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678 results on '"Phipps, Simon"'

151. Confessions of an open source purist

Author

Phipps, Simon

Subjects
Computers and office automation industries
Abstract

Byline: Simon Phipps Writing about my successful migration from a MacBook Pro to a Chromebook -- two years after the original transition -- led to the inevitable denunciations from certain [...]

Published
2014

152. Geeks give back: Be an open source tester

Author

Phipps, Simon

Subjects
Open source software -- Usage, Software testing -- Social aspects, Software product testing, Open source software, Computers and office automation industries
Abstract

Byline: Simon Phipps Are you using open source software for free? Do you wish you could contribute, but dont have the time to learn how a new developer community works? [...]

Published
2014

153. Microsoft vs. DoJ: The battle for privacy in the cloud

Author

Phipps, Simon

Subjects
Privacy, Chambers of commerce, Privacy issue, Computers and office automation industries
Abstract

Byline: Simon Phipps What issue can unite the EFF and BSA? Fox News and The Guardian? Amazon and eBay? The ACLU and the Chamber of Commerce? The issue is the [...]

Published
2014

154. Google's surprise: ODF support launches ahead of schedule

Author

Phipps, Simon

Subjects
Online information services -- International economic relations, Online information service, Computers and office automation industries
Abstract

Byline: Simon Phipps Following the comments by Google's head of open source, Chris DiBona, last week in London, Google has today announced that support for ODF (OpenDocument Format) has now [...]

Published
2014

155. MacBook to Chromebook: No regrets

Author

Phipps, Simon

Subjects
Computers and office automation industries
Abstract

Byline: Simon Phipps One of the most popular stories Ive written explained why I ditched my MacBook Pro for a Chromebook in 2012. Back then I didnt know how long [...]

Published
2014

156. A shadowy consortium opposes your Internet privacy

Author

Phipps, Simon

Subjects
Privacy, Consortia, World Wide Web, Consortium, World Wide Web, Privacy issue, Computers and office automation industries
Abstract

Byline: Simon Phipps Google researchers have devised a replacement for the HTTP protocol that carries the World Wide Web. By default, its encrypted end to end, its very fast, youre [...]

Published
2014

157. Fraudulent apps stalk Apple's App Store

Author

Phipps, Simon

Subjects
Fraud, Computers and office automation industries
Abstract

Byline: Simon Phipps Many people think that the sort of scams Microsoft cleared out of its mobile app store this year could never affect Apple. But how tight is Apple's [...]

Published
2014

158. Now crowdfunding: A laptop that protects your digital rights

Author

Phipps, Simon

Subjects
Digital rights (Intellectual property), Open source software, Crowdfunding, Open source software, Computers and office automation industries
Abstract

Byline: Simon Phipps Do you have any idea what your laptop is doing deep down? Is there any way to find out? Usually, the answer is no. Anything could be [...]

Published
2014

159. PAG1 limits allergen‐induced type 2 inflammation in the murine lung.

Author

Ullah, Md Ashik, Vicente, Cristina T., Collinson, Natasha, Curren, Bodie, Sikder, Md Al Amin, Sebina, Ismail, Simpson, Jennifer, Varelias, Antiopi, Lindquist, Jonathan A., Ferreira, Manuel A. R., and Phipps, Simon

Subjects
PNEUMONIA, INNATE lymphoid cells, HOUSE dust mites, MUCOCILIARY system, T cells, CD14 antigen, MEMBRANE proteins
Abstract

