bluuebunny/crossref_metadata_2025_split huggingface dataset:
Chest pain risk assessment in Indigenous and non‐Indigenous Australians using HEART Score
Authors: Bodapati Sarath Naidu , Gunnarsson Ronny , McBride William John , Stone Richard , Sutcliffe Steven 
Published: January 2016

AbstractObjectiveThe objectives of this study were to investigate factors that correlate to cardiac events within 30 days in Indigenous and non‐Indigenous Australians who present to ED with chest pain and to describe the predictive ability of the HEART Score in these groups.MethodsPatients who presented with chest pain between 1 January 2013 and 16 May 2013 in a university hospital were retrospectively enrolled in the study. HEART Scores were retrospectively assigned to participants. The study's end‐point was Major Adverse Cardiac Events (MACE) within 30 days.ResultsParticipants (678) were enrolled in the study, of which 148 were Indigenous Australian. Twenty‐eight percent of Indigenous Australian participants and 19% of non‐Indigenous Australian participants were diagnosed with MACE within 30 days. Within the Indigenous Australian participant cohort, 1.6% of those with HEART Scores 0–3, 29% of those with HEART Scores 4–6 and 96% of those with HEART Scores 7–10 were diagnosed with MACE within 30 days. Within the non‐Indigenous Australian participant cohort, 0.58% of those with HEART Scores 0–3, 17% of those with HEART Scores 4–6 and 79% of those with HEART Scores 7–10 were diagnosed with MACE within 30 days. The negative predictive value of HEART Scores 0–3 for ruling out MACE within 30 days was 98% for Indigenous participants and 99% for non‐Indigenous participants.ConclusionThe HEART Score is a reliable predictor of patient outcome in both Indigenous and non‐Indigenous Australians. Modification of the HEART Score may not be required for use in the Indigenous Australian population who present to the ED with chest pain.
Dynamics of bacterial populations during bench‐scale bioremediation of oily seawater and desert soil bioaugmented with coastal microbial mats
Authors: Ali Nidaa , Dashti Narjes , Salamah Samar , Sorkhoh Naser , Al‐Awadhi Husain , Radwan Samir 
Published: January 2016

SummaryThis study describes a bench‐scale attempt to bioremediate Kuwaiti, oily water and soil samples through bioaugmentation with coastal microbial mats rich in hydrocarbonoclastic bacterioflora. Seawater and desert soil samples were artificially polluted with 1% weathered oil, and bioaugmented with microbial mat suspensions. Oil removal and microbial community dynamics were monitored. In batch cultures, oil removal was more effective in soil than in seawater. Hydrocarbonoclastic bacteria associated with mat samples colonized soil more readily than seawater. The predominant oil degrading bacterium in seawater batches was the autochthonous seawater species Marinobacter hydrocarbonoclasticus. The main oil degraders in the inoculated soil samples, on the other hand, were a mixture of the autochthonous mat and desert soil bacteria; Xanthobacter tagetidis, Pseudomonas geniculata, Olivibacter ginsengisoli and others. More bacterial diversity prevailed in seawater during continuous than batch bioremediation. Out of seven hydrocarbonoclastic bacterial species isolated from those cultures, only one, Mycobacterium chlorophenolicum, was of mat origin. This result too confirms that most of the autochthonous mat bacteria failed to colonize seawater. Also culture‐independent analysis of seawater from continuous cultures revealed high‐bacterial diversity. Many of the bacteria belonged to the Alphaproteobacteria, Flavobacteria and Gammaproteobacteria, and were hydrocarbonoclastic. Optimal biostimulation practices for continuous culture bioremediation of seawater via mat bioaugmentation were adding the highest possible oil concentration as one lot in the beginning of bioremediation, addition of vitamins, and slowing down the seawater flow rate.
Spontaneous cleavage of proteins at serine and threonine is facilitated by zinc
Authors: Lyons Brian , Kwan Ann H. , Truscott Roger J.W. 
Published: January 2016

