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578 results on '"Reilly, Cavan"'

102. Abstract A25: Collecting gut microbiome in the 10,000 Families Study

Author

Prizment, Anna, primary, Gabrielson, Deanna, additional, Lazovich, DeAnn, additional, Minnerath, Sharon, additional, Nelson, Heather H., additional, Poynter, Jenny N., additional, Reilly, Cavan, additional, Roesler, Michelle, additional, Spector, Logan G., additional, and Thyagarajan, Bharat, additional

Published
2020
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103. Field Application of Digital Technologies for Health Assessment in the 10,000 Families Study

Author

Thyagarajan, Bharat, primary, Nelson, Heather H., additional, Poynter, Jenny N., additional, Prizment, Anna E., additional, Roesler, Michelle A., additional, Cassidy, Erin, additional, Putnam, Sara, additional, Amos, Laura, additional, Hickle, Andrea, additional, Reilly, Cavan, additional, Spector, Logan G., additional, and Lazovich, DeAnn, additional

Published
2020
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108. Simian immunodeficiency virus-induced intestinal cell apoptosis is the underlying mechanism of the regenerative enteropathy of early infection

Author

Li, Qingsheng, Estes, Jacob D., Duan, Lijie, Jessurun, Jose, Pambuccian, Stefan, Forster, Colleen, Wietgrefe, Stephen, Zupancic, Mary, Schacker, Timothy, Reilly, Cavan, Carlis, John V., and Haase, Ashley T.

Subjects
Simian immunodeficiency virus -- Physiological aspects, Apoptosis -- Development and progression, Epithelial cells -- Physiological aspects, Colon (Anatomy) -- Physiological aspects, Health
Published
2008

110. Simian immunodeficiency virus-induced lymphatic tissue fibrosis is mediated by transforming growth factor (beta)1-positive regulatory T cells and begins in early infection

Author

Estes, Jacob D., Wietgrefe, Stephen, Schacker, Timothy, Southern, Peter, Beilman, Greg, Reilly, Cavan, Milush, Jeffrey M., Lifson, Jeffrey D., Sodora, Donald L., Carlis, John V., and Haase, Ashley T.

Subjects
Simian immunodeficiency virus -- Research, Simian immunodeficiency virus -- Health aspects, Simian immunodeficiency virus -- Development and progression, Fibrosis -- Risk factors, Fibrosis -- Research, Growth factors -- Research, Growth factors -- Physiological aspects, T cells -- Research, T cells -- Physiological aspects, Lymphatic diseases -- Research, Lymphatic diseases -- Risk factors, Health
Published
2007

116. Abstract PR09: Field application of digital technologies for health assessment in the 10,000 Families Study

Author

Bharat Thyagarajan, Lazovich DeAnn, Nelson H. Heather, Poynter Jen, Prizment Anna, Roesler Michelle, Cassidy Erin, Putnam Sara, Reilly Cavan, and Spector Logan

Subjects
Oncology, Epidemiology
Abstract

The 10,000 Families Study (10KFS) is a Minnesota-based cohort study designed to study longitudinal changes in health. Here we report our efforts from a pilot study of 10KFS. During health fairs hosted by the study, we measured anthropometrics, blood pressure, and grip strength; collected biospecimens; performed vision and hearing assessments; and measured lung function and cognitive function. We describe the field deployment of digital applications for measurement of cognitive function, lung function, and hearing assessment in 10KFS. We measure cognitive function using the Digital Clock Drawing (dDCT) test (Cognition Technologies Inc.), a multidimensional task that evaluates spatial skills, semantic knowledge, planning, and motor functioning. We perform spirometry to assess lung function using an Air Smart Spirometer (Pond Healthcare Innovation) that uses a spirometry app (NuvoAir) to estimate forced expiratory volume in one second (FEV1), forced vital capacity (FVC) and peak expiratory flow (PEF). We measure hearing using an iPad-enabled audiometry device (Shoebox, Inc.) that allows us to estimate air conduction and bone conduction over a range of tones from 500-8000 Hertz. These digital devices are low cost and the measurements are readily implemented with minimal training of study staff (training time 2-3 hours). To date, we have performed these measurements on 139 10KFS participants (age range: 5 years–100 years) during an in-person clinic visit. A vast majority (88%; n=123) of eligible 10KFS participants successfully completed all these measurements; participants across the age spectrum were comfortable using these digital technologies during their clinic visit. The Digital Clock Drawing test was administered only to adults >40 years old and completion rates were 92% (n=34) for participants between 41-64 years old and 95% (n=35) for those over 65 years old. The Air Smart Spirometer was administered to participants over 4 years old without a contraindication and completion rates were 96% (n=22) for children 5-17 years old, 98% (n=64) for adults 18-64 years old, and 100% (n=36) for adults over the age of 65 years. The audiometry test was administered to participants >3 years old and completion rates were 87% (n=20) for children 4-17 years old, 100% (n=67) for adults 18-64 years old, and 100% (n=37) for adults over the age of 65 years. As compared to traditional methods for collecting information on cognitive function, lung function, and hearing, these devices allow for real-time monitoring of quality-control measures and allow deployment of standardized methods of data collection in a variety of settings that do not require specialized equipment or have space constraints. In the future we anticipate deploying these methods to a broader range of data collection venues that may include in-home visits, remote assessments, and clinic visits. This abstract is also being presented as Poster A28. Citation Format: Bharat Thyagarajan, Lazovich DeAnn, Nelson H. Heather, Poynter Jen, Prizment Anna, Roesler Michelle, Cassidy Erin, Putnam Sara, Reilly Cavan, Spector Logan. Field application of digital technologies for health assessment in the 10,000 Families Study [abstract]. In: Proceedings of the AACR Special Conference on Modernizing Population Sciences in the Digital Age; 2019 Feb 19-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(9 Suppl):Abstract nr PR09.

