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2. An Analysis of In-Game Feedback Provided by Coaches in an Australian Football League Competition

Author

Mason, Robert J., Farrow, Damian, and Hattie, John A. C.

Abstract

Background: Coach observation studies have been a mainstay of coaching science research for decades, with a major focus on the use of instruction and feedback by coaches. However, relatively few studies have investigated feedback provided in a live competition setting, with a majority focussing on the training environment. As such, little is known about the way that feedback changes as a result of the intensity of a competitive setting. Additionally, feedback variables of interest are featured inconsistently between studies. Purpose: The purpose of the current study was to investigate the quantity and nature of feedback from coach to player in an Australian rules football context, specifically the elite-level Australian Football League (AFL) competition. An entire season's worth of coach-player feedback was recorded and coded against a wide range of feedback variables most commonly found in the literature. A secondary aim of the study was to examine changes in feedback against various game metrics (winning/losing quarter, margin). Method: Five coaches from one AFL team, all with several years of experience at the elite level, were recorded across 21 regular-season games from the 2018 season. Feedback quantity, along with several feedback variables of interest (valence, autonomy-support, descriptive/prescriptive, individual/group, etc.), were coded during each quarter of play. Game information (game outcome, quarter outcome, margin at the start of the quarter, point differential for the quarter) was also recorded. Results: Across 84 quarters of football, 1301 coach-player feedback instances were observed. Mean values across all quarters revealed more negative (20%) than positive (13%) feedback, more prescriptive (81%) than descriptive (19%) feedback, more controlling (58%) than autonomy-supportive (8%), and more individual (70%) than group (30%) feedback was provided. Task-related feedback (60%) was more common than process-related (37%), self-regulation feedback (3%) or self-level feedback i.e. praise (2%). More positive feedback was provided in winning quarters than in losing quarters, while more controlling feedback was present during losing quarters than during winning quarters. Coaches provided significantly more feedback overall when the game was in the balance than quarters where the team was 95% or more likely to win or lose. Conclusions: The paper presents novel findings about feedback use in an elite competitive team sport setting. Areas where the use of feedback does not align with current theory and evidence are highlighted, particularly regarding feedback valence and autonomy support. Feedback variables more commonly associated with improved learning and performance in the literature appear to generally be provided more frequently during winning quarters, but a causal relationship is yet to be determined.

Published
2020
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3. Hypoxia-Inducible Factor 1α Signaling Promotes Repair of the Alveolar Epithelium after Acute Lung Injury

Author

McClendon, Jazalle, Jansing, Nicole L, Redente, Elizabeth F, Gandjeva, Aneta, Ito, Yoko, Colgan, Sean P, Ahmad, Aftab, Riches, David WH, Chapman, Harold A, Mason, Robert J, Tuder, Rubin M, and Zemans, Rachel L

Subjects
Biomedical and Clinical Sciences, Regenerative Medicine, Lung, Acute Respiratory Distress Syndrome, Rare Diseases, 2.1 Biological and endogenous factors, Aetiology, Respiratory, Acute Lung Injury, Alveolar Epithelial Cells, Animals, Cell Line, Cell Proliferation, Chemokine CXCL12, Disease Models, Animal, Hypoxia-Inducible Factor 1, alpha Subunit, Mice, Permeability, Pulmonary Alveoli, Rats, Receptors, CXCR4, Signal Transduction, Vascular Endothelial Growth Factor A, Wound Healing, Medical and Health Sciences, Pathology, Biomedical and clinical sciences, Health sciences
Abstract

