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Search Results: 1 - 10 of 475149 matches for " Mark A;Giembycz "
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Signal transduction and activation of the NADPH oxidase in eosinophils
Lindsay, Mark A;Giembycz, Mark A;
Memórias do Instituto Oswaldo Cruz , 1997, DOI: 10.1590/S0074-02761997000800016
Abstract: activation of the eosinophil nadph oxidase and the subsequent release of toxic oxygen radicals has been implicated in the mechanism of parasite killing and inflammation. at present, little is known of the signal transduction pathway that govern agonist-induced activation of the respiratory burst and is the subject of this review. in particular, we focus on the ability of leukotrine b4 to activate the nadph oxidase in guinea-pig peritoneal eosinophils which can be obtained in sufficient number and purity for detailed biochemical experiments to be performed.
Signal transduction and activation of the NADPH oxidase in eosinophils
Lindsay Mark A,Giembycz Mark A
Memórias do Instituto Oswaldo Cruz , 1997,
Abstract: Activation of the eosinophil NADPH oxidase and the subsequent release of toxic oxygen radicals has been implicated in the mechanism of parasite killing and inflammation. At present, little is known of the signal transduction pathway that govern agonist-induced activation of the respiratory burst and is the subject of this review. In particular, we focus on the ability of leukotrine B4 to activate the NADPH oxidase in guinea-pig peritoneal eosinophils which can be obtained in sufficient number and purity for detailed biochemical experiments to be performed.
Roflumilast: first phosphodiesterase 4 inhibitor approved for treatment of COPD
Mark A Giembycz, Stephen K Field
Drug Design, Development and Therapy , 2010, DOI: http://dx.doi.org/10.2147/DDDT.S7667
Abstract: flumilast: first phosphodiesterase 4 inhibitor approved for treatment of COPD Review (6412) Total Article Views Authors: Mark A Giembycz, Stephen K Field Published Date July 2010 Volume 2010:4 Pages 147 - 158 DOI: http://dx.doi.org/10.2147/DDDT.S7667 Mark A Giembycz1, Stephen K Field2 Departments of 1Physiology and Pharmacology and 2Medicine, Airway Inflammation Research Group, Faculty of Medicine, University of Calgary, Alberta, Canada Abstract: In April 2010, the European Medicines Agency Committee for Medicinal Products for Human Use recommended approval of roflumilast, a selective phosphodiesterase 4 -inhibitor, for the “maintenance treatment of severe chronic obstructive pulmonary disease (COPD, FEV1 postbronchodilator less than 50% predicted) associated with chronic bronchitis in adult patients with a history of frequent exacerbations as add-on to bronchodilator treatment”. This -decision was based, in part, on the results of several large, international, multicenter, randomized, -placebo-controlled trials of either six or 12 months’ duration that had been undertaken in COPD patients. Roflumilast 500 μg daily improved lung function and reduced exacerbations in patients with more severe COPD, especially those with chronic bronchitis, frequent exacerbations, or who required frequent rescue inhaler therapy in the placebo-controlled trials. It also improved lung function and reduced exacerbations in patients with moderately severe COPD treated with salmeterol or tiotropium. Advantages of roflumilast over inhaler therapy are that it is an oral tablet and only needs to be taken once daily. While taking roflumilast, the most common adverse effects patients experienced were gastrointestinal upset and headache. Weight loss, averaging 2.2 kg, occurred in patients treated with roflumilast. Patients taking roflumilast were more likely to drop out of the trials than patients in the control groups. Patients who discontinued therapy usually did so during the first few weeks and were more likely to have experienced -gastrointestinal side effects. Roflumilast is the first selective phosphodiesterase 4 inhibitor and will offer physicians another treatment option for patients with more severe COPD.
