bluuebunny/crossref_metadata_2025_split huggingface dataset:
Monitoring the ecological status of rivers with diatom eDNA metabarcoding: A comparison of taxonomic markers and analytical approaches for the inference of a molecular diatom index
Authors: Apothéloz‐Perret‐Gentil Laure , Bouchez Agnès , Cordier Tristan , Cordonier Arielle , Guéguen Julie , Rimet Frederic , Vasselon Valentin , Pawlowski Jan 
Published: September 2020

AbstractRecently, several studies demonstrated the usefulness of diatom eDNA metabarcoding as an alternative to assess the ecological quality of rivers and streams. However, the choice of the taxonomic marker as well as the methodology for data analysis differ between these studies, hampering the comparison of their results and effectiveness. The aim of this study was to compare two taxonomic markers commonly used in diatom metabarcoding and three distinct analytical approaches to infer a molecular diatom index. We used the values of classical morphological diatom index as a benchmark for this comparison. We amplified and sequenced both a fragment of the rbcL gene and the V4 region of the 18S rRNA gene for 112 epilithic samples from Swiss and French rivers. We inferred index values using three analytical approaches: by computing it directly from taxonomically assigned sequences, by calibrating de novo the ecovalues of all metabarcodes, and by using a supervised machine learning algorithm to train predictive models. In general, the values of index obtained using the two “taxonomy‐free” approaches, encompassing molecular assignment and machine learning, were closer correlated to the values of the morphological index than the values based on taxonomically assigned sequences. The correlations of the three analytical approaches were higher in the case of rbcL compared to the 18S marker, highlighting the importance of the reference database which is more complete for the rbcL marker. Our study confirms the effectiveness of diatom metabarcoding as an operational tool for rivers ecological quality assessment and shows that the analytical approaches by‐passing the taxonomic assignments are particularly efficient when reference databases are incomplete.
Westward range expansion from middle latitudes explains the Mississippi River discontinuity in a forest herb of eastern North America
Authors: Prior Carly J. , Layman Nathan C. , Koski Matthew H. , Galloway Laura F. , Busch Jeremiah W. 
Published: September 2020

AbstractIt is often expected that temperate plants have expanded their geographical ranges northward from primarily southern refugia. Evidence for this hypothesis is mixed in eastern North American species, and there is increasing support for colonization from middle latitudes. We studied genome‐wide patterns of variation in RADseq loci to test hypotheses concerning range expansion in a North American forest herb (Campanula americana). First, spatial patterns of genetic differentiation were determined. Then phylogenetic relationships and divergence times were estimated. Spatial signatures of genetic drift were also studied to identify the directionality of recent range expansion and its geographical origins. Finally, spatially explicit scenarios for the spread of plants across the landscape were compared, using variation in the population mutation parameter and Tajima's D. We found strong longitudinal subdivision, with populations clustering into groups west and east of the Mississippi River. While the southeastern region was probably part of a diverse Pleistocene refugium, there is little evidence that range expansion involved founders from these southern locales. Instead, declines in genetic diversity and the loss of rare alleles support a westward colonization wave from a middle latitude refugium near the southern Appalachian Mountains, with subsequent expansion from a Pleistocene staging ground in the Mississippi River Valley (0.51–1.27 million years ago). These analyses implicate stepping stone colonization from middle latitudes as an important mechanism of species range expansion in eastern North America. This study further demonstrates the utility of population genetics as a tool to infer the routes travelled by organisms during geographical range expansion.
FLI1 and ERG protein degradation is regulated via Cathepsin B lysosomal pathway in human dermal microvascular endothelial cells
Authors: Mazzotta Celestina , Marden Grace , Farina Alessandra , Bujor Andreea , Trojanowski Marcin A. , Trojanowska Maria 
Published: September 2020

