bluuebunny/crossref_metadata_2025_split huggingface dataset:
Global MHD simulations of the Response of Jupiter's Magnetosphere and Ionosphere to Changes in the Solar Wind and IMF
Authors: Sarkango Yash , Jia Xianzhe , Toth Gabor 
Published: July 2019

AbstractWe have developed a new global magnetohydrodynamic (MHD) model for Jupiter's magnetosphere based on the BATSRUS code and an ionospheric electrodynamics solver. Our model includes the Io plasma torus at its appropriate location and couples the global magnetosphere with the planetary ionosphere through field‐aligned currents. Through comparisons with available particle and field observations as well as empirical models, we show that the model captures the overall configuration of the magnetosphere reasonably well. In order to understand how the magnetosphere responds to different solar wind drivers, we have carried out time‐dependent simulations using various kinds of upstream conditions, such as a forward shock and a rotation in the interplanetary magnetic field (IMF). Our model predicts that compression of the magnetosphere by a forward shock of typical strength generally weakens the corotation enforcement currents on the dayside and produces an enhancement on the nightside. However, the global response varies depending on the IMF orientation. A forward shock with a typical Parker‐spiral IMF configuration has a larger impact on the magnetospheric configuration and large‐scale current systems than with a parallel IMF configuration. Plasmoids are found to form in the simulation due to tail reconnection and have complex magnetic topology, as they evolve and propagate down tail. For a fixed mass input rate in the Io plasma torus, the frequency of plasmoid occurrence in our simulation is found to vary depending on the upstream solar wind driving.
C-type natriuretic peptide attenuates renal osteodystrophy through inhibition of FGF-23/MAPK signaling
Authors: Zhang Dong Dong , Wu Yang Fang , Chen Wei Xia , Xu Yao , Liu Si Yan , Luo Huang Huang , Jiang Guang Mei , Wu Yue , Hu Peng 
Published: July 2019

AbstractRenal osteodystrophy (ROD) occurs as early as chronic kidney disease (CKD) stage 2 and seems ubiquitous in almost all pediatric patients with CKD stage 5. Fibroblast growth factor (FGF)-23, a bone-derived endocrine regulator of phosphate homeostasis, is overexpressed in CKD and disturbs osteoblast differentiation and matrix mineralization. In contrast, C-type natriuretic peptide (CNP) acts as a potent positive regulator of bone growth. In the present study, we infused CNP into uremic rats and observed whether CNP could attenuate ROD through the inhibition of FGF-23 cascades. In uremic rats, CNP administration significantly alleviated renal dysfunction, calcium phosphate metabolic disorders, hypovitaminosis D, secondary hyperparathyroidism, the decrease in bone turnover markers and retarded bone pathological progression. More importantly, within FGF-23/mitogen-activated protein kinase (MAPK) signaling, the fibroblast growth factor receptor-1, Klotho and alternative (STAT-1/phospho-STAT-1) elements were upregulated by CNP, whereas FGF-23, RAF-1/phospho-RAF-1, and downstream (ERK/phospho-ERK and P38/phospho-P38) elements were paradoxically underexpressed in bone tissue. Therefore, CNP exerts a therapeutic effect on ROD through inhibition of FGF-23/MAPK signaling at the RAF-1 level.
Activating an anterior nucleus gigantocellularis subpopulation triggers emergence from pharmacologically-induced coma in rodents
Authors: Gao S. , Proekt A. , Renier N. , Calderon D. P. , Pfaff D. W. 
Published: July 2019

AbstractMultiple areas within the reticular activating system (RAS) can hasten awakening from sleep or light planes of anesthesia. However, stimulation in individual sites has shown limited recovery from deep global suppression of brain activity, such as coma. Here we identify a subset of RAS neurons within the anterior portion of nucleus gigantocellularis (aNGC) capable of producing a high degree of awakening represented by a broad high frequency cortical reactivation associated with organized movements and behavioral reactivity to the environment from two different models of deep pharmacologically-induced coma (PIC): isoflurane (1.25%–1.5%) and induced hypoglycemic coma. Activating aNGC neurons triggered awakening by recruiting cholinergic, noradrenergic, and glutamatergic arousal pathways. In summary, we identify an evolutionarily conserved population of RAS neurons, which broadly restore cerebral cortical activation and motor behavior in rodents through the coordinated activation of multiple arousal-promoting circuits.
Dietary fatty acids promote lipid droplet diversity through seipin enrichment in an ER subdomain
Authors: Cao Zhe , Hao Yan , Fung Chun Wing , Lee Yiu Yiu , Wang Pengfei , Li Xuesong , Xie Kang , Lam Wen Jiun , Qiu Yifei , Tang Ben Zhong , Shui Guanghou , Liu Pingsheng , Qu Jianan , Kang Byung-Ho , Mak Ho Yi 
Published: July 2019

