bluuebunny/crossref_metadata_2025_split huggingface dataset:
Inhibition of Lactobacillus fermentum SHY10 on the white membrane production of soaked pickled radish
Authors: Yang Yang , Lian Yinyin , Yin Shimei , Suo Huayi , Zeng Fankun , Wang Hongwei , Song Jiajia , Zhang Yu 
Published: March 2022

AbstractThe formation of white bio‐membrane (shenghua) on the surface of pickle leads to uneatable and spoiled products, which has been the key problem restricting the development of Sichuan pickle industry. In this study, the 17 microorganisms in the white membrane of pickled radish were screened and identified, of which Candida parapsilosis was the main strain causing ”shenghua“. The membrane‐forming ability of Candida parapsilosis was determined by crystal violet staining to explore its adaptability to the fermentation environment concerning temperature and oxygen. It was found that Candida parapsilosis had the strongest membrane‐forming capacity under the aerobic condition at 37°C, with the highest OD595 nm value reached to 3.473 ± 0.07 at 72 h post inoculation. This research identified Lactobacillus fermentum SHY10 to be the inhibitor of the membrane production of Candida parapsilosis via the Oxford cup method on a Petri dish, and via co‐inoculation with Candida parapsilosis in pickles. Furthermore, this study specified that the cell‐free supernatant (CFS) of L. fermentum SHY10 had the most significant inhibitory effects and likely to result from protein substances in the CFS. Proteases treated CFS had significantly reduced inhibitory effects against membrane formation, which confirmed that the active component was protein substances. Overall, this study identified a functional LAB strain with significant inhibitory effects against the white membrane formation in pickles, which provide a safe and consumer‐friendly solution for the membrane problem in the fermented vegetable industry.
VIX option‐implied volatility slope and VIX futures returns
Authors: Yoon Jungah , Ruan Xinfeng , Zhang Jin E. 
Published: March 2022

AbstractThis paper documents the dynamics of the term structure of the implied volatility (IV) smirk of Chicago Board Options Exchange Volatility Index (VIX) options. Empirical analysis shows that VIX option–IV slope predicts VIX futures returns over the next day to month, outperforms existing investors' perception proxies in the stock and option markets. The empirical finding is rationalized through time‐varying correlation between the VIX and volatility of VIX (VVIX), VIX jumps, and investors' net positions in VIX futures market.
Secondary analyses for genome‐wide association studies using expression quantitative trait loci
Authors: Ngwa Julius S. , Yanek Lisa R. , Kammers Kai , Kanchan Kanika , Taub Margaret A. , Scharpf Robert B. , Faraday Nauder , Becker Lewis C. , Mathias Rasika A. , Ruczinski Ingo 
Published: March 2022

AbstractGenome‐wide association studies (GWAS) have successfully identified thousands of single nucleotide polymorphisms (SNPs) associated with complex traits; however, the identified SNPs account for a fraction of trait heritability, and identifying the functional elements through which genetic variants exert their effects remains a challenge. Recent evidence suggests that SNPs associated with complex traits are more likely to be expression quantitative trait loci (eQTL). Thus, incorporating eQTL information can potentially improve power to detect causal variants missed by traditional GWAS approaches. Using genomic, transcriptomic, and platelet phenotype data from the Genetic Study of Atherosclerosis Risk family‐based study, we investigated the potential to detect novel genomic risk loci by incorporating information from eQTL in the relevant target tissues (i.e., platelets and megakaryocytes) using established statistical principles in a novel way. Permutation analyses were performed to obtain family‐wise error rates for eQTL associations, substantially lowering the genome‐wide significance threshold for SNP‐phenotype associations. In addition to confirming the well known association between PEAR1 and platelet aggregation, our eQTL‐focused approach identified a novel locus (rs1354034) and gene (ARHGEF3) not previously identified in a GWAS of platelet aggregation phenotypes. A colocalization analysis showed strong evidence for a functional role of this eQTL.
Transcriptomic profiling of a multiethnic pediatric NAFLD cohort reveals genes and pathways associated with disease
Authors: Yao Kangning , Tarabra Elena , Sia Daniela , Morotti Raffaella , Fawaz Rima , Valentino Pamela , Santoro Nicola , Caprio Sonia , Liu Silvia , Yimlamai Dean 
Published: March 2022