During the acute respiratory distress syndrome, epithelial cells, primarily alveolar type (AT) I cells, die and slough off, resulting in enhanced permeability. ATII cells proliferate and spread onto the denuded basement membrane to reseal the barrier. Repair of the alveolar epithelium is critical for clinical recovery; however, mechanisms underlying ATII cell proliferation and spreading are not well understood. We hypothesized that hypoxia-inducible factor (HIF)1α promotes proliferation and spreading of ATII cells during repair after lung injury. Mice were treated with lipopolysaccharide or hydrochloric acid. HIF activation in ATII cells after injury was demonstrated by increased luciferase activity in oxygen degradation domain-Luc (HIF reporter) mice and expression of the HIF1α target gene GLUT1. ATII cell proliferation during repair was attenuated in ATII cell-specific HIF1α knockout (SftpcCreERT2+/-;HIF1αf/f) mice. The HIF target vascular endothelial growth factor promoted ATII cell proliferation in vitro and after lung injury in vivo. In the scratch wound assay of cell spreading, HIF stabilization accelerated, whereas HIF1α shRNA delayed wound closure. SDF1 and its receptor, CXCR4, were found to be HIF1α-regulated genes in ATII cells and were up-regulated during lung injury. Stromal cell-derived factor 1/CXCR4 inhibition impaired cell spreading and delayed the resolution of permeability after lung injury. We conclude that HIF1α is activated in ATII cells after lung injury and promotes proliferation and spreading during repair.

Published
2017

4. IL1RL1 asthma risk variants regulate airway type 2 inflammation

Author

Gordon, Erin D, Palandra, Joe, Wesolowska-Andersen, Agata, Ringel, Lando, Rios, Cydney L, Lachowicz-Scroggins, Marrah E, Sharp, Louis Z, Everman, Jamie L, MacLeod, Hannah J, Lee, Jae W, Mason, Robert J, Matthay, Michael A, Sheldon, Richard T, Peters, Michael C, Nocka, Karl H, Fahy, John V, and Seibold, Max A

Subjects
Asthma, Genetics, Prevention, Human Genome, Lung, 2.1 Biological and endogenous factors, Aetiology, Respiratory, Cells, Cultured, Genetic Predisposition to Disease, Humans, Inflammation, Interleukin-1 Receptor-Like 1 Protein, Interleukin-33, Polymorphism, Single Nucleotide, Quantitative Trait Loci
Abstract

Genome-wide association studies of asthma have identified genetic variants in the IL1RL1 gene, but the molecular mechanisms conferring risk are unknown. IL1RL1 encodes the ST2 receptor (ST2L) for IL-33 and an inhibitory decoy receptor (sST2). IL-33 promotes type 2 inflammation, which is present in some but not all asthmatics. We find that two single nucleotide polymorphisms (SNPs) in IL1RL1 - rs1420101 and rs11685480 - are strongly associated with plasma sST2 levels, though neither is an expression quantitative trait locus (eQTL) in whole blood. Rather, rs1420101 and rs11685480 mark eQTLs in airway epithelial cells and distal lung parenchyma, respectively. We find that the genetically determined plasma sST2 reservoir, derived from the lung, neutralizes IL-33 activity, and these eQTL SNPs additively increase the risk of airway type 2 inflammation among asthmatics. These risk variants define a population of asthmatics at risk of IL-33-driven type 2 inflammation.

Published
2016

5. CD209L (L-SIGN) Is a Receptor for Severe Acute Respiratory Syndrome Coronavirus

Author

Jeffers, Scott A., Tusell, Sonia M., Gillim-Ross, Laura, Hemmila, Erin M., Achenbach, Jenna E., Babcock, Gregory J., Thomas,, William D., Thackray, Larissa B., Young, Mark D., Mason, Robert J., Ambrosino, Donna M., Wentworth, David E., DeMartini, James C., Holmes, Kathryn V., and Palese, Peter

