bluuebunny/crossref_metadata_2025_split huggingface dataset:
Contrasting Upper and Deep Ocean Oxygen Response to Protracted Global Warming
Authors: Frölicher T. L. , Aschwanden M. T. , Gruber N. , Jaccard S. L. , Dunne J. P. , Paynter D. 
Published: August 2020

AbstractIt is well established that the ocean is currently losing dissolved oxygen (O2) in response to ocean warming, but the long‐term, equilibrium response of O2 to a warmer climate is neither well quantified nor understood. Here we use idealized multimillennial global warming simulations with a comprehensive Earth system model to show that the equilibrium response in ocean O2 differs fundamentally from the ongoing transient response. After physical equilibration of the model (>4,000 years) under a two times preindustrial CO2 scenario, the deep ocean is better ventilated and oxygenated compared to preindustrial conditions, even though the deep ocean is substantially warmer. The recovery and overshoot of deep convection in the Weddell Sea and especially the Ross Sea after ~720 years causes a strong increase in deep ocean O2 that overcompensates the solubility‐driven decrease in O2. In contrast, O2 in most of the upper tropical ocean is substantially depleted owing to the warming‐induced O2 decrease dominating over changes in ventilation and biology. Our results emphasize the millennial‐scale impact of global warming on marine life, with some impacts emerging many centuries or even millennia after atmospheric CO2 has stabilized.
Wave‐Particle Interactions Associated With Io's Auroral Footprint: Evidence of Alfvén, Ion Cyclotron, and Whistler Modes
Authors: Sulaiman A. H. , Hospodarsky G. B. , Elliott S. S. , Kurth W. S. , Gurnett D. A. , Imai M. , Allegrini F. , Bonfond B. , Clark G. , Connerney J. E. P. , Ebert R. W. , Gershman D. J. , Hue V. , Janser S. , Kotsiaros S. , Paranicas C. , Santolík O. , Saur J. , Szalay J. R. , Bolton S. J. 
Published: August 2020

AbstractThe electrodynamic coupling between Io and Jupiter gives rise to wave‐particle interactions across multiple spatial scales. Here we report observations during Juno's 12th perijove (PJ) high‐latitude northern crossing of the flux tube connected to Io's auroral footprint. We focus on plasma wave measurements, clearly differentiating between magnetohydrodynamic (MHD), ion, and electron scales. We find (i) evidence of Alfvén waves undergoing a turbulent cascade, suggesting Alfvénic acceleration processes together with observations of bi‐directional, broadband electrons; (ii) intense ion cyclotron waves with an estimated heating rate that is consistent with the generation of ion conics reported by Clark et al. (2020, https://doi.org/10.1029/2020GL090839); and (iii) whistler‐mode auroral hiss radiation excited by field‐aligned electrons. Such high‐resolution wave and particle measurements provide an insight into satellite interactions in unprecedented detail. We further anticipate that these spatially well‐constrained results can be more broadly applied to better understand processes of Jupiter's main auroral oval.
Marine Heatwaves in the Arctic Region: Variation in Different Ice Covers
Authors: Hu Siyu , Zhang Lujun , Qian Shimeng 
Published: August 2020

AbstractThis study analyzes marine heatwaves (MHWs) in the Arctic for its variation in multiyear ice (MYI), first‐year ice (FYI), and open‐water areas. Results show that there is a significant annual growth in MHW frequency, duration, and intensity in the FYI region, especially for intensity. Since 2005, MHW in FYI increases remarkably in summer and the extent of the affected area continues to grow northward. Particularly, severe MHW events mainly occur in the area where sea ice concentration ranges between 0.1 and 0.5. Stratification in the FYI area impedes the deep mixing and downward transmission of energy from solar radiation, resulting in an anomalously high sea surface temperature in the FYI area. The implication is that MHW will keep growing as the extent of FYI in the Arctic increases.
City‐Scale Dark Fiber DAS Measurements of Infrastructure Use During the COVID‐19 Pandemic
Authors: Lindsey Nathaniel J. , Yuan Siyuan , Lellouch Ariel , Gualtieri Lucia , Lecocq Thomas , Biondi Biondo 
Published: August 2020

