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Search Results: 1 - 10 of 475672 matches for " Lindsay Mark A "
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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.
microRNA expression in the aging mouse lung
Andrew E Williams, Mark M Perry, Sterghios A Moschos, Mark A Lindsay
BMC Genomics , 2007, DOI: 10.1186/1471-2164-8-172
Abstract: To address this question, we have used a highly-sensitive, semi-quantitative RT-PCR based approach to measure the expression profile of 256 of the 493 currently identified miRNAs in the lungs from 6 month (adult) and 18 month (aged) old female BALB/c mice. We show that, despite the characteristic changes in anatomy and gene expression associated with lung aging, there were no significant changes in the expression of 256 miRNAs.Overall, these results show that miRNA transcription is unchanged during lung aging and suggests that stable expression of miRNAs might instead buffer age related changes in the expression of protein-encoding genes.MicroRNAs (miRNAs) are 21–23 nucleotide double-stranded RNA molecules produced from endogenous genes by the sequential action of the RNase III enzymes Drosha and Dicer. At the present time, 493 miRNAs have been identified in mammalian tissues (Sanger Institute miRNA Registry, Release 9.1, February 2007) [1] and shown to regulate the post-transcriptional expression of multiple genes through a mechanism similar to RNA interference (RNAi) [2,3]. Indeed, bioinformatics studies suggest that up to a third of all known genes maybe regulated by this mechanism [4]. Post-transcriptional regulation of gene expression is mediated by the RNA-induced silencing complex (RISC), which uses one strand of the miRNA molecule (the guide strand) to target relevant mRNAs at their 3'-untranslated regions. Once mRNA is targeted by miRNAs, the RISC is thought to inhibit protein production either through blocking translation or by reducing mRNA stability [2,3].At the present time, the functions of only a fraction of the identified miRNAs are known. However, it appears that miRNAs play an essential role during development, since studies with Dicer knockout mice have shown that these die prematurely and have a variety of developmental abnormalities [5-7]. Furthermore, tissue specific developmental functions of individual miRNAs have been determined in mice and
Expression profiling in vivo demonstrates rapid changes in lung microRNA levels following lipopolysaccharide-induced inflammation but not in the anti-inflammatory action of glucocorticoids
Sterghios A Moschos, Andrew E Williams, Mark M Perry, Mark A Birrell, Maria G Belvisi, Mark A Lindsay
BMC Genomics , 2007, DOI: 10.1186/1471-2164-8-240
Abstract: To address this question, we have examined the differential expression of 104 miRNAs using real-time PCR during the innate immune response in mouse lung following exposure to aerosilised lipopolysaccharide (LPS). Following challenge, we observed rapid and transient increase in both the mean (4.3-fold) and individual levels of miRNA expression (46 miRNAs) which peaked at 3 hrs. Crucially, this increase was correlated with a reduction in the expression of tumour necrosis factor (TNF)-α, keratinocyte-derived chemokine (KC) and macrophage inflammatory protein (MIP)-2, suggesting a potential role for miRNAs in the regulation of inflammatory cytokine production. Examination of the individual miRNA expression profiles showed time dependent increases in miR-21, -25, -27b, -100, 140, -142-3p, -181c, 187, -194, -214, -223 and -224. Corticosteroid studies showed that pre-treatment with dexamethasone at concentrations that inhibited TNF-α production, had no effect either alone or upon the LPS-induced miRNA expression profile.We have shown that the LPS-induced innate immune response is associated with widespread, rapid and transient increases in miRNA expression in the mouse lung and we speculate that these changes might be involved in the regulation of the inflammatory response. In contrast, the lack of effect of dexamethasone in either control or challenged animals implies that the actions of glucocorticoids per se are not mediated through changes in miRNAs expression and that LPS-induced increases in miRNA expression are not mediated via classical inflammatory transcription factors.RNA interference (RNAi), mediated by 19- to 23- nucleotide double stranded RNA, has been identified as an evolutionarily conserved mechanism for the post-transcriptional regulation of mammalian gene expression [1]. Initial studies implicated RNAi in the cellular response to viral infection following the demonstration that virally-derived double stranded RNA was cleaved by the action of the RNase-II
Regulation of Anthrax Toxin-Specific Antibody Titers by Natural Killer T Cell-Derived IL-4 and IFNγ
T. Scott Devera, Sunil K. Joshi, Lindsay M. Aye, Gillian A. Lang, Jimmy D. Ballard, Mark L. Lang
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0023817