Roflumilast: first phosphodiesterase 4 inhibitor approved for treatment of COPD
Mark A Giembycz,Stephen K Field
Drug Design, Development and Therapy , 2010,
Abstract: Mark A Giembycz1, Stephen K Field2Departments of 1Physiology and Pharmacology and 2Medicine, Airway Inflammation Research Group, Faculty of Medicine, University of Calgary, Alberta, CanadaAbstract: In April 2010, the European Medicines Agency Committee for Medicinal Products for Human Use recommended approval of roflumilast, a selective phosphodiesterase 4 -inhibitor, for the “maintenance treatment of severe chronic obstructive pulmonary disease (COPD, FEV1 postbronchodilator less than 50% predicted) associated with chronic bronchitis in adult patients with a history of frequent exacerbations as add-on to bronchodilator treatment”. This -decision was based, in part, on the results of several large, international, multicenter, randomized, -placebo-controlled trials of either six or 12 months’ duration that had been undertaken in COPD patients. Roflumilast 500 μg daily improved lung function and reduced exacerbations in patients with more severe COPD, especially those with chronic bronchitis, frequent exacerbations, or who required frequent rescue inhaler therapy in the placebo-controlled trials. It also improved lung function and reduced exacerbations in patients with moderately severe COPD treated with salmeterol or tiotropium. Advantages of roflumilast over inhaler therapy are that it is an oral tablet and only needs to be taken once daily. While taking roflumilast, the most common adverse effects patients experienced were gastrointestinal upset and headache. Weight loss, averaging 2.2 kg, occurred in patients treated with roflumilast. Patients taking roflumilast were more likely to drop out of the trials than patients in the control groups. Patients who discontinued therapy usually did so during the first few weeks and were more likely to have experienced -gastrointestinal side effects. Roflumilast is the first selective phosphodiesterase 4 inhibitor and will offer physicians another treatment option for patients with more severe COPD.Keywords: roflumilast, phosphodiesterase 4 inhibitor, chronic obstructive pulmonary disease, exacerbation
Glucocorticoid Repression of Inflammatory Gene Expression Shows Differential Responsiveness by Transactivation- and Transrepression-Dependent Mechanisms
Elizabeth M. King, Joanna E. Chivers, Christopher F. Rider, Anne Minnich, Mark A. Giembycz, Robert Newton
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0053936
Abstract: Binding of glucocorticoid to the glucocorticoid receptor (GR/NR3C1) may repress inflammatory gene transcription via direct, protein synthesis-independent processes (transrepression), or by activating transcription (transactivation) of multiple anti-inflammatory/repressive factors. Using human pulmonary A549 cells, we showed that 34 out of 39 IL-1β-inducible mRNAs were repressed to varying degrees by the synthetic glucocorticoid, dexamethasone. Whilst these repressive effects were GR-dependent, they did not correlate with either the magnitude of IL-1β-inducibility or the NF-κB-dependence of the inflammatory genes. This suggests that induction by IL-1β and repression by dexamethasone are independent events. Roles for transactivation were investigated using the protein synthesis inhibitor, cycloheximide. However, cycloheximide reduced the IL-1β-dependent expression of 13 mRNAs, which, along with the 5 not showing repression by dexamethasone, were not analysed further. Of the remaining 21 inflammatory mRNAs, cycloheximide significantly attenuated the dexamethasone-dependent repression of 11 mRNAs that also showed a marked time-dependence to their repression. Such effects are consistent with repression occurring via the de novo synthesis of a new product, or products, which subsequently cause repression (i.e., repression via a transactivation mechanism). Conversely, 10 mRNAs showed completely cycloheximide-independent, and time-independent, repression by dexamethasone. This is consistent with direct GR transrepression. Importantly, the inflammatory mRNAs showing attenuated repression by dexamethasone in the presence of cycloheximide also showed a significantly greater extent of repression and a higher potency to dexamethasone compared to those mRNAs showing cycloheximide-independent repression. This suggests that the repression of inflammatory mRNAs by GR transactivation-dependent mechanisms accounts for the greatest levels of repression and the most potent repression by dexamethasone. In conclusion, our data indicate roles for both transrepression and transactivation in the glucocorticoid-dependent repression of inflammatory gene expression. However, transactivation appears to account for the more potent and efficacious mechanism of repression by glucocorticoids on these IL-1β-induced genes.
Tumour Necrosis Factor-α Regulates Human Eosinophil Apoptosis via Ligation of TNF-Receptor 1 and Balance between NF-κB and AP-1
Hannu Kankaanranta, Pinja Ilmarinen, Xianzhi Zhang, Ian M. Adcock, Aleksi Lahti, Peter J. Barnes, Mark A. Giembycz, Mark A. Lindsay, Eeva Moilanen
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0090298
Abstract: Eosinophils play a central role in asthma. The present study was performed to investigate the effect of tumour necrosis factor-α (TNF-α) on longevity of isolated human eosinophils. In contrast to Fas, TNF-α inhibited eosinophil apoptosis as evidenced by a combination of flow cytometry, DNA fragmentation assay and morphological analyses. The effect of TNF-α on eosinophil apoptosis was reversed by a TNF-α neutralising antibody. The anti-apoptotic effect of TNF-α was not due to autocrine release of known survival-prolonging cytokines interleukins 3 and 5 or granulocyte-macrophage-colony-stimulatin?gfactor as their neutralisation did not affect the effect of TNF-α. The anti-apoptotic signal was mediated mainly by the TNF-receptor 1. TNF-α induced phosphorylation and degradation of IκB and an increase in NF-κB DNA-binding activity. The survival-prolonging effect of TNF-α was reversed by inhibitors of NF-κB pyrrolidinedithiocarbamate and gliotoxin and by an inhibitor of IκB kinase, BMS-345541. TNF-α induced also an increase in AP-1 DNA-binding activity and the antiapoptotic effect of TNF-α was potentiated by inhibitors of AP-1, SR 11302 and tanshinone IIA and by an inhibitor of c-jun-N-terminal kinase, SP600125, which is an upstream kinase activating AP-1. Our results thus suggest that TNF-α delays human eosinophil apoptosis via TNF-receptor 1 and the resulting changes in longevity depend on yin-yang balance between activation of NF-κB and AP-1.
