bluuebunny/crossref_metadata_2025_split huggingface dataset:
Affective priming and cognitive load: Event‐related potentials suggest an interplay of implicit affect misattribution and strategic inhibition
Authors: Gibbons Henning , Seib‐Pfeifer Laura‐Effi , Koppehele‐Gossel Judith , Schnuerch Robert 
Published: September 2017

AbstractPrior research suggests that the affective priming effect denoting prime‐congruent evaluative judgments about neutral targets preceded by affective primes increases when the primes are processed less deeply. This has been taken as evidence for greater affect misattribution. However, no study so far has combined an experimental manipulation of the depth of prime processing with the benefits of ERPs. Forty‐seven participants made like/dislike responses about Korean ideographs following 800‐ms affective prime words while 64‐channel EEG was recorded. In a randomized within‐subject design, three levels of working‐memory load were applied specifically during prime processing. Affective priming was significant for all loads and even tended to decrease over loads, although efficiency of the load manipulation was confirmed by reduced amplitudes of posterior attention‐sensitive prime ERPs. Moreover, ERPs revealed greater explicit affective discrimination of the prime words as load increased, with strongest valence effects on central/centroparietal N400 and on the parietal/parietooccipital late positive complex under high load. This suggests that (a) participants by default tried to inhibit the processing of the prime's affect, and (b) inhibition more often failed under cognitive load, thus causing emotional breakthrough that resulted in a binding of affect to the prime and, hence, reduced affect misattribution to the target. As a correlate of affective priming in the target ERP, medial‐frontal negativity, a well‐established marker of (low) stimulus value, increased with increasing negative affect of the prime. Findings support implicit prime‐target affect transfer as a major source of affective priming, but also point to the role of strategic top‐down processes.
Blood conservation in cardiac surgery
Authors: Blaudszun G. , Butchart A. , Klein A. A. 
Published: September 2017

SUMMARYThis article aims at reviewing the currently available evidence about blood conservation strategies in cardiac surgery. Pre‐operative anaemia and perioperative allogeneic blood transfusions are associated with worse outcomes after surgery. In addition, transfusions are a scarce and costly resource. As cardiac surgery accounts for a significant proportion of all blood products transfused, efforts should be made to decrease the risk of perioperative transfusion. Pre‐operative strategies focus on the detection and treatment of anaemia. The management of haematological abnormalities, most frequently functional iron deficiency, is a matter for debate. However, iron supplementation therapy is increasingly commonly administered. Intra‐operatively, antifibrinolytics should be routinely used, whereas the cardiopulmonary bypass strategy should be adapted to minimise haemodilution secondary to circuit priming. There is less evidence to recommend minimally invasive surgery. Cell salvage and point‐of‐care tests should also be a part of the routine care. Post‐operatively, any unnecessary iatrogenic blood loss should be avoided.
Analysis of Argonaute 2–microRNA complexes in ex vivo stored red blood cells
Authors: Vu Long , Ragupathy Viswanath , Kulkarni Sandhya , Atreya Chintamani 
Published: September 2017

BACKGROUNDHuman enucleated mature red blood cells (RBCs) contain both mature microRNAs (miRNAs) and mRNAs, and we have previously correlated RBC storage lesion processes such as eryptosis, adenosine 5′‐triphosphate loss, and RBC indices with differentially expressed miRNAs. Here we have characterized Argonaute 2 (AGO2)–miRNA complexes in stored mature RBCs as a first step toward understanding their role, if any.STUDY DESIGN AND METHODSIn this report AGO2‐bound miRNAs in mature RBCs isolated from RBCs collected from three different healthy donors and stored for 24 hours at 4 to 6°C were identified by anti‐AGO2 immunoprecipitation (IP) followed by next‐generation sequencing of the RNA isolated from the IP. The data were analyzed by various bioinformatics tools.RESULTSThe analysis highlighted 28 mature AGO2‐bound miRNAs that are common to all three donors, representing 95.6% of the identified miRNAs. Among these, miR‐16‐5p (20.6%), miR‐451a‐5p (16.7%), miR‐486‐5p (12.6%), and miR‐92a‐3p (12.6%) are the most abundant miRNAs. Functional enrichment analysis for mRNA targets of the 28 common miRNAs identified molecules related to various diseases, biofunctions, and toxicity functions such as cardio‐, hepato‐, and nephrotoxicity.CONCLUSIONOverall, these results demonstrate the existence of multiple intracellular AGO2‐bound miRNAs in 24‐hour‐stored RBCs and warrant further experiments to determine whether AGO2‐miRNAs are functional in RBCs.
Intrarenal Mas and AT1 receptors play a role in mediating the excretory actions of renal interstitial angiotensin‐(1–7) infusion in anaesthetized rats
Authors: O'Neill Julie , Healy Vincent , Johns Edward J. 
Published: September 2017

New Findings
What is the central question of this study?
Dietary sodium manipulation alters the magnitude of angiotensin‐(1–7) [Ang‐(1–7)]‐induced natriuresis. The present study sought to determine whether this was related to relative changes in the activity of intrarenal Mas and/or AT1 receptors.

