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3. Association of Umbilical Cord Milking vs Delayed Umbilical Cord Clamping With Death or Severe Intraventricular Hemorrhage Among Preterm Infants

Author

Katheria, Anup, Reister, Frank, Essers, Jochen, Mendler, Marc, Hummler, Helmut, Subramaniam, Akila, Carlo, Waldemar, Tita, Alan, Truong, Giang, Davis-Nelson, Shareece, Schmölzer, Georg, Chari, Radha, Kaempf, Joseph, Tomlinson, Mark, Yanowitz, Toby, Beck, Stacy, Simhan, Hyagriv, Dempsey, Eugene, OʼDonoghue, Keelin, Bhat, Shazia, Hoffman, Matthew, Faksh, Arij, Arnell, Kathy, Rich, Wade, Finer, Neil, Vaucher, Yvonne, Khanna, Paritosh, Meyers, Mariana, Varner, Michael, Allman, Phillip, Szychowski, Jeff, and Cutter, Gary

Published
2020
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5. Contributors

Author

Abbasi, Soraya, primary, Abbey, James, additional, Adzick, N. Scott, additional, Ahn, Sun-Young, additional, Albertine, Kurt H., additional, Allegaert, Karel, additional, Alper, Seth L., additional, Altit, Gabriel, additional, Altschuler, Steven M., additional, Alvaro, Ruben E., additional, Amorosa, Jennifer M.H., additional, Anbuhl, Kelsey L., additional, Andersen, Claus Yding, additional, Anderson, Richard A., additional, Askenazi, David J., additional, Auten, Richard Lambert, additional, Autmizguine, Julie, additional, Azhibekov, Timur, additional, Back, Stephen A., additional, Badaut, Jérôme, additional, Baker, Peter Russell, additional, Ballard, Philip L., additional, Bancalari, Eduardo H., additional, Barichello, Tatiana, additional, Battaglia, Frederick, additional, Baum, Michel, additional, Beggs, Simon, additional, Bell, Edward F., additional, Benchimol, Corinne, additional, Benders, Manon J.N.L., additional, Bennet, Laura, additional, Bennett, Phillip R., additional, Berger, Melvin, additional, Bernhard, Wolfgang, additional, Bertram, John F., additional, Bhosle, Vikrant K., additional, Bhutani, Vinod K., additional, Black, M. Jane, additional, Bliss, Joseph M., additional, Bolender, David L., additional, Brandenburg, Joline E., additional, Broussard, Delma L., additional, Brown, Laura Davidson, additional, Burrin, Douglas G., additional, Cannon, Barbara, additional, Caplan, Michael, additional, Carlson, Susan E., additional, Carlton, David P., additional, Caruana, Georgina, additional, Cashore, William J., additional, Chaemsaithong, Piya, additional, Chaiyasit, Noppadol, additional, Charlton, Jennifer R., additional, Cheatham, Carol L., additional, Chemtob, Sylvain, additional, Chen, Yi-Yung, additional, Chevalier, Robert L., additional, Chheda, Sadhana, additional, Childs, Andrew J., additional, Christensen, Robert D., additional, Chu, Alison, additional, Chu, David H., additional, Cilio, Maria Roberta, additional, Clark, David A., additional, Cleary-Goldman, Jane, additional, Clemente, Ethel G., additional, Clements, John A., additional, Clyman, Ronald I., additional, Cohen, Susan S., additional, Colombo, John, additional, Cowett, Richard M., additional, Crawford, Peter A., additional, Crowe, James E., additional, Cullen-McEwen, Luise A., additional, Cutfield, Wayne S., additional, D'Alton, Mary E., additional, Danzer, Enrico, additional, Delacourt, Christophe, additional, Devaskar, Sherin U., additional, Diacovo, Thomas G., additional, Docheva, Nikolina, additional, Dormans, John P., additional, Dysart, Kevin, additional, El-Khuffash, Afif, additional, Ellis, Peter James, additional, Empey, Kerry McGarr, additional, Ercal, Baris, additional, Erdős, Melinda, additional, Erickson, Robert P., additional, Fahim, Mohamed A., additional, Faksh, Arij, additional, Frank, Hans-Georg, additional, Friedlich, Philippe