Published
2020

119. Scalable, semi-automated fluorescence reduction neutralization assay for qualitative assessment of Ebola virus-neutralizing antibodies in human clinical samples

Author

Postnikova, Elena N., primary, Pettitt, James, additional, Van Ryn, Collin J., additional, Holbrook, Michael R., additional, Bollinger, Laura, additional, Yú, Shuǐqìng, additional, Caì, Yíngyún, additional, Liang, Janie, additional, Sneller, Michael C., additional, Jahrling, Peter B., additional, Hensley, Lisa E., additional, Kuhn, Jens H., additional, Fallah, Mosoka P., additional, Bennett, Richard S., additional, and Reilly, Cavan, additional

Published
2019
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122. Metabolite profiles associated with disease progression in influenza infection.

Author

Wendt, Chris H., Castro-Pearson, Sandra, Proper, Jennifer, Pett, Sarah, Griffin, Timothy J., Kan, Virginia, Carbone, Javier, Koulouris, Nikolaos, Reilly, Cavan, and Neaton, James D.

Subjects
DISEASE progression, INFLUENZA, INTENSIVE care units, ODDS ratio, MASS spectrometry
Abstract

Background: We performed metabolomic profiling to identify metabolites that correlate with disease progression and death. Methods: We performed a study of adults hospitalized with Influenza A(H1N1)pdm09. Cases (n = 32) were defined by a composite outcome of death or transfer to the intensive care unit during the 60-day follow-up period. Controls (n = 64) were survivors who did not require transfer to the ICU. Four hundred and eight metabolites from eight families were measured on plasma sample at enrollment using a mass spectrometry based Biocrates platform. Conditional logistic regression was used to summarize the association of the individual metabolites and families with the composite outcome and its major two components. Results: The ten metabolites with the strongest association with disease progression belonged to five different metabolite families with sphingolipids being the most common. The acylcarnitines, glycerides, sphingolipids and biogenic metabolite families had the largest odds ratios based on the composite endpoint. The tryptophan odds ratio for the composite is largely associated with death (OR 17.33: 95% CI, 1.60–187.76). Conclusions: Individuals that develop disease progression when infected with Influenza H1N1 have a metabolite signature that differs from survivors. Low levels of tryptophan had a strong association with death. Registry: ClinicalTrials.gov Identifier: NCT01056185 [ABSTRACT FROM AUTHOR]

Published
2021
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123. Gene expression alterations in brains of mice infected with three strains of scrapie

Author

Race Richard E, Chesebro Bruce, Abbassi Hayet, Skinner Pamela J, Reilly Cavan, and Haase Ashley T

Subjects
Biotechnology, TP248.13-248.65, Genetics, QH426-470
Abstract

Abstract Background Transmissible spongiform encephalopathies (TSEs) or prion diseases are fatal neurodegenerative disorders which occur in humans and various animal species. Examples include Creutzfeldt-Jakob disease (CJD) in humans, bovine spongiform encephalopathy (BSE) in cattle, chronic wasting disease (CWD) in deer and elk, and scrapie in sheep, and experimental mice. To gain insights into TSE pathogenesis, we made and used cDNA microarrays to identify disease-associated alterations in gene expression. Brain gene expression in scrapie-infected mice was compared to mock-infected mice at pre-symptomatic and symptomatic time points. Three strains of mouse scrapie that show striking differences in neuropathology were studied: ME7, 22L, and Chandler/RML. Results In symptomatic mice, over 400 significant gene expression alterations were identified. In contrast, only 22 genes showed significant alteration in the pre-symptomatic animals. We also identified genes that showed significant differences in alterations in gene expression between strains. Genes identified in this study encode proteins that are involved in many cellular processes including protein folding, endosome/lysosome function, immunity, synapse function, metal ion binding, calcium regulation and cytoskeletal function. Conclusion These studies shed light on the complex molecular events that occur during prion disease, and identify genes whose further study may yield new insights into strain specific neuropathogenesis and ante-mortem tests for TSEs.