Abstract: Activation of Natural Killer-like T cells (NKT) with the CD1d ligand α-GC leads to enhanced production of anthrax toxin protective Ag (PA)-neutralizing Abs, yet the underlying mechanism for this adjuvant effect is not known. In the current study we examined the role of Th1 and Th2 type responses in NKT-mediated enhancement of antibody responses to PA. First, the contribution of IL-4 and IFNγ to the production of PA-specific toxin-neutralizing Abs was examined. By immunizing C57Bl/6 controls IL-4?/? mice and IFNγ?/? mice and performing passive serum transfer experiments, it was observed that sera containing PA-specific IgG1, IgG2b and IgG2c neutralized toxin in vitro and conferred protection in vivo. Sera containing IgG2b and IgG2c neutralized toxin in vitro but were not sufficient for protection in vivo. Sera containing IgG1 and IgG2b neutralized toxin in vitro and conferred protection in vivo. IgG1 therefore emerged as a good correlate of protection. Next, C57Bl/6 mice were immunized with PA alone or PA plus a Th2-skewing α-GC derivative known as OCH. Neutralizing PA-specific IgG1 responses were modestly enhanced by OCH in C57Bl/6 mice. Conversely, IgG2b and IgG2c were considerably enhanced in PA/OCH-immunized IL-4?/? mice but did not confer protection. Finally, bone marrow chimeras were generated such that NKT cells were unable to express IL-4 or IFNγ. NKT-derived IL-4 was required for OCH-enhanced primary IgG1 responses but not recall responses. NKT-derived IL-4 and IFNγ also influenced primary and recall IgG2b and IgG2c titers. These data suggest targeted skewing of the Th2 response by α-GC derivatives can be exploited to optimize anthrax vaccination.
Prognosis of West Nile virus associated acute flaccid paralysis: a case series
Jennie Johnstone, Steven E Hanna, Lindsay E Nicolle, Michael A Drebot, Binod Neupane, James B Mahony, Mark B Loeb
Journal of Medical Case Reports , 2011, DOI: 10.1186/1752-1947-5-395
Abstract: Between 2003 and 2006, 157 symptomatic patients with West Nile virus were enrolled in a longitudinal cohort study of West Nile virus in Canada. Seven patients (4%) had acute flaccid paralysis. The first patient was a 55-year-old man who presented with left upper extremity weakness. The second patient was a 54-year-old man who presented with bilateral upper extremity weakness. The third patient was a 66-year-old woman who developed bilateral upper and lower extremity weakness. The fourth patient was a 67-year-old man who presented with right lower extremity weakness. The fifth patient was a 60-year-old woman who developed bilateral lower extremity weakness. The sixth patient was a 71-year-old man with a history of Parkinson's disease and acute onset bilateral lower extremity weakness. The seventh patient was a 52-year-old man who presented with right lower extremity weakness. All were Caucasian. Patients were followed for a mean of 1.1 years. At the end of follow-up the mean score on the Physical Component Summary of the Short-Form 36 scale had only slightly increased to 39. In contrast, mean score on the Mental Component Summary of the Short-Form 36 scale at the end of follow-up had normalized to 50.Despite the poor physical prognosis for patients with acute flaccid paralysis, the mental health outcomes are generally favorable.In 1999, West Nile virus caused an outbreak in New York City and has since emerged as an important human pathogen in North America [1,2]. Although most cases of West Nile virus infection are asymptomatic, symptomatic disease can occur and ranges from a mild febrile illness (20% of infected individuals) to severe illness with central nervous system involvement (<1% of all infected cases) [3]. Classically, neurologic manifestations included meningitis and encephalitis; however, in 2002 the first cases of West Nile virus associated acute flaccid paralysis were described [4,5]. Since then, acute flaccid paralysis has become an established complica
Androgen Receptor Phosphorylation at Serine 308 and Serine 791 Predicts Enhanced Survival in Castrate Resistant Prostate Cancer Patients
Pamela McCall,Claire E. Adams,Jennifer M. Willder,Lindsay Bennett,Tahir Qayyum,Clare Orange,Mark A. Underwood,Joanne Edwards
International Journal of Molecular Sciences , 2013, DOI: 10.3390/ijms140816656
Abstract: We previously reported that AR phosphorylation at serine 213 was associated with poor outcome and may contribute to prostate cancer development and progression. This study investigates if specific AR phosphorylation sites have differing roles in the progression of hormone na?ve prostate cancer (HNPC) to castrate resistant disease (CRPC). A panel of phosphospecific antibodies were employed to study AR phosphorylation in 84 matched HNPC and CRPC tumours. Immunohistochemistry measured Androgen receptor expression phosphorylated at serine residues 94 (pAR 94), 308 (pAR 308), 650(pAR 650) and 791 (pAR 791). No correlations with clinical parameters were observed for pAR 94 or pAR 650 in HNPC or CRPC tumours. In contrast to our previous observation with serine 213, high pAR 308 is significantly associated with a longer time to disease specific death ( p = 0.011) and high pAR 791 expression significantly associated with a longer time to disease recurrence ( p = 0.018) in HNPC tumours and longer time to death from disease recurrence ( p = 0.040) in CRPC tumours. This observation in CRPC tumours was attenuated in high apoptotic tumours ( p = 0.022) and low proliferating tumours ( p = 0.004). These results demonstrate that understanding the differing roles of AR phosphorylation is necessary before this can be exploited as a target for castrate resistant prostate cancer.