S., additional, Friedman, Jed, additional, Gao, Yuansheng, additional, Garland, Marianne, additional, Geddes, Donna, additional, Georgieff, Michael K., additional, Gien, Jason, additional, Giussani, Dino A., additional, Goldman, Armond S., additional, González, Efrén, additional, Good, Misty, additional, Grant, Denis M., additional, Green, Lucy R., additional, Grigoriou, Emmanouil, additional, Grimberg, Adda, additional, Gross, Ian, additional, Grunau, Ruth E., additional, Guignard, Jean-Pierre, additional, Gunn, Alistair Jan, additional, Gurtunca, Nursen, additional, Hadchouel, Alice, additional, Haddad, Gabriel G., additional, Hagberg, Henrik, additional, Hale, Thomas, additional, Hambidge, K. Michael, additional, Hammerman, Cathy, additional, Hansen, Thor Willy Ruud, additional, Hanson, Mark A., additional, Harding, Richard, additional, Harris, Mary Catherine, additional, Hartmann, Peter, additional, Hassiotou, Foteini, additional, Haugen, Guttorm, additional, Hawkes, Colin P., additional, Hay, William W., additional, Hayward, Christina E., additional, Heine, Vivi M., additional, Hellström, Ann, additional, Helmrath, Michael A., additional, Hendricks-Muñoz, Karen D., additional, Herrera, Emilio, additional, Hiatt, Michael J., additional, Hoath, Steven B., additional, Hooper, Stuart B., additional, Huang, Stephen A., additional, Iacobellli, Silvia, additional, Inder, Terrie E., additional, Iruela-Arispe, M. Luisa, additional, Jadcherla, Sudarshan R., additional, Jain, Deepak, additional, Jansson, Thomas, additional, Jefferies, John Lynn, additional, Jetton, Jennifer G., additional, Jobe, Alan H., additional, Johnson, Lois H., additional, Johnston, Richard B., additional, Jones, Rebecca Lee, additional, Jose, Pedro A., additional, Kalhan, Satish C., additional, Kallapur, Suhas G., additional, Kaplan, Michael, additional, Kaplan, Stanley, additional, Karpen, Heidi Eigenrauch, additional, Karpen, Saul J., additional, Karumanchi, S. Ananth, additional, Kaskel, Frederick J., additional, Katheria, Anup C., additional, Katz, Lorraine E. Levitt, additional, Keeney, Susan E., additional, Kern, Steven E., additional, Khanjani, Shirin, additional, Kilpatrick, Laurie E., additional, Kim, Chang-Ryul, additional, Kinsella, John P., additional, Kiserud, Torvid, additional, Koenig, Joyce M., additional, Kollmann, Tobias R., additional, Kolls, Jay K., additional, Krebs, Nancy F., additional, Kulik, Thomas J., additional, Kutikov, Jessica Katz, additional, Lakshminrusimha, Satyan, additional, Lamola, Angelo A., additional, Lasunción, Miguel Angel, additional, Lavoie, Pascal M., additional, LeBien, Tucker W., additional, Lee, Mary M., additional, Lee, Matthew K., additional, Lee, Yvonne K., additional, Leibel, Sandra, additional, Levine, Fred, additional, Levy, Ofer, additional, Liu, Yang, additional, Lobritto, Steven, additional, Loomis, Cynthia A., additional, Lopez, Colleen A., additional, MacIntyre, David A., additional, Mahe, Maxime M., additional, Maheshwari, Akhil, additional, Mankouski, Anastasiya, additional, Mantilla, Carlos B., additional, Marchant, Arnaud, additional, Margolis, Kara Gross, additional, Mariscalco, M. Michele, additional, Maródi, László, additional, Maršál, Karel, additional, Martin, Richard J., additional, Matsell, Douglas G., additional, Matthews, Dwight E., additional, McArdle, Harry J., additional, McManaman, James L., additional, McNamara, Patrick J., additional, McQuillen, Patrick S., additional, McQuinn, Tim C., additional, Mercer, Judith S., additional, Meschia, Giacomo, additional, Miller, Steven P., additional, Minoo, Parviz, additional, Monagle, Paul, additional, Mortola, Jacopo P., additional, Muglia, Louis J., additional, Munshi, Upender K., additional, Namgung, Ran, additional, Narasimhan, Sumana, additional, Nedergaard, Jan, additional, Neu, Josef, additional, Nigam, Sanjay