bluuebunny/crossref_metadata_2025_split huggingface dataset:
Trees tolerate an extreme heatwave via sustained transpirational cooling and increased leaf thermal tolerance
Authors: Drake John E. , Tjoelker Mark G. , Vårhammar Angelica , Medlyn Belinda E. , Reich Peter B. , Leigh Andrea , Pfautsch Sebastian , Blackman Chris J. , López Rosana , Aspinwall Michael J. , Crous Kristine Y. , Duursma Remko A. , Kumarathunge Dushan , De Kauwe Martin G. , Jiang Mingkai , Nicotra Adrienne B. , Tissue David T. , Choat Brendan , Atkin Owen K. , Barton Craig V. M. 
Published: January 2018

AbstractHeatwaves are likely to increase in frequency and intensity with climate change, which may impair tree function and forest C uptake. However, we have little information regarding the impact of extreme heatwaves on the physiological performance of large trees in the field. Here, we grew Eucalyptus parramattensis trees for 1 year with experimental warming (+3°C) in a field setting, until they were greater than 6 m tall. We withheld irrigation for 1 month to dry the surface soils and then implemented an extreme heatwave treatment of 4 consecutive days with air temperatures exceeding 43°C, while monitoring whole‐canopy exchange of CO2 and H2O, leaf temperatures, leaf thermal tolerance, and leaf and branch hydraulic status. The heatwave reduced midday canopy photosynthesis to near zero but transpiration persisted, maintaining canopy cooling. A standard photosynthetic model was unable to capture the observed decoupling between photosynthesis and transpiration at high temperatures, suggesting that climate models may underestimate a moderating feedback of vegetation on heatwave intensity. The heatwave also triggered a rapid increase in leaf thermal tolerance, such that leaf temperatures observed during the heatwave were maintained within the thermal limits of leaf function. All responses were equivalent for trees with a prior history of ambient and warmed (+3°C) temperatures, indicating that climate warming conferred no added tolerance of heatwaves expected in the future. This coordinated physiological response utilizing latent cooling and adjustment of thermal thresholds has implications for tree tolerance of future climate extremes as well as model predictions of future heatwave intensity at landscape and global scales.
Levels of malondialdehyde in the gastric juice: Its association with Helicobacter pylori infection and stomach diseases
Authors: Wang Yao‐Kuang , Chiang Wei‐Chih , Kuo Fu‐Chen , Wu Meng‐Chieh , Shih Hsiang‐Yao , Wang Sophie S.W. , Liu Chung‐Jung , Chen Yen‐Hsu , Wu Deng‐Chyang , Su Wei‐Wen , Huang Yeou‐Lih 
Published: January 2018

AbstractBackgroundHelicobacter pylori (H. pylori) infection causes elevation of lipid peroxidation product malondialdehyde (MDA) and this association may be due to the bacterium causing reactive oxygen species‐mediated damage to DNA in the gastric epithelium. The aim of this study was to investigate the gastric juice MDA levels in relation to H. pylori infection and associated gastric diseases.MethodsGastric juice samples were obtained from 117 patients undergoing endoscopy, and gastric juice MDA levels were determined by high‐performance liquid chromatography (HPLC) system. We compared the MDA levels between patients with and without H. pylori infection and assessed the differences of MDA levels between chronic gastritis, gastric intestinal metaplasia, and gastric cancer postsurgical resection.ResultsMalondialdehyde levels in gastric juice were significantly higher in chronic gastritis patients with H. pylori infection than in those without H. pylori infection (P < .0001). In patients without H. pylori infection, patients with gastric intestinal metaplasia and gastric cancer postsurgical resection had significantly higher gastric juice MDA level than patients with chronic gastritis. As a whole, patients with gastric intestinal metaplasia and gastric cancer postsurgical resection also had significantly higher MDA levels in gastric juice as compared to patients with chronic gastritis (P < .01). However, the difference of gastric juice MDA levels between gastric intestinal metaplasia and gastric cancer postsurgical resection was not significant.ConclusionMalondialdehyde in gastric juice could be used as a potential diagnostic biomarker for H. pylori infection and associated gastric diseases. The gastric juice MDA levels increased proportionally with the severity of gastric diseases.
Construal level and collaborative consumption: An exploratory approach
Authors: Sordi Jefferson D. , Perin Marcelo G. , Petrini Maira de C. , Sampaio Claudio H. 
Published: January 2018

