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6. Contributors

Author

Andreoli, Sharon P., primary, Azhibekov, Timur, additional, Bates, Carlton, additional, Baum, Michel, additional, Baumgart, Stephen, additional, Beall, Marie H., additional, Besouw, Martine TP, additional, Bland, Richard D., additional, Bockenhauer, Detlef, additional, Bonilla-Felix, Melvin, additional, Cerqueira, Debora Malta, additional, Costarino, Andrew Thomas, additional, de Jesús-González, Nilka, additional, Flynn, Joseph, additional, Gattineni, Jyothsna, additional, Gouyon, Jean-Bernard, additional, Guignard, Jean-Pierre, additional, Ho, Jacqueline, additional, Jain, Lucky, additional, Jose, Pedro A., additional, Keene, Sarah D., additional, Khalid, Myda, additional, Levenbrown, Yosef, additional, Matsell, Douglas G., additional, Namgung, Ran, additional, Natarajan, Aruna, additional, Oh, William, additional, Puri, Pawan, additional, Quigley, Raymond, additional, Ross, Michael G., additional, Segar, Jeffrey, additional, Seri, Istvan, additional, Tsang, Reginald C., additional, van den Wijngaard, Jeroen P.H.M., additional, van Gemert, Martin, additional, Villar, Van Anthony M., additional, Wolf, Matthias Tilmann, additional, and Zelikovic, Israel, additional

Published
2019
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12. Association of Gestational Diabetes Mellitus With Neonatal Respiratory Morbidity

Author

Werner, Erika F., Romano, Megan E., Rouse, Dwight J., Sandoval, Grecio, Gyamfi-Bannerman, Cynthia, Blackwell, Sean C., Tita, Alan T.N., Reddy, Uma M., Jain, Lucky, Saade, George R., Iams, Jay D., Clark, Erin A.S., Thorp, John M., Jr, Chien, Edward K., Peaceman, Alan M., Swamy, Geeta K., Norton, Mary E., Casey, Brian M., Caritis, Steve N., Tolosa, Jorge E., and Sorokin, Yoram

Published
2019
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14. Contributors