Abstract
Nonalcoholic fatty liver disease (NAFLD) is the most common type of chronic liver disease in children. The mechanisms that drive NAFLD disease progression in this specific patient population remain poorly defined. In this study, we obtained liver biopsy samples from a multiethnic cohort of pediatric patients with NAFLD (n = 52, mean age = 13.6 years) and healthy liver controls (n = 5). We analyzed transcriptomic changes associated with NAFLD stages using high‐throughput RNA sequencing. Unsupervised clustering as well as pairwise transcriptome comparison distinguished NAFLD from healthy livers. We identified perturbations in pathways including calcium and insulin/glucose signaling occurring early in NAFLD disease, before the presence of histopathologic evidence of advanced disease. Transcriptomic comparisons identified a 25‐gene signature associated with the degree of liver fibrosis. We also identified expression of the insulin‐like growth factor binding protein (IGFBP) gene family (1/2/3/7) as correlating with disease stages, and it has the potential to be used as a peripheral biomarker in NAFLD. Comparing our data set with publicly available adult and adolescent transcriptomic data, we identified similarities and differences in pathway enrichment and gene‐expression profiles between adult and pediatric patients with NAFLD. Regulation of genes including interleukin‐32, IGFBP1, IGFBP2, and IGFBP7 was consistently found in both NAFLD populations, whereas IGFBP3 was specific to pediatric NAFLD. Conclusion: This paper expands our knowledge on the molecular mechanisms underlying pediatric NAFLD. It identifies potential biomarkers and directs us toward new therapies in this population.
Investment opportunities in the energy market: What can be learnt from different energy sectors
Authors: Uddin Gazi Salah , Sahamkhadam Maziar , Yahya Muhammad , Tang Ou 
Published: March 2022

AbstractWe construct portfolio strategies consisting of different stocks from four main energy market sectors, including oil and gas, oil and gas related equipment and services, multiline utilities and renewable energy. To construct portfolio strategies, we first forecast assets' returns by using multivariate copula models. These forecasting frameworks enable us to undertake both symmetric and asymmetric tail connectedness in simulating from the joint distribution. Second, we applied four major risk measures including volatility, mean absolute deviation, conditional value‐at‐risk and conditional drawdown‐at‐Risk. Our findings indicate that the consideration of homogeneity of oil and gas sector and oil and gas related equipment and services sector, together with the heterogeneity of multiline utilities sector and renewable energy sector should lead to information decoupling among these sectors, thereby providing portfolio diversification. The mixed copula model results in better out‐of‐sample economic performance, indicating the advantage obtained from modelling both symmetric and asymmetric tail dependence. Our analysis of the portfolio weights, among the energy market sectors, shows that for optimal portfolios, multiline utilities and renewable energy sectors constitute higher portion of the invested assets. The study results provide an encouraging guideline for developing renewable energy sector from the perspective of financial market.
Special issue editorial: Revitalisation of dynamic riverine landscapes—Evaluation of the effects of hydromorphological restoration measures
Authors: Schulz‐Zunkel Christiane , Dziock Frank , Seele‐Dilbat Carolin , Bondar‐Kunze Elisabeth , Scholz Mathias 
Published: March 2022

AbstractThe progressive loss of biodiversity in rivers and their floodplains has not yet been stopped. With the European Biodiversity Strategy and the goal of restoring at least 25,000 km of free‐flowing European rivers by 2030, the first important step has been taken. Now we need to be able to effectively demonstrate a reversal of biodiversity loss as well as the success of urgently needed restoration measures. This special issue presents twelve results of current river and floodplain restoration and evaluation approaches that have successfully combined hydromorphological restoration measures with interdisciplinary research. We report comprehensively on the challenges and opportunities that river and floodplain restoration can offer to protect the biodiversity and ecosystem functioning of these habitats.
Friends know you: Peer nomination of self‐control predict changes in academic achievement and friendship among adolescents
Authors: Park Daeun , Tsukayama Eli , Galla Brian M. 
Published: March 2022

AbstractIntroductionSelf‐control predicts academic achievement and social outcomes in adolescents. Despite the increased role of peers in the lives of adolescents, little is known about whether peers' views of an individual's self‐control have predictive validity for academic and social outcomes.MethodIn a longitudinal study involving over 1500 adolescents (Mage = 13.74), we examined whether peer nomination of self‐control provides incremental predictive validity over and above self‐reports for rank‐order changes in academic achievement and friendship (i.e., the total number of nominations received as a best friend). To do so, we followed 8th graders through the 9th grade, measuring self‐reported self‐control (academic vs. social), peer‐nominated self‐control (academic vs. social), grade point average, and friendship.ResultsPeer‐nominated academic self‐control predicted rank‐order changes in grade point average and peer‐nominated interpersonal self‐control predicted rank‐order changes in friendship over and above self‐reported academic and interpersonal self‐control.ConclusionOur findings demonstrate the predictive utility of peer nominations in research on self‐control.
New insights into arsenic, lead, and iron neurotoxicity: Activation of MAPK signaling pathway and oxidative stress
Authors: Khedr Naglaa F. , Talkan Ola F. A. 
Published: March 2022

