bluuebunny/crossref_metadata_2025_split huggingface dataset:
Moho Depth of Northern Baja California, Mexico, From Teleseismic Receiver Functions
Authors: Ramírez E. E. , Bataille Klaus , Vidal‐Villegas J. A. , Stock J. M. , Ramírez‐Hernández J. 
Published: April 2021

AbstractWe estimated Moho depths from data recorded by permanent and temporary broadband seismic stations deployed in northern Baja California, Mexico, using the receiver function technique. This region is composed of two subregions of contrasting geological and topographical characteristics: the Peninsular Ranges of Baja California (PRBC), a batholith with high elevations (up to 2,600 m); and the Mexicali Valley (MV) region, a sedimentary environment close to sea level. Crustal thickness derived from the P‐to‐S converted phases at 29 seismic stations were analyzed in three profiles: Two that cross the two subregions, in ∼W‐E direction, and the third one that runs over the PRBC in a N‐S direction. For the PRBC, Moho depths vary from 35 to 45 km, from 33°N to 32°N; and from 30 to 46 km depth from 32°N to 30.5°N. From a profile that crosses the subregions in the W‐E direction; Moho depths vary from 45 to ∼34 km under western and eastern PRBC, respectively; with an abrupt change of depth under the Main Gulf Escarpment (30°), from ∼32 to 30 km; and depths of 17–20 km under the MV. Moho depths of the profile in an ∼ W‐E direction at ∼31.5°N are from ∼30 to 40 km, under topography that increases from 0 to 2,600 m; and became shallower (16 km depth) as the profile reaches the Gulf of California. These results show that deeper Moho is related to higher elevations with an abrupt change under the Main Gulf Escarpment, except for western PRBC where the Moho depth is not simply reflecting isostatic compensation.
Paris Agreement's Ambiguity About Aerosols Drives Uncertain Health and Climate Outcomes
Authors: Polonik Pascal , Ricke Katharine , Burney Jennifer 
Published: April 2021

AbstractAnthropogenic aerosols are hazardous to human health but have helped offset warming from greenhouse gases (GHGs), creating a potential regulatory tradeoff. As countries implement their GHG reduction targets under the Paris climate agreement, the co‐emissions of aerosols and their precursors will also change. Since these co‐emissions vary by country and by economic sector, each country will face different tradeoffs between aerosol‐driven health or temperature co‐benefits. We combine simple parameterizations of physical processes and health outcomes to examine three idealized climate policy approaches that are consistent with the Paris Agreement targets, which (i) optimize for local air quality, (ii) reduce global temperature change, or (iii) reduce emissions equally from all domestic economic sectors. We evaluate aerosol impacts on premature mortality and global mean temperature change under these three policy approaches and find that by 2030 the three policies yield differences of over 1 million annual premature deaths and global temperature differences of the same magnitude as those from GHG reductions. We also show that implementing equal reductions between all economic sectors can actually result in less beneficial health and temperature outcomes than either of the other options, especially in less industrialized regions. We therefore conclude that aerosol‐related co‐benefits and aerosol accounting guidelines should be explicitly considered in setting international climate policy.
Coastal Migration due to 21st Century Sea‐Level Rise
Authors: Lincke Daniel , Hinkel Jochen 
Published: April 2021

AbstractRising mean and extreme sea‐levels and induced increased coastal flooding are expected to lead to massive coastal migration if coasts are not protected. Using a wide range of sea‐level rise (SLR) scenarios, socioeconomic pathways and discount rate assumptions, 21st century coastal migration is assessed at global scale assuming local cost‐benefit optimal protection decisions for about 12,000 coastal segments with homogeneous coastal and socioeconomic characteristics. Costs considered include investment and maintenance cost for protection, migration cost in the case of no protection, and expected annual damage to assets by extreme sea‐level events that over‐top existing protection. Robust decisions in favor of protection over all scenarios are found for about 3% of the global coastline, covering 78% of global coastal population and 92% of global coastal floodplain assets. For the remaining 97% of global coastline cumulative 21st century land loss ranges from 60,000 to 415,000 km2 and coastal migration ranges from 17 to 72 million people. Big countries with long uninhabited coastlines suffer the biggest land losses. In absolute terms big countries in South and South‐east Asia account for the highest coastal migration, while in relative terms small island nations suffer most. Global cost of 21st century SLR can be lowered by factor two to four if local cost‐benefit decisions also consider, next to protection, coastal migration as an adaptation option.
Teeth of Past and Present Elephants: Microstructure and Composition of Enamel in Fossilized Proboscidean Molars and Implications for Diagenesis
Authors: Białas Nataniel , Prymak Oleg , Singh Ningthoujam Premjit , Paul Debajyoti , Patnaik Rajeev , Epple Matthias 
Published: April 2021

