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34 results on '"Thompson, Philip J."'

1. Characterisation of the Australian Adult Population Living with Asthma: Severe - Exacerbation Frequency, Long-Term OCS Use and Adverse Effects

Author: Hancock,Kerry L, Bosnic-Anticevich,Sinthia, Blakey,John D, Hew,Mark, Chung,Li Ping, Cvetkovski,Biljana, Claxton,Scott, Del Fante,Peter, Denton,Eve, Doan,Joe, Ranasinghe,Kanchanamala, Morgan,Lucy, Sharma,Anita, Smith,Peter K, Stewart,Deb, Thompson,Philip J, Wiseman,Russell, Upham,John W, Yan,Kwok Y, Carter,Victoria, Dhillon,Kiranjeet, Heraud,Florian, Le,Thao, Vella,Rebecca, Price,David, Hancock,Kerry L, Bosnic-Anticevich,Sinthia, Blakey,John D, Hew,Mark, Chung,Li Ping, Cvetkovski,Biljana, Claxton,Scott, Del Fante,Peter, Denton,Eve, Doan,Joe, Ranasinghe,Kanchanamala, Morgan,Lucy, Sharma,Anita, Smith,Peter K, Stewart,Deb, Thompson,Philip J, Wiseman,Russell, Upham,John W, Yan,Kwok Y, Carter,Victoria, Dhillon,Kiranjeet, Heraud,Florian, Le,Thao, Vella,Rebecca, and Price,David
Abstract: Kerry L Hancock,1 Sinthia Bosnic-Anticevich,2â 4 John D Blakey,5,6 Mark Hew,7,8 Li Ping Chung,9 Biljana Cvetkovski,3 Scott Claxton,10 Peter Del Fante,11 Eve Denton,7,8 Joe Doan,12 Kanchanamala Ranasinghe,13,14 Lucy Morgan,15â 17 Anita Sharma,18 Peter K Smith,19 Deb Stewart,20 Philip J Thompson,21â 23 Russell Wiseman,24 John W Upham,25 Kwok Y Yan,26 Victoria Carter,27 Kiranjeet Dhillon,28 Florian Heraud,28 Thao Le,27 Rebecca Vella,28 David Price27â 30 On behalf of the OPCA Improving Asthma outcomes in Australia Research Group1Chandlers Hill Surgery, Happy Valley, SA, 5159, Australia; 2Sydney Pharmacy School, Faculty of Medicine and Health, The University of Sydney, Sydney, NSW, 2006, Australia; 3Woolcock Institute of Medical Research, Glebe, MSW, 2037, Australia; 4Sydney Local Health District, Camperdown, NSW, 2050, Australia; 5Respiratory Medicine, Sir Charles Gairdner Hospital, Hospital Ave, Nedlands, WA, 6009, Australia; 6Curtin University Medical School, Bentley, Western Australia, 6102, Australia; 7Allergy, Asthma & Clinical Immunology, Alfred Health, Melbourne, VIC, 3004, Australia; 8Public Health and Preventive Medicine, Monash University, Victoria, 3800, Australia; 9Fiona Stanley Hospital, 11 Robin Warren Dr, Murdoch, WA, 6150, Australia; 10Genesis Care Sleep and Respiratory, Joondalup, WA, 6027, Australia; 11Hutt Street General Practice, Adelaide, SA, 5000, Australia; 12HealthPlus Medical Centre, Kogarah, NSW, 2217, Australia; 13School of Medicine, Griffith University, Nathan, QLD, Australia; 14Cannon Hill Family Doctors, Cannon Hill, QLD, 4170, Australia; 15Sydney Medical School, University of Sydney, Sydney, NSW, Australia; 16Department of Thoracic Medicine, Concord Hospital, Sydney, NSW, Australia; 17Australian School of Advanced Medicine, Macquarie University, Sydney, NSW, Australia; 18Platinum Medical Centre, Chermside, QLD, 4032, Australia; 19Griffith University, Southport, QLD, Australia; 20Adjunct Lecturer, School of Medicine, University
Published: 2022

2. Multiancestry association study identifies new asthma risk loci that colocalize with immune-cell enhancer marks

Author: Demenais, Florence, Margaritte-Jeannin, Patricia, Barnes, Kathleen C., Cookson, William O. C., Altmueller, Janine, Ang, Wei, Barr, R. Graham, Beaty, Terri H., Becker, Allan B., Beilby, John, Bisgaard, Hans, Bjornsdottir, Unnur Steina, Bleecker, Eugene, Bonnelykke, Klaus, Boomsma, Dorret I., Bouzigon, Emmanuelle, Brightling, Christopher E., Brossard, Myriam, Brusselle, Guy G., Burchard, Esteban, Burkart, Kristin M., Bush, Andrew, Chan-Yeung, Moira, Chung, Kian Fan, Alves, Alexessander Couto, Curtin, John A., Custovic, Adnan, Daley, Denise, de Jongste, Johan C., Del-Rio-Navarro, Blanca E., Donohue, Kathleen M., Duijts, Liesbeth, Eng, Celeste, Eriksson, Johan G., Farrall, Martin, Fedorova, Yuliya, Feenstra, Bjarke, Ferreira, Manuel A., Freidin, Maxim B., Gajdos, Zofia, Gauderman, Jim, Gehring, Ulrike, Geller, Frank, Genuneit, Jon, Gharib, Sina A., Gilliland, Frank, Granell, Raquel, Graves, Penelope E., Gudbjartsson, Daniel F., Haahtela, Tari, Heckbert, Susan R., Heederik, Dick, Heinrich, Joachim, Heliovaara, Markku, Henderson, John, Himes, Blanca E., Hirose, Hiroshi, Hirschhorn, Joel N., Hofman, Albert, Holt, Patrick, Hottenga, Jouke, Hudson, Thomas J., Hui, Jennie, Imboden, Medea, Ivanov, Vladimir, Jaddoe, Vincent W. V., James, Alan, Janson, Christer, Jarvelin, Marjo-Riitta, Jarvis, Deborah, Jones, Graham, Jonsdottir, Ingileif, Jousilahti, Pekka, Kabesch, Michael, Kahonen, Mika, Kantor, David B., Karunas, Alexandra S., Khusnutdinova, Elza, Koppelman, Gerard H., Kozyrskyj, Anita L., Kreiner, Eskil, Kubo, Michiaki, Kumar, Rajesh, Kumar, Ashish, Kuokkanen, Mikko, Lahousse, Lies, Laitinen, Tarja, Laprise, Catherine, Lathrop, Mark, Lau, Susanne, Lee, Young-Ae, Lehtimaki, Terho, Letort, Sebastien, Levin, Albert M., Li, Guo, Liang, Liming, Loehr, Laura R., London, Stephanie J., Loth, Daan W., Manichaikul, Ani, Marenholz, Ingo, Martinez, Fernando J., Matheson, Melanie C., Mathias, Rasika A., Matsumoto, Kenji, Mbarek, Hamdi, McArdle, Wendy L., Melbye, Mads, Melen, Erik, Meyers, Deborah, Michel, Sven, Mohamdi, Hamida, Musk, Arthur W., Myers, Rachel A., Nieuwenhuis, Maartje A. E., Noguchi, Emiko, O'Connor, George T., Ogorodova, Ludmila M., Palmer, Cameron D., Palotie, Aarno, Park, Julie E., Pennell, Craig E., Pershagen, Goran, Polonikov, Alexey, Postma, Dirkje S., Probst-Hensch, Nicole, Puzyrev, Valery P., Raby, Benjamin A., Raitakari, Olli T., Ramasamy, Adaikalavan, Rich, Stephen S., Robertson, Colin F., Romieu, Isabelle, Salam, Muhammad T., Salomaa, Veikko, Schlunssen, Vivi, Scott, Robert, Selivanova, Polina A., Sigsgaard, Torben, Simpson, Angela, Siroux, Valerie, Smith, Lewis J., Solodilova, Maria, Standl, Marie, Stefansson, Kari, Strachan, David P., Stricker, Bruno H., Takahashi, Atsushi, Thompson, Philip J., Thorleifsson, Gudmar, Thorsteinsdottir, Unnur, Tiesler, Carla M. T., Torgerson, Dara G., Tsunoda, Tatsuhiko, Uitterlinden, Andre G., van der Valk, Ralf J. P., Vaysse, Amaury, Vedantam, Sailaja, von Berg, Andrea, von Mutius, Erika, Vonk, Judith M., Waage, Johannes, Wareham, Nick J., Weiss, Scott T., White, Wendy B., Wickman, Magnus, Widen, Elisabeth, Willemsen, Gonneke, Williams, L. Keoki, Wouters, Inge M., Yang, James J., Zhao, Jing Hua, Moffatt, Miriam F., Ober, Carole, Nicolae, Dan L., Demenais, Florence, Margaritte-Jeannin, Patricia, Barnes, Kathleen C., Cookson, William O. C., Altmueller, Janine, Ang, Wei, Barr, R. Graham, Beaty, Terri H., Becker, Allan B., Beilby, John, Bisgaard, Hans, Bjornsdottir, Unnur Steina, Bleecker, Eugene, Bonnelykke, Klaus, Boomsma, Dorret I., Bouzigon, Emmanuelle, Brightling, Christopher E., Brossard, Myriam, Brusselle, Guy G., Burchard, Esteban, Burkart, Kristin M., Bush, Andrew, Chan-Yeung, Moira, Chung, Kian Fan, Alves, Alexessander Couto, Curtin, John A., Custovic, Adnan, Daley, Denise, de Jongste, Johan C., Del-Rio-Navarro, Blanca E., Donohue, Kathleen M., Duijts, Liesbeth, Eng, Celeste, Eriksson, Johan G., Farrall, Martin, Fedorova, Yuliya, Feenstra, Bjarke, Ferreira, Manuel A., Freidin, Maxim B., Gajdos, Zofia, Gauderman, Jim, Gehring, Ulrike, Geller, Frank, Genuneit, Jon, Gharib, Sina A., Gilliland, Frank, Granell, Raquel, Graves, Penelope E., Gudbjartsson, Daniel F., Haahtela, Tari, Heckbert, Susan R., Heederik, Dick, Heinrich, Joachim, Heliovaara, Markku, Henderson, John, Himes, Blanca E., Hirose, Hiroshi, Hirschhorn, Joel N., Hofman, Albert, Holt, Patrick, Hottenga, Jouke, Hudson, Thomas J., Hui, Jennie, Imboden, Medea, Ivanov, Vladimir, Jaddoe, Vincent W. V., James, Alan, Janson, Christer, Jarvelin, Marjo-Riitta, Jarvis, Deborah, Jones, Graham, Jonsdottir, Ingileif, Jousilahti, Pekka, Kabesch, Michael, Kahonen, Mika, Kantor, David B., Karunas, Alexandra S., Khusnutdinova, Elza, Koppelman, Gerard H., Kozyrskyj, Anita L., Kreiner, Eskil, Kubo, Michiaki, Kumar, Rajesh, Kumar, Ashish, Kuokkanen, Mikko, Lahousse, Lies, Laitinen, Tarja, Laprise, Catherine, Lathrop, Mark, Lau, Susanne, Lee, Young-Ae, Lehtimaki, Terho, Letort, Sebastien, Levin, Albert M., Li, Guo, Liang, Liming, Loehr, Laura R., London, Stephanie J., Loth, Daan W., Manichaikul, Ani, Marenholz, Ingo, Martinez, Fernando J., Matheson, Melanie C., Mathias, Rasika A., Matsumoto, Kenji, Mbarek, Hamdi, McArdle, Wendy L., Melbye, Mads, Melen, Erik, Meyers, Deborah, Michel, Sven, Mohamdi, Hamida, Musk, Arthur W., Myers, Rachel A., Nieuwenhuis, Maartje A. E., Noguchi, Emiko, O'Connor, George T., Ogorodova, Ludmila M., Palmer, Cameron D., Palotie, Aarno, Park, Julie E., Pennell, Craig E., Pershagen, Goran, Polonikov, Alexey, Postma, Dirkje S., Probst-Hensch, Nicole, Puzyrev, Valery P., Raby, Benjamin A., Raitakari, Olli T., Ramasamy, Adaikalavan, Rich, Stephen S., Robertson, Colin F., Romieu, Isabelle, Salam, Muhammad T., Salomaa, Veikko, Schlunssen, Vivi, Scott, Robert, Selivanova, Polina A., Sigsgaard, Torben, Simpson, Angela, Siroux, Valerie, Smith, Lewis J., Solodilova, Maria, Standl, Marie, Stefansson, Kari, Strachan, David P., Stricker, Bruno H., Takahashi, Atsushi, Thompson, Philip J., Thorleifsson, Gudmar, Thorsteinsdottir, Unnur, Tiesler, Carla M. T., Torgerson, Dara G., Tsunoda, Tatsuhiko, Uitterlinden, Andre G., van der Valk, Ralf J. P., Vaysse, Amaury, Vedantam, Sailaja, von Berg, Andrea, von Mutius, Erika, Vonk, Judith M., Waage, Johannes, Wareham, Nick J., Weiss, Scott T., White, Wendy B., Wickman, Magnus, Widen, Elisabeth, Willemsen, Gonneke, Williams, L. Keoki, Wouters, Inge M., Yang, James J., Zhao, Jing Hua, Moffatt, Miriam F., Ober, Carole, and Nicolae, Dan L.
Abstract: We examined common variation in asthma risk by conducting a meta-analysis of worldwide asthma genome-wide association studies (23,948 asthma cases, 118,538 controls) of individuals from ethnically diverse populations. We identified five new asthma loci, found two new associations at two known asthma loci, established asthma associations at two loci previously implicated in the comorbidity of asthma plus hay fever, and confirmed nine known loci. Investigation of pleiotropy showed large overlaps in genetic variants with autoimmune and inflammatory diseases. The enrichment in enhancer marks at asthma risk loci, especially in immune cells, suggested a major role of these loci in the regulation of immunologically related mechanisms.
Published: 2018
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3. Multiancestry association study identifies new asthma risk loci that colocalize with immune-cell enhancer marks

Author: Demenais, Florence, Margaritte-Jeannin, Patricia, Barnes, Kathleen C., Cookson, William O. C., Altmueller, Janine, Ang, Wei, Barr, R. Graham, Beaty, Terri H., Becker, Allan B., Beilby, John, Bisgaard, Hans, Bjornsdottir, Unnur Steina, Bleecker, Eugene, Bonnelykke, Klaus, Boomsma, Dorret I., Bouzigon, Emmanuelle, Brightling, Christopher E., Brossard, Myriam, Brusselle, Guy G., Burchard, Esteban, Burkart, Kristin M., Bush, Andrew, Chan-Yeung, Moira, Chung, Kian Fan, Alves, Alexessander Couto, Curtin, John A., Custovic, Adnan, Daley, Denise, de Jongste, Johan C., Del-Rio-Navarro, Blanca E., Donohue, Kathleen M., Duijts, Liesbeth, Eng, Celeste, Eriksson, Johan G., Farrall, Martin, Fedorova, Yuliya, Feenstra, Bjarke, Ferreira, Manuel A., Freidin, Maxim B., Gajdos, Zofia, Gauderman, Jim, Gehring, Ulrike, Geller, Frank, Genuneit, Jon, Gharib, Sina A., Gilliland, Frank, Granell, Raquel, Graves, Penelope E., Gudbjartsson, Daniel F., Haahtela, Tari, Heckbert, Susan R., Heederik, Dick, Heinrich, Joachim, Heliovaara, Markku, Henderson, John, Himes, Blanca E., Hirose, Hiroshi, Hirschhorn, Joel N., Hofman, Albert, Holt, Patrick, Hottenga, Jouke, Hudson, Thomas J., Hui, Jennie, Imboden, Medea, Ivanov, Vladimir, Jaddoe, Vincent W. V., James, Alan, Janson, Christer, Jarvelin, Marjo-Riitta, Jarvis, Deborah, Jones, Graham, Jonsdottir, Ingileif, Jousilahti, Pekka, Kabesch, Michael, Kahonen, Mika, Kantor, David B., Karunas, Alexandra S., Khusnutdinova, Elza, Koppelman, Gerard H., Kozyrskyj, Anita L., Kreiner, Eskil, Kubo, Michiaki, Kumar, Rajesh, Kumar, Ashish, Kuokkanen, Mikko, Lahousse, Lies, Laitinen, Tarja, Laprise, Catherine, Lathrop, Mark, Lau, Susanne, Lee, Young-Ae, Lehtimaki, Terho, Letort, Sebastien, Levin, Albert M., Li, Guo, Liang, Liming, Loehr, Laura R., London, Stephanie J., Loth, Daan W., Manichaikul, Ani, Marenholz, Ingo, Martinez, Fernando J., Matheson, Melanie C., Mathias, Rasika A., Matsumoto, Kenji, Mbarek, Hamdi, McArdle, Wendy L., Melbye, Mads, Melen, Erik, Meyers, Deborah, Michel, Sven, Mohamdi, Hamida, Musk, Arthur W., Myers, Rachel A., Nieuwenhuis, Maartje A. E., Noguchi, Emiko, O'Connor, George T., Ogorodova, Ludmila M., Palmer, Cameron D., Palotie, Aarno, Park, Julie E., Pennell, Craig E., Pershagen, Goran, Polonikov, Alexey, Postma, Dirkje S., Probst-Hensch, Nicole, Puzyrev, Valery P., Raby, Benjamin A., Raitakari, Olli T., Ramasamy, Adaikalavan, Rich, Stephen S., Robertson, Colin F., Romieu, Isabelle, Salam, Muhammad T., Salomaa, Veikko, Schlunssen, Vivi, Scott, Robert, Selivanova, Polina A., Sigsgaard, Torben, Simpson, Angela, Siroux, Valerie, Smith, Lewis J., Solodilova, Maria, Standl, Marie, Stefansson, Kari, Strachan, David P., Stricker, Bruno H., Takahashi, Atsushi, Thompson, Philip J., Thorleifsson, Gudmar, Thorsteinsdottir, Unnur, Tiesler, Carla M. T., Torgerson, Dara G., Tsunoda, Tatsuhiko, Uitterlinden, Andre G., van der Valk, Ralf J. P., Vaysse, Amaury, Vedantam, Sailaja, von Berg, Andrea, von Mutius, Erika, Vonk, Judith M., Waage, Johannes, Wareham, Nick J., Weiss, Scott T., White, Wendy B., Wickman, Magnus, Widen, Elisabeth, Willemsen, Gonneke, Williams, L. Keoki, Wouters, Inge M., Yang, James J., Zhao, Jing Hua, Moffatt, Miriam F., Ober, Carole, Nicolae, Dan L., Demenais, Florence, Margaritte-Jeannin, Patricia, Barnes, Kathleen C., Cookson, William O. C., Altmueller, Janine, Ang, Wei, Barr, R. Graham, Beaty, Terri H., Becker, Allan B., Beilby, John, Bisgaard, Hans, Bjornsdottir, Unnur Steina, Bleecker, Eugene, Bonnelykke, Klaus, Boomsma, Dorret I., Bouzigon, Emmanuelle, Brightling, Christopher E., Brossard, Myriam, Brusselle, Guy G., Burchard, Esteban, Burkart, Kristin M., Bush, Andrew, Chan-Yeung, Moira, Chung, Kian Fan, Alves, Alexessander Couto, Curtin, John A., Custovic, Adnan, Daley, Denise, de Jongste, Johan C., Del-Rio-Navarro, Blanca E., Donohue, Kathleen M., Duijts, Liesbeth, Eng, Celeste, Eriksson, Johan G., Farrall, Martin, Fedorova, Yuliya, Feenstra, Bjarke, Ferreira, Manuel A., Freidin, Maxim B., Gajdos, Zofia, Gauderman, Jim, Gehring, Ulrike, Geller, Frank, Genuneit, Jon, Gharib, Sina A., Gilliland, Frank, Granell, Raquel, Graves, Penelope E., Gudbjartsson, Daniel F., Haahtela, Tari, Heckbert, Susan R., Heederik, Dick, Heinrich, Joachim, Heliovaara, Markku, Henderson, John, Himes, Blanca E., Hirose, Hiroshi, Hirschhorn, Joel N., Hofman, Albert, Holt, Patrick, Hottenga, Jouke, Hudson, Thomas J., Hui, Jennie, Imboden, Medea, Ivanov, Vladimir, Jaddoe, Vincent W. V., James, Alan, Janson, Christer, Jarvelin, Marjo-Riitta, Jarvis, Deborah, Jones, Graham, Jonsdottir, Ingileif, Jousilahti, Pekka, Kabesch, Michael, Kahonen, Mika, Kantor, David B., Karunas, Alexandra S., Khusnutdinova, Elza, Koppelman, Gerard H., Kozyrskyj, Anita L., Kreiner, Eskil, Kubo, Michiaki, Kumar, Rajesh, Kumar, Ashish, Kuokkanen, Mikko, Lahousse, Lies, Laitinen, Tarja, Laprise, Catherine, Lathrop, Mark, Lau, Susanne, Lee, Young-Ae, Lehtimaki, Terho, Letort, Sebastien, Levin, Albert M., Li, Guo, Liang, Liming, Loehr, Laura R., London, Stephanie J., Loth, Daan W., Manichaikul, Ani, Marenholz, Ingo, Martinez, Fernando J., Matheson, Melanie C., Mathias, Rasika A., Matsumoto, Kenji, Mbarek, Hamdi, McArdle, Wendy L., Melbye, Mads, Melen, Erik, Meyers, Deborah, Michel, Sven, Mohamdi, Hamida, Musk, Arthur W., Myers, Rachel A., Nieuwenhuis, Maartje A. E., Noguchi, Emiko, O'Connor, George T., Ogorodova, Ludmila M., Palmer, Cameron D., Palotie, Aarno, Park, Julie E., Pennell, Craig E., Pershagen, Goran, Polonikov, Alexey, Postma, Dirkje S., Probst-Hensch, Nicole, Puzyrev, Valery P., Raby, Benjamin A., Raitakari, Olli T., Ramasamy, Adaikalavan, Rich, Stephen S., Robertson, Colin F., Romieu, Isabelle, Salam, Muhammad T., Salomaa, Veikko, Schlunssen, Vivi, Scott, Robert, Selivanova, Polina A., Sigsgaard, Torben, Simpson, Angela, Siroux, Valerie, Smith, Lewis J., Solodilova, Maria, Standl, Marie, Stefansson, Kari, Strachan, David P., Stricker, Bruno H., Takahashi, Atsushi, Thompson, Philip J., Thorleifsson, Gudmar, Thorsteinsdottir, Unnur, Tiesler, Carla M. T., Torgerson, Dara G., Tsunoda, Tatsuhiko, Uitterlinden, Andre G., van der Valk, Ralf J. P., Vaysse, Amaury, Vedantam, Sailaja, von Berg, Andrea, von Mutius, Erika, Vonk, Judith M., Waage, Johannes, Wareham, Nick J., Weiss, Scott T., White, Wendy B., Wickman, Magnus, Widen, Elisabeth, Willemsen, Gonneke, Williams, L. Keoki, Wouters, Inge M., Yang, James J., Zhao, Jing Hua, Moffatt, Miriam F., Ober, Carole, and Nicolae, Dan L.
Abstract: We examined common variation in asthma risk by conducting a meta-analysis of worldwide asthma genome-wide association studies (23,948 asthma cases, 118,538 controls) of individuals from ethnically diverse populations. We identified five new asthma loci, found two new associations at two known asthma loci, established asthma associations at two loci previously implicated in the comorbidity of asthma plus hay fever, and confirmed nine known loci. Investigation of pleiotropy showed large overlaps in genetic variants with autoimmune and inflammatory diseases. The enrichment in enhancer marks at asthma risk loci, especially in immune cells, suggested a major role of these loci in the regulation of immunologically related mechanisms.
Published: 2018