What is the main finding and its importance?
Angiotensin‐(1–7)‐induced diuresis and natriuresis is mediated by intrarenal Mas receptors. However, intrarenal AT1 receptor blockade also had an inhibitory effect on Ang‐(1–7)‐induced natriuresis and diuresis. Thus, Ang‐(1–7)‐induced increases in sodium and water excretion are dependent upon functional Mas and AT1 receptors.

We investigated whether angiotensin‐(1–7) [Ang‐(1–7)]‐induced renal haemodynamic and excretory actions were solely dependent upon intrarenal Mas receptor activation or required functional angiotensin II type 1 (AT1) receptors. The renin–angiotensin system was enhanced in anaesthetized rats by prior manipulation of dietary sodium intake. Angiotensin‐(1–7) and AT1 and Mas receptor antagonists were infused into the kidney at the corticomedullary border. Mas receptor expression was measured in the kidney. Mean arterial pressure, urine flow and fractional sodium excretion were 93 ± 4 mmHg, 46.1 ± 15.7 μl min−1 kg−1 and 1.4 ± 0.3%, respectively, in the normal‐sodium group and 91 ± 2 mmHg, 19.1 ± 3.3 μl min−1 kg−1 and 0.7 ± 0.2%, respectively, in the low‐sodium group. Angiotensin‐(1–7) infusion had no effect on mean arterial pressure in rats receiving a normal‐sodium diet but decreased it by 4 ± 5% in rats receiving a low‐sodium diet (P < 0.05). Interstitial Ang‐(1–7) infusion increased urine flow twofold and fractional sodium excretion threefold (P < 0.05) in rats receiving a normal‐sodium diet and to a greater extent, approximately three‐ and fourfold, respectively, in rats receiving the low‐sodium diet (both P < 0.05). Angiotensin‐(1–7)‐induced increases in urine flow and fractional sodium excretion were absent in both dietary groups during intrarenal AT1 or Mas receptor inhibition after either losartan or A‐779, respectively. Thus, AT1 receptor activation, as well as Mas receptor activation, plays an essential role in mediating Ang‐(1–7)‐induced natriuresis and diuresis. Whether this is because Ang‐(1–7) partly antagonizes AT1 receptors or whether Ang‐(1–7)‐induced natriuresis is mediated through AT1–Mas receptor dimerization remains unclear.
Dietary sodium induces a redistribution of the tubular metabolic workload
Authors: Udwan Khalil , Abed Ahmed , Roth Isabelle , Dizin Eva , Maillard Marc , Bettoni Carla , Loffing Johannes , Wagner Carsten A. , Edwards Aurélie , Feraille Eric 
Published: September 2017

Key points
Body Na+ content is tightly controlled by regulated urinary Na+ excretion.
The intrarenal mechanisms mediating adaptation to variations in dietary Na+ intake are incompletely characterized.
We confirmed and expanded observations in mice that variations in dietary Na+ intake do not alter the glomerular filtration rate but alter the total and cell‐surface expression of major Na+ transporters all along the kidney tubule.
Low dietary Na+ intake increased Na+ reabsorption in the proximal tubule and decreased it in more distal kidney tubule segments.
High dietary Na+ intake decreased Na+ reabsorption in the proximal tubule and increased it in distal segments with lower energetic efficiency.
The abundance of apical transporters and Na+ delivery are the main determinants of Na+ reabsorption along the kidney tubule.
Tubular O2 consumption and the efficiency of sodium reabsorption are dependent on sodium diet.
AbstractNa+ excretion by the kidney varies according to dietary Na+ intake. We undertook a systematic study of the effects of dietary salt intake on glomerular filtration rate (GFR) and tubular Na+ reabsorption. We examined the renal adaptive response in mice subjected to 7 days of a low sodium diet (LSD) containing 0.01% Na+, a normal sodium diet (NSD) containing 0.18% Na+ and a moderately high sodium diet (HSD) containing 1.25% Na+. As expected, LSD did not alter measured GFR and increased the abundance of total and cell‐surface NHE3, NKCC2, NCC, α‐ENaC and cleaved γ‐ENaC compared to NSD. Mathematical modelling predicted that tubular Na+ reabsorption increased in the proximal tubule but decreased in the distal nephron because of diminished Na+ delivery. This prediction was confirmed by the natriuretic response to diuretics targeting the thick ascending limb, the distal convoluted tubule or the collecting system. On the other hand, HSD did not alter measured GFR but decreased the abundance of the aforementioned transporters compared to NSD. Mathematical modelling predicted that tubular Na+ reabsorption decreased in the proximal tubule but increased in distal segments with lower transport efficiency with respect to O2 consumption. This prediction was confirmed by the natriuretic response to diuretics. The activity of the metabolic sensor adenosine monophosphate‐activated protein kinase (AMPK) was related to the changes in tubular Na+ reabsorption. Our data show that fractional Na+ reabsorption is distributed differently according to dietary Na+ intake and induces changes in tubular O2 consumption and sodium transport efficiency.
Caenorhabditis elegans as an Emerging Model for Virus-Host Interactions
Authors: Gammon Don B. 
Published: September 2017