Background: Phosphoprotein associated with glycosphingolipid‐enriched microdomains 1 (PAG1) is a transmembrane adaptor protein that affects immune receptor signaling in T and B cells. Evidence from genome‐wide association studies of asthma suggests that genetic variants that regulate the expression of PAG1 are associated with asthma risk. However, it is not known whether PAG1 expression is causally related to asthma pathophysiology. Here, we investigated the role of PAG1 in a preclinical mouse model of house dust mite (HDM)‐induced allergic sensitization and allergic airway inflammation. Methods: Pag1‐deficient (Pag1−/−) and wild‐type (WT) mice were sensitized or sensitized/challenged to HDM, and hallmark features of allergic inflammation were assessed. The contribution of T cells was assessed through depletion (anti‐CD4 antibody) and adoptive transfer studies. Results: Type 2 inflammation (eosinophilia, eotaxin‐2 expression, IL‐4/IL‐5/IL‐13 production, mucus production) in the airways and lungs was significantly increased in HDM sensitized/challenged Pag1−/− mice compared to WT mice. The predisposition to allergic sensitization was associated with increased airway epithelial high‐mobility group box 1 (HMGB1) translocation and release, increased type 2 innate lymphoid cells (ILC2s) and monocyte‐derived dendritic cell numbers in the mediastinal lymph nodes, and increased T‐helper type 2 (TH2)‐cell differentiation. CD4+ T‐cell depletion studies or the adoptive transfer of WT OVA‐specific CD4+ T cells to WT or Pag1−/− recipients demonstrated that the heightened propensity for TH2‐cell differentiation was both T cell intrinsic and extrinsic. Conclusion: PAG1 deficiency increased airway epithelial activation, ILC2 expansion, and TH2 differentiation. As a consequence, PAG1 deficiency predisposed toward allergic sensitization and increased the severity of experimental asthma. [ABSTRACT FROM AUTHOR]

Published
2020
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160. The parasitic 68-mer peptide FhHDM-1 inhibits mixed granulocytic inflammation and airway hyperreactivity in experimental asthma

Author

Tanaka, Akane, primary, Allam, Venkata Sita Rama Raju, additional, Simpson, Jennifer, additional, Tiberti, Natalia, additional, Shiels, Jenna, additional, To, Joyce, additional, Lund, Maria, additional, Combes, Valery, additional, Weldon, Sinead, additional, Taggart, Cliff, additional, Dalton, John P., additional, Phipps, Simon, additional, Sukkar, Maria B., additional, and Donnelly, Sheila, additional

Published
2018
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161. PGD2/DP2 receptor activation promotes severe viral bronchiolitis by suppressing IFN- λ production

Author

Werder, Rhiannon B., primary, Lynch, Jason P., additional, Simpson, Jennifer C., additional, Zhang, Vivian, additional, Hodge, Nick H., additional, Poh, Matthew, additional, Forbes-Blom, Elizabeth, additional, Kulis, Christina, additional, Smythe, Mark L., additional, Upham, John W., additional, Spann, Kirsten, additional, Everard, Mark L., additional, and Phipps, Simon, additional

Published
2018
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163. PD17-08 THE EFFECTS OF MEDICALLY EXPULSIVE THERAPY (MET) ON SPONTANEOUS STONE PASSAGE (SSP) IN PATIENTS PRESENTING WITH ACUTE URETERIC COLIC

