A Nonequilibrium Finite-Rate Carbon Ablation Model for Radiating Earth Re-entry Flows

Vehicles entering planetary atmospheres at high speed require an ablative heat shield in order to withstand the high thermal energy flux to the body. The interaction between the ablative products and the flow field is not well characterized. Numerical simulations were conducted to investigate the influence of carbon ablation on shock layer radiation. Data collected from experiments performed in the X-2 expansion tunnel at the University of Queensland was used to compare to the simulations. The model was a short half-cylinder made of isomolded graphite and was tested in 8.6 km/s Earth entry flow. The model surface was heated within a temperature range of 1770-3280 K. The radiation emitted from the CN violet bands was measured by ultraviolet spectrometry in a spectral range from 353-391 nm. This research develops a novel finite-rate surface kinetic model for determining the chemical state of an ablating boundary layer. The proposed ablation model accounts for competing surface reaction processes such as adsorption/desorption, Eley-Rideal mechanisms, oxidation, nitridation, and sublimation. The included oxidation mechanisms predict CO as the primary oxidized product at the considered surface temperatures, which is in agreement with experiment and theory. A previous model had incorrectly predicted CO2 as the primary oxidized product for a majority of the tested surface temperatures. The ablative gas species predicted by this new surface model results in better agreement with experimental spectral measurements than predictions provided by legacy ablation models, and represents a significant improvement in current modeling capabilities for hypersonic nonequilibrium ablating re-entry flows

Case 3847 - Simopithecus oswaldi Andrews, 1916 (currently Theropithecus oswaldi; Mammalia, Primates, Cercopithecidae), proposed conservation by reversal of precedence with Cynocephalus atlanticus Thomas, 1884

The purpose of this application, under Articles 23.9.3 and 81.1 of the Code, is to conserve the usage of the species-group name Simopithecus oswaldi Andrews, 1916 by giving it precedence over its senior subjective synonym Cynocephalus atlanticus Thomas, 1884. Theropithecus is a common to dominant member of the extinct primate community across Africa after 4 million years ago (Jablonski & Frost, 2010) and often co-occurred with extinct humans (Hominini); fossils are also known rarely across Eurasia (Roberts et al., 2014). Most fossil samples are currently included in Theropithecus oswaldi (Andrews, 1916), which is often divided into chrono-geographic subspecies. Cynocephalus atlanticus Thomas, 1884 was not recognized as a member of Theropithecus until 1973, and this nomen has seldom been used, but if it were shown (as seems likely) to be conspecific with Simopithecus oswaldi Andrews, 1916, widespread paleontological usage would be upset. It is thus proposed to give conditional precedence to the later name, which would still permit the use of Theropithecus atlanticus as a distinct species or subspecies of Theropithecus oswaldi. Lectotypes are designated for Simopithecus oswaldi olduvaiensis Leakey & Whitworth, 1958 and Simopithecus oswaldi hopefieldensis Singer, 1962

Measurements and Computations of Second-Mode Instability Waves in Three Hypersonic Wind Tunnels

High-frequency pressure-fluctuation measurements were made in AEDC Tunnel 9 at Mach 10 and the NASA Langley 15-Inch Mach 6 and 31-Inch Mach 10 tunnels. Measurements were made on a 7deg-half-angle cone model. Pitot measurements of freestream pressure fluctuations were also made in Tunnel 9 and the Langley Mach-6 tunnel. For the first time, second-mode waves were measured in all of these tunnels, using 1-MHz-response pressure sensors. In Tunnel 9, second-mode waves could be seen in power spectra computed from records as short as 80 micro-s. The second-mode wave amplitudes were observed to saturate and then begin to decrease in the Langley tunnels, indicating wave breakdown. Breakdown was estimated to occur near N approx. equals 5 in the Langley Mach-10 tunnel. The unit-Reynolds-number variations in the data from Tunnel 9 were too large to see the same processes. In Tunnel 9, the measured transition locations were found to be at N = 4.5 using thermocouples, and N = 5.3 using 50-kHz-response pressure sensors. What appears to be a very long transitional region was observed at a unit Reynolds number of 13.5 million per meter in Tunnel 9. These results were consistent with the high-frequency pressure fluctuation measurements. High-frequency pressure fluctuation measurements indicated that transition did occur in the Langley Mach-6 tunnel, but the location of transition was not precisely determined. Unit Reynolds numbers in the Langley Mach-10 tunnel were too low to observe transition. More analysis of this data set is expected in the future

