bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hepatic steatosis and liver fat contents in liver transplant recipients are associated with serum adipokines and insulin resistance
Authors: Eshraghian Ahad , Nikeghbalian Saman , Shamsaeefar Alireza , Kazemi Kourosh , Fattahi Mohammad Reza , Malek-Hosseini Seyed Ali 
Published: July 2020

AbstractOur data about pathogenesis of hepatic steatosis after liver transplantation is scarce. This study aimed to investigate the association between serum adipokines and insulin resistance with hepatic steatosis in liver transplant recipients. We investigated the association between insulin resistance, serum adiponectin, insulin, and leptin with hepatic steatosis in a cohort of liver transplant recipients. Homeostatic model assessment of insulin resistance 2 (HOMA 2-IR) was used for estimation of insulin resistance. Hepatic steatosis was determined using ultrasound and controlled attenuation parameter (CAP). A total of 178 patients were included. 79 patients (44.4%) had hepatic steatosis. Serum adiponectin (OR: 0.912; 95% CI 0.869–0.957; P < 0.001), serum leptin (OR: 1.060; 95% CI 1.017–1.102; P = 0.005), HOMA2-IR (OR: 1.671; 95% CI 1.049–2.662; P = 0.031), and post-transplant diabetes mellitus (PTDM) (OR: 5.988; 95% CI 1.680–21.276; P = 0.006) were independently associated with hepatic steatosis after liver transplantation. CAP values were negatively correlated with serum adiponectin (P = 0.011) and positively correlated with serum insulin (P = 0.001), leptin (P < 0.001) and HOMA2-IR (P < 0.001). Insulin resistance and alterations in adipokines might have central role in pathogenesis of hepatic steatosis after liver transplantation and can be targeted for diagnostic and therapeutic purposes.
Factors controlling the spatial distribution of soil organic carbon in Daxing’anling Mountain
Authors: Li Junyao , Zhang Dongyou , Liu Mei 
Published: July 2020

AbstractDaxing’anling Mountain, in the northeastern part of China, contains a large amount of soil organic carbon (SOC). Using data including topography, climate, and vegetation, the spatial distribution of SOC content was modeled using classical and geography-based statistics, as well as a geographically weighted kriging model. The study findings include: (1) SOC content generally ranges 40–70 g/kg, with high SOC content in the southwest and low SOC content in the southeast; (2) Results of principal component analysis suggested the normalized difference vegetation index is the best predictor of patterns in SOC; and (3) The geo-weighted regression Kriging model well reflects factors influencing spatial distribution of SOC content. This study provides important baseline information for environmental protection in the Daxing’anling Mountain area, as well as general information as to important factors that mediate this important reservoir of soil carbon.
Toll-like receptor dual-acting agonists are potent inducers of PBMC-produced cytokines that inhibit hepatitis B virus production in primary human hepatocytes
Authors: Janovec Vaclav , Hodek Jan , Clarova Kamila , Hofman Tomas , Dostalik Pavel , Fronek Jiri , Chlupac Jaroslav , Chaperot Laurence , Durand Sarah , Baumert Thomas F. , Pichova Iva , Lubyova Barbora , Hirsch Ivan , Weber Jan 
Published: July 2020

AbstractRecombinant interferon-α (IFN-α) treatment functionally cures chronic hepatitis B virus (HBV) infection in some individuals and suppresses virus replication in hepatocytes infected in vitro. We studied the antiviral effect of conditioned media (CM) from peripheral blood mononuclear cells (PBMCs) stimulated with agonists of Toll-like receptors (TLRs) 2, 7, 8 and 9. We found that CM from PBMCs stimulated with dual-acting TLR7/8 (R848) and TLR2/7 (CL413) agonists were more potent drivers of inhibition of HBe and HBs antigen secretion from HBV-infected primary human hepatocytes (PHH) than CM from PBMCs stimulated with single-acting TLR7 (CL264) or TLR9 (CpG-B) agonists. Inhibition of HBV in PHH did not correlate with the quantity of PBMC-produced IFN-α, but it was a complex function of multiple secreted cytokines. More importantly, we found that the CM that efficiently inhibited HBV production in freshly isolated PHH via various cytokine repertoires and mechanisms did not reduce covalently closed circular (ccc)DNA levels. We confirmed our data with a cell culture model based on HepG2-NTCP cells and the plasmacytoid dendritic cell line GEN2.2. Collectively, our data show the importance of dual-acting TLR agonists inducing broad cytokine repertoires. The development of poly-specific TLR agonists provides novel opportunities towards functional HBV cure.
Inhibition of acetyl-CoA carboxylase by spirotetramat causes growth arrest and lipid depletion in nematodes
Authors: Gutbrod Philipp , Gutbrod Katharina , Nauen Ralf , Elashry Abdelnaser , Siddique Shahid , Benting Jürgen , Dörmann Peter , Grundler Florian M. W. 
Published: July 2020

