bluuebunny/crossref_metadata_2025_split huggingface dataset:
Predation risk and resource availability explain roost locations of Whimbrel Numenius phaeopus in a tropical mangrove delta
Authors: Johnston‐González Richard , Abril Elizabeth 
Published: September 2018

Roosts are important sites for shorebirds in non‐breeding areas at night and during high tides. How the spatial configuration of food and risk of predation and disturbance influence roost site use in tropical locations remains poorly known. We analysed the locations of nocturnal roosts of Whimbrel Numenius phaeopus in mangroves of Sanquianga National Park, Colombia, with respect to variation in spatial variables related to food resources and risk of predation and disturbance. We contrasted characteristics of all 13 known nocturnal roost locations with those of all other mangrove islands (n = 209) within the limits of the park. We estimated the distance from roosts and other mangrove islands to foraging sites, and sources of predators and human disturbance. Larger areas of feeding habitat surrounded nocturnal roosts than other mangrove islands, and the average distance to individual feeding patches was shorter. Roosts were also more isolated than other islands, but proximity to sources of human disturbance did not differ. We conclude that Whimbrel roost site use in Sanquianga was best explained by a combination of access to feeding territories and isolation from potential sources of mainland predators, but not by avoidance of human disturbance. Beyond identifying factors influencing roost site selection, the large aggregations of individuals in single locations may suggest that presence of conspecifics itself also plays a role in the formation of Whimbrel roosts. We highlight the interaction of food and risk landscapes with intraspecific attraction on the roost site selection by Whimbrels and the importance of mangroves as roosting sites in tropical regions.
STRATEGIC BIDDING AND CONTRACT RENEGOTIATION
Authors: Jung Hojin , Kosmopoulou Georgia , Lamarche Carlos , Sicotte Richard 
Published: September 2018

AbstractWhen firms bid in procurement auctions, they take into account the likelihood of future contract renegotiations. If they anticipate that certain input quantities will change ex post, they have an incentive to strategically skew their itemized bids, thereby increasing profits for themselves and costs for the procuring agency. We develop and estimate a structural model of strategic bidding using a data set of road construction projects in Vermont. We find that bidding strategies lead to increased markups for renegotiated items and reduced markups for nonrenegotiated items, results consistent with bid‐skewing.
Filaggrin gene polymorphisms in Iranian ichthyosis vulgaris and atopic dermatitis patients
Authors: Hassani Bita , Isaian Anna , Shariat Mansoureh , Mollanoori Hasan , Sotoudeh Soheila , Babaei Vahid , Ziaali Arghavan , Teimourian Shahram 
Published: September 2018

AbstractBackgroundFilaggrin is a key structural epidermal protein in terminal differentiation and formation of skin barrier. The important role of filaggrin and its effects in various cutaneous and noncutaneous disorders initiated a cascade of considerable research in recent years. Loss‐of‐function mutations in FLG, the human gene encoding profilaggrin/filaggrin, is the cause of the common skin condition ichthyosis vulgaris (IV) and major genetic predisposing factor for atopic dermatitis (AD). Several null mutations in the FLG gene that lead to a decrease or absence of filaggrin in skin and predispose these conditions have been described.ObjectiveThe aim of this study was to investigative genetic polymorphism of FLG in Iranian patients with IV and AD.MethodsIn the current study, we carried out full sequencing of the entire FLG coding region in 30 IV patients and 30 AD patients, and also 60 healthy controls.ResultsIn our research, we identified 43 variants reported previously and two novel variants.ConclusionIn our study, in the AD and IV patients, loss‐of‐function FLG mutation was not found. This means that another mechanism other than FLG nonsense mutation is involved in the pathogenesis of these patients.
Impact of the carer on length of hospital stay for mental health: Results from two Australian surveys
Authors: Hielscher Emily , Diminic Sandra , Harris Meredith , Castle David , Lee Yong Yi , Kealton Jan , Whiteford Harvey 
Published: September 2018