Author

Shah, Taimur T, primary, Gao, Chuanyu, additional, O' Keefe, Aidan, additional, Manning, Todd, additional, Peacocke, Anthony, additional, Cashman, Sophia, additional, Nambiar, Arjun, additional, Lamb, Ben, additional, Cumberbatch, Marcus, additional, Ivin, Nicholas, additional, Maw, Jonathan, additional, Ali Abdaal, Cissy, additional, Al Hayek, Sami, additional, Christidis, Daniel, additional, Bolton, Damien, additional, Lawrentschuk, Nathan, additional, Khan, Shahid, additional, Demirel, Sibel, additional, Graham, Stuart, additional, Lee, Jonathan Chuo Min, additional, Evans, Simon, additional, Koschel, Samantha, additional, Badgery, Henry, additional, Brennan, Janelle, additional, Wang, Luke, additional, Nzenza, Tatenda, additional, Ruljancich, Paul, additional, Begum, Ruzi, additional, Hamad, Shazia, additional, Shetty, Aarti, additional, Swallow, Daniel, additional, Jessica S, Morrow, additional, Curry, David, additional, Young, Michael, additional, Abboudi, Hamid, additional, Jalil, Rozh, additional, Dasgupta, Ranan, additional, Cameron, Fraser, additional, Shingles, Connie, additional, Ho, Cherrie, additional, Parwaiz, Iram, additional, Henderson, John, additional, Mackenzie, Kenneth R, additional, Reid, Kyle, additional, Umeni-Eronini, Nkemi, additional, Assaf, Nazrin, additional, Oyekan, Adekinte, additional, Sriprasad, Seshadri, additional, Hayat, Zara, additional, Morrison-Jones, Victoria, additional, Steen, Christopher, additional, Alberto, Matthew, additional, Rujancich, Paul, additional, Laird, Alex, additional, Sharma, Abhishek, additional, Phipps, Simon, additional, Harris, Andrew, additional, Rogers, Alistair, additional, Ngweso, Simeon, additional, Nyandoro, Munyaradzi, additional, Hayne, Dickon, additional, Hendry, Jane, additional, Kerr, Lynne, additional, Mcilhenny, Craig, additional, Rodger, Flora, additional, Docherty, Emma, additional, Ng, Alicia, additional, Seaward, Lisette, additional, Eldred-Evans, David, additional, Bultitude, Matthew, additional, Abdelmoteleb, Haitham, additional, Hawary, Amr, additional, Tregunna, Rebecca, additional, Ibrahim, Husam, additional, Mc Grath, Shannon, additional, O’ Brien, Jonathan, additional, Campbell, Angus, additional, Cronbach, Peter, additional, Paget, Amar, additional, Suraparaj, Lokesh, additional, O' Brien, James, additional, Gupta, Suresh K, additional, Tait, Campbell, additional, Sakthivel, Ashok, additional, Pankhania, Rahul, additional, Al-Qassim, Zubair, additional, Rezacova, Monika, additional, Edison, Eric, additional, Sandhu, Sarbjinder, additional, Foley, Robert, additional, Akintimehin, Abisoye, additional, Khan, Azhar, additional, Nkwam, Nkwam, additional, Grice, Peter, additional, Khan, Masood, additional, Kashora, Florence, additional, Manson-Bahr, David, additional, Mc Cauley, Nadine, additional, Nehikhare, Osayuki, additional, Bycroft, John, additional, Tailor, Kishan, additional, Saleemi, Asad, additional, Al-Dhahir, Wesam, additional, Abu Yousif, Mohamed, additional, O' Rourke, John, additional, Chin, Angus On Luk, additional, Pearce, Ian, additional, Olivier, James, additional, Tay, Joel, additional, Cannon, Andrea, additional, Akman, James, additional, Hussain, Zahid, additional, Coode-Bate, Jack, additional, Natarajan, Madhavi, additional, Irving, Stuart, additional, Murtagh, Kevin, additional, Carrie, Anne, additional, Miller, Marek, additional, Malki, Manar, additional, Burge, Frances, additional, Ratan, Harry, additional, Bedi, Nishant, additional, Kavia, Raj, additional, Stonier, Thomas, additional, Simson, Nick, additional, Singh, Harpreet, additional, Hatem, Emer, additional, Arya, Manit, additional, Sadien, Iannish, additional, Miakhil, Iqbal, additional, Sharma, Sunil, additional, Olaniyi, Patrick, additional, Stammeijer, Roelof, additional, Mason, Hannah, additional, Symes, Andrew, additional, Lavan, Lisa, additional, Rowbotham, Carl, additional, Wong, Carol, additional, Al-Shakhshir, Sarah, additional, Belal, Mohammed, additional, Mc Kay, Alastair Crawford, additional, Graham, John, additional, Simmons, Lucy, additional, Khadouri, Sinan, additional, Withington, John, additional, Ajayi, Leye, additional, Tay, Li June, additional, Ward, Alex, additional, Parys, Bo, additional, Liew, Matthew, additional, Simpson, Richard, additional, Ross, David, additional, Adams, Robert, additional, Mirza, Asfand Baig, additional, Acher, Pete, additional, Gallagher, Michael, additional, Premakumar, Yaamini, additional, Ager, Michael, additional, Ayres, Benjamin, additional, Pang, Karl, additional, Patterson, Jake, additional, Kozan, Andrei Adrian, additional, Jaffer, Ata, additional, Din, Waqas, additional, Biyani, Chandra Shekhar, additional, Tam, Johnson Pok-Him, additional, Tudor, Edward, additional, Probert, John Llewellyn, additional, Matanhelia, Mudit, additional, Hegazy, Mohammed, additional, Quinlan, David, additional, Ness, Daniel, additional, Gowardhan, Bharat, additional, Bateman, Kellie, additional, Wozniak, Slawomir, additional, Ellis, Gidon, additional, Smith, Daron, additional, Derbyshire, Laura, additional, Chow, Karyee, additional, Mosey, Rebecca, additional, Osman, Banan, additional, Kynaston, Howard, additional, Clements, Joshua, additional, Hann, Gemma, additional, Gray, Sam, additional, Yassaie, Omid, additional, Weeratunga, George, additional, Udovicich, Cristian, additional, Mbuvi, James, additional, Stewart, Heather, additional, Samsudin, Azizan, additional, Hughes-Hallet, Archie, additional, Kum, Francesca, additional, Symes, Rebecca, additional, Frymann, Rob, additional, Chappell, Barnaby, additional, Rezvani, Sean, additional, Ahmed, Issam, additional, Shergill, Iqbal, additional, Lee, Su-Min, additional, Hussain, Ali, additional, Pickard, Robert, additional, Erotocritou, Paul, additional, and Kasivisvanathan, Veeru, additional

