bluuebunny/crossref_metadata_2025_split huggingface dataset:
Can incivility impair team’s creative performance through paralyzing employee’s knowledge sharing? A multi-level approach
Authors: Sharifirad Mohammad Sadegh 
Published: March 2016

Purpose– The purpose of this paper is to examine how a supervisor’s incivility in teams impact team’s creative performance through the mediating factor of knowledge sharing intention among team members. Moreover, the moderating role of collaborative climate was investigated as protector against leaders’ incivility.Design/methodology/approach– The proposed multi-level model was tested by surveying 312 health care providers nested within 42 work units at eight large hospitals in Iran. Multi-level regression analysis was used to analyze the data.Findings– The findings revealed that those team members experiencing incivility from their supervisors are more likely to show reluctance to share knowledge with team members and as a consequence this response further decreases team’s creative performance. However, the climate of collaboration inside hospitals can buffer the negative impact of incivility on their readiness to share knowledge.Practical implications– In team-based organizations, a supervisor’s incivility can stifle the creative performance of his/her team through blocking the knowledge sharing of members. First, human resource department should have some plans to curtail incivility of supervisors. Second, establishing a climate of collaboration and trust among team members can mitigate the insidious effects of supervisors’ incivility.Originality/value– In prior research studies, the role of incivility on individual outcomes has been highlighted. This paper, according to the best knowledge of the author, is the first considering the negative impact of incivility on team’s performance. Moreover, collaborative climate is a novel moderator considered in this study.
What’s to argue? A comparison of opposing viewpoints in context to the updated points of view reference center, with a nod to the original points of view reference center
Authors: Nuttall Harry D. 
Published: March 2016

Purpose
– The purpose of this paper is to provide an evaluative comparison of databases for argumentative/persuasive rhetoric.

Design/methodology/approach
– This paper reviews and compares the databases in terms of the organization, types of information included and the ease of use.

Findings
– To assist students in learning the rhetorical modes of argument and persuasion, some database vendors have developed proprietary electronic databases specific to this purpose. EBSCOhost’s Points of View Reference Center and Gale/Cengage’s Opposing Viewpoints in Context are two such databases. Which is better largely depends on the dominant user demographic of the educational institution. Both databases have strengths and weaknesses; therefore, the best results can be achieved by using them to complement one another. But if only one database can be selected, then that choice should most be influenced by the user demographic served.

Research limitations/implications
– These databases have value as primers and introductions to research and writing in the rhetorical mode(s) of argumentation and persuasion, but students taking advanced classes should supplement them with more sophisticated searches in standard aggregator databases, which are not examined in detail in this paper.

Originality/value
– This paper offers selectors an apples-to-apples comparison and analysis of two related resources, providing an insight about which can be used in the selection process.
Volatile Compounds Emitted by Pseudomonas aeruginosa Stimulate Growth of the Fungal Pathogen Aspergillus fumigatus
Authors: Briard Benoit , Heddergott Christoph , Latgé Jean-Paul 
Published: March 2016

ABSTRACT

Chronic lung infections with opportunistic bacterial and fungal pathogens are a major cause of morbidity and mortality especially in patients with cystic fibrosis.
Pseudomonas aeruginosa
is the most frequently colonizing bacterium in these patients, and it is often found in association with the filamentous fungus
Aspergillus fumigatus
.
P. aeruginosa
is known to inhibit the growth of
A. fumigatus
in situations of direct contact, suggesting the existence of interspecies communication that may influence disease outcome. Our study shows that the lung pathogens
P. aeruginosa
and
A. fumigatus
can interact at a distance via volatile-mediated communication and expands our understanding of interspecific signaling in microbial communities.

IMPORTANCE
Microbiota studies have shown that pathogens cannot be studied individually anymore and that the establishment and progression of a specific disease are due not to a single microbial species but are the result of the activity of many species living together. To date, the interaction between members of the human microbiota has been analyzed in situations of direct contact or liquid-mediated contact between organisms. This study showed unexpectedly that human opportunistic pathogens can interact at a distance after sensing volatiles emitted by another microbial species. This finding will open a new research avenue for the understanding of microbial communities.
Features of Circulating Parainfluenza Virus Required for Growth in Human Airway
Authors: Palermo Laura M. , Uppal Manik , Skrabanek Lucy , Zumbo Paul , Germer Soren , Toussaint Nora C. , Rima Bert K. , Huey Devra , Niewiesk Stefan , Porotto Matteo , Moscona Anne 
Published: March 2016