4. Multiancestry association study identifies new asthma risk loci that colocalize with immune-cell enhancer marks

Author: Demenais, Florence, Margaritte-Jeannin, Patricia, Barnes, Kathleen C., Cookson, William O. C., Altmueller, Janine, Ang, Wei, Barr, R. Graham, Beaty, Terri H., Becker, Allan B., Beilby, John, Bisgaard, Hans, Bjornsdottir, Unnur Steina, Bleecker, Eugene, Bonnelykke, Klaus, Boomsma, Dorret I., Bouzigon, Emmanuelle, Brightling, Christopher E., Brossard, Myriam, Brusselle, Guy G., Burchard, Esteban, Burkart, Kristin M., Bush, Andrew, Chan-Yeung, Moira, Chung, Kian Fan, Alves, Alexessander Couto, Curtin, John A., Custovic, Adnan, Daley, Denise, de Jongste, Johan C., Del-Rio-Navarro, Blanca E., Donohue, Kathleen M., Duijts, Liesbeth, Eng, Celeste, Eriksson, Johan G., Farrall, Martin, Fedorova, Yuliya, Feenstra, Bjarke, Ferreira, Manuel A., Freidin, Maxim B., Gajdos, Zofia, Gauderman, Jim, Gehring, Ulrike, Geller, Frank, Genuneit, Jon, Gharib, Sina A., Gilliland, Frank, Granell, Raquel, Graves, Penelope E., Gudbjartsson, Daniel F., Haahtela, Tari, Heckbert, Susan R., Heederik, Dick, Heinrich, Joachim, Heliovaara, Markku, Henderson, John, Himes, Blanca E., Hirose, Hiroshi, Hirschhorn, Joel N., Hofman, Albert, Holt, Patrick, Hottenga, Jouke, Hudson, Thomas J., Hui, Jennie, Imboden, Medea, Ivanov, Vladimir, Jaddoe, Vincent W. V., James, Alan, Janson, Christer, Jarvelin, Marjo-Riitta, Jarvis, Deborah, Jones, Graham, Jonsdottir, Ingileif, Jousilahti, Pekka, Kabesch, Michael, Kahonen, Mika, Kantor, David B., Karunas, Alexandra S., Khusnutdinova, Elza, Koppelman, Gerard H., Kozyrskyj, Anita L., Kreiner, Eskil, Kubo, Michiaki, Kumar, Rajesh, Kumar, Ashish, Kuokkanen, Mikko, Lahousse, Lies, Laitinen, Tarja, Laprise, Catherine, Lathrop, Mark, Lau, Susanne, Lee, Young-Ae, Lehtimaki, Terho, Letort, Sebastien, Levin, Albert M., Li, Guo, Liang, Liming, Loehr, Laura R., London, Stephanie J., Loth, Daan W., Manichaikul, Ani, Marenholz, Ingo, Martinez, Fernando J., Matheson, Melanie C., Mathias, Rasika A., Matsumoto, Kenji, Mbarek, Hamdi, McArdle, Wendy L., Melbye, Mads, Melen, Erik, Meyers, Deborah, Michel, Sven, Mohamdi, Hamida, Musk, Arthur W., Myers, Rachel A., Nieuwenhuis, Maartje A. E., Noguchi, Emiko, O'Connor, George T., Ogorodova, Ludmila M., Palmer, Cameron D., Palotie, Aarno, Park, Julie E., Pennell, Craig E., Pershagen, Goran, Polonikov, Alexey, Postma, Dirkje S., Probst-Hensch, Nicole, Puzyrev, Valery P., Raby, Benjamin A., Raitakari, Olli T., Ramasamy, Adaikalavan, Rich, Stephen S., Robertson, Colin F., Romieu, Isabelle, Salam, Muhammad T., Salomaa, Veikko, Schlunssen, Vivi, Scott, Robert, Selivanova, Polina A., Sigsgaard, Torben, Simpson, Angela, Siroux, Valerie, Smith, Lewis J., Solodilova, Maria, Standl, Marie, Stefansson, Kari, Strachan, David P., Stricker, Bruno H., Takahashi, Atsushi, Thompson, Philip J., Thorleifsson, Gudmar, Thorsteinsdottir, Unnur, Tiesler, Carla M. T., Torgerson, Dara G., Tsunoda, Tatsuhiko, Uitterlinden, Andre G., van der Valk, Ralf J. P., Vaysse, Amaury, Vedantam, Sailaja, von Berg, Andrea, von Mutius, Erika, Vonk, Judith M., Waage, Johannes, Wareham, Nick J., Weiss, Scott T., White, Wendy B., Wickman, Magnus, Widen, Elisabeth, Willemsen, Gonneke, Williams, L. Keoki, Wouters, Inge M., Yang, James J., Zhao, Jing Hua, Moffatt, Miriam F., Ober, Carole, Nicolae, Dan L., Demenais, Florence, Margaritte-Jeannin, Patricia, Barnes, Kathleen C., Cookson, William O. C., Altmueller, Janine, Ang, Wei, Barr, R. Graham, Beaty, Terri H., Becker, Allan B., Beilby, John, Bisgaard, Hans, Bjornsdottir, Unnur Steina, Bleecker, Eugene, Bonnelykke, Klaus, Boomsma, Dorret I., Bouzigon, Emmanuelle, Brightling, Christopher E., Brossard, Myriam, Brusselle, Guy G., Burchard, Esteban, Burkart, Kristin M., Bush, Andrew, Chan-Yeung, Moira, Chung, Kian Fan, Alves, Alexessander Couto, Curtin, John A., Custovic, Adnan, Daley, Denise, de Jongste, Johan C., Del-Rio-Navarro, Blanca E., Donohue, Kathleen M., Duijts, Liesbeth, Eng, Celeste, Eriksson, Johan G., Farrall, Martin, Fedorova, Yuliya, Feenstra, Bjarke, Ferreira, Manuel A., Freidin, Maxim B., Gajdos, Zofia, Gauderman, Jim, Gehring, Ulrike, Geller, Frank, Genuneit, Jon, Gharib, Sina A., Gilliland, Frank, Granell, Raquel, Graves, Penelope E., Gudbjartsson, Daniel F., Haahtela, Tari, Heckbert, Susan R., Heederik, Dick, Heinrich, Joachim, Heliovaara, Markku, Henderson, John, Himes, Blanca E., Hirose, Hiroshi, Hirschhorn, Joel N., Hofman, Albert, Holt, Patrick, Hottenga, Jouke, Hudson, Thomas J., Hui, Jennie, Imboden, Medea, Ivanov, Vladimir, Jaddoe, Vincent W. V., James, Alan, Janson, Christer, Jarvelin, Marjo-Riitta, Jarvis, Deborah, Jones, Graham, Jonsdottir, Ingileif, Jousilahti, Pekka, Kabesch, Michael, Kahonen, Mika, Kantor, David B., Karunas, Alexandra S., Khusnutdinova, Elza, Koppelman, Gerard H., Kozyrskyj, Anita L., Kreiner, Eskil, Kubo, Michiaki, Kumar, Rajesh, Kumar, Ashish, Kuokkanen, Mikko, Lahousse, Lies, Laitinen, Tarja, Laprise, Catherine, Lathrop, Mark, Lau, Susanne, Lee, Young-Ae, Lehtimaki, Terho, Letort, Sebastien, Levin, Albert M., Li, Guo, Liang, Liming, Loehr, Laura R., London, Stephanie J., Loth, Daan W., Manichaikul, Ani, Marenholz, Ingo, Martinez, Fernando J., Matheson, Melanie C., Mathias, Rasika A., Matsumoto, Kenji, Mbarek, Hamdi, McArdle, Wendy L., Melbye, Mads, Melen, Erik, Meyers, Deborah, Michel, Sven, Mohamdi, Hamida, Musk, Arthur W., Myers, Rachel A., Nieuwenhuis, Maartje A. E., Noguchi, Emiko, O'Connor, George T., Ogorodova, Ludmila M., Palmer, Cameron D., Palotie, Aarno, Park, Julie E., Pennell, Craig E., Pershagen, Goran, Polonikov, Alexey, Postma, Dirkje S., Probst-Hensch, Nicole, Puzyrev, Valery P., Raby, Benjamin A., Raitakari, Olli T., Ramasamy, Adaikalavan, Rich, Stephen S., Robertson, Colin F., Romieu, Isabelle, Salam, Muhammad T., Salomaa, Veikko, Schlunssen, Vivi, Scott, Robert, Selivanova, Polina A., Sigsgaard, Torben, Simpson, Angela, Siroux, Valerie, Smith, Lewis J., Solodilova, Maria, Standl, Marie, Stefansson, Kari, Strachan, David P., Stricker, Bruno H., Takahashi, Atsushi, Thompson, Philip J., Thorleifsson, Gudmar, Thorsteinsdottir, Unnur, Tiesler, Carla M. T., Torgerson, Dara G., Tsunoda, Tatsuhiko, Uitterlinden, Andre G., van der Valk, Ralf J. P., Vaysse, Amaury, Vedantam, Sailaja, von Berg, Andrea, von Mutius, Erika, Vonk, Judith M., Waage, Johannes, Wareham, Nick J., Weiss, Scott T., White, Wendy B., Wickman, Magnus, Widen, Elisabeth, Willemsen, Gonneke, Williams, L. Keoki, Wouters, Inge M., Yang, James J., Zhao, Jing Hua, Moffatt, Miriam F., Ober, Carole, and Nicolae, Dan L.
Abstract: We examined common variation in asthma risk by conducting a meta-analysis of worldwide asthma genome-wide association studies (23,948 asthma cases, 118,538 controls) of individuals from ethnically diverse populations. We identified five new asthma loci, found two new associations at two known asthma loci, established asthma associations at two loci previously implicated in the comorbidity of asthma plus hay fever, and confirmed nine known loci. Investigation of pleiotropy showed large overlaps in genetic variants with autoimmune and inflammatory diseases. The enrichment in enhancer marks at asthma risk loci, especially in immune cells, suggested a major role of these loci in the regulation of immunologically related mechanisms.
Published: 2018