Published
2006
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129. Assessment and Optimization of the GeneXpert Diagnostic Platform for Detection of Ebola Virus RNA in Seminal Fluid

Author

Pettitt, James, primary, Higgs, Elizabeth, additional, Fallah, Mosoka, additional, Nason, Martha, additional, Stavale, Eric, additional, Marchand, Jonathan, additional, Reilly, Cavan, additional, Jensen, Kenneth, additional, Dighero-Kemp, Bonnie, additional, Tuznik, Kaylie, additional, Logue, James, additional, Bolay, Fatorma, additional, and Hensley, Lisa, additional

Published
2016
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130. Additional file 8: of HIV-1 and HIV-2 exhibit similar mutation frequencies and spectra in the absence of G-to-A hypermutation

Author

Rawson, Jonathan, Landman, Sean, Reilly, Cavan, and Mansky, Louis

Abstract

Figure S3. Dinucleotide contexts of G-to-A mutations not occurring within G-to-A hypermutants. The dinucleotide contexts of all G-to-A mutations from HIV-1 and HIV-2 single mutants (i.e. non-hypermutants) were determined, demonstrating the lack of a bias toward GA and/or GG dinucleotides.

Published
2015
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131. Additional file 2: of Protein relative abundance patterns associated with sucrose-induced dysbiosis are conserved across taxonomically diverse oral microcosm biofilm models of dental caries

Author

Rudney, Joel, Pratik Jagtap, Reilly, Cavan, Ruoqiong Chen, Markowski, Todd, LeeAnn Higgins, Johnson, James, and Griffin, Timothy

Abstract

Heat map of HOMINGS data. The color key is on a logarithmic scale. The Bray-Curtis distance metric was used to generate the dendrograms. Each column represents a plaque, NS, or WS microcosm sample; labels provided for the columns are colored blue for plaque, green for NS, or red for WS. Each row represents one of the 453 HOMINGS probes that were positive for at least one sample (probes that were not detected in any sample are excluded). Row labels are not shown, since they would not be legible. Additional files 3, 4, and 5 list all positive probes.

Published
2015
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132. Additional file 4: of HIV-1 and HIV-2 exhibit similar mutation frequencies and spectra in the absence of G-to-A hypermutation

Author

Rawson, Jonathan, Landman, Sean, Reilly, Cavan, and Mansky, Louis

Abstract

Figure S1. Bias of transversion spectra toward C-to-A and G-to-T mutations. The transversion spectra for HIV-1 and HIV-2 biological samples and plasmid controls are illustrated, revealing a clear bias toward C-to-A and G-to-T transversion types, particularly for the plasmid controls.

Published
2015
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133. Additional file 10: of Protein relative abundance patterns associated with sucrose-induced dysbiosis are conserved across taxonomically diverse oral microcosm biofilm models of dental caries

Author

Rudney, Joel, Pratik Jagtap, Reilly, Cavan, Ruoqiong Chen, Markowski, Todd, LeeAnn Higgins, Johnson, James, and Griffin, Timothy

Abstract

Heat map of MEGAN5 SEED assignments. The color key is on a logarithmic scale. The Bray-Curtis distance metric was used to generate the dendrograms. Each column represents a NS, or WS microcosm sample; labels provided for the columns are colored green for NS or red for WS. Each row represents one of the 1969 SEED-assigned proteins. Row labels are not shown, since they would not be legible. Additional file 9 lists all protein assignments.

Published
2015
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134. Additional file 7: of Protein relative abundance patterns associated with sucrose-induced dysbiosis are conserved across taxonomically diverse oral microcosm biofilm models of dental caries

Author

Rudney, Joel, Pratik Jagtap, Reilly, Cavan, Ruoqiong Chen, Markowski, Todd, LeeAnn Higgins, Johnson, James, and Griffin, Timothy

Abstract

Heat map of species-level MEGAN5 LCA assignments. The color key is on a logarithmic scale. The Bray-Curtis distance metric was used to generate the dendrograms. Each column represents a NS, or WS microcosm sample; labels provided for the columns are colored green for NS or red for WS. Each row represents one of the 303 LCA-assigned species. Row labels are not shown, since they would not be legible. Additional file 6 lists all species assignments.

