bluuebunny/crossref_metadata_2025_split huggingface dataset:
Postsecularity, Political Resistance, and Protest in the Occupy Movement
Authors: Cloke Paul , Sutherland Callum , Williams Andrew 
Published: October 2015

AbstractThis paper examines and critically interprets the interrelations between religion and the Occupy movements of 2011. It presents three main arguments. First, through an examination of the Occupy Movement in the UK and USA—and in particular of the two most prominent Occupy camps (Wall Street and London Stock Exchange)—the paper traces the emergence of postsecularity evidenced in the rapprochement of religious and secular actors, discourses, and practices in the event‐spaces of Occupy. Second, it examines the specific set of challenges that Occupy has posed to the Christian church in the UK and USA, arguing that religious participation in the camps served at least in part to identify wider areas of religious faith that are themselves in need of redemption. Third, the paper considers the challenges posed by religious groups to Occupy, not least in the emphasis on postmaterial values in pathways to resistance against contemporary capitalism.
The challenge of antibiotic resistance in haematology patients
Authors: Blennow Ola , Ljungman Per 
Published: October 2015

SummaryBacterial infections were once a major obstacle to the treatment of acute leukaemia. Improvement in management strategies, including the use of broad‐spectrum antibacterial drugs targeting Gram‐negative bacteria, has reduced the mortality in neutropenic patients developing blood stream infections and other severe infections. In many countries these achievements are threatened by development of multi‐resistant bacteria, such as Klebsiella pneumoniae, Pseudomonas aeruginosa and methicillin‐resistant Staphylococcus aureus. This review addresses the epidemiology, clinical importance and possible management of these multi‐resistant organisms.
Risk factor analysis of cerebral white matter hyperintensities in children with sickle cell disease
Authors: van der Land Veronica , Mutsaerts Henri J. M. M. , Engelen Marc , Heijboer Harriët , Roest Mark , Hollestelle Martine J. , Kuijpers Taco W. , Nederkoorn Paul. J. , Cnossen Marjon H. , Majoie Charles B. L. M. , Nederveen Aart J. , Fijnvandraat Karin 
Published: October 2015

SummarySickle cell disease (SCD) is complicated by silent cerebral infarcts, visible as white matter hyperintensities (WMHs) on magnetic resonance imaging (MRI). Both local vaso‐occlusion, elicited by endothelial dysfunction, and insufficiency of cerebral blood flow (CBF) have been proposed to be involved in the aetiology. We performed an explorative study to investigate the associations between WMHs and markers of endothelial dysfunction and CBF by quantifying WMH volume on 3·0 Tesla MRI. We included 40 children with HbSS or HbSβ0thalassaemia, with a mean age of 12·1 ± 2·6 years. Boys demonstrated an increased risk for WMHs (odds ratio 4·5, 95% confidence interval 1·2–17·4), unrelated to glucose‐6‐phosphate dehydrogenase deficiency. In patients with WMHs, lower fetal haemoglobin (HbF) was associated with a larger WMH volume (regression coefficient = −0·62, R2 = 0·25, P = 0·04). Lower ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13) levels were associated with lower CBF in the white matter (regression coefficient = 0·07, R2 = 0·15, P = 0·03), suggesting that endothelial dysfunction could potentially hamper CBF. The findings of our explorative study suggest that a high level of HbF may be protective for WMHs and that endothelial dysfunction may contribute to the development of WMHs by reducing CBF.
Understanding Aspects of Aluminum Exposure in Alzheimer's Disease Development
Authors: Kandimalla Ramesh , Vallamkondu Jayalakshmi , Corgiat Edwin B , Gill Kiran Dip 
Published: October 2015