SummaryOld proteins are widely distributed in the body. Over time, they deteriorate and many spontaneous reactions, for example isomerisation of Asp and Asn, can be replicated by incubation of peptides under physiological conditions. One of the signatures of long‐lived proteins that has proven to be difficult to replicate in vitro is cleavage on the N‐terminal side of Ser residues, and this is important since cleavage at Ser, and also Thr, has been observed in a number of human proteins. In this study, the autolysis of Ser‐ and Thr‐containing peptides was investigated with particular reference to discovering factors that promote cleavage adjacent to Ser/Thr at neutral pH. It was found that zinc catalyses cleavage of the peptide bond on the N‐terminal side of Ser residues and further that this process is markedly accelerated if a His residue is adjacent to the Ser. NMR analysis indicated that the imidazole group co‐ordinates zinc and that once zinc is co‐ordinated, it can polarize the carbonyl group of the peptide bond in a manner analogous to that observed in the active site of the metalloexopeptidase, carboxypeptidase A. The hydroxyl side chain of Ser/Thr is then able to cleave the adjacent peptide bond. These observations enable an understanding of the origin of common truncations observed in long‐lived proteins, for example truncation on the N‐terminal side of Ser 8 in Abeta, Ser 19 in alpha B crystallin and Ser 66 in alpha A crystallin. The presence of zinc may therefore significantly affect the long‐term stability of cellular proteins.
Characterization of age‐associated exhausted CD8+ T cells defined by increased expression of Tim‐3 and PD‐1
Authors: Lee Kyoo‐A , Shin Kwang‐Soo , Kim Ga‐Young , Song You Chan , Bae Eun‐Ah , Kim Il‐Kyu , Koh Choong‐Hyun , Kang Chang‐Yuil 
Published: January 2016

SummaryAging is accompanied by altered T‐cell responses that result in susceptibility to various diseases. Previous findings on the increased expression of inhibitory receptors, such as programmed cell death protein 1 (PD‐1), in the T cells of aged mice emphasize the importance of investigations into the relationship between T‐cell exhaustion and aging‐associated immune dysfunction. In this study, we demonstrate that T‐cell immunoglobulin mucin domain‐3 (Tim‐3), another exhaustion marker, is up‐regulated on aged T cells, especially CD8+ T cells. Tim‐3‐expressing cells also produced PD‐1, but Tim‐3+PD‐1+ CD8+ T cells had a distinct phenotype that included the expression of CD44 and CD62L, from Tim‐3−PD‐1+ cells. Tim‐3+PD‐1+ CD8+ T cells showed more evident properties associated with exhaustion than Tim‐3−PD‐1+ CD8+ T cells: an exhaustion‐related marker expression profile, proliferative defects following homeostatic or TCR stimulation, and altered production of cytokines. Interestingly, these cells produced a high level of IL‐10 and induced normal CD8+ T cells to produce IL‐10, which might contribute to immune dysregulation in aged mice. The generation of Tim‐3‐expressing CD8+ T cells in aged mice seems to be mediated by encounters with antigens but not by specific infection, based on their high expression of CD49d and their unbiased TCR Vβ usage. In conclusion, we found that a CD8+ T‐cell population with age‐associated exhaustion was distinguishable by its expression of Tim‐3. These results provide clues for understanding the alterations that occur in T‐cell populations with age and for improving dysfunctions related to the aging of the immune system.
Defects in MAP1S‐mediated autophagy cause reduction in mouse lifespans especially when fibronectin is overexpressed
Authors: Li Wenjiao , Zou Jing , Yue Fei , Song Kun , Chen Qi , McKeehan Wallace L. , Wang Fen , Xu Guibin , Huang Hai , Yi Jinglin , Liu Leyuan 
Published: January 2016

SummaryAutophagy is a cellular process that executes the turnover of dysfunctional organelles and misfolded or abnormally aggregated proteins. Microtubule‐associated protein MAP1S interacts with autophagy marker LC3 and positively regulates autophagy flux. LC3 binds with fibronectinmRNA and facilitates its translation. The synthesized fibronectin protein is exported to cell surface to initiate the assembly of fibronectin extracellular matrix. Fibronectin is degraded in lysosomes after it is engulfed into cytosol via endocytosis. Here, we show that defects in MAP1S‐mediated autophagy trigger oxidative stress, sinusoidal dilation, and lifespan reduction. Overexpression of LC3 in wild‐type mice increases the levels of fibronectin and γ‐H2AX, a marker of DNA double‐strand breakage. LC3‐induced fibronectin is efficiently degraded in lysosomes to maintain a balance of fibronectin levels in wild‐type mice so that the mice live a normal term of lifespan. In the LC3 transgenic mice with MAP1S deleted, LC3 enhances the synthesis of fibronectin but the MAP1S depletion causes an impairment of the lysosomal degradation of fibronectin. The accumulation of fibronectin protein promotes liver fibrosis, induces an accumulation of cell population at the G0/G1 stage, and further intensifies oxidative stress and sinusoidal dilatation. The LC3‐induced overexpression of fibronectin imposes stresses on MAP1S‐deficient mice and dramatically reduces their lifespans. Therefore, MAP1S‐mediated autophagy plays an important role in maintaining mouse lifespan especially in the presence of extra amount of fibronectin.
Capital expenditures and firm performance: evidence from a cross‐sectional analysis of stock returns
Authors: Cordis Adriana S. , Kirby Chris 
Published: January 2016