AbstractInformal carers play a vital role in supporting Australians living with a mental illness, including during the acute phases of illness; however, little is known about their impact on length of hospital stay. We aimed to investigate the impact of having a carer and of carer burden on length of hospital stay for mental health. Two Australian datasets were used. Data from the 2010 National Survey of High Impact Psychosis (n = 1825) were used to investigate the impact of having versus not having a carer on length of hospital stay for mental health. Data from the UQ Carer Survey 2016 (n = 105), a convenience sample of mental health carers, were used to investigate the impact of weekly hours of care (a measure of objective carer burden) on length of stay. Multiple logistic regression and correlation analyses were performed to investigate the association between carer status/burden and length of stay. Having a carer was associated with a significantly longer length of hospital stay; however, this relationship was no longer significant after adjusting for diagnosis, global functioning, depressive symptoms, deliberate self‐harm, mental health outpatient contacts and type of admission. Weekly hours of care did not significantly impact on length of stay. Patients with carers had poorer functioning which may be related to longer stays. Our analysis was not able to look at subgroups of carers with different needs. Future work is required to determine other components of the admission and discharge process where having a carer is influential.
What Can We Learn from Art Practices? Exploring New Perspectives on Critical Engagement with Plurality and Difference in Community Art Education
Authors: Wildemeersch Danny 
Published: September 2018

AbstractThe article presents a case of community art education in Leuven, Belgium. Participants who belong to disenfranchised groups of the local community were invited to engage in artistic actions and performances aiming at familiarising them with modern art practices. Such experiments are often disqualified as being irrelevant to the life‐conditions of these families in poverty, and hence as non‐emancipatory. In this article, the emancipatory quality of such initiatives is explored with reference to the art practices of the Belgian/Mexican artist Francis Alÿs and the reflections on emancipation by the French philosopher Jacques Rancière. These reflections help to shed a new light on the emancipatory dimension of community art practices and to consider theoretical concepts such as ‘poor pedagogy’.
Collaborative Amateur Production of Educational Videos, which are Viewed on Mobiles: Addressing Poor Technical Resources for Nigerian Creative Arts Academics
Authors: Chick Anne , Etsename Emmanuel 
Published: September 2018

AbstractThis research was a co‐creation and co‐assessment exercise between the researchers, participating printmaking and weaving academics and their students in a Nigerian university. The poor technical resources and increasingly large student groups in the design department, which severely hampers the delivery of an effective education, were addressed. The academics were supported to learn how to create their own instructional videos for their students, demonstrating identified designer‐maker skills and how to use required equipment. These academics are now empowered and have the knowledge to produce their own instructional videos without professional assistance. This is also irrespective of their previous experiences of using video equipment and developing video content.
On Art and Knowledge
Authors: Szpakowski Michael 
Published: September 2018

AbstractI comment upon the recent blossoming of writing on art, knowledge and research and connect this to its material roots in the changing nature of higher education. I find much of this writing wanting in that it implies a division of art into ‘knowledge‐producing’ and ‘non knowledge‐producing’ art. I examine how art objects might be said to generate knowledge, particularly the kind of propositional knowledge which sits at the centre of both traditional epistemology and ‘knowledge transfer’ in the contemporary academy. Although there are many ways in which artworks might variously generate such knowledge, I conclude that there is none that is common to all. I go on to examine other kinds of knowledge, particularly Gilbert Ryle's ‘knowledge‐how’ and use this as a staging post to suggest that there is yet another kind of knowledge, produced by all works of art. Finally I borrow some ideas from recent work in the philosophy of science to suggest a concrete mechanism by which this knowledge is made available to us.
Co‐Design Education Based on the Changing Designer's Role and Changing Creativity
Authors: Lee Jeehyun , Ahn Jiwon , Kim Jieun , Kho Jeong‐min 
Published: September 2018

AbstractThe field of fashion design relies on the originality of fashion designers and information on design trends, and design education also focuses on the creative ideas of designers; in this field, design through co‐design is a very limited area. However, with the proliferation of participatory culture, the need to diversify fashion design education methods has also emerged. The purpose of this study is to present an educational framework and an instructional strategy for co‐design based on the changing role of the designer and to obtain educational insight through the implementation of an actual education prototype. To do this, we developed an educational prototype and implemented it with six undergraduate students. Through this study, the participants engaged in the process of design development with the consumer and analysed the instructional insight. As a result, this study redefines the roles and design methods of designers for co‐design and identifies creativity characteristics through the co‐design process. The results of this study can be used as basic data for co‐design education and can contribute to the expansion of fashion design educational methods.
Long non‐coding RNA CRNDE promotes the proliferation, migration and invasion of hepatocellular carcinoma cells through miR‐217/MAPK1 axis
Authors: Wang Haihao , Ke Ji , Guo Qiannan , Barnabo Nampoukime Kan‐Paatib , Yang Peiwen , Ma Ke 
Published: September 2018