AbstractAluminum is a ubiquitously abundant nonessential element. Aluminum has been associated with neurodegenerative diseases such as Alzheimer's disease (AD), amyotrophic lateral sclerosis, and dialysis encephalopathy. Many continue to regard aluminum as controversial although increasing evidence supports the implications of aluminum in the pathogenesis of AD. Aluminum causes the accumulation of tau protein and Aβ protein in the brain of experimental animals. Aluminum induces neuronal apoptosis in vivo and in vitro, either by endoplasmic stress from the unfolded protein response, by mitochondrial dysfunction, or a combination of them. Some, people who are exposed chronically to aluminum, either from through water and/or food, have not shown any AD pathology, apparently because their gastrointestinal barrier is more effective. This article is written keeping in mind mechanisms of action of aluminum neurotoxicity with respect to AD.
Mirabegron relaxes urethral smooth muscle by a dual mechanism involving β3‐adrenoceptor activation and α1‐adrenoceptor blockade
Authors: Alexandre E C , Kiguti L R , Calmasini F B , Silva F H , da Silva K P , Ferreira R , Ribeiro C A , Mónica F Z , Pupo A S , Antunes E 
Published: October 2015

Linked ArticleThis article is commented on by Michel, M. C., pp. 429‐430 of this issue. To view this commentary visit http://dx.doi.org/10.1111/bph.13379.Background and PurposeMirabegron is the first β3‐adrenoceptor agonist approved for treatment of overactive bladder syndrome. This study aimed to investigate the effects of β3‐adrenoceptor agonist mirabegron in mouse urethra. The possibility that mirabegron also exerts α1‐adrenoceptor antagonism was also tested in rat smooth muscle preparations presenting α1A‐ (vas deferens and prostate), α1D‐ (aorta) and α1B‐adrenoceptors (spleen).Experimental ApproachFunctional assays were carried out in mouse and rat isolated tissues. Competition assays for the specific binding of [3H]prazosin to membrane preparations of HEK‐293 cells expressing each of the human α1‐adrenoceptors, as well as β‐adrenoceptor mRNA expression and cyclic AMP measurements in mouse urethra, were performed.Key ResultsMirabegron produced concentration‐dependent urethral relaxations that were shifted to the right by the selective β3‐adrenoceptor antagonist L‐748,337 but unaffected by β1‐ and β2‐adrenoceptor antagonists (atenolol and ICI‐118,551 respectively). Mirabegron‐induced relaxations were enhanced by the PDE4 inhibitor rolipram, and the agonist stimulated cAMP synthesis. Mirabegron also produced rightward shifts in urethral contractions induced by the α1‐adrenoceptor agonist phenylephrine. Schild regression analysis revealed that mirabegron behaves as a competitive antagonist of α1‐adrenoceptors in urethra, vas deferens and prostate (α1A‐adrenoceptor, pA2 ≅ 5.6) and aorta (α1D‐adrenoceptor, pA2 ≅ 5.4) but not in spleen (α1B‐adrenoceptor). The affinities estimated for mirabegron in functional assays were consistent with those estimated in radioligand binding with human recombinant α1A‐ and α1D‐adrenoceptors (pKi ≅ 6.0).Conclusion and ImplicationsThe effects of mirabegron in urethral smooth muscle are the result of β3‐adrenoceptor agonism together with α1A and α1D‐adrenoceptor antagonism.
Bcl‐2 phosphorylation confers resistance on chronic lymphocytic leukaemia cells to the BH3 mimetics ABT‐737, ABT‐263 and ABT‐199 by impeding direct binding
Authors: Song Ting , Chai Gaobo , Liu Yubo , Yu Xiaoyan , Wang Ziqian , Zhang Zhichao 
Published: October 2015