AbstractWhat motivates the participation in collaborative consumption, a part of the economy that will move 300 billion dollars by 2025? The literature presents external factors to the consumer as a form of incentive or limitation, such as economic opportunity, search for a sustainable society or emergence of a marketplace with no regulations. A few quantitative articles focused on understanding this access phenomenon, by analyzing the consumer as the main subject of research. However, it is possible to analyze this behaviour in the light of a theory that has not yet being explored within the collaborative consumer literature: The Construal Level Theory (CLT). This article aims to demonstrate that CLT presents a plausible explanation for adoption and access to collaborative consumption. The CLT's main idea is that consumers develop their interpretations on two levels: a higher one, focused on more abstract and simple situations; and a lower one, where judgments are conducted more concretely and complexly. Studies on CLT have shown that attitudes are usually constructed at high levels of interpretation, while behaviour is interpreted within lower levels. We propose that collaborative consumption can be reflected by consumers’ high or low levels and so defining the consumer's behaviour in this context.
Evaluation of ICAM‐1 expression and vascular changes in the skin of patients with plaque, pustular, and erythrodermic psoriasis
Authors: Bressan Aline L. , Picciani Bruna L. S. , Azulay‐Abulafia Luna , Fausto‐Silva Anna K. , Almeida Paula N. , Cunha Karin S. G. , Dias Eliane P. , Carneiro Sueli 
Published: January 2018

AbstractBackgroundPsoriasis is a chronic inflammatory disease. Pustular, erythrodermic, and extensive plaque psoriasis are responsible for systemic complications. Systemic capillary leak syndrome is the complication with greater progression to death and occurs due to vascular changes.PurposeThe aim of this study was to evaluate vascular changes through the expression of CD34 and ICAM‐1 in plaque, pustular, and erythrodermic psoriasis.MethodsThe sample consisted of seven patients with erythrodermic psoriasis, 24 with moderate‐severe plaque psoriasis, 14 with mild plaque psoriasis and 13 with pustular psoriasis. Patients were submitted to physical examination and skin biopsy for histopathological examination and immunohistochemical analysis with anti‐CD34 and anti‐ICAM‐1 antibodies. Subsequently, tissue fragments were organized by groups using the Tissue Macroarray (TMA) technique to perform immunohistochemistry.ResultsIn 58 patients, analysis of vessels using anti‐CD34 demonstrated vascular immunostaining in superficial dermis and between dermal papillae. There were more blood vessels in erythrodermic psoriasis, followed by plaque psoriasis. In erythrodermic psoriasis, there were small and few tortuous blood vessels with great dilatation, while plaque psoriasis presented larger vessels that were less dilated and more tortuous. There was an intense and localized expression of ICAM‐1 in endothelial and lymphocytic cells in all groups, with significant differences.ConclusionsVascular alterations are important in psoriasis, with an increase in the number of blood vessels and ICAM‐1 overexpression, especially in erythrodermic form. Therefore, vascular changes and the expression of intercellular adhesion molecules could help to diagnose the erythrodermic form of psoriasis.
Humility: Our Current Understanding of the Construct and its Role in Organizations
Authors: Nielsen Rob , Marrone Jennifer A. 
Published: January 2018

AbstractSince 2000, researchers and practitioners have shown increased interest in humility. This construct has been studied in disciplines ranging from organizational behaviour to positive psychology, culminating in a wealth of information that can now be analysed and reviewed through the lens of humility in organizations. This review begins by reflecting on existing conceptualizations of humility and presenting a summary of findings that reflects a greater consensus in definitional work than some researchers may realize. It then considers the progress that has been made in measuring humility by specifying key measurement strategies. It next synthesizes existing empirical findings on humility to illuminate the uniqueness of the construct. It also shows that researchers have focused on studying dependent variables that exist at multiple organizational levels and that largely comprise pro‐social and relational variables, emotional well‐being, and learning and performance outcomes. The paper concludes with recommendations for future research.
Multimorbidity, not human immunodeficiency virus (HIV) markers predicts unplanned admission among people with HIV in regional New South Wales
Authors: Edmiston Natalie , Petoumenos Kathy , Smith David J. 
Published: January 2018

