bluuebunny/crossref_metadata_2025_split huggingface dataset:
FeGenie: a comprehensive tool for the identification of iron genes and iron gene neighborhoods in genomes and metagenome assemblies
Authors: Garber Arkadiy I. , Nealson Kenneth H. , Okamoto Akihiro , McAllister Sean M. , Chan Clara S. , Barco Roman A. , Merino Nancy 
Published: September 2019

AbstractIron is a micronutrient for nearly all life on Earth. It can be used as an electron donor and electron acceptor by iron-oxidizing and iron-reducing microorganisms, and is used in a variety of biological processes, including photosynthesis and respiration. While it is the fourth most abundant metal in the Earth’s crust, iron is often limiting for growth in oxic environments because it is readily oxidized and precipitated. Much of our understanding of how microorganisms compete for and utilize iron is based on laboratory experiments. However, the advent of next-generation sequencing and the associated surge in publicly-available sequence data has now made it possible to probe the structure and function of microbial communities in the environment. To bridge the gap between our understanding of iron acquisition and utilization in model microorganisms and the plethora of sequence data available from environmental studies, we have created a comprehensive database of hidden Markov models (HMMs) that is based on genes related to iron acquisition, storage, and reduction/oxidation. Along with this database, we present FeGenie, a bioinformatics tool that accepts genome and metagenome assemblies as input and uses our comprehensive HMM database to annotate the provided datasets with respect to iron-related genes and gene clusters. An important contribution of this tool is the efficient identification of genes involved in iron oxidation and dissimilatory iron reduction, which have been largely overlooked by standard annotation pipelines. While this tool will not replace the reliability of culture-dependent analyses of microbial physiology, it provides reliable predictions derived from the most up-to-date genetic markers. FeGenie’s database will be maintained and continually-updated as new genetic markers are discovered. FeGenie is freely available:https://github.com/Arkadiy-Garber/FeGenie.
Description of Ruminococcus catenae SW178 sp. nov., a new anaerobic species isolated from feral chicken
Authors: Wongkuna Supapit , Ghimire Sudeep , Chankhamhaengdecha Surang , Janvilisri Tavan , Scaria Joy 
Published: September 2019

AbstractA Gram-positive, obligately anaerobic coccobacillus, with the white raised circular colony was isolated from the cecum of feral chickens in Brookings, South Dakota, USA. The 16S rRNA gene sequence analysis suggested that the closest species to strain SW178 was Ruminococcus torques ATCC 27756T (96.94% similarity) that belongs to the family Lachnospiraceae. The genome of strain SW178 is 3.18 Mbp with G+C content of 46.9 mol%. Based on the phylogenetic and phenotypic comparison, we propose that strain SW178 be assigned to the genus Ruminococcus as a novel species, for which the name Ruminococcus catenae is proposed. The type strain is SW178 (= CCOS 1886 T, =DSM 109242T).
β-adrenergic signaling modulates cancer cell mechanotype through a RhoA-ROCK-myosin II axis
Authors: Kim Tae-Hyung , Vazquez-Hidalgo Esteban , Abdou Alexander , Tan Xing Haw Marvin , Christodoulides Alexei , Farris Carly M. , Chiou Pei-Yu , Sloan Erica K. , Katira Parag , Rowat Amy C. 
Published: September 2019

AbstractThe ability of cells to deform and generate forces are key mechanical properties that are implicated in metastasis. While various soluble and mechanical cues are known to regulate cancer cell mechanical phenotype or mechanotype, our knowledge of how cells translate external signals into changes in mechanotype is still emerging. We previously discovered that activation of β-adrenergic signaling, which results from soluble stress hormone cues, causes cancer cells to be stiffer or less deformable; this stiffer mechanotype was associated with increased cell motility and invasion. Here, we characterize how β-adrenergic activation is translated into changes in cellular mechanotype by identifying molecular mediators that regulate key components of mechanotype including cellular deformability, traction forces, and non-muscle myosin II (NMII) activity. Using a micropillar assay and computational modelling, we determine that βAR activation increases cellular force generation by increasing the number of actin-myosin binding events; this mechanism is distinct from how cells increase force production in response to matrix stiffness, suggesting that cells regulate their mechanotype using a complementary mechanism in response to stress hormone cues. To identify the molecules that modulate cellular mechanotype with βAR activation, we use a high throughput filtration platform to screen the effects of pharmacologic and genetic perturbations on βAR regulation of whole cell deformability. Our results indicate that βAR activation decreases cancer cell deformability and increases invasion by signaling through RhoA, ROCK, and NMII. Our findings establish βAR-RhoA-ROCK-NMII as a primary signaling axis that mediates cancer cell mechanotype, which provides a foundation for future interventions to stop metastasis.
Mechanism of Interaction of BMP and Insulin Signaling inC. elegansDevelopment and Homeostasis
Authors: Clark James F. , Ciccarelli Emma J. , Kayastha Peter , Ranepura Gehan , Hasan Muhammad S. , Meléndez Alicia , Savage-Dunn Cathy 
Published: September 2019

