bluuebunny/crossref_metadata_2025_split huggingface dataset:
A Quantitative Comparison and Validation of Finite‐Fault Models: The 2011 Tohoku‐Oki Earthquake
Authors: Wong Jeremy Wing Ching , Fan Wenyuan , Gabriel Alice‐Agnes 
Published: October 2024

AbstractLarge earthquakes rupture faults over hundreds of kilometers within minutes. Finite‐fault models image these processes and provide observational constraints for understanding earthquake physics. However, finite‐fault inversions are subject to non‐uniqueness and uncertainties. The diverse range of published models for the well‐recorded 2011 9.0 Tohoku‐Oki earthquake illustrates this challenge, and its rupture process remains under debate. Here, we comprehensively compare 32 published finite‐fault models of the Tohoku‐Oki earthquake. We aim to identify the most coherent slip features of the Tohoku‐Oki earthquake from these slip models and develop a new method for quantitatively analyzing their variations. We find that the models correlate poorly at 1‐km subfault size, irrespective of the data type. In contrast, model agreement improves significantly with increasing subfault sizes, consistently showing that the largest slip occurs up‐dip of the hypocenter near the trench. We use the set of models to test the sensitivity of available teleseismic, regional seismic, and geodetic observations. For the large Tohoku‐Oki earthquake, we find that the analyzed finite‐fault models are less sensitive to slip features smaller than 64 km. When we use the models to compute synthetic seafloor deformation, we observe strong variations in the synthetics, suggesting their sensitivity to small‐scale slip features. Our newly developed approach offers a quantitative framework to identify common features in distinct finite‐fault slip models and to analyze their robustness using regional and global geophysical observations for megathrust earthquakes. Our results indicate that dense offshore instrumentation is critical for resolving the rupture complexities of megathrust earthquakes.
Elevated plasma bile acids coincide with cardiac stress and inflammation in young Cyp2c70−/− mice
Authors: de Vries Hilde D. , Eijgenraam Tim R. , Bloks Vincent W. , Mulder Niels L. , van Zutphen Tim , Silljé Herman H. W. , Kuipers Folkert , de Boer Jan Freark 
Published: October 2024

Abstract
Background
High plasma bile acids (BAs), for instance due to intrahepatic cholestasis of pregnancy or neonatal cholestasis, are associated with cardiac abnormalities. Here, we exploited the variability in plasma BA levels in Cyp2c70−/− mice with a human-like BA composition to investigate the acute effects of elevated circulating BAs on the heart.

Methods
RNA sequencing was performed on hearts of 3-week-old Cyp2c70−/− mice lacking mouse-specific BA species that show features of neonatal cholestasis. Cardiac transcriptomes were compared between wild-type pups, Cyp2c70−/− pups with low or high plasma BAs, and Cyp2c70−/− pups from dams that were perinatally treated with ursodeoxycholic acid (UDCA).

Results
We identified 1355 genes that were differentially expressed in hearts of Cyp2c70−/− mice with high versus low plasma BAs with enrichment of inflammatory processes. Strikingly, expression of 1053 (78%) of those genes was normalized in hearts of pups of UDCA-treated dams. Moreover, 645 cardiac genes strongly correlated to plasma BAs, of which 172 genes were associated with cardiovascular disease.

Conclusions
Elevated plasma BAs alter gene expression profiles of hearts of mice with a human-like BA profile, revealing cardiac stress and inflammation. Our findings support the notion that high plasma BAs induce cardiac complications in early life.

Impact

Cyp2c70−/− mice with a human-like bile acid composition show features of neonatal cholestasis but the extrahepatic consequences hereof have so far hardly been addressed

Elevated plasma bile acids in Cyp2c70−/− pups coincide with cardiac stress and inflammation

Perinatal treatment with UDCA prevents dysregulated cardiac gene expression patterns in Cyp2c70−/− pups
Loss of EMI1 compromises chromosome stability and is associated with cellular transformation in colonic epithelial cell contexts
Authors: Campos Gudiño Rubi , Neudorf Nicole M. , Andromidas Demi , Lichtensztejn Zelda , McManus Kirk J. 
Published: October 2024

Abstract
Background
Colorectal cancer (CRC) is still a leading cause of cancer deaths worldwide. Thus, identifying the aberrant genes and proteins underlying disease pathogenesis is critical to improve early detection methods and develop novel therapeutic strategies. Chromosome instability (CIN), or ongoing changes in chromosome complements, is a predominant form of genome instability. It is a driver of genetic heterogeneity found in ~85% of CRCs. Although CIN contributes to CRC pathogenesis, the molecular determinants underlying CIN remain poorly understood. Recently, EMI1, an F-box protein, was identified as a candidate CIN gene. In this study, we sought to determine the impact reduced EMI1 expression has on CIN and cellular transformation.