Published
2015
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135. Intravenous aviptadil and remdesivir for treatment of COVID-19-associated hypoxaemic respiratory failure in the USA (TESICO): a randomised, placebo-controlled trial

Author

Brown, Samuel M, Barkauskas, Christina E, Grund, Birgit, Sharma, Shweta, Phillips, Andrew N, Leither, Lindsay, Peltan, Ithan D, Lanspa, Michael, Gilstrap, Daniel L, Mourad, Ahmad, Lane, Kathleen, Beitler, Jeremy R, Serra, Alexis L, Garcia, Ivan, Almasri, Eyad, Fayed, Mohamed, Hubel, Kinsley, Harris, Estelle S, Middleton, Elizabeth A, Barrios, Macy A G, Mathews, Kusum S, Goel, Neha N, Acquah, Samuel, Mosier, Jarrod, Hypes, Cameron, Salvagio Campbell, Elizabeth, Khan, Akram, Hough, Catherine L, Wilson, Jennifer G, Levitt, Joseph E, Duggal, Abhijit, Dugar, Siddharth, Goodwin, Andrew J, Terry, Charles, Chen, Peter, Torbati, Sam, Iyer, Nithya, Sandkovsky, Uriel S, Johnson, Nicholas J, Robinson, Bryce R H, Matthay, Michael A, Aggarwal, Neil R, Douglas, Ivor S, Casey, Jonathan D, Hache-Marliere, Manuel, Georges Youssef, J, Nkemdirim, William, Leshnower, Brad, Awan, Omar, Pannu, Sonal, O'Mahony, Darragh Shane, Manian, Prasad, Awori Hayanga, J W, Wortmann, Glenn W, Tomazini, Bruno M, Miller, Robert F, Jensen, Jens-Ulrik, Murray, Daniel D, Bickell, Nina A, Zatakia, Jigna, Burris, Sarah, Higgs, Elizabeth S, Natarajan, Ven, Dewar, Robin L, Schechner, Adam, Kang, Nayon, Arenas-Pinto, Alejandro, Hudson, Fleur, Ginde, Adit A, Self, Wesley H, Rogers, Angela J, Oldmixon, Cathryn F, Morin, Haley, Sanchez, Adriana, Weintrob, Amy C, Cavalcanti, Alexandre Biasi, Davis-Karim, Anne, Engen, Nicole, Denning, Eileen, Taylor Thompson, B, Gelijns, Annetine C, Kan, Virginia, Davey, Victoria J, Lundgren, Jens D, Babiker, Abdel G, Neaton, James D, Lane, H Clifford, Tierney, John, Vogel, Susan E., McNay, Laura A., Cahill, Kelly, Crew, Page, Sardana, Ratna, Segal Raim, Sharo, Shaw-Saliba, Katy, Atri, Negin, Miller, Mark, Vallee, David, Chung, Lucy, Delph, Yvette, Adam, Stacey J., Read, Sarah, Draghia-Akli, Ruxandra, Harrigan, Rachel, Carlsen, Amy, Carter, Anita, DuChene, Alain, Eckroth, Kate, Frase, Alex, Harrison, Merrie, Meger, Sue, Quan, Kien, Quan, Siu Fun, Reilly, Cavan, Thompson, Greg, Walski, Jamie, Moskowitz, Alan J., Bagiella, Emilia, Moquete, Ellen, O'Sullivan, Karen, Marks, Mary E., Accardi, Evan, Kinzel, Emily, Bedoya, Gabriela, Gupta, Lopa, Overbey, Jessica R., Padillia, Maria L., Santos, Milerva, Gillinov, Marc A., Miller, Marissa A., Taddei-Peters, Wendy C., Fenton, Kathleen, Smith, Peter K., Vekstein, Andrew M., Ko, Emily R., Al-Hegelan, Mashael S., McGowan, Lauren M., Motta, Mary, Howell, Shauna, Bent, Francine, Kalager, Rachel, Chan, Emmanuel, Aloor, Heather L., Griffin, S. Michelle, Covington, Anna, McLendon-Arvik, Beth, Bussadori, Barbara, Miller-Bell, Mary, Sampey, Cathy, Gaver, Vincent, Hollister, Beth A., Giangiacomo, Dana M., Pauley, Alena, Patel, Aashay, Classon, Chris, Frazier, Madison, Osborne, Robyn, Conlon, Debbi