AbstractA small number of peptide growth factor ligands are used repeatedly in development and homeostasis to drive programs of cell differentiation and function. Cells and tissues must integrate inputs from these diverse signals correctly, while failure to do so leads to pathology, reduced fitness, or death. Previous work using the nematodeC. elegansidentified an interaction between the bone morphogenetic protein (BMP) and insulin/IGF-1-like signaling (IIS) pathways in the regulation of lipid homeostasis. The molecular components required for this interaction, however, were not known. Here we report that INS-4, one of 40 insulin-like peptides (ILPs), is regulated by BMP signaling to modulate fat accumulation. Furthermore, we find that the IIS transcription factor DAF-16/FoxO, but not SKN-1/Nrf, acts downstream of BMP signaling in lipid homeostasis. Interestingly, BMP activity alters sensitivity of these two transcription factors to IIS-promoted cytoplasmic retention in opposite ways. Finally, we probe the extent of BMP and IIS interactions by testing two additional IIS functions, dauer formation and autophagy induction. Coupled with our previous work and that of other groups, we conclude that BMP and IIS pathways have at least three modes of interaction: independent, epistatic, and antagonistic. The molecular interactions we identify provide new insight into mechanisms of signaling crosstalk and potential therapeutic targets for IIS-related pathologies such as diabetes and metabolic syndrome.
Contribution of NPY Y5 Receptors to the Reversible Structural Remodeling Of Basolateral Amygdala Dendrites in Male Rats Associated with NPY-mediated Stress Resilience
Authors: Michaelson Sheldon D. , Tapia Ana Pamela Miranda , McKinty Amanda , Villarroel Heika Silveira , Mackay James P. , Urban Janice H. , Colmers William F. 
Published: September 2019

ABSTRACTEndogenous neuropeptide Y (NPY) and corticotrophin-releasing factor (CRF) modulate the responses of the Basolateral amygdala (BLA) to stress, and are associated respectively with the development of stress resilience and vulnerability. We characterized the persistent effects of repeated NPY and CRF treatment on the structure and function of BLA principal neurons (PN) in a novel organotypic slice culture (OTC) model of rat BLA, and examined the contributions of specific NPY receptor subtypes to these neural and behavioral effects. In BLA principal neurons within the OTCs, repeated NPY treatment caused persistent attenuation of excitatory input and induced dendritic hypotrophy via Y5 receptors; conversely, CRF increased excitatory input and induced hypertrophy of BLA PNs. Repeated treatment of OTCs with NPY followed by an identical treatment with CRF, or vice versa inhibited or reversed all structural changes in OTCs. These structural responses to NPY or CRF required calcineurin or CaMKII, respectively. Finally, repeated intra-BLA injections of NPY or a Y5 receptor agonist increased social interaction and recapitulated structural changes in BLA neurons seen in OTCs, while a Y5 receptor antagonist prevented NPY’s effects both on behavior and on structure. These results implicate the Y5 receptor in the long-term, anxiolytic-like effects of NPY in the BLA, consistent with an intrinsic role in stress buffering, and highlight a remarkable mechanism by which BLA neurons may adapt to different levels of stress. Moreover, BLA OTCs offer a robust model to study mechanisms associated with resilience and vulnerability to stress in BLA.Significance StatementWithin the basolateral amygdala (BLA), Neuropeptide Y (NPY) is associated with buffering the neural stress response induced by CRF, and promoting stress resilience. We used a novel organotypic slice culture (OTC) model of BLA, complemented with in vivo studies, to examine the cellular mechanisms associated with the actions of NPY. In OTCs, repeated NPY treatment reduces the complexity of the dendritic extent of anxiogenic BLA principal neurons, making them less excitable. NPY, via activation of Y5 receptors, additionally inhibits and reverses the increases in dendritic extent and excitability induced by the stress hormone, corticotropin releasing factor (CRF). This NPY-mediated neuroplasticity indicates that resilience or vulnerability to stress may thus involve neuropeptide-mediated dendritic remodeling in BLA PNs.
Genetic heterogeneity of the Spy1336/R28 – Spy1337 Virulence Axis inStreptococcus pyogenesand Effect on Gene Transcript Levels and Pathogenesis
Authors: Eraso Jesus M. , Kachroo Priyanka , Olsen Randall J. , Beres Stephen B. , Zhu Luchang , Badu Traci , Shannon Sydney , Cantu Concepcion C. , Saavedra Matthew Ojeda , Kubiak Samantha L. , Porter Adeline R. , DeLeo Frank R. , Musser James M. 
Published: September 2019