AbstractEnamel as hardest biological tissue remains unaltered for millions of years and is therefore an excellent archive for studies on paleodiet, paleoecology, paleoclimate, paleoenvironment, biomechanical, and evolutionary studies. However, diagenetic alterations can influence such interpretations and therefore we analyzed the microstructure and composition (elemental and stable isotopic) of fossil and extant proboscidean teeth to study the extent of diagenesis in them. We report for the first time on the enamel microstructure data of the Indian elephantiformes Anancus, Stegodon, Elephas, and Palaeoloxodon besides analyzing Gomphotherium and Deinotherium from new formations. Furthermore, we compare their microstructure with those of the primitive African taxa of Moeritherium and Palaeomastodon. Our results from depth‐related elemental composition and oxygen isotope ratios of enamel phosphate and carbonate indicate no or only negligible modification. There is also a lack of age‐dependency of these minor alterations within the fossils collected from Siwaliks of the Himalayan Foreland Basin. Overall, our study indicates that diagenesis has not played any significant role on the samples studied here and are therefore well suited for chemical and paleontological studies and proxy for paleoclimate and paleoenvironment reconstruction.
Aerosols and Tides in the Martian Tropics During Southern Hemisphere Spring Equinox From Mars Climate Sounder Data
Authors: Steele L. J. , Kleinböhl A. , Kass D. M. , Zurek R. W. 
Published: April 2021

AbstractWe analyze Mars Climate Sounder temperature and aerosol data in the tropics, and use Fourier analysis at different local times to study atmospheric tides and their relation to the dust and water ice distributions. Our results reveal that Mars year (MY) 29 has large amplitude non‐migrating thermal tides during southern hemisphere spring equinox that are not observed at the same local time in any other year. The nighttime temperatures are the most perturbed compared to other years, with strong temperature inversions at 35–55 km altitude. The nighttime water ice cloud structure is strongly influenced by the eastward‐propagating diurnal Kelvin waves 1 and 2. Increased nighttime radiative cooling from regions of thicker clouds results in stronger downwelling above the clouds, leading to increased adiabatic warming and a strengthening of the temperature inversions. The temperatures and water ice clouds at 3:45 a.m. in MY29 more closely resemble those at 5:00 a.m. in other years, suggesting there was a shift in the phase of the diurnal tide. This phase shift, and the large amplitude non‐migrating thermal tides, appear to be related to early dust activity. Two early dust storms occurred in MY29 around the time there was upwelling over the tropics, associated with the Hadley circulation. This likely enabled the dust to be transported to higher altitudes where it has a larger radiative influence. The early dust activity in MY29 also increased the strength of the westward‐propagating non‐migrating thermal tides.
Bare‐Earth DEM Generation in Urban Areas for Flood Inundation Simulation Using Global Digital Elevation Models
Authors: Liu Yinxue , Bates Paul D. , Neal Jeffery C. , Yamazaki Dai 
Published: April 2021

AbstractAccurate terrain representation is critical to estimating flood risk in urban areas. However, all current global elevation data sets can be regarded as digital surface models in urban areas as they contain building artifacts that cause artificial blocking of flow pathways. By taking surveyed terrain and LIDAR data as “truth,” the vertical error in three popular global DEMs (SRTM 1″, MERIT DEM, and TDM90) was analyzed in six European cities and an Asian city, with RMSE found to be 2.32–5.98 m. To increase the utility of global DEM data for flood modeling, a Random Forest model was developed to correct building artifacts in the MERIT DEM using factors from widely available public datasets, including satellite night‐time lights, global population density, and OpenStreetMap buildings. The proposed correction reduced the vertical errors of MERIT by 15%–67%, despite not using data samples from the target city in training the model. When training data from the target city was included error reduction improved by between 57 and 76 percentage points. The resulting Urban Corrected MERIT DEM improved simulated inundation depth by 18% over original MERIT in a hydrodynamic model of flooding in the UK city of Carlisle, although it did not outperform TDM90 at this site. We conclude that the proposed method has the potential to generate a bare‐earth global DEM in urban areas with improved terrain representation, although in data scarce regions this requires more complete OpenStreetMap building information. In the future, the method should be applied to TDM90.
From bedside to bench: regulation of host factors in SARS-CoV-2 infection
Authors: Ong Samantha Y. Q. , Flyamer Ilya M. , Bickmore Wendy A. , Biddie Simon C. 
Published: April 2021