AbstractObjectivesFriend leukemia integration 1 and erythroblast transformation‐specific, important regulators of endothelial cell homeostasis, are reduced in microvascular endothelial cells in scleroderma patients, and their deficiency has been implicated in disease pathogenesis. The goal of this study was to identify the mechanisms involved in the protein turnover of friend leukemia integration 1 and erythroblast transformation‐specific in microvascular endothelial cells.MethodsThe effects of lysosome and proteosome inhibitors on friend leukemia integration 1 and erythroblast transformation‐specific levels were assessed by Western blotting and capillary morphogenesis. The effect of scleroderma and control sera on the levels of friend leukemia integration 1 and erythroblast transformation‐specific was examined.ResultsThe reduction in the protein levels of friend leukemia integration 1 and erythroblast transformation‐specific in response to interferon α or Poly:(IC) was reversed by blocking either lysosomal (leupeptin and Cathepsin B inhibitor) or proteosomal degradation (MG132). MG132, leupeptin or CTSB‐(i) also counteracted the anti‐angiogenic effects of Poly:(IC) or interferon α. Scleroderma sera reduced protein levels of friend leukemia integration 1 and erythroblast transformation‐specific in comparison to control sera. Treatment with CTSB(i) increased the levels of friend leukemia integration 1 and erythroblast transformation‐specific in a majority of serum‐treated samples.ConclusionsInhibition of cathepsin B was effective in reversing the reduction of friend leukemia integration 1 and erythroblast transformation‐specific protein levels after treatment with interferon α or scleroderma sera, suggesting that targeting cathepsin B may have a beneficial effect in SSc vascular disease.
Transcriptional regulation of the Nε‐fructoselysine metabolism in Escherichia coli by global and substrate‐specific cues
Authors: Graf von Armansperg Benedikt , Koller Franziska , Gericke Nicola , Hellwig Michael , Jagtap Pravin Kumar Ankush , Heermann Ralf , Hennig Janosch , Henle Thomas , Lassak Jürgen 
Published: September 2020

AbstractThermally processed food is an important part of the human diet. Heat‐treatment, however, promotes the formation of so‐called Amadori rearrangement products, such as fructoselysine. The gut microbiota including Escherichia coli can utilize these compounds as a nutrient source. While the degradation route for fructoselysine is well described, regulation of the corresponding pathway genes frlABCD remained poorly understood. Here, we used bioinformatics combined with molecular and biochemical analyses and show that fructoselysine metabolism in E. coli is tightly controlled at the transcriptional level. The global regulator CRP (CAP) as well as the alternative sigma factor σ32 (RpoH) contribute to promoter activation at high cAMP‐levels and inside warm‐blooded hosts, respectively. In addition, we identified and characterized a transcriptional regulator FrlR, encoded adjacent to frlABCD, as fructoselysine‐6‐phosphate specific repressor. Our study provides profound evidence that the interplay of global and substrate‐specific regulation is a perfect adaptation strategy to efficiently utilize unusual substrates within the human gut environment.
Deciphering the Che2 chemosensory pathway and the roles of individual Che2 proteins from Pseudomonas aeruginosa
Authors: Orillard Emilie , Watts Kylie J. 
Published: September 2020

AbstractPseudomonas aeruginosa is an opportunistic pathogen that senses and responds to its environment via four chemosensory systems. Oxygen activates the Che2 chemosensory system by binding to the PAS‐heme domain of the Aer2 receptor. Ostensibly, the output of Che2 occurs via its response regulator CheY2, but controversy persists over CheY2’s exact role. In this study, we show that CheY2 does not interact with the flagellar motor and that the Che2 system does not transfer phosphoryl groups to the chemotaxis (Che) system. We show that CheY2 instead provides feedback control of Aer2 adaptation. In the presence of O2, Aer2 signaling increases the autophosphorylation of the histidine kinase CheA2, followed by CheY2‐mediated dephosphorylation. CheY2 does not stably retain phosphate and may not signal the output of the Che2 system. Rather, CheY2 activity enhances the direct interaction of CheY2 with the adaptation protein CheD (a role often facilitated by CheC, which P. aeruginosa lacks). In the absence of O2, Aer2 does not signal, and CheY2/CheD interactions attenuate. This frees CheD to augment CheR2‐mediated methylation of Aer2, which enhances Aer2 signaling. CheD does not interact with CheR2, but most likely interacts with Aer2 via conserved CheD‐binding motifs to make Aer2 a better methylation substrate.
Impact of biofilm production by Candida species and antifungal therapy on mortality of patients with candidemia
Authors: Lee Chen‐Hsiang , Chen Yi‐Chun , Chen I‐Ling , Chen Fang‐Ju , Chien Chun‐Chih 
Published: September 2020