5. Association Between Telomere Length and Risk of Cancer and Non-Neoplastic Diseases A Mendelian Randomization Study

Author: Haycock, Philip C., Burgess, Stephen, Nounu, Aayah, Zheng, Jie, Okoli, George N., Bowden, Jack, Wade, Kaitlin Hazel, Timpson, Nicholas J., Evans, David M., Willeit, Peter, Aviv, Abraham, Gaunt, Tomr., Hemani, Gibran, Mangino, Massimo, Ellis, Hayley Patricia, Kurian, Kathreena M., Pooley, Karen A., Eeles, Rosalind A., Lee, Jeffrey E., Fang, Shenying, Chen, Wei V., Law, Matthew H., Bowdler, Lisa M., Iles, Mark M., Yang, Qiong, Worrall, Bradford B., Markus, Hugh Stephen, Hung, Rayjean J., Amos, Chris I., Spurdle, Amanda B., Thompson, Deborah J., O'Mara, Tracy A., Wolpin, Brian, Amundadottir, Laufey, Stolzenberg-Solomon, Rachael, Trichopoulou, Antonia, Onland-Moret, Charlotte, Lund, Eiliv, Duell, Eric J., Canzian, Federico, Severi, Gianluca, Overvad, Kim, Gunter, Marc J., Tumino, Rosario, Svenson, Ulrika, van Rij, Andre, Baas, Annette F., Bown, Matthew J., Samani, Nilesh J., van t'Hof, Femke N. G., Tromp, Gerard, Jones, Gregory T., Kuivaniemi, Helena, Elmore, James R., Johansson, Mattias, Mckay, James, Scelo, Ghislaine, carreras-Torres, Robert, Gaborieau, Valerie, Brennan, Paul, Bracci, Paige M., Neale, Rachel E., Olson, Sara H., Gallinger, Steven, Li, Donghui, Petersen, Gloria M., Risch, Harvey A., Klein, Alison P., Han, Jiali, Abnet, Christian C., Freedman, Neal D., Taylor, Philip R., Maris, John M., Aben, Katja K., Kiemeney, Lambertus A., Vermeulen, Sita H., Wiencke, John K., Walsh, Kyle M., Wrensch, Margaret, Rice, Terri, Turnbull, Clare, Litchfield, Kevin, Paternoster, Lavinia, Standl, Marie, Abecasis, Goncalo R., SanGiovanni, John Paul, Li, Yong, Mijatovic, Vladan, Sapkota, Yadav, Low, Siew-Kee, Zondervan, Krina T., Montgomery, Grant W., Nyholt, Dale R., van Heel, David A., Hunt, Karen, Arking, Dan E., Ashar, Foram N., Sotoodehnia, Nona, Woo, Daniel, Rosand, Jonathan, Comeau, Mary E., Brown, W. Mark, Silverman, Edwin K., Hokanson, John E., Cho, Michael H., Hui, Jennie, Ferreira, Manuel A., Thompson, Philip J., Morrison, Alanna C., Felix, Janine F., Smith, Nicholas L., Christiano, Angela M., Petukhova, Lynn, Betz, Regina C., Fan, Xing, Zhang, Xuejun, Zhu, Caihong, Langefeld, Carl D., Thompson, Susan D., Wang, Feijie, Lin, Xu, Schwartz, David A., Fingerlin, Tasha, Rotter, Jerome I., Cotch, Mary Frances, Jensen, Richard A., Munz, Matthias, Dommisch, Henrik, Schaefer, Arne S., Han, Fang, Ollila, Hanna M., Hillary, Ryan P., Albagha, Omar, Ralston, Stuart H., Zeng, Chenjie, Zheng, Wei, Shu, Xiao-Ou, Reis, Andre, Uebe, Steffen, Hueffmeier, Ulrike, Kawamura, Yoshiya, Otowa, Takeshi, Sasaki, Tsukasa, Hibberd, Martin Lloyd, Davila, Sonia, Xie, Gang, Siminovitch, Katherine, Bei, Jin-Xin, Zeng, Yi-Xin, Foersti, Asta, Chen, Bowang, Landi, Stefano, Franke, Andre, Fischer, Annegret, Ellinghaus, David, Flores, Carlos, Noth, Imre, Ma, Shwu-Fan, Foo, Jia Nee, Liu, Jianjun, Kim, Jong-Won, Cox, David G., Delattre, Olivier, Mirabeau, Olivier, Skibola, Christine F., Tang, Clara S., Garcia-Barcelo, Merce, Chang, Kai-Ping, Su, Wen-Hui, Chang, Yu-Sun, Martin, Nicholas G., Gordon, Scott, Wade, Tracey D., Lee, Chaeyoung, Kubo, Michiaki, Cha, Pei-Chieng, Nakamura, Yusuke, Levy, Daniel, Kimura, Masayuki, Hwang, Shih-Jen, Hunt, Steven, Spector, Tim, Soranzo, Nicole, Manichaikul, Aniw., Barr, Graham, Kahali, Bratati, Speliotes, Elizabeth, Yerges-Armstrong, LauraM., Cheng, Ching-Yu, Jonas, Jost B., Wong, Tien Yin, Fogh, Isabella, Lin, Kuang, Powell, John F., Rice, Kenneth, Relton, Caroline L., Martin, Richard M., Smith, George Davey, Haycock, Philip C., Burgess, Stephen, Nounu, Aayah, Zheng, Jie, Okoli, George N., Bowden, Jack, Wade, Kaitlin Hazel, Timpson, Nicholas J., Evans, David M., Willeit, Peter, Aviv, Abraham, Gaunt, Tomr., Hemani, Gibran, Mangino, Massimo, Ellis, Hayley Patricia, Kurian, Kathreena M., Pooley, Karen A., Eeles, Rosalind A., Lee, Jeffrey E., Fang, Shenying, Chen, Wei V., Law, Matthew H., Bowdler, Lisa M., Iles, Mark M., Yang, Qiong, Worrall, Bradford B., Markus, Hugh Stephen, Hung, Rayjean J., Amos, Chris I., Spurdle, Amanda B., Thompson, Deborah J., O'Mara, Tracy A., Wolpin, Brian, Amundadottir, Laufey, Stolzenberg-Solomon, Rachael, Trichopoulou, Antonia, Onland-Moret, Charlotte, Lund, Eiliv, Duell, Eric J., Canzian, Federico, Severi, Gianluca, Overvad, Kim, Gunter, Marc J., Tumino, Rosario, Svenson, Ulrika, van Rij, Andre, Baas, Annette F., Bown, Matthew J., Samani, Nilesh J., van t'Hof, Femke N. G., Tromp, Gerard, Jones, Gregory T., Kuivaniemi, Helena, Elmore, James R., Johansson, Mattias, Mckay, James, Scelo, Ghislaine, carreras-Torres, Robert, Gaborieau, Valerie, Brennan, Paul, Bracci, Paige M., Neale, Rachel E., Olson, Sara H., Gallinger, Steven, Li, Donghui, Petersen, Gloria M., Risch, Harvey A., Klein, Alison P., Han, Jiali, Abnet, Christian C., Freedman, Neal D., Taylor, Philip R., Maris, John M., Aben, Katja K., Kiemeney, Lambertus A., Vermeulen, Sita H., Wiencke, John K., Walsh, Kyle M., Wrensch, Margaret, Rice, Terri, Turnbull, Clare, Litchfield, Kevin, Paternoster, Lavinia, Standl, Marie, Abecasis, Goncalo R., SanGiovanni, John Paul, Li, Yong, Mijatovic, Vladan, Sapkota, Yadav, Low, Siew-Kee, Zondervan, Krina T., Montgomery, Grant W., Nyholt, Dale R., van Heel, David A., Hunt, Karen, Arking, Dan E., Ashar, Foram N., Sotoodehnia, Nona, Woo, Daniel, Rosand, Jonathan, Comeau, Mary E., Brown, W. Mark, Silverman, Edwin K., Hokanson, John E., Cho, Michael H., Hui, Jennie, Ferreira, Manuel A., Thompson, Philip J., Morrison, Alanna C., Felix, Janine F., Smith, Nicholas L., Christiano, Angela M., Petukhova, Lynn, Betz, Regina C., Fan, Xing, Zhang, Xuejun, Zhu, Caihong, Langefeld, Carl D., Thompson, Susan D., Wang, Feijie, Lin, Xu, Schwartz, David A., Fingerlin, Tasha, Rotter, Jerome I., Cotch, Mary Frances, Jensen, Richard A., Munz, Matthias, Dommisch, Henrik, Schaefer, Arne S., Han, Fang, Ollila, Hanna M., Hillary, Ryan P., Albagha, Omar, Ralston, Stuart H., Zeng, Chenjie, Zheng, Wei, Shu, Xiao-Ou, Reis, Andre, Uebe, Steffen, Hueffmeier, Ulrike, Kawamura, Yoshiya, Otowa, Takeshi, Sasaki, Tsukasa, Hibberd, Martin Lloyd, Davila, Sonia, Xie, Gang, Siminovitch, Katherine, Bei, Jin-Xin, Zeng, Yi-Xin, Foersti, Asta, Chen, Bowang, Landi, Stefano, Franke, Andre, Fischer, Annegret, Ellinghaus, David, Flores, Carlos, Noth, Imre, Ma, Shwu-Fan, Foo, Jia Nee, Liu, Jianjun, Kim, Jong-Won, Cox, David G., Delattre, Olivier, Mirabeau, Olivier, Skibola, Christine F., Tang, Clara S., Garcia-Barcelo, Merce, Chang, Kai-Ping, Su, Wen-Hui, Chang, Yu-Sun, Martin, Nicholas G., Gordon, Scott, Wade, Tracey D., Lee, Chaeyoung, Kubo, Michiaki, Cha, Pei-Chieng, Nakamura, Yusuke, Levy, Daniel, Kimura, Masayuki, Hwang, Shih-Jen, Hunt, Steven, Spector, Tim, Soranzo, Nicole, Manichaikul, Aniw., Barr, Graham, Kahali, Bratati, Speliotes, Elizabeth, Yerges-Armstrong, LauraM., Cheng, Ching-Yu, Jonas, Jost B., Wong, Tien Yin, Fogh, Isabella, Lin, Kuang, Powell, John F., Rice, Kenneth, Relton, Caroline L., Martin, Richard M., and Smith, George Davey
Abstract: IMPORTANCE: The causal direction and magnitude of the association between telomere length and incidence of cancer and non-neoplastic diseases is uncertain owing to the susceptibility of observational studies to confounding and reverse causation. OBJECTIVE: To conduct a Mendelian randomization study, using germline genetic variants as instrumental variables, to appraise the causal relevance of telomere length for risk of cancer and non-neoplastic diseases. DATA SOURCES: Genomewide association studies (GWAS) published up to January 15, 2015. STUDY SELECTION: GWAS of noncommunicable diseases that assayed germline genetic variation and did not select cohort or control participants on the basis of preexisting diseases. Of 163 GWAS of noncommunicable diseases identified, summary data from 103 were available. DATA EXTRACTION AND SYNTHESIS: Summary association statistics for single nucleotide polymorphisms (SNPs) that are strongly associated with telomere length in the general population. MAIN OUTCOMES AND MEASURES: Odds ratios (ORs) and 95% confidence intervals (CIs) for disease per standard deviation (SD) higher telomere length due to germline genetic variation. RESULTS: Summary data were available for 35 cancers and 48 non-neoplastic diseases, corresponding to 420 081 cases (median cases, 2526 per disease) and 1 093 105 controls (median, 6789 per disease). Increased telomere length due to germline genetic variation was generally associated with increased risk for site-specific cancers. The strongest associations (ORs [ 95% CIs] per 1-SD change in genetically increased telomere length) were observed for glioma, 5.27 (3.15-8.81); serous low-malignant-potential ovarian cancer, 4.35 (2.39-7.94); lung adenocarcinoma, 3.19 (2.40-4.22); neuroblastoma, 2.98 (1.92-4.62); bladder cancer, 2.19 (1.32-3.66); melanoma, 1.87 (1.55-2.26); testicular cancer, 1.76 (1.02-3.04); kidney cancer, 1.55 (1.08-2.23); and endometrial cancer, 1.31 (1.07-1.61). Associations were stronger for rarer c
Published: 2017
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6. Shared genetic origin of asthma, hay fever and eczema elucidates allergic disease biology

Author: Ferreira, Manuel A, Vonk, Judith M, Baurecht, Hansjörg, Marenholz, Ingo, Tian, Chao, Hoffman, Joshua D, Helmer, Quinta, Tillander, Annika, Ullemar, Vilhelmina, van Dongen, Jenny, Lu, Yi, Rüschendorf, Franz, Esparza-Gordillo, Jorge, Medway, Chris W, Mountjoy, Edward, Burrows, Kimberley, Hummel, Oliver, Grosche, Sarah, Brumpton, Ben M, Witte, John S, Hottenga, Jouke-Jan, Willemsen, Gonneke, Zheng, Jie, Rodríguez, Elke, Hotze, Melanie, Franke, Andre, Revez, Joana A, Beesley, Jonathan, Matheson, Melanie C, Dharmage, Shyamali C, Bain, Lisa M, Fritsche, Lars G, Gabrielsen, Maiken E, Balliu, Brunilda, Nielsen, Jonas B, Zhou, Wei, Hveem, Kristian, Langhammer, Arnulf, Holmen, Oddgeir L, Løset, Mari, Abecasis, Gonçalo R, Willer, Cristen J, Arnold, Andreas, Homuth, Georg, Schmidt, Carsten O, Thompson, Philip J, Martin, Nicholas G, Duffy, David L, Novak, Natalija, Boomsma, Dorret I, 23andMe Research Team, Ferreira, Manuel A, Vonk, Judith M, Baurecht, Hansjörg, Marenholz, Ingo, Tian, Chao, Hoffman, Joshua D, Helmer, Quinta, Tillander, Annika, Ullemar, Vilhelmina, van Dongen, Jenny, Lu, Yi, Rüschendorf, Franz, Esparza-Gordillo, Jorge, Medway, Chris W, Mountjoy, Edward, Burrows, Kimberley, Hummel, Oliver, Grosche, Sarah, Brumpton, Ben M, Witte, John S, Hottenga, Jouke-Jan, Willemsen, Gonneke, Zheng, Jie, Rodríguez, Elke, Hotze, Melanie, Franke, Andre, Revez, Joana A, Beesley, Jonathan, Matheson, Melanie C, Dharmage, Shyamali C, Bain, Lisa M, Fritsche, Lars G, Gabrielsen, Maiken E, Balliu, Brunilda, Nielsen, Jonas B, Zhou, Wei, Hveem, Kristian, Langhammer, Arnulf, Holmen, Oddgeir L, Løset, Mari, Abecasis, Gonçalo R, Willer, Cristen J, Arnold, Andreas, Homuth, Georg, Schmidt, Carsten O, Thompson, Philip J, Martin, Nicholas G, Duffy, David L, Novak, Natalija, Boomsma, Dorret I, and 23andMe Research Team
Abstract: Asthma, hay fever (or allergic rhinitis) and eczema (or atopic dermatitis) often coexist in the same individuals, partly because of a shared genetic origin. To identify shared risk variants, we performed a genome-wide association study (GWAS; n = 360,838) of a broad allergic disease phenotype that considers the presence of any one of these three diseases. We identified 136 independent risk variants (P < 3 × 10-8), including 73 not previously reported, which implicate 132 nearby genes in allergic disease pathophysiology. Disease-specific effects were detected for only six variants, confirming that most represent shared risk factors. Tissue-specific heritability and biological process enrichment analyses suggest that shared risk variants influence lymphocyte-mediated immunity. Six target genes provide an opportunity for drug repositioning, while for 36 genes CpG methylation was found to influence transcription independently of genetic effects. Asthma, hay fever and eczema partly coexist because they share many genetic risk variants that dysregulate the expression of immune-related genes.
Published: 2017
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7. Characteristics associated with clinical severity and inflammatory phenotype of naturally occurring virus-induced exacerbations of asthma in adults

Author: Bjerregaard, Asger, Laing, Ingrid A, Poulsen, Nadia, Backer, Vibeke, Sverrild, Asger, Fally, Markus, Khoo, Siew-Kim, Barrett, Lucy, Baltic, Svetlana, Thompson, Philip J, Chidlow, Glenys, Sikazwe, Chisha, Smith, David W, Bochkov, Yury A, Le Souëf, Peter, Porsbjerg, Celeste, Bjerregaard, Asger, Laing, Ingrid A, Poulsen, Nadia, Backer, Vibeke, Sverrild, Asger, Fally, Markus, Khoo, Siew-Kim, Barrett, Lucy, Baltic, Svetlana, Thompson, Philip J, Chidlow, Glenys, Sikazwe, Chisha, Smith, David W, Bochkov, Yury A, Le Souëf, Peter, and Porsbjerg, Celeste
Abstract: BACKGROUND: In experimental studies viral infections have been shown to induce type 2 inflammation in asthmatics, but whether this is a feature of naturally occurring virus-induced asthma exacerbations is unknown. Thymic stromal lymphopoietin (TSLP) released from the airway epithelium in response to damage, has been suggested as a link between viral infection and type 2 inflammation, but the role of TSLP in asthma exacerbations is unknown.OBJECTIVE: To assess whether type 2 inflammation, as measured by sputum eosinophils and fractional exhaled nitric oxide (FeNO), is a feature of naturally occurring virus-induced exacerbations of asthma and whether TSLP is associated with this type 2 inflammation.METHODS: Patients presenting to hospital with acute asthma were examined during the exacerbation, and after 4 weeks recovery. The assessments included spirometry, FeNO and induced sputum for differential counts and TSLP mRNA levels. Nasal swabs were collected for viral detection.RESULTS: Sputum eosinophils and FeNO were similar between virus-positive (n = 44) and negative patients (n = 44). In virus-positive patients, TSLP expression was lower at exacerbation than follow-up (p = 0.03). High TSLP at exacerbation was associated with lower sputum eosinophils (p = 0.01) and higher FEV1 (p = 0.03). In virus-positive patients, %-predicted FEV1 negatively correlated with both FeNO and sputum eosinophils (p = 0.02 and p = 0.05, respectively).CONCLUSION: Our findings support that type 2 inflammation is present in patients during virus-induced asthma exacerbations, to the same degree as non-viral exacerbations, and correlate negatively with FEV1. However, in virus-positive patients, high TSLP expression during exacerbation was associated with low sputum eosinophils, suggesting that the effect of TSLP in vivo, in the setting of an asthma exacerbation, might be different than the type 2 inducing effects observed in experimental studies.
Published: 2017

8. Meta-analysis identifies seven susceptibility loci involved in the atopic march

Author: Marenholz, Ingo, Esparza-Gordillo, Jorge, Rueschendorf, Franz, Bauerfeind, Anja, Strachan, David P., Spycher, Ben D., Baurecht, Hansjoerg, Margaritte-Jeannin, Patricia, Saaf, Annika, Kerkhof, Marjan, Ege, Markus, Baltic, Svetlana, Matheson, Melanie C., Li, Jin, Michel, Sven, Ang, Wei Q., McArdle, Wendy, Arnold, Andreas, Homuth, Georg, Demenais, Florence, Bouzigon, Emmanuelle, Soderhall, Cilla, Pershagen, Goran, de Jongste, Johan C., Postma, Dirkje S., Braun-Fahrlaender, Charlotte, Horak, Elisabeth, Ogorodova, Ludmila M., Puzyrev, Valery P., Bragina, Elena Yu, Hudson, Thomas J., Morin, Charles, Duffy, David L., Marks, Guy B., Robertson, Colin F., Montgomery, Grant W., Musk, Bill, Thompson, Philip J., Martin, Nicholas G., James, Alan, Sleiman, Patrick, Toskala, Elina, Rodriguez, Elke, Foelster-Holst, Regina, Franke, Andre, Lieb, Wolfgang, Gieger, Christian, Heinzmann, Andrea, Rietschel, Ernst, Keil, Thomas, Cichon, Sven, Noethen, Markus M., Pennell, Craig E., Sly, Peter D., Schmidt, Carsten O., Matanovic, Anja, Schneider, Valentin, Heinig, Matthias, Huebner, Norbert, Holt, Patrick G., Lau, Susanne, Kabesch, Michael, Weidinger, Stefan, Hakonarson, Hakon, Ferreira, Manuel A. R., Laprise, Catherine, Freidin, Maxim B., Genuneit, Jon, Koppelman, Gerard H., Melen, Erik, Dizier, Marie-Helene, Henderson, A. John, Lee, Young Ae, Marenholz, Ingo, Esparza-Gordillo, Jorge, Rueschendorf, Franz, Bauerfeind, Anja, Strachan, David P., Spycher, Ben D., Baurecht, Hansjoerg, Margaritte-Jeannin, Patricia, Saaf, Annika, Kerkhof, Marjan, Ege, Markus, Baltic, Svetlana, Matheson, Melanie C., Li, Jin, Michel, Sven, Ang, Wei Q., McArdle, Wendy, Arnold, Andreas, Homuth, Georg, Demenais, Florence, Bouzigon, Emmanuelle, Soderhall, Cilla, Pershagen, Goran, de Jongste, Johan C., Postma, Dirkje S., Braun-Fahrlaender, Charlotte, Horak, Elisabeth, Ogorodova, Ludmila M., Puzyrev, Valery P., Bragina, Elena Yu, Hudson, Thomas J., Morin, Charles, Duffy, David L., Marks, Guy B., Robertson, Colin F., Montgomery, Grant W., Musk, Bill, Thompson, Philip J., Martin, Nicholas G., James, Alan, Sleiman, Patrick, Toskala, Elina, Rodriguez, Elke, Foelster-Holst, Regina, Franke, Andre, Lieb, Wolfgang, Gieger, Christian, Heinzmann, Andrea, Rietschel, Ernst, Keil, Thomas, Cichon, Sven, Noethen, Markus M., Pennell, Craig E., Sly, Peter D., Schmidt, Carsten O., Matanovic, Anja, Schneider, Valentin, Heinig, Matthias, Huebner, Norbert, Holt, Patrick G., Lau, Susanne, Kabesch, Michael, Weidinger, Stefan, Hakonarson, Hakon, Ferreira, Manuel A. R., Laprise, Catherine, Freidin, Maxim B., Genuneit, Jon, Koppelman, Gerard H., Melen, Erik, Dizier, Marie-Helene, Henderson, A. John, and Lee, Young Ae
Abstract: Eczema often precedes the development of asthma in a disease course called the 'atopic march'. To unravel the genes underlying this characteristic pattern of allergic disease, we conduct a multi-stage genome-wide association study on infantile eczema followed by childhood asthma in 12 populations including 2,428 cases and 17,034 controls. Here we report two novel loci specific for the combined eczema plus asthma phenotype, which are associated with allergic disease for the first time; rs9357733 located in EFHC1 on chromosome 6p12.3 (OR 1.27; P = 2.1 x 10(-8)) and rs993226 between TMTC2 and SLC6A15 on chromosome 12q21.3 (OR 1.58; P = 5.3 x 10(-9)). Additional susceptibility loci identified at genome-wide significance are FLG (1q21.3), IL4/KIF3A (5q31.1), AP5B1/OVOL1 (11q13.1), C11orf30/LRRC32 (11q13.5) and IKZF3 (17q21). We show that predominantly eczema loci increase the risk for the atopic march. Our findings suggest that eczema may play an important role in the development of asthma after eczema.
Published: 2015

