bluuebunny/crossref_metadata_2025_split huggingface dataset:
Interleukin-38 ameliorates poly(I:C) induced lung inflammation: therapeutic implications in respiratory viral infections
Authors: Gao Xun , Chan Paul Kay Sheung , Lui Grace Chung Yan , Hui David Shu Cheong , Chu Ida Miu-Ting , Sun Xiaoyu , Tsang Miranda Sin-Man , Chan Ben Chung Lap , Lam Christopher Wai-Kei , Wong Chun-Kwok 
Published: January 2021

AbstractInterleukin-38 has recently been shown to have anti-inflammatory properties in lung inflammatory diseases. However, the effects of IL-38 in viral pneumonia remains unknown. In the present study, we demonstrate that circulating IL-38 concentrations together with IL-36α increased significantly in influenza and COVID-19 patients, and the level of IL-38 and IL-36α correlated negatively and positively with disease severity and inflammation, respectively. In the co-cultured human respiratory epithelial cells with macrophages to mimic lung microenvironment in vitro, IL-38 was able to alleviate inflammatory responses by inhibiting poly(I:C)-induced overproduction of pro-inflammatory cytokines and chemokines through intracellular STAT1, STAT3, p38 MAPK, ERK1/2, MEK, and NF-κB signaling pathways. Intriguingly, transcriptomic profiling revealed that IL-38 targeted genes were associated with the host innate immune response to virus. We also found that IL-38 counteracts the biological processes induced by IL-36α in the co-culture. Furthermore, the administration of recombinant IL-38 could mitigate poly I:C-induced lung injury, with reduced early accumulation of neutrophils and macrophages in bronchoalveolar lavage fluid, activation of lymphocytes, production of pro-inflammatory cytokines and chemokines and permeability of the alveolar-epithelial barrier. Taken together, our study indicates that IL-38 plays a crucial role in protection from exaggerated pulmonary inflammation during poly(I:C)-induced pneumonia, thereby providing the basis of a novel therapeutic target for respiratory viral infections.
Deletion of IKK2 in haematopoietic cells of adult mice leads to elevated interleukin-6, neutrophilia and fatal gastrointestinal inflammation
Authors: Fischer Karla C. , Daunt Carmel P. , Tremblay Cédric S. , Dias Sheila , Vince James E. , Jabbour Anissa M. 
Published: January 2021

AbstractThe IκB kinase complex, consisting of IKK1, IKK2 and the regulatory subunit NEMO, is required for NF-κB signalling following the activation of several cell surface receptors, such as members of the Tumour Necrosis Factor Receptor superfamily and the Interleukin-1 Receptor. This is critical for haematopoietic cell proliferation, differentiation, survival and immune responses. To determine the role of IKK in the regulation of haematopoiesis, we used the Rosa26Cre-ERT2 Cre/lox recombination system to achieve targeted, haematopoietic cell-restricted deletion of the genes for IKK1 or IKK2 in vivo. We found that the IKK complex plays a critical role in haematopoietic cell development and function. Deletion of IKK2, but not loss of IKK1, in haematopoietic cells led to an expansion of CD11b/Gr-1-positive myeloid cells (neutrophilia), severe anaemia and thrombocytosis, with reduced numbers of long-term haematopoietic stem cells (LT-HSCs), short-term haematopoietic stem cells (ST-HSCs) and multipotential progenitor cells (MPPs), increased circulating interleukin-6 (IL-6) and severe gastrointestinal inflammation. These findings identify distinct functions for the two IKK catalytic subunits, IKK1 and IKK2, in the haematopoietic system.
MicroRNA-153-5p promotes the proliferation and metastasis of renal cell carcinoma via direct targeting of AGO1
Authors: Li Zeyan , Zhao Shuo , Zhu Shiqin , Fan Yidong 
Published: January 2021

