bluuebunny/crossref_metadata_2025_split huggingface dataset:
Stress Release Process Along an Intraplate Fault Analogous to the Plate Boundary: A Case Study of the 2017 M5.2 Akita‐Daisen Earthquake, NE Japan
Authors: Yoshida Keisuke , Taira Taka'aki , Matsumoto Yoshiaki , Saito Tatsuhiko , Emoto Kentaro , Matsuzawa Toru 
Published: April 2020

AbstractStress accumulation and release inside the plate remains poorly understood compared to that at the plate boundaries. Spatiotemporal variations in foreshock and aftershock activities can provide key constraints on time‐dependent stress and deformation processes inside the plate. The 2017 M5.2 Akita‐Daisen intraplate earthquake in NE Japan was preceded by intense foreshock activity and triggered a strong sequence of aftershocks. We examine the spatiotemporal distributions of foreshocks and aftershocks and determine the coseismic slip distribution of the mainshock. Our results indicate that seismicity both before and after the mainshock was concentrated on a planar structure with N‐S strike that dips steeply eastward. We observe a migration of foreshocks toward the mainshock rupture area, suggesting the possibility that foreshocks were triggered by aseismic phenomena preceding the mainshock rupture. The mainshock rupture propagated toward the north, showing less slip beneath foreshock regions. The stress drop of the mainshock was 1.4 MPa, and the radiation efficiency was 0.72. Aftershocks were intensely triggered near the edge of large coseismic slip regions where shear stress increased. The aftershock region expanded along the fault strike, which can be attributed to the postseismic aseismic slip of the mainshock. We find that the foreshocks, mainshock, aftershocks, and postseismic slip released stress at different segments along the fault, which may reflect differences in frictional properties. Obtained results were similar to those observed for interplate earthquakes, which supports the hypothesis that the deformation processes along plate boundaries and intraplate faults are fundamentally the same.
Deficiency in the autophagy modulator Dram1 exacerbates pyroptotic cell death of Mycobacteria-infected macrophages
Authors: Zhang Rui , Varela Monica , Forn-Cuní Gabriel , Torraca Vincenzo , van der Vaart Michiel , Meijer Annemarie H. 
Published: April 2020

AbstractDNA damage regulated autophagy modulator 1 (DRAM1) is a stress-inducible regulator of autophagy and cell death. DRAM1 has been implicated in cancer, myocardial infarction, and infectious diseases, but the molecular and cellular functions of this transmembrane protein remain poorly understood. Previously, we have proposed DRAM1 as a host resistance factor for tuberculosis (TB) and a potential target for host-directed anti-infective therapies. In this study, we generated a zebrafish dram1 mutant and investigated its loss-of-function effects during Mycobacterium marinum (Mm) infection, a widely used model in TB research. In agreement with previous knockdown analysis, dram1 mutation increased the susceptibility of zebrafish larvae to Mm infection. RNA sequencing revealed major effects of Dram1 deficiency on metabolic, immune response, and cell death pathways during Mm infection, and only minor effects on proteinase and metabolic pathways were found under uninfected conditions. Furthermore, unchallenged dram1 mutants did not display overt autophagic defects, but autophagic targeting of Mm was reduced in the absence of Dram1. The phagocytic ability of macrophages in dram1 mutants was unaffected, but acidification of Mm-containing vesicles was strongly reduced, indicating that Dram1 is required for phagosome maturation. By in vivo imaging, we observed that Dram1-deficient macrophages fail to restrict Mm during early stages of infection. The resulting increase in bacterial burden could be reverted by knockdown of inflammatory caspase a (caspa) and gasdermin Eb (gsdmeb), demonstrating pyroptosis as the mechanism underlying premature cell death of Mm-infected macrophages in dram1 mutants. Collectively, these data demonstrate that dissemination of mycobacterial infection in zebrafish larvae is promoted in the absence of Dram1 due to reduced maturation of mycobacteria-containing vesicles, failed intracellular containment, and consequent pyroptotic death of infected macrophages. These results provide new evidence that Dram1 plays a central role in host resistance to intracellular infection, acting at the crossroad of autophagy and cell death.
A necroptotic-independent function of MLKL in regulating endothelial cell adhesion molecule expression
Authors: Dai Jialin , Zhang Chonghe , Guo Lin , He Hao , Jiang Kai , Huang Yingying , Zhang Xixi , Zhang Haibing , Wei Wu , Zhang Yaoyang , Lu Lihua , Hu Junhao 
Published: April 2020