9. Meta-analysis identifies seven susceptibility loci involved in the atopic march

Author: Marenholz, Ingo, Esparza-Gordillo, Jorge, Rueschendorf, Franz, Bauerfeind, Anja, Strachan, David P., Spycher, Ben D., Baurecht, Hansjoerg, Margaritte-Jeannin, Patricia, Saaf, Annika, Kerkhof, Marjan, Ege, Markus, Baltic, Svetlana, Matheson, Melanie C., Li, Jin, Michel, Sven, Ang, Wei Q., McArdle, Wendy, Arnold, Andreas, Homuth, Georg, Demenais, Florence, Bouzigon, Emmanuelle, Soderhall, Cilla, Pershagen, Goran, de Jongste, Johan C., Postma, Dirkje S., Braun-Fahrlaender, Charlotte, Horak, Elisabeth, Ogorodova, Ludmila M., Puzyrev, Valery P., Bragina, Elena Yu, Hudson, Thomas J., Morin, Charles, Duffy, David L., Marks, Guy B., Robertson, Colin F., Montgomery, Grant W., Musk, Bill, Thompson, Philip J., Martin, Nicholas G., James, Alan, Sleiman, Patrick, Toskala, Elina, Rodriguez, Elke, Foelster-Holst, Regina, Franke, Andre, Lieb, Wolfgang, Gieger, Christian, Heinzmann, Andrea, Rietschel, Ernst, Keil, Thomas, Cichon, Sven, Noethen, Markus M., Pennell, Craig E., Sly, Peter D., Schmidt, Carsten O., Matanovic, Anja, Schneider, Valentin, Heinig, Matthias, Huebner, Norbert, Holt, Patrick G., Lau, Susanne, Kabesch, Michael, Weidinger, Stefan, Hakonarson, Hakon, Ferreira, Manuel A. R., Laprise, Catherine, Freidin, Maxim B., Genuneit, Jon, Koppelman, Gerard H., Melen, Erik, Dizier, Marie-Helene, Henderson, A. John, Lee, Young Ae, Marenholz, Ingo, Esparza-Gordillo, Jorge, Rueschendorf, Franz, Bauerfeind, Anja, Strachan, David P., Spycher, Ben D., Baurecht, Hansjoerg, Margaritte-Jeannin, Patricia, Saaf, Annika, Kerkhof, Marjan, Ege, Markus, Baltic, Svetlana, Matheson, Melanie C., Li, Jin, Michel, Sven, Ang, Wei Q., McArdle, Wendy, Arnold, Andreas, Homuth, Georg, Demenais, Florence, Bouzigon, Emmanuelle, Soderhall, Cilla, Pershagen, Goran, de Jongste, Johan C., Postma, Dirkje S., Braun-Fahrlaender, Charlotte, Horak, Elisabeth, Ogorodova, Ludmila M., Puzyrev, Valery P., Bragina, Elena Yu, Hudson, Thomas J., Morin, Charles, Duffy, David L., Marks, Guy B., Robertson, Colin F., Montgomery, Grant W., Musk, Bill, Thompson, Philip J., Martin, Nicholas G., James, Alan, Sleiman, Patrick, Toskala, Elina, Rodriguez, Elke, Foelster-Holst, Regina, Franke, Andre, Lieb, Wolfgang, Gieger, Christian, Heinzmann, Andrea, Rietschel, Ernst, Keil, Thomas, Cichon, Sven, Noethen, Markus M., Pennell, Craig E., Sly, Peter D., Schmidt, Carsten O., Matanovic, Anja, Schneider, Valentin, Heinig, Matthias, Huebner, Norbert, Holt, Patrick G., Lau, Susanne, Kabesch, Michael, Weidinger, Stefan, Hakonarson, Hakon, Ferreira, Manuel A. R., Laprise, Catherine, Freidin, Maxim B., Genuneit, Jon, Koppelman, Gerard H., Melen, Erik, Dizier, Marie-Helene, Henderson, A. John, and Lee, Young Ae
Abstract: Eczema often precedes the development of asthma in a disease course called the 'atopic march'. To unravel the genes underlying this characteristic pattern of allergic disease, we conduct a multi-stage genome-wide association study on infantile eczema followed by childhood asthma in 12 populations including 2,428 cases and 17,034 controls. Here we report two novel loci specific for the combined eczema plus asthma phenotype, which are associated with allergic disease for the first time; rs9357733 located in EFHC1 on chromosome 6p12.3 (OR 1.27; P = 2.1 x 10(-8)) and rs993226 between TMTC2 and SLC6A15 on chromosome 12q21.3 (OR 1.58; P = 5.3 x 10(-9)). Additional susceptibility loci identified at genome-wide significance are FLG (1q21.3), IL4/KIF3A (5q31.1), AP5B1/OVOL1 (11q13.1), C11orf30/LRRC32 (11q13.5) and IKZF3 (17q21). We show that predominantly eczema loci increase the risk for the atopic march. Our findings suggest that eczema may play an important role in the development of asthma after eczema.
Published: 2015

10. Meta-analysis identifies seven susceptibility loci involved in the atopic march

Author: Marenholz, Ingo, Esparza-Gordillo, Jorge, Rüschendorf, Franz, Bauerfeind, Anja, Strachan, David P., Spycher, Ben D., Baurecht, Hansjörg, Margaritte-Jeannin, Patricia, Sääf, Annika, Kerkhof, Marjan, Ege, Markus, Baltic, Svetlana, Matheson, Melanie C., Li, Jin, Michel, Sven, Ang, Wei Q., McArdle, Wendy, Arnold, Andreas, Homuth, Georg, Demenais, Florence, Bouzigon, Emmanuelle, Söderhäll, Cilla, Pershagen, Göran, de Jongste, Johan C., Postma, Dirkje S., Braun-Fahrländer, Charlotte, Horak, Elisabeth, Ogorodova, Ludmila M., Puzyrev, Valery P., Bragina, Elena Yu, Hudson, Thomas J., Morin, Charles, Duffy, David L., Marks, Guy B., Robertson, Colin F., Montgomery, Grant W., Musk, Bill, Thompson, Philip J., Martin, Nicholas G., James, Alan, Sleiman, Patrick, Toskala, Elina, Rodriguez, Elke, Fölster-Holst, Regina, Franke, Andre, Lieb, Wolfgang, Gieger, Christian, Heinzmann, Andrea, Rietschel, Ernst, Keil, Thomas, Cichon, Sven, Nöthen, Markus M., Pennell, Craig E., Sly, Peter D., Schmidt, Carsten O., Matanovic, Anja, Schneider, Valentin, Heinig, Matthias, Hübner, Norbert, Holt, Patrick G., Lau, Susanne, Kabesch, Michael, Weidinger, Stefan, Hakonarson, Hakon, Ferreira, Manuel A. R., Laprise, Catherine, Freidin, Maxim B., Genuneit, Jon, Koppelman, Gerard H., Melén, Erik, Dizier, Marie- Hélène, Henderson, A John, Lee, Young Ae, Marenholz, Ingo, Esparza-Gordillo, Jorge, Rüschendorf, Franz, Bauerfeind, Anja, Strachan, David P., Spycher, Ben D., Baurecht, Hansjörg, Margaritte-Jeannin, Patricia, Sääf, Annika, Kerkhof, Marjan, Ege, Markus, Baltic, Svetlana, Matheson, Melanie C., Li, Jin, Michel, Sven, Ang, Wei Q., McArdle, Wendy, Arnold, Andreas, Homuth, Georg, Demenais, Florence, Bouzigon, Emmanuelle, Söderhäll, Cilla, Pershagen, Göran, de Jongste, Johan C., Postma, Dirkje S., Braun-Fahrländer, Charlotte, Horak, Elisabeth, Ogorodova, Ludmila M., Puzyrev, Valery P., Bragina, Elena Yu, Hudson, Thomas J., Morin, Charles, Duffy, David L., Marks, Guy B., Robertson, Colin F., Montgomery, Grant W., Musk, Bill, Thompson, Philip J., Martin, Nicholas G., James, Alan, Sleiman, Patrick, Toskala, Elina, Rodriguez, Elke, Fölster-Holst, Regina, Franke, Andre, Lieb, Wolfgang, Gieger, Christian, Heinzmann, Andrea, Rietschel, Ernst, Keil, Thomas, Cichon, Sven, Nöthen, Markus M., Pennell, Craig E., Sly, Peter D., Schmidt, Carsten O., Matanovic, Anja, Schneider, Valentin, Heinig, Matthias, Hübner, Norbert, Holt, Patrick G., Lau, Susanne, Kabesch, Michael, Weidinger, Stefan, Hakonarson, Hakon, Ferreira, Manuel A. R., Laprise, Catherine, Freidin, Maxim B., Genuneit, Jon, Koppelman, Gerard H., Melén, Erik, Dizier, Marie- Hélène, Henderson, A John, and Lee, Young Ae
Abstract: Eczema often precedes the development of asthma in a disease course called the ‘atopic march’. To unravel the genes underlying this characteristic pattern of allergic disease, we conduct a multi-stage genome-wide association study on infantile eczema followed by childhood asthma in 12 populations including 2,428 cases and 17,034 controls. Here we report two novel loci specific for the combined eczema plus asthma phenotype, which are associated with allergic disease for the first time; rs9357733 located in EFHC1 on chromosome 6p12.3 (OR 1.27; P=2.1 × 10−8) and rs993226 between TMTC2 and SLC6A15 on chromosome 12q21.3 (OR 1.58; P=5.3 × 10−9). Additional susceptibility loci identified at genome-wide significance are FLG (1q21.3), IL4/KIF3A (5q31.1), AP5B1/OVOL1 (11q13.1), C11orf30/LRRC32 (11q13.5) and IKZF3 (17q21). We show that predominantly eczema loci increase the risk for the atopic march. Our findings suggest that eczema may play an important role in the development of asthma after eczema.
Published: 2015
Full Text: View/download PDF

11. Meta-analysis of genome-wide association studies identifies ten loci influencing allergic sensitization

Author: Bønnelykke, Klaus, Matheson, Melanie C, Pers, Tune H, Granell, Raquel, Strachan, David P, Alves, Alexessander Couto, Linneberg, Allan, Curtin, John A, Warrington, Nicole M, Standl, Marie, Kerkhof, Marjan, Jonsdottir, Ingileif, Bukvic, Blazenka K, Kaakinen, Marika, Sleimann, Patrick, Thorleifsson, Gudmar, Thorsteinsdottir, Unnur, Schramm, Katharina, Baltic, Svetlana, Kreiner-Møller, Eskil, Simpson, Angela, Pourcain, Beate St, Coin, Lachlan, Hui, Jennie, Walters, Eugene H, Tiesler, Carla M T, Duffy, David L, Jones, Graham, Ring, Susan M, McArdle, Wendy L, Price, Loren, Robertson, Colin F, Pekkanen, Juha, Tang, Clara S, Thiering, Elisabeth, Montgomery, Grant W, Hartikainen, Anna-Liisa, Dharmage, Shyamali C, Husemoen, Lise L, Herder, Christian, Kemp, John P, Elliot, Paul, James, Alan, Waldenberger, Melanie, Abramson, Michael J, Fairfax, Benjamin P, Knight, Julian C, Gupta, Ramneek, Thompson, Philip J, Holt, Patrick, Sly, Peter, Hirschhorn, Joel N, Blekic, Mario, Weidinger, Stephan, Hakonarsson, Hakon, Stefansson, Kari, Heinrich, Joachim, Postma, Dirkje S, Custovic, Adnan, Pennell, Craig E, Jarvelin, Marjo-Riitta, Koppelman, Gerard H, Timpson, Nicholas, Ferreira, Manuel A, Bisgaard, Hans, Henderson, A John, (AAGC), Australian Asthma Genetics Consortium, Bønnelykke, Klaus, Matheson, Melanie C, Pers, Tune H, Granell, Raquel, Strachan, David P, Alves, Alexessander Couto, Linneberg, Allan, Curtin, John A, Warrington, Nicole M, Standl, Marie, Kerkhof, Marjan, Jonsdottir, Ingileif, Bukvic, Blazenka K, Kaakinen, Marika, Sleimann, Patrick, Thorleifsson, Gudmar, Thorsteinsdottir, Unnur, Schramm, Katharina, Baltic, Svetlana, Kreiner-Møller, Eskil, Simpson, Angela, Pourcain, Beate St, Coin, Lachlan, Hui, Jennie, Walters, Eugene H, Tiesler, Carla M T, Duffy, David L, Jones, Graham, Ring, Susan M, McArdle, Wendy L, Price, Loren, Robertson, Colin F, Pekkanen, Juha, Tang, Clara S, Thiering, Elisabeth, Montgomery, Grant W, Hartikainen, Anna-Liisa, Dharmage, Shyamali C, Husemoen, Lise L, Herder, Christian, Kemp, John P, Elliot, Paul, James, Alan, Waldenberger, Melanie, Abramson, Michael J, Fairfax, Benjamin P, Knight, Julian C, Gupta, Ramneek, Thompson, Philip J, Holt, Patrick, Sly, Peter, Hirschhorn, Joel N, Blekic, Mario, Weidinger, Stephan, Hakonarsson, Hakon, Stefansson, Kari, Heinrich, Joachim, Postma, Dirkje S, Custovic, Adnan, Pennell, Craig E, Jarvelin, Marjo-Riitta, Koppelman, Gerard H, Timpson, Nicholas, Ferreira, Manuel A, Bisgaard, Hans, Henderson, A John, and (AAGC), Australian Asthma Genetics Consortium
Published: 2013

12. Meta-analysis of genome-wide association studies identifies ten loci influencing allergic sensitization

Author: Bønnelykke, Klaus, Matheson, Melanie C, Pers, Tune H, Granell, Raquel, Strachan, David P, Alves, Alexessander Couto, Linneberg, Allan, Curtin, John A, Warrington, Nicole M, Standl, Marie, Kerkhof, Marjan, Jonsdottir, Ingileif, Bukvic, Blazenka K, Kaakinen, Marika, Sleimann, Patrick, Thorleifsson, Gudmar, Thorsteinsdottir, Unnur, Schramm, Katharina, Baltic, Svetlana, Kreiner-Møller, Eskil, Simpson, Angela, Pourcain, Beate St, Coin, Lachlan, Hui, Jennie, Walters, Eugene H, Tiesler, Carla M T, Duffy, David L, Jones, Graham, Ring, Susan M, McArdle, Wendy L, Price, Loren, Robertson, Colin F, Pekkanen, Juha, Tang, Clara S, Thiering, Elisabeth, Montgomery, Grant W, Hartikainen, Anna-Liisa, Dharmage, Shyamali C, Husemoen, Lise L, Herder, Christian, Kemp, John P, Elliot, Paul, James, Alan, Waldenberger, Melanie, Abramson, Michael J, Fairfax, Benjamin P, Knight, Julian C, Gupta, Ramneek, Thompson, Philip J, Holt, Patrick, Sly, Peter, Hirschhorn, Joel N, Blekic, Mario, Weidinger, Stephan, Hakonarsson, Hakon, Stefansson, Kari, Heinrich, Joachim, Postma, Dirkje S, Custovic, Adnan, Pennell, Craig E, Jarvelin, Marjo-Riitta, Koppelman, Gerard H, Timpson, Nicholas, Ferreira, Manuel A, Bisgaard, Hans, Henderson, A John, (AAGC), Australian Asthma Genetics Consortium, Bønnelykke, Klaus, Matheson, Melanie C, Pers, Tune H, Granell, Raquel, Strachan, David P, Alves, Alexessander Couto, Linneberg, Allan, Curtin, John A, Warrington, Nicole M, Standl, Marie, Kerkhof, Marjan, Jonsdottir, Ingileif, Bukvic, Blazenka K, Kaakinen, Marika, Sleimann, Patrick, Thorleifsson, Gudmar, Thorsteinsdottir, Unnur, Schramm, Katharina, Baltic, Svetlana, Kreiner-Møller, Eskil, Simpson, Angela, Pourcain, Beate St, Coin, Lachlan, Hui, Jennie, Walters, Eugene H, Tiesler, Carla M T, Duffy, David L, Jones, Graham, Ring, Susan M, McArdle, Wendy L, Price, Loren, Robertson, Colin F, Pekkanen, Juha, Tang, Clara S, Thiering, Elisabeth, Montgomery, Grant W, Hartikainen, Anna-Liisa, Dharmage, Shyamali C, Husemoen, Lise L, Herder, Christian, Kemp, John P, Elliot, Paul, James, Alan, Waldenberger, Melanie, Abramson, Michael J, Fairfax, Benjamin P, Knight, Julian C, Gupta, Ramneek, Thompson, Philip J, Holt, Patrick, Sly, Peter, Hirschhorn, Joel N, Blekic, Mario, Weidinger, Stephan, Hakonarsson, Hakon, Stefansson, Kari, Heinrich, Joachim, Postma, Dirkje S, Custovic, Adnan, Pennell, Craig E, Jarvelin, Marjo-Riitta, Koppelman, Gerard H, Timpson, Nicholas, Ferreira, Manuel A, Bisgaard, Hans, Henderson, A John, and (AAGC), Australian Asthma Genetics Consortium
Published: 2013

13. Genome-Wide Association Studies of Asthma in Population-Based Cohorts Confirm Known and Suggested Loci and Identify an Additional Association near HLA

Author: Ramasamy, Adaikalavan, Kuokkanen, Mikko, Vedantam, Sailaja, Gajdos, Zofia K., Alves, Alexessander Couto, Lyon, Helen N., Ferreira, Manuel A. R., Strachan, David P., Zhao, Jing Hua, Abramson, Michael J., Brown, Matthew A., Coin, Lachlan, Dharmage, Shyamali C., Duffy, David L., Haahtela, Tari, Heath, Andrew C., Janson, Christer, Kahonen, Mika, Khaw, Kay-Tee, Laitinen, Jaana, Le Souef, Peter, Lehtimaki, Terho, Madden, Pamela A. F., Marks, Guy B., Martin, Nicholas G., Matheson, Melanie C., Palmer, Cameron D., Palotie, Aarno, Pouta, Anneli, Robertson, Colin F., Viikari, Jorma, Widen, Elisabeth, Wjst, Matthias, Jarvis, Deborah L., Montgomery, Grant W., Thompson, Philip J., Wareham, Nick, Eriksson, Johan, Jousilahti, Pekka, Laitinen, Tarja, Pekkanen, Juha, Raitakari, Olli T., O'Connor, George T., Salomaa, Veikko, Jarvelin, Marjo-Riitta, Hirschhorn, Joel N., Ramasamy, Adaikalavan, Kuokkanen, Mikko, Vedantam, Sailaja, Gajdos, Zofia K., Alves, Alexessander Couto, Lyon, Helen N., Ferreira, Manuel A. R., Strachan, David P., Zhao, Jing Hua, Abramson, Michael J., Brown, Matthew A., Coin, Lachlan, Dharmage, Shyamali C., Duffy, David L., Haahtela, Tari, Heath, Andrew C., Janson, Christer, Kahonen, Mika, Khaw, Kay-Tee, Laitinen, Jaana, Le Souef, Peter, Lehtimaki, Terho, Madden, Pamela A. F., Marks, Guy B., Martin, Nicholas G., Matheson, Melanie C., Palmer, Cameron D., Palotie, Aarno, Pouta, Anneli, Robertson, Colin F., Viikari, Jorma, Widen, Elisabeth, Wjst, Matthias, Jarvis, Deborah L., Montgomery, Grant W., Thompson, Philip J., Wareham, Nick, Eriksson, Johan, Jousilahti, Pekka, Laitinen, Tarja, Pekkanen, Juha, Raitakari, Olli T., O'Connor, George T., Salomaa, Veikko, Jarvelin, Marjo-Riitta, and Hirschhorn, Joel N.
Abstract: Rationale: Asthma has substantial morbidity and mortality and a strong genetic component, but identification of genetic risk factors is limited by availability of suitable studies. Objectives: To test if population-based cohorts with self-reported physician-diagnosed asthma and genome-wide association (GWA) data could be used to validate known associations with asthma and identify novel associations. Methods: The APCAT (Analysis in Population-based Cohorts of Asthma Traits) consortium consists of 1,716 individuals with asthma and 16,888 healthy controls from six European-descent population-based cohorts. We examined associations in APCAT of thirteen variants previously reported as genome-wide significant (P < 5x10(-8)) and three variants reported as suggestive (P < 5 x 10(-7)). We also searched for novel associations in APCAT (Stage 1) and followed-up the most promising variants in 4,035 asthmatics and 11,251 healthy controls (Stage 2). Finally, we conducted the first genome-wide screen for interactions with smoking or hay fever. Main Results: We observed association in the same direction for all thirteen previously reported variants and nominally replicated ten of them. One variant that was previously suggestive, rs11071559 in RORA, now reaches genome-wide significance when combined with our data (P = 2.4x10(-9)). We also identified two genome-wide significant associations: rs13408661 near IL1RL1/IL18R1 (PStage1+Stage2 = 1.1x10(-9)), which is correlated with a variant recently shown to be associated with asthma (rs3771180), and rs9268516 in the HLA region (PStage1+Stage2 = 1.1x10(-8)), which appears to be independent of previously reported associations in this locus. Finally, we found no strong evidence for gene-environment interactions with smoking or hay fever status. Conclusions: Population-based cohorts with simple asthma phenotypes represent a valuable and largely untapped resource for genetic studies of asthma.
Published: 2012
Full Text: View/download PDF