AbstractHepatocellular carcinoma (HCC) is an invasive malignant tumour and the second major cause of cancer‐related deaths over the world. CRNDE and miR‐217 are non‐coding RNAs which play critical roles in cell growth, proliferation, migration. Mitogen‐activated protein kinase 1 (MAPK1) also participates in cancer cell process. Hence, this study aimed at investigating the effect of CRNDE on migration and invasion of HCC and figuring out the role of miR‐217 and MAPK1 in this process. The overexpression of CRNDE was demonstrated by a microarray‐based lncRNA profiling study. CRNDE expression in HCC was verified by qRT‐PCR. MTT assay and BrdU staining were applied to detect cell proliferation level. Transwell assay was utilized to examine cell migration and invasiveness abilities. Wound healing assay was performed for further exploration of cell migration capacity. MiR‐217 was predicted by bioinformatics. The dual luciferase reporter assay was performed to corroborate the targeting relationship between CRNDE, miR‐217 and MAPK1. MAPK1, the downstream target of miR‐217, was predicted using bioinformatics and was further confirmed by qRT‐PCR and Western blot. The interaction between CRNDE, miR‐217 and MAPK1 was studied by qRT‐PCR, Western blot, MTT, BrdU, transwell assay and wound healing assay. CRNDE was up‐regulated in HCC tissues and HCC cell lines. The high expression of CRNDE facilitated cell proliferation, migration and invasion, while the inhibited one affected on the contrary. MiR‐217, negatively correlated with CRNDE expression, was the target of CRNDE and was more lowly expressed in HCC. With the high expression of miR‐217, HCC cell proliferation, migration and invasion were suppressed. MAPK1, the possible target of miR‐217, was negatively correlated with miR‐217 but positively correlated with CRNDE and had the same effect in HCC formation process as CRNDE. Long non‐coding RNA CRNDE promotes the proliferation, migration and invasion of HCC cells through miR‐217/MAPK1 axis.
NEK4 kinase regulates EMT to promote lung cancer metastasis
Authors: Ding Nian‐Hua , Zhang Lu , Xiao Zhi , Rong Zhuo‐Xian , Li Zhi , He Jiang , Chen Lin , Ou Dan‐Min , Liao Wei‐Hua , Sun Lun‐Quan 
Published: September 2018

AbstractEpithelial‐to‐mesenchymal transition (EMT) is a dynamic transitional state from the epithelial to mesenchymal phenotypes. Numerous studies have suggested that EMT and its intermediate states play important roles in tumor invasion and metastasis. To identify novel regulatory molecules of EMT, we screened a siRNA library targeting human 720 kinases in A549 lung adenocarcinoma cells harboring E‐cadherin promoter‐luciferase reporter vectors. NIMA‐related kinase‐4 (NEK4) was identified and characterized as a positive regulator of EMT in the screening. Suppression of NEK4 resulted in the inhibition of cell migration and invasion, accompanying with an increased expression of cell adhesion‐related proteins such as E‐cadherin and ZO1. Furthermore, NEK4 knockdown caused the decreased expression of the transcriptional factor Zeb1 and Smads proteins, which are known to play key roles in EMT regulation. Consistently, overexpression of NEK4 resulted in the decreased expression of E‐cadherin and increased expression of Smad3. Using a mouse model with tail vein injection of NEK4 knockdown stable cell line, we found a lower rate of tumor formation and metastasis of the NEK4‐knockdown cells in vivo. Thus, this study demonstrates NEK4 as a novel kinase involved in regulation of EMT and suggests that NEK4 may be further explored as a potential therapeutic target for lung cancer metastasis.
Galectin‐3 promotes CXCR2 to augment the stem‐like property of renal cell carcinoma
Authors: Huang Chang‐Shuo , Tang Shye‐Jye , Lee Mei‐Hsuan , Chang Wang Chien‐Chih , Sun Guang‐Huan , Sun Kuang‐Hui 
Published: September 2018