Gender and Anxiety: A Comparison of Student Anxiety Levels in Face-to-Face and Video Conferencing Courses  [PDF]
Jodi McKnight, Mark A. McKnight
Creative Education (CE) , 2012, DOI: 10.4236/ce.2012.31015
Abstract: This research focuses on the role of gender in face-to-face instruction and video conferencing instruction on students’ levels of anxiety. This is due, in part, to the fact that gender and anxiety levels of students enrolled in remote video conferencing learning environments has received little attention in either psychological or educational research. A difference in gender as it relates to education is an important focus of research. This is due to the increasing learning opportunities for female students (online in particular). Explored later, further research should investigate various demographics and delivery options for courses.
Forest Fragmentation and Its Potential Implications in the Brazilian Amazon between 2001 and 2010  [PDF]
Izaya Numata, Mark A. Cochrane
Open Journal of Forestry (OJF) , 2012, DOI: 10.4236/ojf.2012.24033
Abstract: In recent decades, human development pressures have results in conversions of vast tracts of Amazonian tropical rain forests to agriculture and other human land uses. In addition to the loss of large forest cover, remaining forests are also fragmented into smaller habitats. Fragmented forests suffer several biological and ecological changes due to edge effects that can exacerbate regional forest degradation. The Brazilian Amazon has had greatly contrasting land cover dynamics in the past decade with the highest historical rates of deforestation (2001-2005) followed by the lowest rates of forest loss in decades, since 2006. Currently, the basin-wide status and implications of forest fragmentation on remnant forests is not well known. We performed a regional forest fragmentation analysis for seven states of the Brazilian Amazon between 2001 and 2010 using a recent deforestation data. During this period, the number of forest fragments (>2 ha) doubled, nearly 125,000 fragments were formed by human activities with more than 50% being smaller than 10 ha. Over the decade, forest edges increased by an average of 36,335 km/year. However, the rate was much greater from 2001-2005 (50,046 km/year) then 2006-2010 (25,365 km/year) when deforestation rates dropped drastically. In 2010, 55% of basin-wide forest edges were < 10 years old due to the creation of large number of small fragments where intensive biological and ecological degradation is ongoing. Over the past decade protected areas have been expanded dramatically over the Brazilian Amazon and, as of 2010, 51% of remaining forests across the basin are within protected areas and only 1.5% of protected areas has been deforested. Conversely, intensive forest cover conversion has been occurred in unprotected forests. While 17% of Amazonian forests are within 1 km of forest edges in 2010, the proportion increases to 34% in unprotected areas varying between 14% and 95% among the studied states. Our results indicate that the Brazilian Amazon now largely consists of two contrasting forest conditions: protected areas with vast undisturbed forests and unprotected forests that are highly fragmented and disturbed landscapes.
The Effects of Forest Thinning Practices and Altered Nutrient Supply on Soil Trace Gas Fluxes in Colorado  [PDF]
Mark A. Gathany, Ingrid C. Burke
Open Journal of Forestry (OJF) , 2014, DOI: 10.4236/ojf.2014.43034
Abstract:

Increases in wildfire activity in the western United States have prompted land managers to reevaluate management practices. In the Colorado Front Range, where population density is high, there is often a great concern regarding wildfire which leads to efforts that will reduce fire hazard. The most common method of achieving this goal is to thin the forest of small diameter trees. Oftentimes these practices are undertaken with little knowledge of the ecological consequences of such treatments. We investigated the effect(s) of three treatments (control, thinning-only and broadcast chipping) on trace gas fluxes (CO2, CH4, and N2O), litter mass, and soil carbon and nitrogen. In a small plot study, we used a 2 × 3 × 3 randomized complete block design to determine the influence of nutrient amendments (woodchips, nitrogen, and phosphorus availability) on trace gas fluxes. The stand-management study revealed that neither thinning-only nor broadcast chipping significantly affected soil carbon or nitrogen, while thinning-only significantly reduced the amount of forest floor litter. Each trace gas flux was significantly affected by the date of sampling (June or August). CO2 and N2O fluxes each had a significant interaction between treatment and sampling date. We attribute this to a difference in moisture availability between the sampling times. In the plot study we found that only the interaction between woodchip addition and phosphorus

A Review of Artificial Immune System Based Security Frameworks for MANET  [PDF]
Lincy Elizebeth Jim, Mark A. Gregory
Int'l J. of Communications, Network and System Sciences (IJCNS) , 2016, DOI: 10.4236/ijcns.2016.91001
Abstract: Mobile ad hoc networks (MANETs) are collections of wireless mobile devices that form a communication network with restricted broadcast range, limited resources and without fixed infrastructure. Routing is a critical function in multi-hop MANETs. At the same time, security in MANETs—especially routing security—presents a number of new and interesting challenges. Communication is achieved by relaying data along routes that are dynamically discovered and maintained through collaboration between the nodes. Advances in the field of artificial immune systems provide an opportunity to improve MANET security and performance. Artificial immune systems mimic the functionality of the human immune system wherein there is clear distinction between self and non self and this delineation is important in a MANET where there is no centralized management. The high level of protection provided to the human body by an evolved immune system can be applied as a security feature in MANET. The current security techniques proposed for MANET have varying degrees of success due to the dynamic nature of a MANET. This paper will review different strategies for the application of artificial immune systems to MANETs.
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