14. Genome-Wide Association Studies of Asthma in Population-Based Cohorts Confirm Known and Suggested Loci and Identify an Additional Association near HLA

Author: Ramasamy, Adaikalavan, Kuokkanen, Mikko, Vedantam, Sailaja, Gajdos, Zofia K., Alves, Alexessander Couto, Lyon, Helen N., Ferreira, Manuel A. R., Strachan, David P., Zhao, Jing Hua, Abramson, Michael J., Brown, Matthew A., Coin, Lachlan, Dharmage, Shyamali C., Duffy, David L., Haahtela, Tari, Heath, Andrew C., Janson, Christer, Kahonen, Mika, Khaw, Kay-Tee, Laitinen, Jaana, Le Souef, Peter, Lehtimaki, Terho, Madden, Pamela A. F., Marks, Guy B., Martin, Nicholas G., Matheson, Melanie C., Palmer, Cameron D., Palotie, Aarno, Pouta, Anneli, Robertson, Colin F., Viikari, Jorma, Widen, Elisabeth, Wjst, Matthias, Jarvis, Deborah L., Montgomery, Grant W., Thompson, Philip J., Wareham, Nick, Eriksson, Johan, Jousilahti, Pekka, Laitinen, Tarja, Pekkanen, Juha, Raitakari, Olli T., O'Connor, George T., Salomaa, Veikko, Jarvelin, Marjo-Riitta, Hirschhorn, Joel N., Ramasamy, Adaikalavan, Kuokkanen, Mikko, Vedantam, Sailaja, Gajdos, Zofia K., Alves, Alexessander Couto, Lyon, Helen N., Ferreira, Manuel A. R., Strachan, David P., Zhao, Jing Hua, Abramson, Michael J., Brown, Matthew A., Coin, Lachlan, Dharmage, Shyamali C., Duffy, David L., Haahtela, Tari, Heath, Andrew C., Janson, Christer, Kahonen, Mika, Khaw, Kay-Tee, Laitinen, Jaana, Le Souef, Peter, Lehtimaki, Terho, Madden, Pamela A. F., Marks, Guy B., Martin, Nicholas G., Matheson, Melanie C., Palmer, Cameron D., Palotie, Aarno, Pouta, Anneli, Robertson, Colin F., Viikari, Jorma, Widen, Elisabeth, Wjst, Matthias, Jarvis, Deborah L., Montgomery, Grant W., Thompson, Philip J., Wareham, Nick, Eriksson, Johan, Jousilahti, Pekka, Laitinen, Tarja, Pekkanen, Juha, Raitakari, Olli T., O'Connor, George T., Salomaa, Veikko, Jarvelin, Marjo-Riitta, and Hirschhorn, Joel N.
Abstract: Rationale: Asthma has substantial morbidity and mortality and a strong genetic component, but identification of genetic risk factors is limited by availability of suitable studies. Objectives: To test if population-based cohorts with self-reported physician-diagnosed asthma and genome-wide association (GWA) data could be used to validate known associations with asthma and identify novel associations. Methods: The APCAT (Analysis in Population-based Cohorts of Asthma Traits) consortium consists of 1,716 individuals with asthma and 16,888 healthy controls from six European-descent population-based cohorts. We examined associations in APCAT of thirteen variants previously reported as genome-wide significant (P < 5x10(-8)) and three variants reported as suggestive (P < 5 x 10(-7)). We also searched for novel associations in APCAT (Stage 1) and followed-up the most promising variants in 4,035 asthmatics and 11,251 healthy controls (Stage 2). Finally, we conducted the first genome-wide screen for interactions with smoking or hay fever. Main Results: We observed association in the same direction for all thirteen previously reported variants and nominally replicated ten of them. One variant that was previously suggestive, rs11071559 in RORA, now reaches genome-wide significance when combined with our data (P = 2.4x10(-9)). We also identified two genome-wide significant associations: rs13408661 near IL1RL1/IL18R1 (PStage1+Stage2 = 1.1x10(-9)), which is correlated with a variant recently shown to be associated with asthma (rs3771180), and rs9268516 in the HLA region (PStage1+Stage2 = 1.1x10(-8)), which appears to be independent of previously reported associations in this locus. Finally, we found no strong evidence for gene-environment interactions with smoking or hay fever status. Conclusions: Population-based cohorts with simple asthma phenotypes represent a valuable and largely untapped resource for genetic studies of asthma.
Published: 2012
Full Text: View/download PDF

15. Genome-Wide Association Studies of Asthma in Population-Based Cohorts Confirm Known and Suggested Loci and Identify an Additional Association near HLA

Author: Ramasamy, Adaikalavan, Kuokkanen, Mikko, Vedantam, Sailaja, Gajdos, Zofia K., Alves, Alexessander Couto, Lyon, Helen N., Ferreira, Manuel A. R., Strachan, David P., Zhao, Jing Hua, Abramson, Michael J., Brown, Matthew A., Coin, Lachlan, Dharmage, Shyamali C., Duffy, David L., Haahtela, Tari, Heath, Andrew C., Janson, Christer, Kahonen, Mika, Khaw, Kay-Tee, Laitinen, Jaana, Le Souef, Peter, Lehtimaki, Terho, Madden, Pamela A. F., Marks, Guy B., Martin, Nicholas G., Matheson, Melanie C., Palmer, Cameron D., Palotie, Aarno, Pouta, Anneli, Robertson, Colin F., Viikari, Jorma, Widen, Elisabeth, Wjst, Matthias, Jarvis, Deborah L., Montgomery, Grant W., Thompson, Philip J., Wareham, Nick, Eriksson, Johan, Jousilahti, Pekka, Laitinen, Tarja, Pekkanen, Juha, Raitakari, Olli T., O'Connor, George T., Salomaa, Veikko, Jarvelin, Marjo-Riitta, Hirschhorn, Joel N., Ramasamy, Adaikalavan, Kuokkanen, Mikko, Vedantam, Sailaja, Gajdos, Zofia K., Alves, Alexessander Couto, Lyon, Helen N., Ferreira, Manuel A. R., Strachan, David P., Zhao, Jing Hua, Abramson, Michael J., Brown, Matthew A., Coin, Lachlan, Dharmage, Shyamali C., Duffy, David L., Haahtela, Tari, Heath, Andrew C., Janson, Christer, Kahonen, Mika, Khaw, Kay-Tee, Laitinen, Jaana, Le Souef, Peter, Lehtimaki, Terho, Madden, Pamela A. F., Marks, Guy B., Martin, Nicholas G., Matheson, Melanie C., Palmer, Cameron D., Palotie, Aarno, Pouta, Anneli, Robertson, Colin F., Viikari, Jorma, Widen, Elisabeth, Wjst, Matthias, Jarvis, Deborah L., Montgomery, Grant W., Thompson, Philip J., Wareham, Nick, Eriksson, Johan, Jousilahti, Pekka, Laitinen, Tarja, Pekkanen, Juha, Raitakari, Olli T., O'Connor, George T., Salomaa, Veikko, Jarvelin, Marjo-Riitta, and Hirschhorn, Joel N.
Abstract: Rationale: Asthma has substantial morbidity and mortality and a strong genetic component, but identification of genetic risk factors is limited by availability of suitable studies. Objectives: To test if population-based cohorts with self-reported physician-diagnosed asthma and genome-wide association (GWA) data could be used to validate known associations with asthma and identify novel associations. Methods: The APCAT (Analysis in Population-based Cohorts of Asthma Traits) consortium consists of 1,716 individuals with asthma and 16,888 healthy controls from six European-descent population-based cohorts. We examined associations in APCAT of thirteen variants previously reported as genome-wide significant (P < 5x10(-8)) and three variants reported as suggestive (P < 5 x 10(-7)). We also searched for novel associations in APCAT (Stage 1) and followed-up the most promising variants in 4,035 asthmatics and 11,251 healthy controls (Stage 2). Finally, we conducted the first genome-wide screen for interactions with smoking or hay fever. Main Results: We observed association in the same direction for all thirteen previously reported variants and nominally replicated ten of them. One variant that was previously suggestive, rs11071559 in RORA, now reaches genome-wide significance when combined with our data (P = 2.4x10(-9)). We also identified two genome-wide significant associations: rs13408661 near IL1RL1/IL18R1 (PStage1+Stage2 = 1.1x10(-9)), which is correlated with a variant recently shown to be associated with asthma (rs3771180), and rs9268516 in the HLA region (PStage1+Stage2 = 1.1x10(-8)), which appears to be independent of previously reported associations in this locus. Finally, we found no strong evidence for gene-environment interactions with smoking or hay fever status. Conclusions: Population-based cohorts with simple asthma phenotypes represent a valuable and largely untapped resource for genetic studies of asthma.
Published: 2012
Full Text: View/download PDF

16. Genome-Wide Association Studies of Asthma in Population-Based Cohorts Confirm Known and Suggested Loci and Identify an Additional Association near HLA

Author: University of Helsinki, Clinicum, University of Helsinki, Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Department of Public Health (-2009), Ramasamy, Adaikalavan, Kuokkanen, Mikko, Vedantam, Sailaja, Gajdos, Zofia K., Alves, Alexessander Couto, Lyon, Helen N., Ferreira, Manuel A. R., Strachan, David P., Zhao, Jing Hua, Abramson, Michael J., Brown, Matthew A., Coin, Lachlan, Dharmage, Shyamali C., Duffy, David L., Haahtela, Tari, Heath, Andrew C., Janson, Christer, Kahonen, Mika, Khaw, Kay-Tee, Laitinen, Jaana, Le Souef, Peter, Lehtimaki, Terho, Madden, Pamela A. F., Marks, Guy B., Martin, Nicholas G., Matheson, Melanie C., Palmer, Cameron D., Palotie, Aarno, Pouta, Anneli, Robertson, Colin F., Viikari, Jorma, Widen, Elisabeth, Wjst, Matthias, Jarvis, Deborah L., Montgomery, Grant W., Thompson, Philip J., Wareham, Nick, Eriksson, Johan, Jousilahti, Pekka, Laitinen, Tarja, Pekkanen, Juha, Raitakari, Olli T., O'Connor, George T., Salomaa, Veikko, Jarvelin, Marjo-Riitta, Hirschhorn, Joel N., Australian Asthma Genetics, University of Helsinki, Clinicum, University of Helsinki, Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Department of Public Health (-2009), Ramasamy, Adaikalavan, Kuokkanen, Mikko, Vedantam, Sailaja, Gajdos, Zofia K., Alves, Alexessander Couto, Lyon, Helen N., Ferreira, Manuel A. R., Strachan, David P., Zhao, Jing Hua, Abramson, Michael J., Brown, Matthew A., Coin, Lachlan, Dharmage, Shyamali C., Duffy, David L., Haahtela, Tari, Heath, Andrew C., Janson, Christer, Kahonen, Mika, Khaw, Kay-Tee, Laitinen, Jaana, Le Souef, Peter, Lehtimaki, Terho, Madden, Pamela A. F., Marks, Guy B., Martin, Nicholas G., Matheson, Melanie C., Palmer, Cameron D., Palotie, Aarno, Pouta, Anneli, Robertson, Colin F., Viikari, Jorma, Widen, Elisabeth, Wjst, Matthias, Jarvis, Deborah L., Montgomery, Grant W., Thompson, Philip J., Wareham, Nick, Eriksson, Johan, Jousilahti, Pekka, Laitinen, Tarja, Pekkanen, Juha, Raitakari, Olli T., O'Connor, George T., Salomaa, Veikko, Jarvelin, Marjo-Riitta, Hirschhorn, Joel N., and Australian Asthma Genetics
Published: 2012

17. Genome-Wide Association Studies of Asthma in Population-Based Cohorts Confirm Known and Suggested Loci and Identify an Additional Association near HLA

Author: Ramasamy, Adaikalavan, Kuokkanen, Mikko, Vedantam, Sailaja, Gajdos, Zofia K., Alves, Alexessander Couto, Lyon, Helen N., Ferreira, Manuel A. R., Strachan, David P., Zhao, Jing Hua, Abramson, Michael J., Brown, Matthew A., Coin, Lachlan, Dharmage, Shyamali C., Duffy, David L., Haahtela, Tari, Heath, Andrew C., Janson, Christer, Kahonen, Mika, Khaw, Kay-Tee, Laitinen, Jaana, Le Souef, Peter, Lehtimaki, Terho, Madden, Pamela A. F., Marks, Guy B., Martin, Nicholas G., Matheson, Melanie C., Palmer, Cameron D., Palotie, Aarno, Pouta, Anneli, Robertson, Colin F., Viikari, Jorma, Widen, Elisabeth, Wjst, Matthias, Jarvis, Deborah L., Montgomery, Grant W., Thompson, Philip J., Wareham, Nick, Eriksson, Johan, Jousilahti, Pekka, Laitinen, Tarja, Pekkanen, Juha, Raitakari, Olli T., O'Connor, George T., Salomaa, Veikko, Jarvelin, Marjo-Riitta, Hirschhorn, Joel N., Ramasamy, Adaikalavan, Kuokkanen, Mikko, Vedantam, Sailaja, Gajdos, Zofia K., Alves, Alexessander Couto, Lyon, Helen N., Ferreira, Manuel A. R., Strachan, David P., Zhao, Jing Hua, Abramson, Michael J., Brown, Matthew A., Coin, Lachlan, Dharmage, Shyamali C., Duffy, David L., Haahtela, Tari, Heath, Andrew C., Janson, Christer, Kahonen, Mika, Khaw, Kay-Tee, Laitinen, Jaana, Le Souef, Peter, Lehtimaki, Terho, Madden, Pamela A. F., Marks, Guy B., Martin, Nicholas G., Matheson, Melanie C., Palmer, Cameron D., Palotie, Aarno, Pouta, Anneli, Robertson, Colin F., Viikari, Jorma, Widen, Elisabeth, Wjst, Matthias, Jarvis, Deborah L., Montgomery, Grant W., Thompson, Philip J., Wareham, Nick, Eriksson, Johan, Jousilahti, Pekka, Laitinen, Tarja, Pekkanen, Juha, Raitakari, Olli T., O'Connor, George T., Salomaa, Veikko, Jarvelin, Marjo-Riitta, and Hirschhorn, Joel N.
Abstract: Rationale: Asthma has substantial morbidity and mortality and a strong genetic component, but identification of genetic risk factors is limited by availability of suitable studies. Objectives: To test if population-based cohorts with self-reported physician-diagnosed asthma and genome-wide association (GWA) data could be used to validate known associations with asthma and identify novel associations. Methods: The APCAT (Analysis in Population-based Cohorts of Asthma Traits) consortium consists of 1,716 individuals with asthma and 16,888 healthy controls from six European-descent population-based cohorts. We examined associations in APCAT of thirteen variants previously reported as genome-wide significant (P < 5x10(-8)) and three variants reported as suggestive (P < 5 x 10(-7)). We also searched for novel associations in APCAT (Stage 1) and followed-up the most promising variants in 4,035 asthmatics and 11,251 healthy controls (Stage 2). Finally, we conducted the first genome-wide screen for interactions with smoking or hay fever. Main Results: We observed association in the same direction for all thirteen previously reported variants and nominally replicated ten of them. One variant that was previously suggestive, rs11071559 in RORA, now reaches genome-wide significance when combined with our data (P = 2.4x10(-9)). We also identified two genome-wide significant associations: rs13408661 near IL1RL1/IL18R1 (PStage1+Stage2 = 1.1x10(-9)), which is correlated with a variant recently shown to be associated with asthma (rs3771180), and rs9268516 in the HLA region (PStage1+Stage2 = 1.1x10(-8)), which appears to be independent of previously reported associations in this locus. Finally, we found no strong evidence for gene-environment interactions with smoking or hay fever status. Conclusions: Population-based cohorts with simple asthma phenotypes represent a valuable and largely untapped resource for genetic studies of asthma.
Published: 2012
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18. Genome-Wide Association Studies of Asthma in Population-Based Cohorts Confirm Known and Suggested Loci and Identify an Additional Association near HLA