AbstractExogenous metabolites from microbial and dietary origins have profound effects on host metabolism. Here, we report that a sub-population of lipid droplets (LDs), which are conserved organelles for fat storage, is defined by metabolite-modulated targeting of the C. elegans seipin ortholog, SEIP-1. Loss of SEIP-1 function reduces the size of a subset of LDs while over-expression of SEIP-1 has the opposite effect. Ultrastructural analysis reveals SEIP-1 enrichment in an endoplasmic reticulum (ER) subdomain, which co-purifies with LDs. Analyses of C. elegans and bacterial genetic mutants indicate a requirement of polyunsaturated fatty acids (PUFAs) and microbial cyclopropane fatty acids (CFAs) for SEIP-1 enrichment, as confirmed by dietary supplementation experiments. In mammalian cells, heterologously expressed SEIP-1 engages nascent lipid droplets and promotes their subsequent expansion in a conserved manner. Our results suggest that microbial and polyunsaturated fatty acids serve unexpected roles in regulating cellular fat storage by promoting LD diversity.
Electroencephalography reflects the activity of sub-cortical brain regions during approach-withdrawal behaviour while listening to music
Authors: Daly Ian , Williams Duncan , Hwang Faustina , Kirke Alexis , Miranda Eduardo R. , Nasuto Slawomir J. 
Published: July 2019

AbstractThe ability of music to evoke activity changes in the core brain structures that underlie the experience of emotion suggests that it has the potential to be used in therapies for emotion disorders. A large volume of research has identified a network of sub-cortical brain regions underlying music-induced emotions. Additionally, separate evidence from electroencephalography (EEG) studies suggests that prefrontal asymmetry in the EEG reflects the approach-withdrawal response to music-induced emotion. However, fMRI and EEG measure quite different brain processes and we do not have a detailed understanding of the functional relationships between them in relation to music-induced emotion. We employ a joint EEG – fMRI paradigm to explore how EEG-based neural correlates of the approach-withdrawal response to music reflect activity changes in the sub-cortical emotional response network. The neural correlates examined are asymmetry in the prefrontal EEG, and the degree of disorder in that asymmetry over time, as measured by entropy. Participants’ EEG and fMRI were recorded simultaneously while the participants listened to music that had been specifically generated to target the elicitation of a wide range of affective states. While listening to this music, participants also continuously reported their felt affective states. Here we report on co-variations in the dynamics of these self-reports, the EEG, and the sub-cortical brain activity. We find that a set of sub-cortical brain regions in the emotional response network exhibits activity that significantly relates to prefrontal EEG asymmetry. Specifically, EEG in the pre-frontal cortex reflects not only cortical activity, but also changes in activity in the amygdala, posterior temporal cortex, and cerebellum. We also find that, while the magnitude of the asymmetry reflects activity in parts of the limbic and paralimbic systems, the entropy of that asymmetry reflects activity in parts of the autonomic response network such as the auditory cortex. This suggests that asymmetry magnitude reflects affective responses to music, while asymmetry entropy reflects autonomic responses to music. Thus, we demonstrate that it is possible to infer activity in the limbic and paralimbic systems from pre-frontal EEG asymmetry. These results show how EEG can be used to measure and monitor changes in the limbic and paralimbic systems. Specifically, they suggest that EEG asymmetry acts as an indicator of sub-cortical changes in activity induced by music. This shows that EEG may be used as a measure of the effectiveness of music therapy to evoke changes in activity in the sub-cortical emotion response network. This is also the first time that the activity of sub-cortical regions, normally considered “invisible” to EEG, has been shown to be characterisable directly from EEG dynamics measured during music listening.
Boundary effects of expectation in human pain perception
Authors: Hird E. J. , Charalambous C. , El-Deredy W. , Jones A. K. P. , Talmi D. 
Published: July 2019

