bluuebunny/crossref_metadata_2025_split huggingface dataset:
DMD-based hyperspectral microscopy with flexible multiline parallel scanning
Authors: Dong Xue , Tong Geng , Song Xuankun , Xiao Xingchen , Yu Yiting 
Published: September 2021

AbstractAs one of the most common hyperspectral microscopy (HSM) techniques, line-scanning HSM is currently utilized in many fields. However, its scanning efficiency is still considered to be inadequate since many biological and chemical processes occur too rapidly to be captured. Accordingly, in this work, a digital micromirror device (DMD) based on microelectromechanical systems (MEMS) is utilized to demonstrate a flexible multiline scanning HSM system. To the best of our knowledge, this is the first line-scanning HSM system in which the number of scanning lines N can be tuned by simply changing the DMD’s parallel scanning units according to diverse applications. This brilliant strategy of effortless adjustability relies only on on-chip scanning methods and totally exploits the benefits of parallelization, aiming to achieve nearly an N-time improvement in the detection efficiency and an N-time decrease in the scanning time and data volume compared with the single-line method under the same operating conditions. To validate this, we selected a few samples of different spectral wavebands to perform reflection imaging, transmission imaging, and fluorescence imaging with varying numbers of scanning lines. The results show the great potential of our DMD-based HSM system for the rapid development of cellular biology, material analysis, and so on. In addition, its on-chip scanning process eliminates the inherent microscopic architecture, making the whole system compact, lightweight, portable, and not subject to site constraints.
Melatonin enhances radiofrequency-induced NK antitumor immunity, causing cancer metabolism reprogramming and inhibition of multiple pulmonary tumor development
Authors: Li Ming , Hao Bingjie , Zhang Menghuan , Reiter Russel J. , Lin Shumeng , Zheng Tiansheng , Chen Xiangyun , Ren Yanbei , Yue Liduo , Abay Baigenzhin , Chen Guojie , Xu Xiao , Shi Yufeng , Fan Lihong 
Published: September 2021

AbstractSurgery is the common treatment for early lung cancer with multiple pulmonary nodules, but it is often accompanied by the problem of significant malignancy of other nodules in non-therapeutic areas. In this study, we found that a combined treatment of local radiofrequency ablation (RFA) and melatonin (MLT) greatly improved clinical outcomes for early lung cancer patients with multiple pulmonary nodules by minimizing lung function injury and reducing the probability of malignant transformation or enlargement of nodules in non-ablated areas. Mechanically, as demonstrated in an associated mouse lung tumor model, RFA not only effectively remove treated tumors but also stimulate antitumor immunity, which could inhibit tumor growth in non-ablated areas. MLT enhanced RFA-stimulated NK activity and exerted synergistic antitumor effects with RFA. Transcriptomics and proteomics analyses of residual tumor tissues revealed enhanced oxidative phosphorylation and reduced acidification as well as hypoxia in the tumor microenvironment, which suggests reprogrammed tumor metabolism after combined treatment with RFA and MLT. Analysis of residual tumor further revealed the depressed activity of MAPK, NF-kappa B, Wnt, and Hedgehog pathways and upregulated P53 pathway in tumors, which was in line with the inhibited tumor growth. Combined RFA and MLT treatment also reversed the Warburg effect and decreased tumor malignancy. These findings thus demonstrated that combined treatment of RFA and MLT effectively inhibited the malignancy of non-ablated nodules and provided an innovative non-invasive strategy for treating early lung tumors with multiple pulmonary nodules. Trial registration: www.chictr.org.cn, identifier ChiCTR2100042695, http://www.chictr.org.cn/showproj.aspx?proj=120931.
Associations between childhood maltreatment and DNA methylation of the oxytocin receptor gene in immune cells of mother–newborn dyads
Authors: Ramo-Fernández Laura , Gumpp Anja M. , Boeck Christina , Krause Sabrina , Bach Alexandra M. , Waller Christiane , Kolassa Iris-Tatjana , Karabatsiakis Alexander 
Published: September 2021