Author: Ramasamy, Adaikalavan, Kuokkanen, Mikko, Vedantam, Sailaja, Gajdos, Zofia K., Alves, Alexessander Couto, Lyon, Helen N., Ferreira, Manuel A. R., Strachan, David P., Zhao, Jing Hua, Abramson, Michael J., Brown, Matthew A., Coin, Lachlan, Dharmage, Shyamali C., Duffy, David L., Haahtela, Tari, Heath, Andrew C., Janson, Christer, Kahonen, Mika, Khaw, Kay-Tee, Laitinen, Jaana, Le Souef, Peter, Lehtimaki, Terho, Madden, Pamela A. F., Marks, Guy B., Martin, Nicholas G., Matheson, Melanie C., Palmer, Cameron D., Palotie, Aarno, Pouta, Anneli, Robertson, Colin F., Viikari, Jorma, Widen, Elisabeth, Wjst, Matthias, Jarvis, Deborah L., Montgomery, Grant W., Thompson, Philip J., Wareham, Nick, Eriksson, Johan, Jousilahti, Pekka, Laitinen, Tarja, Pekkanen, Juha, Raitakari, Olli T., O'Connor, George T., Salomaa, Veikko, Jarvelin, Marjo-Riitta, Hirschhorn, Joel N., Ramasamy, Adaikalavan, Kuokkanen, Mikko, Vedantam, Sailaja, Gajdos, Zofia K., Alves, Alexessander Couto, Lyon, Helen N., Ferreira, Manuel A. R., Strachan, David P., Zhao, Jing Hua, Abramson, Michael J., Brown, Matthew A., Coin, Lachlan, Dharmage, Shyamali C., Duffy, David L., Haahtela, Tari, Heath, Andrew C., Janson, Christer, Kahonen, Mika, Khaw, Kay-Tee, Laitinen, Jaana, Le Souef, Peter, Lehtimaki, Terho, Madden, Pamela A. F., Marks, Guy B., Martin, Nicholas G., Matheson, Melanie C., Palmer, Cameron D., Palotie, Aarno, Pouta, Anneli, Robertson, Colin F., Viikari, Jorma, Widen, Elisabeth, Wjst, Matthias, Jarvis, Deborah L., Montgomery, Grant W., Thompson, Philip J., Wareham, Nick, Eriksson, Johan, Jousilahti, Pekka, Laitinen, Tarja, Pekkanen, Juha, Raitakari, Olli T., O'Connor, George T., Salomaa, Veikko, Jarvelin, Marjo-Riitta, and Hirschhorn, Joel N.
Abstract: Rationale: Asthma has substantial morbidity and mortality and a strong genetic component, but identification of genetic risk factors is limited by availability of suitable studies. Objectives: To test if population-based cohorts with self-reported physician-diagnosed asthma and genome-wide association (GWA) data could be used to validate known associations with asthma and identify novel associations. Methods: The APCAT (Analysis in Population-based Cohorts of Asthma Traits) consortium consists of 1,716 individuals with asthma and 16,888 healthy controls from six European-descent population-based cohorts. We examined associations in APCAT of thirteen variants previously reported as genome-wide significant (P < 5x10(-8)) and three variants reported as suggestive (P < 5 x 10(-7)). We also searched for novel associations in APCAT (Stage 1) and followed-up the most promising variants in 4,035 asthmatics and 11,251 healthy controls (Stage 2). Finally, we conducted the first genome-wide screen for interactions with smoking or hay fever. Main Results: We observed association in the same direction for all thirteen previously reported variants and nominally replicated ten of them. One variant that was previously suggestive, rs11071559 in RORA, now reaches genome-wide significance when combined with our data (P = 2.4x10(-9)). We also identified two genome-wide significant associations: rs13408661 near IL1RL1/IL18R1 (PStage1+Stage2 = 1.1x10(-9)), which is correlated with a variant recently shown to be associated with asthma (rs3771180), and rs9268516 in the HLA region (PStage1+Stage2 = 1.1x10(-8)), which appears to be independent of previously reported associations in this locus. Finally, we found no strong evidence for gene-environment interactions with smoking or hay fever status. Conclusions: Population-based cohorts with simple asthma phenotypes represent a valuable and largely untapped resource for genetic studies of asthma.
Published: 2012
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19. FluCAN 2009: initial results from sentinel surveillance for adult influenza and pneumonia in eight Australian hospitals

Author: Kelly, Paul, Kotsimbos, Tom, Reynolds, Anna, Wood-Baker, Richard, Hancox, Robert J, Brown, Simon GA, Simpson, Graham, Bowler, Simon, Waterer, Grant, Irving, Louis, Jenkins, Christine, Thompson, Philip J, Cheng, Allen, Kelly, Paul, Kotsimbos, Tom, Reynolds, Anna, Wood-Baker, Richard, Hancox, Robert J, Brown, Simon GA, Simpson, Graham, Bowler, Simon, Waterer, Grant, Irving, Louis, Jenkins, Christine, Thompson, Philip J, and Cheng, Allen
Abstract: Objective: To describe the epidemiology of adult patients hospitalised with influenza or pneumonia during a pandemic season in a sentinel network in Australia. Design, participants and setting: Prospective case series of adult hospital admissions to eight acute care general public hospitals (Influenza Complications Alert Network [Flu CAN] sentinel hospitals) in six Australian jurisdictions, 1 July to 4 December 2009. Main outcome measures: Demographic, clinical and outcome measures in patients admitted with laboratory-confirmed pandemic (H1N1) 2009 influenza in the sentinel hospitals compared with data from national notifications and intensive care unit (ICU) surveillance; admissions for influenza and pneumonia over time in each jurisdiction. Results: During 190 hospital-weeks of observation, there were 538 influenza admissions. Of these, 465 patients (86.4%) had the pandemic strain, representing 9.3% of total admissions with pandemic (H1N1) 2009 influenza (n = 4992) recorded nationally in 2009. Of these patients, 250/465 (53.8%) were women, 67/453 (14.8%) were Indigenous, and the median age was 46 years (interquartile range, 29-58 years). Comorbidities were present in 354/464 patients (76.3%), and 40 were pregnant (30.3% of women aged 15-49 years). FluCAN reported that 102 patients (21.9%) were admitted to ICUs, and of patients admitted to hospital, 26 (5.6%) died. FluCAN results were very similar to national notification data and published ICU admissions data. Of those who were followed to 30 days after discharge, 30 (6.5%) were readmitted. Of 1468 patients hospitalised with pneumonia, 718 (48.9%) were tested for influenza and 163 (11.1%) were co-infected with the pandemic strain. Conclusions: Sentinel surveillance systems can provide important and reliable information in a timely fashion and can monitor changes in severity of influenza during a pandemic season.
Published: 2011

20. Effectiveness of H1N1/09 monovalent and trivalent influenza vaccines against hospitalization with laboratory-confirmed H1N1/09 influenza in Australia: A test-negative case control study

Author: Cheng, Allen, Kotsimbos, Tom, Kelly, H, Irving, Louis, Bowler, Simon, Brown, Simon G. A, Holmes, Mark, Jenkins, Christine, Thompson, Philip J, Simpson, Graham, Senanayake, Sanjaya, Kelly, Paul, Wood-Baker, Richard, Senanayake, Sanjaya N., Brady, S.J, Paterson, David, Paterson, D L, Dwyer, Dominic, Dwyer, Dominic E, Waterer, Grant, Cheng, Allen, Kotsimbos, Tom, Kelly, H, Irving, Louis, Bowler, Simon, Brown, Simon G. A, Holmes, Mark, Jenkins, Christine, Thompson, Philip J, Simpson, Graham, Senanayake, Sanjaya, Kelly, Paul, Wood-Baker, Richard, Senanayake, Sanjaya N., Brady, S.J, Paterson, David, Paterson, D L, Dwyer, Dominic, Dwyer, Dominic E, and Waterer, Grant
Abstract: We aimed to estimate the effectiveness of H1N1/09 containing influenza vaccines against hospitalization from influenza in Australia. We performed a test-negative case control study in patients hospitalized in 15 sentinel Australian hospitals between March and November 2010, comparing influenza vaccination (H1N1/09 monovalent or 2010 seasonal trivalent) in hospitalized patients with PCR-confirmed influenza compared to PCR-negative controls. Between March and November 2010, 1169 hospitalized patients were tested for suspected influenza, of which influenza vaccine status was ascertained in 165/238 patients with H1N1/09 influenza, 40/64 with seasonal influenza and 558/867 test negative controls; 24% of H1N1/09 cases, 43% of seasonal influenza cases and 54% of controls were vaccinated. VE against hospitalisation with H1N1/09 influenza after adjusting for age, medical comorbidities and pregnancy status was estimated at 49% (95% CI: 13%, 70%). Influenza vaccination was associated with a reduction in hospitalisation caused by H1N1/09 influenza in the 2010 southern hemisphere winter season.
Published: 2011

21. Meta-analysis of genome-wide association studies identifies three new risk loci for atopic dermatitis

Author: Paternoster, Lavinia, Standl, Marie, Chen, Chih-Mei, Ramasamy, Adaikalavan, Bønnelykke, Klaus, Duijts, Liesbeth, Ferreira, Manuel A, Alves, Alexessander Couto, Thyssen, Jacob P, Albrecht, Eva, Baurecht, Hansjörg, Feenstra, Bjarke, Sleiman, Patrick M A, Hysi, Pirro, Warrington, Nicole M, Curjuric, Ivan, Myhre, Ronny, Curtin, John A, Groen-Blokhuis, Maria M, Kerkhof, Marjan, Sääf, Annika, Franke, Andre, Ellinghaus, David, Fölster-Holst, Regina, Dermitzakis, Emmanouil, Montgomery, Stephen B, Prokisch, Holger, Heim, Katharina, Hartikainen, Anna-Liisa, Pouta, Anneli, Pekkanen, Juha, Blakemore, Alexandra I F, Buxton, Jessica L, Kaakinen, Marika, Duffy, David L, Madden, Pamela A, Heath, Andrew C, Montgomery, Grant W, Thompson, Philip J, Matheson, Melanie C, Le Souëf, Peter, Pourcain, Beate St, Smith, George Davey, Henderson, John, Kemp, John P, Timpson, Nicholas J, Deloukas, Panos, Linneberg, Allan, Menné, Torkil, Bisgaard, Hans, Paternoster, Lavinia, Standl, Marie, Chen, Chih-Mei, Ramasamy, Adaikalavan, Bønnelykke, Klaus, Duijts, Liesbeth, Ferreira, Manuel A, Alves, Alexessander Couto, Thyssen, Jacob P, Albrecht, Eva, Baurecht, Hansjörg, Feenstra, Bjarke, Sleiman, Patrick M A, Hysi, Pirro, Warrington, Nicole M, Curjuric, Ivan, Myhre, Ronny, Curtin, John A, Groen-Blokhuis, Maria M, Kerkhof, Marjan, Sääf, Annika, Franke, Andre, Ellinghaus, David, Fölster-Holst, Regina, Dermitzakis, Emmanouil, Montgomery, Stephen B, Prokisch, Holger, Heim, Katharina, Hartikainen, Anna-Liisa, Pouta, Anneli, Pekkanen, Juha, Blakemore, Alexandra I F, Buxton, Jessica L, Kaakinen, Marika, Duffy, David L, Madden, Pamela A, Heath, Andrew C, Montgomery, Grant W, Thompson, Philip J, Matheson, Melanie C, Le Souëf, Peter, Pourcain, Beate St, Smith, George Davey, Henderson, John, Kemp, John P, Timpson, Nicholas J, Deloukas, Panos, Linneberg, Allan, Menné, Torkil, and Bisgaard, Hans
Abstract: Atopic dermatitis (AD) is a commonly occurring chronic skin disease with high heritability. Apart from filaggrin (FLG), the genes influencing atopic dermatitis are largely unknown. We conducted a genome-wide association meta-analysis of 5,606 affected individuals and 20,565 controls from 16 population-based cohorts and then examined the ten most strongly associated new susceptibility loci in an additional 5,419 affected individuals and 19,833 controls from 14 studies. Three SNPs reached genome-wide significance in the discovery and replication cohorts combined, including rs479844 upstream of OVOL1 (odds ratio (OR) = 0.88, P = 1.1 × 10(-13)) and rs2164983 near ACTL9 (OR = 1.16, P = 7.1 × 10(-9)), both of which are near genes that have been implicated in epidermal proliferation and differentiation, as well as rs2897442 in KIF3A within the cytokine cluster at 5q31.1 (OR = 1.11, P = 3.8 × 10(-8)). We also replicated association with the FLG locus and with two recently identified association signals at 11q13.5 (rs7927894; P = 0.008) and 20q13.33 (rs6010620; P = 0.002). Our results underline the importance of both epidermal barrier function and immune dysregulation in atopic dermatitis pathogenesis.
Published: 2011

22. Meta-analysis of genome-wide association studies identifies three new risk loci for atopic dermatitis

Author: Paternoster, Lavinia, Standl, Marie, Chen, Chih-Mei, Ramasamy, Adaikalavan, Bønnelykke, Klaus, Duijts, Liesbeth, Ferreira, Manuel A, Alves, Alexessander Couto, Thyssen, Jacob P, Albrecht, Eva, Baurecht, Hansjörg, Feenstra, Bjarke, Sleiman, Patrick M A, Hysi, Pirro, Warrington, Nicole M, Curjuric, Ivan, Myhre, Ronny, Curtin, John A, Groen-Blokhuis, Maria M, Kerkhof, Marjan, Sääf, Annika, Franke, Andre, Ellinghaus, David, Fölster-Holst, Regina, Dermitzakis, Emmanouil, Montgomery, Stephen B, Prokisch, Holger, Heim, Katharina, Hartikainen, Anna-Liisa, Pouta, Anneli, Pekkanen, Juha, Blakemore, Alexandra I F, Buxton, Jessica L, Kaakinen, Marika, Duffy, David L, Madden, Pamela A, Heath, Andrew C, Montgomery, Grant W, Thompson, Philip J, Matheson, Melanie C, Le Souëf, Peter, Pourcain, Beate St, Smith, George Davey, Henderson, John, Kemp, John P, Timpson, Nicholas J, Deloukas, Panos, Linneberg, Allan, Menné, Torkil, Bisgaard, Hans, Paternoster, Lavinia, Standl, Marie, Chen, Chih-Mei, Ramasamy, Adaikalavan, Bønnelykke, Klaus, Duijts, Liesbeth, Ferreira, Manuel A, Alves, Alexessander Couto, Thyssen, Jacob P, Albrecht, Eva, Baurecht, Hansjörg, Feenstra, Bjarke, Sleiman, Patrick M A, Hysi, Pirro, Warrington, Nicole M, Curjuric, Ivan, Myhre, Ronny, Curtin, John A, Groen-Blokhuis, Maria M, Kerkhof, Marjan, Sääf, Annika, Franke, Andre, Ellinghaus, David, Fölster-Holst, Regina, Dermitzakis, Emmanouil, Montgomery, Stephen B, Prokisch, Holger, Heim, Katharina, Hartikainen, Anna-Liisa, Pouta, Anneli, Pekkanen, Juha, Blakemore, Alexandra I F, Buxton, Jessica L, Kaakinen, Marika, Duffy, David L, Madden, Pamela A, Heath, Andrew C, Montgomery, Grant W, Thompson, Philip J, Matheson, Melanie C, Le Souëf, Peter, Pourcain, Beate St, Smith, George Davey, Henderson, John, Kemp, John P, Timpson, Nicholas J, Deloukas, Panos, Linneberg, Allan, Menné, Torkil, and Bisgaard, Hans
Abstract: Atopic dermatitis (AD) is a commonly occurring chronic skin disease with high heritability. Apart from filaggrin (FLG), the genes influencing atopic dermatitis are largely unknown. We conducted a genome-wide association meta-analysis of 5,606 affected individuals and 20,565 controls from 16 population-based cohorts and then examined the ten most strongly associated new susceptibility loci in an additional 5,419 affected individuals and 19,833 controls from 14 studies. Three SNPs reached genome-wide significance in the discovery and replication cohorts combined, including rs479844 upstream of OVOL1 (odds ratio (OR) = 0.88, P = 1.1 × 10(-13)) and rs2164983 near ACTL9 (OR = 1.16, P = 7.1 × 10(-9)), both of which are near genes that have been implicated in epidermal proliferation and differentiation, as well as rs2897442 in KIF3A within the cytokine cluster at 5q31.1 (OR = 1.11, P = 3.8 × 10(-8)). We also replicated association with the FLG locus and with two recently identified association signals at 11q13.5 (rs7927894; P = 0.008) and 20q13.33 (rs6010620; P = 0.002). Our results underline the importance of both epidermal barrier function and immune dysregulation in atopic dermatitis pathogenesis.
Published: 2011

23. Meta-analysis of genome-wide association studies identifies three new risk loci for atopic dermatitis

Author: Paternoster, Lavinia, Standl, Marie, Chen, Chih-Mei, Ramasamy, Adaikalavan, Bønnelykke, Klaus, Duijts, Liesbeth, Ferreira, Manuel A, Alves, Alexessander Couto, Thyssen, Jacob P, Albrecht, Eva, Baurecht, Hansjörg, Feenstra, Bjarke, Sleiman, Patrick M A, Hysi, Pirro, Warrington, Nicole M, Curjuric, Ivan, Myhre, Ronny, Curtin, John A, Groen-Blokhuis, Maria M, Kerkhof, Marjan, Sääf, Annika, Franke, Andre, Ellinghaus, David, Fölster-Holst, Regina, Dermitzakis, Emmanouil, Montgomery, Stephen B, Prokisch, Holger, Heim, Katharina, Hartikainen, Anna-Liisa, Pouta, Anneli, Pekkanen, Juha, Blakemore, Alexandra I F, Buxton, Jessica L, Kaakinen, Marika, Duffy, David L, Madden, Pamela A, Heath, Andrew C, Montgomery, Grant W, Thompson, Philip J, Matheson, Melanie C, Le Souëf, Peter, Pourcain, Beate St, Smith, George Davey, Henderson, John, Kemp, John P, Timpson, Nicholas J, Deloukas, Panos, Linneberg, Allan, Menné, Torkil, Bisgaard, Hans, Paternoster, Lavinia, Standl, Marie, Chen, Chih-Mei, Ramasamy, Adaikalavan, Bønnelykke, Klaus, Duijts, Liesbeth, Ferreira, Manuel A, Alves, Alexessander Couto, Thyssen, Jacob P, Albrecht, Eva, Baurecht, Hansjörg, Feenstra, Bjarke, Sleiman, Patrick M A, Hysi, Pirro, Warrington, Nicole M, Curjuric, Ivan, Myhre, Ronny, Curtin, John A, Groen-Blokhuis, Maria M, Kerkhof, Marjan, Sääf, Annika, Franke, Andre, Ellinghaus, David, Fölster-Holst, Regina, Dermitzakis, Emmanouil, Montgomery, Stephen B, Prokisch, Holger, Heim, Katharina, Hartikainen, Anna-Liisa, Pouta, Anneli, Pekkanen, Juha, Blakemore, Alexandra I F, Buxton, Jessica L, Kaakinen, Marika, Duffy, David L, Madden, Pamela A, Heath, Andrew C, Montgomery, Grant W, Thompson, Philip J, Matheson, Melanie C, Le Souëf, Peter, Pourcain, Beate St, Smith, George Davey, Henderson, John, Kemp, John P, Timpson, Nicholas J, Deloukas, Panos, Linneberg, Allan, Menné, Torkil, and Bisgaard, Hans
Abstract: Atopic dermatitis (AD) is a commonly occurring chronic skin disease with high heritability. Apart from filaggrin (FLG), the genes influencing atopic dermatitis are largely unknown. We conducted a genome-wide association meta-analysis of 5,606 affected individuals and 20,565 controls from 16 population-based cohorts and then examined the ten most strongly associated new susceptibility loci in an additional 5,419 affected individuals and 19,833 controls from 14 studies. Three SNPs reached genome-wide significance in the discovery and replication cohorts combined, including rs479844 upstream of OVOL1 (odds ratio (OR) = 0.88, P = 1.1 × 10(-13)) and rs2164983 near ACTL9 (OR = 1.16, P = 7.1 × 10(-9)), both of which are near genes that have been implicated in epidermal proliferation and differentiation, as well as rs2897442 in KIF3A within the cytokine cluster at 5q31.1 (OR = 1.11, P = 3.8 × 10(-8)). We also replicated association with the FLG locus and with two recently identified association signals at 11q13.5 (rs7927894; P = 0.008) and 20q13.33 (rs6010620; P = 0.002). Our results underline the importance of both epidermal barrier function and immune dysregulation in atopic dermatitis pathogenesis.
Published: 2011

