bluuebunny/crossref_metadata_2025_split huggingface dataset:
Transcriptome Analyses of Heart and Liver Reveal Novel Pathways for Regulating Songbird Migration
Authors: Horton William J. , Jensen Matthew , Sebastian Aswathy , Praul Craig A. , Albert Istvan , Bartell Paul A. 
Published: April 2019

AbstractMany birds undertake long biannual voyages during the night. During these times of the year birds drastically reduce their amount of sleep, yet curiously perform as well on tests of physical and cognitive performance than during non-migrating times of the year. This inherent physiological protection disappears when birds are forced to stay awake at other times of the year; thus these protective changes are only associated with the nocturnal migratory state. The goal of the current study was to identify the physiological mechanisms that confer protection against the consequences of sleep loss while simultaneously allowing for the increased physical performance required for migration. We performed RNA-seq analyses of heart and liver collected from birds at different times of day under different migratory states and analyzed these data using differential expression, pathway analysis and WGCNA. We identified changes in gene expression networks implicating multiple systems and pathways. These pathways regulate many aspects of metabolism, immune function, wound repair, and protection of multiple organ systems. Consequently, the circannual program controlling the appearance of the migratory phenotype involves the complex regulation of diverse gene networks associated with the physical demands of migration.
Long intergenic non-coding RNAs regulate human lung fibroblast function: Implications for idiopathic pulmonary fibrosis
Authors: Hadjicharalambous Marina R. , Roux Benoit T. , Csomor Eszter , Feghali-Bostwick Carol A. , Murray Lynne A. , Clarke Deborah L. , Lindsay Mark A. 
Published: April 2019

AbstractPhenotypic changes in lung fibroblasts are believed to contribute to the development of Idiopathic Pulmonary Fibrosis (IPF), a progressive and fatal lung disease. Long intergenic non-coding RNAs (lincRNAs) have been identified as novel regulators of gene expression and protein activity. In non-stimulated cells, we observed reduced proliferation and inflammation but no difference in the fibrotic response of IPF fibroblasts. These functional changes in non-stimulated cells were associated with changes in the expression of the histone marks, H3K4me1, H3K4me3 and H3K27ac indicating a possible involvement of epigenetics. Following activation with TGF-β1 and IL-1β, we demonstrated an increased fibrotic but reduced inflammatory response in IPF fibroblasts. There was no significant difference in proliferation following PDGF exposure. The lincRNAs, LINC00960 and LINC01140 were upregulated in IPF fibroblasts. Knockdown studies showed that LINC00960 and LINC01140 were positive regulators of proliferation in both control and IPF fibroblasts but had no effect upon the fibrotic response. Knockdown of LINC01140 but not LINC00960 increased the inflammatory response, which was greater in IPF compared to control fibroblasts. Overall, these studies demonstrate for the first time that lincRNAs are important regulators of proliferation and inflammation in human lung fibroblasts and that these might mediate the reduced inflammatory response observed in IPF-derived fibroblasts.
Mutation-specific peripheral and ER quality control of hERG channel cell-surface expression
Authors: Foo Brian , Barbier Camille , Guo Kevin , Vasantharuban Jaminie , Lukacs Gergely L. , Shrier Alvin 
Published: April 2019

AbstractImpaired functional plasma membrane (PM) expression of the hERG K+-channel is associated with Long-QT syndrome type-2 (LQT2) and increased risk of cardiac arrhythmia. Reduced PM-expression is primarily attributed to retention and degradation of misfolded channels by endoplasmic reticulum (ER) protein quality control (QC) systems. However, as the molecular pathogenesis of LQT2 was defined using severely-misfolded hERG variants with limited PM-expression, the potential contribution of post-ER (peripheral) QC pathways to the disease phenotype remains poorly established. Here, we investigate the cellular processing of mildly-misfolded Per-Arnt-Sim (PAS)-domain mutant hERGs, which display incomplete ER-retention and PM-expression defects at physiological temperature. We show that the attenuated PM-expression of hERG is dictated by mutation-specific contributions from both the ER and peripheral QC systems. At the ER, PAS-mutants experience inefficient conformational maturation coupled with rapid ubiquitin-dependent proteasomal degradation. In post-ER compartments, they are rapidly endocytosed from the PM via a ubiquitin-independent mechanism and rapidly targeted for lysosomal degradation. Conformational destabilization underlies aberrant cellular processing at both ER- and post-ER compartments, since conformational correction by a hERG-specific pharmacochaperone or low-temperatures can restore WT-like trafficking. Our results demonstrate that the post-ER QC alone or jointly with the ER QC determines the loss-of-PM-expression phenotype of a subset of LQT2 mutations.
Prediction of a typhoon track using a generative adversarial network and satellite images
Authors: Rüttgers Mario , Lee Sangseung , Jeon Soohwan , You Donghyun 
Published: April 2019