H., Joshi, Marybeth, Gottlieb, Robert L., Mack, Michael, Berhe, Mezgebe, Haley, Clinton, Dishner, Emma, Bettacchi, Christopher, Golden, Kevin, Duhaime, Erin, Ryan, Madison, Tallmadge, Catherine, Estrada, Lorie, Jones, Felecia, Villa, Samantha, Wang, Samantha, Robert, Raven, Coleman, Tanquinisha, Clariday, Laura, Baker, Rebecca, Hurutado-Rodriguez, Mariana, Iram, Nazia, Fresnedo, Michelle, Davis, Allyson, Leonard, Kiara, Ramierez, Noelia, Thammavong, Jon, Duque, Krizia, Turner, Emma, Fisher, Tammy, Robinson, Dianna, Ransom, Desirae, Maldonado, Nicholas, Lusk, Erica, Killian, Aaron, Palacios, Adriana, Solis, Edilia, Jerrow, Janet, Watts, Matthew, Whitacre, Heather, Cothran, Elizabeth, Bender, William, Miller, Jeffrey, Nugent, Katherine, Farrington, Woodrow, Baio, Kim T., McBride, Mary K., Fielding, Michele, Mathewson, Sonya, Porte, Kristina, Haley, Elizabeth, Rogers, Susan, Tyler, Derrick, Perin, Emerson, Costello, Briana, Postalian, Alexander, Sohail, Rizwan, Hinsu, Punit, Watson, Carolyn, Kappenman, Casey, Chen, James, Walker, Kim, Fink, Melyssa, Phillip, Gabrielle, Mahon, Kim, Sturgis, Lydia, Maher, Patrick, Rogers, Linda, Ng, Nicole, Marshall, Jason, Bassily-Marcus, Adel, Cohen, Ivy, Ramoo, Shamini, Malhotra, Aryan, Kessler, Jonathan, Goetz, Rebekah, Badhwar, Vinay, Hayanga, Jeremiah, Giblin Sutton, Lisa, Williams, Roger, Berry Bartolo, Elizabeth, Walker, Dmitry, Bunner, Robin, Glaze, Chad, Aucremanne, Tanja, Bishop, James, Kelley, Macey, Peterson, Autumn, Sauerborn, Erica, Reckart, Robin, Miller, Brittany, Mittel, Aaron, Darmanian, Anita, Rosen, Amanda, Madahar, Purnema, Schicchi, John, Gosek, Katarzyna, Dzierba, Amy, Wahab, Romina, Eng, Connie, Al-Saadi, Mukhtar, Zahiruddin, Faisal, Syed, Mohi, George, Michael, Patel, Varsha, Onwunyi, Chisom, Barroso da Costa, Rosa, North, Crystal, Ringwood, Nancy, Fitzgerald, Laura, Muzikansky, Ariela, Morse, Richard, Brower, Roy G., Reineck, Lora A., Bienstock, Karen, Hou, Peter, Steingrub, Jay S., Tidswell, Mark A., Kozikowski, Lori-Ann, Kardos, Cynthia, De Souza, Leslie, Talmor, Daniel, Shapiro, Nathan, Hibbert, Kathryn, Brait, Kelsey, Kone, Mamary, Hendey, Gregory, Kangelaris, Kirsten N., Ashktorab, Kimia, Gropper, Rachel, Agrawal, Anika, Timothy, Kelly, Zhou, Hanjing, Hughes, Alyssa, Garcia, Rebekah, Torres, Adrian, Hernandez-Almaraz, Maria Elena, Vojnik, Rosemary, Perez, Cynthia, McDowell, Jordan, Chang, Steven Y., Vargas, Julia, Moss, Marc, McKeehan, Jeffrey, Higgins, Carrie, Johnson, Emily, Slaughter, Suzanne, Wyles, David, Hiller, Terra, Oakes, Judy, Garcia, Ana, Gravitz, Stephanie, Lyle, Carolynn, Swanson, Diandra, Gong, Michelle Ng., Richardson, Lynnne D., Chen, Jen-Ting, Moskowitz, Ari, Mohamed, Amira, Lopez, Brenda, Amosu, Omowunmi, Tzehaie, Hiwet, Boujid, Sabah, Bixby, Billie, Lopez, Anitza A., Durley, JaVon, Gilson, Boris, Hite, R. Duncan, Wang, Henry, Wiedemann, Hebert P., Mehkri, Omar, Ashok, Kiran, King, Alexander, Brennan, Connery, Exline, Matthew C., Englert, Joshua