ABSTRACT

Since 1999,
Caenorhabditis elegans
has been extensively used to study microbe-host interactions due to its simple culture, genetic tractability, and susceptibility to numerous bacterial and fungal pathogens. In contrast, virus studies have been hampered by a lack of convenient virus infection models in nematodes. The recent discovery of a natural viral pathogen of
C. elegans
and development of diverse artificial infection models are providing new opportunities to explore virus-host interplay in this powerful model organism.
Host Noncoding Retrotransposons Induced by DNA Viruses: a SINE of Infection?
Authors: Tucker Jessica M. , Glaunsinger Britt A. 
Published: September 2017

ABSTRACT
Our genomes are dominated by repetitive elements. The majority of these elements derive from retrotransposons, which expand throughout the genome through a process of reverse transcription and integration. Short interspersed nuclear elements, or SINEs, are an abundant class of retrotransposons that are transcribed by RNA polymerase III, thus generating exclusively noncoding RNA (ncRNA) that must hijack the machinery required for their transposition. SINE loci are generally transcriptionally repressed in somatic cells but can be robustly induced upon infection with multiple DNA viruses. Recent research has focused on the gene expression and signaling events that are modulated by SINE ncRNAs, particularly during gammaherpesvirus infection. Here, we review the biology of these SINE ncRNAs, explore how DNA virus infection may lead to their induction, and describe how novel gene regulatory and immune-related functions of these ncRNAs may impact the viral life cycle.
IKKγ-Mimetic Peptides Block the Resistance to Apoptosis Associated with Kaposi's Sarcoma-Associated Herpesvirus Infection
Authors: Briggs Louise C. , Chan A. W. Edith , Davis Christopher A. , Whitelock Nicholas , Hotiana Hajira A. , Baratchian Mehdi , Bagnéris Claire , Selwood David L. , Collins Mary K. , Barrett Tracey E. 
Published: September 2017

ABSTRACT

Primary effusion lymphoma (PEL) is a lymphogenic disorder associated with Kaposi's sarcoma-associated herpesvirus (KSHV) infection. Key to the survival and proliferation of PEL is the canonical NF-κB pathway, which becomes constitutively activated following overexpression of the viral oncoprotein KSHV vFLIP (ks-vFLIP). This arises from its capacity to form a complex with the modulatory subunit of the IκB kinase (IKK) kinase, IKKγ (or NEMO), resulting in the overproduction of proteins that promote cellular survival and prevent apoptosis, both of which are important drivers of tumorigenesis. Using a combination of cell-based and biophysical assays together with structural techniques, we showed that the observed resistance to cell death is largely independent of autophagy or major death receptor signaling pathways and demonstrated that direct targeting of the ks-vFLIP–IKKγ interaction both in cells and
in vitro
can be achieved using IKKγ-mimetic peptides. Our results further reveal that these peptides not only induce cell killing but also potently sensitize PEL to the proapoptotic agents tumor necrosis factor alpha and etoposide and are the first to confirm ks-vFLIP as a tractable target for the treatment of PEL and related disorders.

