bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Impact of Ocean‐Wave Coupling on the Upper Ocean Circulation During Storm Events
Authors: Bruciaferri D. , Tonani M. , Lewis H. W. , Siddorn J. R. , Saulter A. , Castillo Sanchez J. M. , Valiente N. G. , Conley D. , Sykes P. , Ascione I. , McConnell N. 
Published: June 2021

AbstractMany human activities rely on accurate knowledge of the sea surface dynamics. This is especially true during storm events, when wave‐current interactions might represent a leading order process of the upper ocean. In this study, we assess and analyze the impact of including three wave‐dependent processes in the ocean momentum equation of the Met Office North West European Shelf ocean‐wave forecasting system on the accuracy of the simulated surface circulation. The analysis is conducted using ocean currents and Stokes drift data produced by different implementations of the coupled forecasting systems to simulate the trajectories of surface (iSphere) and 15 m drogued (SVP) drifters affected by four storms selected from winter 2016. Ocean and wave simulations differ only in the degree of coupling and the skills of the Lagrangian simulations are evaluated by comparing model results against the observed drifter tracks. Results show that, during extreme events, ocean‐wave coupling improves the accuracy of the surface dynamics by 4%. Improvements are larger for ocean currents on the shelf (8%) than in the open ocean (4%): this is thought to be due to the synergy between strong tidal currents and more mature decaying waves. We found that the Coriolis‐Stokes forcing is the dominant wave‐current interaction for both type of drifters; for iSpheres the secondary wave effect is the wave‐dependent sea surface roughness while for SVPs the wave‐modulated water‐side stress is more important. Our results indicate that coupled ocean‐wave systems may play a key role for improving the accuracy of particle transport simulations.
Factors Governing Cloud Growth and Entrainment Rates in Shallow Cumulus and Cumulus Congestus During GoAmazon2014/5
Authors: Eissner J. M. , Mechem D. B. , Jensen M. P. , Giangrande S. E. 
Published: June 2021

AbstractShallow cumulus and cumulus congestus clouds play an important role in the large‐scale tropical circulation by mixing heat and moisture vertically and preconditioning the environment for deeper convection. Different representations of these shallow clouds account for much of the spread in General Circulation Model (GCMs) climate sensitivity, potentially because of how entrainment is represented in GCM parameterizations. This study uses observations from the Department of Energy's Atmospheric Radiation Measurement (ARM) mobile facility deployed at Manacapuru, Brazil, during the Green Ocean Amazon (GoAmazon2014/5) Campaign. Environmental thermodynamic profiles and observations of cloud top height (CTH) are used to constrain an entraining plume model to estimate bulk entrainment rates (ERs). Estimates of CTH are obtained from a combination of vertically pointing W‐band ARM cloud radar and 1,290 MHz Radar Wind Profiler observations. A combination of radiosonde, microwave radiometer profiler, and microwave radiometer observations provides new best estimates of the environmental thermodynamic state. We quantify uncertainty in ERs considering uncertainties in estimated CTH, environmental thermodynamic properties, and assumed initial parcel characteristics. We find ERs ranging from 0.16 to 2.8 km−1 with an average of 0.58 ± 0.10 km−1 over a selected population of 469 shallow cumulus and cumulus congestus clouds. Using the retrieved estimates of ER, we evaluate several entrainment closures that are currently used in atmospheric models or have been proposed based on theory or large eddy simulation. Entrainment rates in cumulus clouds are weakly correlated with low‐level buoyancy, cloud depth, and cloud size.
Genetic variations influence brain changes in patients with attention-deficit hyperactivity disorder
Authors: Yadav Santosh K. , Bhat Ajaz A. , Hashem Sheema , Nisar Sabah , Kamal Madeeha , Syed Najeeb , Temanni Mohamed-Ramzi , Gupta Rakesh K. , Kamran Saddat , Azeem Muhammad Waqar , Srivastava Amit K. , Bagga Puneet , Chawla Sanjeev , Reddy Ravinder , Frenneaux Michael P. , Fakhro Khalid , Haris Mohammad 
Published: June 2021