ABSTRACT

Respiratory paramyxoviruses, including the highly prevalent human parainfluenza viruses, cause the majority of childhood croup, bronchiolitis, and pneumonia, yet there are currently no vaccines or effective treatments. Paramyxovirus research has relied on the study of laboratory-adapted strains of virus in immortalized cultured cell lines. We show that findings made in such systems about the receptor interaction and viral fusion requirements for entry and fitness—mediated by the receptor binding protein and the fusion protein—can be drastically different from the requirements for infection
in vivo
. Here we carried out whole-genome sequencing and genomic analysis of circulating human parainfluenza virus field strains to define functional and structural properties of proteins of circulating strains and to identify the genetic basis for properties that confer fitness in the field. The analysis of clinical strains suggests that the receptor binding-fusion molecule pairs of circulating viruses maintain a balance of properties that result in an inverse correlation between fusion in cultured cells and growth
in vivo
. Future analysis of entry mechanisms and inhibitory strategies for paramyxoviruses will benefit from considering the properties of viruses that are fit to infect humans, since a focus on viruses that have adapted to laboratory work provides a distinctly different picture of the requirements for the entry step of infection.

IMPORTANCE
Mechanistic information about viral infection—information that impacts antiviral and vaccine development—is generally derived from viral strains grown under laboratory conditions in immortalized cells. This study uses whole-genome sequencing of clinical strains of human parainfluenza virus 3—a globally important respiratory paramyxovirus—in cell systems that mimic the natural human host and in animal models. By examining the differences between clinical isolates and laboratory-adapted strains, the sequence differences are correlated to mechanistic differences in viral entry. For this ubiquitous and pathogenic respiratory virus to infect the human lung, modulation of the processes of receptor engagement and fusion activation occur in a manner quite different from that carried out by the entry glycoprotein-expressing pair of laboratory strains. These marked contrasts in the viral properties necessary for infection in cultured immortalized cells and in natural host tissues and animals will influence future basic and clinical studies.
Acupuncture for Irritable Bowel Syndrome: 2-Year Follow-Up of a Randomised Controlled Trial
Authors: MacPherson Hugh , Tilbrook Helen , Agbedjro Deborah , Buckley Hannah , Hewitt Catherine , Frost Chris 
Published: March 2016

Background A recent randomised controlled trial (RCT) of acupuncture as a treatment for irritable bowel syndrome (IBS) demonstrated sustained benefits over a period of 12 months post-randomisation. Aim To extend the trial follow-up to evaluate the effects of acupuncture at 24 months post-randomisation. Methods Patients in primary care with ongoing IBS were recruited to a two-arm pragmatic RCT of acupuncture for IBS. Participants were randomised to the offer of up to 10 weekly sessions of acupuncture plus usual care (n=116 patients) or to continue with usual care alone (n=117). The primary outcome was the self-reported IBS symptom severity score (IBS SSS) measured at 24 months post-randomisation. Analysis was by intention-to-treat using an unstructured multivariate linear model incorporating all repeated measures. Results The overall response rate was 61%. The adjusted difference in mean IBS SSS at 24 months was −18.28 (95% CI −40.95 to 4.40) in favour of the acupuncture arm. Differences at earlier time points estimated from the multivariate model were: −27.27 (−47.69 to −6.86) at 3 months; −23.69 (−45.17 to −2.21) at 6 months; −24.09 (−45.59 to −2.59) at 9 months; and −23.06 (−44.52 to −1.59) at 12 months. Conclusions There were no statistically significant differences between the acupuncture and usual care groups in IBS SSS at 24 months post-randomisation, and the point estimate for the mean difference was approximately 80% of the size of the statistically significant results seen at 6, 9 and 12 months. Trial registration number ISRCTN08827905.
Reliability and validity of the Chronic Liver Disease Questionnaire (CLDQ) in adults with non-alcoholic steatohepatitis (NASH)
Authors: Chawla Kashmira S , Talwalkar Jayant A , Keach Jill C , Malinchoc Michael , Lindor Keith D , Jorgensen Roberta 
Published: March 2016

