bluuebunny/crossref_metadata_2025_split huggingface dataset:
Syntropia – acid-dependent diseases and hypertension
Authors: CALIN Ghenadie , ISTRATI Valeriu , STOICA Mihaela , SCURTU Alina , SCORPAN Anatolie , SIRBU Oxana 
Published: July 2022

Introduction. With syntropy of CVD and AH, the pathology of the digestive system can exacerbate the course of AH and develop special conditions for increasing the risk of cardiovascular complications. Pharmacotherapy of HD may affect the course and progression of gastroesophageal reflux disease.
Material and methods. The study was conducted using the PubMed, Z-library, NCIB, Medscape, Mendeley databases using the keywords: “syntropy”, “comorbidity”, “arterial hypertension”, “acid-dependent diseases”, “gastric ulcer”, “gastroesophageal reflux disease”.
Results. AH and CVD are quite often observed together, having, moreover, a conditioned commonality of the mechanisms of formation. The proximity of the location with the heart, the commonality of innervation, in the pathology of the esophagus, can create viscero-visceral reflexes and provoke arrhythmias, imitate coronary heart disease. Pathology of the upper gastrointestinal tract can lead to functional disorders of the cardiovascular system, manifested through the autonomic nervous system. The combined course of AH and CVD, observed, according to various sources, from 11.6% to 50%, is not just random, but may have pathogenetic and etiological patterns. Comorbidity of CVD and AH can enhance the development of the main pathological process and lead to disruption of adaptive mechanisms.
Conclusions. The syntropy of AH and CVD requires thorough scientific studies to discover and elucidate the pathogenetic features of the course and methods of better drug therapy.
An overview of plant tissue culture research trends at Areka Agricultural Research Center, Southern Agricultural Research Institute, Ethiopia 2016-2019
Authors: Mekso Mekibib , Mena Tigist Markos 
Published: July 2022

Plant tissue culture techniques have encountered a lot of obstacles and breakthroughs as a life-giving technology in numerous field of biotechnology research. Tissue culture technology has evolved throughout times in the world, from shoot tip culture to variety creation. Plant tissue culture may be thought of as a collection of techniques/methodologies that make uses distinct rooms and essential facilities.
The Areka tissue culture research laboratory was established with the aim of conducting comprehensive plant biotechnology researches. However, numerous challenges and opportunities have arisen in the course of attempting to conduct tissue culture experiments in the lab. In fact, the lab highlighted several accomplishments in a few key areas while also tracking improvement over time. Therefore, this walk-through review offers an overall picture of the lab in relation to the research plans, status, and trends. As a result, contribute to the provision of baseline information for future study advancement.
Constraining High-redshift Stellar-mass Primordial Black Holes with Next-generation Ground-based Gravitational-wave Detectors
Authors: Ng Ken K. Y. , Franciolini Gabriele , Berti Emanuele , Pani Paolo , Riotto Antonio , Vitale Salvatore 
Published: July 2022

Abstract
The possible existence of primordial black holes in the stellar-mass window has received considerable attention because their mergers may contribute to current and future gravitational-wave detections. Primordial black hole mergers, together with mergers of black holes originating from Population III stars, are expected to dominate at high redshifts (z ≳ 10). However, the primordial black hole merger rate density is expected to rise monotonically with redshift, while Population III mergers can only occur after the birth of the first stars. Next-generation gravitational-wave detectors such as the Cosmic Explorer (CE) and Einstein Telescope (ET) can access this distinctive feature in the merger rates as functions of redshift, allowing for direct measurement of the abundance of the two populations and hence for robust constraints on the abundance of primordial black holes. We simulate four months’ worth of data observed by a CE-ET detector network and perform hierarchical Bayesian analysis to recover the merger rate densities. We find that if the universe has no primordial black holes with masses of


(
10

M

⊙

)

, the projected upper limit on their abundance f
PBH as a fraction of dark matter energy density may be as low as

f

PBH

∼

(

10

−
5

)