Background and PurposeAlthough the ongoing clinical trials of ABT‐263 and ABT‐199 in chronic lymphocytic leukaemia (CLL) have indicated that BH3 mimetics hold considerable promise, understanding the mechanism of CLL resistance to BH3 mimetics remains a challenge.Experimental ApproachThe LD50 values of ABT‐737, ABT‐263 and ABT‐199 in a number of primary CLL cells from 40 patients, were determined. The levels of Bcl‐2 family proteins, including phosphorylated Bcl‐2 (pBcl‐2) and their interactions were measured by immunoblotting and co‐immunoprecipitation. In vitro binding assays were performed by isothermal titration calorimetry and ELISA. BH3 profiling in isolated mitochondria was analysed.Key ResultsThe ratio of (Mcl‐1 + pBcl‐2) to Bcl‐2 expression provided the most significant predictive marker for the cytotoxic potential of ABT‐737, ABT‐263 and ABT‐199 in the panel of CLL samples. Mechanistically, pBcl‐2 inhibited the effects of the ABT compounds on the displacement of Bax and Bim from Bcl‐2, thereby suppressing mitochondrial apoptosis. The ABT compounds exhibited 100–300‐fold lower binding affinity to the glutamic acid, phosphomimetic, mutant of Bcl‐2 (T69E, S70E and S87E; EEE‐Bcl‐2). BH3 peptides exhibited different rank orders of binding affinities to full‐length WT‐Bcl‐2 and full‐length EEE‐Bcl‐2.Conclusions and ImplicationsOur study suggested that a structural alteration in the BH3‐binding groove was induced by phosphorylation of Bcl‐2. Our data also provided a framework to overcome resistance of CLL cells to the ABT compounds by combining pBcl‐2 kinase inhibitors with the ABT compounds.
Enhanced serelaxin signalling in co‐cultures of human primary endothelial and smooth muscle cells
Authors: Sarwar M , Samuel C S , Bathgate R A , Stewart D R , Summers R J 
Published: October 2015

Background and PurposeIn the phase III clinical trial, RELAX‐AHF, serelaxin caused rapid and long‐lasting haemodynamic changes. However, the cellular mechanisms involved are unclear in humans.Experimental ApproachThis study examined the effects of serelaxin in co‐cultures of human primary endothelial cells (ECs) and smooth muscle cells (SMCs) on cAMP and cGMP signalling.Key ResultsStimulation of HUVECs or human coronary artery endothelial cells (HCAECs) with serelaxin, concentration‐dependently increased cGMP accumulation in co‐cultured SMCs to a greater extent than in monocultures of either cell type. This was not observed in human umbilical artery endothelial cells (HUAECs) that do not express the relaxin receptor, RXFP1. Treatment of ECs with l‐NG‐nitro arginine (NOARG; 30 μM, 30 min) inhibited serelaxin‐mediated (30 nM) cGMP accumulation in HUVECs, HCAECs and co‐cultured SMCs. In HCAECs, but not HUVECs, pre‐incubation with indomethacin (30 μM, 30 min) also inhibited cGMP accumulation in SMCs. Pre‐incubation of SMCs with the guanylate cyclase inhibitor ODQ (1 μM, 30 min) had no effect on serelaxin‐mediated (30 nM) cGMP accumulation in HUVECs and HCAECs but inhibited cGMP accumulation in SMCs. Serelaxin stimulation of HCAECs, but not HUVECs, increased cAMP accumulation concentration‐dependently in SMCs. Pre‐incubation of HCAECs with indomethacin, but not l‐NOARG, abolished cAMP accumulation in co‐cultured SMCs, suggesting involvement of prostanoids.Conclusions and ImplicationsIn co‐cultures, treatment of ECs with serelaxin caused marked cGMP accumulation in SMCs and with HCAEC also cAMP accumulation. Responses involved EC‐derived NO and with HCAEC prostanoid production. Thus, serelaxin differentially modulates vascular tone in different vascular beds.
CREB, AP‐1, ternary complex factors and MAP kinases connect transient receptor potential melastatin‐3 (TRPM3) channel stimulation with increased c‐Fos expression
Authors: Rubil Sandra , Rössler Oliver G. , Thiel Gerald 
Published: October 2015