AbstractThe neuropeptide oxytocin (OXT) and its receptor (OXTR) modulate interpersonal relationships, particularly mother–child interactions. DNA methylation (DNAm) changes of theOXTRgene were observed in individuals who experienced Childhood Maltreatment (CM). A modulatory role of single nucleotide polymorphisms (SNP) withinOXTRin association with CM on the regulation of OXTR was also postulated. Whether these CM-induced epigenetic alterations are biologically inherited by the offspring remains unknown. We thus investigated possible intergenerational effects of maternal CM exposure on DNAm andOXTRgene expression, additionally accounting for the possible influence of three SNP: rs53576 and rs2254298 (OXTRgene), and rs2740210 (OXTgene). We used theChildhood Trauma Questionnaireto classify mothers into individuals with (CM+) or without CM (CM−). Maternal peripheral immune cells were isolated from venous blood (N = 117) and fetal immune cells from the umbilical cord (N = 113) after parturition. DNA methylation was assessed using MassARRAY. Taqman assays were performed for genotyping and gene expression analyses. Among mothers, CM was not associated withOXTRmean methylation or gene expression. However, four CpG sites showed different methylation levels in CM− compared to CM+. In mothers, theOXTRrs53576 andOXTrs2740210 allelic variations interacted with CM load on theOXTRmean methylation. Maternal and newborns’ mean methylation ofOXTRwere positively associated within CM− dyads, but not in CM+ dyads. We show gene×environment interactions on the epigenetic regulation of the oxytocinergic signaling and show the intergenerational comparability of theOXTRDNAm might be altered in infants of CM+ mothers.
Osteoblastic glucocorticoid signaling exacerbates high-fat-diet- induced bone loss and obesity
Authors: Kim Sarah , Henneicke Holger , Cavanagh Lauryn L. , Macfarlane Eugenie , Thai Lee Joanne , Foong Daphne , Gasparini Sylvia J. , Fong-Yee Colette , Swarbrick Michael M. , Seibel Markus J. , Zhou Hong 
Published: September 2021

AbstractChronic high-fat diet (HFD) consumption not only promotes obesity and insulin resistance, but also causes bone loss through mechanisms that are not well understood. Here, we fed wild-type CD-1 mice either chow or a HFD (43% of energy from fat) for 18 weeks; HFD-fed mice exhibited decreased trabecular volume (−28%) and cortical thickness (−14%) compared to chow-fed mice. In HFD-fed mice, bone loss was due to reduced bone formation and mineral apposition, without obvious effects on bone resorption. HFD feeding also increased skeletal expression of sclerostin and caused deterioration of the osteocyte lacunocanalicular network (LCN). In mice fed HFD, skeletal glucocorticoid signaling was activated relative to chow-fed mice, independent of serum corticosterone concentrations. We therefore examined whether skeletal glucocorticoid signaling was necessary for HFD-induced bone loss, using transgenic mice lacking glucocorticoid signaling in osteoblasts and osteocytes (HSD2OB/OCY-tg mice). In HSD2OB/OCY-tg mice, bone formation and mineral apposition rates were not suppressed by HFD, and bone loss was significantly attenuated. Interestingly, in HSD2OB/OCY-tg mice fed HFD, both Wnt signaling (less sclerostin induction, increased β-catenin expression) and glucose uptake were significantly increased, relative to diet- and genotype-matched controls. The osteocyte LCN remained intact in HFD-fed HSD2OB/OCY-tg mice. When fed a HFD, HSD2OB/OCY-tg mice also increased their energy expenditure and were protected against obesity, insulin resistance, and dyslipidemia. Therefore, glucocorticoid signaling in osteoblasts and osteocytes contributes to the suppression of bone formation in HFD-fed mice. Skeletal glucocorticoid signaling is also an important determinant of glucose uptake in bone, which influences the whole-body metabolic response to HFD.
Cyclic AMP-binding protein Epac1 acts as a metabolic sensor to promote cardiomyocyte lipotoxicity
Authors: Laudette Marion , Sainte-Marie Yannis , Cousin Grégoire , Bergonnier Dorian , Belhabib Ismahane , Brun Stéphanie , Formoso Karina , Laib Loubna , Tortosa Florence , Bergoglio Camille , Marcheix Bertrand , Borén Jan , Lairez Olivier , Fauconnier Jérémy , Lucas Alexandre , Mialet-Perez Jeanne , Moro Cédric , Lezoualc’h Frank 
Published: September 2021