Using coding and non-coding rare variants to target candidate genes in patients with severe tinnitus

Tinnitus is the phantom percept of an internal non-verbal set of noises and tones. It is reported by 15% of the population and it is usually associated with hearing and/or brain disorders. The role of structural variants (SVs) in coding and non-coding regions has not been investigated in patients with severe tinnitus. In this study, we performed whole-genome sequencing in 97 unrelated Swedish individuals with chronic tinnitus (TIGER cohort). Rare single nucleotide variants (SNV), large structural variants (LSV), and copy number variations (CNV) were retrieved to perform a gene enrichment analysis in TIGER and in a subgroup of patients with severe tinnitus (SEVTIN, n = 34), according to the tinnitus handicap inventory (THI) scores. An independent exome sequencing dataset of 147 Swedish tinnitus patients was used as a replication cohort (JAGUAR cohort) and population-specific datasets from Sweden (SweGen) and Non-Finish Europeans (NFE) from gnomAD were used as control groups. SEVTIN patients showed a higher prevalence of hyperacusis, hearing loss, and anxiety when they were compared to individuals in the TIGER cohort. We found an enrichment of rare missense variants in 6 and 8 high-constraint genes in SEVTIN and TIGER cohorts, respectively. Of note, an enrichment of missense variants was found in the CACNA1E gene in both SEVTIN and TIGER. We replicated the burden of missense variants in 9 high-constrained genes in the JAGUAR cohort, including the gene NAV2, when data were compared with NFE. Moreover, LSVs in constrained regions overlapping CACNA1E, NAV2, and TMEM132D genes were observed in TIGER and SEVTIN.publishedVersio

The Potato Nucleotide-Binding Leucine-Rich Repeat (NLR) Immune Receptor Rx1 is a Pathogen Dependent DNA-Deforming Protein

Plant NLR proteins enable cells to respond to pathogen attack. Several NLRs act in the nucleus, however, conserved nuclear targets that support their role in immunity are unknown. Previously we noted a structural homology between the NB domain of NLRs and DNA replication origin-binding Cdc6/Orc1 proteins. Here we show that the NB-ARC domain of the Rx1 NLR of potato binds nucleic acids. Rx1 induces ATP-dependent bending and melting of DNA in vitro dependent upon a functional P-loop. In situ full-length Rx1 binds nuclear DNA following activation by its cognate pathogen-derived effector protein, the coat protein of potato virus X. In line with its obligatory nucleocytoplasmic distribution, DNA-binding was only observed when Rx1 was allowed to freely translocate between both compartments and was activated in the cytoplasm. Immune activation induced by an unrelated NLR-effector pair did not trigger a Rx1-DNA interaction. DNA-binding is therefore not merely a consequence of immune activation. These data establish a role for DNA distortion in Rx1 immune signalling and defines DNA as a molecular target of an activated NLR

Environment Impacts the Metabolic Dependencies of Ras-Driven Non-Small Cell Lung Cancer