A., Karow, Sarah, Schwartz, Elizabeth, So, Preston, So, Madison, Krol, Olivia F., Briceno Parra, Genesis I., Mills, Emmanuel Nii Lantei, Oh, Minn, Pena, Jose, Martínez, Jesús Alejandro, Jackman, Susan E., Bayoumi, Emad, Pascual, Ethan, Caudill, Antonina, Chen, Po-En, Richardson, Tabia, Clapham, Gregg J., Herrera, Lisa, Ojukwu, Cristabelle, Fine, Devin, Gomez, Millie J., Choi-Kuaea, Yunhee, Weissberg, Gwendolyn, Isip, Katherine, Mattison, Brittany, Tran, Dana, Emilov Dukov, Jennifer, Chung, Paul, Kang, Bo Ran, Escobar, Lauren, Tran, Trung, Baig, Saba, Wallick, Julie A., Duven, Alexandria M., Fletcher, Dakota D., Gundel, Stephanie, Fuentes, Megan, Newton, Maranda, Peterson, Emily, Jiang, Kelsey, Files, D. Clark, Miller, Chadwick, Lematty, Caitlin, Rasberry, April, Warden, Ashley, Bledsoe, Joseph, Knowlton, Kirk, Knox, Daniel B., Klippel, Carolyn, Armbruster, Brent P., Applegate, Darrin, Imel, Karah, Fergus, Melissa, Rahmati, Kasra, Jensen, Hannah, Aston, Valerie T., Jeppson, Joshua, Marshall, J. Hunter, Lumpkin, Jenna, Smith, Cassie, Burke, Tyler, Gray, Andrew, Paine, Robert, Callahan, Sean, Yamane, Misty, Waddoups, Lindsey, Rice, Todd W., Johnson, Jakea, Gray, Christopher, Hays, Margaret, Roth, Megan, Musick, Sarah, Miller, Karen, Semler, Matthew W., Popielski, Laura, Kambo, Amy, Viens, Kimberly, Turner, Melissa, Vjecha, Michael J., Denyer, Rachel, Khosla, Rahul, Rajendran, Bindu, Gonzales, Melissa, Moriarty, Theresa, Biswas, Kousick, Harrington, Cristin, Garcia, Amanda, Bremer, Tammy, Burke, Tara, Koker, Brittany, Pittman, David, Vasudeva, Shikha S., Anholm, James D., Specht, Lennard, Rodriguez, Aimee, Ngo, Han, Duong, Lien, Previte, Matthew, Raben, Dorthe, Nielsen, Charlotte B., Friis Larsen, Jakob, Peters, Lars, Matthews, Gail, Kelleher, Anthony, Polizzotto, Mark, Carey, Catherine, Chang, Christina, Dharan, Nila, Hough, Sally, Virachit, Sophie, Davidson, Sarah, Bice, Daniel J., Ognenovska, Katherine, Cabrera, Gesalit, Flynn, Ruth, Abdelghany, Mazin, Baseler, Beth, Teitelbaum, Marc, Holley, H. Preston, Jankelevich, Shirley, Adams, Amy, Becker, Nancy, Doleny, Suzanne, Hissey, Debbie, Simpson, Shelly, Kim, Mi Ha, Beeler, Joy, Harmon, Liam, Vanderpuye, Sharon, Yeon, Lindsey, Frye, Leanna, Rudzinski, Erin, Buehn, Molly, Eccard-Koons, Vanessa, Frary, Sadie, MacDonalad, Leah, Cash, Jennifer, Hoopengardner, Lisa, Linton, Jessica, Nelson, Michaela, Spinelli-Nadzam, Mary, Proffitt, Calvin, Lee, Christopher, Engel, Theresa, Fontaine, Laura, Osborne, CK, Hohn, Matt, Galcik, Michael, Thompson, DeeDee, Sandrus, Jen, Manchard, Jon, Giri, Jiwan, Kopka, Stacy, Chang, Weizhong, Sherman, Brad T., Rupert, Adam W., Highbarger, Helene, Baseler, Michael, Lallemand, Perrine, Rehman, Tauseef, Imamichi, Tom, Laverdure, Sylvain, Paudel, Sharada, Cook, Kyndal, Haupt, Kendra, Hazen, Allison, Badralmaa, Yunden, Highbarger, Jeroen, McCormack, Ashley, Gerry, Norman P., Smith, Kenneth, Patel, Bhakti, Domeraski, Nadia, Hoover, Marie L., DuChateau, Nadine, Flosi, Adam, Nelson, Rich, Stojanovic, Jelena, and Wenner, Christine