SummaryBackground and ObjectivesFew studies have investigated the clinical outcomes of patients with candidemia caused by Candida species with different levels of biofilm formation. We aimed to investigate the impact of antifungal therapy on the outcome of candidemia caused by Candida species that were categorised as low biofilm formers (LBFs), moderate biofilm formers (MBFs), and high biofilm formers (HBFs).MethodsAdults with candidemia caused by LBF and HBF/MBF Candida species that were susceptible to fluconazole and caspofungin were included to investigate the impact of treatment with fluconazole vs an echinocandin on 30‐day crude mortality.ResultsIn total, 215 patients with candidemia received fluconazole and 116 patients received an echinocandin. In multivariate analysis, Pittsburgh bacteremia score ≥ 4 (adjusted odds ratio [AOR] =2.42; 95% confidence interval [CI], 1.32‐4.41), malignancy (AOR = 3.45; 95% CI, 1.83‐6.51), not removing the central venous catheter within 48 hours of a positive blood culture (AOR = 4.69; 95% CI, 2.61‐8.45), and treatment with fluconazole for candidemia due to HBF/MBF Candida spp. (AOR = 2.23; 95% CI, 1.22‐4.06) were independent factors associated with 30‐day mortality. Of the 165 patients infected by HBF/MBF Candida isolates, those who received azole therapy had a significantly higher sepsis‐related mortality rate than those who received echinocandin therapy (44.9% [49/109] vs 26.8% [15/56], P = .03).ConclusionsThere was a trend of an independent association between fluconazole treatment and poor outcomes in the patients infected by HBF/MBF Candida strains.
Neurogeriatric approach to delirium/dementia in a multi‐faculty university hospital
Authors: Sakakibara Ryuji , Katsuragawa Shuichi , Iimura Ayako , Ogata Tsuyoshi , Terayama Keiichiro , Doi Hirokazu , Suzuki Keiko , Tateno Fuyuki , Aiba Yosuke , Sato Megumi 
Published: September 2020

AbstractObjectiveDelirium/dementia (collectively called cognitive spectrum disorder [CSD]) is a major issue in hospital wards. However, few reports are available on the incidence of CSD on multi‐faculty wards or on the factors contributing to it. The aim of this study was to address these issues by a neurogeriatric team (neurologists, psychiatrists, specialist nurses, and link nurses from all wards).Patients and MethodsThis was a retrospective study with a 12‐month recruiting period, a prospective follow‐up period of 3.0 ± 2.5 weeks, and ≥1×/week visits. We diagnosed acute‐onset delirium by the Confusion Assessment Method and analyzed underlying conditions. We also diagnosed premorbid dementia by neurocognitive examination and neuroimaging following published criteria.ResultsOur subjects were 723 CSD from 15 faculties, accounting for 6.5% of admissions, 393 men and 330 women, mean age 81 years. CSD was prevalent in cardiology/cardiac surgery (CAR), orthopedic surgery (OP), and neurology/neurosurgery (N), with dementia alone in ophthalmology and a combination of delirium/dementia in the other faculties. Premorbid dementia were diagnosed with Alzheimer's disease (AD), white matter disease, dementia with Lewy bodies (DLB), or some combination of these. Delirium was accompanied by worsening of gait difficulty. The ratio of brain (N) versus extra‐brain was 105 (14.5%):618 (85.5%). Severe CSD was common in DLB than AD but without statistical significance.ConclusionTotal 6.5% of hospital admissions showed CSD, with CAR, OP, and N being prevalent. The ratio of brain versus extra‐brain was 14.5%:85.5%. Severe CSD was more prevalent in DLB patients than in AD patients, but without statistical significance.
A novel multi‐exon deletion in the dysferlin gene of a limb‐girdle muscular dystrophy type 2B Filipino patient
Authors: Porto Kristine Joyce L. , Mitsui Jun , Ishiura Hiroyuki , Kubota Akatsuki , Luspian Kathleen Jaye L. , Eduardo Emmanuel , Damian Ludwig , Toda Tatsushi , Tsuji Shoji 
Published: September 2020

AbstractWe present a 34‐year‐old woman, from Philippines, diagnosed limb‐girdle muscular dystrophy type 2B with compound heterozygous nonsense mutation W1478* and novel deletion of exons 43‐46 of the dysferlin gene. These loss‐of‐function mutations do not seem to be predictive of a severer clinical course. We report the first identification of microhomologous region of 2 bp (TG) identical sequences surrounding the breakpoint junction. Detailed analysis of the deleted allele should be pursued in order to better understand the underlying mechanism of genomic rearrangements of the dysferlin gene.
Recurrent severe and long‐lasting cerebellar ataxia attacks in adult‐onset neuronal intranuclear inclusion disease
Authors: Osakada Yosuke , Deguchi Kentaro , Deguchi Shoko , Higaki Fumiyo , Oda Wakako , Yoshida Mari , Ohta Yasuyuki , Yamashita Toru , Abe Koji 
Published: September 2020