AbstractCyclic adenosine monophosphate (cAMP) is a master regulator of mitochondrial metabolism but its precise mechanism of action yet remains unclear. Here, we found that a dietary saturated fatty acid (FA), palmitate increased intracellular cAMP synthesis through the palmitoylation of soluble adenylyl cyclase in cardiomyocytes. cAMP further induced exchange protein directly activated by cyclic AMP 1 (Epac1) activation, which was upregulated in the myocardium of obese patients. Epac1 enhanced the activity of a key enzyme regulating mitochondrial FA uptake, carnitine palmitoyltransferase 1. Consistently, pharmacological or genetic Epac1 inhibition prevented lipid overload, increased FA oxidation (FAO), and protected against mitochondrial dysfunction in cardiomyocytes. In addition, analysis of Epac1 phosphoproteome led us to identify two key mitochondrial enzymes of the the β-oxidation cycle as targets of Epac1, the long-chain FA acyl-CoA dehydrogenase (ACADL) and the 3-ketoacyl-CoA thiolase (3-KAT). Epac1 formed molecular complexes with the Ca2+/calmodulin-dependent protein kinase II (CaMKII), which phosphorylated ACADL and 3-KAT at specific amino acid residues to decrease lipid oxidation. The Epac1-CaMKII axis also interacted with the α subunit of ATP synthase, thereby further impairing mitochondrial energetics. Altogether, these findings indicate that Epac1 disrupts the balance between mitochondrial FA uptake and oxidation leading to lipid accumulation and mitochondrial dysfunction, and ultimately cardiomyocyte death.
Metabolite profiling and transcriptome analyses reveal novel regulatory mechanisms of melatonin biosynthesis in hickory
Authors: Chen Wenchao , Zhang Jiaqi , Zheng Shan , Wang Zhanqi , Xu Chuanmei , Zhang Qixiang , Wu Jiasheng , Lou Heqiang 
Published: September 2021

AbstractStudies have shown that melatonin regulates the expression of various elements in the biosynthesis and catabolism of plant hormones. In contrast, the effects of these different plant hormones on the biosynthesis and metabolism of melatonin and their underlying molecular mechanisms are still unclear. In this study, the melatonin biosynthesis pathway was proposed from constructed metabolomic and transcriptomic libraries from hickory (Carya cathayensis Sarg.) nuts. The candidate pathway genes were further identified by phylogenetic analysis, amino-acid sequence alignment, and subcellular localization. Notably, most of the transcription factor-related genes coexpressed with melatonin pathway genes were hormone-responsive genes. Furthermore, dual-luciferase and yeast one‐hybrid assays revealed that CcEIN3 (response to ethylene) and CcAZF2 (response to abscisic acid) could activate melatonin biosynthesis pathway genes, a tryptophan decarboxylase coding gene (CcTDC1) and an N-acetylserotonin methyltransferase coding gene (CcASMT1), by directly binding to their promoters, respectively. Our results provide a molecular basis for the characterization of novel melatonin biosynthesis regulatory mechanisms and demonstrate for the first time that abscisic acid and ethylene can regulate melatonin biosynthesis.
Downregulated expression of S2-RNase attenuates self-incompatibility in “Guiyou No. 1” pummelo
Authors: Hu Jianbing , Xu Qiang , Liu Chenchen , Liu Binghao , Deng Chongling , Chen Chuanwu , Wei Zhuangmin , Ahmad Muhammad Husnain , Peng Kang , Wen Hao , Chen Xiangling , Chen Peng , Larkin Robert M , Ye Junli , Deng Xiuxin , Chai Lijun 
Published: September 2021

Abstract
Self-incompatibility (SI) substantially restricts the yield and quality of citrus. Therefore, breeding and analyzing self-compatible germplasm is of great theoretical and practical significance for citrus. Here, we focus on the mechanism of a self-compatibility mutation in ‘Guiyou No. 1’ pummelo (Citrus maxima), which is a spontaneous mutant of ‘Shatian’ pummelo (Citrus maxima, self-incompatibility). The rate of fruit set and the growth of pollen tubes in the pistil confirmed that a spontaneous mutation in the pistil is responsible for the self-compatibility of ‘Guiyou No. 1’. Segregation ratios of the S genotype in F1 progeny, expression analysis, and western blotting validated that the reduced levels of S2-RNase mRNA contribute to the loss of SI in ‘Guiyou No. 1’. Furthermore, we report a phased assembly of the ‘Guiyou No. 1’ pummelo genome and obtained two complete and well-annotated S haplotypes. Coupled with an analysis of SV variations, methylation levels, and gene expression, we identified a candidate gene (CgHB40), that may influence the regulation of the S2-RNase promoter. Our data provide evidence that a mutation that affects the pistil led to the loss of SI in ‘Guiyou No. 1’ by influencing a poorly understood mechanism that affects transcriptional regulation. This work significantly advances our understanding of the genetic basis of the SI system in citrus and provides information on the regulation of S-RNase genes.
The use of shared haplotype length information for pedigree reconstruction in asexually propagated outbreeding crops, demonstrated for apple and sweet cherry
Authors: Howard Nicholas P. , Peace Cameron , Silverstein Kevin A. T. , Poets Ana , Luby James J. , Vanderzande Stijn , Durel Charles-Eric , Muranty Hélène , Denancé Caroline , van de Weg Eric 
Published: September 2021