AbstractAttention-deficit hyperactivity disorder (ADHD) is a neurological and neurodevelopmental childhood-onset disorder characterized by a persistent pattern of inattentiveness, impulsiveness, restlessness, and hyperactivity. These symptoms may continue in 55–66% of cases from childhood into adulthood. Even though the precise etiology of ADHD is not fully understood, it is considered as a multifactorial and heterogeneous disorder with several contributing factors such as heritability, auxiliary to neurodevelopmental issues, severe brain injuries, neuroinflammation, consanguineous marriages, premature birth, and exposure to environmental toxins. Neuroimaging and neurodevelopmental assessments may help to explore the possible role of genetic variations on ADHD neuropsychobiology. Multiple genetic studies have observed a strong genetic association with various aspects of neuropsychobiological functions, including neural abnormalities and delayed neurodevelopment in ADHD. The advancement in neuroimaging and molecular genomics offers the opportunity to analyze the impact of genetic variations alongside its dysregulated pathways on structural and functional derived brain imaging phenotypes in various neurological and psychiatric disorders, including ADHD. Recently, neuroimaging genomic studies observed a significant association of brain imaging phenotypes with genetic susceptibility in ADHD. Integrating the neuroimaging-derived phenotypes with genomics deciphers various neurobiological pathways that can be leveraged for the development of novel clinical biomarkers, new treatment modalities as well as therapeutic interventions for ADHD patients. In this review, we discuss the neurobiology of ADHD with particular emphasis on structural and functional changes in the ADHD brain and their interactions with complex genomic variations utilizing imaging genetics methodologies. We also highlight the genetic variants supposedly allied with the development of ADHD and how these, in turn, may affect the brain circuit function and related behaviors. In addition to reviewing imaging genetic studies, we also examine the need for complementary approaches at various levels of biological complexity and emphasize the importance of combining and integrating results to explore biological pathways involved in ADHD disorder. These approaches include animal models, computational biology, bioinformatics analyses, and multimodal imaging genetics studies.
Methylome-wide change associated with response to electroconvulsive therapy in depressed patients
Authors: Sirignano Lea , Frank Josef , Kranaster Laura , Witt Stephanie H. , Streit Fabian , Zillich Lea , Sartorius Alexander , Rietschel Marcella , Foo Jerome C. 
Published: June 2021

AbstractElectroconvulsive therapy (ECT) is a quick-acting and powerful antidepressant treatment considered to be effective in treating severe and pharmacotherapy-resistant forms of depression. Recent studies have suggested that epigenetic mechanisms can mediate treatment response and investigations about the relationship between the effects of ECT and DNA methylation have so far largely taken candidate approaches. In the present study, we examined the effects of ECT on the methylome associated with response in depressed patients (n = 34), testing for differentially methylated CpG sites before the first and after the last ECT treatment. We identified one differentially methylated CpG site associated with the effect of ECT response (defined as >50% decrease in Hamilton Depression Rating Scale score, HDRS), TNKS (q < 0.05; p = 7.15 × 10−8). When defining response continuously (ΔHDRS), the top suggestive differentially methylated CpG site was in FKBP5 (p = 3.94 × 10−7). Regional analyses identified two differentially methylated regions on chromosomes 8 (Šídák’s p = 0.0031) and 20 (Šídák’s p = 4.2 × 10−5) associated with ΔHDRS. Functional pathway analysis did not identify any significant pathways. A confirmatory look at candidates previously proposed to be involved in ECT mechanisms found CpG sites associated with response only at the nominally significant level (p < 0.05). Despite the limited sample size, the present study was able to identify epigenetic change associated with ECT response suggesting that this approach, especially when involving larger samples, has the potential to inform the study of mechanisms involved in ECT and severe and treatment-resistant depression.
Regulation of adipogenic differentiation and adipose tissue inflammation by interferon regulatory factor 3
Authors: Tang Peng , Virtue Sam , Goie Jian Yi Gerald , Png Chin Wen , Guo Jing , Li Ying , Jiao Huipeng , Chua Yen Leong , Campbell Mark , Moreno-Navarrete José Maria , Shabbir Asim , Fernández-Real José-Manuel , Gasser Stephan , Kemeny David Michael , Yang Henry , Vidal-Puig Antonio , Zhang Yongliang 
Published: June 2021