Author

Abman, Steven H., primary, Allegaert, Karel, additional, Arya, Bhawna, additional, Askenazi, David, additional, Azhibekov, Timur, additional, Back, Stephen A., additional, Baldwin, H. Scott, additional, Ballard, Roberta A., additional, Bancalari, Eduardo, additional, Bates, Carlton M., additional, Batra, Maneesh, additional, Bayart, Cheryl B., additional, Bellus, Gary A., additional, Benedetti, Thomas J., additional, Benjamin, John T., additional, Bennett, James T., additional, Berry, Gerard T., additional, Binenbaum, Gil, additional, Boos, Markus D., additional, Bouchard, Maryse, additional, Brandling-Bennett, Heather A., additional, Broughton, Darcy E., additional, Brown, Zane, additional, Campbell, Katherine H., additional, Carmichael, Suzan L., additional, Carter, Brian S., additional, Cederbaum, Stephen, additional, Chabra, Shilpi, additional, Chang, Justine, additional, Cheng, Edith Y., additional, Chisholm, Karen M., additional, Christensen, Robert D., additional, Chun, Terrence, additional, Claure, Nelson, additional, Clyman, Ronald I., additional, Colaizy, Tarah T., additional, Cortezzo, DonnaMaria E., additional, Cotten, C. Michael, additional, Cunningham, Michael L., additional, de Alba Campomanes, Alejandra G., additional, Dees, Ellen, additional, DeMauro, Sara B., additional, Denne, Scott C., additional, Deschmann, Emöke, additional, Cecilia, Carolina, additional, DiBlasi, Robert M., additional, Dimmitt, Reed A., additional, DiVall, Sara A., additional, Djahangirian, Orchid, additional, Doherty, Dan, additional, Eichenwald, Eric C., additional, Engen, Rachel, additional, Engmann, Cyril, additional, Evans, Jacquelyn R., additional, Evans, Kelly N., additional, Farmer, Diana L., additional, Fechner, Patricia Y., additional, Ferrieri, Patricia, additional, Finer, Neil N., additional, Fleishman, Rachel A., additional, Fleiss, Bobbi, additional, Flynn, Joseph T., additional, Flynn-O'Brien, Katherine T., additional, Frey, Mark R., additional, Furman, Lydia, additional, Gallagher, Renata C., additional, Gauda, Estelle B., additional, Gleason, Christine A., additional, Goldberg, Michael J., additional, Goldin, Adam B., additional, Gospe, Sidney M., additional, Gressens, Pierre, additional, Gupta, Deepti, additional, Guttentag, Susan H., additional, Haldeman-Englert, Chad R., additional, Hansen, Thomas N., additional, Hing, Anne V., additional, Hingorani, Sangeeta, additional, Hintz, Susan R., additional, Hirose, Shinjiro, additional, Hodson, W. Alan, additional, Hoppe, Kara K., additional, Hostetter, Margaret K., additional, Huang, Benjamin, additional, Huang, Sarah Bauer, additional, Inder, Terrie E., additional, Inoita, Cristian, additional, Jackson, J. Craig, additional, Jain, Deepak, additional, Jain, Lucky, additional, Javid, Patrick J., additional, Josephson, Cassandra D., additional, Jungheim, Emily S., additional, Juul, Sandra E., additional, Katheria, Anup, additional, Keller, Benjamin A., additional, Keller, Roberta L., additional, Kelly, Thomas F., additional, Khorsand, Kate, additional, Kim, Grace, additional, Kinsella, John P., additional, Koves, Ildiko H., additional, Lam, Christina, additional, Lane, Erin R., additional, Lantos, John D., additional, Ledbetter, Daniel J., additional, Lee, Ben, additional, Levy, Harvey L., additional, Levy, Ofer, additional, Lewin, Mark B., additional, Lewis, David B., additional, Lin, P. Ling, additional, Lin, Tiffany Fangtse, additional, Lorch, Scott A., additional, Maheshwari, Akhil, additional, Maltepe, Emin, additional, Marsh, Ketzela J., additional, Martin, Richard J., additional, Mayock, Dennis E., additional, McAdams, Ryan Michael, additional, McAleer, Irene, additional, McElroy, Steven J., additional, McNelis, Kera M., additional, McQuillen, Patrick, additional, Meadow, William L., additional, Merguerian, Paul A., additional, Merjaneh, Lina, additional, Merritt, J. Lawrence, additional, Mezger, Valerie, additional, Michaels, Marian G., additional, Miller, Steven P., additional, Mohan, Sowmya S., additional, Mollen, Thomas J., additional, Moore, Thomas R., additional, Murray, Jeffrey C., additional, Murray, Karen F., additional, Nandi-Munshi, Debika, additional, Natarajan, Niranjana, additional, Neil, Jeffrey J., additional, Ness, Kathryn D., additional, Neu, Josef, additional, Siu-Ying, Angel, additional, Noori, Shahab, additional, O'Mahony, Lila, additional, Palma, Jonathan P., additional, Paneth, Nigel, additional, Parker, Thomas A., additional, Patel, Ravi Mangal, additional, Penn, Anna A., additional, Pettker, Christian M., additional, Peyvandi, Shabnam, additional, Pihoker, Cate, additional, Plosa, Erin, additional, Poindexter, Brenda B., additional, Posencheg, Michael A., additional, Reinking, Benjamin E., additional, Rice-Townsend, Samuel, additional, Richards, Morgan K., additional, Richardson, C. Peter, additional, Richardson, Kelsey, additional, Riggle, Kevin M., additional, Robbins, Elizabeth, additional, Rollins, Mark D., additional, Rosen, Mark A., additional, Rowe, Courtney K., additional, Sahai, Inderneel, additional, Saitta, Sulagna C., additional, Salehi, Parisa, additional, Sanchez, Pablo, additional, Saxonhouse, Matthew A., additional, Schanler, Richard J., additional, Schleiss, Mark R., additional, Scholz, Thomas, additional, Schwaderer, Andrew L., additional, Selewski, David, additional, Sellers, Zachary M., additional, Seri, Istvan, additional, Shnorhavorian, Margarett, additional, Sibley, Eric, additional, Sidbury, Robert, additional, Simmons, Rebecca, additional, Smith, Caitlin, additional, Sola-Visner, Martha C., additional, Srinivasan, Lakshmi, additional, Steinhorn, Robin H., additional, Stevenson, David K., additional, Stolp, Helen, additional, Taplin, Craig, additional, Tarczy-Hornoch, Peter, additional, Taylor, James A., additional, Thomas, Janet A., additional, Thompson, Tracy, additional, Tiller, George E., additional, Torres, Benjamin A., additional, Traudt, Christopher Michael, additional, van den Anker, John N., additional, Vernon, Margaret M., additional, Vohr, Betty, additional, Walker, Valencia P., additional, Wallen, Linda D., additional, Wallenstein, Matthew B., additional, Wang, Peter (Zhan Tao), additional, Warady, Bradley A., additional, Ward, Robert M., additional, Watchko, Jon F., additional, Wehbi, Elias, additional, Weitkamp, Joern-Hendrik, additional, Werny, David, additional, White, Klane K., additional, Willig, Laurel, additional, Woodrum, David, additional, Woodward, George A., additional, Wright, Clyde J., additional, Wright, Jeffrey A., additional, Yonekawa, Karyn, additional, and Zackai, Elaine H., additional

Published
2018
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19. Evaluation of Hypoglycemia in Neonates of Women at Risk for Late Preterm Delivery: An Antenatal Late Preterm Steroids Trial Cohort Study.