Observations of Binary Stars with the Differential Speckle Survey Instrument. VI. Measures During 2014 at the Discovery Channel Telescope
Elliott P. Horch,Gerard T. van Belle,James W. Davidson, Jr.,Lindsay A. Ciastko,Mark E. Everett,Karen S. Bjorkman
Physics , 2015, DOI: 10.1088/0004-6256/150/5/151
Abstract: We present the results of 938 speckle measures of double stars and suspected double stars drawn mainly from the Hipparcos Catalogue, as well as 208 observations where no companion was noted. One hundred fourteen pairs have been resolved for the first time. The data were obtained during four observing runs in 2014 using the Differential Speckle Survey Instrument (DSSI) at Lowell Observatory's Discovery Channel Telescope. The measurement precision obtained when comparing to ephemeris positions of binaries with very well-known orbits is generally less than 2 mas in separation and 0.5 degrees in position angle. Differential photometry is found to have internal precision of approximately 0.1 magnitudes and to be in very good agreement with Hipparcos measures in cases where the comparison is most relevant. We also estimate the detection limit in the cases where no companion was found. Visual orbital elements are derived for 6 systems.
MicroRNA Expression Profiling in Mild Asthmatic Human Airways and Effect of Corticosteroid Therapy
Andrew E. Williams, Hanna Larner-Svensson, Mark M. Perry, Gaynor A. Campbell, Sarah E. Herrick, Ian M. Adcock, Jonas S. Erjefalt, Kian Fan Chung, Mark A. Lindsay
PLOS ONE , 2009, DOI: 10.1371/journal.pone.0005889
Abstract: Background Asthma is a common disease characterised by reversible airflow obstruction, bronchial hyperresponsiveness and chronic inflammation, which is commonly treated using corticosteroids such as budesonide. MicroRNAs (miRNAs) are a recently identified family of non-protein encoding genes that regulate protein translation by a mechanism entitled RNA interference. Previous studies have shown lung-specific miRNA expression profiles, although their importance in regulating gene expression is unresolved. We determined whether miRNA expression was differentially expressed in mild asthma and the effect of corticosteroid treatment. Methodology/Principal Findings We have examined changes in miRNA using a highly sensitive RT-PCR based approach to measure the expression of 227 miRNAs in airway biopsies obtained from normal and mild asthmatic patients. We have also determined whether the anti-inflammatory action of corticosteroids are mediated through miRNAs by determining the profile of miRNA expression in mild asthmatics, before and following 1 month twice daily treatment with inhaled budesonide. Furthermore, we have analysed the expression of miRNAs from individual cell populations from the airway and lung. We found no significant difference in the expression of 227 miRNAs in the airway biopsies obtained from normal and mild asthmatic patients. In addition, despite improved lung function, we found no significant difference in the miRNA expression following one month treatment with the corticosteroid, budesonide. However, analysis of bronchial and alveolar epithelial cells, airway smooth muscle cells, alveolar macrophages and lung fibroblasts demonstrate a miRNA expression profile that is specific to individual cell types and demonstrates the complex cellular heterogeneity within whole tissue samples. Conclusions Changes in miRNA expression do not appear to be involved in the development of a mild asthmatic phenotype or in the anti-inflammatory action of the corticosteroid budesonide.
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.
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