AbstractPlant-parasitic nematodes pose a significant threat to agriculture causing annual yield losses worth more than 100 billion US$. Nematode control often involves the use of nematicides, but many of them including non-selective fumigants have been phased out, particularly due to ecotoxicological concerns. Thus new control strategies are urgently needed. Spirotetramat (SPT) is used as phloem-mobile systemic insecticide targeting acetyl-CoA carboxylase (ACC) of pest insects and mites upon foliar application. However, in nematodes the mode of action of SPT and its effect on their development have not been studied so far. Our studies revealed that SPT known to be activatedin plantato SPT-enol acts as a developmental inhibitor of the free-living nematodeCaenorhabditis elegansand the plant-parasitic nematodeHeterodera schachtii. Exposure to SPT-enol leads to larval arrest and disruption of the life cycle. Furthermore, SPT-enol inhibits nematode ACC activity, affects storage lipids and fatty acid composition. Silencing ofH. schachtii ACCby RNAi induced similar phenotypes and thus mimics the effects of SPT-enol, supporting the conclusion that SPT-enol acts on nematodes by inhibiting ACC. Our studies demonstrated that the inhibition of de novo lipid biosynthesis by interfering with nematode ACC is a new nematicidal mode of action addressed by SPT, a well-known systemic insecticide for sucking pest control.
CD122-targetted IL-2 signals cause acute and selective apoptosis of B cells in Peyer’s Patches
Authors: Singh Ayushi , Dhume Kunal , Tejero Joanne D. , Strutt Tara M. , McKinstry K. Kai 
Published: July 2020

AbstractInterleukin-2 (IL-2) has both pro- and anti-inflammatory properties that have been harnessed clinically and that are used experimentally to modulate leukocyte subsets in vivo. In mice, the bioavailability and half-life of IL-2 in vivo can be increased by complexing recombinant IL-2 with different clones of anti-IL-2 monoclonal antibodies that differentially target the cytokine to cells expressing different kinds of IL-2 receptors. While the impacts of systemic IL-2: anti-IL-2 antibody complex (IL-2C) administration are well-defined in the spleen and peripheral lymph nodes, how immune cells in the gut and gut-associated lymphoid tissues respond to IL-2C is not well characterized. Here, we analyze how major leukocyte populations in these tissues respond to IL-2C. We find that IL-2C targeting cells expressing IL-2 receptor beta cause an acute decrease in cellularity of Peyer’s Patches while cell numbers in the lamina propria and intraepithelial lymphocytes are unaffected. Cell contraction in Peyer’s Patches is associated with the apoptosis of multiple B cell subsets. Our results are important to consider for understanding off-target impacts of IL-2C regimes in experimental models and for considering how IL-2 may contribute to the etiology or severity of gut-associated conditions such as Crohn’s Disease.
MITF variants cause nonsyndromic sensorineural hearing loss with autosomal recessive inheritance
Authors: Thongpradit Supranee , Jinawath Natini , Javed Asif , Noojarern Saisuda , Khongkraparn Arthaporn , Tim-Aroon Thipwimol , Lertsukprasert Krisna , Suktitipat Bhoom , Jensen Laran T. , Wattanasirichaigoon Duangrurdee 
Published: July 2020

AbstractMITF is a known gene underlying autosomal dominant hearing loss, Waardenburg syndrome (WS). Biallelic MITF mutations have been found associated with a rare hearing loss syndrome consisting eye abnormalities and albinism; and a more severe type of WS whose heterozygous parents were affected with classic WS in both cases. The aims of this study were to identify a new candidate gene causing autosomal recessive nonsyndromic hearing loss (ARNSHL) and confirm its causation by finding additional families affected with the candidate gene and supporting evidences from functional analyses. By using whole exome sequencing, we identified a homozygous c.1022G>A: p.Arg341His variant of MITF, which co-segregated with the hearing loss in five affected children of a consanguineous hearing couple. Targeted exome sequencing in a cohort of 130 NSHL individuals, using our in-house gene panel revealed a second family with c.1021C>T: p.Arg341Cys MITF variant. Functional studies confirmed that the Arg341His and Arg341Cys alleles yielded a normal sized MITF protein, with aberrant cytosolic localization as supported by the molecular model and the reporter assay. In conclusion, we demonstrate MITF as a new cause of ARNSHL, with heterozygous individuals free of symptoms. MITF should be included in clinical testing for NSHL, though it is rare.
Photocatalytic degradation of methylene blue with spent FCC catalyst loaded with ferric oxide and titanium dioxide
Authors: Xu Jiasheng , Zhang Te , Zhang Jie 
Published: July 2020