Author

Gyamfi-Bannerman, Cynthia, Jablonski, Kathleen A., Blackwell, Sean C., Tita, Alan T. N., Reddy, Uma M., Jain, Lucky, Saade, George R., Rouse, Dwight J., Clark, Erin A. S., Thorp Jr., John M., Chien, Edward K., Peaceman, Alan M., Gibbs, Ronald S., Swamy, Geeta K., Norton, Mary E., Casey, Brian M., Caritis, Steve N., Tolosa, Jorge E., Sorokin, Yoram, and VanDorsten, J. Peter

Subjects
HYPOGLYCEMIA treatment, RELATIVE medical risk, PREMATURE infants, CONFIDENCE intervals, BETAMETHASONE, COMPARATIVE studies, HYPOGLYCEMIA, PREGNANCY complications, DESCRIPTIVE statistics, RESEARCH funding, RESPIRATORY distress syndrome, SECONDARY analysis, LONGITUDINAL method, CHILDREN
Abstract

Objective In the antenatal late preterm steroids (ALPS) trial betamethasone significantly decreased short-term neonatal respiratory morbidity but increased the risk of neonatal hypoglycemia, diagnosed only categorically (<40 mg/dL). We sought to better characterize the nature, duration, and treatment for hypoglycemia. Study Design Secondary analysis of infants from ALPS, a multicenter trial randomizing women at risk for late preterm delivery to betamethasone or placebo. This study was a reabstraction of all available charts from the parent trial, all of which were requested. Unreviewed charts included those lost to follow-up or from sites not participating in the reabstraction. Duration of hypoglycemia (<40 mg/dL), lowest value and treatment, if any, were assessed by group. Measures of association and regression models were used where appropriate. Results Of 2,831 randomized, 2,609 (92.2%) were included. There were 387 (29.3%) and 223 (17.3%) with hypoglycemia in the betamethasone and placebo groups, respectively (relative risk [RR]: 1.69, 95% confidence interval [CI]: 1.46–1.96). Hypoglycemia generally occurred in the first 24 hours in both groups: 374/385 (97.1%) in the betamethasone group and 214/222 (96.4%) in the placebo group (p = 0.63). Of 387 neonates with hypoglycemia in the betamethasone group, 132 (34.1%) received treatment, while 73/223 (32.7%) received treatment in placebo group (p = 0.73). The lowest recorded blood sugar was similar between groups. Most hypoglycemia resolved by 24 hours in both (93.0 vs. 89.3% in the betamethasone and placebo groups, respectively, p = 0.18). Among infants with hypoglycemia in the first 24 hours, the time to resolution was shorter in the betamethasone group (2.80 [interquartile range: 2.03–7.03) vs. 3.74 (interquartile range: 2.15–15.08) hours; p = 0.002]. Persistence for >72 hours was rare and similar in both groups, nine (2.4%, betamethasone) and four (1.9%, placebo, p = 0.18). Conclusion In this cohort, hypoglycemia was transient and most received no treatment, with a quicker resolution in the betamethasone group. Prolonged hypoglycemia was uncommon irrespective of steroid exposure. Key Points Hypoglycemia was transient and approximately two-thirds received no treatment. Neonates in the ALPS trial who received betamethasone had a shorter time to resolution than those with hypoglycemia in the placebo group. Prolonged hypoglycemia occurred in approximately 2 out of 100 late preterm newborns, irrespective of antenatal steroid exposure. [ABSTRACT FROM AUTHOR]

Published
2023
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27. Antenatal Betamethasone for Women at Risk for Late Preterm Delivery

Author

Gyamfi-Bannerman, Cynthia, Thom, Elizabeth A., Blackwell, Sean C., Tita, Alan T.N., Reddy, Uma M., Saade, George R., Rouse, Dwight J., McKenna, David S., Clark, Erin A.S., Thorp, John M., Jr., Chien, Edward K., Peaceman, Alan M., Gibbs, Ronald S., Swamy, Geeta K., Norton, Mary E., Casey, Brian M., Caritis, Steve N., Tolosa, Jorge E., Sorokin, Yoram, VanDorsten, Peter J., and Jain, Lucky

Published
2016
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31. Rac1-mediated NADPH oxidase release of [O.sup.-.sub.2] regulates epithelial sodium channel activity in the alveolar epithelium

Author

Takemura, Yoshizumi, Goodson, Preston, Bao, Hui Fang, Jain, Lucky, and Helms, My N.

Subjects
Oxidases -- Physiological aspects, Oxidases -- Health aspects, Pulmonary alveoli -- Chemical properties, Pulmonary alveoli -- Health aspects, Sodium channels -- Research, NADP (Coenzyme) -- Physiological aspects, NADP (Coenzyme) -- Health aspects, Biological sciences
Abstract