IntroductionSignificant impairments in health-related quality of life (HRQL) in patients with non-alcoholic fatty liver disease have been previously described. The disease-specific HRQL among patients with non-alcoholic steatohepatitis (NASH), however, remains unknown.AimTo determine the degree of construct validity of the Chronic Liver Disease Questionnaire (CLDQ) in adults with NASH.MethodsParticipants referred for the evaluation of histology-proven NASH at Mayo Clinic, Rochester, between 1996 and 2000, were evaluated. HRQL assessment by the Short-Form 36 (SF-36) Health Survey and CLD) was performed. The primary outcome was to determine the level of correlation between overall and subscale scores for the CLDQ and SF-36 instruments.ResultsAmong 79 participants (70%) with NASH completing both questionnaires (mean age, 51.2 years with 64% female gender), excellent reliability was noted for the CLDQ instrument. Significant reductions in all SF-36 domains (p<0.05 for all) including PCS and MCS scores (p<0.02 for both) among participants with NASH compared with normative data from an age-matched and sex-matched US general population sample was observed. Highly significant correlations were observed between overall CLDQ score with SF-36 PCS (r=0.82, p<0.0001) and SF-36 MCS (r=0.67, p<0.0001) scores. Similar degrees of correlation were observed between relevant subscales of the CLDQ and SF-36 as well.DiscussionThe CLDQ has excellent reliability and validity of construct for HRQL assessment in adults with NASH when compared with the SF-36. Future investigations among participants with NASH require assessing the responsiveness of the CLDQ to medical therapies and disease progression.
Intubation performance using different laryngoscopes while wearing chemical protective equipment: a manikin study
Authors: Schröder H , Zoremba N , Rossaint R , Deusser K , Stoppe C , Coburn M , Rieg A , Schälte G 
Published: March 2016

ObjectivesThis study aimed to compare visualisation of the vocal cords and performance of intubation by anaesthetists using four different laryngoscopes while wearing full chemical protective equipment.SettingMedical simulation center of a university hospital, department of anaesthesiology.Participants42 anaesthetists (15 females and 27 males) completed the trial. The participants were grouped according to their professional education as anaesthesiology residents with experience of <2 years or <5 years, or as anaesthesiology specialists with experience of >5 years.InterventionsIn a manikin scenario, participants performed endotracheal intubations with four different direct and indirect laryngoscopes (Macintosh (MAC), Airtraq (ATQ), Glidescope (GLS) and AP Advance (APA)), while wearing chemical protective gear, including a body suit, rubber gloves, a fire helmet and breathing apparatus.Primary and secondary outcome measuresWith respect to the manikin, setting time to complete ‘endotracheal intubation’ was defined as primary end point. Glottis visualisation (according to the Cormack-Lehane score (CLS) and impairments caused by the protective equipment, were defined as secondary outcome measures.ResultsThe times to tracheal intubation were calculated using the MAC (31.4 s; 95% CI 26.6 to 36.8), ATQ (37.1 s; 95% CI 28.3 to 45.9), GLS (35.4 s; 95% CI 28.7 to 42.1) and APA (23.6 s; 95% CI 19.1 to 28.1), respectively. Intubation with the APA was significantly faster than with all the other devices examined among the total study population (p<0.05). A significant improvement in visualisation of the vocal cords was reported for the APA compared with the GLS.ConclusionsDespite the restrictions caused by the equipment, the anaesthetists intubated the manikin successfully within adequate time. The APA outperformed the other devices in the time to intubation, and it has been evaluated as an easily manageable device for anaesthetists with varying degrees of experience (low to high), providing good visualisation in scenarios that require the use of chemical protective equipment.
Influence of fault geometries and mechanical anisotropies on the growth and inversion of hanging-wall synclinal basins: insights from sandbox models and natural examples
Authors: Ferrer O. , McClay K. , Sellier N. C. 
Published: March 2016