AbstractAlthough targeted therapy is usually the first‐line treatment for advanced renal cell carcinoma (RCC), some patients can experience drug resistance. Cancer stem cells are tumour‐initiating cells that play a vital role in drug resistance, metastasis and cancer relapse, while galectins (Gal) participate in tumour progression and drug resistance. However, the exact role of galectins in RCC stemness is yet unknown. In this study, we grew a subpopulation of RCC cells as tumour spheres with higher levels of stemness‐related genes, such as Oct4, Sox2 and Nanog. Among the Gal family, Gal‐3 in particular was highly expressed in RCC tumour spheres. To further investigate Gal‐3's role in the stemness of RCC, lentivirus‐mediated knockdown and overexpression of Gal‐3 in RCC cells were used to examine both in vitro and in vivo tumorigenicity. We further assessed Gal‐3 expression in RCC tissue microarray using immunohistochemistry. Upon suppressing Gal‐3 in parental RCC cells, invasion, colony formation, sphere‐forming ability, drug resistance and stemness‐related gene expression were all significantly decreased. Furthermore, CXCL6, CXCL7 and CXCR2 were down‐regulated in Gal‐3‐knockdown tumour spheres, while CXCR2 overexpression in Gal‐3‐knockdown RCC restored the ability of sphere formation. Gal‐3 overexpression in RCC promoted both in vitro and in vivo tumorigenicity, and its expression was correlated with CXCR2 expression and tumour progression in clinical tissues. RCC patients with higher co‐expressions of Gal‐3 and CXCR2 demonstrated a worse survival rate. These results indicate that highly expressed Gal‐3 may up‐regulate CXCR2 to augment RCC stemness. Gal‐3 may be a prognostic and innovative target of combined therapy for treating RCC.
Inhibition of autophagy enhances the antitumour activity of tigecycline in multiple myeloma
Authors: Ma Ruye , Zhang Yu , Wang Wei , Wu Junqing , Yang Qianqian , Xu Wanling , Jiang Songfu , Han Yixiang , Yu Kang , Zhang Shenghui 
Published: September 2018

AbstractAccumulating evidence shows that tigecycline, a first‐in‐class glycylcycline, has potential antitumour properties. Here, we found that tigecycline dramatically inhibited the proliferation of multiple myeloma (MM) cell lines RPMI‐8226, NCI‐H929 and U266 in a dose and time‐dependent manner. Meanwhile, tigecycline also potently impaired the colony formation of these three cell lines. Mechanism analysis found that tigecycline led to cell cycle arrest at G0/G1 with down‐regulation of p21, CDK2 and cyclin D1, rather than induced apoptosis, in MM cells. Importantly, we found that tigecycline induced autophagy and an autophagy inhibitor bafilomycin A1 further amplified the tigecycline‐induced cytotoxicity, suggesting that autophagy plays a cytoprotective role in tigecycline‐treated MM cells. Mechanisms modulating autophagy found that tigecycline enhanced the phosphorylation of AMPK, but did not decrease the phosphorylation of Akt, to inhibit the phosphorylation of mTOR and its two downstream effectors p70S6K1 and 4E‐BP1. Tigecycline effectively inhibited tumour growth in the xenograft tumour model of RPMI‐8226 cells. Autophagy also occurred in tigecycline‐treated tumour xenograft, and autophagy inhibitor chloroquine and tigecycline had a synergistic effect against MM cells in vivo. Thus, our results suggest that tigecycline may be a promising candidate in the treatment of MM.
An alternative renin isoform is cardioprotective by modulating mitochondrial metabolism
Authors: Wanka Heike , Lutze Philipp , Staar Doreen , Grunow Bianka , Peters Barbara S. , Peters Jörg 
Published: September 2018