We examine whether alveolar cells can control release of [O.sup.-.sub.2] through regulated NADPH oxidase (NOX) 2 (NOX2) activity to maintain lung fluid homeostasis. Using FACS to purify alveolar epithelial cells, we show that type 1 cells robustly express each of the critical NOX components that catalyze the production of [O.sup.-.sub.2] (NOX2 or [gp91.sup.phox], [p22.sup.phox], pp67.sup.phox], [p47.sup.phox], and [p40.sup.phox] subunits) as well as Rac1 at substantially higher levels than type 2 cells. Immunohistochemical labeling of lung tissue shows that Rac1 expression is cytoplasmic and resides near the apical surface of type 1 cells, whereas NOX2 coimmunoprecipitates with epithelial sodium channel (ENaC). Since Rac1 is a known regulator of NOX2, and hence [O.sup.-.sub.2] release, we tested whether inhibition or activation of Rac1 influenced ENaC activity. Indeed, 1 [micro]M NSC23766 inhibition of Rac1 decreased [O.sup.-.sub.2] output in lung cells and significantly decreased ENaC activity from 0.87 [+ or -] 0.16 to 0.52 [+ or -] 0.16 [mean number of channels (N) and single-channel open probability ([P.sub.o]) (N[P.sub.o]) [+ or -] SE, n = 6; P < 0.05] in type 2 cells. NSC23766 (10 [micro]M) decreased ENaC N[P.sub.o] from 1.16 [+ or -] 0.27 to 0.38 [+ or -] 0.10 (n = 6 in type 1 cells). Conversely, 10 ng/ml EGF (a known stimulator of both Rac1 and [O.sup.-.sub.2] release) increased ENaC N[P.sub.o] values in both type 1 and 2 cells. N[P.sub.o] values increased from 0.48 [+ or -] 0.21 to 0.91 [+ or -] 0.28 in type 2 cells (P < 0.05; n = 10). In type 1 cells, ENaC activity also significantly increased from 0.40 [+ or -] 0.15 to 0.60 [+ or -] + 0.23 following EGF treatment (n = 7). Sequestering [O.sup.-.sub.2] using 2,2,6,6-tetramethylpiperidineN-oxyl (TEMPO) compound prevented EGF activation of ENaC in both type 1 and 2 cells. In conclusion, we report that Rac1-mediated NOX2 activity is an important component in [O.sup.-.sub.2] regulation of ENaC. doi: 10.1152/ajplung.00230.2009 redox; NOX2; lung slice; fluorescence-activated cell sorting; single-channel patch

Published
2010

35. Effects of cardiogenic edema fluid on ion and fluid transport in the adult lung

Author

Gandhi, Shephali G., Rafii, Bijan, Harris, Michael S., Garces, Alexandra, Mahuran, Don, Chen, Xi-Juan, Bao, Hui-Fang, Jain, Lucky, Eaton, Douglas C., Otulakowski, Gail, and O'Brodovich, Hugh

Subjects
Pulmonary edema -- Research, Sodium channels -- Research, Epithelial cells -- Research, Cellular control mechanisms -- Research, Pulmonary alveoli -- Research, Biological sciences
Abstract

We have previously shown that cardiogenic pulmonary edema fluid (EF) increases [Na.sup.+] and fluid transport by fetal distal lung epithelia (FDLE) (Rafii B, Gillie DJ, Sulowski C, Hannam V, Cheung T, Otulakowski G, Barker PM and O'Brodovich H. J Physiol 544: 537-548, 2002). We now report the effect of EF on [Na.sup.+] and fluid transport by the adult lung. We first studied primary cultures of adult type II (ATII) epithelium and found that overnight exposure to EF increased [N.sup.+]. transport, and this effect was mainly due to factors other than catecholamines. Plasma did not stimulate [N.sup.+]. transport in ATII. Purification of EF demonstrated that at least some agent(s) responsible for the amiloride-insensitive component resided within the globulin fraction. ATII exposed to globulins demonstrated a conversion of amiloride-sensitive short-circuit current ([I.sub.SC]) to amiloride-insensitive L~ with no increase in total [I.sub.SC]. Patch-clamp studies showed that ATII exposed to EF for 18 h had increased the number of highly selective Nan channels in their apical membrane. In situ acute exposure to EF increased the open probability of [N.sup.+].-permeant ion channels in ATII within rat lung slices. EF did increase, by amiloride-sensitive pathways, the alveolar fluid clearance from the lungs of adult rats. We conclude that cardiogenic EF increases [N.sup.+]. transport by adult lung epithelia in primary cell culture, in situ and in vivo. pulmonary edema fluid: alveolar type ii epithelium; sodium channels; lung fluid clearance

Published
2007

36. Dopamine activates amiloride-sensitive sodium channels in alveolar type I cells in lung slice preparations

Author

Helms, My N., Self, Julie, Bao, Hui Fang, Job, Lauren C., Jain, Lucky, and Eaton, Douglas C.

Subjects
Sodium channels -- Research, Epithelial cells -- Research, Amiloride -- Research, Biological sciences
Abstract

Active [Na.sup.+] reabsorption by alveolar epithelial cells generates the driving force used to clear fluids from the air space. Using single-channel methods, we examined epithelial [Na.sup.+] channel (ENaC) activity of alveolar type I (AT1) cells from live 250- to 300-[micro]m sections of lung tissue, circumventing concerns that protracted cell isolation procedures might compromise the innate transport properties of native lung cells. We used fluorescein-labeled Erythrina crystagalli lectin to positively identify AT1 cells for single-channel patch-clamp analysis. We demonstrated, for the first time, single-channel recordings of highly selective and nonselective amiloride-sensitive ENaC channels (HSC and NSC, respectively) from AT1 cells in situ, with mean conductances of 8.2 [+ or -] 2.5 and 22 [+ or -] 3.2 pS, respectively. Additionally, 25 nM amiloride in the patch electrode blocked [Na.sup.+] channel activity in AT1 cells. Immunohistochemical studies demonstrated the presence of dopamine [D.sub.1] and [D.sub.2] receptors on the surface of AT1 cells, and single-channel recordings showed that 10 [micro]M dopamine increased [Na.sup.+] channel activity [product of the number of channels and single-channel open probability ([NP.sub.o])] from 0.31 [+ or -] 0.19 to 0.60 [+ or -] 0.21 (P < 0.001). The [D.sub.1] receptor antagonist SCH-23390 (10 [micro]M) blocked the stimulatory effect of dopamine on AT1 cells, but the [D.sub.2] receptor antagonist sulpiride did not. AT1 cells; epithelial sodium channel; single-channel recording; Erythrina crystagalli lectin; dopamine [D.sub.1] and [D.sub.2] receptors

Published
2006

37. Integrating acute lung injury and regulation of alveolar fluid clearance

Author

Guidot, David M., Folkesson, Hans G., Jain, Lucky, Sznajder, Jacob I., Pittet, Jean-Francois, and Matthay, Michael A.