AbstractThe zoonotic coronavirus SARS-CoV-2 (severe acute respiratory syndrome coronavirus-2), which causes COVID-19 (coronavirus disease-2019), has resulted in a pandemic. This has led to an urgent need to understand the molecular determinants of SARS-CoV-2 infection, factors associated with COVID-19 heterogeneity and severity, and therapeutic options for these patients. In this review, we discuss the role of host factors in SARS-CoV-2 infection and describe variations in host factor expression as mechanisms underlying the symptoms and severity of COVID-19. We focus on two host factors, angiotensin-converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2), implicated in SARS-CoV-2 infection. We also discuss genetic variants associated with COVID-19 severity revealed in selected patients and based on genome-wide association studies (GWASs). Furthermore, we highlight important advances in cell and chromatin biology, such as single-cell RNA and chromatin sequencing and chromosomal conformation assays, as methods that may aid in the discovery of viral–host interactions in COVID-19. Understanding how regulation of host factor genes varies in physiological and pathological states might explain the heterogeneity observed in SARS-CoV-2 infection, help identify pathways for therapeutic development, and identify patients most likely to progress to severe COVID-19.
Kv1.3 voltage-gated potassium channels link cellular respiration to proliferation through a non-conducting mechanism
Authors: Styles Faye L. , Al-Owais Moza M. , Scragg Jason L. , Chuntharpursat-Bon Eulashini , Hettiarachchi Nishani T. , Lippiat Jonathan D. , Minard Aisling , Bon Robin S. , Porter Karen , Sukumar Piruthivi , Peers Chris , Roberts Lee D. 
Published: April 2021

AbstractCellular energy metabolism is fundamental for all biological functions. Cellular proliferation requires extensive metabolic reprogramming and has a high energy demand. The Kv1.3 voltage-gated potassium channel drives cellular proliferation. Kv1.3 channels localise to mitochondria. Using high-resolution respirometry, we show Kv1.3 channels increase oxidative phosphorylation, independently of redox balance, mitochondrial membrane potential or calcium signalling. Kv1.3-induced respiration increased reactive oxygen species production. Reducing reactive oxygen concentrations inhibited Kv1.3-induced proliferation. Selective Kv1.3 mutation identified that channel-induced respiration required an intact voltage sensor and C-terminal ERK1/2 phosphorylation site, but is channel pore independent. We show Kv1.3 channels regulate respiration through a non-conducting mechanism to generate reactive oxygen species which drive proliferation. This study identifies a Kv1.3-mediated mechanism underlying the metabolic regulation of proliferation, which may provide a therapeutic target for diseases characterised by dysfunctional proliferation and cell growth.
Loss of FoxO3a prevents aortic aneurysm formation through maintenance of VSMC homeostasis
Authors: Lu Weiling , Zhou Yu , Zeng Shan , Zhong Lintao , Zhou Shiju , Song Haoyu , Ding Rongming , Zhong Gaojun , Li Qingrui , Hu Yuhua , Wen Zhongyu , Liao Qin , Wang Yalan , Lyu Lianglliang , Zhong Yiming , Hu Gonghua , Liao Yulin , Xie Dongming , Xie Jiahe 
Published: April 2021