AbstractUsing a simple two‐period model of investment, we show that there should be a nonlinear relation between a firm's investment‐to‐capital ratio and its subsequent stock returns. This prediction finds substantial empirical support. The evidence indicates that the slope of the investment function is negative at low investment levels, close to zero at intermediate investment levels and negative at high investment levels. Our results, which are robust to the use of narrowly‐ and broadly‐defined measures of capital investment, pose a challenge to the hypothesis that the negative cross‐sectional correlation between investment and stock returns is attributable to some sort of overinvestment phenomenon.
Striatal activation and frontostriatal connectivity during non‐drug reward anticipation in alcohol dependence
Authors: Becker Alena , Kirsch Martina , Gerchen Martin Fungisai , Kiefer Falk , Kirsch Peter 
Published: January 2016

AbstractAccording to prevailing neurobiological theories of addiction, altered function in neural reward circuitry is a central mechanism of alcohol dependence. Growing evidence postulates that the ventral striatum (VS), as well as areas of the prefrontal cortex, contribute to the increased incentive salience of alcohol‐associated cues, diminished motivation to pursue non‐drug rewards and weakened strength of inhibitory cognitive control, which are central to addiction. The present study aims to investigate the neural response and functional connectivity underlying monetary, non‐drug reward processing in alcohol dependence. We utilized a reward paradigm to investigate the anticipation of monetary reward in 32 alcohol‐dependent inpatients and 35 healthy controls. Functional magnetic resonance imaging was used to measure task‐related brain activation and connectivity. Alcohol‐dependent patients showed increased activation of the VS during anticipation of monetary gain compared with healthy controls. Generalized psychophysiological interaction analyses revealed decreased functional connectivity between the VS and the dorsolateral prefrontal cortex in alcohol dependent patients relative to controls. Increased activation of the VS and reduced frontostriatal connectivity were associated with increased craving. These findings provide evidence that alcohol dependence is rather associated with disrupted integration of striatal and prefrontal processes than with a global reward anticipation deficit.
Influence of a Rotational Speed Modulation System Used With an Implantable Continuous‐Flow Left Ventricular Assist Device on von Willebrand Factor Dynamics
Authors: Naito Noritsugu , Mizuno Toshihide , Nishimura Takashi , Kishimoto Satoru , Takewa Yoshiaki , Eura Yuka , Kokame Koichi , Miyata Toshiyuki , Date Kazuma , Umeki Akihide , Ando Masahiko , Ono Minoru , Tatsumi Eisuke 
Published: January 2016

AbstractWe have developed a rotational speed (RS) modulation system for a continuous‐flow left ventricular assist device (EVAHEART) that can change RS in synchronization with a patient's electrocardiogram. Although EVAHEART is considered not to cause significant acquired von Willebrand syndrome, there remains a concern that the repeated acceleration and deceleration of the impeller may degrade von Willebrand factor (vWF) multimers. Accordingly, we evaluated the influence of our RS modulation system on vWF dynamics. A simple mock circulation was used. The circulation was filled with whole bovine blood (650 mL), and the temperature was maintained at 37 ± 1°C. EVAHEART was operated using the electrocardiogram‐synchronized RS modulation system with an RS variance of 500 rpm and a pulse frequency of 60 bpm (EVA‐RSM; n = 4). The pumps were operated at a mean flow rate of 5.0 ± 0.2 L/min against a mean pressure head of 100 ± 3 mm Hg. The continuous‐flow mode of EVAHEART (EVA‐C; n = 4) and ROTAFLOW (ROTA; n = 4) was used as controls. Whole blood samples were collected at baseline and every 60 min for 6 h. Complete blood counts (CBCs), normalized indexes of hemolysis (NIH), vWF antigen (vWF:Ag), vWF ristocetin cofactor (vWF:Rco), the ratio of vWF:Rco to vWF:Ag (Rco/Ag), and high molecular weight multimers (HMWM) of vWF were evaluated. There were no significant changes in CBCs throughout the 6‐h test period in any group. NIH levels of EVA‐RSM, EVA‐C, and ROTA were 0.0035 ± 0.0018, 0.0031 ± 0.0007, and 0.0022 ± 0.0011 g/100 L, respectively. Levels of vWF:Ag, vWF:Rco, and Rco/Ag did not change significantly during the test. Immunoblotting analysis of vWF multimers showed slight degradation of HMWM in all groups, but there were no significant differences between groups in the ratios of HMWM to low molecular weight multimers, calculated by densitometry. This study suggests that our RS modulation system used with EVAHEART does not have marked adverse influences on vWF dynamics. The low NIH and the absence of significant decreases in CBCs indicate that EVAHEART is hemocompatible, regardless of whether it is operated with the RS modulation system.
Bilaminar Device of Poly(Lactic‐co‐Glycolic Acid)/Collagen Cultured With Adipose‐Derived Stem Cells for Dermal Regeneration
Authors: Domingues Juliana A. , Cherutti Giselle , Motta Adriana C. , Hausen Moema A. , Oliveira Rômulo T.D. , Silva‐Zacarin Elaine C.M. , Barbo Maria Lourdes P. , Duek Eliana A.R. 
Published: January 2016