Published
2004

17. Contributors

Author

Adams, Lewis, primary, Adler, Dan Elie, additional, Agusti, Alvar, additional, Akoumianaki, Evangelia, additional, Alberg, Anthony J., additional, Albertine, Kurt H., additional, Alexander, Barbara D., additional, Alfille, Paul H., additional, Anantham, Devanand, additional, Arenberg, Douglas A., additional, Ayas, Najib T., additional, Bagchi, Aranya, additional, Balmes, John Randolph, additional, Banaei, Niaz, additional, Barnett, Christopher F., additional, Baughman, Robert P., additional, Becklake, Margaret R., additional, Benditt, Joshua O., additional, Benowitz, Neal L., additional, Bhakta, Nirav R., additional, Bhave, Anant D., additional, Blanc, Paul D., additional, Bleecker, Eugene R., additional, Bove, Alfred A., additional, Bradley, T. Douglas, additional, Brambilla, Elisabeth, additional, Broaddus, V. Courtney, additional, Brochard, Laurent, additional, Brock, Malcolm V., additional, Brown, Kevin K., additional, Brunetta, Paul G., additional, Cadranel, Jacques, additional, Celli, Bartolome, additional, Chan, Edward D., additional, Channick, Richard N., additional, Chastre, Jean, additional, Cheng, Guang-Shing, additional, Chin, Kelly, additional, Chung, Kian Fan, additional, Clerici, Christine, additional, Colby, Thomas V., additional, Collard, Harold R., additional, Cool, Carlyne D., additional, Cordier, Jean-François, additional, Cordioli, Ricardo Luiz, additional, Corte, Tamera J., additional, Cottin, Vincent, additional, Courey, Mark S., additional, Cowie, Robert L., additional, Crothers, Kristina, additional, Curley, Gerard F., additional, Daley, Charles L., additional, Davis, J. Lucian, additional, De Marco, Teresa, additional, Deresinski, Stanley C., additional, Deroose, Christophe, additional, Dobbs, Leland G., additional, Dooms, Christophe, additional, Downey, Gregory P., additional, du Bois, Roland M., additional, Dulohery, Megan M., additional, Effros, Richard M., additional, Eisner, Mark D., additional, Elicker, Brett M., additional, Ernst, Armin, additional, Ernst, Joel D., additional, Fahy, John V., additional, Fedullo, Peter F., additional, Feller-Kopman, David, additional, Fenster, Brett E., additional, Fingerlin, Tasha E., additional, Fontenot, Andrew P., additional, Frankel, Stephen K., additional, Garcia, Joe G.N., additional, Gebhart, G.F., additional, Gilstrap, Daniel Lee, additional, Girard, Nicolas, additional, Gladwin, Mark T., additional, Glenny, Robb W., additional, Gold, Warren M., additional, Gotway, Michael B., additional, Grasselli, Giacomo, additional, Greenberg, James M., additional, Griffith, David E., additional, Gruden, James F., additional, Han, MeiLan King, additional, Henderson, William, additional, Hill, Nicholas S., additional, Hoover, Wynton, additional, Hopewell, Philip C., additional, Horan-Saullo, Jennifer L., additional, Horner, Richard L., additional, Huang, Laurence, additional, Huchon, Gérard, additional, Inoue, Yoshikazu, additional, Iseman, Michael D., additional, Jackson, James E., additional, Jakubzick, Claudia V., additional, Janssen, Julius P., additional, Jett, James R., additional, Jones, Kirk, additional, Judson, Marc A., additional, Kato-Maeda, Midori, additional, Kavanagh, Brian P., additional, Keshavjee, Shaf, additional, Kim, Kami, additional, Kimoff, R. John, additional, King, Talmadge E., additional, Klein, Jeffrey S., additional, Koth, Laura L., additional, Kotloff, Robert M., additional, Kraft, Monica, additional, Küpeli, Elif, additional, Laffey, John G., additional, Lapinsky, Stephen