Methods
Coupling siRNA-based silencing and CRISPR/Cas9 knockout clones with quantitative imaging microscopy we evaluated the impact reduced EMI1 expression has on CIN and cellular transformation in four colonic epithelial cell contexts.

Results
Quantitative imaging microscopy data revealed that reduced EMI1 expression induces increases in CIN phenotypes in both transient (siRNA) and constitutive (CRISPR/Cas9) cell models that are associated with increases in DNA damage and cellular transformation phenotypes in long-term studies.

Conclusions
This study determined that reduced EMI1 expression induces CIN and promotes cellular transformation, which is consistent with a role in early CRC development.
Inhibition of poly(ADP-Ribosyl)ation reduced vascular smooth muscle cells loss and improves aortic disease in a mouse model of human accelerated aging syndrome
Authors: Cardoso Déborah , Guilbert Solenn , Guigue Philippe , Carabalona Aurélie , Harhouri Karim , Peccate Cécile , Tournois Johana , Guesmia Zoheir , Ferreira Lino , Bartoli Catherine , Levy Nicolas , Colleaux Laurence , Nissan Xavier , Muchir Antoine 
Published: October 2024

AbstractHutchinson-Gilford progeria syndrome (HGPS) is an extremely rare genetic disorder associated with features of accelerated aging. HGPS is an autosomal dominant disease caused by a de novo mutation of LMNA gene, encoding A-type lamins, resulting in the truncated form of pre-lamin A called progerin. While asymptomatic at birth, patients develop symptoms within the first year of life when they begin to display accelerated aging and suffer from growth retardation, and severe cardiovascular complications including loss of vascular smooth muscle cells (VSMCs). Recent works reported the loss of VSMCs as a major factor triggering atherosclerosis in HGPS. Here, we investigated the mechanisms by which progerin expression leads to massive VSMCs loss. Using aorta tissue and primary cultures of murine VSMCs from a mouse model of HGPS, we showed increased VSMCs death associated with increased poly(ADP-Ribosyl)ation. Poly(ADP-Ribosyl)ation is recognized as a post-translational protein modification that coordinates the repair at DNA damage sites. Poly-ADP-ribose polymerase (PARP) catalyzes protein poly(ADP-Ribosyl)ation by utilizing nicotinamide adenine dinucleotide (NAD+). Our results provided the first demonstration linking progerin accumulation, augmented poly(ADP-Ribosyl)ation and decreased nicotinamide adenine dinucleotide (NAD+) level in VSMCs. Using high-throughput screening on VSMCs differentiated from iPSCs from HGPS patients, we identified a new compound, trifluridine able to increase NAD+ levels through decrease of PARP-1 activity. Lastly, we demonstrate that trifluridine treatment in vivo was able to alleviate aortic VSMCs loss and clinical sign of progeria, suggesting a novel therapeutic approach of cardiovascular disease in progeria.
A Drosophila computational brain model reveals sensorimotor processing
Authors: Shiu Philip K. , Sterne Gabriella R. , Spiller Nico , Franconville Romain , Sandoval Andrea , Zhou Joie , Simha Neha , Kang Chan Hyuk , Yu Seongbong , Kim Jinseop S. , Dorkenwald Sven , Matsliah Arie , Schlegel Philipp , Yu Szi-chieh , McKellar Claire E. , Sterling Amy , Costa Marta , Eichler Katharina , Bates Alexander Shakeel , Eckstein Nils , Funke Jan , Jefferis Gregory S. X. E. , Murthy Mala , Bidaye Salil S. , Hampel Stefanie , Seeds Andrew M. , Scott Kristin 
Published: October 2024