Published
2018
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165. Plasmacytoid dendritic cells protect from viral bronchiolitis and asthma through semaphorin 4a–mediated T reg expansion

Author

Lynch, Jason P., primary, Werder, Rhiannon B., additional, Loh, Zhixuan, additional, Sikder, Md. Al Amin, additional, Curren, Bodie, additional, Zhang, Vivian, additional, Rogers, Matthew J., additional, Lane, Katie, additional, Simpson, Jennifer, additional, Mazzone, Stuart B., additional, Spann, Kirsten, additional, Hayball, John, additional, Diener, Kerrilyn, additional, Everard, Mark L., additional, Blyth, Christopher C., additional, Forstner, Christian, additional, Dennis, Paul G., additional, Murtaza, Nida, additional, Morrison, Mark, additional, Ó Cuív, Páraic, additional, Zhang, Ping, additional, Haque, Ashraful, additional, Hill, Geoffrey R., additional, Sly, Peter D., additional, Upham, John W., additional, and Phipps, Simon, additional

Published
2017
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166. RAGE deficiency predisposes mice to virus-induced paucigranulocytic asthma

Author

Arikkatt, Jaisy, Ullah, Md, Short, Kirsty, Zhang, Vivian, Gan, Wan Jun, Loh, Zhixuan (Ken), Werder, Rhiannon, Simpson, Jennifer, Sly, Peter, Mazzone, Stuart, Spann, Kirsten, Ferreira, Manuel, Upham, John, Sukkar, Maria, Phipps, Simon, Arikkatt, Jaisy, Ullah, Md, Short, Kirsty, Zhang, Vivian, Gan, Wan Jun, Loh, Zhixuan (Ken), Werder, Rhiannon, Simpson, Jennifer, Sly, Peter, Mazzone, Stuart, Spann, Kirsten, Ferreira, Manuel, Upham, John, Sukkar, Maria, and Phipps, Simon

Abstract

Asthma is a chronic inflammatory disease. Although many patients with asthma develop type-2 dominated eosinophilic inflammation, a number of individuals develop paucigranulocytic asthma, which occurs in the absence of eosinophilia or neutrophilia. The aetiology of paucigranulocytic asthma is unknown. However, both respiratory syncytial virus (RSV) infection and mutations in the receptor for advanced glycation endproducts (RAGE) are risk factors for asthma development. Here, we show that RAGE deficiency impairs anti-viral immunity during an early-life infection with pneumonia virus of mice (PVM; a murine analogue of RSV). The elevated viral load was associated with the release of high mobility group box-1 (HMGB1) which triggered airway smooth muscle remodelling in early-life. Re-infection with PVM in later-life induced many of the cardinal features of asthma in the absence of eosinophilic or neutrophilic inflammation. Anti-HMGB1 mitigated both early-life viral disease and asthma-like features, highlighting HMGB1 as a possible novel therapeutic target.

Published
2017

167. Allergen-encoding bone marrow transfer inactivates allergic T cell responses, alleviating airway inflammation

Author

Al Kouba, Jane, Wilkinson, Andrew, Starkey, Malcolm, Rudraraju, Rajeev, Werder, Rhiannon, Liu, Xiao, Law, Soi-Cheng, Horvat, Jay, Brooks, Jeremy, Hill, Geoffrey, Davies, Janet, Phipps, Simon, Hansbro, Philip, Steptoe, Raymond, Al Kouba, Jane, Wilkinson, Andrew, Starkey, Malcolm, Rudraraju, Rajeev, Werder, Rhiannon, Liu, Xiao, Law, Soi-Cheng, Horvat, Jay, Brooks, Jeremy, Hill, Geoffrey, Davies, Janet, Phipps, Simon, Hansbro, Philip, and Steptoe, Raymond

