jet, a poleward shift in storm tracks, a poleward expansion of the Hadley cell, and many others. While these changes have been extensively related with anthropogenic warming resulting from the increase in greenhouse gases, their potential link to stratospheric cooling resulting from ozone depletion has only recently been examined and a comprehensive picture is still lacking. Examining model output from the coupled climate models participating in the Intergovernmental Panel on Climate Change (IPCC) Fourth Assessment (AR4), and grouping them depending on the stratospheric ozone forcing used, we here show that stratospheric ozone affects the entire atmospheric circulation in the SH, from the polar regions to the subtropics, and from the stratosphere to the surface. Furthermore, model projections suggest that the anticipated ozone recovery, resulting from the implementation of the Montreal Protocol, will likely decelerate future climate change resulting from increased greenhouse gases, although it might accelerate surface warming over Antarctica

The Fine-Scale Structure of the Global Tropopause Derived from COSMIC GPS Radio Occultation Measurements

The spatiotemporal structure of the lapse-rate tropopause is examined by using state-of-the-art Global Positioning System radio occultation measurements from the Constellation Observing System for Meteorology, Ionosphere and Climate (COSMIC) Formosa Satellite Mission 3 mission. The high temporal and spatial resolutions of the data reveal the detailed structure of tropopause properties such as pressure (pt), temperature (Tt), and sharpness (Nt^2) and their relationships to upper tropospheric and lower stratospheric processes. The overall results are generally in good agreement with previous studies. The climatology of all three tropopause properties shows largely homogeneous structure in the zonal direction: noticeable asymmetries are found only in the tropics and the Northern Hemisphere extratropics during boreal winter owing to localized tropospheric processes. This contrasts with the seasonal cycles of tropopause properties which are significantly influenced by stratospheric processes such as the Brewer-Dobson circulation, the polar vortex, and the radiative processes near the tropopause. On intraseasonal time scales, pt and Tt exhibit significant variability over the Asian summer monsoon and the subtropics where double tropopauses frequently occur. In contrast, Nt^2 shows maximum variability in the tropics where pt and Tt have minimum variability, possibly a consequence of vertically propagating waves. The tropopause properties derived from COSMIC observations are further applied to evaluate tropopause data directly available from the NCEP-NCAR Reanalysis (NNR). Although the NNR tropopause data have been widely used in climate studies, they are found to have significant and systematic biases, especially in the subtropics. This suggests that the NNR tropopause data should be treated with great caution in any quantitative studies

Discovery of Novel MicroRNAs in Rat Kidney Using Next Generation Sequencing and Microarray Validation

MicroRNAs (miRNAs) are small non-coding RNAs that regulate a variety of biological processes. The latest version of the miRBase database (Release 18) includes 1,157 mouse and 680 rat mature miRNAs. Only one new rat mature miRNA was added to the rat miRNA database from version 16 to version 18 of miRBase, suggesting that many rat miRNAs remain to be discovered. Given the importance of rat as a model organism, discovery of the completed set of rat miRNAs is necessary for understanding rat miRNA regulation. In this study, next generation sequencing (NGS), microarray analysis and bioinformatics technologies were applied to discover novel miRNAs in rat kidneys. MiRanalyzer was utilized to analyze the sequences of the small RNAs generated from NGS analysis of rat kidney samples. Hundreds of novel miRNA candidates were examined according to the mappings of their reads to the rat genome, presence of sequences that can form a miRNA hairpin structure around the mapped locations, Dicer cleavage patterns, and the levels of their expression determined by both NGS and microarray analyses. Nine novel rat hairpin precursor miRNAs (pre-miRNA) were discovered with high confidence. Five of the novel pre-miRNAs are also reported in other species while four of them are rat specific. In summary, 9 novel pre-miRNAs (14 novel mature miRNAs) were identified via combination of NGS, microarray and bioinformatics high-throughput technologies

Basic science232. Certolizumab pegol prevents pro-inflammatory alterations in endothelial cell function

