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Increased hypoxia-inducible factor 1α expression in lung cells of horses with recurrent airway obstruction
Marie Toussaint, Laurence Fievez, Christophe J Desmet, Dimitri Pirottin, Frédéric Farnir, Fabrice Bureau, Pierre Lekeux
BMC Veterinary Research , 2012, DOI: 10.1186/1746-6148-8-64
Abstract: In vitro, we observed that Hif is expressed in equine myeloid cells after hay dust stimulation and regulates genes such as tumor necrosis factor alpha (TNF-α), interleukin-8 (IL-8) and vascular endothelial growth factor A (VEGF-A). We further showed in vivo that airway challenge with hay dust upregulated Hif1-α mRNA expression in myeloid cells from the bronchoalveolar lavage fluid (BALF) of healthy and RAO-affected horses, with a more pronounced effect in cells from RAO-affected horses. Finally, Hif1-α mRNA expression in BALF cells from challenged horses correlated positively with lung dysfunction.Taken together, our results suggest an important role for Hif1-α in myeloid cells during hay dust-induced inflammation in horses with RAO. We therefore propose that future research aiming at functional inactivation of Hif1 in lung myeloid cells could open new therapeutic perspectives for RAO.Recurrent airway obstruction (RAO) or heaves is a well-known respiratory disease in horses that shares any pathophysiological similarities with asthma in humans [1-3]. RAO is a severe, potentially debilitating, chronic inflammatory airway disease typically affecting middle-aged horses. Acute exacerbations are characterized by neutrophilic airway inflammation, coughing, periods of labored breathing at rest and exercise intolerance due to bronchospasm and mucus accumulation in the airways [4]. It is initiated following exposure to organic dusts, molds, and lipopolysaccharides (LPS) in hay [5]. Periods of acute exacerbation are interspersed by periods of remission, when horses are kept away from the causative environment [3]. The immunological processes responsible for the persistent airway inflammation are still largely unknown [6]. RAO is thought to result from an aberrant immune response orchestrated by antigen-specific T lymphocytes via the secretion of pro-inflammatory cytokines. Whether these T lymphocytes have a type 1 or type 2 phenotype and cytokine secretion profile is still a m
Ir-LBP, an Ixodes ricinus Tick Salivary LTB4-Binding Lipocalin, Interferes with Host Neutrophil Function
Jér?me Beaufays, Beno?t Adam, Catherine Menten-Dedoyart, Laurence Fievez, Amélie Grosjean, Yves Decrem, Pierre-Paul Prév?t, Sébastien Santini, Robert Brasseur, Michel Brossard, Michel Vanhaeverbeek, Fabrice Bureau, Ernst Heinen, Laurence Lins, Luc Vanhamme, Edmond Godfroid
PLOS ONE , 2008, DOI: 10.1371/journal.pone.0003987
Abstract: Background During their blood meal, ticks secrete a wide variety of proteins that can interfere with their host's defense mechanisms. Among these proteins, lipocalins play a major role in the modulation of the inflammatory response. Methodology/Principal Findings We previously identified 14 new lipocalin genes in the tick Ixodes ricinus. One of them codes for a protein that specifically binds leukotriene B4 with a very high affinity (Kd: ±1 nM), similar to that of the neutrophil transmembrane receptor BLT1. By in silico approaches, we modeled the 3D structure of the protein and the binding of LTB4 into the ligand pocket. This protein, called Ir-LBP, inhibits neutrophil chemotaxis in vitro and delays LTB4-induced apoptosis. Ir-LBP also inhibits the host inflammatory response in vivo by decreasing the number and activation of neutrophils located at the tick bite site. Thus, Ir-LBP participates in the tick's ability to interfere with proper neutrophil function in inflammation. Conclusions/Significance These elements suggest that Ir-LBP is a “scavenger” of LTB4, which, in combination with other factors, such as histamine-binding proteins or proteins inhibiting the classical or alternative complement pathways, permits the tick to properly manage its blood meal. Moreover, with regard to its properties, Ir-LBP could possibly be used as a therapeutic tool for illnesses associated with an increased LTB4 production.