Abstract

This article is free to read on the publishers website Memory Th2 cell responses underlie the development and perpetuation of allergic diseases. Because these states result from immune dysregulation, established Th2 cell responses represent a significant challenge for conventional immunotherapies. New approaches that overcome the detrimental effects of immune dysregulation are required. We tested whether memory Th2 cell responses were silenced using a therapeutic approach where allergen expression in DCs is transferred to sensitized recipients using BM cells as a vector for therapeutic gene transfer. Development of allergen-specific Th2 responses and allergen-induced airway inflammation was blocked by expression of allergen in DCs. Adoptive transfer studies showed that Th2 responses were inactivated by a combination of deletion and induction of T cell unresponsiveness. Transfer of BM encoding allergen expression targeted to DCs terminated, in an allergen-specific manner, Th2 responses in sensitized recipients. Importantly, when preexisting airway inflammation was present, there was effective silencing of Th2 cell responses, airway inflammation was alleviated, and airway hyperreactivity was reversed. The effectiveness of DC-targeted allergen expression to terminate established Th2 responses in sensitized animals indicates that exploiting cell-intrinsic T cell tolerance pathways could lead to development of highly effective immunotherapies.

Published
2017

168. Human metapneumovirus impairs apoptosis of nasal epithelial cells in asthma via HSP70

Author

Baturcam, Engin, Snape, Natale, Yeo, Tiong Han, Schagen, Johanna, Thomas, Emma, Logan, Jayden, Galbraith, Sally, Collinson, Natasha, Phipps, Simon, Fantino, Emmanuelle, Sly, Peter, Spann, Kirsten, Baturcam, Engin, Snape, Natale, Yeo, Tiong Han, Schagen, Johanna, Thomas, Emma, Logan, Jayden, Galbraith, Sally, Collinson, Natasha, Phipps, Simon, Fantino, Emmanuelle, Sly, Peter, and Spann, Kirsten

Abstract

Asthmatics are highly susceptible to respiratory viral infections, possibly due to impaired innate immunity. However, the exact mechanisms of susceptibility are likely to differ amongst viruses. Therefore, we infected primary nasal epithelial cells (NECs) from adults with mild-to-moderate asthma, with respiratory syncytial virus (RSV) or human metapneumovirus (hMPV) in vitro and investigated the antiviral response. NECs from these asthmatics supported elevated hMPV but not RSV infection, compared to non-asthmatic controls. This correlated with reduced apoptosis and reduced activation of caspase-9 and caspase-3/7 in response to hMPV, but not RSV. The expression of heat shock protein 70 (HSP70), a known inhibitor of caspase activation and subsequent apoptosis, was amplified in response to hMPV infection. Chemical inhibition of HSP70 function restored caspase activation and reduced hMPV infection in NECs from asthmatic subjects. There was no impairment in the production of IFN by NECs from asthmatics in response to either hMPV or RSV, demonstrating that increased infection of asthmatic airway cells by hMPV is IFN-independent. This study demonstrates, for the first time, a mechanism for elevated hMPV infection in airway epithelial cells from adult asthmatics and identifies HSP70 as a potential target for antiviral and asthma therapies.

Published
2017

169. Little Suse wakes up, Linux shakes up

Author

Phipps, Simon

Subjects
Linux (Operating system), Linux (Operating system), Computers and office automation industries
Abstract

Byline: Simon Phipps Thursday saw the start of the next phase of life for Suse Linux with completion of the merger of its owner into the British company Micro Focus. [...]

Published
2014

170. Twitter emoji: 5 lessons for effective open source

Author

Phipps, Simon

Subjects
Computers and office automation industries
Abstract

Byline: Simon Phipps It may not seem like serious business to you, but for Twitter and other social media companies, emoji -- the cute icons that texters include in their [...]

Published
2014

171. Suse jumps into software-defined storage

Author

Phipps, Simon

Subjects
Linux (Operating system), Linux (Operating system), Computers and office automation industries
Abstract

Byline: Simon Phipps At the SuseCon conference in Orlando, Linux distributor Suse today announced it's jumping into software-defined storage. Currently at the beta test stage, Suse Storage is a self-healing, [...]

Published
2014

172. Microsoft must finish the job of opening .Net

Author

Phipps, Simon

Subjects
Operating systems (Software), 64-bit operating system, 32-bit operating system, Operating system, Computers and office automation industries
Abstract

Byline: Simon Phipps As you will have read elsewhere, Microsoft has announced that much of .Net will become open source, hosted at the .Net Foundation. It has also announced it [...]

