bluuebunny/crossref_metadata_2025_split huggingface dataset:
Decision support system for flood risk reduction policies: The case of a flood protection measure in the area of Vicenza
Authors: Pantalona Georgia , Tsalakanidou Filareti , Nikolopoulos Spiros , Kompatsiaris Ioannis , Lombardo Francesca , Norbiato Daniele , Ferri Michele , Kovats Laszlo , Haberstock Holger 
Published: October 2021

Abstract
Climate change is one of the most significant and pressing issues faced by humanity; it frequently results in major natural disasters, such as catastrophic floods, which require the establishment of effective management policies by local and national authorities. These policies involve complex multistep decision-making processes that require combined assessment of various sources of data by different stakeholders. Even though an abundance of data is being collected to monitor climate change and estimate its consequences on the society, the environment, and the economy, policy-making is still largely based on intuition rather than evidence due to lack of a structured approach for modeling the decision-making process and considering the appropriate use of data in every step of the process. The goal of this work is to introduce a novel decision support system that can guide policy makers through a structured data-driven decision-making process aiming to create policies for flood risk management. The proposed system is a multifacet platform that guides policy makers through five phases—inform, advise, monitor, evaluate, and revise—of the policy cycle. For each phase, different dashboards provide relevant information regarding the environmental, social, and economic conditions. To demonstrate the potential of the proposed system, we use it to assess a flood protection policy in the city of Vicenza, Italy. The results reveal the benefits and challenges of the proposed decision support tool for public administrations involved in flood risk management.
Necrotising otitis externa and how to reduce length of hospital stay: a complete audit cycle of 77 hospital admissions
Authors: Mohammed H , Chean Khun Ng J , Qureshi M H , Yates P 
Published: October 2021

AbstractBackgroundNecrotising otitis externa is a serious condition that requires hospital admission. Longer hospital stays are associated with increased complications.MethodThis was a closed audit cycle in a tertiary ENT centre of patients presenting with necrotising otitis externa to the ENT department between 2015 and 2019. The aim was to audit the length of hospital stay in comparison to national figures as well as the time needed for investigations.ResultsThe number of patients with necrotising otitis externa is increasing in England. Length of stay, however, appears to be more stable. A total of 66 admissions occurred over the study period for 48 patients in total, and mean length of stay was 12.4 days. After implementation of a new protocol, length of stay was reduced to 7.1 days.ConclusionPatients with necrotising otitis externa require prompt diagnosis and management in order to shorten length of stay in hospital and avoid serious complications. Multi-disciplinary protocol development and implementation could help in reducing length of stay of necrotising otitis externa patients.
Stigmatization of Voluntarily Childfree Women and Men in the	UK
Authors: Ekelund Malin , Ask Karl 
Published: October 2021

Abstract. People who choose not to have children may face negative social judgment. Using a UK sample, Study 1 ( N = 199) successfully replicated Ashburn-Nardo’s (2017) finding that childfree targets are perceived as less psychologically fulfilled than targets with children. The effect, however, appeared limited to expected decision regret rather than general fulfillment, which was later confirmed in Study 2 ( N = 329). In contrast to Ashburn-Nardo , our results did not indicate that moral outrage mediates the effect (Study 1), but exploratory findings suggested that perceivers who intend to have children of their own perceive the childfree as morally inferior and less likable (Study 2). Participants’ endorsement of conservative values was not consistently related to negative perceptions of childfree targets.
Slow Slip Triggers the 2018 Mw 6.9 Zakynthos Earthquake Within the Weakly Locked Hellenic Subduction System, Greece
Authors: Saltogianni Vasso , Mouslopoulou Vasiliki , Dielforder Armin , Bocchini Gian Maria , Bedford Jonathan , Oncken Onno 
Published: October 2021

AbstractSlow slip events (SSEs) at subduction zones can precede large‐magnitude earthquakes and may serve as precursor indicators, but the triggering of earthquakes by slow slip remains insufficiently understood. Here, we combine geodetic, Coulomb wedge and Coulomb failure‐stress models with seismological data to explore the potential causal relationship between two SSEs and the 2018 Mw 6.9 Zakynthos Earthquake within the Hellenic Subduction System. We show that both SSEs released up to 10 mm of aseismic slip on the plate‐interface and were accompanied by an increase in upper‐plate seismicity rate. While the first SSE in late 2014 generated only mild Coulomb failure stress changes (≤3 kPa), that were nevertheless sufficient to destabilize faults of various kinematics in the overriding plate, the second SSE in 2018 caused stress changes up to 25 kPa prior to the mainshock. Collectively, these stress changes affected a highly overpressured and mechanically weak forearc, whose state of stress fluctuated between horizontal deviatoric compression and tension during the years preceding the Zakynthos Earthquake. We conclude that this configuration facilitated episodes of aseismic and seismic deformation that ultimately triggered the Zakynthos Earthquake.
A Spherical Harmonic Model of Earth's Lithospheric Magnetic Field up to Degree 1050
Authors: Thébault E. , Hulot G. , Langlais B. , Vigneron P. 
Published: October 2021