AbstractToxic metals cause neurodegeneration via formation of toxic complexes with the cellular compounds and production of highly reactive oxygen species. The present study aimed to investigate the role of mitogen‐activated protein kinase (MAPK) signaling pathway in iron, lead, and arsenic induced neurotoxicity. Also, to explore their effect on brain enzymes, inducible nitric oxide synthase (iNOS) and nuclear factor κB (NF‐κB) in rat brains. Rats were divided into four groups (n = 8): Control group, lead group (30 mg/kg lead acetate), arsenic group (5 mg/kg sodium arsenite), and iron group (100 mg/kg ferric hydroxide). Treatments were given three times/week orally for 2 months. Brain tissues were assessed for reduced glutathione and malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD), alkaline phosphatase (ALP), acid phosphatase (ACP), Na+/K+activated adenosine 5′‐triphosphatase (Na+/K+‐ATPase) and acetylcholinesterase (AChE) activities, expression of iNOS and NF‐κB, and Western blot analysis of c‐Jun NH(2)‐terminal kinase (JNK) and extracellular signal‐regulated protein kinase (ERK) proteins. Levels of arsenic, iron, and lead were significantly (p = 0.000) increased in blood and brain tissues. Levels of MDA, SOD, CAT, iNOS, and NF‐κB gene expression, phosphorylated JNK and phosphorylated ERK proteins were increased significantly in lead, arsenic, and iron treated rat groups compared to control. ALP, ACP, AChE, and ATPase activities in brain were significantly altered in metal‐treated rat groups compared to control. Iron, lead, and arsenic induced neurotoxicity activated the pro‐inflammatory mediators NF‐κB, iNOS, and MAPK pathway and altered the activity of brain ALP, ACP, Na+/K+‐ATPase, CAT, SOD, and AChE.
HEPES‐buffering of bicarbonate‐containing culture medium perturbs lysosomal glucocerebrosidase activity
Authors: van der Lienden Martijn J. C. , Aten Jan , Boot Rolf G. , van Eijk Marco , Aerts Johannes M. F. G. , Kuo Chi‐Lin 
Published: March 2022

AbstractGlucocerebrosidase (GCase), encoded by the GBA gene, degrades the ubiquitous glycosphingolipid glucosylceramide. Inherited GCase deficiency causes Gaucher disease (GD). In addition, carriers of an abnormal GBA allele are at increased risk for Parkinson's disease. GCase undergoes extensive modification of its four N‐glycans en route to and inside the lysosome that is reflected in changes in molecular weight as detected with sodium dodecyl sulfate‐polyacrylamide gel electrophoresis. Fluorescent activity‐based probes (ABPs) that covalently label GCase in reaction‐based manner in vivo and in vitro allow sensitive visualization of GCase molecules. Using these ABPs, we studied the life cycle of GCase in cultured fibroblasts and macrophage‐like RAW264.7 cells. Specific attention was paid to the impact of 4‐(2‐hydroxyethyl)‐1‐piperazineethanesulfonic acid (HEPES) supplementation to bicarbonate‐buffered medium. Here, we report how HEPES‐buffered medium markedly influences processing of GCase, its lysosomal degradation, and the total cellular enzyme level. HEPES‐containing medium was also found to reduce maturation of other lysosomal enzymes (α‐glucosidase and β‐glucuronidase) in cells. The presence of HEPES in bicarbonate containing medium increases GCase activity in GD‐patient derived fibroblasts, illustrating how the supplementation of HEPES complicates the use of cultured cells for diagnosing GD.
Hsa_circ_0007142 contributes to cisplatin resistance in esophageal squamous cell carcinoma via miR‐494‐3p/LASP1 axis
Authors: Chang Na , Ge Ning , Zhao Yufei , Yang Liu , Qin Wei , Cui Yayun 
Published: March 2022

