bluuebunny/crossref_metadata_2025_split huggingface dataset:
Gene Coexpression Analysis Reveals Complex Metabolism of the Monoterpene Alcohol Linalool inArabidopsisFlowers
Authors: Ginglinger Jean-François , Boachon Benoit , Höfer René , Paetz Christian , Köllner Tobias G. , Miesch Laurence , Lugan Raphael , Baltenweck Raymonde , Mutterer Jérôme , Ullmann Pascaline , Beran Franziska , Claudel Patricia , Verstappen Francel , Fischer Marc J.C. , Karst Francis , Bouwmeester Harro , Miesch Michel , Schneider Bernd , Gershenzon Jonathan , Ehlting Jürgen , Werck-Reichhart Danièle 
Published: November 2013

AbstractThe cytochrome P450 family encompasses the largest family of enzymes in plant metabolism, and the functions of many of its members in Arabidopsis thaliana are still unknown. Gene coexpression analysis pointed to two P450s that were coexpressed with two monoterpene synthases in flowers and were thus predicted to be involved in monoterpenoid metabolism. We show that all four selected genes, the two terpene synthases (TPS10 and TPS14) and the two cytochrome P450s (CYP71B31 and CYP76C3), are simultaneously expressed at anthesis, mainly in upper anther filaments and in petals. Upon transient expression in Nicotiana benthamiana, the TPS enzymes colocalize in vesicular structures associated with the plastid surface, whereas the P450 proteins were detected in the endoplasmic reticulum. Whether they were expressed in Saccharomyces cerevisiae or in N. benthamiana, the TPS enzymes formed two different enantiomers of linalool: (−)-(R)-linalool for TPS10 and (+)-(S)-linalool for TPS14. Both P450 enzymes metabolize the two linalool enantiomers to form different but overlapping sets of hydroxylated or epoxidized products. These oxygenated products are not emitted into the floral headspace, but accumulate in floral tissues as further converted or conjugated metabolites. This work reveals complex linalool metabolism in Arabidopsis flowers, the ecological role of which remains to be determined.
A Genomics Approach to Deciphering Lignin Biosynthesis in Switchgrass
Authors: Shen Hui , Mazarei Mitra , Hisano Hiroshi , Escamilla-Trevino Luis , Fu Chunxiang , Pu Yunqiao , Rudis Mary R. , Tang Yuhong , Xiao Xirong , Jackson Lisa , Li Guifen , Hernandez Tim , Chen Fang , Ragauskas Arthur J. , Stewart C. Neal , Wang Zeng-Yu , Dixon Richard A. 
Published: November 2013

Abstract
It is necessary to overcome recalcitrance of the biomass to saccharification (sugar release) to make switchgrass (Panicum virgatum) economically viable as a feedstock for liquid biofuels. Lignin content correlates negatively with sugar release efficiency in switchgrass, but selecting the right gene candidates for engineering lignin biosynthesis in this tetraploid outcrossing species is not straightforward. To assist this endeavor, we have used an inducible switchgrass cell suspension system for studying lignin biosynthesis in response to exogenous brassinolide. By applying a combination of protein sequence phylogeny with whole-genome microarray analyses of induced cell cultures and developing stem internode sections, we have generated a list of candidate monolignol biosynthetic genes for switchgrass. Several genes that were strongly supported through our bioinformatics analysis as involved in lignin biosynthesis were confirmed by gene silencing studies, in which lignin levels were reduced as a result of targeting a single gene. However, candidate genes encoding enzymes involved in the early steps of the currently accepted monolignol biosynthesis pathway in dicots may have functionally redundant paralogues in switchgrass and therefore require further evaluation. This work provides a blueprint and resources for the systematic genome-wide study of the monolignol pathway in switchgrass, as well as other C4 monocot species.
Interpreting genetics in the context of eating disorders: evidence of disease, not diversity
Authors: Easter Michele 
Published: November 2013