AbstractTracks of typhoons are predicted using a generative adversarial network (GAN) with satellite images as inputs. Time series of satellite images of typhoons which occurred in the Korea Peninsula in the past are used to train the neural network. The trained GAN is employed to produce a 6-hour-advance track of a typhoon for which the GAN was not trained. The predicted track image of a typhoon favorably identifies the future location of the typhoon center as well as the deformed cloud structures. Errors between predicted and real typhoon centers are measured quantitatively in kilometers. An averaged error of 95.6 km is achieved for tested 10 typhoons. Predicting sudden changes of the track in westward or northward directions is identified as a challenging task, while the prediction is significantly improved, when velocity fields are employed along with satellite images.
First report of Salmonella 1,4,[5],12:i:- in free-ranging striped dolphins (Stenella coeruleoalba), Italy
Authors: Grattarola C. , Gallina S. , Giorda F. , Pautasso A. , Ballardini M. , Iulini B. , Varello K. , Goria M. , Peletto S. , Masoero L. , Serracca L. , Romano A. , Dondo A. , Zoppi S. , Garibaldi F. , Scaglione F. E. , Marsili L. , Di Guardo G. , Lettini A. A. , Mignone W. , Fernandez A. , Casalone C. 
Published: April 2019

AbstractBetween 2015 and the beginning of 2018 (January-March), 30 cetaceans were found stranded along the Ligurian Sea coast of Italy. Necropsies were performed in 22 cases and infectious diseases resulted the most common cause of death. Three striped dolphins, showed a severe coinfection involving the monophasic variant of Salmonella Typhimurium (Salmonella 1,4,[5],12:i:-). The isolates were characterized based on antimicrobial resistance, Multiple-Locus Variable-number tandem-repeat Analysis (MLVA) and whole-genome sequencing (WGS). All isolates demonstrated the same multidrug resistant genotype (ASSuT isolates), showed three different MLVA profiles, two of which closely related, and were identified as Sequence Type 34. Moreover, Single nucleotide polymorphisms (SNP) analysis confirmed strong correlations between two out of the three isolates. To our knowledge, S. 1,4,[5],12:i:-, one of the most common serovars in cases of human infection and food sources worldwide, has not previously been described in marine mammals, and reports of Salmonella-associated disease in free-ranging cetaceans are rare. These results highlight the role of cetaceans as sentinel species for zoonotic and terrestrial pathogens in the marine environment, suggest a potential risk for cetaceans and public health along the North Western Italian coastline and indicate cetaceans as a novel potential reservoir for one of the most widespread Salmonella serovars.
Functional compartmentalization in the hemocoel of insects
Authors: Pendar Hodjat , Aviles Jessica , Adjerid Khaled , Schoenewald Caroline , Socha John J. 
Published: April 2019

AbstractThe insect circulatory system contains an open hemocoel, in which the mechanism of hemolymph flow control is ambiguous. As a continuous fluidic structure, this cavity should exhibit pressure changes that propagate quickly. Narrow-waisted insects create sustained pressure differences across segments, but their constricted waist provides an evident mechanism for compartmentalization. Insects with no obvious constrictions between segments may be capable of functionally compartmentalizing the body, which could explain complex hemolymph flows. Here, we test the hypothesis of functional compartmentalization by measuring pressures in a beetle and recording abdominal movements. We found that the pressure is indeed uniform within the abdomen and thorax, congruent with the predicted behavior of an open system. However, during some abdominal movements, pressures were on average 62% higher in the abdomen than in the thorax, suggesting that functional compartmentalization creates a gradient within the hemocoel. Synchrotron tomography and dissection show that the arthrodial membrane and thoracic muscles may contribute to this dynamic pressurization. Analysis of volume change suggests that the gut may play an important role in regulating pressure by translating between body segments. Overall, this study suggests that functional compartmentalization may provide an explanation for how fluid flows are managed in an open circulatory system.
Intra- and interobserver reproducibility of pancreatic perfusion by computed tomography
Authors: Garcia Tiago S. , Engelholm Jean-Luc , Vouche Michaël , Hirakata Vânia N. , Leitão Cristiane B. 
Published: April 2019