AbstractMixed-lineage kinase domain-like protein (MLKL) is known as the terminal executor of necroptosis. However, its function outside of necroptosis is still not clear. Herein, we demonstrate that MLKL promotes vascular inflammation by regulating the expression of adhesion molecules ICAM1, VCAM1, and E-selectin in endothelial cells (EC). MLKL deficiency suppresses the expression of these adhesion molecules, thereby reducing EC-leukocyte interaction in vitro and in vivo. Mechanistically, we show that MLKL interacts with RBM6 to promote the mRNA stability of adhesion molecules. In conclusion, this study identified a novel role of MLKL in regulating endothelial adhesion molecule expression and local EC-leukocyte interaction during acute inflammation.
CACNA1H downregulation induces skeletal muscle atrophy involving endoplasmic reticulum stress activation and autophagy flux blockade
Authors: Li Suting , Hao Menglei , Li Bingshu , Chen Mao , Chen Jue , Tang Jianming , Hong Shasha , Min Jie , Hu Ming , Hong Li 
Published: April 2020

AbstractMultiple vaginal delivery (MVD) is an important factor for pelvic floor muscle (PFM) function decline and pelvic floor dysfunction (PFD). PFD is common in middle-aged and elderly women, but its pathogenesis is not clear. In this study, we found that the expression of CACNA1H was lower in the PFM of old mice after MVD compared with old or adult mice. In in-vitro studies, we found that treatment with the T-type Ca2+ channel (T-channel) inhibitor NNC-55 or downregulation of the CACNA1H gene by siRNA intervention promoted myotube atrophy and apoptosis. Mechanistically, we revealed that NNC-55 increased the expression of GRP78 and DDIT3 in myotubes, indicating endoplasmic reticulum stress (ERS) activation, and that the IRE1 and PERK pathways might be involved in this effect. NNC-55 induced the formation of autophagosomes but inhibited autophagy flux. Moreover, rapamycin, an autophagy activator, did not rescue myotube atrophy or apoptosis induced by NNC-55, and the autophagy inhibitors 3-MA and HCQ accelerated this damage. Further studies showed that the ERS inhibitors 4-PBA and TUDAC relieved NNC-55-induced damage and autophagy flux blockade. Finally, we found multisite muscle atrophy and decreased muscle function in Cacna1h−/− (TH-null) mice, as well as increased autophagy inhibition and apoptotic signals in the PFM of old WT mice after MVD and TH-null mice. Taken together, our results suggest that MVD-associated PFD is partially attributed to CACNA1H downregulation-induced PFM atrophy and that ERS is a potential therapeutic target for this disease.
Record thermopower found in an IrMn-based spintronic stack
Authors: Tu Sa , Ziman Timothy , Yu Guoqiang , Wan Caihua , Hu Junfeng , Wu Hao , Wang Hanchen , Liu Mengchao , Liu Chuanpu , Guo Chenyang , Zhang Jianyu , Cabero Z. Marco A. , Zhang Youguang , Gao Peng , Liu Song , Yu Dapeng , Han Xiufeng , Hallsteinsen Ingrid , Gilbert Dustin A. , Matsuo Mamoru , Ohnuma Yuichi , Wölfle Peter , Wang Kang L. , Ansermet Jean-Philippe , Maekawa Sadamichi , Yu Haiming 
Published: April 2020

AbstractThe Seebeck effect converts thermal gradients into electricity. As an approach to power technologies in the current Internet-of-Things era, on-chip energy harvesting is highly attractive, and to be effective, demands thin film materials with large Seebeck coefficients. In spintronics, the antiferromagnetic metal IrMn has been used as the pinning layer in magnetic tunnel junctions that form building blocks for magnetic random access memories and magnetic sensors. Spin pumping experiments revealed that IrMn Néel temperature is thickness-dependent and approaches room temperature when the layer is thin. Here, we report that the Seebeck coefficient is maximum at the Néel temperature of IrMn of 0.6 to 4.0 nm in thickness in IrMn-based half magnetic tunnel junctions. We obtain a record Seebeck coefficient 390 (±10) μV K−1 at room temperature. Our results demonstrate that IrMn-based magnetic devices could harvest the heat dissipation for magnetic sensors, thus contributing to the Power-of-Things paradigm.
Mapping the spreading routes of lymphatic metastases in human colorectal cancer
Authors: Zhang Chong , Zhang Lin , Xu Tianlei , Xue Ruidong , Yu Liang , Zhu Yuelu , Wu Yunlong , Zhang Qingqing , Li Dongdong , Shen Shuohao , Tan Dongfeng , Bai Fan , Zhang Haizeng 
Published: April 2020