Abstract

There is a clinical need for therapeutics for COVID-19 patients with acute hypoxemic respiratory failure whose 60-day mortality remains at 30-50%. Aviptadil, a lung-protective neuropeptide, and remdesivir, a nucleotide prodrug of an adenosine analog, were compared with placebo among patients with COVID-19 acute hypoxaemic respiratory failure.

Published
2024
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136. Tryptophan catabolism in acute exacerbations of chronic obstructive pulmonary disease

Author

Gulcev,Makedonka, Reilly,Cavan, Griffin,Timothy, Broeckling,Corey, Sandri,Brian, Witthuhn,Bruce, Hodgson,Shane, Woodruff,Prescott, Wendt,Chris, Gulcev,Makedonka, Reilly,Cavan, Griffin,Timothy, Broeckling,Corey, Sandri,Brian, Witthuhn,Bruce, Hodgson,Shane, Woodruff,Prescott, and Wendt,Chris

Abstract

Makedonka Gulcev,1 Cavan Reilly,2 Timothy J Griffin,3 Corey D Broeckling,4 Brian J Sandri,1 Bruce A Witthuhn,3 Shane W Hodgson,1 Prescott G Woodruff,5 Chris H Wendt1,6,* 1Department of Medicine, 2Division of Biostatistics, School of Public Health, 3Department of Biochemistry, Molecular Biology and Biophysics, University of Minnesota, Minneapolis, MN, USA; 4Department of Computer Science, Colorado State University, Fort Collins, CO, USA; 5Division of Pulmonary, Critical Care, Sleep and Allergy, Department of Medicine and the CVRI, University of California, San Francisco, CA, USA; 6Department of Medicine, Minneapolis VA Medical Center, Minneapolis, MN, USA *For the COPD Clinical Research Network Introduction: Exacerbations are a leading cause of morbidity in COPD. The objective of this study was to identify metabolomic biomarkers of acute exacerbations of COPD (AECOPD). Methods: We measured metabolites via mass spectrometry (MS) in plasma drawn within 24 hours of admission to the hospital for 33 patients with an AECOPD (day 0) and 30 days later and for 65 matched controls. Individual metabolites were measured via selective reaction monitoring with mass spectrometry. We used a mixed-effect model to compare metabolite levels in cases compared to controls and a paired t-test to test for differences between days 0 and 30 in the AECOPD group. Results: We identified 377 analytes at a false discovery rate of 5% that differed between cases (day 0) and controls, and 31 analytes that differed in the AECOPD cases between day 0 and day 30 (false discovery rate: 5%). Tryptophan was decreased at day 0 of AECOPD compared to controls corresponding to an increase in indoleamine 2,3-dioxygenase activity. Conclusion: Patients with AECOPD have a unique metabolomic signature that includes a decrease in tryptophan levels consistent with an increase in indoleamine 2,3-dioxygenase activity. Keywords: Chronic Obstructive Pulmonary Disease, metabolomics, tryptophan

Published
2016

137. Live SIV vaccine correlate of protection: local antibody production and concentration on the path of virus entry

Author

Li, Qingsheng, Zeng, Ming, Duan, Lijie, Voss, James E., Smith, Anthony J., Pambuccian, Stefan, Shang, Liang, Wietgrefe, Stephen, Southern, Peter J., Reilly, Cavan S., Skinner, Pamela J., Zupancic, Mary L., Carlis, John V., Piatak, Michael, Waterman, Diane, Reeves, R. Keith, Masek-Hammerman, Katherine, Derdeyn, Cynthia A., Alpert, Michael D., Evans, David T., Kohler, Heinz, Muller, Sybille, Robinson, James, Lifson, Jeffrey D., Burton, Dennis R., Johnson, R. Paul, and Haase, Ashley T.

Subjects
Mucous Membrane, Vaccination, SAIDS Vaccines, Simian Acquired Immunodeficiency Syndrome, HIV Infections, Cervix Uteri, Antibodies, Viral, Vaccines, Attenuated, Antibodies, Neutralizing, Macaca mulatta, Article, HIV Envelope Protein gp41, Immunoglobulin G, Antibody Formation, Vagina, HIV-1, Animals, Female, Simian Immunodeficiency Virus
Abstract

We sought design principles for a vaccine to prevent HIV transmission to women by identifying correlates of protection conferred by a highly effective live attenuated SIV vaccine in the rhesus macaque animal model. We show that SIVmac239Δnef vaccination recruits plasma cells and induces ectopic lymphoid follicle formation beneath the mucosal epithelium in the rhesus macaque female reproductive tract. The plasma cells and ectopic follicles produce IgG antibodies reactive with viral envelope glycoprotein gp41 trimers, and these antibodies are concentrated on the path of virus entry by the neonatal Fc receptor (FcRn) in cervical reserve epithelium and in vaginal epithelium. This local antibody production and delivery system correlated spatially and temporally with the maturation of local protection against high dose pathogenic SIV vaginal challenge. Thus, designing vaccines to elicit production and concentration of antibodies at mucosal frontlines could aid development of an effective vaccine to protect women against HIV-1.