AbstractBackgroundChemoresistance is one of the major obstacles for tumor treatment. Circular RNAs (circRNAs) have been confirmed to play vital roles in chemoresistance of cancer, including esophageal squamous cell carcinoma (ESCC). We investigated the roles and mechanisms of circ_0007142 in cisplatin (DDP) resistance of ESCC.MethodsQuantitative real‐time polymerase chain reaction (qRT‐PCR) was conducted to determine the levels of circ_0007142, DOCK1 mRNA, microRNA‐494‐3p (miR‐494‐3p) and LIM And SH3 Protein 1 (LASP1) mRNA. RNase R assay was conducted to analyze the characteristic of circ_0007142. Cell Counting Kit‐8 (CCK‐8) assay was performed to evaluate IC50 of DDP. Flow cytometry analysis, 5‐ethynyl‐2’‐deoxyuridine (EdU) assay and transwell assay were carried out to examine cell apoptosis, proliferation and invasion, respectively. Dual‐luciferase reporter assay was employed to verify the association between miR‐494‐3p and circ_0007142 or LASP1. Murine xenograft assay was conducted to investigate the role of circ_0007142 in DDP resistant in vivo. The protein level of LASP1 in tumors was measured by Immunohistochemistry (IHC) analysis.ResultsCirc_0007142 was upregulated in DDP‐resistant ESCC tissues and cells. Circ_0007142 knockdown improved DDP sensitivity, induced cell apoptosis and hampered cell proliferation and invasion in DDP‐resistant ESCC cells. Circ_0007142 functioned as the sponge for miR‐494‐3p and miR‐494‐3p inhibition reversed the impacts of circ_0007142 knockdown on DDP resistance, cell apoptosis, proliferation, and invasion. LASP1 was a target of miR‐494‐3p, and the effects on DDP resistance, cell apoptosis, growth, and invasion mediated by LASP1 downregulation were rescued by miR‐494‐3p inhibition. Moreover, circ_0007142 knockdown enhanced DDP sensitivity in vivo.ConclusionCirc_0007142 improved DDP resistance of ESCC by upregulating LASP1 via sponging miR‐494‐3p.
CircRNA hsa_circ_0018289 exerts an oncogenic role in cervical cancer progression through miR‐1294/ICMT axis
Authors: Li Yujuan , Gao Xiangrong , Yang Chaochao , Yan Hua , Li Cui 
Published: March 2022

AbstractBackgroundcircRNA hsa_circ_0018289‐mediated growth and metastasis of CC cells were investigated, as well as the mechanistic pathway.MethodsQuantitative real‐time reverse transcription‐polymerase chain reaction (qRT‐PCR) was carried out to examine the expression of hsa_circ_0018289, microRNA (miR)‐1294, and isoprenylcysteine carboxyl methyltransferase (ICMT). CC cell proliferation, migration, and invasion were evaluated by 5‐ethynyl‐2’‐deoxyuridine (EdU) incorporation, colony formation, transwell assays, Western blot analysis of ICMT, and glycolysis‐associated proteins. Dual‐luciferase reporter or RNA pull‐down analysis of the target interaction between miR‐1294 and hsa_hsa_circ_0018289 or ICMT. Xenograft model assay was implemented to assess the role of hsa_circ_0018289 in vivo. Immunofluorescence (IHC) was employed to detect the level of Ki‐67.ResultsHsa_circ_0018289 was elevated in CC tissues and cells, its deficiency could repress growth, metastasis, and glycolysis of CC cells in vitro, as well as hamper tumor growth in vivo. Hsa_circ_0018289 sponged miR‐1294 while miR‐1294 bound with ICMT, and the inhibition of miR‐1294 or addition of ICMT could partially relieve the effect caused by hsa_circ_0018289 depletion.ConclusionHsa_circ_0018289 contributes to malignant development by regulating the miR‐1294/ICMT axis, affording novel insight into CC therapy.
Human adipose and synovial mesenchymal stem cells improve osteoarthritis in rats by reducing chondrocyte reactive oxygen species and inhibiting inflammatory response
Authors: Liu Xunzhi , Liu Yaqing , He Huabin , Xiang Weiwei , He Cheng 
Published: March 2022