Background and PurposeThe rise in intracellular Ca2+ stimulates the expression of the transcription factor c‐Fos. Depending on the mode of entry of Ca2+ into the cytosol, distinct signal transducers and transcription factors are required. Here, we have analysed the signalling pathway connecting a Ca2+ influx via activation of transient receptor potential melastatin‐3 (TRPM3) channels with enhanced c‐Fos expression.Experimental ApproachTranscription of c‐Fos promoter/reporter genes that were integrated into the chromatin via lentiviral gene transfer was analysed in HEK293 cells overexpressing TRPM3. The transcriptional activation potential of c‐Fos was measured using a GAL4‐c‐Fos fusion protein.Key ResultsThe signalling pathway connecting TRPM3 stimulation with enhanced c‐Fos expression requires the activation of MAP kinases. On the transcriptional level, three Ca2+‐responsive elements, the cAMP‐response element and the binding sites for the serum response factor (SRF) and AP‐1, are essential for the TRPM3‐mediated stimulation of the c‐Fos promoter. Ternary complex factors are additionally involved in connecting TRPM3 stimulation with the up‐regulation of c‐Fos expression. Stimulation of TRPM3 channels also increases the transcriptional activation potential of c‐Fos.Conclusions and ImplicationsSignalling molecules involved in connecting TRPM3 with the c‐Fos gene are MAP kinases and the transcription factors CREB, SRF, AP‐1 and ternary complex factors. As c‐Fos constitutes, together with other basic region leucine zipper transcription factors, the AP‐1 transcription factor complex, the results of this study explain TRPM3‐induced activation of AP‐1 and connects TRPM3 with the biological functions regulated by AP‐1. © 2015 The British Pharmacological Society
Young Children's Preferences: Gender, Race, and Social Status
Authors: Shutts Kristin 
Published: October 2015

AbstractIn this article, I consider how two aspects of society—social categories (in particular, gender and race) and social status—guide young children's preferences. Research on children's social categories reveals that gender‐based social preferences emerge earlier than race‐based preferences. Recent studies also show that children are attuned to social status, and the association of race with status differences could explain why race influences children's social preferences. I conclude with questions and suggestions for research.
Pathogenic T helper type 17 cells contribute to type 1 diabetes independently of interleukin-22
Authors: Bellemore S M , Nikoopour E , Krougly O , Lee-Chan E , Fouser L A , Singh B 
Published: October 2015

Summary
We have shown that pathogenic T helper type 17 (Th17) cells differentiated from naive CD4+ T cells of BDC2·5 T cell receptor transgenic non-obese diabetic (NOD) mice by interleukin (IL)-23 plus IL-6 produce IL-17, IL-22 and induce type 1 diabetes (T1D). Neutralizing interferon (IFN)-γ during the polarization process leads to a significant increase in IL-22 production by these Th17 cells. We also isolated IL-22-producing Th17 cells from the pancreas of wild-type diabetic NOD mice. IL-27 also blocked IL-22 production from diabetogenic Th17 cells. To determine the functional role of IL-22 produced by pathogenic Th17 cells in T1D we neutralized IL-22 in vivo by using anti-IL-22 monoclonal antibody. We found that blocking IL-22 did not alter significantly adoptive transfer of disease by pathogenic Th17 cells. Therefore, IL-22 is not required for T1D pathogenesis. The IL-22Rα receptor for IL-22 however, increased in the pancreas of NOD mice during disease progression and based upon our and other studies we suggest that IL-22 may have a regenerative and protective role in the pancreatic islets.
Quantification of normal cerebral oxygen extraction and oxygen metabolism by phase‐based MRI susceptometry: evaluation of repeatability using two different imaging protocols
Authors: Kämpe Robin , Lind Emelie , Ståhlberg Freddy , van Westen Danielle , Knutsson Linda , Wirestam Ronnie 
Published: October 2015