Cultured cells convert glucose to lactate, and glutamine is the major source of tricarboxylic acid (TCA)-cycle carbon, but whether the same metabolic phenotype is found in tumors is less studied. We infused mice with lung cancers with isotope-labeled glucose or glutamine and compared the fate of these nutrients in tumor and normal tissue. As expected, lung tumors exhibit increased lactate production from glucose. However, glutamine utilization by both lung tumors and normal lung was minimal, with lung tumors showing increased glucose contribution to the TCA cycle relative to normal lung tissue. Deletion of enzymes involved in glucose oxidation demonstrates that glucose carbon contribution to the TCA cycle is required for tumor formation. These data suggest that understanding nutrient utilization by tumors can predict metabolic dependencies of cancers in vivo. Furthermore, these data argue that the in vivo environment is an important determinant of the metabolic phenotype of cancer cells.National Science Foundation (U.S.) (Grant T32GM007287

Quantification of CH4 emissions from waste disposal sites near the city of Madrid using ground- and space-based observations of COCCON, TROPOMI and IASI

We use different methane ground- and space-based remote sensing data sets for investigating the emission strength of three waste disposal sites close to Madrid. We present a method that uses wind-assigned anomalies for deriving emission strengths from satellite data and estimating their uncertainty to 9–14 %. The emission strengths estimated from the remote sensing data sets are significantly larger than the values published in the official register.ESA support through the COCCON-PROCEEDS and COCCON-PROCEEDS II projects. In addition, this research was funded by the Ministerio de Economía y Competitividad from Spain through the INMENSE project (CGL2016-80688-P). This research has largely benefit from funds of the Deutsche Forschungsgemeinschaft (provided for the two projects MOTIV and TEDDY with IDs/290612604 and 416767181, respectively)

Fibrocytes and the tissue niche in lung repair

Human fibrocytes are bone marrow-derived mesenchymal progenitor cells that express a variety of markers related to leukocytes, hematopoietic stem cells and a diverse set of fibroblast phenotypes. Fibrocytes can be recruited from the circulation to the tissue where they further can differentiate and proliferate into various mesenchymal cell types depending on the tissue niche. This local tissue niche is important because it modulates the fibrocytes and coordinates their role in tissue behaviour and repair. However, plasticity of a niche may be co-opted in chronic airway diseases such as asthma, idiopathic pulmonary fibrosis and obliterative bronchiolitis. This review will therefore focus on a possible role of fibrocytes in pathological tissue repair processes in those diseases

Ezh2 is essential for the generation of functional yolk sac derived erythro-myeloid progenitors

From Springer Nature via Jisc Publications RouterHistory: received 2020-05-19, accepted 2021-10-27, registration 2021-11-08, collection 2021-12, pub-electronic 2021-12-02, online 2021-12-02Publication status: PublishedFunder: Kay Kendall Leukaemia Fund (KKLF); doi: https://doi.org/10.13039/501100000402; Grant(s): KKL811Funder: RCUK | Medical Research Council (MRC); doi: https://doi.org/10.13039/501100000265; Grant(s): MR/L006340/1, MC_UU_12009/5Funder: Cancer Research UK (CRUK); doi: https://doi.org/10.13039/501100000289; Grant(s): C42639/A26988, C5759/A27412Funder: Bloodwise; doi: https://doi.org/10.13039/501100007903; Grant(s): 19014Abstract: Yolk sac (YS) hematopoiesis is critical for the survival of the embryo and a major source of tissue-resident macrophages that persist into adulthood. Yet, the transcriptional and epigenetic regulation of YS hematopoiesis remains poorly characterized. Here we report that the epigenetic regulator Ezh2 is essential for YS hematopoiesis but dispensable for subsequent aorta–gonad–mesonephros (AGM) blood development. Loss of EZH2 activity in hemogenic endothelium (HE) leads to the generation of phenotypically intact but functionally deficient erythro-myeloid progenitors (EMPs), while the generation of primitive erythroid cells is not affected. EZH2 activity is critical for the generation of functional EMPs at the onset of the endothelial-to-hematopoietic transition but subsequently dispensable. We identify a lack of Wnt signaling downregulation as the primary reason for the production of non-functional EMPs. Together, our findings demonstrate a critical and stage-specific role of Ezh2 in modulating Wnt signaling during the generation of EMPs from YS HE