bluuebunny/crossref_metadata_2025_split huggingface dataset:
Long non‐coding RNA PVT1: Emerging biomarker in digestive system cancer
Authors: Zhou Dan‐Dan , Liu Xiu‐fen , Lu Cheng‐wei , Pant Om Prakash , Liu Xiao‐dong 
Published: October 2017

AbstractThe digestive system cancers are leading cause of cancer‐related death worldwide, and have high risks of morbidity and mortality. More and more long non‐coding RNAs (lncRNAs) have been studied to be abnormally expressed in cancers and play a key role in the process of digestive system tumour progression. Plasmacytoma variant translocation 1 (PVT1) seems fairly novel. Since 1984, PVT1 was identified to be an activator of MYC in mice. Its role in human tumour initiation and progression has long been a subject of interest. The expression of PVT1 is elevated in digestive system cancers and correlates with poor prognosis. In this review, we illustrate the various functions of PVT1 during the different stages in the complex process of digestive system tumours (including oesophageal cancer, gastric cancer, colorectal cancer, hepatocellular carcinoma and pancreatic cancer). The growing evidence shows the involvement of PVT1 in both proliferation and differentiation process in addition to its involvement in epithelial to mesenchymal transition (EMT). These findings lead us to conclude that PVT1 promotes proliferation, survival, invasion, metastasis and drug resistance in digestive system cancer cells. We will also discuss PVT1's potential in diagnosis and treatment target of digestive system cancer. There was a great probability PVT1 could be a novel biomarker in screening tumours, prognosis biomarkers and future targeted therapy to improve the survival rate in cancer patients.
Oedema‐fibrosis in Duchenne Muscular Dystrophy: Role of cardiovascular magnetic resonance imaging
Authors: Mavrogeni Sophie , Papavasiliou Antigoni , Giannakopoulou Katerina , Markousis‐Mavrogenis George , Pons Maria Roser , Karanasios Evangelos , Nikas Ioannis , Papadopoulos George , Kolovou Genovefa , Chrousos George P. 
Published: October 2017

AbstractDuchenne muscular dystrophy (DMD) is an X‐linked muscle disorder characterized by progressive, irreversible loss of cardiac and skeletal muscular function. Muscular enlargement in DMD is attributed to oedema, due to the increased cytoplasmic Na+ concentration. The aim of this review was to present the current experience and emphasize the role of cardiovascular magnetic resonance (CMR) in the diagnosis of this condition. DMD patients' survival depends on ventilatory assistance, as respiratory muscle dysfunction was the most common cause of death in the past. Currently, due to improved ventilatory assistance, cardiomyopathy has become the main cause of death, even though clinically overt heart failure may be absent. CMR is the technique of choice to assess the pathophysiologic phenomena taking place in DMD, such as myocardial oedema and subepicardial fibrosis. The classic index to assess oedema is the T2‐weighted short‐tau inversion recovery (T2w‐STIR), as it suppresses the signal from flowing blood and resident fat and enhances sensitivity to tissue fluid. Furthermore, CMR is the most reliable technique to detect and quantify fibrosis in DMD. Recently, the new indices T2, T1 mapping (native and postcontrast) and the extracellular volume (ECV) allow a more accurate approach of myocardial oedema and fibrosis. To conclude, the assessment of cardiac oedema and subepicardial fibrosis in the inferolateral wall of the left heart ventricle are the most important early finding in DMD with preserved ventricular function, and CMR, using both the classic and the new indices, is the best technique to detect and monitor these lesions.
Ecological plant epigenetics: Evidence from model and non‐model species, and the way forward
Authors: Richards Christina L. , Alonso Conchita , Becker Claude , Bossdorf Oliver , Bucher Etienne , Colomé‐Tatché Maria , Durka Walter , Engelhardt Jan , Gaspar Bence , Gogol‐Döring Andreas , Grosse Ivo , van Gurp Thomas P. , Heer Katrin , Kronholm Ilkka , Lampei Christian , Latzel Vít , Mirouze Marie , Opgenoorth Lars , Paun Ovidiu , Prohaska Sonja J. , Rensing Stefan A. , Stadler Peter F. , Trucchi Emiliano , Ullrich Kristian , Verhoeven Koen J. F. 
Published: October 2017