, about two orders of magnitude lower than the current upper limits in this mass range. If instead f
PBH ≳ 10−4, future gravitational-wave observations would exclude f
PBH = 0 at the 95% credible interval.
Jansky Very Large Array Detections of CO(1–0) Emission in H i-absorption-selected Galaxies at z ≳ 2
Authors: Kaur B. , Kanekar N. , Rafelski M. , Neeleman M. , Prochaska J. X. , Revalski M. 
Published: July 2022

Abstract
We report a Karl G. Jansky Very Large Array search for redshifted CO(1–0) emission from three H i-absorption-selected galaxies at z ≈ 2, identified earlier in their CO(3–2) or CO(4–3) emission. We detect CO(1–0) emission from DLA B1228-113 at z ≈ 2.1933 and DLA J0918+1636 at z ≈ 2.5848; these are the first detections of CO(1–0) emission in high-z H i-selected galaxies. We obtain high molecular gas masses, M
mol ≈ 1011 × (α
CO/4.36) M
⊙, for the two objects with CO(1–0) detections, which are a factor of ≈1.5–2 lower than earlier estimates. We determine the excitation of the mid-J CO rotational levels relative to the J = 1 level, r

J1, in H i-selected galaxies for the first time, obtaining r
31 = 1.00 ± 0.20 and r
41 = 1.03 ± 0.23 for DLA J0918+1636, and r
31 = 0.86 ± 0.21 for DLA B1228-113. These values are consistent with thermal excitation of the J = 3 and J = 4 levels. The excitation of the J = 3 level in the H i-selected galaxies is similar to that seen in massive main-sequence and submillimeter galaxies at z≳2, but higher than that in main-sequence galaxies at z ≈ 1.5; the higher excitation of the galaxies at z ≳ 2 is likely to be due to their higher star formation rate (SFR) surface density. We use Hubble Space Telescope Wide Field Camera 3 imaging to detect the rest-frame near-ultraviolet (NUV) emission of DLA B1228-113, obtaining an NUV SFR of 4.44 ± 0.47 M
⊙ yr−1, significantly lower than that obtained from the total infrared luminosity, indicating significant dust extinction in the z ≈ 2.1933 galaxy.
Characterizing the Breakdown of Quasi-universality in Postmerger Gravitational Waves from Binary Neutron Star Mergers
Authors: Raithel Carolyn A. , Most Elias R. 
Published: July 2022

Abstract
The postmerger gravitational wave (GW) emission from a binary neutron star merger is expected to provide exciting new constraints on the dense-matter equation of state (EoS). Such constraints rely, by and large, on the existence of quasi-universal relations, which relate the peak frequencies of the postmerger GW spectrum to properties of the neutron star structure in a model-independent way. In this work, we report on violations of existing quasi-universal relations between the peak spectral frequency, f
2, and the stellar radius, for EoS models with backwards-bending slopes in their mass–radius relations (such that the radius increases at high masses). The violations are extreme, with variations in f
2 of up to ∼600 Hz between EoSs that predict the same radius for a 1.4 M
⊙ neutron star but that have significantly different radii at higher masses. Quasi-universality can be restored by adding in a second parameter to the fitting formulae that depends on the slope of the mass–radius curve. We further find strong evidence that quasi-universality is better maintained for the radii of very massive stars (with masses 2 M
⊙). Both statements imply that f
2 is mainly sensitive to the high-density EoS. Combined with observations of the binary neutron star inspiral, these generalized quasi-universal relations can be used to simultaneously infer the characteristic radius and slope of the neutron star mass–radius relation.
A dataset of sea turtle occurrences around the Taiwan coast
Authors: Hoh Daphne Z. , Fong Chia-Ling , Su Huai , Chen Pengyu , Tsai Chia-Chen , Tseng Kelly W. H. , Liu Melissa J. Y. 
Published: July 2022

