bluuebunny/crossref_metadata_2025_split huggingface dataset:
Normal fault growth influenced by basement fabrics: The importance of preferential nucleation from pre‐existing structures
Authors: Collanega Luca , Siuda Katherine , A.‐L. Jackson Christopher , Bell Rebecca E. , Coleman Alexander J. , Lenhart Antje , Magee Craig , Breda Anna 
Published: November 2018

AbstractReactivation of pre‐existing intra‐basement structures can influence the evolution of rift basins, yet the detailed kinematic relationship between these structures and overlying rift‐related faults remains poorly understood. Understanding the kinematic as well as geometric relationship between intra‐basement structures and rift‐related fault networks is important, with the extension direction in many rifted provinces typically thought to lie normal to fault strike. We here investigate this problem using a borehole‐constrained, 3D seismic reflection dataset from the Taranaki Basin, offshore New Zealand. Excellent imaging of intra‐basement structures and a relatively weakly deformed, stratigraphically simple sedimentary cover allow us to: (a) identify a range of interaction styles between intra‐basement structures and overlying, Plio‐Pleistocene rift‐related normal faults; and (b) examine the cover fault kinematics associated with each interaction style. Some of the normal faults parallel and are physically connected to intra‐basement reflections, which are interpreted as mylonitic reverse faults formed during Mesozoic subduction and basement terrane accretion. These geometric relationships indicate pre‐existing intra‐basement structures locally controlled the position and attitude of Plio‐Pleistocene rift‐related normal faults. However, through detailed 3D kinematic analysis of selected normal faults, we show that: (a) normal faults only nucleated above intra‐basement structures that experienced late Miocene compressional reactivation, (b) despite playing an important role during subsequent rifting, intra‐basement structures have not been significantly extensionally reactivated, and (c) preferential nucleation and propagation of normal faults within late Miocene reverse faults and folds appears to be the key genetic relationship between contractionally reactivated intra‐basement structures and rift‐related normal faults. Our analysis shows that km‐scale, intra‐basement structures can control the nucleation and development of newly formed, rift‐related normal faults, most likely due to a local perturbation of the regional stress field. Because of this, simply inverting fault strike for causal extension direction may be incorrect, especially in provinces where pre‐existing, intra‐basement structures occur. We also show that a detailed kinematic analysis is key to deciphering the temporal as well as simply the spatial or geometric relationship between structures developed at multiple structural levels.
Monocytes show immunoregulatory capacity on CD4+ T cells in a humanin-vitromodel of extracorporeal photopheresis
Authors: Wiese F , Reinhardt-Heller K , Volz M , Gille C , Köstlin N , Billing H , Handgretinger R , Holzer U 
Published: November 2018

SummaryExtracorporeal photopheresis (ECP) is a widely used immunomodulatory therapy for the treatment of various T cell-mediated disorders such as cutaneous T cell lymphoma (CTCL), graft-versus-host disease (GvHD) or systemic sclerosis. Although clinical benefits of ECP are already well described, the underlying mechanism of action of ECP is not yet fully understood. Knowledge on the fate of CD14+ monocytes in the context of ECP is particularly limited and controversial. Here, we investigated the immunoregulatory function of ECP treated monocytes on T cells in an in-vitro ECP model. We show that ECP-treated monocytes significantly induce proinflammatory T cell types in co-cultured T cells, while anti-inflammatory T cells remain unaffected. Furthermore, we found significantly reduced proliferation rates of T cells after co-culture with ECP-treated monocytes. Both changes in interleukin secretion and proliferation were dependent on cell-contact between monocytes and T cells. Interestingly, blocking interactions of programmed death ligand 1 (PD-L1) to programmed death 1 (PD-1) in the in-vitro model led to a significant recovery of T cell proliferation. These results set the base for further studies on the mechanism of ECP, especially the regulatory role of ECP-treated monocytes.
Effect of methacrylated chitosan incorporated in experimental composite and adhesive on mechanical properties and biofilm formation
Authors: Stenhagen Ida S. R. , Rukke Håkon V. , Dragland Inger S. , Kopperud Hilde M. 
Published: November 2018