AbstractGrowing evidence shows that epigenetic mechanisms contribute to complex traits, with implications across many fields of biology. In plant ecology, recent studies have attempted to merge ecological experiments with epigenetic analyses to elucidate the contribution of epigenetics to plant phenotypes, stress responses, adaptation to habitat, and range distributions. While there has been some progress in revealing the role of epigenetics in ecological processes, studies with non‐model species have so far been limited to describing broad patterns based on anonymous markers of DNA methylation. In contrast, studies with model species have benefited from powerful genomic resources, which contribute to a more mechanistic understanding but have limited ecological realism. Understanding the significance of epigenetics for plant ecology requires increased transfer of knowledge and methods from model species research to genomes of evolutionarily divergent species, and examination of responses to complex natural environments at a more mechanistic level. This requires transforming genomics tools specifically for studying non‐model species, which is challenging given the large and often polyploid genomes of plants. Collaboration among molecular geneticists, ecologists and bioinformaticians promises to enhance our understanding of the mutual links between genome function and ecological processes.
The risk of Stevens‐Johnson syndrome and toxic epidermal necrolysis in new users of antiepileptic drugs
Authors: Frey Noel , Bodmer Michael , Bircher Andreas , Rüegg Stephan , Jick Susan S. , Meier Christoph R. , Spoendlin Julia 
Published: October 2017

SummaryObjectiveOlder antiepileptic drugs (AEDs) are known to cause Stevens‐Johnson syndrome and toxic epidermal necrolysis (SJS/TEN). However, evidence for newer AED is sparse. We quantified risks of SJS/TEN in association with use of all AEDs in the United Kingdom.MethodsIn a matched case‐control study of 480 previously validated SJS/TEN cases (1995–2013) we used conditional logistic regression to calculate odds ratios (ORs) with 95% confidence intervals (CIs), and calculated absolute risks of SJS/TEN within separate cohorts of new users of 28 AEDs. We assessed causality between drugs and SJS/TEN in each exposed case, using an adapted version of the algorithm of drug causality for epidermal necrolysis (ALDEN) score.ResultsWe observed a strong association between SJS/TEN and new use of carbamazepine (OR 92.57, 95% CI 19.89–∞), phenytoin (OR 49.96, 95% CI 10.13–∞), and lamotrigine (OR 26.90, 95% CI 4.88–∞), where causality, according to the ALDEN score, was very probable or probable for most exposed cases. Absolute risks for SJS/TEN were highest for phenytoin (45.86 cases/100,000 exposed), lamotrigine (44.17 cases/100,000 exposed), and carbamazepine (20.38 cases/100,000 exposed). Despite increased ORs for valproate (40,941 exposed), gabapentin (116,037 exposed), pregabalin (59,967 exposed), and clobazam (4,300 exposed), ALDEN suggested no causal association. There were no observed cases of SJS/TEN among new users of levetiracetam (n = 96,77), clonazepam (n = 18,075), or topiramate (n = 11,307).SignificanceThe results of our study are consistent with those of previous studies of SJS/TEN, which found increased risks of SJS/TEN in new use of carbamazepine, phenytoin, and lamotrigine. Despite frequent use, no ALDEN‐score confirmed cases were observed in new users of valproate, gabapentin, pregabalin, levetiracetam, topiramate, or clonazepam.
Too big to fail: Measures, remedies, and consequences for efficiency and stability*
Authors: Barth James R. , Wihlborg Clas 
Published: October 2017

AbstractThis paper evaluates whether reform efforts addressing “too big to fail” actually enhance the stability of the financial system, and whether trade‐offs exist between stability and efficiency. We also present and discuss various measures of bank size and complexity since such measures are essential for implementing appropriate corrective remedies. As we will show, there are no unambiguous measures of size or complexity that can fully capture a bank's contribution to systemic risk. Their effects on efficiency are also impossible to capture with certainty. While we recognize the need for additional research and empirical evidence, we do identify weaknesses and strengths of proposed and implemented reforms that could have consequences for bank stability and efficiency.
State uncertainty models and mark‐resight models for understanding non‐breeding site use by Piping Plovers
Authors: Cohen Jonathan B. , Maddock Sidney B. , Bimbi Melissa K. , Golder W. Walker , Ledee Olivia E. , Cuthbert Francesca J. , Catlin Daniel H. , Fraser James D. , Gratto‐Trevor Cheri L. 
Published: October 2017