Abstract
Salt is mechanically weaker than other sedimentary rocks in rift basins. It commonly acts as a strain localizer, and decouples supra- and sub-salt deformation. In the rift basins discussed in this paper, sub-salt faults commonly form wide and deep ramp synclines controlled by the thickness and strength of the overlying salt section, as well as by the shapes of the extensional faults, and the magnitudes and slip rates along the faults. Upon inversion of these rift basins, the inherited extensional architectures, and particularly the continuity of the salt section, significantly controls the later contractional deformation.
This paper utilizes scaled sandbox models to analyse the interplay between sub-salt structures and supra-salt units during both extension and inversion. Series 1 experiments involved baseline models run using isotropic sand packs for simple and ramp-flat listric faults, as well as for simple planar and kinked planar faults. Series 2 experiments involved the same fault geometries but also included a pre-extension polymer layer to simulate salt in the stratigraphy. In these experiments, the polymer layer decoupled the extensional and contractional strains, and inhibited the upwards propagation of sub-polymer faults. In all Series 2 experiments, the extension produced a synclinal hanging-wall basin above the polymer layer as a result of polymer migration during the deformation. During inversion, the supra-polymer synclinal basin was uplifted, folded and detached above the polymer layer. Changes in thickness of the polymer layer during the inversion produced primary welds and these permitted the sub-polymer deformation to propagate upwards into the supra-salt layers.
The experimental results are compared with examples from the Parentis Basin (Bay of Biscay), the Broad Fourteens Basin (southern North Sea), the Feda Graben (central North Sea) and the Cameros Basin (Iberian Range, Spain).
MIF Maintains the Tumorigenic Capacity of Brain Tumor–Initiating Cells by Directly Inhibiting p53
Authors: Fukaya Raita , Ohta Shigeki , Yaguchi Tomonori , Matsuzaki Yumi , Sugihara Eiji , Okano Hideyuki , Saya Hideyuki , Kawakami Yutaka , Kawase Takeshi , Yoshida Kazunari , Toda Masahiro 
Published: March 2016

Abstract
Tumor-initiating cells thought to drive brain cancer are embedded in a complex heterogeneous histology. In this study, we isolated primary cells from 21 human brain tumor specimens to establish cell lines with high tumorigenic potential and to identify the molecules enabling this capability. The morphology, sphere-forming ability upon expansion, and differentiation potential of all cell lines were indistinguishable in vitro. However, testing for tumorigenicity revealed two distinct cell types, brain tumor–initiating cells (BTIC) and non-BTIC. We found that macrophage migration inhibitory factor (MIF) was highly expressed in BTIC compared with non-BTIC. MIF bound directly to both wild-type and mutant p53 but regulated p53-dependent cell growth by different mechanisms, depending on glioma cell line and p53 status. MIF physically interacted with wild-type p53 in the nucleus and inhibited its transcription-dependent functions. In contrast, MIF bound to mutant p53 in the cytoplasm and abrogated transcription-independent induction of apoptosis. Furthermore, MIF knockdown inhibited BTIC-induced tumor formation in a mouse xenograft model, leading to increased overall survival. Collectively, our findings suggest that MIF regulates BTIC function through direct, intracellular inhibition of p53, shedding light on the molecular mechanisms underlying the tumorigenicity of certain malignant brain cells. Cancer Res; 76(9); 2813–23. ©2016 AACR.
TGFβ Signaling in the Pancreatic Tumor Microenvironment Promotes Fibrosis and Immune Evasion to Facilitate Tumorigenesis
Authors: Principe Daniel R. , DeCant Brian , Mascariñas Emman , Wayne Elizabeth A. , Diaz Andrew M. , Akagi Naomi , Hwang Rosa , Pasche Boris , Dawson David W. , Fang Deyu , Bentrem David J. , Munshi Hidayatullah G. , Jung Barbara , Grippo Paul J. 
Published: March 2016

Abstract
In early pancreatic carcinogenesis, TGFβ acts as a tumor suppressor due to its growth-inhibitory effects in epithelial cells. However, in advanced disease, TGFβ appears to promote tumor progression. Therefore, to better understand the contributions of TGFβ signaling to pancreatic carcinogenesis, we generated mouse models of pancreatic cancer with either epithelial or systemic TGFBR deficiency. We found that epithelial suppression of TGFβ signals facilitated pancreatic tumorigenesis, whereas global loss of TGFβ signaling protected against tumor development via inhibition of tumor-associated fibrosis, stromal TGFβ1 production, and the resultant restoration of antitumor immune function. Similarly, TGFBR-deficient T cells resisted TGFβ-induced inactivation ex vivo, and adoptive transfer of TGFBR-deficient CD8+ T cells led to enhanced infiltration and granzyme B–mediated destruction of developing tumors. These findings paralleled our observations in human patients, where TGFβ expression correlated with increased fibrosis and associated negatively with expression of granzyme B. Collectively, our findings suggest that, despite opposing the proliferation of some epithelial cells, TGFβ may promote pancreatic cancer development by affecting stromal and hematopoietic cell function. Therefore, the use of TGFBR inhibition to target components of the tumor microenvironment warrants consideration as a potential therapy for pancreatic cancer, particularly in patients who have already lost tumor-suppressive TGFβ signals in the epithelium. Cancer Res; 76(9); 2525–39. ©2016 AACR.
The Prosurvival IKK-Related Kinase IKKϵ Integrates LPS and IL17A Signaling Cascades to Promote Wnt-Dependent Tumor Development in the Intestine
Authors: Göktuna Serkan Ismail , Shostak Kateryna , Chau Tieu-Lan , Heukamp Lukas C. , Hennuy Benoit , Duong Hong-Quan , Ladang Aurélie , Close Pierre , Klevernic Iva , Olivier Fabrice , Florin Alexandra , Ehx Grégory , Baron Frédéric , Vandereyken Maud , Rahmouni Souad , Vereecke Lars , van Loo Geert , Büttner Reinhard , Greten Florian R. , Chariot Alain 
Published: March 2016