Published
2014

142. Defining HIV and SIV Reservoirs in Lymphoid Tissues

Author

Deleage, Claire, primary, Wietgrefe, Stephen W., additional, Del Prete, Gregory, additional, Morcock, David R., additional, Hao, Xing-Pei, additional, Piatak, Jr., Michael, additional, Bess, Julian, additional, Anderson, Jodi L., additional, Perkey, Katherine, additional, Reilly, Cavan, additional, McCune, Joseph M., additional, Haase, Ashley T., additional, Lifson, Jeffrey D., additional, Schacker, Timothy W., additional, and Estes, Jacob D., additional

Published
2016
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147. The Immunosuppressive Role of IL-32 in Lymphatic Tissue during HIV-1 Infection1

Author

Smith, Anthony J., Toledo, Chad M., Wietgrefe, Stephen W., Duan, Lijie, Schacker, Timothy W., Reilly, Cavan S., and Haase, Ashley T.

Subjects
Adult, Male, Membrane Glycoproteins, Time Factors, Lymphoid Tissue, Gene Expression Profiling, Interleukins, Rectum, HIV Infections, Middle Aged, Virus Replication, Article, Ileum, Host-Pathogen Interactions, HIV-1, Humans, Indoleamine-Pyrrole 2,3,-Dioxygenase, RNA, Viral, Female, Lymph Nodes, Receptors, Immunologic, In Situ Hybridization, Oligonucleotide Array Sequence Analysis
Abstract

One pathological hallmark of HIV-1 infection is chronic activation of the immune system, driven, in part, by increased expression of pro-inflammatory cytokines. The host attempts to counterbalance this prolonged immune activation through compensatory mediators of immune suppression. We recently identified a gene encoding the pro-inflammatory cytokine IL-32 in microarray studies of HIV-1 infection in lymphatic tissue (LT) and show here that increased expression of IL-32 in both gut and LT of HIV-1-infected individuals may have a heretofore unappreciated role as a mediator of immune suppression. We show that: (i) IL-32 expression is increased in T cells, B cells, macrophages, dendritic cells, and epithelial cells in vivo; (ii) IL-32 induces the expression of immunosuppressive molecules indoleamine 2, 3-dioxygenase (IDO) and immunoglobulin-like transcript 4 (ILT4) in immune cells in vitro; (iii) in vivo, IL-32-associated IDO/ILT4 expression in LT macrophages and gut epithelial cells decreases immune activation but also may impair host defenses, supporting productive viral replication, thereby accounting for the correlation between IL-32 levels and HIV-1 replication in LT. Thus, during HIV-1 infection, we propose that IL-32 moderates chronic immune activation to avert associated immunopathology but at the same time dampens the antiviral immune response and thus paradoxically supports HIV-1 replication and viral persistence.

Published
2011

148. Host Genes Associated with HIV-1 Replication in Lymphatic Tissue1

Author

Smith, Anthony J., Li, Qingsheng, Wietgrefe, Stephen W., Schacker, Timothy W., Reilly, Cavan S., and Haase, Ashley T.

Subjects
Adult, Male, Gene Expression Profiling, Fluorescent Antibody Technique, Gene Expression, HIV Infections, Middle Aged, Viral Load, Virus Replication, Article, Young Adult, HIV-1, Humans, Female, Lymph Nodes, RNA, Messenger, Oligonucleotide Array Sequence Analysis
Abstract

Much effort has been spent recently in identifying host factors required for HIV-1 to effectively replicate in cultured human cells. However, much less is known about the genetic factors in vivo that impact viral replication in lymphatic tissue, the primary anatomical site of virus-host interactions where the bulk of viral replication and pathogenesis occurs. To identify genetic determinants in lymphatic tissue that critically affect HIV-1 replication, we used microarrays to transcriptionally profile and identify host genes expressed in inguinal lymph nodes that were associated determinants of viral load. Strikingly, ∼95% of the transcripts (558) in this data set (592 transcripts total) were negatively associated with HIV-1 replication. Genes in this subset 1) inhibit cellular activation/proliferation (e.g., TCFL5, SOCS5 and SCOS7, KLF10), 2) promote heterochromatin formation (e.g., HIC2, CREBZF, ZNF148/ZBP-89), 3) increase collagen synthesis (e.g., PLOD2, POSTN, CRTAP), and 4) reduce cellular transcription and translation. Potential anti-HIV-1 restriction factors were also identified (e.g., NR3C1, HNRNPU, PACT). Only ∼5% of the transcripts (34) were positively associated with HIV-1 replication. Paradoxically, nearly all of these genes function in innate and adaptive immunity, particularly highlighting heightened gene expression in the IFN system. We conclude that this conventional host response cannot contain HIV-1 replication and, in fact, could well contribute to increased replication through immune activation. More importantly, genes that have a negative association with virus replication point to target cell availability and potentially new viral restriction factors as principal determinants of viral load.

Published
2010

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