AbstractConservation of beach‐nesting medium‐distance migrants has focused on breeding areas because protection of nests is more tractable than protection of non‐breeding habitat. As breeding ground management has encountered diminishing returns, interest in understanding threats in non‐breeding areas has increased. However, robust estimates of non‐breeding demographic rates and abundance are generally lacking, hindering the study of limiting factors. Estimating such rates is made more difficult by complex population dynamics at non‐breeding sites. In South Carolina, endangered Piping Plovers Charadrius melodus start arriving in July and some depart prior to December (the autumn‐only population) while others remain through at least March (the wintering population). State uncertainty capture‐mark‐recapture models provide a means for estimating vital rates for such co‐occurring populations. We estimated the proportion of the population entering the study area per survey (entry probability) and proportion remaining per survey (persistence rate) for both populations during autumn, and abundance of the wintering population, at four sites in South Carolina in 2006/7 and 2007/8, taking advantage of birds previously colour‐ringed on the breeding grounds. We made fairly precise estimates of entry and persistence rates with small sample sizes. Cumulative entry probability was ~50% by the end of July and reached 95% for both populations by October. Estimated stopover duration for birds in the autumn‐only population was 35 days in year 1 and 42 days in year 2. We estimated a wintering super‐population size of 71 ± 16 se birds in the first year and 75 ± 16 in the second. If ringing programmes on the breeding grounds continue, standardized resighting surveys in the non‐breeding period and mark‐recapture models can provide robust estimates of entry and persistence rates and abundance. Habitat protection intended to benefit non‐breeding Piping Plovers at our coastal sites should be in effect by late summer, as many birds are resident from July to the end of winter.
Sintering behavior and microwave dielectric properties of MgTiO3 obtained from coprecipitation method with additives
Authors: Nikzad Leila , Majidian Hudsa , Ghofrani Samaneh , Ebadzadeh Touradj 
Published: October 2017

AbstractMnO2 and ZnO additives, at three different weight percentages of 0.7, 1.4, and 2.1 wt%, were added to pure MgTiO3 ceramic obtained by coprecipitation method. Effects of these additives on microstructure, density, and dielectric properties of bulk products were investigated. The density of sample prepared from the synthesized MgTiO3 powder was 3.65 g/cm3 after sintering at low temperature of 1050 ̊C. Results showed that the density of samples consolidated from MgTiO3 submicrometer particles (less than 200 nm) containing 2.1 wt% MnO2 and ZnO was increased to 3.71 g/cm3 and 3.78 g/cm3, respectively, at low sintering temperature of 1050̊C. Also, the dielectric properties of sample containing 2.1 wt% ZnO were the best with εr of 16.9 and Q×f of 141000 GHz.
Migration, masculinity and social class: Insights from Pikine, Senegal
Authors: Prothmann Sebastian 
Published: October 2017

AbstractIn the shattered economy of Dakar, many young men feel stuck in prolonged bachelorhood. Handed‐down role expectations can often not be met due to dire economic prospects. Drawing on fieldwork in Pikine, an urban area within the Dakar region of Senegal, between 2011 and 2013, this article reflects upon the relation between risk, migration, social class and masculinity. Through migration to unknown destinations and by enduring the many challenges and hardships associated with it, in the hope of eventually reaching a higher social class upon return, young men wish to fix and rewrite their masculine identities. To pursue this aim even the oddest job in Europe becomes acceptable. At home, however, many work opportunities are considered to be beneath their social class. Most male urbanites seek jobs that are rewarded with respect and authority, and often assemble their choices about pursuing certain income‐generating activities considering notions of class.
Managing the National Status Group: Immigration Policy in Germany
Authors: Elrick Jennifer , Winter Elke 
Published: October 2017

AbstractThis article challenges the established convention in immigration policy scholarship of treating economic utility and identity maintenance as logically distinct concerns. Drawing on work by Weber, Wallerstein and Bourdieu, we argue that concerns about economic utility and identity maintenance interact in the immigration policies of Western liberal democratic states, leading to policies designed to build and maintain middle‐class national status groups. Using the example of contemporary immigration policy in Germany, we illustrate how this impulse to build the middle‐class status group affects immigrant inclusion/exclusion in nuanced ways at both the group and individual levels, along class/status, ethnic and gender lines. We conclude by considering the policy implications of growing and shaping populations according to middle‐class ideals, particularly for the statistical monitoring of immigrant populations for integration benchmarking purposes.
Cell death and immunity in cancer: From danger signals to mimicry of pathogen defense responses
Authors: Garg Abhishek D. , Agostinis Patrizia 
Published: October 2017