The lifespan of a resin‐based restoration is limited, with the main reason for failure being secondary caries. Biofilm formation at the tooth–material interface is a necessary etiological agent for caries development. Dental materials with antimicrobial properties may reduce formation of biofilm and thus increase the longevity of restorations. This study aimed to investigate the effect of methacrylated chitosan (CH‐MA), incorporated into the polymeric network of an experimental dental composite and adhesive, on biofilm growth of Streptococcus mutans and to assess the mechanical properties of the modified materials. The methacrylation of low‐molecular‐weight chitosan was achieved and biofilm studies confirmed the antibacterial effect of the modified polymer in solution. Methacrylated chitosan was incorporated into an experimental composite and adhesive, and the modified materials reduced the formation of S. mutans biofilm. The incorporation of CH‐MA did not alter the bond strength of the adhesives. However, the amount of CH‐MA in composite that is required to elicit an antibacterial response challenges the mechanical properties of the material. The hardness and flexural strength of the composite decreased with increasing amounts of CH‐MA. However, flexural strength values still met the requirement in the ISO standard.
The Unity We Have Not Found: The Ontology of Relation in Koinonia
Authors: Ahola Miika 
Published: November 2018

AbstractThe search for the unity of the church is foundational to the World Council of Churches. This vocation has led the council to form unity statements that describe the motivation, requirements, and goals of unity. Subsequently, many models of unity have been created to meet these requirements. Koinonia ecclesiology provides the possibility to overcome the problems that have hindered these models of unity from becoming a reality. The relational ontology of koinonia has much to offer the churches in their search for visible communion. At its best, koinonia could bring together different facets of the council's work: the doctrinal, the ethical, the diaconal, the liturgical, the structural, and the contextual.
An Instrument of the Ecumenical Movement: The Joint Working Group between the Roman Catholic Church and the World Council of Churches
Authors: Mayer Annemarie C. 
Published: November 2018

AbstractFor 53 years of its 70‐year existence, the World Council of Churches (WCC) has had a Joint Working Group (JWG) with the Roman Catholic Church. This article offers a brief overview of various dates, facts, and figures about the JWG before turning to the beginnings of the JWG, explaining how it came about and some crucial turning points and shifts during its history of more than half a century. It focuses on some theological highlights of the work of the JWG and outlines its current work in progress. An issue that arises logically from the existence of the JWG is that of Roman Catholic membership in the WCC. This will be dealt with by examining the steps taken by the JWG to address this question. The article concludes by reflecting on some of the achievements and challenges, underlining what the JWG is and what it is not.
A roadmap for urban evolutionary ecology
Authors: Rivkin L. Ruth , Santangelo James S. , Alberti Marina , Aronson Myla F. J. , de Keyzer Charlotte W. , Diamond Sarah E. , Fortin Marie‐Josée , Frazee Lauren J. , Gorton Amanda J. , Hendry Andrew P. , Liu Yang , Losos Jonathan B. , MacIvor J. Scott , Martin Ryan A. , McDonnell Mark J. , Miles Lindsay S. , Munshi‐South Jason , Ness Robert W. , Newman Amy E. M. , Stothart Mason R. , Theodorou Panagiotis , Thompson Ken A. , Verrelli Brian C. , Whitehead Andrew , Winchell Kristin M. , Johnson Marc T. J. 
Published: November 2018

AbstractUrban ecosystems are rapidly expanding throughout the world, but how urban growth affects the evolutionary ecology of species living in urban areas remains largely unknown. Urban ecology has advanced our understanding of how the development of cities and towns change environmental conditions and alter ecological processes and patterns. However, despite decades of research in urban ecology, the extent to which urbanization influences evolutionary and eco‐evolutionary change has received little attention. The nascent field of urban evolutionary ecology seeks to understand how urbanization affects the evolution of populations, and how those evolutionary changes in turn influence the ecological dynamics of populations, communities, and ecosystems. Following a brief history of this emerging field, this Perspective article provides a research agenda and roadmap for future research aimed at advancing our understanding of the interplay between ecology and evolution of urban‐dwelling organisms. We identify six key questions that, if addressed, would significantly increase our understanding of how urbanization influences evolutionary processes. These questions consider how urbanization affects nonadaptive evolution, natural selection, and convergent evolution, in addition to the role of urban environmental heterogeneity on species evolution, and the roles of phenotypic plasticity versus adaptation on species’ abundance in cities. Our final question examines the impact of urbanization on evolutionary diversification. For each of these six questions, we suggest avenues for future research that will help advance the field of urban evolutionary ecology. Lastly, we highlight the importance of integrating urban evolutionary ecology into urban planning, conservation practice, pest management, and public engagement.
A novel role of angiotensin II in epidermal cell lineage determination: Angiotensin II promotes the differentiation of mesenchymal stem cells into keratinocytes through the p38 MAPK, JNK and JAK2 signalling pathways
Authors: Jiang Xiao , Wu Fan , Xu Yuan , Yan Jian‐Xin , Wu Yin‐Di , Li Sheng‐Hong , Liao Xuan , Liang Jun‐Xian , Li Ze‐Hua , Liu Hong‐Wei 
Published: November 2018