AbstractThroughout the recent COVID‐19 pandemic, real‐time measurements about shifting use of roads, hospitals, grocery stores, and other public infrastructure became vital for government decision makers. Mobile phone locations are increasingly assimilated for this purpose, but an alternative, unexplored, natively anonymous, absolute method would be to use geophysical sensing to directly measure public infrastructure usage. In this paper, we demonstrate how fiber‐optic distributed acoustic sensing (DAS) connected to a telecommunication cable beneath Palo Alto, CA, successfully monitored traffic over a 2‐month period, including major reductions associated with COVID‐19 response. Continuous DAS recordings of over 450,000 individual vehicles were analyzed using an automatic template‐matching detection algorithm based on roadbed strain. In one commuter sector, we found a 50% decrease in vehicles immediately following the order, but near Stanford Hospital, the traffic persisted. The DAS measurements correlate with mobile phone locations and urban seismic noise levels, suggesting geophysics would complement future digital city sensing systems.
Daily and Monthly Variations of the Equatorial Ionization Anomaly (EIA) Over the Brazilian Sector During the Descending Phase of the Solar Cycle 24
Authors: Dias M. A. L. , Fagundes P. R. , Venkatesh K. , Pillat V. G. , Ribeiro B. A. G. , Seemala G. K. , Arcanjo M. O. 
Published: August 2020

AbstractIt has been noticed recently that the equatorial ionization anomaly (EIA) in the Brazilian eastern, middle, and western sectors present significant longitudinal variability within a short separation due to the presence of typical magnetic field structure over South America. Therefore, the main motivation of this study is to investigate day‐to‐day and month‐to‐month characteristics of the EIA in three closely spaced longitudinal sectors over the Brazilian region during the year 2016 in the descending phase of the solar activity. These three longitudinal sectors are perpendicular to the magnetic equator at its largest declination over the globe. The EIA showed a semiannual variation in all sectors with a major maximum during the summer, a minimum during the winter, and secondary maximum during spring. In addition, the EIA shows its classical behavior with a trough around the magnetic equator and crests at low latitudes (from ±15° to ±20°). When the EIA is not developed, the maximum ionization is located around the dip equatorial latitudes and the anomaly crest is absent. The number of days within 1 year that showed clear EIA development in the west, middle, and east sectors is 248 (78.2%), 236 (74.4%), and 265 (83.6%), respectively. The undeveloped/absence of EIA is also found often during the months of winter, and the numbers of such days during 2016 in the west, middle, and east are 69 (21.8%), 81 (25.6%), and 52 (16.4%), respectively. Also, the shape, strength, extent, and lifetimes of EIA crest have shown significant variabilities between the three sectors during different seasons. Further, a comparative analysis is carried out on the variations of EIA crest and lifetime between GPS observations and IRI‐2016 model, and the results are discussed.
Systematical Analyses of Global Ionospheric Disturbance Current Systems Caused by Multiple Processes: Penetration Electric Fields, Solar Wind Pressure Impulses, Magnetospheric Substorms, and ULF Waves
Authors: Huang Chao‐Song 
Published: August 2020

AbstractWe present the first systematic analysis of global ionospheric disturbance current systems caused by multiple processes of solar and magnetospheric origin, including reorientations of the interplanetary magnetic field (IMF), sudden changes in the solar wind dynamic pressure, magnetospheric sawtooth substorms, and ultralow frequency (ULF) waves. Measurements from global magnetometer networks are used to derive the equivalent disturbance currents from the polar cap to the equator. A surprising result is that the equivalent disturbance current systems are very similar, although the driving processes are completely different. The equivalent disturbance current system in response to IMF reorientation or substorm onset is characterized by a large vortex on the dayside and evening sector and a smaller vortex near dawn, and the polarity of the current vortices depends on the IMF direction. The equivalent disturbance current system caused by a sudden change in the solar wind pressure or by ULF waves consists of a single vortex at middle and low latitudes and a very small vortex above ~60° magnetic latitude near dawn. The similar disturbance current systems caused by different solar wind and magnetospheric processes suggest that the global distribution of the ionospheric currents is determined by the intrinsic property of the ionosphere. The global current system takes only ~1 min to completely reconstruct, indicating that the current system can reach a new steady state within 1 min. A scenario is proposed to explain the global distribution and fast reconstruction of the current systems.
NF-κB-dependent miR-31/155 biogenesis is essential for TNF-α-induced impairment of endothelial progenitor cell function
Authors: Kim Ji-Hee , Kim Ji-Yoon , Park Minsik , Kim Suji , Kim Taesam , Kim Joohwan , Choi Seunghwan , Park Wonjin , Hwang Jong Yun , Choe Jongseon , Ha Kwon-Soo , Won Moo-Ho , Ryoo Sungwoo , Kwon Young-Guen , Kim Young-Myeong 
Published: August 2020