E., additional, Lazarus, Stephen C., additional, Lee, Frances Eun-Hyung, additional, Lee, Jarone, additional, Lee, Y.C. Gary, additional, Lee, Warren L., additional, Lee-Chiong, Teofilo L., additional, Lemière, Catherine, additional, Light, Richard W., additional, Limper, Andrew H., additional, Loddenkemper, Robert, additional, Lugogo, Njira, additional, Luisetti, Maurizio, additional, Luks, Andrew M., additional, Luyt, Charles-Edouard, additional, Machado, Roberto F., additional, MacIntyre, Neil R., additional, MacNee, William, additional, Madtes, David K., additional, Maier, Lisa A., additional, Maldonado, Fabien, additional, Malhotra, Atul, additional, Martin, Thomas R., additional, Maskell, Nick A., additional, Mason, Robert J., additional, Massion, Pierre P., additional, Matthay, Michael A., additional, Matthay, Richard A., additional, Mayer, Annyce S., additional, Mazzone, Stuart B., additional, McCool, F. Dennis, additional, McCormack, Francis Xavier, additional, Mehta, Atul C., additional, Menéndez, Rosario, additional, Morgenthau, Adam S., additional, Morris, Alison, additional, Morris, Timothy A., additional, Muncey, Aaron R., additional, Murray, John F., additional, Myers, Jeffrey L., additional, Nadel, Jay A., additional, Nelson-Piercy, Catherine, additional, Neuman, Tom S., additional, Nosanchuk, Joshua D., additional, O'Riordan, Thomas G., additional, Ortega, Victor Enrique, additional, Panse, Prasad M., additional, Pao, William, additional, Paré, Peter A., additional, Park, David R., additional, Pastis, Nicholas J., additional, Patroniti, Nicolò, additional, Patterson, Karen C., additional, Pesenti, Antonio, additional, Pickens, Allan, additional, Pinsky, Benjamin A., additional, Pletcher, Steven D., additional, Powell, Frank L., additional, Que, Loretta G., additional, Redente, Elizabeth F., additional, Riches, David W.H., additional, Robinson, Bruce W.S., additional, Rodriguez-Roisin, Roberto, additional, Rose, Cecile S., additional, Routes, John M., additional, Rowe, Steven M., additional, Ryan, Clodagh M., additional, Ryu, Jay H., additional, Samet, Jonathan M., additional, Sandrock, Christian E., additional, Schoene, Robert B., additional, Schwartz, David A., additional, Schwartzstein, Richard M., additional, Schwarz, Marvin I., additional, Selman, Moisés, additional, Sequist, Lecia V., additional, Shannon, John M., additional, Shovlin, Claire L., additional, Silvestri, Gerard A., additional, Simonian, Philip L., additional, Singer, Jonathan P., additional, Slutsky, Arthur S., additional, Smaldone, Gerald C., additional, Solomon, George M., additional, Sorscher, Eric J., additional, Swenson, Erik R., additional, Tanner, Nichole T., additional, Tanowitz, Herbert B., additional, Torres, Antoni, additional, Trapnell, Bruce C., additional, Travis, William David, additional, Treanor, John J., additional, Tzelepis, George E., additional, Vandenplas, Olivier, additional, Vansteenkiste, Johan F., additional, Varghese, Thomas K., additional, Vestbo, Jørgen, additional, Wagner, Peter D., additional, Wahidi, Momen M., additional, Wallace, W. Dean, additional, Weiss, Louis M., additional, Weiss, Scott T., additional, Wells, Athol U., additional, West, John B., additional, White, Douglas B., additional, Wiener-Kronish, Jeanine P., additional, Wikenheiser-Brokamp, Kathryn A., additional, Woodruff, Prescott G., additional, Wunderink, Richard G., additional, Yeh, D. Dante, additional, Zemans, Rachel L., additional, Zimmerman, Leslie, additional, and Zuwallack, Richard L., additional