AbstractThe spent fluid catalytic cracking (FCC) catalyst has been loaded with ferric oxide (Fe2O3) and titanium dioxide (TiO2). Fe-Ti/SF composite (loaded with 5 wt% TiO2 and 5 wt% Fe2O3), Fe/SF composite (loaded with10 wt% Fe2O3) and Ti/SF composite (loaded with 10 wt% TiO2) have been fabricated via a modified-impregnation method. The band gaps of the Fe-Ti/SF, Fe/SF and Ti/SF composites (evaluated by the energy versus [F(R∞)hv]n) are 2.23, 1.98 and 3.0 eV, respectively. Electrochemical impedance spectroscopy shows that the Fe-Ti/SF has lower electron transfer resistance, it has the small charge transfer resistance and fast charge transfer rate. The interparticle electrons transfer between the Fe2O3 and TiO2, which can improve the separation of the photo-electrons and holes. The holes transfer from valence band of TiO2 to the valence band of Fe2O3, which can provide more active sites around the adsorbed molecules. The methylene blue degradation efficiencies (with the Fe-Ti/SF, Fe/SF and Ti/SF composites) are ~ 94.2%, ~ 22.3% and ~ 54.0% in 120 min, respectively. This work reveals that the spent FCC catalyst as supporter can be loaded with Fe2O3 and TiO2. This composite is highly suitable for degradation of methylene blue, which can provide a potential method to dispose the spent FCC catalyst in industry.
Development and long-term evaluation of a new 68Ge/68Ga generator based on nano-SnO2 for PET imaging
Authors: Romero Eduardo , Martínez Alfonso , Oteo Marta , Ibañez Marta , Santos Mirentxu , Morcillo Miguel Ángel 
Published: July 2020

AbstractRadionuclide generator systems can routinely provide radionuclides on demand such as 68Ga produced by a 68Ge/68Ga generator without the availability of an on-site accelerator or a research reactor. Thus, in this work nano-SnO2 was used to develop a new 68Ge/68Ga generator which was evaluated over a period of 17 months and 305 elution cycles. The elution yield was 91.1 ± 1.8% in the first 7 mL (1 M HCl as eluent) when the generator was new and then it decreased with time and use to 73.8 ± 1.9%. Around 80% of the elutable 68Ga activity was obtained in 1 mL and the 68Ge content in the eluate did not exceed 1 × 10–4% over the investigation period when it was eluted regularly. The described generator provided adequate results for radiolabelling of DOTA-TOC with direct use of eluate. In addition, [68Ga]Ga-DOTA-TOC was tested satisfactorily for in vivo tumor detection by microPET/CT imaging in a lung cancer mouse model.
Genetic tropicalisation following a marine heatwave
Authors: Coleman Melinda A. , Minne Antoine J. P. , Vranken Sofie , Wernberg Thomas 
Published: July 2020

AbstractExtreme events are increasing globally with devastating ecological consequences, but the impacts on underlying genetic diversity and structure are often cryptic and poorly understood, hindering assessment of adaptive capacity and ecosystem vulnerability to future change. Using very rare “before” data we empirically demonstrate that an extreme marine heatwave caused a significant poleward shift in genetic clusters of kelp forests whereby alleles characteristic of cool water were replaced by those that predominated in warm water across 200 km of coastline. This “genetic tropicalisation” was facilitated by significant mortality of kelp and other co-occurring seaweeds within the footprint of the heatwave that opened space for rapid local proliferation of surviving kelp genotypes or dispersal and recruitment of spores from warmer waters. Genetic diversity declined and inbreeding increased in the newly tropicalised site, but these metrics were relative stable elsewhere within the footprint of the heatwave. Thus, extreme events such as marine heatwaves not only lead to significant mortality and population loss but can also drive significant genetic change in natural populations.
Genetic diversity and population structure of Aedes aegypti after massive vector control for dengue fever prevention in Yunnan border areas
Authors: Lv Rui-chen , Zhu Chang -qiang , Wang Chun-hui , Ai Le-le , Lv Heng , Zhang Bing , Li Chun-min , An Jing , Wang Pei-gang , Hu Dan , Tan Xian-zhe , Yang Lu , Zhou Hong-ning , Tan Wei-long 
Published: July 2020