Abstract
Constitutive Wnt signaling promotes intestinal cell proliferation, but signals from the tumor microenvironment are also required to support cancer development. The role that signaling proteins play to establish a tumor microenvironment has not been extensively studied. Therefore, we assessed the role of the proinflammatory Ikk-related kinase Ikkϵ in Wnt-driven tumor development. We found that Ikkϵ was activated in intestinal tumors forming upon loss of the tumor suppressor Apc. Genetic ablation of Ikkϵ in β-catenin-driven models of intestinal cancer reduced tumor incidence and consequently extended survival. Mechanistically, we attributed the tumor-promoting effects of Ikkϵ to limited TNF-dependent apoptosis in transformed intestinal epithelial cells. In addition, Ikkϵ was also required for lipopolysaccharide (LPS) and IL17A-induced activation of Akt, Mek1/2, Erk1/2, and Msk1. Accordingly, genes encoding pro-inflammatory cytokines, chemokines, and anti-microbial peptides were downregulated in Ikkϵ-deficient tissues, subsequently affecting the recruitment of tumor-associated macrophages and IL17A synthesis. Further studies revealed that IL17A synergized with commensal bacteria to trigger Ikkϵ phosphorylation in transformed intestinal epithelial cells, establishing a positive feedback loop to support tumor development. Therefore, TNF, LPS, and IL17A-dependent signaling pathways converge on Ikkϵ to promote cell survival and to establish an inflammatory tumor microenvironment in the intestine upon constitutive Wnt activation. Cancer Res; 76(9); 2587–99. ©2016 AACR.
Oncoprotein HBXIP Modulates Abnormal Lipid Metabolism and Growth of Breast Cancer Cells by Activating the LXRs/SREBP-1c/FAS Signaling Cascade
Authors: Zhao Yu , Li Hang , Zhang Yingyi , Li Leilei , Fang Runping , Li Yinghui , Liu Qian , Zhang Weiying , Qiu Liyan , Liu Fabao , Zhang Xiaodong , Ye Lihong 
Published: March 2016

Abstract
Abnormal lipid metabolism is a hallmark of tumorigenesis. Accumulating evidence demonstrates that fatty acid synthase (FAS, FASN) is a metabolic oncogene that supports the growth and survival of tumor cells and is highly expressed in many cancers. Here, we report that the oncoprotein, hepatitis B X-interacting protein (HBXIP, LAMTOR5) contributes to abnormal lipid metabolism. We show that high expression of HBXIP in 236 breast cancer patients was significantly associated with decreased overall survival and progression-free survival. Interestingly, the expression of HBXIP was positively related to that of FAS in clinical breast cancer tissues, and HBXIP overexpression in breast cancer cells resulted in FAS upregulation. Mechanistically, HBXIP upregulated SREBP-1c (SREBF1), which activates the transcription of FAS, by directly interacting with and coactivating nuclear receptor (NR) liver X receptors (LXR). Physiologically, LXRs are activated via a coactivator containing NR motif in a ligand-dependent manner. However, in breast cancer cells, HBXIP containing the corepressor/nuclear receptor motif with special flanking sequence could coactivate LXRs independent of ligand. Moreover, overexpressed SREBP-1c was able to activate the transcription of HBXIP, forming a positive-feedback loop. Functionally, HBXIP enhanced lipogenesis, resulting in the growth of breast cancer cells in vitro and in vivo. Thus, we conclude that the oncoprotein HBXIP contributes to the abnormal lipid metabolism in breast cancer through LXRs/SREBP-1c/FAS signaling, providing new insights into the mechanisms by which cancer cells reprogram lipid metabolism in their favor. Cancer Res; 76(16); 4696–707. ©2016 AACR.