AbstractHow is genetic involvement interpreted for disorders whose medicalisation is contested? Framing psychiatric and behavioural disorders in terms of genetics is expected to make them seem more medical. Yet a genetic aetiology can also be used to frame behaviour as acceptable human variation, rather than a medical problem (for example, sexual orientation). I analyse responses to the idea that there is a genetic component in anorexia and bulimia nervosa (AN or BN) via semi‐structured interviews with a sample of 50 women diagnosed with an eating disorder (25 had recovered). All but three volunteered that genetics would medicalise AN or BN by (i) making eating disorders seem more like ‘real diseases’; implying that these disorders need (ii) professional treatment or (iii) a biologically based treatment. The results also indicate there are several counter‐logics by which genetic framing could support non‐medical definitions of AN or BN. I argue that genetic framing reduces perceived individual responsibility, which can support definitions of behaviour as either a reflection of disease (which entails intervention) or a reflection of normal human diversity (which does not). In the context of public scepticism as to the ‘reality’ of AN or BN, genetic involvement was taken as evidence of disease in ongoing negotiations about the medical and moral status of people with eating disorders.
Learning by Doing and Fragmentation
Authors: Bond Eric W. , Ma Yan 
Published: November 2013

AbstractWe analyse the competitive equilibrium and socially optimal allocation of production fragments in a two‐country model where there is learning by doing with spillovers between fragments in the home country. We distinguish between forward and backward knowledge linkages, where learning results from producing products that are less (more) complex than the current knowledge frontier with forward (backward) linkages. We compare the pattern of comparative advantage in the competitive and socially optimal cases, and compare the intensive and extensive margins of fragments produced at home in the two cases. We establish a sufficient condition for the range of fragments produced at home to be non‐decreasing with forward linkages. We also show that with backward linkages, the home country will produce some fragments in the neighbourhood of the steady state that are more complex than those produced in the steady state.
Emission Taxes and Border Tax Adjustments for Oligopolistic Industries
Authors: Yomogida Morihiro , Tarui Nori 
Published: November 2013

AbstractWe examine the welfare consequences of an emission tax with and without a border tax adjustment (BTA) for an imperfectly competitive industry, where intra‐industry trade arises between countries. BTA allows a government to impose a pollution‐content tariff on imports and refund an emission tax for export sales. We analyse the structure of an optimal emission tax with BTA when a government chooses its emission tax rate to maximize its national welfare. We show that the optimal emission tax policy with BTA achieves greater national welfare and higher environmental quality than the optimal policy without BTA.
The Only Way Is Up? Ordinary Topologies of Ramallah
Authors: Harker Christopher 
Published: November 2013

AbstractThis article seeks to conceptualize and value some of the quotidian geographies responsible for contemporary forms of urban change. The starting point for the argument is an attempt to account for recent urban change in the Palestinian city of Ramallah, particularly the proliferation of apartment buildings, using emerging work on verticality. It is argued that work on verticality focuses empirically on prominent cities and spaces of violent conflict, invokes the vertical as politically suspect and offers a theorization of space that is topographical in nature. Consequently, accounts of verticality have produced narratives that obscure topological spatial relations. This article seeks to make space for such topologies, which it is argued are crucial to producing urban and political life itself in many contexts. The concept of ordinary topologies is proposed as a means of attending to the complex and undervalued practices that are thought to be normal (but not static) and common within and across intensive or qualitative spatio‐temporal relations. This approach is fleshed out through a discussion of changing topographic–topological landscapes in Ramallah. In particular, it is argued that the increasingly verticalized landscape of the city, embodied in rapidly proliferating apartment buildings, must be understood in relation to frequent journeys to other places and changing family relations.
Loss of NDG‐4 extends lifespan and stress resistance in Caenorhabditis elegans
Authors: Brejning Jeanette , Nørgaard Steffen , Schøler Lone , Morthorst Tine H. , Jakobsen Helle , Lithgow Gordon J. , Jensen Louise T. , Olsen Anders 
Published: November 2013