AbstractDengue fever is a mosquito-borne disease caused by the dengue virus. Aedes aegypti (Ae. Aegypti) is considered the primary vector of Dengue virus transmission in Yunnan Province, China. With increased urbanization, Ae. aegypti populations have significantly increased over the last 20 years. Despite all the efforts that were made for controlling the virus transmission, especially on border areas between Yunnan and Laos, Vietnam, and Myanmar (dengue-endemic areas), the epidemic has not yet been eradicated. Thus, further understanding of the genetic diversity, population structure, and invasive strategies of Ae. aegypti populations in the border areas was vital to uncover the vector invasion and distribution dynamic, and essential for controlling the infection. In this study, we analyzed genetic diversity and population structure of eight adult Ae. Aegypti populations collected along the border areas of Yunnan Province in 2017 and 2018. Nine nuclear microsatellite loci and mitochondrial DNA (mtDNA) sequences were used to achieve a better understanding of the genetic diversity and population structure. One hundred and fourteen alleles were found in total. The polymorphic information content value, together with the expected heterozygosity (He) and observed heterozygosity (Ho) values showed high genetic diversity in all mosquito populations. The clustering analysis based on Bayesian algorithm, the UPGMA and DAPC analysis revealed that all the eight Ae. aegypti populations can be divided into three genetic groups. Based on the mtDNA results, all Ae. aegypti individuals were divided into 11 haplotypes. The Ae. aegypti populations in the border areas of Yunnan Province presented with high genetic diversity, which might be ascribed to the continuous incursion of Ae. aegypti.
NHF-derived carbon dots: prevalidation approach in breast cancer treatment
Authors: Tiron Crina Elena , Luta Gabriel , Butura Mihail , Zugun-Eloae Florin , Stan Corneliu S. , Coroaba Adina , Ursu Elena-Laura , Stanciu Gabriela Dumitrita , Tiron Adrian 
Published: July 2020

AbstractMetastatic breast cancer dominates the female cancer-related mortality. Tumour-associated molecules represents a crucial for early disease detection and identification of novel therapeutic targets. Nanomaterial technologies provide promising novel approaches to disease diagnostics and therapeutics. In the present study we extend the investigations of antitumoral properties of Carbon Dots prepared from N-hydroxyphthalimide (CD-NHF) precursor. We evaluate the effect of CD-NHF on tumour cell migration and invasion in vitro and their impact on tumour progression using an in vivo model. Furthermore, we investigate the molecular mechanisms involved in CD-NHF antitumour effects. In vivo mammary tumours were induced in Balb/c female mice by injecting 4T1 cells into the mammary fat pad. Conditional treatment with CD-NHF significantly impair both migration and invasion of metastatic breast cancer cells. The presence of CD-NHF within the 3D cell cultures strongly inhibited the malignant phenotype of MDA-MB-231, 4T1 and MCF-7 cells in 3D culture, resulting in culture colonies lacking invasive projections and reduction of mammospheres formation. Importantly, breast tumour growth and metastasis dissemination was significantly reduced upon CD-NHF treatments in a syngeneic mouse model and is associated with down-regulation of Ki67 and HSP90 expression. CD-NHF nanostructures provide exciting perspective for improving treatment outcome in breast cancer.
Fatty acid mimetic PBI-4547 restores metabolic homeostasis via GPR84 in mice with non-alcoholic fatty liver disease
Authors: Simard Jean-Christophe , Thibodeau Jean-François , Leduc Martin , Tremblay Mikael , Laverdure Alexandre , Sarra-Bournet François , Gagnon William , Ouboudinar Jugurtha , Gervais Liette , Felton Alexandra , Letourneau Sylvie , Geerts Lilianne , Cloutier Marie-Pier , Hince Kathy , Corpuz Ramon , Blais Alexandra , Quintela Vanessa Marques , Duceppe Jean-Simon , Abbott Shaun D. , Blais Amélie , Zacharie Boulos , Laurin Pierre , Laplante Steven R. , Kennedy Christopher R. J. , Hébert Richard L. , Leblond François A. , Grouix Brigitte , Gagnon Lyne 
Published: July 2020