AbstractThe aim of this study was to measure intra- and interobserver agreement among radiologists in the assessment of pancreatic perfusion by computed tomography (CT). Thirty-nine perfusion CT scans were analyzed. The following parameters were measured by three readers: blood flow (BF), blood volume (BV), mean transit time (MTT) and time to peak (TTP). Statistical analysis was performed using the Bland-Altman method, linear mixed model analysis, and intraclass correlation coefficient (ICC). There was no significant intraobserver variability for the readers regarding BF, BV or TTP. There were session effects for BF in the pancreatic body and MTT in the pancreatic tail and whole pancreas. There were reader effects for BV in the pancreatic head, pancreatic body and whole pancreas. There were no effects for the interaction between session and reader for any perfusion parameter. ICCs showed substantial agreement for the interobserver measurements and moderate to substantial agreement for the intraobserver measurements, with the exception of MTT. In conclusion, satisfactory reproducibility of measurements was observed for TTP in all pancreatic regions, for BF in the head and BV in the tail, and these parameters seem to ensure a reasonable estimation of pancreatic perfusion.
MeshMonk: Open-source large-scale intensive 3D phenotyping
Authors: White Julie D. , Ortega-Castrillón Alejandra , Matthews Harold , Zaidi Arslan A. , Ekrami Omid , Snyders Jonatan , Fan Yi , Penington Tony , Van Dongen Stefan , Shriver Mark D. , Claes Peter 
Published: April 2019

AbstractDense surface registration, commonly used in computer science, could aid the biological sciences in accurate and comprehensive quantification of biological phenotypes. However, few toolboxes exist that are openly available, non-expert friendly, and validated in a way relevant to biologists. Here, we report a customizable toolbox for reproducible high-throughput dense phenotyping of 3D images, specifically geared towards biological use. Given a target image, a template is first oriented, repositioned, and scaled to the target during a scaled rigid registration step, then transformed further to fit the specific shape of the target using a non-rigid transformation. As validation, we use n = 41 3D facial images to demonstrate that the MeshMonk registration is accurate, with 1.26 mm average error, across 19 landmarks, between placements from manual observers and using the MeshMonk toolbox. We also report no variation in landmark position or centroid size significantly attributable to landmarking method used. Though validated using 19 landmarks, the MeshMonk toolbox produces a dense mesh of vertices across the entire surface, thus facilitating more comprehensive investigations of 3D shape variation. This expansion opens up exciting avenues of study in assessing biological shapes to better understand their phenotypic variation, genetic and developmental underpinnings, and evolutionary history.
Dysregulation of Neuronal Gαo Signaling by Graphene Oxide in Nematode Caenorhabditis elegans
Authors: Liu Peidang , Shao Huimin , Ding Xuecheng , Yang Ruilong , Rui Qi , Wang Dayong 
Published: April 2019

AbstractExposure to graphene oxide (GO) induced some dysregulated microRNAs (miRNAs), such as the increase in mir-247, in nematode Caenorhabditis elegans. We here further identified goa-1 encoding a Gαo and pkc-1 encoding a serine/threonine protein kinase as the targets of neuronal mir-247 in the regulation of GO toxicity. GO exposure increased the expressions of both GOA-1 and PKC-1. Mutation of goa-1 or pkc-1 induced a susceptibility to GO toxicity, and suppressed the resistance of mir-247 mutant to GO toxicity. GOA-1 and PKC-1 could also act in the neurons to regulate the GO toxicity, and neuronal overexpression of mir-247 could not affect the resistance of nematodes overexpressing neuronal goa-1 or pkc-1 lacking 3′-UTR to GO toxicity. In the neurons, GOA-1 acted upstream of diacylglycerol kinase/DGK-1 and PKC-1 to regulate the GO toxicity. Moreover, DGK-1 and GOA-1 functioned synergistically in the regulation of GO toxicity. Our results highlight the crucial role of neuronal Gαo signaling in response to GO in nematodes.
Gene co-expression networks contributing to the expression of compensatory growth in metabolically active tissues in cattle
Authors: Keogh Kate , Kenny David A. , Waters Sinead M. 
Published: April 2019