AbstractEndothelial progenitor cell (EPC) dysfunction impairs vascular function and remodeling in inflammation-associated diseases, including preeclampsia. However, the underlying mechanism of this inflammation-induced dysfunction remains unclear. In the present study, we found increases in TNF-α and miR-31/155 levels and reduced numbers of circulating EPCs in patients with preeclampsia. Patient-derived mononuclear cells (MNCs) cultured in autologous serum had decreased endothelial nitric oxide synthase (eNOS) expression, nitric oxide production, and differentiation into EPCs with angiogenic potential, and these effects were inhibited by a TNF-α-neutralizing antibody and miR-31/155 inhibitors. Moreover, TNF-α treatment of normal MNCs increased miR-31/155 biogenesis, decreased eNOS expression, reduced EPC differentiation, and impaired angiogenic potential. The TNF-α-induced impairment of EPC differentiation and function was rescued by NF-κB p65 knockdown or miR-31/155 inhibitors. In addition, treatment of MNCs with synthetic miR-31/155 or an eNOS inhibitor mimicked the inhibitory effects of TNF-α on eNOS expression and EPC functions. Moreover, transplantation of EPCs that had been differentiated from TNF-α-treated MNCs decreased neovascularization and blood perfusion in ischemic mouse hindlimbs compared with those of normally differentiated EPCs. These findings suggest that NF-κB activation is required for TNF-α-induced impairment of EPC mobilization, differentiation, and function via miR-31/155 biogenesis and eNOS downregulation. Our data provide a new role for NF-κB-dependent miR-31/155 in EPC dysfunction under the pathogenic conditions of inflammation-associated vascular diseases, including preeclampsia.
Mutant p53 induces Golgi tubulo-vesiculation driving a prometastatic secretome
Authors: Capaci Valeria , Bascetta Lorenzo , Fantuz Marco , Beznoussenko Galina V. , Sommaggio Roberta , Cancila Valeria , Bisso Andrea , Campaner Elena , Mironov Alexander A. , Wiśniewski Jacek R. , Ulloa Severino Luisa , Scaini Denis , Bossi Fleur , Lees Jodi , Alon Noa , Brunga Ledia , Malkin David , Piazza Silvano , Collavin Licio , Rosato Antonio , Bicciato Silvio , Tripodo Claudio , Mantovani Fiamma , Del Sal Giannino 
Published: August 2020

AbstractTP53 missense mutations leading to the expression of mutant p53 oncoproteins are frequent driver events during tumorigenesis. p53 mutants promote tumor growth, metastasis and chemoresistance by affecting fundamental cellular pathways and functions. Here, we demonstrate that p53 mutants modify structure and function of the Golgi apparatus, culminating in the increased release of a pro-malignant secretome by tumor cells and primary fibroblasts from patients with Li-Fraumeni cancer predisposition syndrome. Mechanistically, interacting with the hypoxia responsive factor HIF1α, mutant p53 induces the expression of miR-30d, which in turn causes tubulo-vesiculation of the Golgi apparatus, leading to enhanced vesicular trafficking and secretion. The mut-p53/HIF1α/miR-30d axis potentiates the release of soluble factors and the deposition and remodeling of the ECM, affecting mechano-signaling and stromal cells activation within the tumor microenvironment, thereby enhancing tumor growth and metastatic colonization.
A blood miRNA signature associates with sporadic Creutzfeldt-Jakob disease diagnosis
Authors: Norsworthy Penny J. , Thompson Andrew G. B. , Mok Tze H. , Guntoro Fernando , Dabin Luke C. , Nihat Akin , Paterson Ross W. , Schott Jonathan M. , Collinge John , Mead Simon , Viré Emmanuelle A. 
Published: August 2020