AbstractLymphatic metastases are closely associated with tumor relapse and reduced survival in colorectal cancer (CRC). How tumor cells disseminate within the lymphatic network remains largely unknown. Here, we analyze the subclonal structure of 94 tumor samples, covering the primary tumors, lymph node metastases (LNMs), and liver metastases from 10 CRC patients. We portray a high-resolution lymphatic metastatic map for CRC by dividing LNMs into paracolic, intermediate, and central subgroups. Among the 61 metastatic routes identified, 38 (62.3%) are initiated from the primary tumors, 22 (36.1%) from LNMs, and 1 from liver metastasis (1.6%). In 5 patients, we find 6 LNMs that reseed 2 or more LNMs. We summarize 3 diverse modes of metastasis in CRC and show that skip spreading of tumor cells within the lymphatic network is common. Our study sheds light on the complicated metastatic pattern in CRC and has great clinical implications.
Perceptual saccadic suppression starts in the retina
Authors: Idrees Saad , Baumann Matthias P. , Franke Felix , Münch Thomas A. , Hafed Ziad M. 
Published: April 2020

AbstractVisual sensitivity, probed through perceptual detectability of very brief visual stimuli, is strongly impaired around the time of rapid eye movements. This robust perceptual phenomenon, called saccadic suppression, is frequently attributed to active suppressive signals that are directly derived from eye movement commands. Here we show instead that visual-only mechanisms, activated by saccade-induced image shifts, can account for all perceptual properties of saccadic suppression that we have investigated. Such mechanisms start at, but are not necessarily exclusive to, the very first stage of visual processing in the brain, the retina. Critically, neural suppression originating in the retina outlasts perceptual suppression around the time of saccades, suggesting that extra-retinal movement-related signals, rather than causing suppression, may instead act to shorten it. Our results demonstrate a far-reaching contribution of visual processing mechanisms to perceptual saccadic suppression, starting in the retina, without the need to invoke explicit motor-based suppression commands.
Chemical modifications of adenine base editor mRNA and guide RNA expand its application scope
Authors: Jiang Tingting , Henderson Jordana M. , Coote Kevin , Cheng Yi , Valley Hillary C. , Zhang Xiao-Ou , Wang Qin , Rhym Luke H. , Cao Yueying , Newby Gregory A. , Bihler Hermann , Mense Martin , Weng Zhiping , Anderson Daniel G. , McCaffrey Anton P. , Liu David R. , Xue Wen 
Published: April 2020

AbstractCRISPR-Cas9-associated base editing is a promising tool to correct pathogenic single nucleotide mutations in research or therapeutic settings. Efficient base editing requires cellular exposure to levels of base editors that can be difficult to attain in hard-to-transfect cells or in vivo. Here we engineer a chemically modified mRNA-encoded adenine base editor that mediates robust editing at various cellular genomic sites together with moderately modified guide RNA, and show its therapeutic potential in correcting pathogenic single nucleotide mutations in cell and animal models of diseases. The optimized chemical modifications of adenine base editor mRNA and guide RNA expand the applicability of CRISPR-associated gene editing tools in vitro and in vivo.
A mycorrhizae-like gene regulates stem cell and gametophore development in mosses
Authors: Wang Shuanghua , Guan Yanlong , Wang Qia , Zhao Jinjie , Sun Guiling , Hu Xiangyang , Running Mark P. , Sun Hang , Huang Jinling 
Published: April 2020

AbstractPlant colonization of land has been intimately associated with mycorrhizae or mycorrhizae-like fungi. Despite the pivotal role of fungi in plant adaptation, it remains unclear whether and how gene acquisition following fungal interaction might have affected the development of land plants. Here we report a macro2 domain gene in bryophytes that is likely derived from Mucoromycota, a group that includes some mycorrhizae-like fungi found in the earliest land plants. Experimental and transcriptomic evidence suggests that this macro2 domain gene in the moss Physcomitrella patens, PpMACRO2, is important in epigenetic modification, stem cell function, cell reprogramming and other processes. Gene knockout and over-expression of PpMACRO2 significantly change the number and size of gametophores. These findings provide insights into the role of fungal association and the ancestral gene repertoire in the early evolution of land plants.
The Difficulty of Effectively Using Allocentric Prior Information in a Spatial Recall Task
Authors: Negen James , Bird Laura-Ashleigh , King Eleanor , Nardini Marko 
Published: April 2020