ABSTRACTStreptococcus pyogenesis a strict human pathogen responsible for more than 700 million infections annually worldwide. Strains of serotype M28S. pyogenesare typically among the five more abundant types causing invasive infections and pharyngitis in adults and children. Type M28 strains also have an unusual propensity to cause puerperal sepsis and neonatal disease. We recently discovered that a one-nucleotide indel in an intergenic homopolymeric tract located between genesSpy1336/R28andSpy1337altered virulence in a mouse model of infection. In the present study, we analyzed size variation in this homopolymeric tract and determined the extent of heterogeneity in the number of tandemly-repeated 79-amino acid domains in the coding region ofSpy1336/R28in large samples of strains recovered from humans with invasive infections. Both repeat sequence elements are highly polymorphic in natural populations of M28 strains. Variation in the homopolymeric tract results in (i) changes in transcript levels ofSpy1336/R28andSpy1337 in vitro,(ii) differences in virulence in a mouse model of necrotizing myositis, and (iii) global transcriptome changes as shown by RNAseq analysis of isogenic mutant strains. Variation in the number of tandem repeats in the coding sequence ofSpy1336/R28is responsible for size variation of R28 protein in natural populations. Isogenic mutant strains in which genes encoding R28 or transcriptional regulator Spy1337 are inactivated are significantly less virulent in a nonhuman primate model of necrotizing myositis. Our findings provide impetus for additional studies addressing the role of R28 and Spy1337 variation in pathogen-host interactions.
Transcriptome and translatome profiling and translational network analysis during seed maturation reveals conserved transcriptional and distinct translational regulatory patterns
Authors: Bai Bing , van der Horst Sjors , Delhomme Nicolas , Robles Alexander Vergara , Bentsink Leónie , Hanson Johannes 
Published: September 2019

AbstractSeed maturation is an important plant developmental process that follows embryo development. It is associated with a series of physiological changes such as the establishment of desiccation tolerance, seed longevity and seed dormancy. However, the translational dynamics associated with seed maturation, especially its connection with seed germination remains largely elusive. Here transcriptome and translatome profiling were performed during seed maturation. During seed maturation we observed a gradual disappearance of polysomes and a relative increase of monosomes, indicating a gradual reduction of global translation. Comparing the levels of polysomal associated mRNAs with total mRNA levels showed that thousands of genes are translationally regulated at early sates of maturation, as judged by dramatic changes in polysomal occupancy. By including previous published data from germination and seedling establishment, a translational regulatory network: SeedTransNet was constructed. Network analysis identified hundreds of gene modules with distinct functions and transcript sequence features indicating the existence of separate translational regulatory circuits possibly acting through specific regulatory elements. The regulatory potential of one such element was confirmed in vivo. The network identified several seed maturation associated genes as central nodes, and we could confirm the importance of many of these hub genes with a maturation associated seed phenotype by mutant analysis. One of the identified regulators an AWPM19 family protein PM19-Like1 (PM19L1) was shown to regulate seed dormancy and longevity. This putative RBP also affects the transitional regulation of one its, by the SeedTransNet identified, target mRNAs. Our data shows the usefulness of SeedTransNet in identifying regulatory pathways during seed phase transitions.
Dopamine Promotes Cognitive Effort by Biasing the Benefits Versus Costs of Cognitive Work
Authors: Westbrook A. , van den Bosch R. , Määttä J. I. , Hofmans L. , Papadopetraki D. , Cools R. , Frank M. J. 
Published: September 2019