AbstractSporadic Creutzfeldt-Jakob disease (sCJD) presents as a rapidly progressive dementia which is usually fatal within six months. No clinical blood tests are available for diagnosis or disease monitoring. Here, we profile blood microRNA (miRNA) expression in sCJD. Sequencing of 57 sCJD patients, and healthy controls reveals differential expression of hsa-let-7i-5p, hsa-miR-16-5p, hsa-miR-93-5p and hsa-miR-106b-3p. Downregulation of hsa-let-7i-5p, hsa-miR-16-5p and hsa-miR-93-5p replicates in an independent cohort using quantitative PCR, with concomitant upregulation of four mRNA targets. Absence of correlation in cross-sectional analysis with clinical phenotypes parallels the lack of association between rate of decline in miRNA expression, and rate of disease progression in a longitudinal cohort of samples from 21 patients. Finally, the miRNA signature shows a high level of accuracy in discriminating sCJD from Alzheimer’s disease. These findings highlight molecular alterations in the periphery in sCJD which provide information about differential diagnosis and improve mechanistic understanding of human prion diseases.
Molecular architecture and activation of the insecticidal protein Vip3Aa from Bacillus thuringiensis
Authors: Núñez-Ramírez Rafael , Huesa Juanjo , Bel Yolanda , Ferré Juan , Casino Patricia , Arias-Palomo Ernesto 
Published: August 2020

AbstractBacillus thuringiensis Vip3 (Vegetative Insecticidal Protein 3) toxins are widely used in biotech crops to control Lepidopteran pests. These proteins are produced as inactive protoxins that need to be activated by midgut proteases to trigger cell death. However, little is known about their three-dimensional organization and activation mechanism at the molecular level. Here, we have determined the structures of the protoxin and the protease-activated state of Vip3Aa at 2.9 Å using cryo-electron microscopy. The reconstructions show that the protoxin assembles into a pyramid-shaped tetramer with the C-terminal domains exposed to the solvent and the N-terminal region folded into a spring-loaded apex that, after protease activation, drastically remodels into an extended needle by a mechanism akin to that of influenza haemagglutinin. These results provide the molecular basis for Vip3 activation and function, and serves as a strong foundation for the development of more efficient insecticidal proteins.
Likely weakening of the Florida Current during the past century revealed by sea-level observations
Authors: Piecuch Christopher G. 
Published: August 2020

AbstractThe Florida Current marks the beginning of the Gulf Stream at Florida Straits, and plays an important role in climate. Nearly continuous measurements of Florida Current transport are available at 27°N since 1982. These data are too short for assessing possible multidecadal or centennial trends. Here I reconstruct Florida Current transport during 1909–2018 using probabilistic methods and principles of ocean physics applied to the available transport data and longer coastal sea-level records. Florida Current transport likely declined steadily during the past century. Transport since 1982 has likely been weaker on average than during 1909–1981. The weakest decadal-mean transport in the last 110 y likely took place in the past two decades. Results corroborate hypotheses that the deep branch of the overturning circulation declined over the recent past, and support relationships observed in climate models between the overturning and surface western boundary current transports at multidecadal and longer timescales.
ABL1-dependent OTULIN phosphorylation promotes genotoxic Wnt/β-catenin activation to enhance drug resistance in breast cancers
Authors: Wang Wei , Li Mingqi , Ponnusamy Suriyan , Chi Yayun , Xue Jingyan , Fahmy Beshoy , Fan Meiyun , Miranda-Carboni Gustavo A. , Narayanan Ramesh , Wu Jiong , Wu Zhao-Hui 
Published: August 2020

AbstractDysregulated Wnt/β-catenin activation plays a critical role in cancer progression, metastasis, and drug resistance. Genotoxic agents such as radiation and chemotherapeutics have been shown to activate the Wnt/β-catenin signaling although the underlying mechanism remains incompletely understood. Here, we show that genotoxic agent-activated Wnt/β-catenin signaling is independent of the FZD/LRP heterodimeric receptors and Wnt ligands. OTULIN, a linear linkage-specific deubiquitinase, is essential for the DNA damage-induced β-catenin activation. OTULIN inhibits linear ubiquitination of β-catenin, which attenuates its Lys48-linked ubiquitination and proteasomal degradation upon DNA damage. The association with β-catenin is enhanced by OTULIN Tyr56 phosphorylation, which depends on genotoxic stress-activated ABL1/c-Abl. Inhibiting OTULIN or Wnt/β-catenin sensitizes triple-negative breast cancer xenograft tumors to chemotherapeutics and reduces metastasis. Increased OTULIN levels are associated with aggressive molecular subtypes and poor survival in breast cancer patients. Thus, OTULIN-mediated Wnt/β-catenin activation upon genotoxic treatments promotes drug resistance and metastasis in breast cancers.
Adolescent frontal top-down neurons receive heightened local drive to establish adult attentional behavior in mice
Authors: Nabel Elisa M. , Garkun Yury , Koike Hiroyuki , Sadahiro Masato , Liang Ana , Norman Kevin J. , Taccheri Giulia , Demars Michael P. , Im Susanna , Caro Keaven , Lopez Sarah , Bateh Julia , Hof Patrick R. , Clem Roger L. , Morishita Hirofumi 
Published: August 2020