AbstractPerception of sensory stimulation is influenced by numerous psychological variables. One example is placebo analgesia, where expecting low pain causes a painful stimulus to feel less painful. Yet, because pain evolved to signal threats to survival, it should be maladaptive for highly-erroneous expectations to yield unrealistic pain experiences. Therefore, we hypothesised that a cue followed by a highly discrepant stimulus intensity, which generates a large prediction error, will have a weaker influence on the perception of that stimulus. To test this hypothesis we collected two independent pain-cueing datasets. The second dataset and the analysis plan were preregistered (https://osf.io/5r6z7/). Regression modelling revealed that reported pain intensities were best explained by a quartic polynomial model of the prediction error. The results indicated that the influence of cues on perceived pain decreased when stimulus intensity was very different from expectations, suggesting that prediction error size has an immediate functional role in pain perception.
Genome-wide Association Study of Change in Fasting Glucose over time in 13,807 non-diabetic European Ancestry Individuals
Authors: Liu Ching-Ti , Merino Jordi , Rybin Denis , DiCorpo Daniel , Benke Kelly S. , Bragg-Gresham Jennifer L. , Canouil Mickaël , Corre Tanguy , Grallert Harald , Isaacs Aaron , Kutalik Zoltan , Lahti Jari , Marullo Letizia , Marzi Carola , Rasmussen-Torvik Laura J. , Rocheleau Ghislain , Rueedi Rico , Scapoli Chiara , Verweij Niek , Vogelzangs Nicole , Willems Sara M. , Yengo Loïc , Bakker Stephan J. L. , Beilby John , Hui Jennie , Kajantie Eero , Müller-Nurasyid Martina , Rathmann Wolfgang , Balkau Beverley , Bergmann Sven , Eriksson Johan G. , Florez Jose C. , Froguel Philippe , Harris Tamara , Hung Joseph , James Alan L. , Kavousi Maryam , Miljkovic Iva , Musk Arthur W. , Palmer Lyle J. , Peters Annette , Roussel Ronan , van der harst Pim , van Duijn Cornelia M. , Vollenweider Peter , Barroso Inês , Prokopenko Inga , Dupuis Josée , Meigs James B. , Bouatia-Naji Nabila 
Published: July 2019

AbstractType 2 diabetes (T2D) affects the health of millions of people worldwide. The identification of genetic determinants associated with changes in glycemia over time might illuminate biological features that precede the development of T2D. Here we conducted a genome-wide association study of longitudinal fasting glucose changes in up to 13,807 non-diabetic individuals of European descent from nine cohorts. Fasting glucose change over time was defined as the slope of the line defined by multiple fasting glucose measurements obtained over up to 14 years of observation. We tested for associations of genetic variants with inverse-normal transformed fasting glucose change over time adjusting for age at baseline, sex, and principal components of genetic variation. We found no genome-wide significant association (P < 5 × 10−8) with fasting glucose change over time. Seven loci previously associated with T2D, fasting glucose or HbA1c were nominally (P < 0.05) associated with fasting glucose change over time. Limited power influences unambiguous interpretation, but these data suggest that genetic effects on fasting glucose change over time are likely to be small. A public version of the data provides a genomic resource to combine with future studies to evaluate shared genetic links with T2D and other metabolic risk traits.
Pharmacologic treatment with CPI-613 and PS48 decreases mitochondrial membrane potential and increases quantity of autolysosomes in porcine fibroblasts
Authors: Mordhorst Bethany R. , Kerns Karl C. , Schauflinger Martin , Zigo Michal , Murphy Stephanie L. , Ross Renee M. , Wells Kevin D. , Green Jonathan A. , Sutovsky Peter , Prather Randall S. 
Published: July 2019