Published
2016
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19. Preface to the Sixth Edition

Author

Murray, John F., primary, Nadel, Jay A., additional, Broaddus, V. Courtney, additional, Mason, Robert J., additional, Ernst, Joel D., additional, King, Talmadge E., additional, Lazarus, Stephen C., additional, Slutsky, Arthur S., additional, and Gotway, Michael B., additional

Published
2016
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31. Differential requirement for the activation of the inflammasome for processing and release of IL-1β in monocytes and macrophages

Author

Netea, Mihai G., Nold-Petry, Claudia A., Nold, Marcel F., Joosten, Leo A.B., Opitz, Bastian, van der Meer, Jonathan H.M., van de Veerdonk, Frank L., Ferwerda, Gerben, Heinhuis, Bas, Devesa, Isabel, Funk, C. Joel, Mason, Robert J., Kullberg, Bart Jan, Rubartelli, Anna, van der Meer, Jos W.M., and Dinarello, Charles A.

Published
2009
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37. LPCAT1 regulates surfactant phospholipids synthesis and is required for transitioning to air breathing in mice

Author

Bridges, James P., Ikegami, Machiko, Brilli, Lauren L., Chen, Xueni, Mason, Robert J., and Shannon, John M.

Subjects
Phospholipids -- Properties -- Research -- Health aspects, Surface active agents -- Health aspects -- Research, Biological control systems -- Research -- Health aspects, Respiratory physiology -- Research -- Health aspects, Health care industry
Abstract

Respiratory distress syndrome (RDS), which is the leading cause of death in premature infants, is caused by surfactant deficiency. The most critical and abundant phospholipid in pulmonary surfactant is saturated phosphatidylcholine (SatPC), which is synthesized in alveolar type II cells de novo or by the deacylation-reacylation of existing phosphatidylcholine species. We recently cloned and partially characterized a mouse enzyme with characteristics of a lung lysophosphatidylcholine acyltransferase (LPCAT1) that we predicted would be involved in surfactant synthesis. Here, we describe our studies investigating whether LPCAT1 is required for pulmonary surfactant homeostasis. To address this issue, we generated mice bearing a hypomorphic allele of Lpcat1 (referred to herein as [Lpcat1.sup.[GT/GT]] mice) using a genetrap strategy. Newborn [Lpcat1.sup.[GT/GT]] mice showed varying perinatal mortality from respiratory failure, with affected animals demonstrating hallmarks of respiratory distress such as atelectasis and hyaline membranes. Lpcat1 mRNA levels were reduced in newborn [Lpcat1.sup.[GT/GT]] mice and directly correlated with SatPC content, LPCAT1 activity, and survival. Surfactant isolated from dead [Lpcat1.sup.[GT/GT]] mice failed to reduce minimum surface tension to wild-type levels. Collectively, these data demonstrate that full LPCAT1 activity is required to achieve the levels of SatPC essential for the transition to air breathing., Introduction Maintenance of alveolar patency is critical for gas exchange. Pulmonary surfactant is a lipoprotein complex that coats the luminal surface of alveoli to reduce surface tension to near 0 [...]

Published
2010
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39. Alveolar type II cells inhibit fibroblast proliferation: role of IL-1[alpha]

Author

Portnoy, Joshua, Pan, Tianli, Dinarello, Charles A., Shannon, John M., Westcott, Jay Y., Zhang, Lening, and Mason, Robert J.

Subjects
Fibroblasts -- Research, Prostaglandins -- Research, Keratinocytes -- Research, Biological sciences
Abstract

Alveolar type II (ATII) cells inhibit fibroblast proliferation in coculture by releasing or secreting a factor(s) that stimulates fibroblast production of prostaglandin [E.sub.2] ([PGE.sub.2]). In the present study, we sought to determine the factors released from ATII cells that stimulate [PGE.sub.2] production in fibroblasts. Exogenous addition of rat IL-1[alpha] to cultured lung fibroblasts induced [PGE.sub.2] secretion in a dose-response manner. When fibroblasts were cocultured with rat ATII cells, IL-1[alpha] protein was detectable in ATII cells and in the coculture medium between days 8 and 12 of culture, correlating with the highest levels of [PGE.sub.2]. Furthermore, under coculture conditions, IL-1[alpha] gene expression increased in ATII cells (but not fibroblasts) compared with either cell cultured alone. In both mixed species (human fibroblasts-rat ATII cells) and same species cocultures (rat fibroblasts and ATII cells), [PGE.sub.2] secretion was inhibited by the presence of IL-1 receptor antagonist (IL-1Ra) or selective neutralizing antibody directed against rat IL-1[alpha] (but not IL-1[beta]). Conditioned media from cocultures inhibited fibroblast proliferation, and this effect was abrogated by the addition of IL-IRa. Addition of keratinocyte growth factor (KGF) resulted in an earlier increase in [PGE.sub.2] secretion and fibroblast inhibition (day 8 of coculture). This effect was inhibited by indomethacin but was not altered by IL-IRa. We conclude that in this coculture system, IL-1[alpha] secretion by ATII cells is one factor that stimulates [PGE.sub.2] production by lung fibroblasts, thereby inhibiting fibroblast proliferation. In addition, these studies demonstrate that KGF enhances ATII cell [PGE.sub.2] production through an IL-1[alpha]-independent pathway. interleukin-1[beta]; interleukin-l[alpha]; keratinocyte growth factor; prostaglandin [E.sub.2]; cyclooxygenase-2