AbstractMicroRNAs (miRNAs) have been demonstrated to affect the biological processes of cancers and showed great potential for prognostic biomarkers. In this study, we screened differentially expressed miRNAs in ccRCC based on three dimensions of metastasis, prognosis, and differential expression compared to normal tissue using bioinformatics algorithms. MiR-153-5p was identified as a candidate miRNA to promote ccRCC occurrence and progression. Clinically, we found that miR-153-5p was significantly upregulated and related to unfavorable clinical features in ccRCC. Besides, miR-153-5p served as an independent prognostic biomarker. Functionally, miR-153-5p depletion remarkably inhibited the proliferation and metastasis of ccRCC via the phosphatidylinositol 3-kinase (PI3K)/Akt signaling. Furthermore, AGO1 was proved to be a direct target of miR-153-5p. AGO1 is associated with favorable clinical features and exhibited independent prognostic value in ccRCC. Besides, we observed that AGO1 knockdown significantly promoted tumor proliferation and metastasis. Downregulation of AGO1 partly abolished the oncogenic effects of miR-153-5p knockdown. Furthermore, miR-153-5p combined with AGO1 showed more robust prognostic significance in ccRCC. In conclusion, we found that the newly identified miR-153-5p/AGO1 axis was responsible for tumor occurrence and progression via PI3K/Akt signaling, which may therefore provide promising therapeutic targets and prognostic biomarkers for patients with ccRCC.
METTL14-regulated PI3K/Akt signaling pathway via PTEN affects HDAC5-mediated epithelial–mesenchymal transition of renal tubular cells in diabetic kidney disease
Authors: Xu Zhaoxia , Jia Keqi , Wang Hui , Gao Feng , Zhao Song , Li Fan , Hao Jun 
Published: January 2021

AbstractHistone deacetylase 5 (HDAC5) belongs to class II HDAC subfamily and is reported to be increased in the kidneys of diabetic patients and animals. However, little is known about its function and the exact mechanism in diabetic kidney disease (DKD). Here, we found that HDAC5 was located in renal glomeruli and tubular cells, and significantly upregulated in diabetic mice and UUO mice, especially in renal tubular cells and interstitium. Knockdown of HDAC5 ameliorated high glucose-induced epithelial–mesenchymal transition (EMT) of HK2 cells, indicated in the increased E-cadherin and decreased α-SMA, via the downregulation of TGF-β1. Furthermore, HDAC5 expression was regulated by PI3K/Akt signaling pathway and inhibition of PI3K/Akt pathway by LY294002 treatment or Akt phosphorylation mutation reduced HDAC5 and TGF-β1 expression in vitro high glucose-cultured HK2 cells. Again, high glucose stimulation downregulated total m6A RNA methylation level of HK2 cells. Then, m6A demethylase inhibitor MA2 treatment decreased Akt phosphorylation, HDAC5, and TGF-β1 expression in high glucose-cultured HK2 cells. In addition, m6A modification-associated methylase METTL3 and METTL14 were decreased by high glucose at the levels of mRNA and protein. METTL14 not METTL3 overexpression led to PI3K/Akt pathway inactivation in high glucose-treated HK2 cells by enhancing PTEN, followed by HDAC5 and TGF-β1 expression downregulation. Finally, in vivo HDACs inhibitor TSA treatment alleviated extracellular matrix accumulation in kidneys of diabetic mice, accompanied with HDAC5, TGF-β1, and α-SMA expression downregulation. These above data suggest that METTL14-regulated PI3K/Akt signaling pathway via PTEN affected HDAC5-mediated EMT of renal tubular cells in diabetic kidney disease.
Downregulation of microRNA-9-5p promotes synaptic remodeling in the chronic phase after traumatic brain injury
Authors: Wu Jingchuan , Li Hui , He Junchi , Tian Xiaocui , Luo Shuilian , Li Jiankang , Li Wei , Zhong Jianjun , Zhang Hongrong , Huang Zhijian , Sun Xiaochuan , Jiang Tao 
Published: January 2021