AbstractBackgroundMultimorbidity and unplanned admissions are common among people with human immunodeficiency virus (PWH).AimsTo determine factors predictive of unplanned admission among PWH in regional New South Wales and compare care coordination between people with and without unplanned admissions.MethodsA prospective cohort study of PWH attending a regional human immunodeficiency virus (HIV) service was conducted. Baseline HIV‐specific results and multimorbidity markers including Cumulative Illness Rating Scale (CIRS) were assessed as predictors of time to first unplanned admission using Cox regression analysis. Care coordination markers were compared between people with and without unplanned admission, using χ2 statistic for proportions and t‐test for means.ResultsA cohort of 181 PWH was followed for a maximum of 5 years. During a total of 739 person‐years of follow up, 39 (20.6%) patients reached the endpoint of unplanned admission. In multivariate analysis, the baseline CIRS score was predictive of unplanned admission (P < 0.001). Age, HIV‐specific markers and missed visits were not predictive of unplanned admission. For patients with an unplanned admission, discharge summaries were documented for 22/39 (56.4%). Of 180 PWH with a visit after baseline, 131 (72.8%) had a letter to a general practitioner and 79 (43.7%) had two or more prescribers. Having two or more prescribers was more common in people with an unplanned admission than in those without (64.1% vs 38.0%, P = 0.004).ConclusionUnplanned admission among PWH is predicted by multimorbidity. Care for PWH should include coordinated management of other health conditions in order to reduce their severity and prevent unplanned admissions.
Improved methods for predicting peptide binding affinity to MHC class II molecules
Authors: Jensen Kamilla Kjærgaard , Andreatta Massimo , Marcatili Paolo , Buus Søren , Greenbaum Jason A. , Yan Zhen , Sette Alessandro , Peters Bjoern , Nielsen Morten 
Published: January 2018

SummaryMajor histocompatibility complex class II (MHC‐II) molecules are expressed on the surface of professional antigen‐presenting cells where they display peptides to T helper cells, which orchestrate the onset and outcome of many host immune responses. Understanding which peptides will be presented by the MHC‐II molecule is therefore important for understanding the activation of T helper cells and can be used to identify T‐cell epitopes. We here present updated versions of two MHC–II–peptide binding affinity prediction methods, NetMHCII and NetMHCIIpan. These were constructed using an extended data set of quantitative MHC–peptide binding affinity data obtained from the Immune Epitope Database covering HLA‐DR, HLA‐DQ, HLA‐DP and H‐2 mouse molecules. We show that training with this extended data set improved the performance for peptide binding predictions for both methods. Both methods are publicly available at www.cbs.dtu.dk/services/NetMHCII-2.3 and www.cbs.dtu.dk/services/NetMHCIIpan-3.2.
Autoimmunity and autoimmune co‐morbidities in psoriasis
Authors: Furue Kazuhisa , Ito Takamichi , Tsuji Gaku , Kadono Takafumi , Nakahara Takeshi , Furue Masutaka 
Published: January 2018

SummaryPsoriasis is characterized by widespread scaly erythematous plaques that cause significant physical and psychological burdens for the affected individuals. Accelerated inflammation driven by the tumour necrosis factor‐α/interleukin‐23/interleukin‐17 axis is now known to be the major mechanism in the development of psoriasis. In addition, psoriasis has an autoimmune nature that manifests as autoreactive T cells and is co‐morbid with other autoimmune diseases, such as autoimmune bullous diseases, vitiligo, alopecia and thyroiditis. In this article, we review the recent topics on autoimmunity and autoimmune co‐morbidities in psoriasis.
The American Inventors Protection Act: A Natural Experiment on Innovation Disclosure and the Cost of Debt
Authors: Hoffmann Arvid O. I. , Kleimeier Stefanie , Mimiroglu Nagihan , Pennings Joost M. E. 
Published: January 2018