24. Influenza A/H1N1_09: Australia and New Zealand's Winter of Discontent

Author: Kotsimbos, Tom, Waterer, Grant, Jenkins, Christine, Kelly, Paul, Cheng, Allen, Hancox, Robert J, Holmes, Mark, Wood-Baker, Richard, Bowler, Simon, Irving, Louis, Thompson, Philip J, Kotsimbos, Tom, Waterer, Grant, Jenkins, Christine, Kelly, Paul, Cheng, Allen, Hancox, Robert J, Holmes, Mark, Wood-Baker, Richard, Bowler, Simon, Irving, Louis, and Thompson, Philip J
Abstract: Influenza A/H1N1-09 emerged in Mexico at the end of the Northern Hemisphere winter.Within weeks, the focus shifted to the Southern Hemisphere as the introduction of the novel virus coincided with the beginning of the influenza season. Intensive public health and health services planning had occurred in Australia and New Zealand as preparation for an influenza pandemic before 2009. However, this first pandemic wave was quite different to what had been expected. Key elements of the pandemic and response are outlined from the perspective of clinicians working at the frontline of patient care. In particular, they examine why past influenza pandemics and recent history are poor predictors of the current pandemic, the discordance between potential for transmission and disease severity, the broad clinical spectrum of H1N1-09 infection, clinical and health service management issues, and the relationship between health care and government policy. Finally, they address the need for the respiratory community to show leadership in times of crisis. Lessons learned in Australia and New Zealand during 2009 have important messages for similarly resourced countries in the Northern Hemisphere in the coming months as they face their own influenza season.
Published: 2010

25. Sequence variants affecting eosinophil numbers associate with asthma and myocardial infarction

Author: Gudbjartsson, Daniel F., Bjornsdottir, Unnur S., Halapi, Eva, Helgadottir, Anna, Sulem, Patrick, Jonsdottir, Gudrun M., Thorleifsson, Gudmar, Helgadottir, Hafdis, Steinthorsdottir, Valgerdur, Stefansson, Hreinn, Williams, Carolyn, Hui, Jennie, Beilby, John, Warrington, Nicole M., James, Alan, Palmer, Lyle J., Koppelman, Gerard H., Heinzmann, Andrea, Krueger, Marcus, Boezen, H. Marike, Wheatley, Amanda, Altmuller, Janine, Shin, Hyoung Doo, Uh, Soo-Taek, Cheong, Hyun Sub, Jonsdottir, Brynja, Gislason, David, Park, Choon-Sik, Rasmussen, Linda M., Porsbjerg, Celeste, Hansen, Jakob W., Backer, Vibeke, Werge, Thomas, Janson, Christer, Jönsson, Ulla-Britt, Ng, Maggie C. Y., Chan, Juliana, So, Wing Yee, Ma, Ronald, Shah, Svati H., Granger, Christopher B., Quyyumi, Arshed A., Levey, Allan I., Vaccarino, Viola, Reilly, Muredach P., Rader, Daniel J., Williams, Michael J. A., van Rij, Andre M., Jones, Gregory T., Trabetti, Elisabetta, Malerba, Giovanni, Pignatti, Pier Franco, Boner, Attilio, Pescollderungg, Lydia, Girelli, Domenico, Olivieri, Oliviero, Martinelli, Nicola, Ludviksson, Bjorn R., Ludviksdottir, Dora, Eyjolfsson, Gudmundur I., Arnar, David, Thorgeirsson, Gudmundur, Deichmann, Klaus, Thompson, Philip J., Wjst, Matthias, Hall, Ian P., Postma, Dirkje S., Gislason, Thorarinn, Gulcher, Jeffrey, Kong, Augustine, Jonsdottir, Ingileif, Thorsteinsdottir, Unnur, Stefansson, Kari, Gudbjartsson, Daniel F., Bjornsdottir, Unnur S., Halapi, Eva, Helgadottir, Anna, Sulem, Patrick, Jonsdottir, Gudrun M., Thorleifsson, Gudmar, Helgadottir, Hafdis, Steinthorsdottir, Valgerdur, Stefansson, Hreinn, Williams, Carolyn, Hui, Jennie, Beilby, John, Warrington, Nicole M., James, Alan, Palmer, Lyle J., Koppelman, Gerard H., Heinzmann, Andrea, Krueger, Marcus, Boezen, H. Marike, Wheatley, Amanda, Altmuller, Janine, Shin, Hyoung Doo, Uh, Soo-Taek, Cheong, Hyun Sub, Jonsdottir, Brynja, Gislason, David, Park, Choon-Sik, Rasmussen, Linda M., Porsbjerg, Celeste, Hansen, Jakob W., Backer, Vibeke, Werge, Thomas, Janson, Christer, Jönsson, Ulla-Britt, Ng, Maggie C. Y., Chan, Juliana, So, Wing Yee, Ma, Ronald, Shah, Svati H., Granger, Christopher B., Quyyumi, Arshed A., Levey, Allan I., Vaccarino, Viola, Reilly, Muredach P., Rader, Daniel J., Williams, Michael J. A., van Rij, Andre M., Jones, Gregory T., Trabetti, Elisabetta, Malerba, Giovanni, Pignatti, Pier Franco, Boner, Attilio, Pescollderungg, Lydia, Girelli, Domenico, Olivieri, Oliviero, Martinelli, Nicola, Ludviksson, Bjorn R., Ludviksdottir, Dora, Eyjolfsson, Gudmundur I., Arnar, David, Thorgeirsson, Gudmundur, Deichmann, Klaus, Thompson, Philip J., Wjst, Matthias, Hall, Ian P., Postma, Dirkje S., Gislason, Thorarinn, Gulcher, Jeffrey, Kong, Augustine, Jonsdottir, Ingileif, Thorsteinsdottir, Unnur, and Stefansson, Kari
Abstract: Eosinophils are pleiotropic multifunctional leukocytes involved in initiation and propagation of inflammatory responses and thus have important roles in the pathogenesis of inflammatory diseases. Here we describe a genome-wide association scan for sequence variants affecting eosinophil counts in blood of 9,392 Icelanders. The most significant SNPs were studied further in 12,118 Europeans and 5,212 East Asians. SNPs at 2q12 (rs1420101), 2q13 (rs12619285), 3q21 (rs4857855), 5q31 (rs4143832) and 12q24 (rs3184504) reached genome-wide significance (P = 5.3 x 10(-14), 5.4 x 10(-10), 8.6 x 10(-17), 1.2 x 10(-10) and 6.5 x 10(-19), respectively). A SNP at IL1RL1 associated with asthma (P = 5.5 x 10(-12)) in a collection of ten different populations (7,996 cases and 44,890 controls). SNPs at WDR36, IL33 and MYB that showed suggestive association with eosinophil counts were also associated with atopic asthma (P = 4.2 x 10(-6), 2.2 x 10(-5) and 2.4 x 10(-4), respectively). We also found that a nonsynonymous SNP at 12q24, in SH2B3, associated significantly (P = 8.6 x 10(-8)) with myocardial infarction in six different populations (6,650 cases and 40,621 controls).
Published: 2009
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26. Sequence variants affecting eosinophil numbers associate with asthma and myocardial infarction

Author: Gudbjartsson, Daniel F, Bjornsdottir, Unnur S, Halapi, Eva, Helgadottir, Anna, Sulem, Patrick, Jonsdottir, Gudrun M, Thorleifsson, Gudmar, Helgadottir, Hafdis, Steinthorsdottir, Valgerdur, Stefansson, Hreinn, Williams, Carolyn, Hui, Jennie, Beilby, John, Warrington, Nicole M, James, Alan, Palmer, Lyle J, Koppelman, Gerard H, Heinzmann, Andrea, Krueger, Marcus, Boezen, H Marike, Wheatley, Amanda, Altmuller, Janine, Shin, Hyoung Doo, Uh, Soo-Taek, Cheong, Hyun Sub, Jonsdottir, Brynja, Gislason, David, Park, Choon-Sik, Rasmussen, Linda M, Porsbjerg, Celeste, Hansen, Jakob W, Backer, Vibeke, Werge, Thomas, Janson, Christer, Jönsson, Ulla-Britt, Ng, Maggie C Y, Chan, Juliana, So, Wing Yee, Ma, Ronald, Shah, Svati H, Granger, Christopher B, Quyyumi, Arshed A, Levey, Allan I, Vaccarino, Viola, Reilly, Muredach P, Rader, Daniel J, Williams, Michael J A, van Rij, Andre M, Jones, Gregory T, Trabetti, Elisabetta, Malerba, Giovanni, Pignatti, Pier Franco, Boner, Attilio, Pescollderungg, Lydia, Girelli, Domenico, Olivieri, Oliviero, Martinelli, Nicola, Ludviksson, Bjorn R, Ludviksdottir, Dora, Eyjolfsson, Gudmundur I, Arnar, David, Thorgeirsson, Gudmundur, Deichmann, Klaus, Thompson, Philip J, Wjst, Matthias, Hall, Ian P, Postma, Dirkje S, Gislason, Thorarinn, Gulcher, Jeffrey, Kong, Augustine, Jonsdottir, Ingileif, Thorsteinsdottir, Unnur, Stefansson, Kari, Gudbjartsson, Daniel F, Bjornsdottir, Unnur S, Halapi, Eva, Helgadottir, Anna, Sulem, Patrick, Jonsdottir, Gudrun M, Thorleifsson, Gudmar, Helgadottir, Hafdis, Steinthorsdottir, Valgerdur, Stefansson, Hreinn, Williams, Carolyn, Hui, Jennie, Beilby, John, Warrington, Nicole M, James, Alan, Palmer, Lyle J, Koppelman, Gerard H, Heinzmann, Andrea, Krueger, Marcus, Boezen, H Marike, Wheatley, Amanda, Altmuller, Janine, Shin, Hyoung Doo, Uh, Soo-Taek, Cheong, Hyun Sub, Jonsdottir, Brynja, Gislason, David, Park, Choon-Sik, Rasmussen, Linda M, Porsbjerg, Celeste, Hansen, Jakob W, Backer, Vibeke, Werge, Thomas, Janson, Christer, Jönsson, Ulla-Britt, Ng, Maggie C Y, Chan, Juliana, So, Wing Yee, Ma, Ronald, Shah, Svati H, Granger, Christopher B, Quyyumi, Arshed A, Levey, Allan I, Vaccarino, Viola, Reilly, Muredach P, Rader, Daniel J, Williams, Michael J A, van Rij, Andre M, Jones, Gregory T, Trabetti, Elisabetta, Malerba, Giovanni, Pignatti, Pier Franco, Boner, Attilio, Pescollderungg, Lydia, Girelli, Domenico, Olivieri, Oliviero, Martinelli, Nicola, Ludviksson, Bjorn R, Ludviksdottir, Dora, Eyjolfsson, Gudmundur I, Arnar, David, Thorgeirsson, Gudmundur, Deichmann, Klaus, Thompson, Philip J, Wjst, Matthias, Hall, Ian P, Postma, Dirkje S, Gislason, Thorarinn, Gulcher, Jeffrey, Kong, Augustine, Jonsdottir, Ingileif, Thorsteinsdottir, Unnur, and Stefansson, Kari
Abstract: Eosinophils are pleiotropic multifunctional leukocytes involved in initiation and propagation of inflammatory responses and thus have important roles in the pathogenesis of inflammatory diseases. Here we describe a genome-wide association scan for sequence variants affecting eosinophil counts in blood of 9,392 Icelanders. The most significant SNPs were studied further in 12,118 Europeans and 5,212 East Asians. SNPs at 2q12 (rs1420101), 2q13 (rs12619285), 3q21 (rs4857855), 5q31 (rs4143832) and 12q24 (rs3184504) reached genome-wide significance (P = 5.3 x 10(-14), 5.4 x 10(-10), 8.6 x 10(-17), 1.2 x 10(-10) and 6.5 x 10(-19), respectively). A SNP at IL1RL1 associated with asthma (P = 5.5 x 10(-12)) in a collection of ten different populations (7,996 cases and 44,890 controls). SNPs at WDR36, IL33 and MYB that showed suggestive association with eosinophil counts were also associated with atopic asthma (P = 4.2 x 10(-6), 2.2 x 10(-5) and 2.4 x 10(-4), respectively). We also found that a nonsynonymous SNP at 12q24, in SH2B3, associated significantly (P = 8.6 x 10(-8)) with myocardial infarction in six different populations (6,650 cases and 40,621 controls).
Published: 2009

27. Sequence variants affecting eosinophil numbers associate with asthma and myocardial infarction

Author: Gudbjartsson, Daniel F, Bjornsdottir, Unnur S, Halapi, Eva, Helgadottir, Anna, Sulem, Patrick, Jonsdottir, Gudrun M, Thorleifsson, Gudmar, Helgadottir, Hafdis, Steinthorsdottir, Valgerdur, Stefansson, Hreinn, Williams, Carolyn, Hui, Jennie, Beilby, John, Warrington, Nicole M, James, Alan, Palmer, Lyle J, Koppelman, Gerard H, Heinzmann, Andrea, Krueger, Marcus, Boezen, H Marike, Wheatley, Amanda, Altmuller, Janine, Shin, Hyoung Doo, Uh, Soo-Taek, Cheong, Hyun Sub, Jonsdottir, Brynja, Gislason, David, Park, Choon-Sik, Rasmussen, Linda M, Porsbjerg, Celeste, Hansen, Jakob W, Backer, Vibeke, Werge, Thomas, Janson, Christer, Jönsson, Ulla-Britt, Ng, Maggie C Y, Chan, Juliana, So, Wing Yee, Ma, Ronald, Shah, Svati H, Granger, Christopher B, Quyyumi, Arshed A, Levey, Allan I, Vaccarino, Viola, Reilly, Muredach P, Rader, Daniel J, Williams, Michael J A, van Rij, Andre M, Jones, Gregory T, Trabetti, Elisabetta, Malerba, Giovanni, Pignatti, Pier Franco, Boner, Attilio, Pescollderungg, Lydia, Girelli, Domenico, Olivieri, Oliviero, Martinelli, Nicola, Ludviksson, Bjorn R, Ludviksdottir, Dora, Eyjolfsson, Gudmundur I, Arnar, David, Thorgeirsson, Gudmundur, Deichmann, Klaus, Thompson, Philip J, Wjst, Matthias, Hall, Ian P, Postma, Dirkje S, Gislason, Thorarinn, Gulcher, Jeffrey, Kong, Augustine, Jonsdottir, Ingileif, Thorsteinsdottir, Unnur, Stefansson, Kari, Porsbjerg, Celeste Michala, Gudbjartsson, Daniel F, Bjornsdottir, Unnur S, Halapi, Eva, Helgadottir, Anna, Sulem, Patrick, Jonsdottir, Gudrun M, Thorleifsson, Gudmar, Helgadottir, Hafdis, Steinthorsdottir, Valgerdur, Stefansson, Hreinn, Williams, Carolyn, Hui, Jennie, Beilby, John, Warrington, Nicole M, James, Alan, Palmer, Lyle J, Koppelman, Gerard H, Heinzmann, Andrea, Krueger, Marcus, Boezen, H Marike, Wheatley, Amanda, Altmuller, Janine, Shin, Hyoung Doo, Uh, Soo-Taek, Cheong, Hyun Sub, Jonsdottir, Brynja, Gislason, David, Park, Choon-Sik, Rasmussen, Linda M, Porsbjerg, Celeste, Hansen, Jakob W, Backer, Vibeke, Werge, Thomas, Janson, Christer, Jönsson, Ulla-Britt, Ng, Maggie C Y, Chan, Juliana, So, Wing Yee, Ma, Ronald, Shah, Svati H, Granger, Christopher B, Quyyumi, Arshed A, Levey, Allan I, Vaccarino, Viola, Reilly, Muredach P, Rader, Daniel J, Williams, Michael J A, van Rij, Andre M, Jones, Gregory T, Trabetti, Elisabetta, Malerba, Giovanni, Pignatti, Pier Franco, Boner, Attilio, Pescollderungg, Lydia, Girelli, Domenico, Olivieri, Oliviero, Martinelli, Nicola, Ludviksson, Bjorn R, Ludviksdottir, Dora, Eyjolfsson, Gudmundur I, Arnar, David, Thorgeirsson, Gudmundur, Deichmann, Klaus, Thompson, Philip J, Wjst, Matthias, Hall, Ian P, Postma, Dirkje S, Gislason, Thorarinn, Gulcher, Jeffrey, Kong, Augustine, Jonsdottir, Ingileif, Thorsteinsdottir, Unnur, Stefansson, Kari, and Porsbjerg, Celeste Michala
Abstract: Udgivelsesdato: 2009-Mar, Eosinophils are pleiotropic multifunctional leukocytes involved in initiation and propagation of inflammatory responses and thus have important roles in the pathogenesis of inflammatory diseases. Here we describe a genome-wide association scan for sequence variants affecting eosinophil counts in blood of 9,392 Icelanders. The most significant SNPs were studied further in 12,118 Europeans and 5,212 East Asians. SNPs at 2q12 (rs1420101), 2q13 (rs12619285), 3q21 (rs4857855), 5q31 (rs4143832) and 12q24 (rs3184504) reached genome-wide significance (P = 5.3 x 10(-14), 5.4 x 10(-10), 8.6 x 10(-17), 1.2 x 10(-10) and 6.5 x 10(-19), respectively). A SNP at IL1RL1 associated with asthma (P = 5.5 x 10(-12)) in a collection of ten different populations (7,996 cases and 44,890 controls). SNPs at WDR36, IL33 and MYB that showed suggestive association with eosinophil counts were also associated with atopic asthma (P = 4.2 x 10(-6), 2.2 x 10(-5) and 2.4 x 10(-4), respectively). We also found that a nonsynonymous SNP at 12q24, in SH2B3, associated significantly (P = 8.6 x 10(-8)) with myocardial infarction in six different populations (6,650 cases and 40,621 controls).
Published: 2009