K., additional, Nogee, Lawrence M., additional, Noori, Shahab, additional, O'Brien, Barbara M., additional, Ohls, Robin K., additional, Ortega-Senovilla, Henar, additional, O'Sullivan, Justin M., additional, Owusu, Sarah A., additional, Pal, Abhijeet, additional, Panitch, Howard B., additional, Penn, Anna A., additional, Penn, Raymond B., additional, Pernia, Cameron, additional, Philipps, Anthony F., additional, Picoraro, Joseph A., additional, Pisani, Francesco, additional, Pleasure, David, additional, Pleasure, Jeanette R., additional, Pleasure, Samuel J., additional, Pomeroy, Scott L., additional, Post, Martin, additional, Prakash, Y.S., additional, Prozialeck, Joshua D., additional, Pysher, Theodore J., additional, Quigley, Raymond, additional, Rabinovitch, Marlene, additional, Raffay, Thomas M., additional, Raj, J. Usha, additional, Ramsey, Haley, additional, Rana, Sarosh, additional, Randis, Tara Marie, additional, Ranger, Manon, additional, Ratner, Adam J., additional, Regnault, Timothy R.H., additional, Rigatto, Henrique, additional, Rintoul, Natalie E., additional, Romero, Roberto, additional, Rose, James C., additional, Rosenfeld, Charles R., additional, Ross, A. Catharine, additional, Rozycki, Henry J., additional, Ryan, Thomas D., additional, Sahni, Rakesh, additional, Sajti, Eniko, additional, Sarnat, Harvey B., additional, Satlin, Lisa M., additional, Saugstad, Ola Didrik, additional, Schierding, William, additional, Schmalstieg, Frank C., additional, Schwartz, George J., additional, Schwartz, Jeffrey, additional, Segar, Jeffrey L., additional, Selewski, David T., additional, Seri, Istvan, additional, Shaffer, Thomas H., additional, Shah, Kara N., additional, Shearer, Martin J., additional, Shojaie, Sharareh, additional, Shroyer, Noah F., additional, Sibley, Colin P., additional, Sieck, Gary C., additional, Simmons, Rebecca A., additional, Sivieri, Emidio M., additional, Smith, Francine G., additional, Smith, Lois E.H., additional, Smyth, Ian M., additional, Snarr, Brian S., additional, Snyder, Evan Y., additional, Sola-Visner, Martha, additional, Solhaug, Michael J., additional, Sperling, Mark A., additional, Srinivasan, Lakshmi, additional, Stahl, Andreas, additional, Stanley, Charles A., additional, Steinhorn, Robin H., additional, Stonestreet, Barbara S., additional, Strasburger, Janette F., additional, Styne, Dennis M., additional, Sussel, Lori, additional, Tam, Emily W.Y., additional, Tan, Libo, additional, Thornton, Claire, additional, Tollin, Daniel J., additional, Tóth, Beáta, additional, Towbin, Jeffrey A., additional, Trocle, Ashley, additional, Truog, William E., additional, Tsang, Reginald C., additional, Uhler, Kristin M., additional, Van Den Anker, John N., additional, van Goudoever, Johannes (Hans) B., additional, Vannucci, Susan J., additional, Vickers, Mark H., additional, Virgintino, Daniela, additional, Volpe, Joseph J., additional, Vora, Neeta L., additional, Vyas, Neha V., additional, Wacker-Gussmann, Annette, additional, Wallace, Megan J., additional, Walsh, Brian H., additional, Wang, Alice M., additional, Warburton, David, additional, Ward, Robert M., additional, Watterberg, Kristi L., additional, Werner, Lynne A., additional, Wershil, Barry K., additional, Wert, Susan E., additional, Wessels, Andy, additional, Whitsett, Jeffrey A., additional, Wise, Michael, additional, Wolf, Matthias T., additional, Wolfson, Marla R., additional, Wong, Hector R., additional, Wynn, James L., additional, Yeo, Lami, additional, Yip, Stephen, additional, Yoder, Bradley A, additional, Yoder, Mervin C., additional, Yoshimoto, Momoko, additional, Yuskaitis, Christopher J., additional, Zhou, Dan, additional, and Zovein, Ann, additional