AbstractA metabolic phenomenon known as the Warburg effect has been characterized in certain cancerous cells, embryonic stem cells, and other rapidly proliferative cell types. Previously, our attempts to induce a Warburg-like state pharmaceutically via CPI-613 and PS48 treatment did augment metabolite production and gene expression; however, this treatment demonstrated a Reverse Warburg effect phenotype observed in cancer-associated stroma. In the current study, we inquired whether the mitochondria were affected by the aforementioned pharmaceutical treatment as observed in cancerous stromal fibroblasts. While the pharmaceutical agents decreased mitochondrial membrane potential in porcine fetal fibroblasts, the number and size of mitochondria were similar, as was the overall cell size. Moreover, the fibroblasts that were treated with CPI-613 and PS48 for a week had increased numbers of large autolysosome vesicles. This coincided with increased intensity of LysoTracker staining in treated cells as observed by flow cytometry. Treated fibroblasts thus may utilize changes in metabolism and autophagy to mitigate the damage of treatment with pharmaceutical agents. These findings shed light on how these pharmaceutical agents interact and how treated cells augment metabolism to sustain viability.
Oviductal extracellular vesicles interact with the spermatozoon’s head and mid-piece and improves its motility and fertilizing ability in the domestic cat
Authors: Ferraz M. de A. M. M. , Carothers A. , Dahal R. , Noonan M. J. , Songsasen N. 
Published: July 2019

AbstractFertilization and early embryo development are regulated by a unique maternal-gamete/embryo cross-talk within the oviduct. Recent studies have shown that extracellular vesicles (EVs) within the oviduct play important roles in mediating this developmental process. Here, we examined the influence of oviductal EVs on sperm function in the domestic cat. We demonstrated that (1) EVs are enriched in proteins related to energy metabolism, membrane modification, and reproductive function; (2) EVs bound and fused with the membranes of the acrosome and mid piece; and (3) incubating sperm with EVs improved motility, fertilizing capacity of cat spermatozoa and prevented acrosomal exocytosisin vitro. These findings indicated that oviductal EVs mediate sperm function and fertilization in the cat and provides new insights to improve sperm cryopreservation andin vitrofertilization in the domestic and wild felids and human.
Automated high-throughput high-content autophagy and mitophagy analysis platform
Authors: Arias-Fuenzalida Jonathan , Jarazo Javier , Walter Jonas , Gomez-Giro Gemma , Forster Julia I. , Krueger Rejko , Antony Paul M. A. , Schwamborn Jens C. 
Published: July 2019

AbstractAutophagic processes play a central role in cellular homeostasis. In pathological conditions, the flow of autophagy can be affected at multiple and distinct steps of the pathway. Current analyses tools do not deliver the required detail for dissecting pathway intermediates. The development of new tools to analyze autophagic processes qualitatively and quantitatively in a more straightforward manner is required. Defining all autophagy pathway intermediates in a high-throughput manner is technologically challenging and has not been addressed yet. Here, we overcome those requirements and limitations by the developed of stable autophagy and mitophagy reporter-iPSC and the establishment of a novel high-throughput phenotyping platform utilizing automated high-content image analysis to assess autophagy and mitophagy pathway intermediates.
The Interplay between Incipient Species and Social Polymorphism in the Desert Ant Cataglyphis
Authors: Reiner Brodetzki Tali , Inbar Shani , Cohen Pnina , Aron Serge , Privman Eyal , Hefetz Abraham 
Published: July 2019

AbstractIn social insects, due to considerable polyphenism as well as high level of hybridization, the delimitation of species can be challenging. The genus Cataglyphis presents a high level of diversification, making it an excellent model with which to study evolutionary paths. Israel appears to be a “hot spot” for recent speciation in this genus. Although previous studies have described multiple species of Cataglyphis in Israel, a recent genetic study has questioned the existence of some of these historically described species. The present study focuses on an apparent species complex, the C. niger species complex which includes C. niger, C. savigyi, and C. drusus that are distinguishable by their mitochondrial DNA (and therefore named mitotypes) but not by their nuclear DNA. Using a multi-method approach (genetics, chemistry and behavior), we show that these mitotypes also differ in their social structures and are readily distinguishable by their cuticular hydrocarbons profiles. While most populations of the different mitotypes are allopatric, at our study site they are sympatric, but nonetheless maintain the observed differences between them. This raises the evolutionary question: Are these incipient species that have diverged with gene flow, or is this a case of social and chemical polymorphism that is maintained within a single species? Unveiling the interplay between social polyphenism and species segregation is at the core of evolutionary biology.
PSD-95 deficiency disrupts PFC-associated function and behavior during neurodevelopment
Authors: Coley Austin A. , Gao Wen-Jun 
Published: July 2019