AbstractCompensatory growth (CG) is an accelerated growth phenomenon which occurs in animals upon re-alimentation following a period of dietary restriction. The objective of this study was to perform gene co-expression analysis on metabolic tissues of animals undergoing CG, in order to elucidate the molecular control governing this phenomenon. Thirty Holstein Friesian bulls were fed a restricted diet for 125 days, after which they received feed ad libitum. Following 55 days of ad libitum feeding all animals were slaughtered. RNAseq and gene co-expression analyses were performed on tissue samples collected at slaughter including liver, rumen papillae and jejunum epithelium tissues. A period of CG resulted in 15 networks of co-expressed genes. One network of genes, involved in proteasome core complex, signal transduction and protein synthesis was found to be similar across liver and jejunum tissue datasets (r = 0.68, P = 0.04). Results from this study also showed that a large portion of co-expressed genes had not previously been implicated in the expression of CG, thus this study identifies novel genes involved in controlling CG across tissues, with hub genes holding potential for use as biomarkers for the selection of animals with a greater propensity to display CG.
Selenium nanoparticles for targeted stroke therapy through modulation of inflammatory and metabolic signaling
Authors: Amani Hamed , Habibey Rouhollah , Shokri Fereshteh , Hajmiresmail Seyed Javad , Akhavan Omid , Mashaghi Alireza , Pazoki-Toroudi Hamidreza 
Published: April 2019

AbstractIschemic cerebral stroke is a major cause of death and morbidity. Currently, no neuroprotective agents have been shown to impact the clinical outcomes in cerebral stroke cases. Here, we report therapeutic effects of Se nanoparticles on ischemic stroke in a murine model. Anti-transferrin receptor monoclonal antibody (OX26)-PEGylated Se nanoparticles (OX26-PEG-Se NPs) were designed and synthesized and their neuroprotective effects were measured using in vitro and in vivo approaches. We demonstrate that administration of the biodegradable nanoparticles leads to resolution of brain edema, protection of axons in hippocampus region, and myelination of hippocampal area after cerebral ischemic stroke. Our nanoparticle design ensures efficient targeting and minimal side effects. Hematological and biochemical analyses revealed no undesired NP-induced changes. To gain mechanistic insights into the therapeutic effects of these particles, we characterized the changes to the relevant inflammatory and metabolic signaling pathways. We assessed metabolic regulator mTOR and related signaling pathways such as hippo, Ubiquitin-proteasome system (ERK5), Tsc1/Tsc2 complex, FoxO1, wnt/β-catenine signaling pathway. Moreover, we examined the activity of jak2/stat3 signaling pathways and Adamts1, which are critically involved in inflammation. Together, our study provides a promising treatment strategy for cerebral stroke based on Se NP induced suppression of excessive inflammation and oxidative metabolism.
Citrate synthase from Synechocystis is a distinct class of bacterial citrate synthase
Authors: Ito Shoki , Koyama Naoto , Osanai Takashi 
Published: April 2019

AbstractCitrate synthase (CS, EC 2.3.3.1) catalyses the initial reaction of the tricarboxylic acid (TCA) cycle. Although CSs from heterotrophic bacteria have been extensively studied, cyanobacterial CSs are not well-understood. Cyanobacteria can produce various metabolites from carbon dioxide. Synechocystis sp. PCC 6803 (Synechocystis 6803) is a cyanobacterium used to synthesize metabolites through metabolic engineering techniques. The production of acetyl-CoA-derived metabolites in Synechocystis 6803 has been widely examined. However, the biochemical mechanisms of reactions involving acetyl-CoA in Synechocystis 6803 are poorly understood. We characterised the CS from Synechocystis 6803 (SyCS) and compared its characteristics with other bacterial CSs. SyCS catalysed only the generation of citrate, and did not catalyse the cleavage of citrate. It is suggested that SyCS is not related to the reductive TCA cycle. The substrate affinity and turnover number of SyCS were lower than those of CSs from heterotrophic bacteria. SyCS was activated by MgCl2 and CaCl2, which inhibit various bacterial CSs. SyCS was not inhibited by ATP and NADH; which are typical feedback inhibitors of other bacterial CSs. SyCS was inhibited by phosphoenolpyruvate and activated by ADP, which has not been reported for CSs from heterotrophic bacteria. Thus, SyCS showed unique characteristics, particularly its sensitivity to effectors.
Precise definition of PTEN C-terminal epitopes and its implications in clinical oncology
Authors: Mingo Janire , Luna Sandra , Gaafar Ayman , Nunes-Xavier Caroline E. , Torices Leire , Mosteiro Lorena , Ruiz Rebeca , Guerra Isabel , Llarena Roberto , Angulo Javier C. , López José I. , Pulido Rafael 
Published: April 2019