Published
2014

173. Why all software needs a license

Author

Phipps, Simon

Subjects
Copyrights, Patent/copyright issue, Computers and office automation industries
Abstract

Byline: Simon Phipps If you want your code to be open source, it needs an OSI-approved copyright license. Code with no license to the copyright isn't open source. That may [...]

Published
2014

174. Joyent open-sources its core technology

Author

Phipps, Simon

Subjects
Computers and office automation industries
Abstract

Byline: Simon Phipps Not all the action is happening at the OpenStack Summit in Paris. In a bold move, cloud specialist Joyent has announced it's open-sourcing its core technology. That [...]

Published
2014

175. Microsoft 'loves' Linux? Then stop attacking open source

Author

Phipps, Simon

Subjects
Linux (Operating system), Middleware, Linux (Operating system), Middleware, Database middleware, Computers and office automation industries
Abstract

Byline: Simon Phipps According to Satya Nadella, Microsoft loves Linux. He said as much, complete with pictures -- and his team backs him up. In itself, it's a remarkable statement. [...]

Published
2014

176. Patent trolls have one fewer legal loophole to hide behind

Author

Phipps, Simon

Subjects
Computers and office automation industries
Abstract

Byline: Simon Phipps The war on (some) trolls continues unabated. This week, author and activist Cory Doctorow spotted a subtle rule change that could make patent trolls' lives really difficult. [...]

Published
2014

177. What Google's petition to the Supreme Court really means

Author

Phipps, Simon

Subjects
Copyright infringement, Copyrights, Open source software, Patent/copyright issue, Open source software, Computers and office automation industries
Abstract

Byline: Simon Phipps In a move that could have significant long-term consequences for open source software, Google applied to the U.S. Supreme Court (SCOTUS) for a writ of certiorari -- [...]

Published
2014

178. As patent trolls fade, a group formed to combat them thrives

Author

Phipps, Simon

Subjects
Patents, Patent law, Patent/copyright issue, Computers and office automation industries
Abstract

Byline: Simon Phipps Remember the Open Invention Network (OIN)? That's the defensive software patent community set up to protect Linux against patent aggressors. Well, it recently passed 1,000 members, growing [...]

Published
2014

179. LibreOffice's superlow defect rate puts proprietary software to shame

Author

Phipps, Simon

Subjects
Software industry, Computers and office automation industries
Abstract

Byline: Simon Phipps For old-timers, the venerable OpenOffice.org codebase comes with a folk-memory of instability and resource greed. But the LibreOffice project -- founded four years ago this weekend -- [...]

Published
2014

180. Alice is killing the trolls -- but expect patent lawyers to strike back

Author

Phipps, Simon

Subjects
Lawyers, Open source software, Software industry -- Intellectual property, Open source software, Computers and office automation industries
Abstract

Byline: Simon Phipps Open source software developers rejoice: Alice Corp. v CLS Bank is fast becoming a landmark decision for patent cases in the United States. The Court of Appeals [...]

Published
2014

181. No, Citrix did not kill CloudStack

Author

Phipps, Simon

Subjects
Computers and office automation industries
Abstract

Byline: Simon Phipps Much ink has been spilled about the recent Citrix shakeup around its CloudStack business, calling into question the long-term health of the Apache IaaS project. From the [...]

Published
2014

182. LibreOffice cash-for-code strategy tests open source ethic

Author

Phipps, Simon

Subjects
Charitable foundations, Computers and office automation industries
Abstract

Byline: Simon Phipps The Document Foundation's tender for the development of an Android implementation of LibreOffice begs serious questions, namely: Can an influx of cash into open source code creation [...]

Published
2014

183. Nude photos, phone records, NSA data offer essential lessons for admins

Author

Phipps, Simon

Subjects
Computer crimes, Privacy, Privacy issue, Computer crime, Computers and office automation industries
Abstract

Byline: Simon Phipps As you've heard many times by now, someone with no life or ethics appears to have hacked into numerous celebrity accounts on Apple's iCloud service and copied [...]