AbstractThe recent assembly of the adult Drosophila melanogaster central brain connectome, containing more than 125,000 neurons and 50 million synaptic connections, provides a template for examining sensory processing throughout the brain1,2. Here we create a leaky integrate-and-fire computational model of the entire Drosophila brain, on the basis of neural connectivity and neurotransmitter identity3, to study circuit properties of feeding and grooming behaviours. We show that activation of sugar-sensing or water-sensing gustatory neurons in the computational model accurately predicts neurons that respond to tastes and are required for feeding initiation4. In addition, using the model to activate neurons in the feeding region of the Drosophila brain predicts those that elicit motor neuron firing5—a testable hypothesis that we validate by optogenetic activation and behavioural studies. Activating different classes of gustatory neurons in the model makes accurate predictions of how several taste modalities interact, providing circuit-level insight into aversive and appetitive taste processing. Additionally, we applied this model to mechanosensory circuits and found that computational activation of mechanosensory neurons predicts activation of a small set of neurons comprising the antennal grooming circuit, and accurately describes the circuit response upon activation of different mechanosensory subtypes6–10. Our results demonstrate that modelling brain circuits using only synapse-level connectivity and predicted neurotransmitter identity generates experimentally testable hypotheses and can describe complete sensorimotor transformations.
RNA m5C oxidation by TET2 regulates chromatin state and leukaemogenesis
Authors: Zou Zhongyu , Dou Xiaoyang , Li Ying , Zhang Zijie , Wang Juan , Gao Boyang , Xiao Yu , Wang Yiding , Zhao Lijie , Sun Chenxi , Liu Qinzhe , Yu Xianbin , Wang Hao , Hong Juyeong , Dai Qing , Yang Feng-Chun , Xu Mingjiang , He Chuan 
Published: October 2024

AbstractMutation of tet methylcytosine dioxygenase 2 (encoded by TET2) drives myeloid malignancy initiation and progression1–3. TET2 deficiency is known to cause a globally opened chromatin state and activation of genes contributing to aberrant haematopoietic stem cell self-renewal4,5. However, the open chromatin observed in TET2-deficient mouse embryonic stem cells, leukaemic cells and haematopoietic stem and progenitor cells5 is inconsistent with the designated role of DNA 5-methylcytosine oxidation of TET2. Here we show that chromatin-associated retrotransposon RNA 5-methylcytosine (m5C) can be recognized by the methyl-CpG-binding-domain protein MBD6, which guides deubiquitination of nearby monoubiquitinated Lys119 of histone H2A (H2AK119ub) to promote an open chromatin state. TET2 oxidizes m5C and antagonizes this MBD6-dependent H2AK119ub deubiquitination. TET2 depletion thereby leads to globally decreased H2AK119ub, more open chromatin and increased transcription in stem cells. TET2-mutant human leukaemia becomes dependent on this gene activation pathway, with MBD6 depletion selectively blocking proliferation of TET2-mutant leukaemic cells and largely reversing the haematopoiesis defects caused by Tet2 loss in mouse models. Together, our findings reveal a chromatin regulation pathway by TET2 through retrotransposon RNA m5C oxidation and identify the downstream MBD6 protein as a feasible target for developing therapies specific against TET2 mutant malignancies.
Three spectrophotometric quantitative analysis of bisoprolol fumarate and telmisartan in fixed-dose combination utilizing ratio spectra manipulation methods
Authors: Sattar Osama I. Abdel , Abuseada Hamed H. M. , Ramzy Sherif , Abuelwafa Mahmoud M. 
Published: October 2024

AbstractHypertension is a chronic condition with multiple drug regimens. Limiting these medicines is critical to patient compliance. Therefore, bisoprolol and telmisartan were recently developed in a fixed-dose combination to control blood pressure. The UV absorption spectra of bisoprolol and telmisartan overlapped significantly. Thus, three spectrophotometric methods have been developed for simultaneous determination of bisoprolol and telmisartan without prior separation. Method A is ratio difference of ratio spectra (RD), which measures the amplitude difference between (210–224) nm for bisoprolol and between (255–365) nm for telmisartan. Method B, the first derivative of ratio spectra (1DD), measures amplitude signals at 232 and 243 nm for bisoprolol and telmisartan, respectively. Method C is the mean centering of ratio spectra (MC), which measures the mean-centered ratio spectra's values at 223 nm for bisoprolol and 245 nm for telmisartan. The applied methods showed good linearity 2–20 µg/mL for bisoprolol, 4–32 µg/mL for telmisartan, with sufficient accuracy and precision. The methods were sensitive, with LOD values of 0.243 µg/mL and 0.596 µg/mL in RD method, 0.313 µg/mL and 0.914 µg/mL in 1DD method, and 0.406 and 0.707 µg/mL in MC method for bisoprolol and telmisartan, respectively, the methods were validated per ICH criteria. The novel methods are precise and accurate and can be used for routine analysis and quality control of bisoprolol and telmisartan in pure and dosage form. Furthermore, the greenness of the approaches was evaluated using Analytical Greenness assessment (AGREE), and the suggested method received a high greenness score.
The role of TiO2 and gC3N4 bimetallic catalysts in boosting antibiotic resistance gene removal through photocatalyst assisted peroxone process
Authors: Cong Xiaoyu , Mazierski Paweł , Miodyńska Magdalena , Zaleska-Medynska Adriana , Horn Harald , Schwartz Thomas , Gmurek Marta 
Published: October 2024