We describe a dataset of sea turtle sightings around the coast of Taiwan and its islands. The data was collected by citizen scientists and reported to TurtleSpot Taiwan, a citizen science initiative that collects sea turtle sighting data mainly through the Facebook group. This dataset includes 3,515 sighting data dated from March 2010, except most of the data (n=3,128; 89%) falls were between June 2017 to December 2021. A standardized format of basic sighting information was suggested to anyone who wishes to report the occurrence. We also request photos and videos for turtle species identification and to record any physical abnormality. In addition to the basic data often associated with an occurrence, TurtleSpot aims to identify each sea turtle up to the individual level using the Photo ID method. Hence, if a good quality photo of left- and right-facial scutes were available, the sighted individual can be identified and given a unique Turtle ID. In total, 762 turtle individuals were assigned a turtle ID, comprising 723 green, 38 hawksbill, and 1 olive ridley turtles. The data of TurtleSpot Taiwan has allowed some ecological observations of sea turtles in the wild, such as witnessing the recovery of some injured turtles, behaviours, intra- and inter-species interactions, and physical abnormality. These data will offer essential information that helps to understand the foraging ecology of sea turtles and assists in the development of conservation measures.
This dataset contains 3,515 occurrence records of sea turtles and is currently the largest public dataset of sea turtle sighting records in Taiwan. Post-publication of this dataset to the Global Biodiversity Information Facility (GBIF) demonstrated that the number of green sea turtle Chelonia mydas occurrence records is few of the top in the world. The data served as the foundation for understanding sea turtle ecology in Taiwan's coastal waters.
Archivo Español de Arqueología. Un análisis historiográfico
Authors: Salas Álvarez Jesús , Durán Cabello Rosalía María 
Published: July 2022

El objetivo del presente trabajo es ofrecer un análisis historiográfico preliminar de la revista Archivo Español de Arqueología desde su nacimiento en 1925 como Archivo Español de Arte y Arqueología hasta el año 2019. Este largo periodo se ha dividido en varias etapas en razón de los cambios en su estructura, organización y orientación temática, relacionándolas con los cambios que ha experimentado la Arqueología española durante casi un siglo. Finalmente se avanzan algunas consideraciones generales, estableciendo futuras líneas de investigación historiográfica para analizar de forma más detallada en el futuro.
Crítica de la economía política y relaciones de fuerzas en el «regreso a Marx» de Gramsci
Authors: Sánchez Berrocal Alejandro 
Published: July 2022

El presente artículo se centra en el papel que desempeñan la crítica de la economía política y la filosofía marxiana en la redefinición de la filosofía política de Gramsci en el momento intelectual denominado como «regreso a Marx». Por un lado, se muestra la importancia teórica del concepto de mercado determinado en la formación de nociones como «sociedad civil» y «relaciones de fuerzas». Por otro, evaluamos la relectura carcelaria de algunas obras de Marx a cargo del filósofo italiano y sus efectos en la revisión de ciertos temas como el de la relación entre estructura-superestructura o la teoría de la hegemonía. El objetivo es presentar una interpretación de la ontología social gramsciana la cual, a través de una original interpretación de la crítica de la economía política y actualizando los principios teóricos del «materialismo histórico» en una «filosofía de la praxis», es capaz de aportar una teoría sobre la génesis, reproducción y crisis de una determinada formación social.
Qui fait « la police pour les Anglais » ?
Authors: Grard Héloïse 
Published: July 2022