IMPORTANCE
KSHV vFLIP (ks-vFLIP) has been shown to have a crucial role in cellular transformation, in which it is vital for the survival and proliferation of primary effusion lymphoma (PEL), an aggressive malignancy associated with infection that is resistant to the majority of chemotherapeutic drugs. It operates via subversion of the canonical NF-κB pathway, which requires a physical interaction between ks-vFLIP and the IKK kinase modulatory subunit IKKγ. While this interaction has been directly linked to protection against apoptosis, it is unclear whether the suppression of other cell death pathways implicated in ks-vFLIP pathogenesis is an additional contributor. We demonstrate that the interaction between ks-vFLIP and IKKγ is pivotal in conferring resistance to apoptosis. Additionally, we show that the ks-vFLIP–IKKγ complex can be disrupted using peptides leading to direct killing and the sensitization of PEL cells to proapoptotic agents. Our studies thus provide a framework for future therapeutic interventions.
Comparative Transcriptomics Highlights the Role of the Activator Protein 1 Transcription Factor in the Host Response to Ebolavirus
Authors: Wynne James W. , Todd Shawn , Boyd Victoria , Tachedjian Mary , Klein Reuben , Shiell Brian , Dearnley Megan , McAuley Alexander J. , Woon Amanda P. , Purcell Anthony W. , Marsh Glenn A. , Baker Michelle L. 
Published: September 2017

ABSTRACT

Ebolavirus
and
Marburgvirus
comprise two genera of negative-sense single-stranded RNA viruses that cause severe hemorrhagic fevers in humans. Despite considerable research efforts, the molecular events following Ebola virus (EBOV) infection are poorly understood. With the view of identifying host factors that underpin EBOV pathogenesis, we compared the transcriptomes of EBOV-infected human, pig, and bat kidney cells using a transcriptome sequencing (RNA-seq) approach. Despite a significant difference in viral transcription/replication between the cell lines, all cells responded to EBOV infection through a robust induction of extracellular growth factors. Furthermore, a significant upregulation of activator protein 1 (AP1) transcription factor complex members
FOS
and
JUN
was observed in permissive cell lines. Functional studies focusing on human cells showed that EBOV infection induces protein expression, phosphorylation, and nuclear accumulation of JUN and, to a lesser degree, FOS. Using a luciferase-based reporter, we show that EBOV infection induces AP1 transactivation activity within human cells at 48 and 72 h postinfection. Finally, we show that JUN knockdown decreases the expression of EBOV-induced host gene expression. Taken together, our study highlights the role of AP1 in promoting the host gene expression profile that defines EBOV pathogenesis.

IMPORTANCE
Many questions remain about the molecular events that underpin filovirus pathophysiology. The rational design of new intervention strategies, such as postexposure therapeutics, will be significantly enhanced through an in-depth understanding of these molecular events. We believe that new insights into the molecular pathogenesis of EBOV may be possible by examining the transcriptomic response of taxonomically diverse cell lines (derived from human, pig, and bat). We first identified the responsive pathways using an RNA-seq-based transcriptomics approach. Further functional and computational analysis focusing on human cells highlighted an important role for the AP1 transcription factor in mediating the transcriptional response to EBOV infection. Our study sheds new light on how host transcription factors respond to and promote the transcriptional landscape that follows viral infection.
Non-invasive high-frequency oscillatory ventilation in preterm infants: a randomised controlled cross-over trial
Authors: Klotz Daniel , Schneider Hendryk , Schumann Stefan , Mayer Benjamin , Fuchs Hans 
Published: September 2017

ObjectiveNon-invasive high-frequency oscillatory ventilation (nHFOV) has recently been described as a novel mode of respiratory support for premature infants. This study was designed to determine whether nHFOV decreases CO2 partial pressure (pCO2) in premature infants more effectively than non-invasive continuous positive airway pressure (nCPAP).DesignNon-blinded prospective randomised controlled cross-over study.SettingUniversity Medical Center tertiary neonatal intensive care unit.Patients26 premature infants of 27±2 weeks of gestational age after extubation or non-invasive surfactant treatment.InterventionsInfants were treated with 4 hours of nHFOV and 4 hours of nCPAP in a cross-over design. The sequence of the ventilation mode was randomly allocated.Main outcome measuresThe primary outcome measure was pCO2 of arterial or arterialised blood 4 hours after commencing the respective mode of respiratory support. Secondary outcome criteria included events of apnoea and bradycardia, respiratory rate, heart rate, pain and/or discomfort, mean airway pressure, fraction of inspired oxygen and failure of non-invasive respiratory support.ResultspCO2 after 4 hours of nHFOV was similar compared with 4 hours of nCPAP (p=0.33). pCO2 was 54.8 (14.6) vs 52.7 (9.3) mm Hg mean (SD) for the nHFOV–nCPAP period (n=13) and 49.0 (8.1) vs 47.7 (9.5) mm Hg for the nCPAP–nHFOV period (n=13). There was no difference in any of the secondary outcome measures. nHFOV was terminated prematurely in five cases for predefined failure criteria (p=0.051).ConclusionsWe could not demonstrate an increased carbon dioxide clearance applying nHFOV compared with nCPAP in this cohort of preterm infants.Trial registration numberDRKS00007171, results.
Genetic polymorphisms associated with the risk of concussion in 1056 college athletes: a multicentre prospective cohort study
Authors: Terrell Thomas Roland , Abramson Ruth , Barth Jeffery T , Bennett Ellen , Cantu Robert C , Sloane Richard , Laskowitz Daniel T , Erlanger David M , McKeag Douglas , Nichols Gregory , Valentine Verle , Galloway Leslie 
Published: September 2017