AbstractThe level of microRNA-9-5p (miRNA-9-5p) in brain tissues is significantly changed in the chronic phase after traumatic brain injury (TBI). However, the effect of miRNA-9-5p on brain function after TBI has not been elucidated. In this study, we used a controlled cortical impact (CCI) model to induce TBI in Sprague–Dawley rats. Brain microvascular endothelial cells (BMECs), astrocytes, and neurons were extracted from immature Sprague–Dawley rats and cocultured to reconstruct the neurovascular unit (NVU) in vitro. The results showed that downregulation of miRNA-9-5p in the chronic phase contributed to neurological function recovery by promoting astrocyte proliferation and increasing the release of astrocyte-derived neurotrophic factors around injured brain tissues after TBI. A dual-luciferase reporter assay validated that miRNA-9-5p was a post-transcriptional modulator of thrombospondin 2 (Thbs-2), and downregulation of miRNA-9-5p promoted Thbs-2 expression in astrocytes. Furthermore, we verified that Thbs-2 can promote Notch pathway activation by directly binding to Jagged and Notch. Through in vitro experiments, we found that the expression of synaptic proteins and the number of synaptic bodies were increased in neurons in the NVU, which was constructed using astrocytes pretreated with miRNA-9-5p inhibitor. Moreover, we also found that downregulation of miRNA-9-5p promoted Thbs-2 expression in astrocytes, which activated the Notch/cylindromatosis/transforming growth factor-β-activated kinase 1 pathway in neurons and promoted the expression of synaptic proteins, including post-synaptic density protein 95 and synaptotagmin. Based on these results, miRNA-9-5p may be a new promising prognostic marker and treatment target for TBI.
Apoptosis inhibitor of macrophage (AIM) contributes to IL-10-induced anti-inflammatory response through inhibition of inflammasome activation
Authors: Kim Tae-Hyun , Yang Kyungwon , Kim Minsuk , Kim Hee-Sun , Kang Jihee Lee 
Published: January 2021

AbstractApoptosis inhibitor of macrophage (AIM) modulates the signaling in inflammatory responses, including infection, cancer, or other immune diseases. Recent studies suggest that like interleukin-10 (IL-10), AIM is involved in alternatively activated (M2) macrophage polarization. We aimed to understand whether and how AIM is involved in IL-10-induced inhibition of inflammasome activation and resolution of inflammation. First, we demonstrated that IL-10 induced increases in mRNA and protein expression of AIM in murine bone marrow-derived macrophages (BMDM). In addition, genetic and pharmacologic inhibition of STAT3 (signal transducer and activator of transcription 3) reduced IL-10-induced AIM expression. We also found that IL-10-induced STAT3 activity enhanced the AIM promoter activity by directly binding the promoter of the AIM gene. Additionally, reduction of LPS/adenosine triphosphate (ATP)-induced IL-1β production and caspase-1 activation by IL-10 was reversed in BMDM from AIM−/− mice. Treatment of BMDM from both wild type (WT) and IL-10−/− mice with recombinant AIM showed the inhibitory effects on IL-1β and IL-18 production and caspase-1 activation. Endogenous and exogenous AIM inhibited apoptosis-associated speck-like protein containing a caspase activation and recruitment domain (ASC) speck formation. In LPS-induced acute peritonitis, inhibition of IL-1β and IL-18 production in peritoneal lavage fluid (PLF) and serum, reduction of caspase-1 activation in peritoneal macrophages, and reduction of numbers of neutrophils and peritoneal macrophages in PLF by administration of IL-10 were not evident in AIM−/− mice. Our in vitro and in vivo data reveal a novel role of AIM in the inhibition of inflammasome-mediated caspase-1 activation and IL-1β and IL-18 production.
MicroRNA-93/STAT3 signalling pathway mediates retinal microglial activation and protects retinal ganglion cells in an acute ocular hypertension model
Authors: Wang Yayi , Chen Shida , Wang Jiawei , Liu Yaoming , Chen Yang , Wen Tao , Fang Xiuli , Vidal-Sanz Manuel , Jonas Jost B. , Zhang Xiulan 
Published: January 2021

AbstractGlaucoma is a common neurodegenerative disease and a leading cause of irreversible blindness worldwide. Retinal microglia-mediated neuroinflammation is involved in the process of optic nerve damage, but the mechanisms driving this microglial activation remain mostly elusive. Previous investigations reported that microRNAs are associated with the retinal microglial reaction and neural apoptosis. In the present study, we found that microRNA-93-5p (miR-93) played a key role in the reaction of retinal microglial cells in vivo and in vitro. The miR-93 level was significantly reduced in the retinae of rat acute ocular hypertension (AOH) models, which were accompanied by retinal microglial activation, overproduction of inflammatory cytokines, and subsequent retinal ganglion cells (RGCs) death, versus the retinae of controls. The induction of miR-93 overexpression significantly reduced microglial proliferation, migration and cytokine release, inhibited the expression of the target gene signal transducer and activator of transcription 3 (STAT3) and p-STAT3, and was associated with a reduced loss of RGCs. Treatment with a STAT3 inhibitor also decreased retinal microglial activation after AOH injury. Taken together, these results suggest that the miR-93/STAT3 pathway is directly related to the downregulation of retinal microglia-mediated neuro-inflammation and showed a neuroprotective effect. Regulating microglial activation through miR-93 may serve as a target for neuroprotective therapy in pathological ocular hypertension.
Distributed resilient flocking control of multi‐agent systems through event/self‐triggered communication
Authors: Amirian Neda , Shamaghdari Saeed 
Published: January 2021