AbstractBackgroundWe explored the therapeutic effects of Adipose‐derived mesenchymal stem cells (ADMSCs) and Synovial‐derived mesenchymal stem cells (SDMSCs) on osteoarthritis (OA).MethodsSDMSCs and ADMSCs were co‐cultured with chondrocytes and stimulated with interleukin (IL)‐1β. An OA model was established on rats by intra‐articular injection with ADMSCs and SDMSCs. After 8 weeks, the joint diameter difference was detected, and histological staining was used to observe the pathological changes in cartilage tissue. Enzyme‐linked immunosorbent assay (ELISA) was used to detect the expressions of IL‐6, tumor necrosis factor (TNF)‐α and IL‐1β in joint fluid. The expressions of COL2A1, Aggrecan, Matrix metalloproteinase (MMP)‐13, SOX9, IL‐6, TNF‐α and IL‐1β were detected by qRT‐PCR and Western blotting in cartilage tissue. Reactive oxygen species (ROS) content in cells and cartilage tissues was detected by ROS kit.ResultsSDMSCs and ADMSCs co‐cultured with chondrocytes could reduce MMP‐13 expression, increase the expressions of COL2A1, Aggrecan and SOX9, as well as reverse the effects of IL‐1β on promoting ROS content and inflammatory factors levels. After the OA model was established, the injection of ADMSCs and SDMSCs reduced the differences in joint diameter and tissue lesions in OA rats. The OA model led to increased levels of IL‐6, TNF‐α and IL‐1β in joint fluid and cartilage tissue, while the injection of ADMSCs and SDMSCs inhibited the inflammatory factor levels in OA rats, and increased the expressions of COL2A1, Aggrecan and SOX9 in OA rats.ConclusionADMSCs and SDMSCs improve osteoarthritis in rats by reducing chondrocyte ROS and inhibiting inflammatory response.
β‐catenin‐controlled tubular cell‐derived exosomes play a key role in fibroblast activation via the OPN‐CD44 axis
Authors: Chen Shuangqin , Zhang Meijia , Li Jiemei , Huang Jiewu , Zhou Shan , Hou Xiaotao , Ye Huiyun , Liu Xi , Xiang Shaowei , Shen Weiwei , Miao Jinhua , Hou Fan Fan , Liu Youhua , Zhou Lili 
Published: March 2022

AbstractTubular injury and peripheral fibroblast activation are the hallmarks of chronic kidney disease (CKD), suggesting intimate communication between the two types of cells. However, the underlying mechanisms remain to be determined. Exosomes play a role in shuttling proteins and other materials to recipient cells. In our study, we found that exosomes were aroused by β‐catenin in renal tubular cells. Osteopontin (OPN), especially its N‐terminal fragment (N‐OPN), was encapsulated in β‐catenin‐controlled tubular cell‐derived exosome cargo, and subsequently passed to fibroblasts. Through binding with CD44, exosomal OPN promoted fibroblast proliferation and activation. Gene deletion of β‐catenin in tubular cells (Ksp‐β‐catenin−/−) or gene ablation of CD44 (CD44−/−) greatly ameliorated renal fibrosis. Notably, N‐OPN was carried by exosome and secreted into the urine of patients with CKD, and negatively correlated with kidney function. The urinary exosomes from patients with CKD greatly accelerated renal fibrosis, which was blocked by CD44 deletion. These results suggest that exosome‐mediated activation of the OPN/CD44 axis plays a key role in renal fibrosis, which is controlled by β‐catenin.
Physiological stress responses to nonmimetic model brood parasite eggs: Leukocyte profiles and heat‐shock protein Hsp70 levels
Authors: Ruiz‐Raya Francisco , Abaurrea Teresa , Vigo Ramón , Soler Manuel 
Published: March 2022

AbstractObligate avian brood parasites lay their eggs in the nest of other bird species, known as hosts. Brood parasitism often imposes severe fitness costs on hosts, selecting for the evolution of effective antiparasitic defences, such as recognition and rejection of brood parasite eggs. Glucocorticoids have been recently found to mediate host physiological and behavioral adjustments in response to brood parasite eggs; however, it remains unclear whether brood parasitism triggers a general response involving multiple physiological elements. In this study, we experimentally investigated whether a salient brood parasitic stimulus (the presence of a nonmimetic model egg in the nest) causes physiological adjustments in adult Eurasian blackbirds (Turdus merula) at immune (leukocyte profiles) and cellular (heat‐shock protein Hsp70 synthesis) level. Also, we explored whether these physiological changes are mediated by variations in corticosterone (CORT) levels. We found that experimental brood parasitism caused an increase in heterophils and a decrease in lymphocytes, leading to higher heterophils and lymphocytes ratios in parasitized birds. Nevertheless, we did not find tradeoffs between immune function and CORT levels. Hsp70 synthesis was not affected by our experimental manipulation. Our findings provide evidence that brood parasite eggs trigger a general stress response in egg‐rejecter hosts, including changes in cellular immune profiles.