AbstractNon-alcoholic Fatty Liver Disease (NAFLD) is the most common form of liver disease and is associated with metabolic dysregulation. Although G protein-coupled receptor 84 (GPR84) has been associated with inflammation, its role in metabolic regulation remains elusive. The aim of our study was to evaluate the potential of PBI-4547 for the treatment of NAFLD and to validate the role of its main target receptor, GPR84. We report that PBI-4547 is a fatty acid mimetic, acting concomitantly as a GPR84 antagonist and GPR40/GPR120 agonist. In a mouse model of diet-induced obesity, PBI-4547 treatment improved metabolic dysregulation, reduced hepatic steatosis, ballooning and NAFLD score. PBI-4547 stimulated fatty acid oxidation and induced gene expression of mitochondrial uncoupling proteins in the liver. Liver metabolomics revealed that PBI-4547 improved metabolic dysregulation induced by a high-fat diet regimen. In Gpr84−/− mice, PBI-4547 treatment failed to improve various key NAFLD-associated parameters, as was observed in wildtype littermates. Taken together, these results highlight a detrimental role for the GPR84 receptor in the context of meta-inflammation and suggest that GPR84 antagonism via PBI-4547 may reflect a novel treatment approach for NAFLD and its related complications.
Stress loading history of earthquake faults influenced by fault/shear zone geometry and Coulomb pre-stress
Authors: Sgambato Claudia , Faure Walker Joanna Phoebe , Mildon Zoë Keiki , Roberts Gerald Patrick 
Published: July 2020

AbstractWhether the stress-loading of faults to failure in earthquakes appears to be random or to an extent explainable, given constraints on fault/shear-zone interaction and the build-up and release of stress over many earthquake cycles, is a key question for seismic hazard assessment. Here we investigate earthquake recurrence for a system of 25 active normal faults arranged predominantly along strike from each other, allowing us to isolate the effects of stress-loading due to regional strain versus across- and along-strike fault interaction. We calculate stress changes over 6 centuries due to interseismic loading and 25 > Mw 5.5 earthquakes. Where only one fault exists across strike, stress-loading is dominated by the regional tectonics through slip on underlying shear zones and fault planes have spatially smooth stress with predominantly time-dependent stress increase. Conversely, where faults are stress-loaded by across-strike fault interactions, fault planes have more irregular stress patterns and interaction-influenced stress loading histories. Stress-loading to failure in earthquakes is not the same for all faults and is dependent on the geometry of the fault/shear-zone system.
Serum levels of cytokines in infants treated with conbercept for retinopathy of prematurity
Authors: Cheng Yong , Zhu Xuemei , Linghu Dandan , Xu Yongsheng , Liang Jianhong 
Published: July 2020

AbstractIntravitreal anti-vascular endothelial growth factor (VEGF) agents have revolutionized the treatment of retinopathy of prematurity (ROP); however, there are concerns regarding the potential systemic complications caused by those treatments. This study aimed to determine the serum concentrations of cytokines in infants with ROP and to evaluate the changes in serum VEGF concentrations after intravitreal conbercept (IVC). Sixty infants with ROP treated with IVC 0.25 mg were included. Blood samples were collected before treatment as well as 1 week and 4 weeks after treatment. Serum levels of 45 types of cytokines were measured by a multiplex bead assay. We observed that IVC 0.25 mg in ROP patients suppressed the circulating levels of VEGF-A and VEGF-D as of 1 week after injection, and these growth factor levels returned to baseline at 4 weeks. No significant differences were observed in the serum levels of the other cytokines between baseline and 1 or 4 weeks after IVC.
PTEN suppresses epithelial–mesenchymal transition and cancer stem cell activity by downregulating Abi1
Authors: Qi Yanmei , Liu Jie , Chao Joshua , Scheuerman Mark P. , Rahimi Saum A. , Lee Leonard Y. , Li Shaohua 
Published: July 2020

AbstractThe epithelial–mesenchymal transition (EMT) is an embryonic program frequently reactivated during cancer progression and is implicated in cancer invasion and metastasis. Cancer cells can also acquire stem cell properties to self-renew and give rise to new tumors through the EMT. Inactivation of the tumor suppressor PTEN has been shown to induce the EMT, but the underlying molecular mechanisms are less understood. In this study, we reconstituted PTEN-deficient breast cancer cells with wild-type and mutant PTEN, demonstrating that restoration of PTEN expression converted cancer cells with mesenchymal traits to an epithelial phenotype and inhibited cancer stem cell (CSC) activity. The protein rather than the lipid phosphatase activity of PTEN accounts for the reversal of the EMT. PTEN dephosphorylates and downregulates Abi1 in breast cancer cells. Gain- and loss-of-function analysis indicates that upregulation of Abi1 mediates PTEN loss-induced EMT and CSC activity. These results suggest that PTEN may suppress breast cancer invasion and metastasis via dephosphorylating and downregulating Abi1.