Fondé sur une enquête ethnographique dans un port qui est aussi une frontière entre la France et le Royaume-Uni, l’article analyse les doubles processus de privatisation et de sécurisation des frontières et l’émergence de nouveaux métiers de la frontière. L’enquête auprès des agents d’escales et de sécurité vise à comprendre comment des agents privés composent avec l’exercice de fonctions publiques qui leur sont déléguées, notamment celle du contrôle migratoire. L’article montre comment ces « petits professionnels de l’international », à mi-chemin entre le secteur public et le secteur privé, s’approprient ou rejettent ces nouvelles fonctions, quelles marges de manœuvre ils réussissent à négocier, et finalement, comment ils construisent quotidiennement la frontière.
Therapeutic Effect of Anti-CD52 Monoclonal Antibody in Multiple Sclerosis and Its Animal Models Is Mediated via T Regulatory Cells
Authors: Kiapour Nazanin , Wu Bing , Wang Yan , Seyedsadr Maryamsadat , Kapoor Sahil , Zhang Xin , Elzoheiry Manal , Kasimoglu Ezgi , Wan Yisong , Markovic-Plese Silva 
Published: July 2022

Abstract
The objective of this study is to determine the mechanism of action of anti-CD52 mAb treatment in patients with relapsing-remitting multiple sclerosis (RRMS). Experimental autoimmune encephalomyelitis (EAE), an animal model of the disease, was used to address the role of T regulatory cells (Tregs) in the anti-CD52 mAb–induced suppression of the disease. In vitro studies on PBMCs from RRMS patients and matched healthy controls determined the effect of IL-7 on the expansion of CD4+CD25+CD127− Tregs and induction of their suppressive phenotype. This study using EAE animal models of MS has shown that mouse anti-CD52 mAb suppression of clinical disease was augmented by coadministration of IL-7 and partially reversed by anti-IL-7 mAb. In vitro human studies showed that IL-7 induced expansion of CD4+CD25+CD127− Tregs and increased their FOXP3, GITIR, CD46, CTLA-4, granzyme B, and perforin expression. Anti-CD52 mAb treatment of mice with relapsing-remitting EAE induced expansion of Foxp3+CD4+ Tregs and the suppression of IL-17A+CD4+ and IFN-γ+CD4+ cells in peripheral immune organs and CNS infiltrates. The effect was detected immediately after the treatment and maintained over long-term follow-up. Foxp3+CD4+ Treg-mediated suppression of IL-17A+CD4+ and IFN-γ+CD4+ cells in the spinal cord infiltrates was reversed after inducible Foxp3 depletion. Our results demonstrated that the therapeutic effect of U.S. Food and Drug Administration–approved anti-CD52 mAb is dependent on the presence of Tregs.
miR-146a Maintains Immune Tolerance of Kupffer Cells and Facilitates Hepatitis B Virus Persistence in Mice
Authors: Liu Yongai , Qin Lijuan , Wang Jiuru , Xie Xialin , Zhang Yu , Li Changfei , Guan Zeliang , Qian Liyuan , Chen Lizhao , Hu Jun , Meng Songdong 
Published: July 2022

Abstract
Kupffer cells (KCs), the largest tissue-resident macrophage population in the body, play a central role in maintaining a delicate balance between immune tolerance and immunity in the liver. However, the underlying molecular mechanism remains elusive. In this study, we show that KCs express high levels of miR-146a, which is under control of the PU.1 transcription factor. miR-146a deficiency promoted KCs differentiation toward a proinflammatory phenotype; conversely, miR-146a overexpression suppressed this phenotypic differentiation. We found that hepatitis B virus (HBV) persistence or HBV surface Ag treatment significantly upregulated miR-146a expression and thereby impaired polarization of KCs toward a proinflammatory phenotype. Furthermore, in an HBV carrier mouse model, KCs depletion by clodronate liposomes dramatically promoted HBV clearance and enhanced an HBV-specific hepatic CD8+ T cell and CD4+ T cell response. Consistent with this finding, miR-146a knockout mice cleared HBV faster and elicited a stronger adaptive antiviral immunity than wild-type mice. In vivo IL-12 blockade promoted HBV persistence and tempered the HBV-specific CTL response in the liver of miR-146a knockout mice. Taken together, our results identified miR-146a as a critical intrinsic regulator of an immunosuppressive phenotype in KCs under inflammatory stimuli, which may be beneficial in maintenance of liver homeostasis under physiological condition. Meanwhile, during HBV infection, miR-146a contributed to viral persistence by inhibiting KCs proinflammatory polarization, highlighting its potential as a therapeutic target in HBV infection.
Carbon Dioxide Sensing by Immune Cells Occurs through Carbonic Anhydrase 2–Dependent Changes in Intracellular pH
Authors: Strowitzki Moritz J , Nelson Ross , Garcia Mario P , Tuffs Christopher , Bleul Marc B , Fitzsimons Stephen , Navas Javier , Uzieliene Ilona , Ritter Alina S , Phelan David , Kierans Sarah J , Blanco Alfonso , Bernotiene Eiva , Belton Orina , Schneider Martin , Cummins Eoin P , Taylor Cormac T 
Published: July 2022