AbstractThis paper proposes a distributed control scheme for multi‐agent systems to achieve resilient flocking behaviour via event‐based communication. The control scheme can provide the required connectivity conditions to form a flock in the presence of cyberattacks in the network. This method is presented in a fully distributed manner to avoid the use of global data. The developed event‐triggered update rules can mitigate the influence of the non‐cooperative agents with the weighted mean subsequence‐reduced algorithm and reduce unnecessary communication among them. It is proved that under the proposed method, convergence is guaranteed and there is no Zeno behaviour exhibited inherently. To relax the requirement of continuous monitoring of self‐state, a self‐triggered mechanism is proposed further. Simulation results are given to illustrate the theoretical analysis and show the advantages of the event‐ and self‐triggered controllers.
Visual‐attention GAN for interior sketch colourisation
Authors: Li Xinrong , Li Hong , Wang Chiyu , Hu Xun , Zhang Wei 
Published: January 2021

AbstractIn the professional field of interior designing, sketch colouring is often a time‐consuming and vapidity task. The traditional neural network does not handle the semantic relationship of sketch lines well, and the colouring effect is unsatisfactory. This paper proposes visual‐attention generative adversarial network (VAGAN), which enhances the processing effect of edge semantics, strengthens the network to line edge recognition ability, as well as reduces colour overflow and improved model colouring result. In addition, a two‐stage training mode is used to simplify the training of rare samples. The simple line draft input into the trained VAGAN, output natural, realistic colour pictures. The experimental results show that, compared with the existing methods, the proposed method can better deal with the problem of sketch and generate stable and reliable images.
Deep spectral unmixing framework via 3D denoising convolutional autoencoder
Authors: Jia Peiyuan , Zhang Miao , Shen Yi 
Published: January 2021

AbstractHyperspectral unmixing is an important technique which attempts to acquire pure spectra of distinct substances (endmembers) and estimate fractional abundances from highly mixed pixels. This paper proposed a novel deep network‐based framework for unmixing problem. It contains two parts: a three‐dimensional convolutional autoencoder for hyperspectral denoising (denoising 3D CAE) which aims to recover data from highly noised input imagery through an unsupervised manner, and a restrictive non‐negative sparse autoencoder which extracts endmembers and abundances from the scene simultaneously. The proposed denoising 3D CAE network integrates 3D operations in each layer, which allows manipulating volumetric representation of the image data directly and facilitates hierarchical exploration for latent information. Being trained with corrupted hyperspectral image data, the denoising 3D CAE network has strong capacity of capturing the principle and robust local features in spatial and spectral domains efficiently, and it shows superior performance for image recovery with high noise disturbance. Moreover, a part‐based non‐negative autoencoder is concatenated, and the ‐norm penalty is imposed for sparsity enhancement of the solution. Comparative experiments are conducted both on synthetic and real‐world hyperspectral data, which demonstrate the applicability and effectiveness of the proposed unmixing framework.
A nearby galaxy perspective on dust evolution
Authors: Galliano Frédéric , Nersesian Angelos , Bianchi Simone , De Looze Ilse , Roychowdhury Sambit , Baes Maarten , Casasola Viviana , Cassará Letizia P. , Dobbels Wouter , Fritz Jacopo , Galametz Maud , Jones Anthony P. , Madden Suzanne C. , Mosenkov Aleksandr , Xilouris Emmanuel M. , Ysard Nathalie 
Published: January 2021