AbstractAntibiotics are extensively used in human medicine, aquaculture, and animal husbandry, leading to the release of antimicrobial resistance into the environment. This contributes to the rapid spread of antibiotic-resistant genes (ARGs), posing a significant threat to human health and aquatic ecosystems. Conventional wastewater treatment methods often fail to eliminate ARGs, prompting the adoption of advanced oxidation processes (AOPs) to address this growing risk. The study investigates the efficacy of visible light-driven photocatalytic systems utilizing two catalyst types (TiO2-Pd/Cu and g-C3N4-Pd/Cu), with a particular emphasis on their effectiveness in eliminating blaTEM, ermB, qnrS, tetM. intl1, 16 S rDNA and 23 S rDNA through photocatalytic ozonation and peroxone processes. Incorporating O3 into photocatalytic processes significantly enhances target removal efficiency, with the photocatalyst-assisted peroxone process emerging as the most effective AOP. The reemergence of targeted contaminants following treatment highlights the pivotal importance of AOPs and the meticulous selection of catalysts in ensuring sustained treatment efficacy. Furthermore, Polymerase Chain Reaction-Denaturing Gradient Gel Electrophoresis (PCR-DGGE) analysis reveals challenges in eradicating GC-rich bacteria with TiO2 and g-C3N4 processes, while slight differences in Cu/Pd loadings suggest g-C3N4-based ozonation improved antibacterial effectiveness. Terminal Restriction Fragment Length Polymorphism analysis highlights the efficacy of the photocatalyst-assisted peroxone process in treating diverse samples.
Human bias and CNNs’ superior insights in satellite based poverty mapping
Authors: Sarmadi Hamid , Wahab Ibrahim , Hall Ola , Rögnvaldsson Thorsteinn , Ohlsson Mattias 
Published: October 2024

AbstractSatellite imagery is a potent tool for estimating human wealth and poverty, especially in regions lacking reliable data. This study compares a range of poverty estimation approaches from satellite images, spanning from expert-based to fully machine learning-based methodologies. Human experts ranked clusters from the Tanzania DHS survey using high-resolution satellite images. Then expert-defined features were utilized in a machine learning algorithm to estimate poverty. An explainability method was applied to assess the importance and interaction of these features in poverty prediction. Additionally, a convolutional neural network (CNN) was employed to estimate poverty from medium-resolution satellite images of the same locations. Our analysis indicates that increased human involvement in poverty estimation diminishes accuracy compared to machine learning involvement, exemplified with the case of Tanzania. Expert defined features exhibited significant overlap and poor interaction when used together in a classifier. Conversely, the CNN-based approach outperformed human experts, demonstrating superior predictive capability with medium-resolution images. These findings highlight the importance of leveraging machine learning explainability methods to identify predictive elements that may be overlooked by human experts. This study advocates for the integration of emerging technologies with traditional methodologies to optimize data collection and analysis of poverty and welfare.
CHK1 controls zygote pronuclear envelope breakdown by regulating F-actin through interacting with MICAL3
Authors: Zhang Honghui , Cui Ying , Yang Bohan , Hou Zhenzhen , Zhang Mengge , Su Wei , Chen Tailai , Bian Yuehong , Li Mei , Chen Zi-Jiang , Zhao Han , Zhao Shigang , Wu Keliang 
Published: October 2024

AbstractCHK1 mutations could cause human zygote arrest at the pronuclei stage, a phenomenon that is not well understood at the molecular level. In this study, we conducted experiments where pre-pronuclei from zygotes with CHK1 mutation were transferred into the cytoplasm of normal enucleated fertilized eggs. This approach rescued the zygote arrest caused by the mutation, resulting in the production of a high-quality blastocyst. This suggests that CHK1 dysfunction primarily disrupts crucial biological processes occurring in the cytoplasm. Further investigation reveals that CHK1 mutants have an impact on the F-actin meshwork, leading to disturbances in pronuclear envelope breakdown. Through co-immunoprecipitation and mass spectrometry analysis of around 6000 mouse zygotes, we identified an interaction between CHK1 and MICAL3, a key regulator of F-actin disassembly. The gain-of-function mutants of CHK1 enhance their interaction with MICAL3 and increase MICAL3 enzymatic activity, resulting in excessive depolymerization of F-actin. These findings shed light on the regulatory mechanism behind pronuclear envelope breakdown during the transition from meiosis to the first mitosis in mammals.
Investigating the consistency of the shape and flux of X-ray reflection spectra in the hard state with an accretion disk reaching close to the black hole
Authors: Datta Sudeb Ranjan , Dovčiak Michal , Bursa Michal , Zhang Wenda , Horák Jiří , Karas Vladimír 
Published: October 2024