Continuous Maps on Digital Simple Closed Curves  [PDF]
Laurence Boxer
Applied Mathematics (AM) , 2010, DOI: 10.4236/am.2010.15050
Abstract: We give digital analogues of classical theorems of topology for continuous functions defined on spheres, for digital simple closed curves. In particular, we show the following. ? A digital simple closed curve of more than 4 points is not contractible, i.e., its identity map is not nullhomotopic in . ? Let and be digital simple closed curves, each symmetric with respect to the origin, such that (where is the number of points in ). Let be a digitally continuous antipodal map. Then is not nullho- motopic in . ? Let be a digital simple closed curve that is symmetric with respect to the origin. Let be a digitally continuous map. Then there is a pair of antipodes such that .
Modelling Visible Foliar Injury Effects on Canopy Photosynthesis and Potential Crop Yield Losses Resulting from Fluoride Exposure  [PDF]
David Doley, Laurence Rossato
Journal of Environmental Protection (JEP) , 2012, DOI: 10.4236/jep.2012.39113
Abstract: Crop production models are highly developed to account for different nitrogen, light, temperature and water availability conditions and, in some species, disease or air pollutant effects. There is very limited knowledge on responses of many tropical crops, such as oil palm (Elaeis guineensis), to air pollutants although predictions of these effects are essential for industrial planning in several countries. In the absence of limitations due to water supply, the effects of leaf area loss due to necrosis and chlorosis are much more important to canopy photosynthesis than are changes in the physiological attributes that influence the efficiency of light use. Therefore, potential losses of crop production due to air pollutants such as fluoride can be inferred usefully from the extent of visible injury to foliage that may be associated with different levels of pollutant exposure.
The Cross-Sectional Risk Premium of Decomposed Market Volatility in UK Stock Market  [PDF]
Yan Yang, Laurence Copeland
Open Journal of Social Sciences (JSS) , 2014, DOI: 10.4236/jss.2014.27006
Abstract:

We decompose UK market volatility into short- and long-run components using EGARCH component model and examine the cross-sectional prices of the two components. Our empirical results suggest that these two components are significantly priced in the cross-section and the negative risk premia are consistent with the existing literature. The Fama-French three-factor model is improved by the inclusion of the two volatility components. However, our ICAPM model using market excess return and the decomposed volatility components as state variables compares inferiorly to the traditional three-factor model.

Role of the Lower and Upper Intestine in the Production and Absorption of Gut Microbiota-Derived PUFA Metabolites
Céline Druart, Audrey M. Neyrinck, Bruno Vlaeminck, Veerle Fievez, Patrice D. Cani, Nathalie M. Delzenne
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0087560
Abstract: In vitro studies have suggested that isolated gut bacteria are able to metabolize PUFA into CLA (conjugated linoleic acids) and CLnA (conjugated linolenic acids). However, the bioavailability of fatty acid metabolites produced in vivo by the gut microbes remains to be studied. Therefore, we measured intestinal concentration and plasma accumulation of bacterial metabolites produced from dietary PUFA in mice, first injected with a lipoprotein lipase inhibitor, then force-fed with either sunflower oil (200 μl) rich in n-6 PUFA or linseed oil (200 μl) rich in n-3 PUFA. The greatest production of bacterial metabolites was observed in the caecum and colon, and at a much lesser extent in the jejunum and ileum. In the caecal content, CLA proportions were higher in sunflower oil force-fed mice whereas CLnA proportions were higher in linseed oil force-fed mice. The accumulation of the main metabolites (CLA cis-9,trans-11-18:2 and CLnA cis-9,trans-11,cis-15-18:3) in the caecal tissue was not associated with their increase in the plasma, therefore suggesting that, if endogenously produced CLA and CLnA have any biological role in host metabolism regulation, their effect would be confined at the intestinal level, where the microbiota is abundant.