SummaryThe immunogenicity of cancer cells is an emerging determinant of anti‐cancer immunotherapy. Beyond developing immunostimulatory regimens like dendritic cell‐based vaccines, immune‐checkpoint blockers, and adoptive T‐cell transfer, investigators are beginning to focus on the immunobiology of dying cancer cells and its relevance for the success of anticancer immunotherapies. It is currently accepted that cancer cells may die in response to anti‐cancer therapies through regulated cell death programs, which may either repress or increase their immunogenic potential. In particular, the induction of immunogenic cancer cell death (ICD), which is hallmarked by the emission of damage‐associated molecular patterns (DAMPs); molecules analogous to pathogen‐associated molecular patterns (PAMPs) acting as danger signals/alarmins, is of great relevance in cancer therapy. These ICD‐associated danger signals favor immunomodulatory responses that lead to tumor‐associated antigens (TAAs)‐directed T‐cell immunity, which paves way for the removal of residual, treatment‐resistant cancer cells. It is also emerging that cancer cells succumbing to ICD can orchestrate “altered‐self mimicry” i.e. mimicry of pathogen defense responses, on the levels of nucleic acids and/or chemokines (resulting in type I interferon/IFN responses or pathogen response‐like neutrophil activity). In this review, we exhaustively describe the main molecular, immunological, preclinical, and clinical aspects of immunosuppressive cell death or ICD (with respect to apoptosis, necrosis and necroptosis). We also provide an extensive historical background of these fields, with special attention to the self/non‐self and danger models, which have shaped the field of cell death immunology.
Dysregulated cellular functions and cell stress pathways provide critical cues for activating and targeting natural killer cells to transformed and infected cells
Authors: Raulet David H. , Marcus Assaf , Coscoy Laurent 
Published: October 2017

SummaryNatural killer (NK) cells recognize and kill cancer cells and infected cells by engaging cell surface ligands that are induced preferentially or exclusively on these cells. These ligands are recognized by activating receptors on NK cells, such as NKG2D. In addition to activation by cell surface ligands, the acquisition of optimal effector activity by NK cells is driven in vivo by cytokines and other signals. This review addresses a developing theme in NK cell biology: that NK‐activating ligands on cells, and the provision of cytokines and other signals that drive high effector function in NK cells, are driven by abnormalities that arise from transformation or the infected state. The pathways include genomic damage, which causes self DNA to be exposed in the cytosol of affected cells, where it activates the DNA sensor cGAS. The resulting signaling induces NKG2D ligands and also mobilizes NK cell activation. Other key pathways that regulate NKG2D ligands include PI‐3 kinase activation, histone acetylation, and the integrated stress response. This review summarizes the roles of these pathways and their relevance in both viral infections and cancer.
High‐mobility group box 1 protein orchestrates responses to tissue damage via inflammation, innate and adaptive immunity, and tissue repair
Authors: Bianchi Marco E. , Crippa Massimo P. , Manfredi Angelo A. , Mezzapelle Rosanna , Rovere Querini Patrizia , Venereau Emilie 
Published: October 2017

SummaryA single protein, HMGB1, directs the triggering of inflammation, innate and adaptive immune responses, and tissue healing after damage. HMGB1 is the best characterized damage‐associated molecular pattern (DAMP), proteins that are normally inside the cell but are released after cell death, and allow the immune system to distinguish between antigens that are dangerous or not. Notably, cells undergoing severe stress actively secrete HMGB1 via a dedicated secretion pathway: HMGB1 is relocated from the nucleus to the cytoplasm and then to secretory lysosomes or directly to the extracellular space. Extracellular HMGB1 (either released or secreted) triggers inflammation and adaptive immunological responses by switching among multiple oxidation states, which direct the mutually exclusive choices of different binding partners and receptors. Immune cells are first recruited to the damaged tissue and then activated; thereafter, HMGB1 supports tissue repair and healing, by coordinating the switch of macrophages to a tissue‐healing phenotype, activation and proliferation of stem cells, and neoangiogenesis. Inevitably, HMGB1 also orchestrates the support of stressed but illegitimate tissues: tumors. Concomitantly, HMGB1 enhances the immunogenicity of mutated proteins in the tumor (neoantigens), promoting anti‐tumor responses and immunological memory. Tweaking the activities of HMGB1 in inflammation, immune responses and tissue repair could bring large rewards in the therapy of multiple medical conditions, including cancer.
Metabolic regulation of macrophage phenotype and function
Authors: Saha Shilpi , Shalova Irina N. , Biswas Subhra K. 
Published: October 2017