AbstractFrontal top-down cortical neurons projecting to sensory cortical regions are well-positioned to integrate long-range inputs with local circuitry in frontal cortex to implement top-down attentional control of sensory regions. How adolescence contributes to the maturation of top-down neurons and associated local/long-range input balance, and the establishment of attentional control is poorly understood. Here we combine projection-specific electrophysiological and rabies-mediated input mapping in mice to uncover adolescence as a developmental stage when frontal top-down neurons projecting from the anterior cingulate to visual cortex are highly functionally integrated into local excitatory circuitry and have heightened activity compared to adulthood. Chemogenetic suppression of top-down neuron activity selectively during adolescence, but not later periods, produces long-lasting visual attentional behavior deficits, and results in excessive loss of local excitatory inputs in adulthood. Our study reveals an adolescent sensitive period when top-down neurons integrate local circuits with long-range connectivity to produce attentional behavior.
Elevated rates of autism, other neurodevelopmental and psychiatric diagnoses, and autistic traits in transgender and gender-diverse individuals
Authors: Warrier Varun , Greenberg David M. , Weir Elizabeth , Buckingham Clara , Smith Paula , Lai Meng-Chuan , Allison Carrie , Baron-Cohen Simon 
Published: August 2020

AbstractIt is unclear whether transgender and gender-diverse individuals have elevated rates of autism diagnosis or traits related to autism compared to cisgender individuals in large non-clinic-based cohorts. To investigate this, we use five independently recruited cross-sectional datasets consisting of 641,860 individuals who completed information on gender, neurodevelopmental and psychiatric diagnoses including autism, and measures of traits related to autism (self-report measures of autistic traits, empathy, systemizing, and sensory sensitivity). Compared to cisgender individuals, transgender and gender-diverse individuals have, on average, higher rates of autism, other neurodevelopmental and psychiatric diagnoses. For both autistic and non-autistic individuals, transgender and gender-diverse individuals score, on average, higher on self-report measures of autistic traits, systemizing, and sensory sensitivity, and, on average, lower on self-report measures of empathy. The results may have clinical implications for improving access to mental health care and tailoring adequate support for transgender and gender-diverse individuals.
Epsin-mediated degradation of IP3R1 fuels atherosclerosis
Authors: Dong Yunzhou , Lee Yang , Cui Kui , He Ming , Wang Beibei , Bhattacharjee Sudarshan , Zhu Bo , Yago Tadayuki , Zhang Kun , Deng Lin , Ouyang Kunfu , Wen Aiyun , Cowan Douglas B. , Song Kai , Yu Lili , Brophy Megan L. , Liu Xiaolei , Wylie-Sears Jill , Wu Hao , Wong Scott , Cui Guanglin , Kawashima Yusuke , Matsumoto Hiroyuki , Kodera Yoshio , Wojcikiewicz Richard J. H. , Srivastava Sanjay , Bischoff Joyce , Wang Da-Zhi , Ley Klaus , Chen Hong 
Published: August 2020

AbstractThe epsin family of endocytic adapter proteins are widely expressed, and interact with both proteins and lipids to regulate a variety of cell functions. However, the role of epsins in atherosclerosis is poorly understood. Here, we show that deletion of endothelial epsin proteins reduces inflammation and attenuates atherosclerosis using both cell culture and mouse models of this disease. In atherogenic cholesterol-treated murine aortic endothelial cells, epsins interact with the ubiquitinated endoplasmic reticulum protein inositol 1,4,5-trisphosphate receptor type 1 (IP3R1), which triggers proteasomal degradation of this calcium release channel. Epsins potentiate its degradation via this interaction. Genetic reduction of endothelial IP3R1 accelerates atherosclerosis, whereas deletion of endothelial epsins stabilizes IP3R1 and mitigates inflammation. Reduction of IP3R1 in epsin-deficient mice restores atherosclerotic progression. Taken together, epsin-mediated degradation of IP3R1 represents a previously undiscovered biological role for epsin proteins and may provide new therapeutic targets for the treatment of atherosclerosis and other diseases.