AbstractSeveral materials are commercially available as substitutes for skin. However, new strategies are needed to improve the treatment of skin wounds. In this study, we developed and characterized a new device consisting of poly(lactic‐co‐glycolic acid) (PLGA) and collagen associated with mesenchymal stem cells derived from human adipose tissue. To develop the bilaminar device, we initially obtained a membrane of PLGA by dissolving the copolymer in chloroform and then produced a collagen type I scaffold by freeze‐drying. The materials were characterized physically by gel permeation chromatography, scanning electron microscopy, and mass loss. Biological activity was assessed by cell proliferation assay. A preliminary study in vivo was performed with a pig model in which tissue regeneration was assessed macroscopically and histologically, the commercial device Integra being used as a control. The PLGA/collagen bilaminar material was porous, hydrolytically degradable, and compatible with skin growth. The polymer complex allowed cell adhesion and proliferation, making it a potentially useful cell carrier. In addition, the transparency of the material allowed monitoring of the lesion when the dressings were changed. Xenogeneic mesenchymal cells cultured on the device (PLGA/collagen/ASC) showed a reduced granulomatous reaction to bovine collagen, down‐regulation of α‐SMA, enhancement in the number of neoformed blood vessels, and collagen organization as compared with normal skin; the device was superior to other materials tested (PLGA/collagen and Integra) in its ability to stimulate the formation of new cutaneous tissue.
GOVERNANCE OF PRODUCTION CO‐OPERATIVES IN RUSSIAN AGRICULTURE
Authors: NILSSON Jerker , GOLOVINA Svetlana , HESS Sebastian , WOLZ Axel 
Published: January 2016

ABSTRACTMany Soviet kolkhozy and sovkhozy were transformed into agricultural production co‐operatives, because the farm workers would have had large transaction costs in any other type of organization. These co‐operatives still hold a strong market position. This study explores the hypothesis that this market strength could be due to low governance costs, obtained through strong manager power. As managers want the co‐operative to survive, they make limited investments in the co‐operative and pay low wages. The members, however, do not consider this to be problematic. They appreciate the community within the village, their private plots of land and the co‐operative's services. Hence the existence of the co‐operatives is not threatened.
EMPLOYMENT STABILIZATION INSIDE FIRMS: AN EMPIRICAL INVESTIGATION OF WORKER COOPERATIVES
Authors: NAVARRA Cecilia 
Published: January 2016

ABSTRACTThere is evidence that worker cooperatives provide a greater stabilization of employment compared to capital‐managed firms. While the reasons of this behaviour can be ascribed to their property and governance structure, less is known of the tools to put it into practice. I discuss two possible ways to guarantee employment insurance: by letting wages fluctuate, or by accumulating reinvested profits into an income stabilizing fund that copes with downturns without firing and without reducing wages. In this second case, I find out that asset locks play a wage smoothing role. This may explain the large share of profits that are reinvested in this indivisible and not appropriable fund. I provide evidence for this mechanism by means of original data at the firm level and of first‐hand collected survey data at the individual level on risk perception in a sample of Italian cooperatives.
THE FORECASTING PERFORMANCE OF SETAR MODELS: AN EMPIRICAL APPLICATION
Authors: Boero Gianna , Lampis Federico 
Published: January 2016