AbstractVascular smooth muscle cell (VSMC) phenotypic switching plays a critical role in the formation of abdominal aortic aneurysms (AAAs). FoxO3a is a key suppressor of VSMC homeostasis. We found that in human and animal AAA tissues, FoxO3a was upregulated, SM22α and α-smooth muscle actin (α-SMA) proteins were downregulated and synthetic phenotypic markers were upregulated, indicating that VSMC phenotypic switching occurred in these diseased tissues. In addition, in cultured VSMCs, significant enhancement of FoxO3a expression was found during angiotensin II (Ang II)-induced VSMC phenotypic switching. In vivo, FoxO3a overexpression in C57BL/6J mice treated with Ang II increased the formation of AAAs, whereas FoxO3a knockdown exerted an inhibitory effect on AAA formation in ApoE−/− mice infused with Ang II. Mechanistically, FoxO3a overexpression significantly inhibited the expression of differentiated smooth muscle cell (SMC) markers, activated autophagy, the essential repressor of VSMC homeostasis, and promoted AAA formation. Our study revealed that FoxO3a promotes VSMC phenotypic switching to accelerate AAA formation through the P62/LC3BII autophagy signaling pathway and that therapeutic approaches that decrease FoxO3a expression may prevent AAA formation.
Silencing PTEN in the fallopian tube promotes enrichment of cancer stem cell-like function through loss of PAX2
Authors: Russo Angela , Colina Jose A. , Moy Junlone , Baligod Seth , Czarnecki Austin A. , Varughese Peter , Lantvit Daniel D. , Dean Matthew J. , Burdette Joanna E. 
Published: April 2021

AbstractHigh-grade serous ovarian cancer (HGSOC) is the most lethal gynecological malignancy that is primarily detected at the metastatic stage. Most HGSOC originates from the fallopian tube epithelium (FTE) and metastasizes to the ovary before invading the peritoneum; therefore, it is crucial to study disease initiation and progression using FTE-derived models. We previously demonstrated that loss of PTEN from the FTE leads to ovarian cancer. In the present study, loss of PTEN in FTE led to the enrichment of cancer stem cell markers such as LGR5, WNT4, ALDH1, CD44. Interestingly, loss of the transcription factor PAX2, which is a common and early alteration in HGSOC, played a pivotal role in the expression of cancer stem-like cells (CSC) markers and cell function. In addition, loss of PTEN led to the generation of two distinct subpopulations of cells with different CSC marker expression, tumorigenicity, and chemoresistance profiles. Taken together, these data suggest that loss of PTEN induces reprogramming of the FTE cells into a more stem-like phenotype due to loss of PAX2 and provides a model to study early events during the FTE-driven ovarian cancer tumor formation.
Ferroptosis contributes to isoflurane-induced neurotoxicity and learning and memory impairment
Authors: Liu Pengfei , Yuan Jing , Feng Yetong , Chen Xin , Wang Guangsuo , Zhao Lei 
Published: April 2021

AbstractFerroptosis is a novel type of programmed cell death, which is different from apoptosis and autophagic cell death. Recently, ferroptosis has been indicated to contribute to the in vitro neurotoxicity induced by isoflurane, which is one of the most common anesthetics in clinic. However, the in vivo position of ferroptosis in isoflurane-induced neurotoxicity as well as learning and memory impairment remains unclear. In this study, we mainly explored the relationship between ferroptosis and isoflurane-induced learning and memory, as well as the therapeutic methods in mouse model. Our results indicated that isoflurane induced the ferroptosis in a dose-dependent and time-dependent manner in hippocampus, the organ related with learning and memory ability. In addition, the activity of cytochrome c oxidase/Complex IV in mitochondrial electron transport chain (ETC) was increased by isoflurane, which might further contributed to cysteine deprivation-induced ferroptosis caused by isoflurane exposure. More importantly, isoflurane-induced ferroptosis could be rescued by both ferroptosis inhibitor (ferrostatin-1) and mitochondria activator (dimethyl fumarate), which also showed effective therapeutic action against isoflurane-induced learning and memory impairment. Taken together, our data indicate the close association among ferroptosis, mitochondria and isoflurane, and provide a novel insight into the therapy mode against isoflurane-induced learning and memory impairment.
Impact of physical activity on course and outcome of pregnancy from pre- to postnatal
Authors: Ferrari Nina , Joisten Christine 
Published: April 2021