AbstractPostsynaptic density protein-95 (PSD-95) is a major regulator in the maturation of excitatory synapses by interacting and trafficking N-methyl-D-aspartic acid receptors (NMDAR) and α-amino-3-hydroxy-5-methyl-4-isox-azoleproprionic acid receptors (AMPAR) to the postsynaptic membrane. PSD-95 disruption has recently been associated with neuropsychiatric disorders such as schizophrenia and autism. However, the effects of PSD-95 deficiency on the prefrontal cortex (PFC)-associated functions, including cognition, working memory, and sociability, has yet to be investigated. Using a PSD-95 knockout mouse model (PSD-95−/−), we examined how PSD-95 deficiency affects NMDAR and AMPAR expression and function in the medial prefrontal cortex (mPFC) during juvenile and adolescent periods of development. We found significant increases in total protein levels of NMDAR subunits GluN1, and GluN2B, accompanied by decreases in AMPAR subunit GluA1 during adolescence. Correspondingly, there is a significant increase in NMDAR/AMPAR-mediated current amplitude ratio that progresses from juvenile-to-adolescence. Behaviorally, PSD-95−/− mice exhibit a lack of sociability, as well as learning and working memory deficits. Together, our data indicate that PSD-95 deficiency disrupts mPFC synaptic function and related behavior at a critical age of development. This study highlights the importance of PSD-95 during neurodevelopment in the mPFC and its potential link in the pathogenesis associated with schizophrenia and/or autism.
Uridine as a protector against hypoxia-induced lung injury
Authors: Rozova Ekaterina V. , Mankovskaya Irina N. , Belosludtseva Natalia V. , Khmil Natalya V. , Mironova Galina D. 
Published: July 2019

AbstractThe effect of the activation of the mitochondrial ATP-dependent potassium channel (mitoKATP) on the ultrastructure of rat lung in acute hypoxic hypoxia (7% of oxygen in nitrogen, exposure 30 min) was studied. It was shown that uridine, a precursor of the mitoKATP activator UDP, exerted a protective effect against hypoxic damage to the lung. The administration of uridine to animals prior to hypoxia decreased the number of mitochondria with altered ultrastructure and prevented the hypoxia-induced mitochondrial swelling. Uridine also protected the epithelial, interstitial and endothelial layers of the air–blood barrier from the hypoxia-induced hyperhydration. The protective action of uridine against hypoxia-induced lung injury was eliminated by the selective blocker of mitoKATP 5-hydroxydecanoate. These data suggest that one of the mechanisms of the positive effect of uridine is related to the activation of the mitoKATP channel, which, according to the literature and our data, is involved in the protection of tissues from hypoxia and leads to adaptation to it. A possible role of uridine in the maintenance of the mitochondrial structure upon hypoxia-induced lung injury and the optimization of oxygen supply of the organism is discussed.
Sulfuric acid decomposition chemistry above Junge layer in Earth's atmosphere concerning ozone depletion and healing
Authors: Hazra Montu K. , Ghoshal Sourav , Mahata Prabhash , Maiti Biswajit 
Published: July 2019

AbstractSulfuric acid (H2SO4) is the seed molecule for formation of stratospheric sulfate aerosol layer that assists ozone depletion by activation of halogen species. The impact of increased stratospheric sulfate aerosols due to large volcanic eruptions and possible side effect claimed in the geoengineering scheme of global climate using man-made injected stratospheric sulfate aerosols is ozone depletion. Given that both volcanic eruptions and geoengineering scheme are ultimately connected with increased upper stratospheric concentrations of H2SO4, here we show by theoretical approach that the pressure-independent H2SO4 + O(1D) insertion/addition reactions via barrierless formation of peroxysulfuric acid (H2SO5) or HSO4 + OH radicals or sulfur trioxide (SO3) + hydrogen peroxide (H2O2) molecules are the potential routes towards H2SO4 loss above the stratospheric sulfate aerosol layer, and for the regeneration or transportation of consumed lower-middle stratospheric OH radical in the upper stratosphere at the cost of O(1D)/ozone.