AbstractBackgroundRecent evidence suggests that angiotensin II (Ang II) plays a role in cutaneous wound healing. Mesenchymal stem cells (MSCs) are known as a rich source of cells that re‐establish healed skin. However, the potential impact of Ang II on MSC differentiation into keratinocytes is still unknown.ObjectiveThe present study was conducted to explore the effect of Ang II on the differentiation of bone marrow‐derived MSCs (BM‐MSCs) into keratinocytes.MethodsBone marrow‐derived MSCs were isolated from rat bone marrow and cultured. The expression of Ang II type 1 (AT1) and type 2 (AT2) receptors was examined by immunofluorescence staining. The differentiation of BM‐MSCs into keratinocytes was investigated by flow cytometry or/and histological observation.ResultsThe BM‐MSCs constitutively expressed both AT1 and AT2 receptors. The differentiation of BM‐MSCs into keratinocytes was successfully induced. Interestingly, incubation of BM‐MSCs with Ang II further promoted the differentiation of BM‐MSCs into keratinocyte, which was abolished by pretreament with losartan, an AT1 receptor antagonist, but not by PD123319, an AT2 receptor antagonist. Moreover, the p38 mitogen‐activated protein kinase (MAPK) inhibitor SB203580, the c‐Jun N‐terminal kinase (JNK) inhibitor SP600125 and the Janus‐activated kinase (JAK)2 inhibitor AG490 suppressed Ang II‐induced differentiation of BM‐MSCs into keratinocytes. The phosphoinositide‐3 kinase (PI3K) inhibitor wortmannin and MEK1/2 inhibitor U0126 had no effect on BM‐MSC differentiation into keratinocytes.ConclusionsOur data demonstrated for the first time that Ang II plays a promotive role in the differentiation of BM‐MSC into keratinocytes through the AT1 receptor, and that the p38 MAPK, JNK and JAK2 signalling pathways are involved in this process.
The absence of Rab27a accelerates the degradation of Melanophilin
Authors: Park Jong il , Lee Ji Eun , Myung Cheol hwan , Jo Chan song , Jang Hye Sung , Hwang Jae Sung 
Published: November 2018

AbstractMelanophilin (Mlph) forms an interaction with Rab27a and the actin‐based motor protein MyosinVa (MyoVa) on mature melanosome membranes and the tripartite complex regulates melanosome transport in melanocytes. In this study, we found that Rab27a siRNA decreased Mlph and Rab27a protein levels, but Mlph mRNA levels were not changed. Other Rab27a siRNA sequences also showed the same results. When Rab27a siRNA was treated with melan‐a melanocytes, Rab27a protein was decreased within 6 hours and Mlph protein was decreased within 24 hours. To determine whether the absence of Rab27a promotes Mlph degradation, we inhibited protein degradation by treatment with proteasome (MG132) and lysosomal enzyme (E64D and Pepstatin A) inhibitors in melan‐a melanocytes. MG132 inhibited the degradation of Mlph, but E64D and Pepstatin A had no effect on Mlph. The absence of Rab27a enhanced ubiquitination of Mlph and induced proteasomal degradation. From these results, we concluded that Mlph interaction with Rab27a is important for Mlph stability and melanosome transport.
Carbon sequestration in riparian forests: A global synthesis and meta‐analysis
Authors: Dybala Kristen E. , Matzek Virginia , Gardali Thomas , Seavy Nathaniel E. 
Published: November 2018