AbstractDetailed mapping of the Earth's magnetic field brings key constraints on the composition, dynamics, and history of the crust. Satellite and near‐surface measurements detect different length scales and are complementary. Here, we build a model, selecting and processing magnetic field measurements from the German CHAMP and ESA Swarm satellites, which we merge with near‐surface scalar anomaly data. We follow a regional approach for modeling the magnetic field measurements and next transform the series of regional models into a unique set of spherical harmonic (SH) Gauss coefficients. This produces the first global model to SH degree 1050 derived by inversion of all available measurements. The new model agrees with previous satellite‐based models at large wavelengths and fits the CHAMP and Swarm satellite data down to expected noise levels. Further assessment in the geographical and spectral domains shows the model to be stable when downward continued to the Earth's surface.
Carbon Dioxide and Methane Release Following Abrupt Thaw of Pleistocene Permafrost Deposits in Arctic Siberia
Authors: Knoblauch Christian , Beer Christian , Schuett Alexander , Sauerland Lewis , Liebner Susanne , Steinhof Axel , Rethemeyer Janet , Grigoriev Mikhail N. , Faguet Alexey , Pfeiffer Eva‐Maria 
Published: October 2021

AbstractThe decomposition of thawing permafrost organic matter (OM) to the greenhouse gases (GHG) carbon dioxide (CO2) and methane forms a positive feedback to global climate change. Data on in situ GHG fluxes from thawing permafrost OM are scarce and OM degradability is largely unknown, causing high uncertainties in the permafrost‐carbon climate feedback. We combined in situ CO2 and methane flux measurements at an abrupt permafrost thaw feature with laboratory incubations and dynamic modeling to quantify annual CO2 release from thawing permafrost OM, estimate its in situ degradability and evaluate the explanatory power of incubation experiments. In July 2016 and 2019, CO2 fluxes ranged between 0.24 and 2.6 g CO2‐C m−2 d−1. Methane fluxes were low, which coincided with the absence of active methanogens in the Pleistocene permafrost. CO2 fluxes were lower three years after initial thaw after normalizing these fluxes to thawed carbon, indicating the depletion of labile carbon. Higher CO2 fluxes from thawing Pleistocene permafrost than from Holocene permafrost indicate OM preservation for millennia and give evidence that microbial activity in the permafrost was not substantial. Short‐term incubations overestimated in situ CO2 fluxes but underestimated methane fluxes. Two independent models simulated median annual CO2 fluxes of 160 and 184 g CO2‐C m−2 from the thaw slump, which include 25%–31% CO2 emissions during winter. Annual CO2 fluxes represent 0.8% of the carbon pool thawed in the surface soil. Our results demonstrate the potential of abrupt thaw processes to transform the tundra from carbon neutral into a substantial GHG source.
Streams as Mirrors: Reading Subsurface Water Chemistry From Stream Chemistry
Authors: Stewart Bryn , Shanley James B. , Kirchner James W. , Norris David , Adler Thomas , Bristol Caitlin , Harpold Adrian A. , Perdrial Julia N. , Rizzo Donna M. , Sterle Gary , Underwood Kristen L. , Wen Hang , Li Li 
Published: October 2021