AbstractPrior information represents the long-term statistical structure of an environment. For example, colds develop more often than throat cancer, making the former a more likely diagnosis for a sore throat. There is ample evidence for effective use of prior information during a variety of perceptual tasks, including the ability to recall locations using an egocentric (self-based) frame. However, it is not yet known if people can use prior information effectively when using an allocentric (world-based) frame. Forty-eight adults were shown sixty sets of three target locations in a sparse virtual environment with three beacons. The targets were drawn from one of four prior distributions. They were then asked to point to the targets after a delay and a change in perspective. While searches were biased towards the beacons, we did not find any evidence that participants successfully exploited the prior distributions of targets. These results suggest that allocentric reasoning does not conform to normative Bayesian models: we saw no evidence for use of priors in our cognitively-complex (allocentric) task, unlike in previous, simpler (egocentric) recall tasks. It is possible that this reflects the high biological cost of processing precise allocentric information.
Study on the relationship between hyperthyroidism and vascular endothelial cell damage
Authors: Yu Tianlong , Jing Miao , Gao Yunyan , Liu Chang , Liu Lanchun , Jia Haihan , Liu Peng , Chang Manli 
Published: April 2020

AbstractThe aim of the research is to explore the relationship between hyperthyroidism, iodine, antithyroid drugs (propylthiouracil) and vascular endothelial injury. In total, 136 SD rats were randomly allocated into the control group, the hyperthyroidism group, the hyperthyroidism propylthiouracil group, the hyperthyroidism low iodine group, the high iodine group, and the endothelial injury group. Rats were raised for 60 days. Afterward, indicators concerning endothelial damage were determined, including the von Willebrand Factor (vWF), thrombomodulin (TM), nitric oxide (NO), endothelin 1 (ET-1), and P-selectin, as well as the plant hemagglutinin sample type oxidized low-density lipoprotein receptor 1 (LOX-1) from the aorta and the number of endothelial progenitor cells (EPCs) in whole blood. The hyperthyroidism group had significantly higher values for vWF, TM, NO, ET-1, and P-selectin in serum and a higher number of EPCs in whole blood compared with the control group, similar to the LOX-1 expression in abdominal aorta. The hyperthyroidism low iodine group had significantly higher values for vWF, ET-1, and P-selectin in serum and a higher number of EPCs in whole blood compared with those of the control group, as was the case for LOX-1 expression in the abdominal aorta. The hyperthyroidism propylthiouracil group had significantly higher values for FT4 in the serum compared with those in the control group. The electron microscope showed that hyperthyroidism caused a certain degree of endothelial injury to the abdominal aorta in rats. Hyperthyroidism can damage the vascular endothelium and is a high-risk factor for cardio-cerebrovascular disease. Propylthiouracil could be used in the treatment of hyperthyroidism, thus protecting endothelial cells from damage.
PIBS: Proton and ion beam spectroscopy for in vivo measurements of oxygen, carbon, and calcium concentrations in the human body
Authors: Magalhaes Martins Paulo , Dal Bello Riccardo , Ackermann Benjamin , Brons Stephan , Hermann German , Kihm Thomas , Seco Joao 
Published: April 2020

AbstractProton and ion beam therapy has proven to benefit tumour control with lower side-effects, mostly in paediatrics. Here we demonstrate a feasible technique for proton and ion beam spectroscopy (PIBS) capable of determining the elemental compositions of the irradiated tissues during particle therapy. This follows the developments in prompt gamma imaging for online range verification and the inheritance from prompt gamma neutron activation analysis. Samples of water solutions were prepared to emulate varying oxygen and carbon concentrations. The irradiation of those samples and other tissue surrogate inserts by protons and ion beams under clinical conditions clearly showed a logarithmic relationship between the target elemental composition and the prompt gamma production. This finding is in line with the known logarithmic dependence of the pH with the proton molar concentration. Elemental concentration changes of 1% for calcium and 2% for oxygen in adipose, brain, breast, liver, muscle and bone-related tissue surrogates were clearly identified. Real-time in vivo measurements of oxygen, carbon and calcium concentrations will be evaluated in a pre-clinical and clinical environment. This technique should have an important impact in the assessment of tumour hypoxia over the course of several treatment fractions and the tracking of calcifications in brain metastases.
Critical behavior and magnetocaloric effect across the magnetic transition in Mn1+xFe4−xSi3
Authors: Singh Vikram , Bag Pallab , Rawat R. , Nath R. 
Published: April 2020