AbstractWe examine the impact of innovation disclosure through patenting on firms' cost of debt, focusing on the American Inventors Protection Act (AIPA) as an exogenous shock in innovation disclosure regulation. Post‐AIPA, firms have an incentive to apply for patents only if commercial success is likely. Accordingly, we expect post‐AIPA patents to be a better proxy for successful innovation activity, and thus to have a stronger effect on reducing the cost of debt than pre‐AIPA patents. Indeed, we find that pre‐AIPA patents reduce the cost of debt only for the most innovative firms, while post‐AIPA, this effect holds for all firms.
Geological effects influence population genetic connectivity more than Pleistocene glaciations in the water strider Metrocoris sichuanensis (Insecta: Hemiptera: Gerridae)
Authors: Ye Zhen , Yuan Juanjuan , Li Min , Damgaard Jakob , Chen Pingping , Zheng Chenguang , Yu Haibin , Fu Siying , Bu Wenjun 
Published: January 2018

AbstractAimPalaeoclimatic and palaeogeological events have been identified as two main factors that influence the genetic structuring of extant organisms. We studied a montane stream‐dwelling insect, Metrocoris sichuanensis, to explore the relative roles played by these two factors in population genetic connectivity.LocationSichuan Basin, China.MethodsMitochondrial (COI, COII, Cytb, 16S) and nuclear (EF‐1α, ITS1) markers were sequenced from 208 individuals. Suitable habitat shifts from the Last Glacial Maximum (LGM) to the present were predicted through fine‐tuned ecological niche modelling (ENM). Phylogenetic and phylogeographical analyses were conducted to reveal the population genetic structure. Intraspecific divergence and expansion times were estimated using beast. Finally, the least cost path (LCP) method coupled with migrate analysis was used to identify possible dispersal corridors and estimate the asymmetric gene flow.ResultsOur ENM results suggested that population habitat connectivity did not change both in the LGM and current conditions. Whole haplotypes were separated into four highly supported clades/haplogroups that exhibited strong geographical structure. The splitting events between the four lineages likely date back to the Early Pleistocene. Bayesian skyline plot (BSP) indicated a moderate demographic growth from the LGM to the present. A putative dispersal corridor was detected along the Longmen Mountains thrust belt, with unidirectional gene flow from north to south.Main conclusionOur findings support the geographical isolation of the genetic lineages and a deep early Pleistocene split in M. sichuanensis. Landscape connectivity analysis incorporating the genetic data and the ENM prediction revealed that population genetic connectivity was strongly associated with stable climatic habitats shaped by complex topography. The drainage system might have assisted the rapid movement of populations along the Longmen Mountains thrust belt. A strategy for researching the population genetic connectivity of narrow endemics, such as M. sichuanensis, in global biodiversity hotspots is proposed and discussed in this paper.
Sexual inhibition of female Queensland fruit flies mated by males treated with raspberry ketone supplements as immature adults
Authors: Akter H. , Taylor P. W. 
Published: January 2018

AbstractRaspberry ketone (RK) dietary supplements accelerate the emergence of sexual behaviour in developing Queensland fruit fly (Q‐fly) males and show promise as a pre‐release supplement for use in sterile insect technique (SIT) programs. However, the value of RK supplements in SIT programs would be greatly reduced if RK‐treated males are ineffective at inducing sexual inhibition in mated females. To test the effectiveness of matings by RK‐treated males, we here investigate the remating propensity of females mated by RK‐treated (1.25% or 5% RK in food) and RK‐untreated (control) males. Tested males received RK supplements mixed in sugar and yeast hydrolysate for 2 days after emerging and then received only sugar. To test for male age‐dependent effects, virgin females were mated to treated and untreated males that were 6, 8, 10, 20 or 30 days old. To test for persistence of sexual inhibition, mated females were tested for remating propensity at 1, 7 or 15 days after their first mating. RK‐treated males did not differ from control males in copula duration, and females mated by RK‐treated males did not differ from those mated by control males in remating propensity, second copula latency or second copula duration. RK‐treated Q‐fly males not only mate at younger ages but also their matings are as effective as those of untreated controls at inducing sexual inhibition in mates.
Retracted: Palmitate‐induced C/EBP homologous protein activation leads to NF‐κB‐mediated increase in BACE1 activity and amyloid beta genesis
Authors: Marwarha Gurdeep , Schommer Jared , Lund Jonah , Schommer Trevor , Ghribi Othman 
Published: January 2018