SummaryNDG‐4 is a predicted transmembrane acyltransferase protein that acts in the distribution of lipophilic factors. Consequently, ndg‐4 mutants lay eggs with a pale appearance due to lack of yolk, and they are resistant to sterility caused by dietary supplementation with the long‐chain omega‐6 polyunsaturated fatty acid dihommogamma‐linolenic acid (DGLA). Two other proteins, NRF‐5 and NRF‐6, a homolog of a mammalian secreted lipid binding protein and a NDG‐4 homolog, respectively, have previously been shown to function in the same lipid transport pathway. Here, we report that mutation of the NDG‐4 protein results in increased organismal stress resistance and lifespan. When NDG‐4 function and insulin/IGF‐1 signaling are reduced simultaneously, maximum lifespan is increased almost fivefold. Thus, longevity conferred by mutation of ndg‐4 is partially overlapping with insulin signaling. The nuclear hormone receptor NHR‐80 (HNF4 homolog) is required for longevity in germline less animals. We find that NHR‐80 is also required for longevity of ndg‐4 mutants. Moreover, we find that nrf‐5 and nrf‐6 mutants also have extended lifespan and increased stress resistance, suggesting that altered lipid transport and metabolism play key roles in determining lifespan.
Acquired aquagenic syringeal acrokeratoderma: A case series of 10 patients
Authors: Ertürk‐Özdemir Emel , Özcan Deren , Seçkin Deniz 
Published: November 2013

AbstractAquagenic syringeal acrokeratoderma is a rare acquired disorder that predominantly affects young women. It is most commonly localised on the palms. It is characterised by translucent papules, oedematous plaques and keratoderma developing after brief exposure to water and resolving shortly after drying. We have observed 10 patients with this disorder within 13 months. We think that aquagenic syringeal acrokeratoderma is a more common condition than was originally anticipated as one can easily underdiagnose this entity due to the transient nature of its clinical findings.
Deletion of thioredoxin‐interacting protein preserves retinal neuronal function by preventing inflammation and vascular injury
Authors: El‐Azab M F , Baldowski B R B , Mysona B A , Shanab A Y , Mohamed I N , Abdelsaid M A , Matragoon S , Bollinger K E , Saul A , El‐Remessy A B 
Published: November 2013

Background and PurposeRetinal neurodegeneration is an early and critical event in several diseases associated with blindness. Clinically, therapies that target neurodegeneration fail. We aimed to elucidate the multiple roles by which thioredoxin‐interacting protein (TXNIP) contributes to initial and sustained retinal neurodegeneration.Experimental ApproachNeurotoxicity was induced by intravitreal injection of NMDA into wild‐type (WT) and TXNIP‐knockout (TKO) mice. The expression of apoptotic and inflammatory markers was assessed by immunohistochemistry, elisa and Western blot. Microvascular degeneration was assessed by periodic acid‐Schiff and haematoxylin staining and retinal function by electroretinogram.Key ResultsNMDA induced early (1 day) and significant retinal PARP activation, a threefold increase in TUNEL‐positive nuclei and 40% neuronal loss in ganglion cell layer (GCL); and vascular permeability in WT but not TKO mice. NMDA induced glial activation, expression of TNF‐α and IL‐1β that co‐localized with Müller cells in WT but not TKO mice. In parallel, NMDA triggered the expression of NOD‐like receptor protein (NLRP3), activation of caspase‐1, and release of IL‐1β and TNF‐α in primary WT but not TKO Müller cultures. After 14 days, NMDA induced 1.9‐fold microvascular degeneration, 60% neuronal loss in GCL and increased TUNEL‐labelled cells in the GCL and inner nuclear layer in WT but not TKO mice. Electroretinogram analysis showed more significant reductions in b‐wave amplitudes in WT than in TKO mice.Conclusion and ImplicationsTargeting TXNIP expression prevented early retinal ganglion cell death, glial activation, retinal inflammation and secondary neuro/microvascular degeneration and preserved retinal function. TXNIP is a promising new therapeutic target for retinal neurodegenerative diseases.
Impact of intracellular domain flexibility upon properties of activated human 5‐HT3 receptors
Authors: Kozuska J L , Paulsen I M , Belfield W J , Martin I L , Cole D J , Holt A , Dunn S M J 
Published: November 2013