AbstractPedigree information is of fundamental importance in breeding programs and related genetics efforts. However, many individuals have unknown pedigrees. While methods to identify and confirm direct parent–offspring relationships are routine, those for other types of close relationships have yet to be effectively and widely implemented with plants, due to complications such as asexual propagation and extensive inbreeding. The objective of this study was to develop and demonstrate methods that support complex pedigree reconstruction via the total length of identical by state haplotypes (referred to in this study as “summed potential lengths of shared haplotypes”, SPLoSH). A custom Python script, HapShared, was developed to generate SPLoSH data in apple and sweet cherry. HapShared was used to establish empirical distributions of SPLoSH data for known relationships in these crops. These distributions were then used to estimate previously unknown relationships. Case studies in each crop demonstrated various pedigree reconstruction scenarios using SPLoSH data. For cherry, a full-sib relationship was deduced for ‘Emperor Francis, and ‘Schmidt’, a half-sib relationship for ‘Van’ and ‘Windsor’, and the paternal grandparents of ‘Stella’ were confirmed. For apple, 29 cultivars were found to share an unknown parent, the pedigree of the unknown parent of ‘Cox’s Pomona’ was reconstructed, and ‘Fameuse’ was deduced to be a likely grandparent of ‘McIntosh’. Key genetic resources that enabled this empirical study were large genome-wide SNP array datasets, integrated genetic maps, and previously identified pedigree relationships. Crops with similar resources are also expected to benefit from using HapShared for empowering pedigree reconstruction.
The Arabidopsis pattern recognition receptor EFR enhances fire blight resistance in apple
Authors: Piazza Stefano , Campa Manuela , Pompili Valerio , Costa Lorenza Dalla , Salvagnin Umberto , Nekrasov Vladimir , Zipfel Cyril , Malnoy Mickael 
Published: September 2021

AbstractFire blight disease, caused by the bacterium Erwinia amylovora (E. amylovora), is responsible for substantial losses in cultivated apples worldwide. An important mechanism of plant immunity is based on the recognition of conserved microbial molecules, named pathogen-associated or microbe-associated molecular patterns (PAMPs or MAMPs), through pattern recognition receptors (PRRs), leading to pattern-triggered immunity (PTI). The interspecies transfer of PRRs represents a promising strategy to engineer broad-spectrum and durable disease resistance in crops. EFR, the Arabidopsis thaliana PRR for the PAMP elf18 derived from the elongation factor thermal unstable (EF-Tu) proved to be effective in improving bacterial resistance when expressed into Solanaceae and other plant species. In this study, we tested whether EFR can affect the interaction of apple with E. amylovora by its ectopic expression in the susceptible apple rootstock M.26. Stable EFR expression led to the activation of PAMP-triggered immune response in apple leaves upon treatment with supernatant of E. amylovora, as measured by the production of reactive oxygen species and the induction of known defense genes. The amount of tissue necrosis associated with E. amylovora infection was significantly reduced in the EFR transgenic rootstock compared to the wild-type. Our results show that the expression of EFR in apple rootstock may be a valuable biotechnology strategy to improve the resistance of apple to fire blight.
EpiScanpy: integrated single-cell epigenomic analysis
Authors: Danese Anna , Richter Maria L. , Chaichoompu Kridsadakorn , Fischer David S. , Theis Fabian J. , Colomé-Tatché Maria 
Published: September 2021

AbstractEpiScanpy is a toolkit for the analysis of single-cell epigenomic data, namely single-cell DNA methylation and single-cell ATAC-seq data. To address the modality specific challenges from epigenomics data, epiScanpy quantifies the epigenome using multiple feature space constructions and builds a nearest neighbour graph using epigenomic distance between cells. EpiScanpy makes the many existing scRNA-seq workflows from scanpy available to large-scale single-cell data from other -omics modalities, including methods for common clustering, dimension reduction, cell type identification and trajectory learning techniques, as well as an atlas integration tool for scATAC-seq datasets. The toolkit also features numerous useful downstream functions, such as differential methylation and differential openness calling, mapping epigenomic features of interest to their nearest gene, or constructing gene activity matrices using chromatin openness. We successfully benchmark epiScanpy against other scATAC-seq analysis tools and show its outperformance at discriminating cell types.
Exceptional dynamical quantum phase transitions in periodically driven systems
Authors: Hamazaki Ryusuke 
Published: September 2021