28. Sequence variants affecting eosinophil numbers associate with asthma and myocardial infarction

Author: Gudbjartsson, Daniel F, Bjornsdottir, Unnur S, Halapi, Eva, Helgadottir, Anna, Sulem, Patrick, Jonsdottir, Gudrun M, Thorleifsson, Gudmar, Helgadottir, Hafdis, Steinthorsdottir, Valgerdur, Stefansson, Hreinn, Williams, Carolyn, Hui, Jennie, Beilby, John, Warrington, Nicole M, James, Alan, Palmer, Lyle J, Koppelman, Gerard H, Heinzmann, Andrea, Krueger, Marcus, Boezen, H Marike, Wheatley, Amanda, Altmuller, Janine, Shin, Hyoung Doo, Uh, Soo-Taek, Cheong, Hyun Sub, Jonsdottir, Brynja, Gislason, David, Park, Choon-Sik, Rasmussen, Linda M, Porsbjerg, Celeste, Hansen, Jakob W, Backer, Vibeke, Werge, Thomas, Janson, Christer, Jönsson, Ulla-Britt, Ng, Maggie C Y, Chan, Juliana, So, Wing Yee, Ma, Ronald, Shah, Svati H, Granger, Christopher B, Quyyumi, Arshed A, Levey, Allan I, Vaccarino, Viola, Reilly, Muredach P, Rader, Daniel J, Williams, Michael J A, van Rij, Andre M, Jones, Gregory T, Trabetti, Elisabetta, Malerba, Giovanni, Pignatti, Pier Franco, Boner, Attilio, Pescollderungg, Lydia, Girelli, Domenico, Olivieri, Oliviero, Martinelli, Nicola, Ludviksson, Bjorn R, Ludviksdottir, Dora, Eyjolfsson, Gudmundur I, Arnar, David, Thorgeirsson, Gudmundur, Deichmann, Klaus, Thompson, Philip J, Wjst, Matthias, Hall, Ian P, Postma, Dirkje S, Gislason, Thorarinn, Gulcher, Jeffrey, Kong, Augustine, Jonsdottir, Ingileif, Thorsteinsdottir, Unnur, Stefansson, Kari, Gudbjartsson, Daniel F, Bjornsdottir, Unnur S, Halapi, Eva, Helgadottir, Anna, Sulem, Patrick, Jonsdottir, Gudrun M, Thorleifsson, Gudmar, Helgadottir, Hafdis, Steinthorsdottir, Valgerdur, Stefansson, Hreinn, Williams, Carolyn, Hui, Jennie, Beilby, John, Warrington, Nicole M, James, Alan, Palmer, Lyle J, Koppelman, Gerard H, Heinzmann, Andrea, Krueger, Marcus, Boezen, H Marike, Wheatley, Amanda, Altmuller, Janine, Shin, Hyoung Doo, Uh, Soo-Taek, Cheong, Hyun Sub, Jonsdottir, Brynja, Gislason, David, Park, Choon-Sik, Rasmussen, Linda M, Porsbjerg, Celeste, Hansen, Jakob W, Backer, Vibeke, Werge, Thomas, Janson, Christer, Jönsson, Ulla-Britt, Ng, Maggie C Y, Chan, Juliana, So, Wing Yee, Ma, Ronald, Shah, Svati H, Granger, Christopher B, Quyyumi, Arshed A, Levey, Allan I, Vaccarino, Viola, Reilly, Muredach P, Rader, Daniel J, Williams, Michael J A, van Rij, Andre M, Jones, Gregory T, Trabetti, Elisabetta, Malerba, Giovanni, Pignatti, Pier Franco, Boner, Attilio, Pescollderungg, Lydia, Girelli, Domenico, Olivieri, Oliviero, Martinelli, Nicola, Ludviksson, Bjorn R, Ludviksdottir, Dora, Eyjolfsson, Gudmundur I, Arnar, David, Thorgeirsson, Gudmundur, Deichmann, Klaus, Thompson, Philip J, Wjst, Matthias, Hall, Ian P, Postma, Dirkje S, Gislason, Thorarinn, Gulcher, Jeffrey, Kong, Augustine, Jonsdottir, Ingileif, Thorsteinsdottir, Unnur, and Stefansson, Kari
Abstract: Eosinophils are pleiotropic multifunctional leukocytes involved in initiation and propagation of inflammatory responses and thus have important roles in the pathogenesis of inflammatory diseases. Here we describe a genome-wide association scan for sequence variants affecting eosinophil counts in blood of 9,392 Icelanders. The most significant SNPs were studied further in 12,118 Europeans and 5,212 East Asians. SNPs at 2q12 (rs1420101), 2q13 (rs12619285), 3q21 (rs4857855), 5q31 (rs4143832) and 12q24 (rs3184504) reached genome-wide significance (P = 5.3 x 10(-14), 5.4 x 10(-10), 8.6 x 10(-17), 1.2 x 10(-10) and 6.5 x 10(-19), respectively). A SNP at IL1RL1 associated with asthma (P = 5.5 x 10(-12)) in a collection of ten different populations (7,996 cases and 44,890 controls). SNPs at WDR36, IL33 and MYB that showed suggestive association with eosinophil counts were also associated with atopic asthma (P = 4.2 x 10(-6), 2.2 x 10(-5) and 2.4 x 10(-4), respectively). We also found that a nonsynonymous SNP at 12q24, in SH2B3, associated significantly (P = 8.6 x 10(-8)) with myocardial infarction in six different populations (6,650 cases and 40,621 controls).
Published: 2009

29. Sequence variants affecting eosinophil numbers associate with asthma and myocardial infarction

Author: Gudbjartsson, Daniel F, Bjornsdottir, Unnur S, Halapi, Eva, Helgadottir, Anna, Sulem, Patrick, Jonsdottir, Gudrun M, Thorleifsson, Gudmar, Helgadottir, Hafdis, Steinthorsdottir, Valgerdur, Stefansson, Hreinn, Williams, Carolyn, Hui, Jennie, Beilby, John, Warrington, Nicole M, James, Alan, Palmer, Lyle J, Koppelman, Gerard H, Heinzmann, Andrea, Krueger, Marcus, Boezen, H Marike, Wheatley, Amanda, Altmuller, Janine, Shin, Hyoung Doo, Uh, Soo-Taek, Cheong, Hyun Sub, Jonsdottir, Brynja, Gislason, David, Park, Choon-Sik, Rasmussen, Linda M, Porsbjerg, Celeste, Hansen, Jakob W, Backer, Vibeke, Werge, Thomas, Janson, Christer, Jönsson, Ulla-Britt, Ng, Maggie C Y, Chan, Juliana, So, Wing Yee, Ma, Ronald, Shah, Svati H, Granger, Christopher B, Quyyumi, Arshed A, Levey, Allan I, Vaccarino, Viola, Reilly, Muredach P, Rader, Daniel J, Williams, Michael J A, van Rij, Andre M, Jones, Gregory T, Trabetti, Elisabetta, Malerba, Giovanni, Pignatti, Pier Franco, Boner, Attilio, Pescollderungg, Lydia, Girelli, Domenico, Olivieri, Oliviero, Martinelli, Nicola, Ludviksson, Bjorn R, Ludviksdottir, Dora, Eyjolfsson, Gudmundur I, Arnar, David, Thorgeirsson, Gudmundur, Deichmann, Klaus, Thompson, Philip J, Wjst, Matthias, Hall, Ian P, Postma, Dirkje S, Gislason, Thorarinn, Gulcher, Jeffrey, Kong, Augustine, Jonsdottir, Ingileif, Thorsteinsdottir, Unnur, Stefansson, Kari, Porsbjerg, Celeste Michala, Gudbjartsson, Daniel F, Bjornsdottir, Unnur S, Halapi, Eva, Helgadottir, Anna, Sulem, Patrick, Jonsdottir, Gudrun M, Thorleifsson, Gudmar, Helgadottir, Hafdis, Steinthorsdottir, Valgerdur, Stefansson, Hreinn, Williams, Carolyn, Hui, Jennie, Beilby, John, Warrington, Nicole M, James, Alan, Palmer, Lyle J, Koppelman, Gerard H, Heinzmann, Andrea, Krueger, Marcus, Boezen, H Marike, Wheatley, Amanda, Altmuller, Janine, Shin, Hyoung Doo, Uh, Soo-Taek, Cheong, Hyun Sub, Jonsdottir, Brynja, Gislason, David, Park, Choon-Sik, Rasmussen, Linda M, Porsbjerg, Celeste, Hansen, Jakob W, Backer, Vibeke, Werge, Thomas, Janson, Christer, Jönsson, Ulla-Britt, Ng, Maggie C Y, Chan, Juliana, So, Wing Yee, Ma, Ronald, Shah, Svati H, Granger, Christopher B, Quyyumi, Arshed A, Levey, Allan I, Vaccarino, Viola, Reilly, Muredach P, Rader, Daniel J, Williams, Michael J A, van Rij, Andre M, Jones, Gregory T, Trabetti, Elisabetta, Malerba, Giovanni, Pignatti, Pier Franco, Boner, Attilio, Pescollderungg, Lydia, Girelli, Domenico, Olivieri, Oliviero, Martinelli, Nicola, Ludviksson, Bjorn R, Ludviksdottir, Dora, Eyjolfsson, Gudmundur I, Arnar, David, Thorgeirsson, Gudmundur, Deichmann, Klaus, Thompson, Philip J, Wjst, Matthias, Hall, Ian P, Postma, Dirkje S, Gislason, Thorarinn, Gulcher, Jeffrey, Kong, Augustine, Jonsdottir, Ingileif, Thorsteinsdottir, Unnur, Stefansson, Kari, and Porsbjerg, Celeste Michala
Abstract: Udgivelsesdato: 2009-Mar, Eosinophils are pleiotropic multifunctional leukocytes involved in initiation and propagation of inflammatory responses and thus have important roles in the pathogenesis of inflammatory diseases. Here we describe a genome-wide association scan for sequence variants affecting eosinophil counts in blood of 9,392 Icelanders. The most significant SNPs were studied further in 12,118 Europeans and 5,212 East Asians. SNPs at 2q12 (rs1420101), 2q13 (rs12619285), 3q21 (rs4857855), 5q31 (rs4143832) and 12q24 (rs3184504) reached genome-wide significance (P = 5.3 x 10(-14), 5.4 x 10(-10), 8.6 x 10(-17), 1.2 x 10(-10) and 6.5 x 10(-19), respectively). A SNP at IL1RL1 associated with asthma (P = 5.5 x 10(-12)) in a collection of ten different populations (7,996 cases and 44,890 controls). SNPs at WDR36, IL33 and MYB that showed suggestive association with eosinophil counts were also associated with atopic asthma (P = 4.2 x 10(-6), 2.2 x 10(-5) and 2.4 x 10(-4), respectively). We also found that a nonsynonymous SNP at 12q24, in SH2B3, associated significantly (P = 8.6 x 10(-8)) with myocardial infarction in six different populations (6,650 cases and 40,621 controls).
Published: 2009

30. Expression of kinin B1 and B2 receptors in immature, monocyte-derived dendritic cells and bradykinin-mediated increase in intracellular Ca2+ and cell migration

Author: Bertram, Cornelia M., Baltic, Svetlana, Misso, Neil L A, Bhoola, Kanti D., Foster, Paul S, Thompson, Philip J, Fogel-Petrovic, Mirjana, Bertram, Cornelia M., Baltic, Svetlana, Misso, Neil L A, Bhoola, Kanti D., Foster, Paul S, Thompson, Philip J, and Fogel-Petrovic, Mirjana
Abstract: The kinins, bradykinin (BK) and Lysdes[ Arg9]-BK, are important inflammatory mediators that act via two specific G protein-coupled kinins, B1 and B2 receptors (B2R). Kinins influence the activity of immune cells by stimulating the synthesis of cytokines
Published: 2007

31. Changes in bronchial hyperresponsiveness following high- and low-sulphite wine challenges in wine-sensitive asthmatic patients

Author: Vally, Hassan, Thompson, Philip J, Misso, Neil L A, Vally, Hassan, Thompson, Philip J, and Misso, Neil L A
Abstract: Background: Previous studies suggest that challenge of most wine-sensitive asthmatic patients may not result in a reduction in forced expiratory volume in 1 s (FEV1). Objective: The aim of this study was to assess whether changes in bronchial hyperresponsiveness (BHR) occur following wine challenge of asthmatic patients who report sensitivity to wine, and whether such changes could help clarify the role of sulphite additives in wine-induced asthmatic responses. Methods: Eight self-reporting wine-sensitive asthmatic patients completed double-blind challenges with high- and low-sulphite wines on separate days. FEV1 and histamine PC20 were measured before and after consumption of 150 mL of wine. Results: None of the eight subjects demonstrated a clinically significant (≥15%) reduction in FEV1 following challenge with either high- or low-sulphite wine. In contrast, one patient demonstrated clinically significant increase in BHR following challenge with both high- and low-sulphite wines, and a smaller increase in BHR following placebo challenge. A second patient showed a significant increase, while another showed a significant decrease in BHR following challenge with low-sulphite wine. A fourth patient showed borderline increases in BHR following challenge with both high- and low-sulphite wines. Conclusions: Although changes in BHR, in the absence of reductions in FEV1, were observed in some asthmatic patients following wine challenge, these changes were not consistent with a single aetiology. Consequently, this study did not support a major role for the sulphite additives in wine-induced asthmatic responses in the patients studied. The aetiology of wine-induced asthma is likely to be complex and appears to vary among individuals who are sensitive to these drinks.
Published: 2007

32. Inhibition of Arginase I Activity by RNA Interference Attenuates IL-13-Induced Airways Hyperresponsiveness

Author: Yang, Ming, Rangasamy, Danny, Matthaei, Klaus, Frew, Ailsa, Zimmermann, Nives, Mahalingam, Surendran, Webb, Dianne, Tremethick, David, Thompson, Philip J, Hogan, Simon, Rosenberg, Marc E, Cowden, William, Foster, Paul S, Yang, Ming, Rangasamy, Danny, Matthaei, Klaus, Frew, Ailsa, Zimmermann, Nives, Mahalingam, Surendran, Webb, Dianne, Tremethick, David, Thompson, Philip J, Hogan, Simon, Rosenberg, Marc E, Cowden, William, and Foster, Paul S
Abstract: Increased arginase I activity is associated with allergic disorders such as asthma. How arginase I contributes to and is regulated by allergic inflammatory processes remains unknown. CD4+ Th2 lymphocytes (Th2 cells) and IL-13 are two crucial immune regulators that use STAT6-dependent pathways to induce allergic airways inflammation and enhanced airways responsiveness to spasmogens (airways hyperresponsiveness (AHR)). This pathway is also used to activate arginase I in isolated cells and in hepatic infection with helminths. In the present study, we show that arginase I expression is also regulated in the lung in a STAT6-dependent manner by Th2-induced allergic inflammation or by IL-13 alone. IL-13-induced expression of arginase I correlated directly with increased synthesis of urea and with reduced synthesis of NO. Expression of arginase I, bat not eosinophilia or mucus hypersecretion, temporally correlated with the development, persistence, and resolution of IL-13-induced AHR. Pharmacological supplementation with L-arginine or with NO donors amplified or attenuated IL-13-induced AHR, respectively. Moreover, inducing loss of function of arginase I specifically in the lung by using RNA interference abrogated the development of IL-13-induced AHR. These data suggest an important role for metabolism of L-arginine by arginase I in the modulation of IL-13-induced AHR and identify a potential pathway distal to cytokine receptor interactions for the control of IL-13-mediated bronchoconstriction in asthma.
Published: 2006

33. Alcoholic drink consumption: a role in the development of allergic disease?

Author: Vally, Hassan, Thompson, Philip J, Vally, Hassan, and Thompson, Philip J
Published: 2003

34. Allergic and asthmatic reactions to alcoholic drinks

Author: Vally, Hassan, Thompson, Philip J, Vally, Hassan, and Thompson, Philip J
Abstract: Alcoholic drinks are capable of triggering a wide range of allergic and allergic-like responses, including rhinitis, itching, facial swelling, headache, cough and asthma. Limited epidemiological data suggests that many individuals are affected and that sensitivities occur to a variety of drinks, including wine, beer and spirits. In surveys of asthmatics, over 40% reported the triggering of allergic or allergic-like symptoms following alcoholic drink consumption and 30-35% reported worsening of their asthma. Sensitivity to ethanol itself can play a role in triggering adverse responses, particularly in Asians, which is due mainly to a reduced capacity to metabolize acetaldehyde. In Caucasians, specific non-alcohol components are the main cause of sensitivities to alcoholic drinks. Allergic sensitivities to specific components of beer, spirits and distilled liquors have been described. Wine is clearly the most commonly reported trigger for adverse responses. Sensitivities to wine appear to be due mainly to pharmacological intolerances to specific components, such as biogenic amines and the sulphite additives. Histamine in wine has been associated with the triggering of a wide spectrum of adverse symptoms, including sneezing, rhinitis, itching, flushing, headache and asthma. The sulphite additives in wine have been associated with triggering asthmatic responses. Clinical studies have confirmed sensitivities to the sulphites in wine in limited numbers of individuals, but the extent to which the sulphites contribute to wine sensitivity overall is not clear. The aetiology of wine-induced asthmatic responses may be complex and may involve several co-factors.
Published: 2003

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34 results on '"Thompson, Philip J."'

1. Characterisation of the Australian Adult Population Living with Asthma: Severe - Exacerbation Frequency, Long-Term OCS Use and Adverse Effects

2. Multiancestry association study identifies new asthma risk loci that colocalize with immune-cell enhancer marks

3. Multiancestry association study identifies new asthma risk loci that colocalize with immune-cell enhancer marks

4. Multiancestry association study identifies new asthma risk loci that colocalize with immune-cell enhancer marks

5. Association Between Telomere Length and Risk of Cancer and Non-Neoplastic Diseases A Mendelian Randomization Study

6. Shared genetic origin of asthma, hay fever and eczema elucidates allergic disease biology

7. Characteristics associated with clinical severity and inflammatory phenotype of naturally occurring virus-induced exacerbations of asthma in adults

8. Meta-analysis identifies seven susceptibility loci involved in the atopic march

9. Meta-analysis identifies seven susceptibility loci involved in the atopic march

10. Meta-analysis identifies seven susceptibility loci involved in the atopic march

11. Meta-analysis of genome-wide association studies identifies ten loci influencing allergic sensitization

12. Meta-analysis of genome-wide association studies identifies ten loci influencing allergic sensitization

13. Genome-Wide Association Studies of Asthma in Population-Based Cohorts Confirm Known and Suggested Loci and Identify an Additional Association near HLA

14. Genome-Wide Association Studies of Asthma in Population-Based Cohorts Confirm Known and Suggested Loci and Identify an Additional Association near HLA

15. Genome-Wide Association Studies of Asthma in Population-Based Cohorts Confirm Known and Suggested Loci and Identify an Additional Association near HLA

16. Genome-Wide Association Studies of Asthma in Population-Based Cohorts Confirm Known and Suggested Loci and Identify an Additional Association near HLA

17. Genome-Wide Association Studies of Asthma in Population-Based Cohorts Confirm Known and Suggested Loci and Identify an Additional Association near HLA

18. Genome-Wide Association Studies of Asthma in Population-Based Cohorts Confirm Known and Suggested Loci and Identify an Additional Association near HLA

19. FluCAN 2009: initial results from sentinel surveillance for adult influenza and pneumonia in eight Australian hospitals

20. Effectiveness of H1N1/09 monovalent and trivalent influenza vaccines against hospitalization with laboratory-confirmed H1N1/09 influenza in Australia: A test-negative case control study

21. Meta-analysis of genome-wide association studies identifies three new risk loci for atopic dermatitis

22. Meta-analysis of genome-wide association studies identifies three new risk loci for atopic dermatitis

23. Meta-analysis of genome-wide association studies identifies three new risk loci for atopic dermatitis

24. Influenza A/H1N1_09: Australia and New Zealand's Winter of Discontent

25. Sequence variants affecting eosinophil numbers associate with asthma and myocardial infarction

26. Sequence variants affecting eosinophil numbers associate with asthma and myocardial infarction

27. Sequence variants affecting eosinophil numbers associate with asthma and myocardial infarction

28. Sequence variants affecting eosinophil numbers associate with asthma and myocardial infarction

29. Sequence variants affecting eosinophil numbers associate with asthma and myocardial infarction

30. Expression of kinin B1 and B2 receptors in immature, monocyte-derived dendritic cells and bradykinin-mediated increase in intracellular Ca2+ and cell migration

31. Changes in bronchial hyperresponsiveness following high- and low-sulphite wine challenges in wine-sensitive asthmatic patients

32. Inhibition of Arginase I Activity by RNA Interference Attenuates IL-13-Induced Airways Hyperresponsiveness

33. Alcoholic drink consumption: a role in the development of allergic disease?

34. Allergic and asthmatic reactions to alcoholic drinks

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