Background and PurposeIt has been proposed that arginine residues lining the intracellular portals of the homomeric 5‐HT3A receptor cause electrostatic repulsion of cation flow, accounting for a single‐channel conductance substantially lower than that of the 5‐HT3AB heteromer. However, comparison of receptor homology models for wild‐type pentamers suggests that salt bridges in the intracellular domain of the homomer may impart structural rigidity, and we hypothesized that this rigidity could account for the low conductance.Experimental ApproachMutations were introduced into the portal region of the human 5‐HT3A homopentamer, such that putative salt bridges were broken by neutralizing anionic partners. Single‐channel and whole cell currents were measured in transfected tsA201 cells and in Xenopus oocytes respectively. Computational simulations of protein flexibility facilitated comparison of wild‐type and mutant receptors.Key ResultsSingle‐channel conductance was increased substantially, often to wild‐type heteromeric receptor values, in most 5‐HT3A mutants. Conversely, introduction of arginine residues to the portal region of the heteromer, conjecturally creating salt bridges, decreased conductance. Gating kinetics varied significantly between different mutant receptors. EC50 values for whole‐cell responses to 5‐HT remained largely unchanged, but Hill coefficients for responses to 5‐HT were usually significantly smaller in mutants. Computational simulations suggested increased flexibility throughout the protein structure as a consequence of mutations in the intracellular domain.Conclusions and ImplicationsThese data support a role for intracellular salt bridges in maintaining the quaternary structure of the 5‐HT3 receptor and suggest a role for the intracellular domain in allosteric modulation of cooperativity and agonist efficacy.Linked ArticleThis article is commented on by Vardy and Kenakin, pp. 1614–1616 of volume 171 issue 7. To view this commentary visit http://dx.doi.org/10.1111/bph.12550.
Inter‐organizational partnership for children with medical complexity: the integrated complex care model
Authors: Kingsnorth S. , Lacombe‐Duncan A. , Keilty K. , Bruce‐Barrett C. , Cohen E. 
Published: November 2013

AbstractBackgroundIntegrated care has important implications for children with medical complexity (CMC) who rely on care and service delivery involving multiple providers in different places over time. Most studies describing complex care programmes focus on the effectiveness of care co‐ordination rather than the process of system integration. This pilot study explores the implementation process of the Integrated Complex Care Model: a voluntary partnership between acute, rehabilitative and community care aimed at system integration through a key worker model to improve care co‐ordination for CMC.MethodsThis descriptive study used qualitative analyses and syntheses to explore the process of inter‐organizational collaboration under ‘real‐life’ circumstances. Multiple methods and sources of data were gathered to support triangulation in understanding of enablers and barriers to model implementation. Forty hours of meeting minutes and administrative databases housing patient records were reviewed. Baseline demographic information was available for 23 families, including child health‐related quality of life and healthcare utilization. A subset of 12 parental caregivers and 21 additional key informants participated in individual interviews or focus groups. Findings are presented using King and Meyer's description of system integration and care co‐ordination.ResultsModel enablers included dedication, timing, leadership and electronic care plan use/communication among key workers, families and health providers. Barriers included assumptions about partner organizations, differing organizational structures and client information systems, constrained project resources and limited engagement of primary care. Parents perceived an electronic care plan as a facilitator of timely and effective care for CMC across multiple settings.ConclusionsAt a systems level, the integrated model fostered collaboration between partner organizations. At a family level, development of inter‐organizational management structures and communication platforms; provision of adequate resourcing; and increased engagement of primary care may enable high level organizational integration aimed at improved care co‐ordination for CMC.
Medium‐ and Long‐Term Complications in Full‐Arch Rehabilitations Supported by Upright and Tilted Implants
Authors: Francetti Luca , Corbella Stefano , Taschieri Silvio , Cavalli Nicolò , Del Fabbro Massimo 
Published: November 2013