Published
2006

44. Contributors

Author

Adams, Lewis, primary, Alberg, Anthony J., additional, Albert, Richard K., additional, Albertine, Kurt H., additional, Anantham, Devanand, additional, Arenberg, Douglas, additional, Ayas, Najib T., additional, Balkissoon, Ronald C., additional, Balmes, John R., additional, Bapoje, Srinivas R., additional, Barberà, Joan Albert, additional, Barnes, Peter J., additional, Baroody, Fuad M., additional, Becklake, Margaret R., additional, Benditt, Joshua O., additional, Benowitz, Neal L., additional, Blanc, Paul D., additional, Boucher, Richard C., additional, Bove, Alfred A., additional, Brambilla, Elisabeth, additional, Broaddus, V. Courtney, additional, Brown, Kevin K., additional, Brunetta, Paul G., additional, Cadranel, Jacques, additional, Carbone, David P., additional, Celli, Bartolome R., additional, Chan, Edward D., additional, Chan-Yeung, Moira, additional, Channick, Richard N., additional, Chastre, Jean, additional, Chung, Kian Fan, additional, Cirino-Marcano, Maria, additional, Coleman, R. Edward, additional, Collard, Harold R., additional, Cool, Carlyne D., additional, Cordier, Jean-François, additional, Corte, Tamera J., additional, Cottin, Vincent, additional, Cowie, Robert L., additional, Crapo, Robert O., additional, Crothers, Kristina, additional, Daley, Charles L., additional, Davies, Scott F., additional, De Marco, Teresa, additional, Sorbo, Lorenzo Del, additional, Downey, Gregory P., additional, Drake, Wonder, additional, du Bois, Roland M., additional, Duffin, James, additional, Effros, Richard M., additional, Eisner, Mark D., additional, Elicker, Brett M., additional, Ernst, Armin, additional, Fedullo, Peter F., additional, Fenton, Matthew J., additional, Fertel, Daniel, additional, Folkesson, Hans G., additional, Folz, Rodney J., additional, Fontenot, Andrew P., additional, Garcia, Joe G.N., additional, Gebhart, Gerald F., additional, Giordano, Thomas J., additional, Girard, Nicolas, additional, Gladwin, Mark T., additional, Gotway, Michael B., additional, Greenberg, James M., additional, Griffith, David E., additional, Groshong, Stephen, additional, Hegewald, Matthew J., additional, Henson, Peter M., additional, Hill, Nicholas S., additional, Hopewell, Philip C., additional, Huang, Laurence, additional, Inoue, Yoshikazu, additional, Iseman, Michael D., additional, Jackson, James E., additional, Jacobson, Jeffrey R., additional, Jett, James R., additional, Karnak, Demet, additional, Kato-Maeda, Midori, additional, Kavuru, Mani S., additional, King, Talmadge E., additional, Knowles, Michael R., additional, Knox, Kenneth S., additional, Kotloff, Robert M., additional, Kraft, Monica, additional, Kupeli, Elif, additional, Lapinsky, Stephen E., additional, Lara, Abigail R., additional, Lazarus, Stephen C., additional, Eun-Hyung Lee, F., additional, Lee, Warren L., additional, Lee, Y.C. Gary, additional, Lee-Chiong, Teofilo, additional, Lewis, James F., additional, Light, Richard W., additional, Limper, Andrew H., additional, Loddenkemper, Robert, additional, Luce, John