ABSTRACTThe aim of this paper is to evaluate the forecasting performance of SETAR models with an application to the Industrial Production Index (IPI) of four major European countries over a period which includes the last Great Recession. Both point and interval forecasts are considered at different horizons against those obtained from two linear models. We follow the approach suggested by Teräsvirta et al. (2005) according to which a dynamic specification may improve the forecast performance of the nonlinear models with respect to the linear models. We re‐specify the models every twelve months and we find that the advantages of this procedure are particularly evident in the forecast rounds immediately following the re‐specification.
Contribution of adrenomedullin to the switch of G protein‐coupled μ‐opioid receptors from Gi to Gs in the spinal dorsal horn following chronic morphine exposure in rats
Authors: Wang Dongmei , Zeng Juan , Li Qi , Huang Jianzhong , Couture Réjean , Hong Yanguo 
Published: January 2016

Background and PurposeChronic exposure to morphine increases spinal adrenomedullin (AM) bioactivity resulting in the development and maintenance of morphine tolerance. This study investigated the possible involvement of AM in morphine‐evoked alteration in μ‐opioid receptor‐coupled G proteins.Experimental ApproachAgents were administered intrathecally (i.t.) in rats. Nociceptive behaviours and cumulative dose–response of morphine analgesia were assessed. Neurochemicals in the spinal dorsal horn were assayed by immunoprecipitation, Western blot analysis and ELISA.Key ResultsIntrathecal injection of AM (8 μg) for 9 days decreased and increased the levels of μ receptor‐coupled Gi and Gs proteins respectively. Morphine stimulation (5 μg) after chronic treatment with AM also induced an increase in cAMP production in the spinal dorsal horn. Co‐administration of the selective AM receptor antagonist AM22–52 inhibited chronic morphine‐evoked switch of G protein‐coupled μ receptor from Gi to Gs. Chronic exposure to AM increased the phosphorylation of cAMP‐responsive element‐binding protein (CREB) and ERK. Co‐administration of the PKA inhibitor H‐89 (5 μg) or MEK1 inhibitor PD98059 (1 μg) reversed the AM‐induced thermal/mechanical hypersensitivity, decline in morphine analgesic potency, switch of G protein‐coupled μ receptor and increase in cAMP.Conclusions and ImplicationsThe present study supports the hypothesis that an increase in AM activity in the spinal dorsal horn contributes to the switch of the μ receptor‐coupled G protein from Gi to Gs protein via the activation of cAMP/PKA/CREB and ERK signalling pathways in chronic morphine use.
Single administration of recombinant IL‐6 restores the gene expression of lipogenic enzymes in liver of fasting IL‐6‐deficient mice
Authors: Gavito AL , Cabello R , Suarez J , Serrano A , Pavón F J , Vida M , Romero M , Pardo V , Bautista D , Arrabal S , Decara J , Cuesta AL , Valverde A M , Rodríguez de Fonseca F , Baixeras E 
Published: January 2016

Background and PurposeLipogenesis is intimately controlled by hormones and cytokines as well as nutritional conditions. IL‐6 participates in the regulation of fatty acid metabolism in the liver. We investigated the role of IL‐6 in mediating fasting/re‐feeding changes in the expression of hepatic lipogenic enzymes.Experimental ApproachGene and protein expression of lipogenic enzymes were examined in livers of wild‐type (WT) and IL‐6‐deficient (IL‐6−/−) mice during fasting and re‐feeding conditions. Effects of exogenous IL‐6 administration on gene expression of these enzymes were evaluated in vivo. The involvement of STAT3 in mediating these IL‐6 responses was investigated by using siRNA in human HepG2 cells.Key ResultsDuring feeding, the up‐regulation in the hepatic expression of lipogenic genes presented similar time kinetics in WT and IL‐6−/− mice. During fasting, expression of lipogenic genes decreased gradually over time in both strains, although the initial drop was more marked in IL‐6−/− mice. Protein levels of hepatic lipogenic enzymes were lower in IL‐6−/− than in WT mice at the end of the fasting period. In WT, circulating IL‐6 levels paralleled gene expression of hepatic lipogenic enzymes. IL‐6 administration in vivo and in vitro showed that IL‐6‐mediated signalling was associated with the up‐regulation of hepatic lipogenic enzyme genes. Moreover, silencing STAT3 in HepG2 cells attenuated IL‐6 mediated up‐regulation of lipogenic gene transcription levels.Conclusions and ImplicationsIL‐6 sustains levels of hepatic lipogenic enzymes during fasting through activation of STAT3. Our findings indicate that clinical use of STAT3‐associated signalling cytokines, particularly against steatosis, should be undertaken with caution.