Background/aimTo evaluate the association of genetic polymorphisms APOE,APOEG-219T promoter, microtubule associated protein(MAPT)/tauexon 6 Ser53Pro, MAPT/tauHist47Tyr,IL-6572 G/C andIL-6RAsp358Alawith the risk of concussion in college athletes.MethodsA 23-centre prospective cohort study of 1056 college athletes with genotyping was completed between August 2003 and December 2012. All athletes completed baseline medical and concussion questionnaires, and post-concussion data were collected for athletes with a documented concussion.ResultsThe study cohort consisted of 1056 athletes of mean±SD age 19.7±1.5 years,89.3% male, 59.4% Caucasian, 35.0% African-American, 5.6% other race. The athletes participated in American football, soccer, basketball, softball, men’s wrestling and club rugby. A total of 133 (12.1% prevalence) concussions occurred during an average surveillance of 3 years per athlete. We observed a significant positive association betweenIL-6RCC (p=0.001) and a negative association betweenAPOE4 (p=0.03) and the risk of concussion. Unadjusted and adjusted logistic regression analysis showed a significant association betweenIL-6RCC and concussion (OR 3.48; 95% CI 1.58 to 7.65; p=0.002) and between the APOE4 allele and concussion (OR 0.61; 95% CI 0.38 to 0.96; p=0.04), which persisted after adjustment for confounders.ConclusionsIL-6RCC was associated with a three times greater concussion risk andAPOE4 with a 40% lower risk.
Efficacy of individualised diets in patients with irritable bowel syndrome: a randomised controlled trial
Authors: Ali Ather , Weiss Theresa R , McKee Douglas , Scherban Alisa , Khan Sumiya , Fields Maxine R , Apollo Damian , Mehal Wajahat Z 
Published: September 2017

BackgroundPatients with irritable bowel syndrome (IBS) are often placed on diets guided by food intolerance assays, although these have not been validated. We assessed the effects of individualised diets in patients with IBS guided by a leucocyte activation test.MethodsThis is a parallel-group, double-blind, randomised controlled trial of 58 adults with IBS seen at an academic health centre in Northeast USA. Peripheral venous blood was analysed using a leucocyte activation test; individual foods were reported to produce positive or negative results. Participants were randomised to a 4-week diet with either individualised guidance to eliminate foods with positive assay results and allow foods with negative assay results (intervention), or with individualised guidance, matched in rigour and complexity, to eliminate foods with negative assay results and allow foods with positive assay results (comparison). The primary outcome was between-group differences in the IBS Global Improvement Scale (GIS). Secondary outcomes included reductions in IBS Symptom Severity Scale (SSS) scores and increases in IBS Adequate Relief (AR) and Quality of Life (QOL) scores. An aptamer-based proteomic analysis was conducted in strong responders.ResultsThe intervention group had significantly greater increases in mean GIS score after 4 weeks (0.86 vs comparison; 95% CI 0.05 to 1.67; p=0.04) and 8 weeks (1.22 vs comparison; 95% CI 0.22 to 2.22; p=0.02). The intervention group also had significantly greater reductions in mean SSS score at 4 weeks (–61.78 vs comparison; 95% CI –4.43 to –119.14; p=0.04) and 8 weeks (–66.42 vs comparison; 95% CI –5.75 to –127.09; p=0.03). There were no significant differences between intervention and comparison groups in mean AR or QOL scores. A reduction in neutrophil elastase concentration was associated with reduced symptoms.ConclusionsElimination diets guided by leucocyte activation tests reduced symptoms. These findings could lead to insights into the pathophysiology of IBS.Trial registration numberNCT02186743.