Versatility of RNA-Binding Proteins in Cancer
Laurence Wurth
Comparative and Functional Genomics , 2012, DOI: 10.1155/2012/178525
Abstract: Posttranscriptional gene regulation is a rapid and efficient process to adjust the proteome of a cell to a changing environment. RNA-binding proteins (RBPs) are the master regulators of mRNA processing and translation and are often aberrantly expressed in cancer. In addition to well-studied transcription factors, RBPs are emerging as fundamental players in tumor development. RBPs and their mRNA targets form a complex network that plays a crucial role in tumorigenesis. This paper describes mechanisms by which RBPs influence the expression of well-known oncogenes, focusing on precise examples that illustrate the versatility of RBPs in posttranscriptional control of cancer development. RBPs appeared very early in evolution, and new RNA-binding domains and combinations of them were generated in more complex organisms. The identification of RBPs, their mRNA targets, and their mechanism of action have provided novel potential targets for cancer therapy.
Mouse Models of Human Autoimmune Diseases: Essential Tools That Require the Proper Controls
Laurence Morel
PLOS Biology , 2012, DOI: 10.1371/journal.pbio.0020241
Abstract:
Hereditary angioedema in women
Laurence Bouillet
Allergy, Asthma & Clinical Immunology , 2010, DOI: 10.1186/1710-1492-6-17
Abstract: Hereditary angioedema (HAE) is inherited in an autosomal dominant manner: consequently both women and men can be affected. However, published series of hereditary angioedema report a clear female predominance (60%) [1,2]. This might be explained by the fact that women are more likely to be symptomatic than men. In HAE associated with C1 Inh deficiency, Professor Bork has shown that women have more clinical episodes than men (p < 0.02) [2].Hormonal factors play a significant role in the precipitation or worsening of the condition in women. There appear to be variation in overall frequency of angioedema symptoms according to the different female life stages of childhood, puberty, menses, pregnancies and menopause. Reports have noted a close relationship between female hormones and angioedema: a mother and her daughter whose HAE-related symptoms appeared to be sex hormone dependent [3]. Their first attack happened around puberty; angioedema worsened premenstrual and when they took combined oral contraceptives. The case of a woman [4] with HAE and Turner's syndrome is also very interesting: starting physiological oestrogen replacement at the age of 34 years old, this woman experienced a worsening both in the severity and in the frequency of angioedema attacks. McGlinchey and al [5] described a patient whose symptoms of HAE emerged after starting hormone replacement therapy (HRT).Female sex hormones are known to affect the synthesis of many proteins. In the context of bradykinin mediated angioedema, they act on the kallikrein-kinin system by increasing synthesis of bradykinin. In ovariectomized rats, studies showed that 17β-estradiol increases Hageman factor levels by stimulation of gene transcription [6-9]. This hormone also increases kininogen and kallikrein levels [10]. Additionally oestrogens regulate B2 receptor gene expression and function: the vasodepressor response to bradykinin and the B2 receptor mRNA levels are reduced in ovariectomized rats, and restored by o
A framework for evolutionary systems biology
Laurence Loewe
BMC Systems Biology , 2009, DOI: 10.1186/1752-0509-3-27
Abstract: Here I propose a novel framework that brings together evolutionary theory and current systems biology approaches in order to quantify small effects of mutations and their epistatic interactions in silico. Central to this approach is the definition of fitness correlates that can be computed in some current systems biology models employing the rigorous algorithms that are at the core of much work in computational systems biology. The framework exploits synergies between the realism of such models and the need to understand real systems in evolutionary theory. This framework can address many longstanding topics in evolutionary biology by defining various 'levels' of the adaptive landscape. Addressed topics include the distribution of mutational effects on fitness, as well as the nature of advantageous mutations, epistasis and robustness. Combining corresponding parameter estimates with population genetics models raises the possibility of testing evolutionary hypotheses at a new level of realism.EvoSysBio is expected to lead to a more detailed understanding of the fundamental principles of life by combining knowledge about well-known biological systems from several disciplines. This will benefit both evolutionary theory and current systems biology. Understanding robustness by analysing distributions of mutational effects and epistasis is pivotal for drug design, cancer research, responsible genetic engineering in synthetic biology and many other practical applications.Mutations with weak effects on fitness that interact with each other are of great interest to evolutionary genetics and genomics, as their long-term consequences are much harder to predict than those of mutations with large effects. These mutations with small effects are also much more frequent [1,2]. Systems biology has accumulated much data on mutations with relatively large effects by using experimental methods and theoretical tools like flux balance analysis, which analyses the flux of metabolites in b
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