Subjects
Acute respiratory distress syndrome -- Research, Pulmonary alveolar proteinosis -- Research, Lung diseases -- Research, Biological sciences
Abstract

The acute respiratory distress syndrome (ARDS) is characterized by non-cardiogenic pulmonary edema and flooding of the alveolar air spaces with proteinaceous fluid. ARDS develops in response to inflammatory stresses including sepsis, trauma, and severe pneumonia, and despite aggressive critical care management, it still has a mortality of 30-50%. At the time of its original description in 1967, relatively little was known about the specific mechanisms by which the alveolar epithelium regulated lung fluid balance. Over the last 20 years, substantial advances in our understanding of the alveolar epithelium have provided major new insights into how molecular and cellular mechanisms regulate the active transport of solutes and fluid across the alveolar epithelium under both normal and pathological conditions. Beginning with the elucidation of active sodium transport as a major driving force for the transport of water from the air space to the interstitium, elegant work by multiple investigators has revealed a complex and integrated network of membrane channels and pumps that coordinately regulates sodium, chloride, and water flux in both a cell- and condition-specific manner. At the Experimental Biology Meeting in San Francisco on April 4, 2006, a symposium was held to discuss some of the most recent advances. Although there is still much to learn about the mechanisms that impair normal alveolar fluid clearance under pathological conditions, the compelling experimental findings presented in this symposium raise the prospect that we are now poised to test and develop therapeutic strategies to improve outcome in patients with acute lung injury. doi:10.1152/ajplung.00153.2006

Published
2006

38. Dopamine regulation of amiloride-sensitive sodium channels in lung cells

Author

Helms, My N., Chen, Xi-Juan, Ramosevac, Semra, Eaton, Douglas C., and Jain, Lucky

Subjects
Ionic mobility -- Research, Ionic mobility -- Analysis, Epithelium -- Research, Epithelium -- Analysis, Dopamine -- Dosage and administration, Dopamine -- Complications and side effects, Dopamine -- Analysis, Biological sciences
Abstract

Dopamine increases lung fluid clearance. This is partly due to activation of basolateral Na-K-ATPase. However, activation of Na-K-ATPase by itself is unlikely to produce large changes in transepithelial transport. Therefore, we examined apical and basolateral dopamine's effect on apical, highly selective sodium channels [epithelial sodium channels (ENaC)] in monolayers of an alveolar type 2 cell line (L2). Dopamine increased channel open probability ([P.sub.o]) without changing the unitary current. The [D.sub.1] receptor blocker SCH-23390 blocked the dopamine effect, but the [D.sub.2] receptor blocker sulpiride did not. The dopamine-mediated increase in ENaC activity was not a secondary effect of dopamine stimulation of Na-K-ATPase, since ouabain applied to the basolateral surface to block the activity of Na-K-ATPase did not alter dopamine-mediated ENaC activity. Protein kinase A (PKA) was not responsible for dopamine's effect since a PKA inhibitor, H89, did not reduce dopamine's effect. However, cpt-2-O-Me-cAMP, which selectively binds and activates EPAC (exchange protein activated by cAMP) but not PKA, increased ENaC [P.sub.o]. An Src inhibitor, PP2, and the phosphatidylinositol-3-kinase inhibitor, LY-294002, blocked dopamine's effect on ENaC. In addition, an MEK blocker, U0126, an inhibitor of phospholipase [A.sub.2], and a protein phosphatase inhibitor also blocked the effect of dopamine on ENaC Po. Finally, since the cAMP-EPAC-Rap1 pathway also activates DARPP32 (32-kDa dopamine response protein phosphatase), we confirmed that dopamine phosphorylates DARPP32, and okadaic acid, which blocks phosphatases (DARPP32), also blocks dopamine's effect. In summary, dopamine increases ENaC activity by a cAMP-mediated alternative signaling pathway involving EPAC and Rap1, signaling molecules usually associated with growth-factor-activated receptors. single channel recording; ion transport; epithelial sodium channels; L2 lung cells; exchange protein activated by cAMP