Published
2017
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6. Perinatal oxygen in the developing lung

Author

Vogel, Elizabeth R., Britt, Jr., Rodney D., Trinidad, Mari Charisse, Faksh, Arij, Martin, Richard J., MacFarlane, Peter M., Pabelick, Christina M., and Prakash, Y.S.

Subjects
Oxygen -- Health aspects, Lung diseases -- Physiological aspects, Biological sciences
Abstract

Lung diseases, such as bronchopulmonary dysplasia (BPD), wheezing, and asthma, remain significant causes of morbidity and mortality in the pediatric population, particularly in the setting of premature birth. Pulmonary outcomes in these infants are highly influenced by perinatal exposures including prenatal inflammation, postnatal intensive care unit interventions, and environmental agents. Here, there is strong evidence that perinatal supplemental oxygen administration has significant effects on pulmonary development and health. This is of particular importance in the preterm lung, where premature exposure to room air represents a hyperoxic insult that may cause harm to a lung primed to develop in a hypoxic environment. Preterm infants are also subject to increased episodes of hypoxia, which may also result in pulmonary damage and disease. Here, we summarize the current understanding of the effects of oxygen on the developing lung and how low vs. high oxygen may predispose to pulmonary disease that may extend even into adulthood. Better understanding of the underlying mechanisms will help lead to improved care and outcomes in this vulnerable population. Key words: neonatal, bronchopulmonary dysplasia, asthma, hypoxia, hyperoxia. Les maladies pulmonaires telles la dysplasie broncho-pulmonaire, la respiration sifflante et l'asthme, demeurent des causes significatives de morbidite et de mortalite chez la population pediatrique, particulierement dans les cas de naissance prematuree. Les consequences sur le plan pulmonaire chez ces bebes sont fortement influencees par des expositions perinatales incluant l'inflammation prenatale, les soins intensifs postnataux et les agents environnementaux. Il y a ici de fortes preuves que l'administration perinatale d'oxygene d'appoint a des effets significatifs sur le developpement et la sante pulmonaires. Ceci est particulierement important chez le poumon premature, ou l'exposition prematuree a l'air ambiant represente un choc hyperoxique qui pourrait etre dommageable a un poumon habitue a un environnement hypoxique. Les bebes prematures sont aussi sujets a des periodes accrues d'hypoxie, qui peuvent aussi resulter en dommage et maladies pulmonaires. Les auteurs resument ici les connaissances actuelles des effets de l'oxygene sur le poumon en developpement, et discutent comment une concentration elevee d'oxygene, par rapport a une faible concentration, peut predisposer a une maladie pulmonaire qui peut persister meme jusqu'a l'age adulte. Une meilleure comprehension des mecanismes sous-jacents aidera a ameliorer les soins et les consequences chez cette population vulnerable. [Traduit par la Redaction] Mots-cles: neonatal, dysplasie broncho-pulmonaire, asthme, hypoxie, hyperoxie., Introduction Premature birth (defined as birth prior to 37 weeks gestational age) continues to be a significant source of morbidity and mortality in neonatal and pediatric populations. Neonatal lung diseases, [...]

Published
2015
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9. Optical spectroscopy of long polyenes

Author

Christensen, Ronald L., Faksh, Arij, Meyers, John A., Samuel, Ifor D.W., Wood, Philip, Schrock, Richard R., and Hultzsch, Kai C.

Subjects
Oligomers -- Chemical properties, Optical spectrometers -- Usage, Polyenes -- Chemical properties, Chemicals, plastics and rubber industries
Abstract

A homologous series of soluble, linearly conjugated oligomers and related polymers using molybdenum alkylidene catalysts are examined. HPCL procedures are developed to isolate the oligomers according to their chain lengths and have obtained the absorption spectra of the purified oligomers in room temperature solutions and in 77 K glasses.