SummaryStudies in the last 20 years have given us a remarkable insight into the functional and phenotypic diversity of macrophages which reflects their integral role in host defence, homeostasis and pathogenesis. Mouse genetics, transcriptomic and epigenetic studies have provided an ontogenic and molecular perspective to the phenotypic diversity of these cells. Recently, metabolic studies have revealed the crucial role of metabolism and metabolites in shaping the phenotype and function of macrophages. Evidence pertaining to this aspect will be reviewed here.
Transformation through Repetition: Walking, Listening and Drawing on Tlicho Lands
Authors: Ruiz Adolfo 
Published: October 2017

AbstractAs part of my PhD practice‐based research on Tlicho lands (a self‐governed Indigenous region in Canada's Northwest Territories), drawing is being used to embody intangible cultural heritage (which includes activities such as oral history and the social practice of walking). Recent work to emerge from this research consists of two drawings created by Tlicho elders, and an animated film made of 900 graphite drawings referencing regional oral history. The process of rendering these drawings embodied experiences on the land that are repetitive, albeit transformative, such as walking or listening to multiple versions of a single story. The entanglement of continually moving lines, evident through the animation, provides a counter‐narrative to colonial interpretations of the land – particularly narratives constructed through Cartesian coordinate systems (on which computer graphics and the geometry of built environments are based). This article will describe the production of this film, while also inquiring into how line‐making provides a trace of memory, rhythmic movement and epistemology.
Drawing Analogies to Deepen Learning
Authors: Fava Michelle 
Published: October 2017

AbstractThis article offers examples of how drawing can facilitate thinking skills that promote analogical reasoning to enable deeper learning. The instructional design applies cognitive principles, briefly described here. The workshops were developed iteratively, through feedback from student and teacher participants. Elements of theUKNational Curriculum's key stage 3 science were covered in these examples, but the method of ‘drawing analogies’ can theoretically be applied in any subject.
No need for stepping stones: Direct, joint dispersal of the lichen‐forming fungus Mastodia tessellata (Ascomycota) and its photobiont explains their bipolar distribution
Authors: Garrido‐Benavent Isaac , de los Ríos Asunción , Fernández‐Mendoza Fernando , Pérez‐Ortega Sergio 
Published: October 2017

AbstractAimThe hypotheses proposed to explain the high percentage of bipolar lichens in Antarctica have never been explicitly tested. We used the strictly bipolar, coastal lichenized fungus Mastodia tessellata (Verrucariaceae, Ascomycota) and its photobionts (Prasiola, Trebouxiophyceae, Chlorophyta) as model species to discern whether this extraordinary disjunction originated from vicariance or long‐distance dispersal.LocationCoasts of Antarctica, Tierra del Fuego (Chile), Alaska (USA) and British Columbia (Canada).MethodsBased on a comprehensive geographical (315 specimens and 16 populations from Antarctica, Tierra del Fuego and North America) and molecular sampling (three and four loci for the fungus and algae respectively), we implemented explicit Bayesian methods to compare alternative hypotheses of speciation and migration, and performed dating analyses for the fungal and algal partner, in order to infer the timing of the colonization events and the direction of gene flow among distant, disjunct areas.ResultsMastodia tessellata comprises two fungal species which in turn associate with three photobiont lineages along the studied distribution range. Independent estimation of divergence ages for myco‐ and photobionts indicated a middle to latest Miocene species split in the Southern Hemisphere, and a late Miocene to Pleistocene acquisition of the bipolar distribution. Comparison of migration models and genetic diversity patterns suggested an austral origin for the bipolar species.Main conclusionsThe complex evolutionary history of Mastodia tessellata s.l. can be explained by a combination of vicariant and long‐distance dispersal mechanisms. We provide novel evidence of a pre‐Pleistocene long‐term evolution of lichens in Antarctica as well as for bipolar distributions shaped by Southern to Northern Hemisphere migratory routes without the need for stepping stones.