Published
2006

40. Contributors

Author

Andreoli, Sharon P., primary, Baumgart, Stephen, additional, Beall, Marie H., additional, Bland, Richard D., additional, Boubred, Farid, additional, Buffat, Christophe, additional, Chevalier, Robert L., additional, Costarino, Andrew T., additional, Dotta, Andrea, additional, Emma, Francesco, additional, Feig, Daniel I., additional, Flynn, Joseph T., additional, Gouyon, Jean-Bernard, additional, Guignard, Jean-Pierre, additional, Jain, Lucky, additional, Jose, Pedro A., additional, Keene, Sarah D., additional, Levenbrown, Yosef, additional, Lorenz, John M., additional, Namgung, Ran, additional, Natarajan, Aruna, additional, Oh, William, additional, Ross, Michael G., additional, Seri, Istvan, additional, Simeoni, Umberto, additional, Sulyok, Endre, additional, Tsang, Reginald C., additional, Vaiman, Daniel, additional, van den Wijngaard, Jeroen P.H.M., additional, van Gemert, Martin, additional, Zaffanello, Marc, additional, and Zelikovic, Israel, additional

Published
2012
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42. Contributors

Author

Abman, Steven H., primary, Ahmed, Amina, additional, Allen, Marilee C., additional, Askenazi, David, additional, Back, Stephen A., additional, Baldwin, H. Scott, additional, Ballard, Roberta A., additional, Bancalari, Eduardo, additional, Bates, Carlton M., additional, Batisky, Donald L., additional, Baumgart, Stephen, additional, Benedetti, Thomas J., additional, Berry, Gerard T., additional, Bianchi, Diana W., additional, Binenbaum, Gil, additional, Bollepalli, Sureka, additional, Bonifacio, Sonia L., additional, Cairo, Mitchell S., additional, Campbell, Katherine H., additional, Caplan, Michael, additional, Cederbaum, Stephen, additional, Chandra, Sudhish, additional, Chen, Ming, additional, Claure, Nelson, additional, Clyman, Ronald I., additional, Cohen, Bernard A., additional, Cole, F. Sessions, additional, Copelovitch, Lawrence, additional, Cunningham, Michael, additional, de Alba Campomanes, Alejandra G., additional, Dees, Ellen, additional, Denne, Scott C., additional, Devaskar, Sherin U., additional, DiBlasi, Robert M., additional, Dimmitt, Reed A., additional, Eichenwald, Eric C., additional, Eisenstein, Eli M., additional, Evans, Jacquelyn R., additional, Evans, Kelly, additional, Farmer, Diana L., additional, Ferrieri, Patricia, additional, Ferriero, Donna M., additional, Finer, Neil N., additional, Fraga, Maria Victoria, additional, Furman, Lydia, additional, Furth, Susan, additional, Gauda, Estelle B., additional, Glader, Bertil, additional, Gleason, Christine A., additional, Goldberg, Michael J., additional, Gonzalez, Fernando, additional, Gopalani, Sameer, additional, Grant, P. Ellen, additional, Greene, Carol L., additional, Guevara-Gallardo, Salvador, additional, Guignard, Jean-Pierre, additional, Guttentag, Susan, additional, Haldeman-Englert, Chad R., additional, Hansen, Thomas, additional, Hing, Anne V., additional, Hohimer, A. Roger, additional, Hostetter, Margaret K., additional, Hull, Andrew D., additional, Jackson, J. Craig, additional, Jain, Lucky, additional, Jain, Vandana, additional, Janjua, Halima Saadia, additional, Juul, Sandra E., additional, Kalkunte, Satyan, additional, Kaplan, Bernard S., additional, Keller, Roberta L., additional, Kelly, Thomas F., additional, Kern, Steven E., additional, Kerkar, Nanda, additional, Kinsella, John P., additional, Kirsch, Roxanne, additional, Kleinman, Monica E., additional, Klitzner, Thomas S., additional, Lambert, Sarah M., additional, Lantos, John D., additional, Leone, Tina A., additional, Leppert, Mary, additional, Levy, Harvey L., additional, Lewin, Mark, additional, Lin-Su, Karen, additional, L. Loh, Mignon, additional, Lorch, Scott A., additional, Lugo, Ralph A., additional, Mai, Volker, additional, Marino, Bradley S., additional, Markovitz, Barry, additional, Marquard, Kerri, additional, Martin, Camilia R., additional, Martin, Richard J., additional, Matthay, Katherine K., additional, Matthews, Dana C., additional, Mayock, Dennis E., additional, Meadow, William L., additional, Menon, Ram K., additional, Mercuri, Eugenio, additional, Mohan, Sowmya S., additional, Moley, Kelle, additional, Mollen, Thomas J., additional, Moore, Jeremy P., additional, Moore, Thomas R., additional, Munson, David A., additional, Murray, Jeffrey C., additional, Neu, Josef, additional, New, Maria I., additional, Nguyen-Vermillion, Annie, additional, Niklas, Victoria, additional, Nimkarn, Saroj, additional, Padbury, James F., additional, Pane, Marika, additional, Paneth, Nigel, additional, Parker, Thomas A., additional, Patterson, Janna C., additional, Pettker, Christian M., additional, Plawner, Lauren L., additional, Poenaru, Dan, additional, Poindexter, Brenda B., additional, Posencheg, Michael A., additional, Prabhu, Sanjay P., additional, Püttgen, Katherine B., additional, Quinn, Graham E., additional, Raju, Tonse N.K., additional, Ramos, Gladys A., additional, Reinking, Benjamin E., additional, Richardson, C. Peter, additional, Rimoin, David L., additional, Robbins, Elizabeth, additional, Robertson, Richard L., additional, Rollins, Mark D., additional, Rose, Susan R., additional, Rosen, Mark A., additional, Rubin, Lewis P., additional, Sahai, Inderneel, additional, Saitta, Sulagna C., additional, Sánchez, Pablo J., additional, Satou, Gary M., additional, Schanler, Richard J., additional, Scher, Mark S., additional, Schleiss, Mark R., additional, Scholz, Thomas D., additional, Schwaderer, Andrew L., additional, Seri, Istvan, additional, Sharma, Surendra, additional, Shereck, Evan B., additional, Sibley, Eric, additional, Signore, Caroline, additional, Simmons, Rebecca, additional, Smith, Jeffrey B., additional, Smith, Lorie B., additional, Song, Clara, additional, Steinhorn, Robin H., additional, Suchy, Frederick J., additional, Sulyok, Endre, additional, Tarczy-Hornoch, Peter, additional, Taylor, George A., additional, Taylor, James A., additional, Thomas, Janet A., additional, Tiller, George E., additional, Tran, Mark M., additional, Trautman, Michael Stone, additional, Upperman, Jeffrey S., additional, van de Ven, Carmella, additional, Vernon, Margaret M., additional, Allan Walker, W., additional, Wallen, Linda D., additional, Waller, Sarah A., additional, Warady, Bradley A., additional, Ward, Robert M., additional, Watchko, Jon F., additional, Wernovsky, Gil, additional, White, Klane K., additional, Williams, Calvin B., additional, Woodrum, David, additional, Woodward, George A., additional, Wright, Dakara Rucker, additional, Wright, Jeffrey A., additional, Wright, Linda L., additional, Young, Christopher M., additional, Young, Guy, additional, Zackai, Elaine H., additional, and Zderic, Stephen A., additional