AbstractThe etiology of Alzheimer's disease (AD) is egregiously comprehended, but epidemiological studies have posited that diets rich in the saturated fatty acid palmitic acid (palmitate) are a significant risk factor. The production and accumulation of amyloid beta peptide (Aβ) is considered the core pathological molecular event in the pathogenesis of AD. The rate‐limiting step in Aβ genesis from amyloid‐β precursor protein (AβPP) is catalyzed by the enzyme β‐site amyloid precursor protein cleaving enzyme 1 (BACE1), the expression and enzymatic activity of which is significantly up‐regulated in the AD brain. In this study, we determined the molecular mechanisms that potentially underlie the palmitate‐induced up‐regulation in BACE1 expression and augmented Aβ production. We demonstrate that a palmitate‐enriched diet and exogenous palmitate treatment evoke an increase in BACE1 expression and activity leading to enhanced Aβ genesis in the mouse brain and SH‐SY5Y‐APPSwe cells, respectively, through the activation of the transcription factor NF‐κB. Chromatin immunoprecipitation (ChIP) assays and luciferase reporter assays revealed that palmitate enhances BACE1 expression by increasing the binding of NF‐κB in the BACE1 promoter followed by an enhancement in the transactivation of the BACE1 promoter. Elucidation and delineation of upstream molecular events unveiled a critical role of the endoplasmic reticulum stress‐associated transcription factor, C/EBP homologous protein (CHOP) in the palmitate‐induced NF‐κB activation, as CHOP knock‐down cells and Chop−/− mice do not exhibit the same degree of NF‐κB activation in response to the palmitate challenge. Our study delineates a novel CHOP‐NF‐κB signaling pathway that mediates palmitate‐induced up‐regulation of BACE1 expression and Aβ genesis.
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HFE Genotype Restricts the Response to Paraquat in a Mouse Model of Neurotoxicity
Authors: Nixon Anne M. , Meadowcroft Mark D. , Neely Elizabeth B. , Snyder Amanda M. , Purnell Carson J. , Wright Justin , Lamendella Regina , Nandar Wint , Huang Xuemei , Connor James R. 
Published: January 2018

AbstractParkinson's disease is marked clinically by motor dysfunction and pathologically by dopaminergic cell loss in the substantia nigra and iron accumulation in the substantia nigra. The driver underlying iron accumulation remains unknown and could be genetic or environmental. The HFE protein is critical for the regulation of cellular iron uptake. Mutations within this protein are associated with increased iron accumulation including in the brain. We have focused on the commonly occurring H63D variant of the HFE gene as a disease modifier in a number of neurodegenerative diseases. To investigate the role of H63D HFE genotype, we generated a mouse model in which the wild‐type (WT) HFE gene is replaced by the H67D gene variant (mouse homolog of the human H63D gene variant). Using paraquat toxicity as the model for Parkinson's disease, we found that WT mice responded as expected with significantly greater motor function, loss of tyrosine hydroxylase staining and increase microglial staining in the substantia nigra, and an increase in R2 relaxation rate within the substantia nigra of the paraquat‐treated mice compared to their saline‐treated counterparts. In contrast, the H67D mice showed a remarkable resistance to paraquat treatment; specifically differing from the WT mice with no changes in motor function or changes in R2 relaxation rates following paraquat exposure. At baseline, there were differences between the H67D HFE mice and WT mice in gut microbiome profile and increased L‐ferritin staining in the substantia nigra that could account for the resistance to paraquat. Of particular note, the H67D HFE mice regardless of whether or not they were treated with paraquat had significantly less tyrosine hydroxylase immunostaining than WT. Our results clearly demonstrate that the HFE genotype impacts the expression of tyrosine hydroxylase in the substantia nigra, the gut microbiome and the response to paraquat providing additional support that the HFE genotype is a disease modifier for Parkinson's disease. Moreover, the finding that the HFE mutant mice are resistant to paraquat may provide a model in which to study resistant mechanisms to neurotoxicants.
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