Abstract
CO2, the primary gaseous product of respiration, is a major physiologic gas, the biology of which is poorly understood. Elevated CO2 is a feature of the microenvironment in multiple inflammatory diseases that suppresses immune cell activity. However, little is known about the CO2-sensing mechanisms and downstream pathways involved. We found that elevated CO2 correlates with reduced monocyte and macrophage migration in patients undergoing gastrointestinal surgery and that elevated CO2 reduces migration in vitro. Mechanistically, CO2 reduces autocrine inflammatory gene expression, thereby inhibiting macrophage activation in a manner dependent on decreased intracellular pH. Pharmacologic or genetic inhibition of carbonic anhydrases (CAs) uncouples a CO2-elicited intracellular pH response and attenuates CO2 sensitivity in immune cells. Conversely, CRISPR-driven upregulation of the isoenzyme CA2 confers CO2 sensitivity in nonimmune cells. Of interest, we found that patients with chronic lung diseases associated with elevated systemic CO2 (hypercapnia) display a greater risk of developing anastomotic leakage following gastrointestinal surgery, indicating impaired wound healing. Furthermore, low intraoperative pH levels in these patients correlate with reduced intestinal macrophage infiltration. In conclusion, CO2 is an immunomodulatory gas sensed by immune cells through a CA2-coupled change in intracellular pH.
Activation of CD4+ T Cell–Derived Cannabinoid Receptor 2 Signaling Exacerbates Sepsis via Inhibiting IL-10
Authors: Chen Jincheng , Wang Fuxiang , Zhang Su , Lin Qiao , Xu Hui , Zhu Tengfei , Peng Ling , Cen Fulan , Li Fang , Wang Zhaoqin , Feng Carl G , Yin Zhinan , Liu Yingxia , Zhang Guoliang 
Published: July 2022

Abstract
The cannabinoid receptor 2 (CB2) is a receptor mainly expressed in immune cells and believed to be immunosuppressive in infective or inflammatory models. However, its role in sepsis has not been fully elucidated. In this study, we delineate the function and mechanism of CB2 in the cecal ligation and puncture–induced septic model in mice. The activation of CB2 signaling with HU308 led to decreased survival rates and more severe lung injury in septic mice, and lower IL-10 levels in peritoneal lavage fluid were observed in the CB2 agonist group. The mice with conditional knockout of CB2-encoding gene CNR2 in CD4+ T cells (CD4 Cre CNR2fl/fl) improved survival, enhanced IL-10 production, and ameliorated pulmonary damage in the sepsis model after CB2 activation. In addition, double-knockout of the CNR2 gene (Lyz2 Cre CD4 Cre CNR2fl/fl) decreased the susceptibility to sepsis compared with Lyz2 Cre CNR2fl/fl mice. Mechanistically, the blockade of IL-10 with the anti–IL-10 Ab abolished its protection in CD4 Cre CNR2fl/fl mice. In accordance with the animal study, in vitro results revealed that the lack of CNR2 in CD4+ cells elevated IL-10 production, and CB2 activation inhibited CD4+ T cell–derived IL-10 production. Furthermore, in the clinical environment, septic patients expressed enhanced CB2 mRNA levels compared with healthy donors in PBMCs, and their CB2 expression was inversely correlated with IL-10. These results suggested that the activation of CD4+ T cell–derived CB2 increased susceptibility to sepsis through inhibiting IL-10 production.
Extracellular Nucleotides and Histamine Suppress TLR3- and RIG-I–Mediated Release of Antiviral IFNs from Human Airway Epithelial Cells
Authors: Kountz Timothy S , Biyasheva Assel , Schleimer Robert P , Prakriya Murali 
Published: July 2022