Published
2014

184. Gene-based analysis of regulatory variants identifies four putative novel asthma risk genes related to nucleotide synthesis and signaling

Author

Ferreira, Manuel A.R., Jansen, Rick, Willemsen, Gonneke, Penninx, Brenda, Bain, Lisa M, Vicente, Cristina T, Revez, Joana A, Matheson, Melanie C., Hui, Jennie, Tung, Joyce Y., Baltic, Svetlana, Le Souëf, Peter, Montgomery, Grant W., Martin, Nicholas G., Robertson, Colin F., James, Alan, Thompson, Philip J., Boomsma, Dorret I., Hopper, John L., Hinds, David A., Werder, Rhiannon B., and Phipps, Simon

Subjects
Nucleotides, Receptors, Purinergic P2, Quantitative Trait Loci, Genetic Variation, Mitochondrial Proton-Translocating ATPases, Article, Asthma, Mice, Inbred C57BL, Mice, Receptors, Purinergic P2Y, Animals, Humans, Genetic Predisposition to Disease, Software, Genome-Wide Association Study
Abstract

Hundreds of genetic variants are thought to contribute to variation in asthma risk by modulating gene expression. Methods that increase the power of genome-wide association studies (GWASs) to identify risk-associated variants are needed.We sought to develop a method that aggregates the evidence for association with disease risk across expression quantitative trait loci (eQTLs) of a gene and use this approach to identify asthma risk genes.We developed a gene-based test and software package called EUGENE that (1) is applicable to GWAS summary statistics; (2) considers both cis- and trans-eQTLs; (3) incorporates eQTLs identified in different tissues; and (4) uses simulations to account for multiple testing. We applied this approach to 2 published asthma GWASs (combined n = 46,044) and used mouse studies to provide initial functional insights into 2 genes with novel genetic associations.We tested the association between asthma and 17,190 genes that were found to have cis- and/or trans-eQTLs across 16 published eQTL studies. At an empirical FDR of 5%, 48 genes were associated with asthma risk. Of these, for 37, the association was driven by eQTLs located in established risk loci for allergic disease, including 6 genes not previously implicated in disease cause (eg, LIMS1, TINF2, and SAFB). The remaining 11 significant genes represent potential novel genetic associations with asthma. The association with 4 of these replicated in an independent GWAS: B4GALT3, USMG5, P2RY13, and P2RY14, which are genes involved in nucleotide synthesis or nucleotide-dependent cell activation. In mouse studies, P2ry13 and P2ry14-purinergic receptors activated by adenosine 5-diphosphate and UDP-sugars, respectively-were upregulated after allergen challenge, notably in airway epithelial cells, eosinophils, and neutrophils. Intranasal exposure with receptor agonists induced the release of IL-33 and subsequent eosinophil infiltration into the lungs.We identified novel associations between asthma and eQTLs for 4 genes related to nucleotide synthesis/signaling and demonstrated the power of gene-based analyses of GWASs.

Published
2016

188. Allergen-encoding bone marrow transfer inactivates allergic T cell responses, alleviating airway inflammation

Author

AL-Kouba, Jane, primary, Wilkinson, Andrew N., additional, Starkey, Malcolm R., additional, Rudraraju, Rajeev, additional, Werder, Rhiannon B., additional, Liu, Xiao, additional, Law, Soi-Cheng, additional, Horvat, Jay C., additional, Brooks, Jeremy F., additional, Hill, Geoffrey R., additional, Davies, Janet M., additional, Phipps, Simon, additional, Hansbro, Philip M., additional, and Steptoe, Raymond J., additional

Published
2017
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192. MP62-16 SHOCK WAVE LITHOTRIPSY IS EFFICACIOUS FOR TREATING OBESE PATIENTS WITH UPPER URETERIC CALCULI : 5 YEAR PROSPECTIVE OUTCOMES FROM A DEDICATED CENTRE TREATING PATIENTS WITH A SKIN-TO-STONE DISTANCE OF MORE THAN 14CM

Author

Gietzmann, William KM, primary, Sharma, Abishek, additional, Mains, Edward, additional, El-Mokadem, ismail, additional, Thomas, Ben G, additional, Phipps, Simon, additional, Tolley, David A, additional, and Cutress, Mark L, additional

Published
2017
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193. Gene-based analysis of regulatory variants identifies 4 putative novel asthma risk genes related to nucleotide synthesis and signaling