M., additional, Lugogo, Njira, additional, Luks, Andrew M., additional, Luyt, Charles-Edouard, additional, Machado, Roberto F., additional, MacIntyre, Neil R., additional, Maier, Lisa A., additional, Maldonado, Fabien, additional, Malo, Jean-Luc, additional, Martin, Erica L., additional, Martin, Thomas R., additional, Mason, Robert J., additional, Massion, Pierre P., additional, Matthay, Michael A., additional, Matthay, Richard A., additional, Mayer, Annyce S., additional, McCarthy, James, additional, McCool, F. Dennis, additional, McCormack, Francis X., additional, McGlothlin, Dana, additional, Mehta, Atul C., additional, Menéndez, Rosario, additional, Morris, Alison, additional, Morris, Timothy A., additional, Morrison, Lake D., additional, Moss, Marc, additional, Murray, Jill, additional, Murray, John F., additional, Myers, Jeffrey L., additional, Nadel, Jay A., additional, Nakata, Koh, additional, Neuman, Thomas S., additional, Newman, Lee S., additional, Noble, Paul W., additional, Noppen, Marc, additional, Nutman, Thomas B., additional, O’Riordan, Thomas G., additional, Pack, Allan I., additional, Paré, Peter D., additional, Park, David R., additional, Patz, Edward F., additional, Phillipson, Eliot A., additional, Pickens, Allan, additional, Pien, Grace W., additional, Powell, Frank L., additional, Pritt, Bobbi S., additional, Que, Loretta G., additional, Ranieri, V. Marco, additional, Reilly, John J., additional, Rennard, Stephen I., additional, Reynolds, Susan D., additional, Riches, David W.H., additional, Rizk, Norman W., additional, Robinson, Bruce W.S., additional, Rodriguez-Roisin, Roberto, additional, Rose, Cecile S., additional, Roussos, Charis, additional, Routes, John M., additional, Rubin, Lewis J., additional, Samet, Jonathan M., additional, Sandrock, Christian, additional, Sarosi, George A., additional, Sawyer, Richard T., additional, Schmidt, Gregory A., additional, Schoene, Robert B., additional, Schraufnagel, Dean E., additional, Schwartz, David A., additional, Schwartzstein, Richard M., additional, Schwarz, Marvin I., additional, Selman, Moises, additional, Shannon, John M., additional, Shapiro, Steven D., additional, Shepherd, Kenneth E., additional, Shovlin, Claire L., additional, Sietsema, Kathy E., additional, Silvestri, Gerard A., additional, Simonian, Philip L., additional, Slutsky, Arthur S., additional, Smaldone, Gerald C., additional, Sullivan, Eugene J., additional, Swenson, Erik R., additional, Togias, Alkis, additional, Torres, Antoni, additional, Trapnell, Bruce C., additional, Treanor, John, additional, Tuder, Rubin M., additional, Tzelepis, George E., additional, Vallières, Eric, additional, Wagner, Peter D., additional, Weiss, Scott T., additional, Wells, Athol U., additional, West, John B., additional, White, Douglas B., additional, Widdicombe, John G., additional, Wiener-Kronish, Jeanine P., additional, Wunderink, Richard, additional, Yankaskas, James R., additional, Yao, Joseph D.C., additional, Zakynthinos, Spyros G., additional, Zimmerman, Leslie, additional, and ZuWallack, Richard L., additional