AbstractNeuronal intranuclear inclusion disease (NIID) is a progressive neurodegenerative disease that is characterized by eosinophilic hyaline intranuclear inclusions. NIID presents highly variable clinical manifestations such as dementia, ataxia, convulsion, neuropathy, and autonomic dysfunction. A 60‐year‐old woman developed recurrent severe cerebellar ataxia (SARA score: 30/40 points). She was diagnosed with adult‐onset NIID by a characteristic brain diffusion‐weighed imaging hyperintensity lesion in subcortical white matter and intranuclear inclusion bodies in a skin biopsy. Her ataxia was more severe and lasted longer (additional 19 days) than a previous case, although she showed remarkable improvement.
Lotus japonicus Nuclear Factor YA1, a nodule emergence stage‐specific regulator of auxin signalling
Authors: Shrestha Arina , Zhong Sihui , Therrien Jasmine , Huebert Terry , Sato Shusei , Mun Terry , Andersen Stig U. , Stougaard Jens , Lepage Agnes , Niebel Andreas , Ross Loretta , Szczyglowski Krzysztof 
Published: September 2020

Summary

Organogenesis of legume root nodules begins with the nodulation factor‐dependent stimulation of compatible root cells to initiate divisions, signifying an early nodule primordium formation event. This is followed by cellular differentiation, including cell expansion and vascular bundle formation, and we previously showed that Lotus japonicus NF‐YA1 is essential for this process, presumably by regulating three members of the SHORT INTERNODES/STYLISH (STY) transcription factor gene family.

In this study, we used combined genetics, genomics and cell biology approaches to characterize the role of STY genes during root nodule formation and to test a hypothesis that they mediate nodule development by stimulating auxin signalling.

We show here that L. japonicus STYs are required for nodule emergence. This is attributed to the NF‐YA1‐dependent regulatory cascade, comprising STY genes and their downstream targets, YUCCA1 and YUCCA11, involved in a local auxin biosynthesis at the post‐initial cell division stage. An analogous NF‐YA1/STY regulatory module seems to operate in Medicago truncatula in association with the indeterminate nodule patterning.

Our data define L. japonicus and M. truncatula NF‐YA1 genes as important nodule emergence stage‐specific regulators of auxin signalling while indicating that the inductive stage and subsequent formation of early nodule primordia are mediated through an independent mechanism(s).
CERBERUS is critical for stabilization of VAPYRIN during rhizobial infection in Lotus japonicus
Authors: Liu Miaoxia , Jia Ning , Li Xiaolin , Liu Ruijun , Xie Qi , Murray Jeremy D. , Downie J. Allan , Xie Fang 
Published: September 2020

Summary

CERBERUS (also known as LIN) and VAPYRIN (VPY) are essential for infection of legumes by rhizobia and arbuscular mycorrhizal fungi (AMF). Medicago truncatula LIN (MtLIN) was reported to interact with MtVPY, but the significance of this interaction is unclear and the function of VPY in Lotus japonicus has not been studied.

We demonstrate that CERBERUS has auto‐ubiquitination activity in vitro and is localized within distinct motile puncta in L. japonicus root hairs and in Nicotiana benthamiana leaves. CERBERUS colocalized with the trans‐Golgi network/early endosome markers.

In L. japonicus, two VPY orthologs (LjVPY1 and LjVPY2) were identified. CERBERUS interacted with and colocalized with both LjVPY1 and LjVPY2. Co‐expression of CERBERUS with LjVPY1 or LjVPY2 in N. benthamiana led to increased protein levels of LjVPY1 and LjVPY2, which accumulated as mobile punctate bodies in the cytoplasm. Conversely, LjVPY2 protein levels decreased in cerberus roots after rhizobial inoculation. Mutant analysis indicates that LjVPY1 and LjVPY2 are required for rhizobial infection and colonization by AMF.