Author

Ferreira, Manuel A.R., primary, Jansen, Rick, additional, Willemsen, Gonneke, additional, Penninx, Brenda, additional, Bain, Lisa M., additional, Vicente, Cristina T., additional, Revez, Joana A., additional, Matheson, Melanie C., additional, Hui, Jennie, additional, Tung, Joyce Y., additional, Baltic, Svetlana, additional, Le Souëf, Peter, additional, Montgomery, Grant W., additional, Martin, Nicholas G., additional, Robertson, Colin F., additional, James, Alan, additional, Thompson, Philip J., additional, Boomsma, Dorret I., additional, Hopper, John L., additional, Hinds, David A., additional, Werder, Rhiannon B., additional, and Phipps, Simon, additional

Published
2017
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195. RAGE deficiency predisposes mice to virus-induced paucigranulocytic asthma

Author

Arikkatt, Jaisy, primary, Ullah, Md Ashik, additional, Short, Kirsty Renfree, additional, Zhang, Vivan, additional, Gan, Wan Jun, additional, Loh, Zhixuan, additional, Werder, Rhiannon B, additional, Simpson, Jennifer, additional, Sly, Peter D, additional, Mazzone, Stuart B, additional, Spann, Kirsten M, additional, Ferreira, Manuel AR, additional, Upham, John W, additional, Sukkar, Maria B, additional, and Phipps, Simon, additional

Published
2017
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197. Author response: RAGE deficiency predisposes mice to virus-induced paucigranulocytic asthma

Author

Arikkatt, Jaisy, primary, Ullah, Md Ashik, additional, Short, Kirsty Renfree, additional, Zhang, Vivan, additional, Gan, Wan Jun, additional, Loh, Zhixuan, additional, Werder, Rhiannon B, additional, Simpson, Jennifer, additional, Sly, Peter D, additional, Mazzone, Stuart B, additional, Spann, Kirsten M, additional, Ferreira, Manuel AR, additional, Upham, John W, additional, Sukkar, Maria B, additional, and Phipps, Simon, additional

Published
2016
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198. Performing Englishness

Author

Winter, Trish and Keegan-Phipps, Simon

Subjects
sub_mediaandculturalstudies
Published
2015

199. Software Freedom Means Business Value

Author

Phipps, Simon

Subjects
Information Technology
Abstract

At a time when open source has "won", when the majority of businesses are using and even planning to contribute to open source and when corporate trade associations are racing to start new "foundations" (actually trade associations) as they did a decade ago with standards bodies, it is more important than ever to return to the principle of software freedom. That doesn't mean preferring ideology over business effectiveness. I'll be explaining why. Simon Phipps

Published
2015
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200. A maternal high-fat diet predisposes to infant lung disease via increased neutrophil-mediated IL-6 trans-signaling

Author

Curren, Bodie, Ahmed, Tufael, Rashid, Ridwan B., Sebina, Ismail, Al Amin Sikder, Md., Howard, Daniel R., Alorro, Mariah, Ullah, Md. Ashik, Bissell, Alec, Rahman, Muhammed Mahfuzur, Pearen, Michael A., Ramm, Grant A., Varelias, Antiopi, Rose-John, Stefan, MacDonald, Kelli P.A., Hoelzle, Robert, Cuív, Páraic Ó., Spann, Kirsten M., Dennis, Paul G., and Phipps, Simon

Abstract

Poor maternal diet during pregnancy predisposes to severe lower respiratory tract infections (sLRI) in infancy, which in turn, increases childhood asthma risk, however the underlying mechanisms remain poorly understood. Here, we show that the offspring of high fat diet (HFD)-fed mothers (‘HFD-reared pups’) developed a sLRI following pneumovirus inoculation in early-life and subsequent asthma in later-life upon allergen exposure. Prior to infection, HFD-reared pups developed microbial dysbiosis and low-grade systemic inflammation (LGSI), characterized by hyper-neutropoiesis in the liver and elevated inflammatory cytokine expression, most notably G-CSF, IL-17A, IL-6 and sIL-6R (indicative of IL-6 trans-signaling) in the circulation and multiple organs, but most prominently the liver. Inhibition of IL-6 trans-signaling, using sgp130Fc transgenic mice or via specific genetic deletion of IL-6Ra on neutrophils, conferred protection against both diseases. Taken together, our findings suggest that a maternal HFD induces neonatal LGSI that predisposes to sLRI and subsequent asthma via neutrophil-mediated IL-6 trans-signaling.

Published
2024
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