AbstractRestoration of deforested and degraded landscapes is a globally recognized strategy to sequester carbon, improve ecological integrity, conserve biodiversity, and provide additional benefits to human health and well‐being. Investment in riparian forest restoration has received relatively little attention, in part due to their relatively small spatial extent. Yet, riparian forest restoration may be a particularly valuable strategy because riparian forests have the potential for rapid carbon sequestration, are hotspots of biodiversity, and provide numerous valuable ecosystem services. To inform this strategy, we conducted a global synthesis and meta‐analysis to identify general patterns of carbon stock accumulation in riparian forests. We compiled riparian biomass and soil carbon stock data from 117 publications, reports, and unpublished data sets. We then modeled the change in carbon stock as a function of vegetation age, considering effects of climate and whether or not the riparian forest had been actively planted. On average, our models predicted that the establishment of riparian forest will more than triple the baseline, unforested soil carbon stock, and that riparian forests hold on average 68–158 Mg C/ha in biomass at maturity, with the highest values in relatively warm and wet climates. We also found that actively planting riparian forest substantially jump‐starts the biomass carbon accumulation, with initial growth rates more than double those of naturally regenerating riparian forest. Our results demonstrate that carbon sequestration should be considered a strong co‐benefit of riparian restoration, and that increasing the pace and scale of riparian forest restoration may be a valuable investment providing both immediate carbon sequestration value and long‐term ecosystem service returns.
Acute kidney injury in HIV‐infected patients: a critical review
Authors: Gameiro J , Agapito Fonseca J , Jorge S , Lopes JA 
Published: November 2018

Acute kidney injury (AKI) is characterized by a rapid decline of renal function associated with worse outcomes. The purpose of the authors is to perform a critical review of the incidence, risk factors, pathogenesis and outcome of AKI in HIV‐infected patients. Human immunodeficiency virus (HIV)‐infected patients have an increased risk of developing AKI, to which contribute both HIV‐dependent and HIV‐independent factors as well as the nephrotoxicity of drugs used. The increased risk of AKI in HIV‐infected patients and its negative impact on prognosis highlights the need for identification of patients at risk, creation of prevention strategies and management.HIV‐infected patients have an increased risk of developing AKI, to which both HIV‐dependent and HIV‐independent factors contribute, as well as the nephrotoxicity of drugs used.The increased risk of AKI in HIV‐infected patients and its negative impact on prognosis highlight the need for identification of patients at risk, creation of prevention strategies and management.
Effects of preparation with the Self‐Adjusting File, TRUShape and XP‐endo Shaper systems, and a supplementary step with XP‐endo Finisher R on filling material removal during retreatment of mandibular molar canals
Authors: Machado A. G. , Guilherme B. P. S. , Provenzano J. C. , Marceliano‐Alves M. F. , Gonçalves L. S. , Siqueira J. F. , Neves M. A. S. 
Published: November 2018

AbstractAimTo compare the effects of three instrumentation systems, and a supplementary approach with a finishing instrument, on filling material removal during retreatment of mandibular molar canals.MethodsSixty mesial canals from mandibular molars (Vertucci's type IV anatomy) were instrumented, filled and subjected to retreatment. After initial removal of the root canal filling material using the D‐RaCe system, the canals were randomly distributed into three groups (n = 20) according to the instrument system used for preparation: the Self‐Adjusting File (SAF), TRUShape or XP‐endo Shaper. The filling material volume in the apical 5 mm of the canals was assessed by means of micro‐computed tomography (micro‐CT) before and after retreatment. All specimens with residual filling material were subjected to a supplementary approach with the XP‐endo Finisher R instrument and another micro‐CT scan was taken. Data on the volumes of filling material and incidence of total removal were compared between groups by the general linear model for paired data and the Fisher's exact test. The effects of the refinement step were evaluated by the Wilcoxon Signed Ranks test.ResultsThe amount of removed material was 92.4%, 96.9% and 96.9% for the SAF, TRUShape and XP‐endo Shaper, respectively. There were no significant differences between them (P > 0.05). Canals were completely cleaned of filling material in 70% of the specimens for XP‐endo Shaper, 55% for SAF and 30% for TRUShape; the difference between XP‐endo Shaper and TRUShape was significant (P = 0.03). The supplementary step with the XP‐endo Finisher R instrument was associated with additional filling material removal of 38% (P < 0.001). Six more canals were rendered free of filling material after using this finishing instrument.ConclusionsThe tested systems were equally effective in removing the mass of filling material from the apical 5 mm of molar canals. The supplementary step with the XP‐endo Finisher R instrument enhanced filling material removal.
Atherosclerosis as a predictor of transient exacerbation of overactive bladder symptoms after robot‐assisted laparoscopic radical prostatectomy
Authors: Koguchi Tomoyuki , Haga Nobuhiro , Matsuoka Kanako , Yabe Michihiro , Hoshi Seiji , Ogawa Soichiro , Kataoka Masao , Akaihata Hidenori , Sato Yuichi , Hata Junya , Ishibashi Kei , Kojima Yoshiyuki 
Published: November 2018