Abstract
Respiratory viruses stimulate the release of antiviral IFNs from the airway epithelium. Previous studies have shown that asthmatic patients show diminished release of type I and type III IFNs from bronchial epithelia. However, the mechanism of this suppression is not understood. In this study, we report that extracellular nucleotides and histamine, which are elevated in asthmatic airways, strongly inhibit release of type I and type III IFNs from human bronchial airway epithelial cells (AECs). Specifically, ATP, UTP, and histamine all inhibited the release of type I and type III IFNs from AECs induced by activation of TLR3, retinoic acid–inducible gene I (RIG-I), or cyclic GMP-AMP synthase–STING. This inhibition was at least partly mediated by Gq signaling through purinergic P2Y2 and H1 receptors, but it did not involve store-operated calcium entry. Pharmacological blockade of protein kinase C partially reversed inhibition of IFN production. Conversely, direct activation of protein kinase C with phorbol esters strongly inhibited TLR3- and RIG-I–mediated IFN production. Inhibition of type I and type III IFNs by ATP, UTP, histamine, and the proteinase-activated receptor 2 (PAR2) receptor agonist SLIGKV also occurred in differentiated AECs grown at an air–liquid interface, indicating that the suppression is conserved following mucociliary differentiation. Importantly, histamine and, more strikingly, ATP inhibited type I IFN release from human airway cells infected with live influenza A virus or rhinovirus 1B. These results reveal an important role for extracellular nucleotides and histamine in attenuating the induction of type I and III IFNs from AECs and help explain the molecular basis of the suppression of IFN responses in asthmatic patients.
Type I IFN Signaling Is Essential for Preventing IFN-γ Hyperproduction and Subsequent Deterioration of Antibacterial Immunity during Postinfluenza Pneumococcal Infection
Authors: Palani Sunil , Bansal Shruti , Verma Atul K , Bauer Christopher , Shao Shengjun , Uddin Md Bashir , Sun Keer 
Published: July 2022

Abstract
Postinfluenza bacterial pneumonia is a significant cause of hospitalization and death in humans. The mechanisms underlying this viral and bacterial synergy remain incompletely understood. Recent evidence indicates that influenza-induced IFNs, particularly type I IFN (IFN-I) and IFN-γ, suppress antibacterial defenses. In this study, we have investigated the relative importance and interplay of IFN-I and IFN-γ pathways in influenza-induced susceptibility to Streptococcus pneumoniae infection. Using gene-deficient mouse models, as well as in vivo blocking Abs, we show that both IFN-I and IFN-γ signaling pathways contribute to the initial suppression of antibacterial immunity; however, IFN-γ plays a dominant role in the disease deterioration, in association with increased TNF-α production and alveolar macrophage (AM) depletion. We have previously shown that IFN-γ impairs AM antibacterial function and thereby acute bacterial clearance. The findings in this study indicate that IFN-γ signaling also impairs AM viability and αβ T cell recruitment during the progression of influenza/S. pneumoniae coinfection. Macrophages insensitive to IFN-γ mice express a dominant-negative mutant IFN-γR in mononuclear phagocytes. Interestingly, macrophages insensitive to IFN-γ mice exhibited significantly improved recovery and survival from coinfection, despite delayed bacterial clearance. Importantly, we demonstrate that IFN-I receptor signaling is essential for preventing IFN-γ hyperproduction and animal death during the progression of postinfluenza pneumococcal pneumonia.