Published
2004

10. Association of Umbilical Cord Milking vs Delayed Umbilical Cord Clamping With Death or Severe Intraventricular Hemorrhage Among Preterm Infants

Author

Katheria, Anup, primary, Reister, Frank, additional, Essers, Jochen, additional, Mendler, Marc, additional, Hummler, Helmut, additional, Subramaniam, Akila, additional, Carlo, Waldemar, additional, Tita, Alan, additional, Truong, Giang, additional, Davis-Nelson, Shareece, additional, Schmölzer, Georg, additional, Chari, Radha, additional, Kaempf, Joseph, additional, Tomlinson, Mark, additional, Yanowitz, Toby, additional, Beck, Stacy, additional, Simhan, Hyagriv, additional, Dempsey, Eugene, additional, O’Donoghue, Keelin, additional, Bhat, Shazia, additional, Hoffman, Matthew, additional, Faksh, Arij, additional, Arnell, Kathy, additional, Rich, Wade, additional, Finer, Neil, additional, Vaucher, Yvonne, additional, Khanna, Paritosh, additional, Meyers, Mariana, additional, Varner, Michael, additional, Allman, Phillip, additional, Szychowski, Jeff, additional, and Cutter, Gary, additional

Published
2019
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16. Persistent Notochord in a Fetus with COL2A1 Mutation

Author

Codsi, Elisabeth, Brost, Brian C., Faksh, Arij, Volk, Amber K., and Borowski, Kristi S.

Subjects
musculoskeletal diseases, animal structures, Article Subject, fungi, embryonic structures, musculoskeletal system
Abstract

Multiple anomalies including micromelia, poor mineralization of the vertebrae, and a persistent notochord were identified on second trimester ultrasound in a fetus with a COL2A1 mutation. To our knowledge, this represents the first case of a persistent notochord associated with a COL2A1 mutation in humans. In this case report, we describe ultrasound and postmortem findings and review the pathogenesis associated with a persistent notochord.

Published
2015
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19. Reply

Author

Rose, Carl H., primary, Faksh, Arij, additional, Traynor, Kyle D., additional, Cabrera, Daniel, additional, Arendt, Katherine W., additional, and Brost, Brian C., additional

Published
2016
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29. 288: Synthetic double stranded RNA increases chemokine expression in human fetal airway smooth muscle cells

Author

Faksh, Arij, primary, Britt, Rodney, additional, Vogel, Elizabeth, additional, Trinidad, Mari Charisse, additional, Codsi, Elisabeth, additional, White, Wendy, additional, Brost, Brian, additional, Davies, Norman, additional, Rose, Carl, additional, Borowski, Kristi, additional, Pabelick, Christina, additional, and Prakash, YS., additional

Published
2015
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30. 158: Genome wide maternal leukocyte DNA methylation analysis performed longitudinally throughout normal pregnancy

Author

White, Wendy, primary, Raghuraman, Sriram, additional, Harris, R. Alan, additional, Milosavljevic, Aleksandar, additional, Baldwin, Elizabeth, additional, Faksh, Arij, additional, Trinidad, Mari Charisse, additional, Brost, Brian, additional, Rose, Carl, additional, Borowski, Kristi, additional, Davies, Norman, additional, and Garovic, Vesna, additional

Published
2014
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33. 759: Unexpected finding in vaginal microbiome assessment in PPROM

Author

Baldwin, Elizabeth, primary, Walther-Antonio, Marina, additional, Brost, Brian, additional, Faksh, Arij, additional, Trinidad, Mari Charisse, additional, White, Wendy, additional, Davies, Norman, additional, Rose, Carl, additional, Borowski, Kristi, additional, Chia, Nicholas, additional, and Creedon, Douglas, additional

Published
2014
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35. 630: Flt-1 expressing microparticle levels correlate with plasma sFlt-1 concentrations and may contribute to VEGF regulation in preeclampsia

Author

O'Brien, Jonathan, primary, White, Wendy, additional, Baldwin, Elizabeth, additional, Faksh, Arij, additional, Boseman, Peter, additional, Jayachandran, Muthuvel, additional, Miller, Virginia, additional, Brost, Brian, additional, Rose, Carl, additional, Davies, Norman, additional, and Garovic, Vesna, additional

Published
2013
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38. Moderate hyperoxia induces extracellular matrix remodeling by human fetal airway smooth muscle cells

Author

Vogel, Elizabeth R., Britt, Rodney D., Faksh, Arij, Kuipers, Ine, Pandya, Hitesh, Prakash, Y.S., Martin, Richard J., and Pabelick, Christina M.