Stimulants like methylphenidate are increasingly used for cognitive enhancement, but precise mechanisms are unknown. We found that methylphenidate boosts willingness to expend cognitive effort by altering the benefit-to-cost ratio of cognitive work. Willingness to expend effort was greater for participants with higher striatal dopamine synthesis capacity, while methylphenidate and sulpiride – a selective D2 receptor antagonist – increased cognitive motivation more for participants with lower synthesis capacity. A sequential sampling model informed by momentary gaze revealed that decisions to expend effort are related to amplification of benefit-versus-cost information attended early in the decision process, while the effect of benefits is strengthened with higher synthesis capacity and by methylphenidate. These findings demonstrate that methylphenidate boosts the perceived benefits-versus-costs of cognitive effort by modulating striatal dopamine signaling.One Sentence SummaryStriatal dopamine increases cognitive effort by respectively amplifying and attenuating the subjective benefits and costs of cognitive control.
The Effect of Eucalyptol on Nursing Home Residents
Authors: Goto Seiko , Suzuki Hinako , Nakagawa Toshinori , Shimizu Kuniyoshi 
Published: September 2019

AbstractEucalyptol is one of the most popular volatile components used in many essential oils for relieving sinus and lung congestion caused by variety of conditions. This pilot study aims to analyze clinical evidence of the effect of the scent of eucalyptol on dementia patients to answer two questions: 1) whether eucalyptol aroma is an effectiveness at reducing the symptoms of dementia, and 2) if so, how it mitigates those symptoms. 27 nursing-home residents with dementia were recruited to assess the efficacy of the scent of eucalyptol. Two one-week experiments were performed: the scent was diffused only at wake-up time in the first experiment and at wake-up time and bedtime in the second experiment. Results showed MMSE, DBD, CMAI scores slightly improved in the first experiment and significantly improved in the second experiment even though no subject reported perceiving the scent in either experiment. The present results indicate that eucalyptol is effective in mitigating dementia symptoms in an elder population with an impaired sense of smell.
Flossing DNA in a Dual Nanopore Device
Authors: Liu Xu , Zimny Philip , Zhang Yuning , Rana Ankit , Nagel Roland , Reisner Walter , Dunbar William B. 
Published: September 2019

AbstractSolid-state nanopores are a single-molecule technique that can provide access to biomolecular information that is otherwise masked by ensemble averaging. A promising application uses pores and barcoding chemistries to map molecular motifs along single DNA molecules. Despite recent research breakthroughs, however, it remains challenging to overcome molecular noise to fully exploit single molecule data. Here we present an active control technique termed “flossing” that uses a dual nanopore device to trap a protein-tagged DNA molecule and perform up to 100’s of back-and-forth electrical scans of the molecule in a few seconds. The protein motifs bound to 48 kb λDNA are used as detectable features for active triggering of the bidirectional control. Molecular noise is suppressed by averaging the multi-scan data to produce averaged inter-tag distance estimates that are comparable to their known values. Since nanopore feature-mapping applications require DNA linearization when passing through the pore, a key advantage of flossing is that trans-pore linearization is increased to >98% by the second scan, compared to 35% for single nanopore passage of the same set of molecules. In concert with barcoding methods, the dual-pore flossing technique could enable genome mapping and structural variation applications, or mapping loci of epigenetic relevance.
Analysis of continuous infusion functional PET (fPET) in the human brain
Authors: Li Shenpeng , Jamadar Sharna D. , Ward Phillip G.D. , Premaratne Malin , Egan Gary F. , Chen Zhaolin 
Published: September 2019