SummaryIntroductionGlobal oxygen extraction fraction (OEF) and cerebral metabolic rate of oxygen (CMRO2) were quantified in a test–retest study. Cerebral blood flow (CBF) data, required for CMRO2 estimation, were obtained using dynamic susceptibility contrast MRI (DSC‐MRI). OEF and CMRO2 were quantified using two separate data sets, that is, conventional high‐resolution (HR) gradient echo (GRE) phase maps as well as echo planar imaging (EPI) phase maps taken from the baseline (precontrast) part of the DSC‐MRI time series. The EPI phase data were included to elucidate whether an extra HR‐GRE scan is needed to obtain information about OEF and CMRO2, or if this information can be extracted from the DSC‐MRI experiment only.MethodsTwenty healthy volunteers were scanned using 3 T MRI on two occasions. Oxygen saturation levels were obtained from phase data measured in the great cerebral vein of Galen, based on HR‐GRE as well as EPI phase maps. In combination with DSC‐MRI CBF, this allowed for calculation of OEF and CMRO2.ResultsHigh‐resolution‐gradient echo‐ and EPI‐based phase images resulted in similar OEF spread and repeatability, with coefficients of variation/intraclass correlation coefficients of 0·26/0·95 and 0·23/0·81, respectively. Absolute OEF values (HR‐GRE: 0·40 ± 0·11, EPI: 0·35 ± 0·08) were consistent with literature data. CMRO2 showed similar repeatability, somewhat increased spread and reasonable absolute values (HR‐GRE: 3·23 ± 1·26 ml O2/100 g min−1, EPI: 2·79 ± 0·89 ml O2/100 g min−1).DiscussionIn general, the results obtained by HR‐GRE and EPI showed comparable characteristics. The EPI methodology could potentially be improved using a slightly modified DSC‐MRI protocol (e.g. with regard to spatial resolution and slice gap).
Filgrastim versus TBO‐filgrastim to reduce the duration of neutropenia after autologous hematopoietic stem cell transplantation: TBO, or not TBO, that is the question
Authors: Trifilio Steven , Zhou Zheng , Galvin John , Fong Jessica L. , Monreal Joanne , Mehta Jayesh 
Published: October 2015

AbstractAfter a hospital‐wide formulary change resulted in the replacement of filgrastim with TBO‐filgrastim for all on‐ and off‐label indications, we performed a retrospective comparison of patients with myeloma receiving 200 mg/m2 melphalan with autologous hematopoietic stem cell transplantation to see whether the type of growth factor used post‐transplant made a difference. One hundred and eighty‐two consecutive patients with myeloma were studied, 91 receiving filgrastim immediately prior to the change and 91 receiving TBO‐filgrastim afterward. The CD34+ cell dose was comparable, as were other characteristics. Although the overall time to neutrophil recovery was similar for both groups, early engraftment (≤12 d) occurred more often (p = 0.05), and late engraftment (≥14 d) less often (p = 0.09) in filgrastim‐treated patients. The number of documented infections was significantly less in the TBO‐filgrastim group. Day 100 mortality and hospital stay were similar for the two groups. These data indicate that there is no material difference between filgrastim and TBO‐filgrastim in this clinical setting.
Practicable methods for delimiting a plant invasion
Authors: Hauser Cindy E. , Giljohann Katherine M. , Rigby Michael , Herbert Karen , Curran Iris , Pascoe Charlie , Williams Nicholas S. G. , Cousens Roger D. , Moore Joslin L. 
Published: October 2015