Abstract

Background:Premature infants are at increased risk for airway diseases, such as wheezing and asthma, because of early exposure to risk factors including hyperoxia. As in adult asthma, airway remodeling and increased extracellular matrix (ECM) deposition is involved.Methods:We assessed the impact of 24–72 h of moderate hyperoxia (50%) on human fetal airway smooth muscle (fASM) ECM deposition through western blot, modified in-cell western, and zymography techniques.Results:Hyperoxia exposure significantly increased collagen I and collagen III deposition, increased pro- and cleaved matrix metalloproteinase 9 (MMP9) activity, and decreased endogenous MMP inhibitor, TIMP1, expression. Hyperoxia-induced change in caveolin-1 (CAV1) expression was assessed as a potential mechanism for the changes in ECM deposition. CAV1 expression was decreased following hyperoxia. Supplementation of CAV1 activity with caveolar scaffolding domain (CSD) peptide abrogated the hyperoxia-mediated ECM changes.Conclusion:These results demonstrate that moderate hyperoxia enhances ECM deposition in developing airways by altering the balance between MMPs and their inhibitors (TIMPs), and by increasing collagen deposition. These effects are partly mediated by a hyperoxia-induced decrease in CAV1 expression. In conjunction with prior data demonstrating increased fASM proliferation with hyperoxia, these data further demonstrate that hyperoxia is an important instigator of remodeling in developing airways.

Published
2017
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39. Perinatal oxygen in the developing lung1.

Author

Britt, Rodney D., Trinidad, Mari Charisse, Martin, Richard J., MacFarlane, Peter M., Vogel, Elizabeth R., Pabelick, Christina M., Prakash, Y.S., and Faksh, Arij

Subjects
LUNG development, BRONCHOPULMONARY dysplasia, NEONATAL infections, HYPOXEMIA, HYPEROXIA, ASTHMA
Abstract

Copyright of Canadian Journal of Physiology & Pharmacology is the property of Canadian Science Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Published
2015
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40. Effects of antenatal lipopolysaccharide and postnatal hyperoxia on airway reactivity and remodeling in a neonatal mouse model

Author

Faksh, Arij, Britt, Rodney D., Vogel, Elizabeth R., Kuipers, Ine, Thompson, Michael A., Sieck, Gary C., Pabelick, Christina M., Martin, Richard J., and Prakash, Y. S.

Abstract

Background:Antenatal inflammation and preterm birth are associated with the development of airway diseases such as wheezing and asthma. Utilizing a newborn mouse model, we assessed the effects of maternal inflammation and postnatal hyperoxia on the neonatal airway.Methods:Pregnant C57/Bl6 dams were injected with lipopolysaccharide (LPS) or saline on embryonic day 16. Offspring were placed in room air or hyperoxia (50% O2) for 7 d and then returned to normoxia. Airway mechanics, histology, and laser capture micro-dissection (LCM) were performed.Results:At postnatal day 21, maternal LPS- and 50% O2-exposed pups exhibited increased resistance and decreased compliance compared to 21% O2pups; however their effects were not synergistic. LPS and hyperoxia each increased the thickness of airway smooth muscle (ASM), but not the airway epithelial layer. Structural changes were largely limited to the conducting airways. Upregulation of inflammatory markers in the lung was observed at birth. LCM revealed increased collagen-3, transforming growth factor ß, and connective tissue growth factor expression with LPS and hyperoxia within the ASM layer.Conclusion:These novel studies provide functional, structural, and molecular evidence that antenatal inflammation is detrimental to the developing airway. Exposure to moderate hyperoxia does not exacerbate LPS effects on the airway.

Published
2016
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42. Perinatal oxygen in the developing lung1.

Author

Britt, Rodney D., Trinidad, Mari Charisse, Martin, Richard J., MacFarlane, Peter M., Vogel, Elizabeth R., Pabelick, Christina M., Prakash, Y.S., and Faksh, Arij

Subjects
*LUNG development, *BRONCHOPULMONARY dysplasia, *NEONATAL infections, *HYPOXEMIA, *HYPEROXIA, *ASTHMA
Abstract