AbstractThe renin‐angiotensin system promotes oxidative stress, apoptosis, necrosis, fibrosis, and thus heart failure. Secretory renin plays a central role in these processes, initiating the generation of angiotensins. Nevertheless, alternative renin transcripts exist, which code for a cytosolically localized renin isoform (cyto‐renin) that is cardioprotective. We tested the hypothesis that the protective effects are associated with a beneficial switch of metabolic and mitochondrial functions. To assess H9c2 cell mitochondrial parameters, we used the Seahorse XF analyser. Cardiac H9c2 cells overexpressing cyto‐renin exhibited enhanced nonmitochondrial oxygen consumption, lactate accumulation, and LDH activity, reflecting a switch to more aerobic glycolysis known as Warburg effect. Additionally, mitochondrial spare capacity and cell respiratory control ratio were enhanced, indicating an increased potential to tolerate stress conditions. Renin knockdown induced opposite effects on mitochondrial functions without influencing metabolic parameters. Thus, the protective effects of cyto‐renin are associated with an altered bioenergetic profile and an enhanced stress tolerance, which are favourable under ischaemic conditions. Therefore, cyto‐renin is a promising new target for the prevention of ischaemia‐induced myocardial damage.
C5aR1 interacts with TLR2 in osteoblasts and stimulates the osteoclast‐inducing chemokine CXCL10
Authors: Mödinger Yvonne , Rapp Anna , Pazmandi Julia , Vikman Anna , Holzmann Karlheinz , Haffner‐Luntzer Melanie , Huber‐Lang Markus , Ignatius Anita 
Published: September 2018

AbstractThe anaphylatoxin C5a is generated upon activation of the complement system, a crucial arm of innate immunity. C5a mediates proinflammatory actions via the C5a receptor C5aR1 and thereby promotes host defence, but also modulates tissue homeostasis. There is evidence that the C5a/C5aR1 axis is critically involved both in physiological bone turnover and in inflammatory conditions affecting bone, including osteoarthritis, periodontitis, and bone fractures. C5a induces the migration and secretion of proinflammatory cytokines of osteoblasts. However, the underlying mechanisms remain elusive. Therefore, in this study we aimed to determine C5a‐mediated downstream signalling in osteoblasts. Using a whole‐genome microarray approach, we demonstrate that C5a activates mitogen‐activated protein kinases (MAPKs) and regulates the expression of genes involved in pathways related to insulin, transforming growth factor‐β and the activator protein‐1 transcription factor. Interestingly, using coimmunoprecipitation, we found an interaction between C5aR1 and Toll‐like receptor 2 (TLR2) in osteoblasts. The C5aR1‐ and TLR2‐signalling pathways converge on the activation of p38 MAPK and the generation of C‐X‐C motif chemokine 10, which functions, among others, as an osteoclastogenic factor. In conclusion, C5a‐stimulated osteoblasts might modulate osteoclast activity and contribute to immunomodulation in inflammatory bone disorders.
High glucose‐induced complement component 3 up‐regulation via RAGE‐p38MAPK‐NF‐κB signalling in astrocytes: In vivo and in vitro studies
Authors: Zhao Yuxing , Luo Cheng , Chen Jinliang , Sun Yue , Pu Die , Lv Ankang , Zhu Shiyu , Wu Jing , Wang Meili , Zhou Jing , Liao Zhiyin , Zhao Kexiang , Xiao Qian 
Published: September 2018

AbstractDiabetes is considered as a risk for cognitive decline, which is characterized by neurodegenerative alteration and innate immunity activation. Recently, complement 3 (C3), the critical central component of complement system, has been reported to play a key role in neurodegenerative alterations under pathological condition. Receptor for advanced glycation end products (RAGE) activation is confirmed to mediate several inflammatory cytokines production. However, whether C3 activation participates in the diabetic neuropathology and whether this process is regulated by RAGE activation remains unknown. The present study aimed to investigate the role of C3 in streptozotocin‐induced diabetic mice and high glucose‐induced primary astrocytes and the underlying modulatory mechanisms. The decreased synaptophysin density and increased C3 deposition at synapses were observed in the diabetic brain compared to the control brain. Furthermore, the elevated C3 was co‐localized with GFAP‐positive astrocytes in the diabetic brain slice in vivo and high glucose‐induced astrocytes culture in vitro. Diabetes/high glucose‐induced up‐regulation of C3 expression at gene, protein and secretion levels, which were attenuated by pre‐treatment with RAGE, p38MAPK and NF‐κB inhibitors separately. These results demonstrate that high glucose induces C3 up‐regulation via RAGE‐ p38MAPK‐NF‐κB signalling in vivo and in vitro, which might be associated with synaptic protein loss.