AbstractThe nature of the magnetic transition, critical scaling of magnetization, and magnetocaloric effect in Mn1+xFe4−xSi3 (x = 0 to 1) are studied in detail. Our measurements show no thermal hysteresis across the magnetic transition for the parent compound which is in contrast with the previous report and corroborate the second order nature of the transition. The magnetic transition could be tuned continuously from 328 K to 212 K with Mn substitution at the Fe site. The Mn substitution leads to a linear increase in the unit cell volume and a slight reduction in the effective moment. A detailed critical analysis of the magnetization data for x = 0.0 and 0.2 is performed in the critical regime using the modified Arrott plots, Kouvel-Fisher plot, universal curve scaling, and scaling analysis of magnetocaloric effect. The magnetization isotherms follow modified Arrott plots with critical exponent (β$$\simeq $$≃ 0.308, γ$$\simeq $$≃ 1.448, and δ$$\simeq $$≃ 5.64) for the parent compound (x = 0.0) and (β$$\simeq $$≃ 0.304, γ$$\simeq $$≃ 1.445, and δ$$\simeq $$≃ 5.64) for x = 0.2. The Kouvel-Fisher and universal scaling plots of the magnetization isotherms further confirm the reliability of our critical analysis and values of the exponents. These values of the critical exponents are found to be same for both the parent and doped samples which do not fall under any of the standard universality classes. The exchange interaction decays as J(r) ~ r−3.41 following the renormalization group theory and the observed critical exponents correspond to lattice dimensionality d = 2, spin dimensionality n = 1, and the range of interaction σ = 1.41. This value of σ(<2) indicates long-range interaction between magnetic spins. A reasonable magnetocaloric effect ΔSm$$\simeq $$≃ −6.67 J/Kg-K and −5.84 J/Kg-K for x = 0.0 and 0.2 compounds, respectively, with a huge relative cooling power (RCP ~ 700 J/Kg) for 9 T magnetic field change is observed. The universal scaling of magnetocaloric effect further mimics the second order character of the magnetic transition. The obtained critical exponents from the critical analysis of magnetocaloric effect agree with the values deduced from the magnetic isotherm analysis.
Neuroligin-1 is altered in the hippocampus of Alzheimer’s disease patients and mouse models, and modulates the toxicity of amyloid-beta oligomers
Authors: Dufort-Gervais Julien , Provost Chloé , Charbonneau Laurence , Norris Christopher M. , Calon Frédéric , Mongrain Valérie , Brouillette Jonathan 
Published: April 2020

AbstractSynapse loss occurs early and correlates with cognitive decline in Alzheimer’s disease (AD). Synaptotoxicity is driven, at least in part, by amyloid-beta oligomers (Aβo), but the exact synaptic components targeted by Aβo remain to be identified. We here tested the hypotheses that the post-synaptic protein Neuroligin-1 (NLGN1) is affected early in the process of neurodegeneration in the hippocampus, and specifically by Aβo, and that it can modulate Aβo toxicity. We found that hippocampal NLGN1 was decreased in patients with AD in comparison to patients with mild cognitive impairment and control subjects. Female 3xTg-AD mice also showed a decreased NLGN1 level in the hippocampus at an early age (i.e., 4 months). We observed that chronic hippocampal Aβo injections initially increased the expression of one specific Nlgn1 transcript, which was followed by a clear decrease. Lastly, the absence of NLGN1 decreased neuronal counts in the dentate gyrus, which was not the case in wild-type animals, and worsens impairment in spatial learning following chronic hippocampal Aβo injections. Our findings support that NLGN1 is impacted early during neurodegenerative processes, and that Aβo contributes to this effect. Moreover, our results suggest that the presence of NLGN1 favors the cognitive prognosis during Aβo-driven neurodegeneration.