ObjectivesTo assess whether atherosclerosis is involved in the development of overactive bladder and the function of lower urinary tract after robot‐assisted radical prostatectomy.MethodsThe present cohort consisted of 80 consecutive participants. The preoperative cardio‐ankle vascular index was used to evaluate the presence of atherosclerosis. The present cohort was split into two groups, the atherosclerotic group, whose cardio‐ankle vascular index was ≥9.0, and the control group, whose index was <9.0. The overactive bladder symptom score and lower urinary tract function were compared for 12 months after surgery.ResultsThe total score of the questionnaire was significantly higher at 6 and 9 months after surgery in the atherosclerosis group (P = 0.04, P = 0.03, respectively). Both the urgency and urgency incontinence subscores of the questionnaire showed a parallel tendency to that of the total score after surgery. At 3 months after surgery, there was a significant increase in the prevalence of de novo overactive bladder in the atherosclerosis group (P = 0.04). At 9 and 12 months after surgery, there was a significant decrease of voided volume in the atherosclerotic group (P < 0.01, P = 0.04, respectively).ConclusionsAtherosclerosis delays the improvement in both overactive bladder symptoms and storage function postoperatively, and it is involved in the transient increase in the prevalence of de novo overactive bladder. Atherosclerosis might be a predictor of the development of overactive bladder after robot‐assisted radical prostatectomy.
Frailty is associated with reduced prospect of discharge home after in‐hospital cardiac arrest
Authors: Smith Roger J. , Reid David A. , Santamaria John D. 
Published: November 2018

AbstractBackgroundFrailty is common among acute hospital patients and might adversely affect recovery from inpatient cardiac arrest.AimTo assess the relationship between hospital admission characteristics, including frailty, and discharge outcome after in‐hospital cardiac arrest.MethodsProspectively collected data were retrospectively analysed for all separations from a tertiary hospital during 2008–2017 that involved rapid response team attendance for cardiac arrest. Hospital Frailty Risk Score (HFRS) and Charlson index of comorbidity were calculated from ‘primary’ and ‘associated’ International Classification of Diseases, 10th revision, Australian Modification diagnoses. HFRS ≥5 was taken to signify frailty. Discharge home from hospital and death in hospital were modelled using logistic regression.ResultsThere were 388 in‐hospital arrest patients: 91% were aged ≥50 years, 34% were previously discharged in the past 6 months, 66% were unplanned admissions, 63% were non‐cardiology‐cardiothoracic admissions, 45% had a Charlson comorbidity index ≥2 and 19% were identified as frail. Discharge home occurred in 22%, discharge to another hospital 17% and death 62%. Of the frail patients, only 3 (4%) were discharged home, 12 (17%) were discharged to another hospital and 57 (79%) died in hospital. Fewer frail patients were discharged home compared with non‐frail patients (4 vs 26%; odds ratio (OR) 0.13, P = 0.001). On multivariable analysis, patients were less likely to be discharged home if they had frailty (OR 0.24, P = 0.02), age ≥ 50 years (OR 0.36, P = 0.01), non‐cardiology‐cardiothoracic unit admission (OR 0.40, P = 0.001) and unplanned admission (OR 0.57, P = 0.04). Frail patients discharged to another hospital spent a median of 15 days (interquartile range 11–23) in the hospital post‐arrest before leaving to continue inpatient care elsewhere. Frailty was associated with death in hospital on univariate analysis (79 vs 58%; OR 2.80, P = 0.001) but not after controlling for other factors.ConclusionFrail patients are unlikely to make a good recovery after in‐hospital arrest. This should be taken into account when planning care with patients and their families.