AbstractAnti-PTEN monoclonal antibodies (mAb) are arising as important tools for immunohistochemistry (IHC) and protein quantification routine analysis in clinical oncology. Although an effort has been made to document the reliability of tumor tissue section immunostaining by anti-PTEN mAb, and to standardize their IHC use in research and in the clinical practice, the precise topological and biochemical definition of the epitope recognized by each mAb has been conventionally overlooked. In this study, six commercial anti-PTEN mAb have been validated and characterized for sensitivity and specificity by IHC and FISH, using a set of prostate and urothelial bladder tumor specimens, and by immunoblot, using PTEN positive and PTEN negative human cell lines. Immunoblot precise epitope mapping, performed using recombinant PTEN variants and mutations, revealed that all mAb recognized linear epitopes of 6–11 amino acid length at the PTEN C-terminus. Tumor-associated or disease-associated mutations at the PTEN C-terminus did not affect subcellular localization or PIP3 phosphatase activity of PTEN in cells, although resulted in specific loss of reactivity for some mAb. Furthermore, specific mimicking-phosphorylation mutations at the PTEN C-terminal region also abolished binding of specific mAb. Our study adds new evidence on the relevance of a precise epitope mapping in the validation of anti-PTEN mAb for their use in the clinics. This will be substantial to provide a more accurate diagnosis in clinical oncology based on PTEN protein expression in tumors and biological fluids.
Laterally confined photonic crystal surface emitting laser incorporating monolayer tungsten disulfide
Authors: Ge Xiaochen , Minkov Momchil , Fan Shanhui , Li Xiuling , Zhou Weidong 
Published: April 2019

AbstractWith an ultimately thin active region, monolayer transition metal dichalcogenide lasers have the potential of realizing ultralow lasing threshold and power consumption. The flexibility also enables integration possibilities on unconventional substrates. Here, we report a photonic crystal surface emitting laser using monolayer tungsten disulfide as the gain medium. The cavity design utilizes a heterostructure in the photonic crystal lattice to provide lateral confinement for a high quality factor with a compact active region. Room-temperature continuous wave lasing is realized after integrating monolayer tungsten disulfide flakes onto the silicon nitride photonic crystal on a quartz substrate. Highly directional, near surface-normal emission has also been experimentally demonstrated. The work reported here demonstrates that a large-area single-mode directional laser can be realized from a monolayer gain medium, which is critical for laser scaling for on-chip integration in data and sensing applications.
miR-20a regulates sensitivity of colorectal cancer cells to NK cells by targeting MICA
Authors: Tang Siwen , Fu Hongyu , Xu Qihua , Zhou Ying 
Published: April 2019

Abstract
Colorectal cancer (CRC) is one of the leading cancer-related causes of deaths in the world. Recently, microRNAs have been reported to regulate the tumor growth, invasion and the immunosuppression. In the present study, we found that miR-20a was increased in human CRC specimens compared with the healthy normal tissues. However, miR-20a overexpression and knockdown did not impair the CRC cell growth in vitro. Our results indicated that CD107a+ NK cells are increased in CRC group. Furthermore, cytotoxicity assays demonstrated that miR-20a knockdown promoted the CRC cells sensitive to NK cells, whereas miR-20a overexpression showed the opposite results. Our results suggest that the regulation of NK cells by miR-20a depends on NKG2D. Luciferase reporter assays revealed that the NKG2D ligand Major Histocompatibility Complex (MHC) class I-related chain genes A (MICA) is the direct target of miR-20a. Flow cytometry showed the MICA protein level is significantly reduced in miR-20a-overexpressing CRC cells and increased in miR-20a knockdown CRC cells. Taken together, our results suggest that miR-20a regulates sensitivity of CRC cells to NK cells by targeting MICA.