Published
2012
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44. Influenza virus inhibits ENaC and lung fluid clearance

Author

Chen, Xi-Juan, Seth, Shaguna, Yue, Gang, Kamat, Pradip, Compans, Richard W., Guidot, David, Brown, Lou Ann, Eaton, Douglas C., and Jain, Lucky

Subjects
Sodium channels -- Research, Protein kinases -- Research, Influenza -- Research, Biological sciences
Abstract

Fluid-free alveolar space is critical for normal gas exchange. Influenza virus alters fluid transport across respiratory epithelia producing rhinorrhea, middle ear effusions, and alveolar flooding. However, the mechanism of fluid retention remains unclear. We investigated influenza virus strain A/PR/8/34, which can attach and enter mammalian cells but is incapable of viral replication and productive infection in mammalian epithelia, on epithelial sodium channels (ENaC) in rat alveolar type II (ATII) cells. In parallel, we determined the effects of virus on amiloride-sensitive (i.e., ENaC-mediated) fluid clearance in rat lungs in vivo. Although influenza virus did not change the inulin permeability of ATII monolayers, it rapidly reduced the net volume transport across monolayers. Virus reduced the open probability of single ENaC channels in apical cell-attached patches. U-73122, a phospholipase C (PLC) inhibitor, and PP2, a Src inhibitor, blocked the effect of virus on ENaC. GF-109203X, a protein kinase C (PKC) inhibitor, also blocked the effect, suggesting a PKC-mediated mechanism. In parallel, intratracheal administration of influenza virus produced a rapid inhibition of amiloride-sensitive (i.e., ENaC-dependent) lung fluid transport. Together. these results show that influenza virus rapidly inhibits ENaC in ATII cells via a PLC- and Src-mediated activation of PKC but does not increase epithelial permeability in this same rapid time course. We speculate that this rapid inhibition of ENaC and formation of edema when the virus first attaches to the alveolar epithelium might facilitate subsequent influenza infection and may exacerbate influenza-mediated alveolar flooding that can lead to acute respiratory failure and death. phospholipase C; protein kinase C; epithelial sodium channels; hemagglutinin; acute respiratory distress syndrome; single channels