Our data suggest that CERBERUS stabilizes LjVPY1 and LjVPY2 within the trans‐Golgi network/early endosome, where they might function to regulate endocytic trafficking and/or the formation or recycling of signaling complexes during rhizobial and AMF symbiosis.
CircCDK8 regulates osteogenic differentiation and apoptosis of PDLSCs by inducing ER stress/autophagy during hypoxia
Authors: Zheng Jingjing , Zhu Ximei , He Yani , Hou Siyu , Liu Ting , Zhi Keqian , Hou Tiezhou , Gao Ling 
Published: September 2020

AbstractMounting evidence indicates that circular RNAs (circRNAs) have essential roles in several diseases, including periodontitis. Periodontal ligament stem cells (PDLSCs) exhibit potential for treating periodontitis accompanied by hypoxia. However, it is unclear how circRNA affects the osteogenesis of PDLSCs under hypoxia. In this study, a novel circRNA, hsa_circ_0003489, was found located at the gene for cyclin‐dependent kinase 8 (CDK8) and referred to as circCDK8. The expression levels of circCDK8 and hypoxia‐inducible factor‐1α were significantly increased in periodontitis tissues, and the expression of circCDK8 was further confirmed in a hypoxia model using cobalt chloride (CoCl2). Interestingly, the results showed that the expression levels of osteoblast markers (RUNX2, ALP, OCN, and COL1A1) were increased in CoCl2‐treated PDLSCs at 6 and 12 h, but decreased at 24, 48, and 72 h. On the basis of bioinformatics and functional experiments, CoCl2 also induced endoplasmic reticulum stress, autophagy, and apoptosis of PDLSCs; the inhibition of autophagy promoted the osteogenic differentiation of CoCl2‐treated PDLSCs. Furthermore, circCDK8 overexpression induced autophagy and apoptosis through mTOR signaling, and circCDK8 silencing reversed the inhibitory effects of CoCl2 on osteogenic differentiation of PDLSCs. In conclusion, our results indicate that circCDK8 represses the osteogenic differentiation of PDLSCs by triggering autophagy activation in a hypoxic microenvironment. CircCDK8 could be a new therapeutic target of periodontitis.
Changes in DNA methylation accompany changes in gene expression during chondrocyte hypertrophic differentiation in vitro
Authors: Singh Purva , Lessard Samantha G. , Mukherjee Piali , Rourke Brennan , Otero Miguel 
Published: September 2020

AbstractDuring osteoarthritis (OA), articular chondrocytes undergo phenotypic changes that resemble developmental patterns characteristic of growth plate chondrocytes. These phenotypic alterations lead to a hypertrophy‐like phenotype characterized by altered production of extracellular matrix constituents and increased collagenase activity, which, in turn, results in cartilage destruction in OA disease. Recent studies have shown that the phenotypic instability and dysregulated gene expression in OA are associated with changes in DNA methylation patterns. Subsequent efforts have aimed to identify changes in DNA methylation with functional impact in OA disease, to potentially uncover therapeutic targets. Here, we paired an in vitro 3D/pellet culture system that mimics chondrocyte hypertrophy with RNA sequencing (RNA‐Seq) and enhanced reduced representation of bisulfite sequencing (ERRBS) to identify transcriptomic and epigenomic changes in murine primary articular chondrocytes undergoing hypertrophy‐like differentiation. We identified hypertrophy‐associated changes in DNA methylation patterns in vitro. Integration of RNA‐Seq and ERRBS datasets identified associations between changes in methylation and gene expression. Our integrative analyses showed that hypertrophic differentiation of articular chondrocytes is accompanied by transcriptomic and epigenomic changes in vitro. We believe that our integrative approaches have the potential to uncover new targets for therapeutic intervention.
Polyamines in the virulence of bacterial pathogens of respiratory tract
Authors: Banerji Rajashri , Kanojiya Poonam , Patil Amrita , Saroj Sunil D. 
Published: September 2020

AbstractPolyamines are positively charged hydrocarbons that are essential for the growth and cellular maintenance in prokaryotes and eukaryotes. Polyamines have been demonstrated to play a role in bacterial pathogenicity and biofilm formation. However, the role of extracellular polyamines as a signaling molecule in the regulation of virulence is not investigated in detail. The bacterial pathogens residing in the respiratory tract remain asymptomatic for an extended period; however, the factors that lead to symptomatic behavior are poorly understood. Further investigation to understand the relation between the host‐secreted factors and virulence of pathogenic bacteria in the respiratory tract may provide insights into the pathogenesis of respiratory tract infections. Polyamines produced within the bacterial cell are generally sequestered. Therefore, the pool of extracellular polyamines formed by secretion of the commensals and the host may be one of the signaling molecules that might contribute toward the alterations in the expression of virulence factors in bacterial pathogens. Besides, convergent mechanisms of polyamine biosynthesis do exist across the border of species and genus level. Also, several novel polyamine transporters in the host and bacteria remain yet to be identified. The review focuses on the role of polyamines in the expression of virulence phenotypes and biofilm formation of the respiratory tract pathogens.