AbstractFunctional positron emission tomography (fPET) is a neuroimaging method involving continuous infusion of 18-F-fluorodeoxyglucose (FDG) radiotracer during the course of the PET examination. Compared with the conventional bolus administered static FDG PET which provides only a snapshot of the averaged glucose uptake into the brain in a limited dynamic time window, fPET offers a significantly wider time window to study the dynamics of glucose uptake. Several earlier studies have applied fPET to investigate brain FDG uptake and study its relationship with functional magnetic resonance imaging (fMRI). However, due to the unique characteristics of fPET signals, modelling of the fPET signal is a complex task and poses challenges for accurate interpretation of the results. This study applies independent component analysis (ICA) to analyze resting state fPET data, and to compare the performance of ICA and general linear modelling (GLM) for estimation of brain activation in response to tasks. The fPET signal characteristics were compared using GLM and ICA methods to model the fPET visual activation data. Our aim was to evaluate GLM and ICA methods for analyzing task fPET datasets and present ICA method in the analysis of resting state fPET datasets. Using both simulation and in-vivo experimental datasets, we show that both methods can successfully identify task related brain activation. We report fPET metabolic resting state brain networks analyzed using the fPET ICA method in a cohort of healthy subjects. Functional PET provides a unique method to map dynamic changes of glucose uptake in the resting human brain and in response to extrinsic stimulation.
Role of Chemokine and TNF signaling pathway in oral squamous cell carcinoma: A RNA deep sequencing analysis of oral buccal mucosa squamous carcinoma model of Chinese hamster
Authors: Xu Guoqiang , Wei Jianing , Huangfu Bing , Gao Jiping , Wang Xiaotang , Xiao Lanfei , Xuan Ruijing , Chen Zhaoyang , Song Guohua 
Published: September 2019

AbstractOral cancer is one of the most common cancers in the world, meanwhile, differentially expressed genes are thought to regulate the development and progression of oral squamous cell carcinomas (OSCC). In this study we screened RNA transcripts from the oral buccal mucosa of healthy male Chinese hamster, divided into 3 groups: a control group with no disposal, a solvent control group coated with acetone solvent, and an experimental group coated with 0.5% DMBA acetone solution by high-throughput RNA sequencing. Tophat and Bowtie were used to align the high-quality reads into transcripts, DEseq was used to analysis the expression of differential gene. Then, the Gene Ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were conducted. The chemokine and TNF signaling pathway were differentially expression and the mRNA expression of CXCL1, CXCL2, CXCL3, CCL7, MMP9, monitored by qRT-PCR, increased remarkably in the cancer group and coincided with the result of RNA-Sequencing. Meanwhile, the CXCL1, CXCL2, CXCL3, and CCL7 are significantly enriched in the chemokine signaling pathway, and CXCL1, CXCL2, CXCL3, and MMP9 are significantly enriched in the tumor necrosis factor (TNF) signaling pathway. The differentially expression of the chemokine and TNF signaling pathway was a response to the invasion of the organism immune system due to oral buccal mucosa squamous carcinoma. All the findings provided novel insights for further molecular researches of oral cancer.
Bub3 and Bub1 maintain the balance of kinetochore-localized Aurora B Kinase and Protein Phosphatase I to Regulate Chromosome Segregation and Anaphase Onset in Meiosis
Authors: Cairo Gisela , MacKenzie Anne M. , Lacefield Soni 
Published: September 2019

AbstractAccurate chromosome segregation depends on proper attachment of kinetochores to spindle microtubules prior to anaphase onset. The Ipl1/Aurora B kinase corrects improper attachments by phosphorylating kinetochore components and so releasing aberrant kinetochore-microtubule interactions. The localization of Ipl1 to kinetochores in budding yeast depends upon multiple pathways, including the Bub1/Bub3 pathway. We show here that in meiosis, Bub3 is crucial for correction of attachment errors. Depletion of Bub3 results in reduced levels of kinetochore-localized Ipl1, and concomitant massive chromosome mis-segregation caused by incorrect chromosome-spindle attachments. Depletion of Bub3 also results in shorter metaphase I and metaphase II due to premature localization of protein phosphatase 1 (PP1) to kinetochores, which antagonizes Ipl1-mediated phosphorylation. We propose a new role for the Bub1-Bub3 pathway in maintaining the balance between kinetochore-localization of Ipl1 and PP1, a balance that is essential for accurate meiotic chromosome segregation and timely anaphase onset.SummaryCairoet alshow that inS. cerevisiaemeiosis, spindle checkpoint proteins Bub1 and Bub3 have an essential role in preventing chromosome mis-segregation and setting the normal duration of anaphase I and anaphase II onset by regulating the kinetochore-localization of Ipl1 and PP1.