Context. The observed spectra from black hole (BH) X-ray binaries (XRBs) typically consist of two primary components. A multitemperature blackbody originating from the accretion disk in the soft X-ray, and a power law-like component in the hard X-ray, due to the Comptonization of soft photons by the hot corona. The illumination of the disk by the corona gives rise to another key component known as reflection. A fraction of the incident hard X-ray radiation is naturally absorbed and re-emitted as a blackbody at lower energies and referred to as the “reprocessed blackbody”.
Aims. For densities relevant to XRBs and typical ionization values, the reprocessed blackbody may become significant in the soft X-ray region (approximately 0.1–1.0 keV) and should be noticeable in the observed spectra as a consequence of reflection. The absence of any blackbody component in the low/hard state of a BH XRB may not be consistent with the reflection of highly irradiating flux, observed as a power law from an appropriately dense disk of XRB.
Methods. We focus on the low/hard state of the BH XRB MAXI J1820+070. In contrast to previous works, we simultaneously fit the shape and flux of the reflection spectra. This allowed us to estimate the correct density and ionization of the slab as well as the corresponding reprocessed blackbody.
Results. Our fitting of the representative observation of the BH XRB low/hard state suggests that the disk may, in principle, extend very close to the BH, even though the reprocessed thermal emission (due to disk illumination) remains cold (and thus low) enough to be consistent with the data in contrast to the results of a previous study. The inner reflection component is highly ionized and its fit is primarily driven by its contribution to the continuum, rather than by the shape of the relativistic iron line.
Conclusions. The reprocessed blackbody cannot help determine whether the disk extends close to the BH or not in the hard state. For this specific observation, the flux in inner reflection component turns out to be quite low with respect to the outer reflection or power law. The outflowing slab corona covering the inner region of the disk could be the plausible geometry of the source, with the underlying disk approaching near to the BH.
Merging galaxies in isolated environments
Authors: Calderón-Castillo Paula , Smith Rory 
Published: October 2024

Context. It is now well known that certain massive galaxies undergo enormous enhancements in their star formation rate (SFR) when they undergo major mergers. These enhancements can be as high as 100 times the SFR of unperturbed galaxies of the same stellar mass. Previous works have found that the size of this boost in star formation (SF) is related to the morphology of and the proximity to the companion. The same trend has also been observed for the fraction of active galactic nuclei (AGN), where galaxies that are closer together tend to have higher AGN fractions.
Aims. We aim to analyse the SF enhancement and AGN fraction evolution during the merger process by using a more timeline-like merger sequence. Additionally, we aim to determine the relation between the SF enhancement in mergers and the morphology of the galaxies involved.
Methods. Taking advantage of the stellar masses (M*) and SFRs of the ∼600 nearby isolated mergers obtained in our previous study, we calculated the distance of each of our galaxies from the star-forming main sequence (MS; specific SFR (sSFR)/sSFRMS), which werefer to as the SF mode. We then analysed how the SF mode varies during the merger process as a function of morphology and M*. Additionally, we analysed the AGN content of our mergers, using multiple diagnostics based on emission line ratios and WISE colours.
Results. We observed that, overall, merging galaxies show an SF mode that is governed by their morphology. Spirals typically show high SF mode values, while highly disturbed (HD) galaxies are generally even more enhanced (median values of +0.8 dex and +1.08 dex above the MS, respectively). In contrast, elliptical and lenticular galaxies show the lowest SF modes, as expected. However, even they show SF enhancement compared to their unperturbed counterparts. For example, their median SF mode is just within the 1-sigma scatter of the MS, and this can occur even before the galaxies have coalesced. We observed a trend for the SF mode to gradually increase with increasing merger stage. We did not find a clear dependency of the observed AGN fraction on the merger stage for the majority of our classification methods.
Conclusions. We find mergers can significantly enhance SF in galaxies of all morphologies. For early-type galaxies, this could suggest that some gas was present prior to the merger, which may be triggered to form stars by the tidal interaction. As the SF enhancement continues throughout the merger process, this suggests that the enhancement may be a long-lived event, contrary to the short starbursts seen in some models.