AbstractExtending notions of phase transitions to nonequilibrium realm is a fundamental problem for statistical mechanics. While it was discovered that critical transitions occur even for transient states before relaxation as the singularity of a dynamical version of free energy, their nature is yet to be elusive. Here, we show that spontaneous symmetry breaking can occur at a short-time regime and causes universal dynamical quantum phase transitions in periodically driven unitary dynamics. Unlike conventional phase transitions, the relevant symmetry is antiunitary: its breaking is accompanied by a many-body exceptional point of a nonunitary operator obtained by space-time duality. Using a stroboscopic Ising model, we demonstrate the existence of distinct phases and unconventional singularity of dynamical free energy, whose signature can be accessed through quasilocal operators. Our results open up research for hitherto unknown phases in short-time regimes, where time serves as another pivotal parameter, with their hidden connection to nonunitary physics.
Major restructuring of marine plankton assemblages under global warming
Authors: Benedetti Fabio , Vogt Meike , Elizondo Urs Hofmann , Righetti Damiano , Zimmermann Niklaus E. , Gruber Nicolas 
Published: September 2021

AbstractMarine phytoplankton and zooplankton form the basis of the ocean’s food-web, yet the impacts of climate change on their biodiversity are poorly understood. Here, we use an ensemble of species distribution models for a total of 336 phytoplankton and 524 zooplankton species to determine their present and future habitat suitability patterns. For the end of this century, under a high emission scenario, we find an overall increase in plankton species richness driven by ocean warming, and a poleward shift of the species’ distributions at a median speed of 35 km/decade. Phytoplankton species richness is projected to increase by more than 16% over most regions except for the Arctic Ocean. In contrast, zooplankton richness is projected to slightly decline in the tropics, but to increase strongly in temperate to subpolar latitudes. In these latitudes, nearly 40% of the phytoplankton and zooplankton assemblages are replaced by poleward shifting species. This implies that climate change threatens the contribution of plankton communities to plankton-mediated ecosystem services such as biological carbon sequestration.
Microglia-neuron interaction at nodes of Ranvier depends on neuronal activity through potassium release and contributes to remyelination
Authors: Ronzano R. , Roux T. , Thetiot M. , Aigrot M. S. , Richard L. , Lejeune F. X. , Mazuir E. , Vallat J. M. , Lubetzki C. , Desmazières A. 
Published: September 2021

AbstractMicroglia, the resident immune cells of the central nervous system, are key players in healthy brain homeostasis and plasticity. In neurological diseases, such as Multiple Sclerosis, activated microglia either promote tissue damage or favor neuroprotection and myelin regeneration. The mechanisms for microglia-neuron communication remain largely unkown. Here, we identify nodes of Ranvier as a direct site of interaction between microglia and axons, in both mouse and human tissues. Using dynamic imaging, we highlight the preferential interaction of microglial processes with nodes of Ranvier along myelinated fibers. We show that microglia-node interaction is modulated by neuronal activity and associated potassium release, with THIK-1 ensuring their microglial read-out. Altered axonal K+flux following demyelination impairs the switch towards a pro-regenerative microglia phenotype and decreases remyelination rate. Taken together, these findings identify the node of Ranvier as a major site for microglia-neuron interaction, that may participate in microglia-neuron communication mediating pro-remyelinating effect of microglia after myelin injury.
Processive dynamics of the usher assembly platform during uropathogenic Escherichia coli P pilus biogenesis
Authors: Du Minge , Yuan Zuanning , Werneburg Glenn T. , Henderson Nadine S. , Chauhan Hemil , Kovach Amanda , Zhao Gongpu , Johl Jessica , Li Huilin , Thanassi David G. 
Published: September 2021

AbstractUropathogenic Escherichia coli assemble surface structures termed pili or fimbriae to initiate infection of the urinary tract. P pili facilitate bacterial colonization of the kidney and pyelonephritis. P pili are assembled through the conserved chaperone-usher pathway. Much of the structural and functional understanding of the chaperone-usher pathway has been gained through investigations of type 1 pili, which promote binding to the bladder and cystitis. In contrast, the structural basis for P pilus biogenesis at the usher has remained elusive. This is in part due to the flexible and variable-length P pilus tip fiber, creating structural heterogeneity, and difficulties isolating stable P pilus assembly intermediates. Here, we circumvent these hindrances and determine cryo-electron microscopy structures of the activated PapC usher in the process of secreting two- and three-subunit P pilus assembly intermediates, revealing processive steps in P pilus biogenesis and capturing new conformational dynamics of the usher assembly machine.