Context.The efficiency of the different processes responsible for the evolution of interstellar dust on the scale of a galaxy are, to date, very uncertain, spanning several orders of magnitude in the literature. Yet, precise knowledge of the grain properties is key to addressing numerous open questions about the physics of the interstellar medium and galaxy evolution.Aims.This article presents an empirical statistical study, aimed at quantifying the timescales of the main cosmic dust evolution processes as a function of the global properties of a galaxy.Methods.We modeled a sample of ≃800 nearby galaxies, spanning a wide range of metallicities, gas fractions, specific star formation rates, and Hubble stages. We derived the dust properties of each object from its spectral energy distribution. Through an additional level of analysis, we inferred the timescales of dust condensation in core-collapse supernova ejecta, grain growth in cold clouds, and dust destruction by shock waves. Throughout this paper, we have adopted a hierarchical Bayesian approach, resulting in a single large probability distribution of all the parameters of all the galaxies, to ensure the most rigorous interpretation of our data.Results.We confirm the drastic evolution with metallicity of the dust-to-metal mass ratio (by two orders of magnitude), found by previous studies. We show that dust production by core-collapse supernovae is efficient only at very low metallicity, a single supernova producing on average less than ≃0.03 M⊙/SN of dust. Our data indicate that grain growth is the dominant formation mechanism at metallicity above ≃1/5 solar, with a grain growth timescale shorter than ≃50 Myr at solar metallicity. Shock destruction is relatively efficient, a single supernova clearing dust on average in at least ≃1200 M⊙/SN of gas. These results are robust when assuming different stellar initial mass functions. In addition, we show that early-type galaxies are outliers in several scaling relations. This feature could result from grain thermal sputtering in hot X-ray emitting gas, which is a hypothesis supported by a negative correlation between the dust-to-stellar mass ratio and the X-ray photon rate per grain. Finally, we confirm the well-known evolution of the aromatic-feature-emitting grain mass fraction as a function of metallicity and interstellar radiation field intensity. Our data indicate that the relation with metallicity is significantly stronger.Conclusions.Our results provide valuable constraints for simulations of galaxies. They imply that grain growth is the likely dust production mechanism in dusty high-redshift objects. We also emphasize the determinant role of local, low metallicity systems in order to address these questions.
Process Model of the Economic Efficiency of the Financial Administration of an EU Member State
Authors: Kot Sebastian , Dobrovič Ján 
Published: January 2021

The current reform of Slovakia’s tax system is a part of the country’s comprehensive tax and levies reform. The reform should contribute to improving and making public finances more efficient. However, its implementation in practice is problematic due to the attitudes and problems of both the professional public and business entities. The aim of this contribution is to help students and business entities to understand the tax system reforms. The contribution is based on information from the main actors of the tax reforms. The data were obtained during 3 months (2019 – 2020) using the questionnaire method. These were processed using basic statistical methods of the descriptive type, followed by an analysis of the principal factors and factor analysis. The factor analysis was crucial for our contribution because it identified 5 significant indicators with regards to the assessment of the reforms and the functioning of the tax system. Subsequently, a correspondence analysis was conducted of the factor “Electronisation/computerisation – greater user comfort” to find out the differences in the perception hereof among the respondents. The contribution therefore provides a new perspective on the evaluation and functioning of the reforms of the Financial Administration’s management system in the Slovak Republic.
Within the framework of the research into this matter, and with a view to increasing the efficiency of the system globally, we also looked at the existing functional organizational structures and tax administration systems in Hungary, Poland, Czech Republic and Slovenia. On the basis of trend analysis, we can assume that the upcoming reform of the Tax and Customs Administrations will significantly contribute to the increasing efficiency of the system and to the positive perception of taxes, which are currently viewed as a socially unpopular obligation.
The Push and Pull Factors Affecting the Migration of Mongolians to the Republic of South Korea
Authors: Zanabazar Altanchimeg , Kho Nam Son , Jigjiddorj Sarantuya 
Published: January 2021

Migration, which is a rational labour issue within society, has become a hot topic globally. In recent years there has been an increase in labour migration due to globalization, disparities in the development levels of countries, culture and environment, social instability, political regimes and war. The objective of the presented study was to research the push & pull factors affecting the migration of Mongolians to the Republic of South Korea. The survey was conducted among 498 Mongolians living and working in the Jeollanamеdu and Jeollabugdu districts of the metropolitan cities of Incheon and Ulsan, as well as in the capital city Seoul.Numerous statistical techniques were applied to test the reliability and validity of the data, as well as factor analysis to confirm that the concepts of each variable were correctly measured, correlation analysis to assess the strength of the relationship between the independent and dependent variables, and multiple regression analysis to predict the value of variables used in the study.The results of the study showed that the major push factor was an economic one, for which the main motives for migration were low or instable income, the economic downturn and poverty. Likewise, the pull factors were also economic, whereby the motivation to migrate to South Korea was driven by high wages, wellbeing, the opportunity to save and/ or social factors, such as access to quality education, the cultural experience and joining family members who had already settled in the country.