Lung diseases, such as bronchopulmonary dysplasia (BPD), wheezing, and asthma, remain significant causes of morbidity and mortality in the pediatric population, particularly in the setting of premature birth. Pulmonary outcomes in these infants are highly influenced by perinatal exposures including prenatal inflammation, postnatal intensive care unit interventions, and environmental agents. Here, there is strong evidence that perinatal supplemental oxygen administration has significant effects on pulmonary development and health. This is of particular importance in the preterm lung, where premature exposure to room air represents a hyperoxic insult that may cause harm to a lung primed to develop in a hypoxic environment. Preterm infants are also subject to increased episodes of hypoxia, which may also result in pulmonary damage and disease. Here, we summarize the current understanding of the effects of oxygen on the developing lung and how low vs. high oxygen may predispose to pulmonary disease that may extend even into adulthood. Better understanding of the underlying mechanisms will help lead to improved care and outcomes in this vulnerable population. [ABSTRACT FROM AUTHOR]

Published
2015
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43. Caveolin-1 scaffolding domain peptide prevents hyperoxia-induced airway remodeling in a neonatal mouse model.

Author

Vogel ER, Manlove LJ, Kuipers I, Thompson MA, Fang YH, Freeman MR, Britt RD Jr, Faksh A, Yang B, Prakash YS, and Pabelick CM

Subjects
Airway Remodeling drug effects, Airway Remodeling immunology, Animals, Animals, Newborn, Bronchial Hyperreactivity etiology, Bronchial Hyperreactivity genetics, Bronchial Hyperreactivity immunology, Bronchoconstrictor Agents pharmacology, Caveolin 1 genetics, Caveolin 1 immunology, Disease Models, Animal, Female, Gene Expression Regulation, Humans, Hyperoxia etiology, Hyperoxia genetics, Hyperoxia immunology, Injections, Intraperitoneal, Lung immunology, Lung pathology, Male, Membrane Proteins genetics, Membrane Proteins immunology, Methacholine Chloride pharmacology, Mice, Oxygen adverse effects, RNA-Binding Proteins genetics, RNA-Binding Proteins immunology, Signal Transduction, Anti-Inflammatory Agents pharmacology, Bronchial Hyperreactivity drug therapy, Caveolin 1 pharmacology, Hyperoxia drug therapy, Lung drug effects, Peptide Fragments pharmacology
Abstract

Reactive airway diseases are significant sources of pulmonary morbidity in neonatal and pediatric patients. Supplemental oxygen exposure in premature infants contributes to airway diseases such as asthma and promotes development of airway remodeling, characterized by increased airway smooth muscle (ASM) mass and extracellular matrix (ECM) deposition. Decreased plasma membrane caveolin-1 (CAV1) expression has been implicated in airway disease and may contribute to airway remodeling and hyperreactivity. Here, we investigated the impact of clinically relevant moderate hyperoxia (50% O 2 ) on airway remodeling and caveolar protein expression in a neonatal mouse model. Within 12 h of birth, litters of B6129SF2J mice were randomized to room air (RA) or 50% hyperoxia exposure for 7 days with or without caveolin-1 scaffolding domain peptide (CSD; caveolin-1 mimic; 10 µl, 0.25 mM daily via intraperitoneal injection) followed by 14 days of recovery in normoxia. Moderate hyperoxia significantly increased airway reactivity and decreased pulmonary compliance at 3 wk. Histologic assessment demonstrated airway wall thickening and increased ASM mass following hyperoxia. RNA from isolated ASM demonstrated significant decreases in CAV1 and cavin-1 in hyperoxia-exposed animals while cavin-3 was increased. Supplementation with intraperitoneal CSD mitigated both the physiologic and histologic changes observed with hyperoxia. Overall, these data show that moderate hyperoxia is detrimental to developing airway and may predispose to airway reactivity and remodeling. Loss of CAV1 is one mechanism through which hyperoxia produces these deleterious effects. Supplementation of CAV1 using CSD or similar analogs may represent a new therapeutic avenue for blunting hyperoxia-induced pulmonary damage in neonates.

Published
2019
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44. TLR3 activation increases chemokine expression in human fetal airway smooth muscle cells.