Published
2010
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45. Preface to the Fifth Edition

Author

Murray, John F., primary, Nadel, Jay A., additional, Mason, Robert J., additional, Broaddus, V. Courtney, additional, Martin, Thomas R., additional, King, Talmadge E., additional, and Schraufnagel, Dean E., additional

Published
2010
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46. Respiratory epithelial cell responses to SARS-CoV-2 in COVID-19.

Author

Bridges, James P., Vladar, Eszter K., Hua Huang, Mason, Robert J., and Huang, Hua

Subjects
EPITHELIAL cells, PULMONARY surfactant-associated protein D, CORONAVIRUS disease treatment, CELL receptors, IMMUNOGLOBULIN M, MIDDLE East respiratory syndrome
Abstract

COVID-19 has different clinical stages, and effective therapy depends on the location and extent of the infection. The purpose of this review is to provide a background for understanding the progression of the disease throughout the pulmonary epithelium and discuss therapeutic options. The prime sites for infection that will be contrasted in this review are the conducting airways and the gas exchange portions of the lung. These two sites are characterised by distinct cellular composition and innate immune responses, which suggests the use of distinct therapeutic agents. In the nose, ciliated cells are the primary target cells for SARS-CoV-2 viral infection, replication and release. Infected cells shed their cilia, which disables mucociliary clearance. Evidence further points to a suppressed or incompletely activated innate immune response to SARS-CoV-2 infection in the upper airways. Asymptomatic individuals can still have a productive viral infection and infect others. In the gas exchange portion of the lung, the alveolar type II epithelial cell is the main target cell type. Cell death and marked innate immune response during infection likely contribute to alveolar damage and resultant acute respiratory distress syndrome. Alveolar infection can precipitate a hyperinflammatory state, which is the target of many therapies in severe COVID-19. Disease resolution in the lung is variable and may include scaring and long-term sequalae because the alveolar type II cells are also progenitor cells for the alveolar epithelium. [ABSTRACT FROM AUTHOR]

Published
2022
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49. Serum SP-D is a marker of lung injury in rats

Author

Pan, Tianli, Nielsen, Larry D., Allen, Martin J., Shannon, Kathleen M., Shannon, John M., Selman, Moises, and Mason, Robert J.

Subjects
Physiology -- Research, Pulmonary surfactant -- Research, Keratinocytes -- Research, Biological sciences
Abstract

Pulmonary surfactant protein D (SP-D) is expressed in alveolar type II and bronchiolar epithelial cells and is secreted into alveoli and conducting airways. However, SP-D has also been measured in serum and is increased in patients with acute respiratory distress syndrome, pulmonary fibrosis, and alveolar proteinosis. To demonstrate that SP-D can be measured in rat serum, we instilled rats with keratinocyte growth factor, which produces type II cell hyperplasia and an increase in SP-D in bronchoalveolar lavage fluid (BALF). To evaluate serum SP-D as a biomarker of lung injury, we examined several injury models. In rats treated with I unit of bleomycin, serum SP-D was elevated on days 3, 7, 14, and 28 after instillation, and SP-D mRNA was increased in focal areas as detected by in situ hybridization. However, there was no increase in whole lung SP-D mRNA when the expression was normalized to whole lung 18S rRNA. After instillation of 2 units of bleomycin, the serum levels of SP-D were higher, and SP-D was also increased in BALF and lung homogenates. In another model of subacute injury, serum SP-D was increased in rats treated with paraquat plus oxygen. Finally to evaluate acute lung injury, we instilled rats with IICI; SP-D was increased at 4 h after instillation. Our data indicate that serum SP-D may be a useful indicator of lung injury and type II cell hyperplasia in rats. bleomycin injury; paraquat injury; HCI injury; keratinocyte growth factor; alveolar type II cells; surfactant protein D

Published
2002

50. Responses to prison for environmental criminals: impacts of incident, perpetrator, and respondent characteristics

Author

Taylor, Ralph B. and Mason, Robert J.

Subjects
Psychological research, Social science research, Offenses against the environment -- Interpretation and construction, Offenses against the environment -- Research, Offenses against the environment -- Cases, Company legal issue, Architecture and design industries, Environmental issues, Psychology and mental health, Sociology and social work
Abstract

Qualitative work with water quality inspectors suggests that structured discretion shapes the transition from informal to administrative sanctions and depends both on impressions formed about the morality of the polluter and the seriousness of the incident. Undergraduates (n = 118) at a diverse, urban university judged vignettes based on an actual prosecution. In a fully between 2 x 2 x 2 randomized design, the authors manipulated incident damage, polluter criminal history, and polluter-regulator relationship. These features influenced respondents' perceptions of offender cooperativeness and event seriousness. Cooperativeness influenced reactions to the appropriateness of prison; event seriousness influenced reactions to the appropriateness of a long prison term. Results suggest the factors influencing reactions to the transition from civil to severe criminal sanctions are somewhat similar to the factors influencing regulators' transitioning from informal to administrative sanctioning; in both sets of processes impressions formed of the incident and the offender mediate the relevant dynamics.

Published
2002

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