AbstractDysfunction of adipocytes and adipose tissue is a primary defect in obesity and obesity-associated metabolic diseases. Interferon regulatory factor 3 (IRF3) has been implicated in adipogenesis. However, the role of IRF3 in obesity and obesity-associated disorders remains unclear. Here, we show that IRF3 expression in human adipose tissues is positively associated with insulin sensitivity and negatively associated with type 2 diabetes. In mouse pre-adipocytes, deficiency of IRF3 results in increased expression of PPARγ and PPARγ-mediated adipogenic genes, leading to increased adipogenesis and altered adipocyte functionality. The IRF3 knockout (KO) mice develop obesity, insulin resistance, glucose intolerance, and eventually type 2 diabetes with aging, which is associated with the development of white adipose tissue (WAT) inflammation. Increased macrophage accumulation with M1 phenotype which is due to the loss of IFNβ-mediated IL-10 expression is observed in WAT of the KO mice compared to that in wild-type mice. Bone-marrow reconstitution experiments demonstrate that the nonhematopoietic cells are the primary contributors to the development of obesity and both hematopoietic and nonhematopoietic cells contribute to the development of obesity-related complications in IRF3 KO mice. This study demonstrates that IRF3 regulates the biology of multiple cell types including adipocytes and macrophages to prevent the development of obesity and obesity-related complications and hence, could be a potential target for therapeutic interventions for the prevention and treatment of obesity-associated metabolic disorders.
Adipocyte death triggers a pro-inflammatory response and induces metabolic activation of resident macrophages
Authors: Lindhorst Andreas , Raulien Nora , Wieghofer Peter , Eilers Jens , Rossi Fabio M. V. , Bechmann Ingo , Gericke Martin 
Published: June 2021

AbstractA chronic low-grade inflammation within adipose tissue (AT) seems to be the link between obesity and some of its associated diseases. One hallmark of this AT inflammation is the accumulation of AT macrophages (ATMs) around dead or dying adipocytes, forming so-called crown-like structures (CLS). To investigate the dynamics of CLS and their direct impact on the activation state of ATMs, we established a laser injury model to deplete individual adipocytes in living AT from double reporter mice (GFP-labeled ATMs and tdTomato-labeled adipocytes). Hence, we were able to detect early ATM-adipocyte interactions by live imaging and to determine a precise timeline for CLS formation after adipocyte death. Further, our data indicate metabolic activation and increased lipid metabolism in ATMs upon forming CLS. Most importantly, adipocyte death, even in lean animals under homeostatic conditions, leads to a locally confined inflammation, which is in sharp contrast to other tissues. We identified cell size as cause for the described pro-inflammatory response, as the size of adipocytes is above a critical threshold size for efferocytosis, a process for anti-inflammatory removal of dead cells during tissue homeostasis. Finally, experiments on parabiotic mice verified that adipocyte death leads to a pro-inflammatory response of resident ATMs in vivo, without significant recruitment of blood monocytes. Our data indicate that adipocyte death triggers a unique degradation process and locally induces a metabolically activated ATM phenotype that is globally observed with obesity.
Cisplatin remodels the tumor immune microenvironment via the transcription factor EB in ovarian cancer
Authors: Liu Wei , Wang Yanqiu , Xie Yunkai , Dai Tianyu , Fan Mingjun , Li Changzhong , Zou Yonghui 
Published: June 2021

AbstractThe mortality rate of ovarian cancer (OC) remains the highest among all gynecological malignancies. Platinum-based chemotherapies are effective in treating most OC cases. However, chemoresistance is still a major challenge for successful OC treatments. Emerging evidence has highlighted that the modulation of the tumor immune microenvironment is involved in chemoresistance, but the mechanism remains unclear. This study aimed to investigate whether resistance to cisplatin (CDDP), the standard treatment for OC, is due to the remodeling of the tumor immune microenvironment by the transcription factor EB (TFEB). We hypothesized that TFEB is not essential for tumor survival but is associated with CDDP resistance. We collected 20 tissue samples of OC patients who had not undergone chemotherapy or radiotherapy prior to surgery. We cultured OC cell lines and performed cell transfection and assays as well as analytical, fluorescence microscopy, and immunohistochemical techniques to explore a novel function of TFEB in remodeling the tumor immune microenvironment in OC. We found a positive correlation between TFEB and programmed cell death-ligand 1 (PD-L1), PD-L2, and HLA-A expression in OC cells and tissues. We also found that CDDP treatment induced TFEB nuclear translocation, thus increasing PD-L1 and PD-L2 expression to foster an immunosuppressive tumor microenvironment, which mediates tumor immune evasion and drug resistance. Interestingly, TFEB also regulated HLA-A expression, which increases the tumor immunogenicity of OC. Finally, in a syngenic murine model of OC, we observed the therapeutic benefit of CDDP plus programmed cell death-1 (PD-1) inhibitor, which enhanced the cytolytic activity of CD8+ T cells and inhibited tumor growth. Our study illustrates the important role of TFEB in regulating the tumor immune microenvironment in OC.
Metabolic protein phosphoglycerate kinase 1 confers lung cancer migration by directly binding HIV Tat specific factor 1
Authors: Chang Yu-Chan , Chan Ming-Hsien , Li Chien-Hsiu , Yang Chih-Jen , Tseng Yu-Wen , Tsai Hsing-Fang , Chiou Jean , Hsiao Michael 
Published: June 2021