Author

Faksh A, Britt RD Jr, Vogel ER, Thompson MA, Pandya HC, Martin RJ, Pabelick CM, and Prakash YS

Subjects
Cells, Cultured, Cytokines metabolism, Humans, Lipopolysaccharides pharmacology, NF-kappa B metabolism, Signal Transduction drug effects, Chemokines metabolism, Lung metabolism, Myocytes, Smooth Muscle metabolism, Toll-Like Receptor 3 metabolism
Abstract

Viral infections, such as respiratory syncytial virus and rhinovirus, adversely affect neonatal and pediatric populations, resulting in significant lung morbidity, including acute asthma exacerbation. Studies in adults have demonstrated that human airway smooth muscle (ASM) cells modulate inflammation through their ability to secrete inflammatory cytokines and chemokines. The role of ASM in the developing airway during infection remains undefined. In our study, we used human fetal ASM cells as an in vitro model to examine the effect of Toll-like receptor (TLR) agonists on chemokine secretion. We found that fetal ASM express multiple TLRs, including TLR3 and TLR4, which are implicated in the pathogenesis of respiratory syncytial virus and rhinovirus infection. Cells were treated with TLR agonists, polyinosinic-polycytidylic acid [poly(I:C)] (TLR3 agonist), lipopolysaccharide (TLR4 agonist), or R848 (TLR7/8 agonist), and IL-8 and chemokine (C-C motif) ligand 5 (CCL5) secretion were evaluated. Interestingly, poly(I:C), but neither lipopolysaccharide nor R848, increased IL-8 and chemokine (C-C motif) ligand 5 secretion. Examination of signaling pathways suggested that the poly(I:C) effects in fetal ASM involve TLR and ERK signaling, in addition to another major inflammatory pathway, NF-κB. Moreover, there are variations between fetal and adult ASM with respect to poly(I:C) effects on signaling pathways. Pharmacological inhibition suggested that ERK pathways mediate poly(I:C) effects. Overall, our data show that poly(I:C) initiates activation of proinflammatory pathways in developing ASM, which may contribute to immune responses to infection and exacerbation of asthma., (Copyright © 2016 the American Physiological Society.)

Published
2016
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45. Pregnancy in Desmin-Related Cardiomyopathy.

Author

Faksh A, Codsi E, Barsoum MK, and Brost BC

Abstract

The course of desmin-related restrictive cardiomyopathy (DRCM) during pregnancy has not been described previously because of the rarity of the condition. Following an episode of heart failure antecedent to conception, a 28-year-old primigravida with DRCM presented to establish prenatal care during the first trimester. Prenatal management consisted of β-blocker and diuretic therapy, with serial echocardiography to monitor cardiac function. Spontaneous labor ensued at 39 weeks' gestation, and vacuum-assisted delivery was performed for fetal indication. Postpartum blood transfusion was required for symptomatic anemia because of uterine atony, and subsequent maternal and neonatal courses were uncomplicated. Cardiac evaluation postpartum demonstrated stable maternal status. Pregnancy in women with controlled DRCM is not contraindicated, however, it requires careful planning and monitoring during the antenatal, intrapartum, and postpartum periods. On the basis of this report, pregnancy does not appear to exert a permanent deleterious effect on cardiac function in women with DRCM.

Published
2015
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46. Preterm premature rupture of membranes ≥ 32 weeks' gestation: impact of revised practice guidelines.

Author

Faksh A, Wax JR, Lucas FL, Cartin A, and Pinette MG

Subjects
Adult, Female, Gestational Age, Humans, Practice Guidelines as Topic, Pregnancy, Pregnancy Trimester, Third, Retrospective Studies, Fetal Membranes, Premature Rupture therapy, Guideline Adherence
Abstract

Objective: The purpose of this study was to determine the perinatal impact of the 2007 American College of Obstetricians and Gynecologists Practice Bulletin on preterm premature membrane rupture., Study Design: Perinatal outcomes were compared in women who had experienced preterm membrane rupture in the 3 years before the 2007 Practice Bulletin to similar women who experienced preterm premature rupture of membranes in the 3 years after the issue and implementation of the guideline., Results: After adjustment for gestational age at membrane rupture and steroids, composite severe morbidity (death, respiratory distress syndrome, assisted ventilation for ≥ 6 hours, sepsis, pneumonia, grade 3 or 4 intraventricular hemorrhage, or necrotizing enterocolitis) was similar by group. Infants in the "after" group experienced less pneumonia and sepsis, similar respiratory morbidity, but more labor inductions and postpartum hemorrhage., Conclusion: The new guideline significantly decreases severe neonatal infections but is associated with more frequent labor induction and postpartum hemorrhage., (Copyright © 2011 Mosby, Inc. All rights reserved.)

Published
2011
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