AbstractA healthy lifestyle that includes physical activity has numerous positive effects on the mother and child during and after pregnancy. In this context physical activity plays a central role due to its influence on body composition. While visceral fatty tissue has a pro-inflammatory effect via so-called adipokines, myokines seem to have a more anti-inflammatory effect and thus prevent numerous diseases such as gestational hypertension or gestational diabetes. However, many women show a decreased level of physical activity during pregnancy when compared to pre-gestation levels. The reasons underlying this change are manifold and include concern about the effects of physical exertion on the unborn child. Gynaecologists and midwives are also often uncertain about what specific advice to give regarding physical activity. The present review describes, besides the underlying mechanisms, current physical activity recommendations and corresponding evidence with a focus on weight development in terms of obesity, gestational diabetes and foetal outcome.
Structural variant evolution after telomere crisis
Authors: Dewhurst Sally M. , Yao Xiaotong , Rosiene Joel , Tian Huasong , Behr Julie , Bosco Nazario , Takai Kaori K. , de Lange Titia , Imieliński Marcin 
Published: April 2021

AbstractTelomere crisis contributes to cancer genome evolution, yet only a subset of cancers display breakage-fusion-bridge (BFB) cycles and chromothripsis, hallmarks of experimental telomere crisis identified in previous studies. We examine the spectrum of structural variants (SVs) instigated by natural telomere crisis. Eight spontaneous post-crisis clones did not show prominent patterns of BFB cycles or chromothripsis. Their crisis-induced genome rearrangements varied from infrequent simple SVs to more frequent and complex SVs. In contrast, BFB cycles and chromothripsis occurred in MRC5 fibroblast clones that escaped telomere crisis after CRISPR-controlled telomerase activation. This system revealed convergent evolutionary lineages altering one allele of chromosome 12p, where a short telomere likely predisposed to fusion. Remarkably, the 12p chromothripsis and BFB events were stabilized by independent fusions to chromosome 21. The data establish that telomere crisis can generate a wide spectrum of SVs implying that a lack of BFB patterns and chromothripsis in cancer genomes does not indicate absence of past telomere crisis.
Myofibril and mitochondria morphogenesis are coordinated by a mechanical feedback mechanism in muscle
Authors: Avellaneda Jerome , Rodier Clement , Daian Fabrice , Brouilly Nicolas , Rival Thomas , Luis Nuno Miguel , Schnorrer Frank 
Published: April 2021

AbstractComplex animals build specialised muscles to match specific biomechanical and energetic needs. Hence, composition and architecture of sarcomeres and mitochondria are muscle type specific. However, mechanisms coordinating mitochondria with sarcomere morphogenesis are elusive. Here we useDrosophilamuscles to demonstrate that myofibril and mitochondria morphogenesis are intimately linked. In flight muscles, the muscle selectorspaltinstructs mitochondria to intercalate between myofibrils, which in turn mechanically constrain mitochondria into elongated shapes. Conversely in cross-striated leg muscles, mitochondria networks surround myofibril bundles, contacting myofibrils only with thin extensions. To investigate the mechanism causing these differences, we manipulated mitochondrial dynamics and found that increased mitochondrial fusion during myofibril assembly prevents mitochondrial intercalation in flight muscles. Strikingly, this causes the expression of cross-striated muscle specific sarcomeric proteins. Consequently, flight muscle myofibrils convert towards a partially cross-striated architecture. Together, these data suggest a biomechanical feedback mechanism downstream ofspaltsynchronizing mitochondria with myofibril morphogenesis.
Widespread reorganisation of pluripotent factor binding and gene regulatory interactions between human pluripotent states
Authors: Chovanec Peter , Collier Amanda J. , Krueger Christel , Várnai Csilla , Semprich Claudia I. , Schoenfelder Stefan , Corcoran Anne E. , Rugg-Gunn Peter J. 
Published: April 2021

AbstractThe transition from naive to primed pluripotency is accompanied by an extensive reorganisation of transcriptional and epigenetic programmes. However, the role of transcriptional enhancers and three-dimensional chromatin organisation in coordinating these developmental programmes remains incompletely understood. Here, we generate a high-resolution atlas of gene regulatory interactions, chromatin profiles and transcription factor occupancy in naive and primed human pluripotent stem cells, and develop a network-graph approach to examine the atlas at multiple spatial scales. We uncover highly connected promoter hubs that change substantially in interaction frequency and in transcriptional co-regulation between pluripotent states. Small hubs frequently merge to form larger networks in primed cells, often linked by newly-formed Polycomb-associated interactions. We identify widespread state-specific differences in enhancer activity and interactivity that correspond with an extensive reconfiguration of OCT4, SOX2 and NANOG binding and target gene expression. These findings provide multilayered insights into the chromatin-based gene regulatory control of human pluripotent states.