AbstractPhosphoglycerate kinase (PGK) is involved in glycolytic and various metabolic events. Dysfunction of PGK may induce metabolic reprogramming and the Warburg effect. In this study, we demonstrated that PGK1, but not PGK2, may play a key role in tumorigenesis and is associated with metastasis. We observed an inverse correlation between PGK1 and the survival rate in several clinical cohorts through bioinformatics statistical and immunohistochemical staining analyses. Surprisingly, we found that PGK1 was significantly increased in adenocarcinoma compared with other subtypes. Thus, we established a PGK1-based proteomics dataset by a pull-down assay. We further investigated HIV-1 Tat Specific Factor 1 (HTATSF1), a potential binding partner, through protein–protein interactions. Then, we confirmed that PGK1 indeed bound to HTATSF1 by two-way immunoprecipitation experiments. In addition, we generated several mutant clones of PGK1 through site-directed mutagenesis, including mutagenesis of the N-terminal region, the enzyme catalytic domain, and the C-terminal region. We observed that even though the phosphoglycerate kinase activity had been inhibited, the migration ability induced by PGK1 was maintained. Moreover, our immunofluorescence staining also indicated the translocation of PGK1 from the cytoplasm to the nucleus and its colocalization with HTATSF1. From the results presented in this study, we propose a novel model in which the PGK1 binds to HTATSF1 and exerts functional control of cancer metastasis. In addition, we also showed a nonenzymatic function of PGK1.
Lanthanide-doping enables kinetically controlled growth of deep-blue two-monolayer halide perovskite nanoplatelets
Authors: Cao Qinxuan , Ilyas Asif , Zhang Shuai , Ju Zhijie , Sun Fangling , Liu Tianyu , Yang Yang(Michael) , Lu Yunhao , Liu Xinfeng , Deng Renren 
Published: June 2021

The doping of lanthanides enables the preparation of high-quality deep-blue emitting 2-monolayer CsPbBr3 nanoplatelets by enhancing the energy barrier for intermediates in the transformation of 2-monolayer to 3-monolayer CsPbBr3 nanoplatelets.
Bearing estimation of low probability of intercept sources via polynomial matrices and sparse linear arrays
Authors: Coventry William , Clemente Carmine , Soraghan John , Cade Neil 
Published: June 2021

AbstractRecent years have seen a steady convergence of Radar and Communications band Radio Frequency (RF) transceiver systems. Not only have Communications systems colonised large swathes of previously allocated Radar bands but there is also a convergence of technologies driven by the relatively low cost of software‐defined transceivers and solid‐sate RF sources. Thus, where conventional radar transmissions are characterised by short narrowband pulses with high peak power, new classes of ‘pulse‐compression’ radar are being developed to exploit this new technology. The resulting Low Probability of Intercept waveforms are designed to spread energy in both time and frequency, yielding a very low instantaneous power spectral density. Methods to detect, analyse and distinguish such sources require longer acquisition periods to collect more energy from the sources. Here, a novel solution is provided for detection and separation based on direction‐finding utilising polynomial matrix methods in conjunction with sparse array geometries. This approach provides enhanced detection, separation and direction finding while using relatively few antenna elements.
Cotton leaf curl Gezira virus.
Authors: Brown Judith K. 
Published: June 2021

Abstract

Cotton leaf curl Gezira virus (CLCuGV) is endemic to the African Sahel region (Idris et al., 2000). It is an economically important cotton-infecting begomovirus, and poses a serious threat to cotton production. It causes yield loss in all affected cotton-growing areas in Africa. Losses are difficult to assess, but estimates range up to 20% when infection occurs early in the growing season and/or with highly susceptible cultivars.
Governance of artificial intelligence
Authors: Taeihagh Araz 
Published: June 2021