Background: Cardiovascular disease is a major comorbidity of rheumatoid arthritis (RA) and a leading cause of death. Chronic systemic inflammation involving tumour necrosis factor alpha (TNF) could contribute to endothelial activation and atherogenesis. A number of anti-TNF therapies are in current use for the treatment of RA, including certolizumab pegol (CZP), (Cimzia ®; UCB, Belgium). Anti-TNF therapy has been associated with reduced clinical cardiovascular disease risk and ameliorated vascular function in RA patients. However, the specific effects of TNF inhibitors on endothelial cell function are largely unknown. Our aim was to investigate the mechanisms underpinning CZP effects on TNF-activated human endothelial cells. Methods: Human aortic endothelial cells (HAoECs) were cultured in vitro and exposed to a) TNF alone, b) TNF plus CZP, or c) neither agent. Microarray analysis was used to examine the transcriptional profile of cells treated for 6 hrs and quantitative polymerase chain reaction (qPCR) analysed gene expression at 1, 3, 6 and 24 hrs. NF-κB localization and IκB degradation were investigated using immunocytochemistry, high content analysis and western blotting. Flow cytometry was conducted to detect microparticle release from HAoECs. Results: Transcriptional profiling revealed that while TNF alone had strong effects on endothelial gene expression, TNF and CZP in combination produced a global gene expression pattern similar to untreated control. The two most highly up-regulated genes in response to TNF treatment were adhesion molecules E-selectin and VCAM-1 (q 0.2 compared to control; p > 0.05 compared to TNF alone). The NF-κB pathway was confirmed as a downstream target of TNF-induced HAoEC activation, via nuclear translocation of NF-κB and degradation of IκB, effects which were abolished by treatment with CZP. In addition, flow cytometry detected an increased production of endothelial microparticles in TNF-activated HAoECs, which was prevented by treatment with CZP. Conclusions: We have found at a cellular level that a clinically available TNF inhibitor, CZP reduces the expression of adhesion molecule expression, and prevents TNF-induced activation of the NF-κB pathway. Furthermore, CZP prevents the production of microparticles by activated endothelial cells. This could be central to the prevention of inflammatory environments underlying these conditions and measurement of microparticles has potential as a novel prognostic marker for future cardiovascular events in this patient group. Disclosure statement: Y.A. received a research grant from UCB. I.B. received a research grant from UCB. S.H. received a research grant from UCB. All other authors have declared no conflicts of interes

Genome-wide Scan of 29,141 African Americans Finds No Evidence of Directional Selection since Admixture

The extent of recent selection in admixed populations is currently an unresolved question. We scanned the genomes of 29,141 African Americans and failed to find any genome-wide-significant deviations in local ancestry, indicating no evidence of selection influencing ancestry after admixture. A recent analysis of data from 1,890 African Americans reported that there was evidence of selection in African Americans after their ancestors left Africa, both before and after admixture. Selection after admixture was reported on the basis of deviations in local ancestry, and selection before admixture was reported on the basis of allele-frequency differences between African Americans and African populations. The local-ancestry deviations reported by the previous study did not replicate in our very large sample, and we show that such deviations were expected purely by chance, given the number of hypotheses tested. We further show that the previous study’s conclusion of selection in African Americans before admixture is also subject to doubt. This is because the FST statistics they used were inflated and because true signals of unusual allele-frequency differences between African Americans and African populations would be best explained by selection that occurred in Africa prior to migration to the Americas

Формирование эмоциональной культуры как компонента инновационной культуры студентов

Homozygosity has long been associated with rare, often devastating, Mendelian disorders1 and Darwin was one of the first to recognise that inbreeding reduces evolutionary fitness2. However, the effect of the more distant parental relatedness common in modern human populations is less well understood. Genomic data now allow us to investigate the effects of homozygosity on traits of public health importance by observing contiguous homozygous segments (runs of homozygosity, ROH), which are inferred to be homozygous along their complete length. Given the low levels of genome-wide homozygosity prevalent in most human populations, information is required on very large numbers of people to provide sufficient power3,4. Here we use ROH to study 16 health-related quantitative traits in 354,224 individuals from 102 cohorts and find statistically significant associations between summed runs of homozygosity (SROH) and four complex traits: height, forced expiratory lung volume in 1 second (FEV1), general cognitive ability (g) and educational attainment (nominal p<1 × 10−300, 2.1 × 10−6, 2.5 × 10−10, 1.8 × 10−10). In each case increased homozygosity was associated with decreased trait value, equivalent to the offspring of first cousins being 1.2 cm shorter and having 10 months less education. Similar effect sizes were found across four continental groups and populations with different degrees of genome-wide homozygosity, providing convincing evidence for the first time that homozygosity, rather than confounding, directly contributes to phenotypic variance. Contrary to earlier reports in substantially smaller samples5,6, no evidence was seen of an influence of genome-wide homozygosity on blood pressure and low density lipoprotein (LDL) cholesterol, or ten other cardio-metabolic traits. Since directional dominance is predicted for traits under directional evolutionary selection7, this study provides evidence that increased stature and cognitive function have been positively selected in human evolution, whereas many important risk factors for late-onset complex diseases may not have been