AbstractThe shallow and deep hypothesis suggests that stream concentration‐discharge (CQ) relationships are shaped by distinct source waters from different depths. Under this hypothesis, baseflows are typically dominated by groundwater and mostly reflect groundwater chemistry, whereas high flows are typically dominated by shallow soil water and mostly reflect soil water chemistry. Aspects of this hypothesis draw on applications like end member mixing analyses and hydrograph separation, yet direct data support for the hypothesis remains scarce. This work tests the shallow and deep hypothesis using co‐located measurements of soil water, groundwater, and streamwater chemistry at two intensively monitored sites, the W‐9 catchment at Sleepers River (Vermont, United States) and the Hafren catchment at Plynlimon (Wales). At both sites, depth profiles of subsurface water chemistry and stream CQ relationships for the 10 solutes analyzed are broadly consistent with the hypothesis. Solutes that are more abundant at depth (e.g., calcium) exhibit dilution patterns (concentration decreases with increasing discharge). Conversely, solutes enriched in shallow soils (e.g., nitrate) generally exhibit flushing patterns (concentration increases with increasing discharge). The hypothesis may hold broadly true for catchments that share such biogeochemical stratifications in the subsurface. Soil water and groundwater chemistries were estimated from high‐ and low‐flow stream chemistries with average relative errors ranging from 24% to 82%. This indicates that streams mirror subsurface waters: stream chemistry can be used to infer scarcely measured subsurface water chemistry, especially where there are distinct shallow and deep end members.
The Upper Tail of Flood Peaks Over China: Hydrology, Hydrometeorology, and Hydroclimatology
Authors: Yang Long , Yang Yixin , Smith James 
Published: October 2021

AbstractCharacterizing the upper tail of flood peak distributions remains a challenge due to the elusive nature of extreme floods. China has experienced some of the most extreme floods on Earth and is therefore an important setting for extreme flood research. Here, we examine the upper tail of flood peaks over China based on a comprehensive flood dataset that integrates systematic observations from 1759 stream gaging stations and 14,779 historical flood surveys. Floods with large upper tail ratios (i.e., flood peak discharge normalized by sample 10‐yr flood) cluster spatially in the windward regions of mountainous terrain with basin mean annual rainfall of around 550 mm. Large upper tail ratio floods are associated with a mixture of rainfall generation processes. These processes are characterized by anomalous moisture transport (e.g., zonal water vapor pathways) and/or synoptic configurations (e.g., blocking), with respect to flood‐producing storms for annual flood peaks. Downscaling simulations with the Weather Research and Forecasting model for the 1939, 1963, and 2016 floods over the North China Plain region highlight the role of interactions between complex terrain and large‐scale environment in defining the world envelope curve of flood peaks. The upper‐tail floods demonstrate a combination of ingredients producing extreme rainfall. Our results provide important insights to extreme floods in China and a frame of reference for assessing the largest floods on Earth.
Role of GALNT4 in protecting against cardiac hypertrophy through ASK1 signaling pathway
Authors: Zhang Bin-Bin , Gao Lu , Yang Qin , Liu Yuan , Yu Xiao-Yue , Shen Ji-Hong , Zhang Wen-Cai , Han Zhan-Ying , Chen Shao-Ze , Guo Sen 
Published: October 2021

AbstractPathological myocardial hypertrophy is regulated by multiple pathways. However, its underlying pathogenesis has not been fully explored. The goal of this work was to elucidate the function of polypeptide N-acetylgalactosaminyltransferase 4 (GALNT4) in myocardial hypertrophy and its underlying mechanism of action. We illustrated that GALNT4 was upregulated in the models of hypertrophy. Two cardiac hypertrophy models were established through partial transection of the aorta in GALNT4-knockout (GALNT4-KO) mice and adeno-associated virus 9-GALNT4 (AAV9-GALNT4) mice. The GALNT4-KO mice demonstrated accelerated cardiac hypertrophy, dysfunction, and fibrosis, whereas the opposite phenotype was observed in AAV9-GALNT4 mice. Similarly, GALNT4 overexpression mitigated the degree of phenylephrine-induced cardiomyocyte hypertrophy in vitro whereas GALNT4 knockdown aggravated the hypertrophy. In terms of mechanism, GALNT4 deficiency increased the phosphorylation and activation of ASK1 and its downstream targets (JNK and p38), whereas GALNT4 overexpression inhibited activation of the ASK1 pathway. Furthermore, we demonstrated that GALNT4 can directly bind to ASK1 inhibiting its N-terminally mediated dimerization and the subsequent phosphorylation of ASK1. Finally, an ASK1 inhibitor (iASK1) was able to reverse the effects of GALNT4 in vitro. In summary, GALNT4 may serve as a new regulatory factor and therapeutic target by blocking the activation of the ASK1 signaling cascade.
ERK5 modulates IL-6 secretion and contributes to tumor-induced immune suppression
Authors: Riegel Kristina , Yurugi Hajime , Schlöder Janine , Jonuleit Helmut , Kaulich Manuel , Kirschner Friederike , Arnold-Schild Danielle , Tenzer Stefan , Schild Hansjörg , Rajalingam Krishnaraj 
Published: October 2021