ABSTRACT
The rapid developments in Artificial Intelligence (AI) and the intensification in the adoption of AI in domains such as autonomous vehicles, lethal weapon systems, robotics and alike pose serious challenges to governments as they must manage the scale and speed of socio-technical transitions occurring. While there is considerable literature emerging on various aspects of AI, governance of AI is a significantly underdeveloped area. The new applications of AI offer opportunities for increasing economic efficiency and quality of life, but they also generate unexpected and unintended consequences and pose new forms of risks that need to be addressed. To enhance the benefits from AI while minimising the adverse risks, governments worldwide need to understand better the scope and depth of the risks posed and develop regulatory and governance processes and structures to address these challenges. This introductory article unpacks AI and describes why the Governance of AI should be gaining far more attention given the myriad of challenges it presents. It then summarises the special issue articles and highlights their key contributions. This special issue introduces the multifaceted challenges of governance of AI, including emerging governance approaches to AI, policy capacity building, exploring legal and regulatory challenges of AI and Robotics, and outstanding issues and gaps that need attention. The special issue showcases the state-of-the-art in the governance of AI, aiming to enable researchers and practitioners to appreciate the challenges and complexities of AI governance and highlight future avenues for exploration.
Pulling things together: regional policy coordination approaches and drivers in Europe
Authors: Ferry Martin 
Published: June 2021

ABSTRACTCoordination is a long-term issue for regional policy that has gained traction in academic and practitioner circles in recent years. The capacity challenges of responding to a broadening set of issues that cut across sectoral and administrative boundaries focus attention on regional policy coordination. Various concepts have emerged to study policy coordination processes, but efforts are ongoing to bring these together into overarching analytical frameworks. This paper contributes to these efforts by disaggregating coordination mechanisms according to different components of regional policy design and delivery (rule-based coordination, organisational arrangements, strategic policy coordination and policy instrument coordination) and by identifying cognitive, political and institutional factors that drive their use. The paper explores the relationship between coordination mechanisms and these drivers in the regional policy systems of three countries: Germany, Poland and the United Kingdom. It assesses the different dynamics at work and notes the importance of administrative capacity as a prerequisite for effective coordination.
Circulating myokines IL‐6, IL‐15 and FGF21 response to training is altered by exercise type but not by menopause in women with obesity
Authors: Pérez‐López Alberto , Gonzalo‐Encabo Paola , Pérez‐Köhler Bárbara , García‐Honduvilla Natalio , Valadés David 
Published: June 2021

ABSTRACTTo examine the effects of a time‐matched endurance vs. concurrent training on circulating IL‐6, IL‐13, IL‐15, IL‐15Ra, FGF21 levels in postmenopausal women with obesity, and to determine these myokines response to endurance training pre‐ and postmenopause. Thirty‐five sedentary postmenopausal women with obesity were randomly divided into endurance training (EN1, N = 10), concurrent training (CON, N = 13) or no training group (CT, N = 12). Additionally, twelve sedentary premenopausal women with obesity were added to an endurance training group (EN2, N = 12). Participants took part in a 12‐week supervised intervention, performing 3 sessions/week of 60 min/session. Before and after the interventions, body composition and fitness were assessed, and blood samples obtained to measure serum myokines levels. Total fat mass decreased in all exercised groups (CON,−5.2%; EN1,−5.3%; EN2,−5.6%). In postmenopausal women, serum IL‐6, IL‐15 and IL‐15Ra decreased after training (P<0.01), finding a pronounced reduction in IL‐6 (−42% vs. −16%) and IL‐15 (−50% vs. −31%) when comparing EN1 to CON (P<0.05). Serum FGF21 was only reduced in the EN1 (−27%; P=0.012). While EN1 and EN2 comparison, reported differences for IL‐15Rα concentration (−28% vs. −40%; P=0.023). Finally, in EN2, the delta change of fat mass and IL‐6, IL‐15 and IL‐15Rα were associated (r = 0.605; r = 0.546; r = 0.515; P<0.05). IL‐13 showed undetected concentrations. Circulating IL‐6, IL‐15 and FGF21 response to training is altered by exercise type but not by menopause in women with obesity. Endurance training promotes a higher reduction of these myokines, potentially activating their intricate immune and fat mass regulation roles in postmenopausal women with obesity.