AbstractAimInvasive populations are often irregularly distributed due to sporadic dispersal events and patchy distribution of suitable habitat, making it difficult to recognize the population boundary and effectively target management. We designed a survey prioritization that addresses these irregularities and tested it on an invasive King Devil Hawkweed (Hieracium praealtum) population.LocationBogong High Plains, Victoria, Australia.MethodsOur optimal design prioritized discovery of infestations beyond the known population boundary, while accounting for the diminishing likelihood of occurrence, plant detectability and the search resources available. Hawkweed management agencies implemented this design in the field. We evaluated its practicality and their progress towards delimitation.ResultsThe survey design favoured locations outside the known population boundary with a relatively high likelihood of species occurrence and high capacity to detect individuals. Difficult‐to‐search sites were selected for intensive survey when the likelihood of occurrence was sufficiently high. The GPS tracks recorded by managing agencies during the survey corresponded well with the priority rankings, but did not include search effort information. In subsequent surveys, managing agencies have improved recording protocols and expanded their performance metrics. This will facilitate future evaluation of progress towards delimitation and eradication.Main conclusionsOur optimization method effectively identified priorities for delimiting an invading population, accounting for the agencies' budget and the risk of detection failures. Probabilistic maps proved useful for communicating search priorities, and GPS track logs provided valuable spatial data for inferring where the species is likely to be absent. When comprehensive spatio‐temporal data are available, survey findings can be used to update species occurrence models and thus our quantitative understanding of the population's extent. A probabilistic map provides a more nuanced view of delimitation than drawing a strict boundary around known infestations. Burgman et al.'s extended delimitation score is a promising summary statistic for reporting.
Facial speech gestures: the relation between visual speech processing, phonological awareness, and developmental dyslexia in 10‐year‐olds
Authors: Schaadt Gesa , Männel Claudia , van der Meer Elke , Pannekamp Ann , Friederici Angela D. 
Published: October 2015

AbstractSuccessful communication in everyday life crucially involves the processing of auditory and visual components of speech. Viewing our interlocutor and processing visual components of speech facilitates speech processing by triggering auditory processing. Auditory phoneme processing, analyzed by event‐related brain potentials (ERP), has been shown to be associated with impairments in reading and spelling (i.e. developmental dyslexia), but visual aspects of phoneme processing have not been investigated in individuals with such deficits. The present study analyzed the passive visual Mismatch Response (vMMR) in school children with and without developmental dyslexia in response to video‐recorded mouth movements pronouncing syllables silently. Our results reveal that both groups of children showed processing of visual speech stimuli, but with different scalp distribution. Children without developmental dyslexia showed a vMMR with typical posterior distribution. In contrast, children with developmental dyslexia showed a vMMR with anterior distribution, which was even more pronounced in children with severe phonological deficits and very low spelling abilities. As anterior scalp distributions are typically reported for auditory speech processing, the anterior vMMR of children with developmental dyslexia might suggest an attempt to anticipate potentially upcoming auditory speech information in order to support phonological processing, which has been shown to be deficient in children with developmental dyslexia.
Difficult temperament and negative parenting in early childhood: a genetically informed cross‐lagged analysis
Authors: Micalizzi Lauren , Wang Manjie , Saudino Kimberly J. 
Published: October 2015

AbstractA genetically informed longitudinal cross‐lagged model was applied to twin data to explore etiological links between difficult temperament and negative parenting in early childhood. The sample comprised 313 monozygotic (MZ) and dizygotic (DZ) twin pairs. Difficult temperament and negative parenting were assessed at ages 2 and 3 using parent ratings. Both constructs were interrelated within and across age (rs .34–.47) and showed substantial stability (rs .65–.68). Difficult temperament and negative parenting were influenced by genetic and environmental factors at ages 2 and 3. The genetic and nonshared environmental correlations (rs .21–.76) at both ages suggest overlap at the level of etiology between the phenotypes. Significant bidirectional associations between difficult temperament and negative parenting were found. The cross‐lagged association from difficult temperament at age 2 to negative parenting at age 3 and from negative parenting at age 2 and difficult temperament at age 3 were due to genetic, shared environmental, and nonshared environmental factors. Substantial novel genetic and nonshared environmental influences emerged at age 3 and suggest change in the etiology of these constructs over time.