AbstractTumors exhibit a variety of strategies to dampen antitumor immune responses. With an aim to identify factors that are secreted from tumor cells, we performed an unbiased mass spectrometry-based secretome analysis in lung cancer cells. Interleukin-6 (IL-6) has been identified as a prominent factor secreted by tumor cells and cancer-associated fibroblasts isolated from cancer patients. Incubation of dendritic cell (DC) cultures with tumor cell supernatants inhibited the production of IL-12p70 in DCs but not the surface expression of other activation markers which is reversed by treatment with IL-6 antibody. Defects in IL-12p70 production in the DCs inhibited the differentiation of Th1 but not Th2 and Th17 cells from naïve CD4+ T cells. We also demonstrate that the classical mitogen-activated protein kinase, ERK5/MAPK7, is required for IL-6 production in tumor cells. Inhibition of ERK5 activity or depletion of ERK5 prevented IL-6 production in tumor cells, which could be exploited for enhancing antitumor immune responses.
CHD8 safeguards early neuroectoderm differentiation in human ESCs and protects from apoptosis during neurogenesis
Authors: Ding Song , Lan Xianchun , Meng Yajing , Yan Chenchao , Li Mao , Li Xiang , Chen Jian , Jiang Wei 
Published: October 2021

AbstractThe chromatin remodeler CHD8, which belongs to the ATP-dependent chromatin remodelers CHD family, is one of the most high-risk mutated genes in autism spectrum disorders. However, the role of CHD8 in neural differentiation and the mechanism of CHD8 in autism remains unclear, despite there are a few studies based on the CHD8 haploinsufficient models. Here, we generate the CHD8 knockout human ESCs by CRISPR/Cas9 technology and characterize the effect of loss-of-function of CHD8 on pluripotency maintenance and lineage determination by utilizing efficient directed differentiation protocols. The results show loss-of-function of CHD8 does not affect human ESC maintenance although having slight effect on proliferation and cell cycle. Interestingly, CHD8 depletion results in defective neuroectoderm differentiation, along with severe cell death in neural progenitor stage. Transcriptome analysis also indicates CHD8 does not alter the expression of pluripotent genes in ESC stage, but in neural progenitor cells depletion of CHD8 induces the abnormal expression of the apoptosis genes and suppresses neuroectoderm-related genes. These results provide the evidence that CHD8 plays an essential role in the pluripotency exit and neuroectoderm differentiation as well as the regulation of apoptosis during neurogenesis.
The emerging roles of neutrophil extracellular traps in wound healing
Authors: Zhu Shuainan , Yu Ying , Ren Yun , Xu Liying , Wang Huilin , Ling Xiaomin , Jin Lin , Hu Yan , Zhang Hao , Miao Changhong , Guo Kefang 
Published: October 2021

AbstractDelayed wound healing causes problems for many patients both physically and psychologically, contributing to pain, economic burden, loss of function, and even amputation. Although many factors affect the wound healing process, abnormally prolonged or augmented inflammation in the wound site is a common cause of poor wound healing. Excessive neutrophil extracellular trap (NET) formation during this phase may amplify inflammation and hinder wound healing. However, the roles of NETs in wound healing are still unclear. Herein, we briefly introduce NET formation and discuss the possible NET-related mechanisms in wound healing. We conclude with a discussion of current studies, focusing on the roles of NETs in diabetic and normoglycemic wounds and the effectiveness of NET-targeting treatments in wound healing.
CPAP enhances and maintains chronic inflammation in hepatocytes to promote hepatocarcinogenesis
Authors: Chen Ruo-Yu , Yen Chia-Jui , Lin Yih-Jyh , Wang Ju-Ming , Tasi Ting-Fen , Huang Yu-Chuan , Liu Yao-Wen , Tsai Hung-Wen , Lee Ming-Hao , Hung Liang-Yi 
Published: October 2021