AbstractPurposeThe purpose of this retrospective investigation was to present the incidence of biological and technical complications in patients treated with implant‐supported, immediately loaded full‐arch restorations.Materials and MethodsClinical data of all patients treated with full‐arch, immediately loaded rehabilitations supported by a combination of upright and tilted implants were screened. Data on both technical and biological complications (such as peri‐implant mucositis and peri‐implantitis) and their onset and frequency of occurrence were recorded and analyzed.ResultsThe clinical records of 86 patients (95 prosthetic rehabilitations) were included in this study. There were 61 mandibular rehabilitations and 34 maxillary ones, all of them immediately loaded within 8 to 48 hours of the surgical intervention. The follow‐up time varied from 16.3 to 112 months of function (mean 65.36 months). The most common biological complications were hygiene‐related (n = 81; 30.2% of patients displayed peri‐implant mucositis and 10.4% peri‐implantitis). Among all prosthetic complications, the detachment of an element of the definitive prosthesis was the most frequent event (n = 20; 23.2% of patients). The total number of prosthetic complications was 42. Most complications were reversible and did not affect the overall implant/prosthesis survival rate.ConclusionsThe occurrence in well‐maintained patients of technical and biological complications in full‐arch rehabilitations supported by a combination of tilted and upright implants in the medium to long term is lower than previously reported by the pertinent literature. Further studies are needed to confirm this result.
Expression of basic fibroblastic growth factor, syndecan 1 and tumour necrosis factor α in resected acute colonic diverticulitis
Authors: Tursi A. , Elisei W. , Giorgetti G. M. , Inchingolo C. D. , Nenna R. , Picchio M. , Giorgio F. , Ierardi E. , Brandimarte G. 
Published: November 2013

AbstractAimInflammation and fibrosis are present in both colonic diverticulitis and Crohn's disease (CD). The molecular pattern of basic fibroblastic growth factor (bFGF) and syndecan 1 (SD1) expression is altered in stenosing CD, but their expression in resected complicated colonic diverticulitis (ACD) is unknown.MethodThe expression of bFGF, SD1 and tumour necrosis factor α (TNF‐α) in 20 patients after resection of ACD was compared with 15 patients having a resection for CD. Analysis was conducted using real‐time reverse transcriptase polymerase chain reaction in biopsy samples.ResultsLymphocytic and neutrophil inflammation scores were similar in both groups (P = 0.771 and P = 0.562). TNF‐α and bFGF expression was significantly higher in ACD than in CD (P < 0.0001 and P = 0.009). SD1 expression was similar in both groups (P = 0.841).ConclusionTNF‐α and bFGF are significantly overexpressed in ACD with respect to CD, whilst SD1 levels do not differ. The findings confirm that inflammation and its association with altered molecular patterns of mucosal healing may play an important role in the phenotype of the diseases.
Influence of exercise intensity on systemic oxidative stress and antioxidant capacity
Authors: Parker Lewan , McGuckin Teneale A. , Leicht Anthony S. 
Published: November 2013

SummaryThe aim of the current study was to examine the influence of exercise intensity on systemic oxidative stress (OS) and endogenous antioxidant capacity. Non‐smoking, sedentary healthy adult males (n = 14) participated in two exercise sessions using an electronically braked cycle ergometer. The first session consisted of a graded exercise test to determine maximal power output and oxygen consumption (VO2max). One week later, participants undertook 5‐min cycling bouts at 40%, 55%, 70%, 85% and 100% of VO2max, with passive 12‐min rest between stages. Measures of systemic OS reactive oxygen metabolites (dROM), biological antioxidant potential (BAP), heart rate (HR), VO2, blood lactate and rating of perceived exertion were assessed at rest and immediately following each exercise stage. Significant (P<0·05) differences between exercise bouts were examined via repeated measures ANOVA and post hoc pairwise comparisons with Bonferroni correction. Increasing exercise intensity significantly augmented HR (P<0·001), VO2 (P<0·001), blood lactate (P<0·001) and perceived exertion (P<0·001) with no significant effect on dROM levels compared with resting values. In contrast, increasing exercise intensity resulted in significantly (P<0·01) greater BAP at 70% (2427 ± 106), 85% (2625 ± 121) and 100% (2651 ± 92) of VO2max compared with resting levels (2105 ± 57 μmol Fe2+/L). The current results indicate that brief, moderate‐to‐high‐intensity exercise significantly elevates endogenous antioxidant defences, possibly to counteract increased levels of exercise‐induced reactive oxygen species. Regular moderate‐to‐high‐intensity exercise may protect against chronic OS associated diseases via activation, and subsequent upregulation of the endogenous antioxidant defence system.