Published
2004

47. Contributors

Author

Abu-Shaweesh, Jalal M., primary, Accornero, Veronica H., additional, Als, Heidelise, additional, Anderson, Brenna L., additional, Aranda, Jacob V., additional, Arnold, James E., additional, Arora, Sundeep, additional, Bajaj, Komal, additional, Baley, Jill E., additional, Bancalari, Eduardo H., additional, Bandstra, Emmalee S., additional, Barksdale, Edward M., additional, Bearer, Cynthia F., additional, Blickstein, Isaac, additional, Blumer, Jeffrey L., additional, Butler, Samantha, additional, Calkins, Kara, additional, Caplan, Michael S., additional, Carlo, Waldemar A., additional, Chelimsky, Gisela, additional, Chock, Valerie Y., additional, Chwals, Walter J., additional, Cohen, Alan R., additional, Cooperman, Daniel R., additional, Crombleholme, Timothy M., additional, Curtis, Mario De, additional, Vries, Linda S. de, additional, Dell, Katherine MacRae, additional, Denne, Scott, additional, Devaskar, Sherin U., additional, Fiore, Juliann Di, additional, Donn, Steven M., additional, Edwards, Morven S., additional, Edwards, William H., additional, Erenberg, Francine, additional, Fanaroff, Avroy A., additional, Fanaroff, Jonathan M., additional, Fasano, Ross, additional, Flidel-Rimon, Orna, additional, Friedman, Smadar, additional, Gerber, Susan E., additional, Goldsmith, Jay P., additional, Gonik, Bernard, additional, Gould, Jeffrey B., additional, Gressens, Pierre, additional, Gross, Susan J., additional, Gruslin, Andrée M., additional, Gupta, Balaji K., additional, Hack, Maureen, additional, Halamek, Louis P., additional, Hamvas, Aaron, additional, Hellmann, Jonathan, additional, Hintz, Susan R., additional, Hoath, Steven B., additional, Horbar, Jeffrey D., additional, Hoyt, McCallum R., additional, Hüppi, Petra S., additional, Jain, Lucky, additional, Jobe, Alan H., additional, Judge, Nancy E., additional, Kaplan, Michael, additional, Kalhan, Satish C., additional, Kapur, Reuben, additional, Karunamuni, Ganga, additional, Kaufman, Lawrence M., additional, Kennedy, Kathleen A., additional, Kennell, John H., additional, Kitterman, Joseph A., additional, Klaus, Marshall H., additional, Kliegman, Robert M., additional, Langer, Oded, additional, Lazebnik, Noam, additional, Levene, Malcolm I., additional, Lim, Foong-Yen, additional, Lissauer, Tom, additional, Lopez, Suzanne M., additional, Lotze, Timothy E., additional, Naomi Luban, L.C., additional, Luchtman-Jones, Lori, additional, Magnuson, David K., additional, Mangurten, Henry H., additional, McClary, Jacquelyn, additional, Miller, Geoffrey, additional, Miller, Marilyn T., additional, Mohamed, Mohamed W., additional, Moore, Thomas R., additional, Morley, Colin J., additional, Morrison, Stuart C., additional, Narang, Anil, additional, Narendran, Vivek, additional, Nock, Mary L., additional, Palmert, Mark R., additional, Parikh, Aditi S., additional, Parry, Robert L., additional, Phelps, Dale L., additional, Poindexter, Brenda, additional, Polin, Richard A., additional, Puppala, Bhagya L., additional, Raju, Tonse N.K., additional, Ramachandrappa, Ashwin, additional, Redline, Raymond W., additional, Rigo, Jacques, additional, Robinson, Barrett K., additional, Rose, Susan R., additional, Rothenberg, Florence, additional, Safder, Shaista, additional, Saugstad, Ola Didrik, additional, Schaefer, Katherine S., additional, Scher, Mark S., additional, Sedin, Gunnar, additional, Shah, Dinesh M., additional, Shinwell, Eric S., additional, Shulman, Rayzel M., additional, Sibley, Eric, additional, Sinha, Sunil K., additional, Sivit, Carlos J., additional, Siwik, Ernest S., additional, Sprecher, Robert C., additional, Steinhorn, Robin H., additional, Stevenson, David K., additional, Stork, Eileen K., additional, Stork, John E., additional, Pas, Arjan B. te, additional, Thompson, George H., additional, Toltzis, Philip, additional, Turbow, Robert, additional, Tyson, Jon E., additional, Hare, George F. Van, additional, Vento, Maximo, additional, Vidyasagar, Dharmapuri, additional, Vogt, Beth A., additional, Vohr, Betty, additional, Walsh, Michele C., additional, Watanabe, Michiko, additional, Wherrett, Diane K., additional, White, Robert D., additional, Wiesner, Georgia L., additional, Wikenheiser, Jamie C., additional, Wilson, David B., additional, Wilson-Costello, Deanne, additional, Wolf, Richard B., additional, Wong, Ronald J., additional, Yoder, Mervin C., additional, Young, Thomas, additional, Zahka, Kenneth G., additional, and Zinn, Arthur B., additional

Published
2011
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49. Regulation of ion channel structure and function by reactive oxygen-nitrogen species

Author

Matalon, Sadis, Hardiman, Karin M., Jain, Lucky, Eaton, Douglas C., Kotlikoff, Michael, Eu, Jerry P., Sun, Junhui, Meissner, Gerhard, and Stamler, Jonathan S.

Subjects
Ion channels -- Research, Biological sciences
Abstract

Ion channels subserve diverse cellular functions. Reactive oxygen and nitrogen species modulate ion channel function by a number of mechanisms including 1) transcriptional regulation of gene expression, 2) posttranslational modifications of channel proteins, i.e. nitrosylation, nitration, and oxidation of key amino acid residues, 3) by altering the gain in other signaling pathways that may in turn lead to changes in channel activity or channel gene expression, and 4) by modulating trafficking or turnover of channel proteins, as typified by oxygen radical activation of NF-kB, with subsequent changes in proteasomal degradation of channel degradation. Regardless of the mechanism, as was discussed in a symposium at the 2003 Experimental Biology Meeting in San Diego, CA, changes in the cellular level of reactive oxygen and nitrogen species can have profound effects on the activity of ion channels and cellular function. calcium channels; potassium channels; sodium channels; chloride channels; nitric oxide; cystic fibrosis transmembrane conductance regulator

Published
2003

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