AbstractChronic and persistent inflammation is a well-known carcinogenesis promoter. Hepatocellular carcinoma (HCC) is one of the most common inflammation-associated cancers; most HCCs arise in the setting of chronic inflammation and hepatic injury. Both NF-κB and STAT3 are important regulators of inflammation. Centrosomal P4.1-associated protein (CPAP), a centrosomal protein that participates primarily in centrosome functions, is overexpressed in HCC and can increase TNF-α-mediated NF-κB activation and IL-6-induced STAT3 activation. A transgenic (Tg) mouse model with hepatocyte-specific CPAP expression was established to investigate the physiological role of CPAP in hepatocarcinogenesis. Obvious inflammatory cell accumulation and fatty change were observed in the livers of CPAP Tg mice. The alanine aminotransferase (ALT) level and the expression levels of inflammatory genes, such as IL-6, IL-1β and TNF-α, were higher in CPAP Tg mice than in wild type (WT) mice. High-dose/short-term treatment with diethylnitrosamine (DEN) increased the ALT level, proinflammatory gene expression levels, and STAT3 and NF-κB activation in CPAP Tg mice; low-dose/long-term DEN treatment induced more severe liver tumor formation in CPAP Tg mice than in WT mice. CPAP can increase the expression of chemokine (C-C motif) ligand 16 (CCL-16), an important chemotactic cytokine, in human hepatocytes. CCL-16 expression is positively correlated with CPAP and TNF-α mRNA expression in the peritumoral part of HCC. In summary, these results suggest that CPAP may promote hepatocarcinogenesis through enhancing the inflammation pathway via increasing the expression of CCL-16.
Effect of tumor-associated macrophages on lncRNA PURPL/miR-363/PDZD2 axis in osteosarcoma cells
Authors: He Fan , Ding Guoming , Jiang Wu , Fan Xiaoliang , Zhu Liulong 
Published: October 2021

AbstractTumor-associated macrophages (TAMs) are known to participate in osteosarcoma (OS) progression. As demonstrated in our previous research, miR-363 played a tumor inhibitory effect in OS cells via lowering the PDZ domain containing 2 (PDZD2) expression. The regulatory roles of TAMs on miR-363/PDZD2 and the internal mechanism relating to long noncoding RNA p53 upregulated regulator of P53 levels (lncRNA PURPL) are examined in this study. TAM-like macrophages were formed by inducing CD14+ peripheral blood mononuclear cells (PBMCs). The TAMs migration was detected after MG-63 cells transfected with miR-363 mimics or inhibitors. We then analyzed the regulatory activity of PURPL on miR-363 expression. We also tested the influences of PURPL overexpression/knockdown on MG-63 cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT), as well as TAMs migration. Silence in PDZD2 expression was used to confirm the effects of PURPL on MG-63 cells. We successfully induced TAM-like macrophages. MG-63 cells transfecting miR-363 mimics suppressed TAMs migration while transfecting a converse effect was seen in miR-363 inhibitor. TAMs raised PURPL expression in MG-63 cells, which was an upstream regulator of miR-363. Along with TAMs migration, PURPL overexpression promoted MG-63 cell proliferation, migration, invasion, and EMT. An opposite influence was seen due to the PURPL knockdown. The silence of PDZD2 weakened the influences of PURPL overexpression on MG-63 cells and TAMs migration. On modulating the PURPL/miR-363/PDZD2 axis, TAMs-promoted OS development might be achieved.
A small molecule produced by Lactobacillus species blocks Candida albicans filamentation by inhibiting a DYRK1-family kinase
Authors: MacAlpine Jessie , Daniel-Ivad Martin , Liu Zhongle , Yano Junko , Revie Nicole M. , Todd Robert T. , Stogios Peter J. , Sanchez Hiram , O’Meara Teresa R. , Tompkins Thomas A. , Savchenko Alexei , Selmecki Anna , Veri Amanda O. , Andes David R. , Fidel Paul L. , Robbins Nicole , Nodwell Justin , Whitesell Luke , Cowen Leah E. 
Published: October 2021

AbstractThe fungus Candida albicans is an opportunistic pathogen that can exploit imbalances in microbiome composition to invade its human host, causing pathologies ranging from vaginal candidiasis to fungal sepsis. Bacteria of the genus Lactobacillus are colonizers of human mucosa and can produce compounds with bioactivity against C. albicans. Here, we show that some Lactobacillus species produce a small molecule under laboratory conditions that blocks the C. albicans yeast-to-filament transition, an important virulence trait. It remains unexplored whether the compound is produced in the context of the human host. Bioassay-guided fractionation of Lactobacillus-conditioned medium linked this activity to 1-acetyl-β-carboline (1-ABC). We use genetic approaches to show that filamentation inhibition by 1-ABC requires Yak1, a DYRK1-family kinase. Additional biochemical characterization of structurally related 1-ethoxycarbonyl-β-carboline confirms that it inhibits Yak1 and blocks C. albicans biofilm formation. Thus, our findings reveal Lactobacillus-produced 1-ABC can prevent the yeast-to-filament transition in C. albicans through inhibition of Yak1.