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462 results on '"Karp, Christopher L."'

1. A BAFF/APRIL axis regulates obesogenic diet-driven weight gain

Author

Chan, Calvin C., Harley, Isaac T. W., Pfluger, Paul T., Trompette, Aurelien, Stankiewicz, Traci E., Allen, Jessica L., Moreno-Fernandez, Maria E., Damen, Michelle S. M. A., Oates, Jarren R., Alarcon, Pablo C., Doll, Jessica R., Flick, Matthew J., Flick, Leah M., Sanchez-Gurmaches, Joan, Mukherjee, Rajib, Karns, Rebekah, Helmrath, Michael, Inge, Thomas H., Weisberg, Stuart P., Pamp, Sünje J., Relman, David A., Seeley, Randy J., Tschöp, Matthias H., Karp, Christopher L., and Divanovic, Senad

Published
2021
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2. Microbiota maintain colonic homeostasis by activating TLR2/MyD88/PI3K signaling in IL-10-producing regulatory B cells

Author

Mishima, Yoshiyuki, Oka, Akihiko, Liu, Bo, Herzog, Jeremy W., Eun, Chang Soo, Fan, Ting-Jia, Bulik-Sullivan, Emily, Carroll, Ian M., Hansen, Jonathan J., Chen, Liang, Wilson, Justin E., Fisher, Nancy C., Ting, Jenny P.Y., Nochi, Tomonori, Wahl, Angela, Garcia, J. Victor, Karp, Christopher L., and Sartor, R. Balfour

Subjects
Thermo Fisher Scientific Inc., Bacteria -- Analysis, Homeostasis -- Analysis, Genetic research -- Analysis, Cytokines -- Analysis, B cells -- Analysis, Inflammation -- Analysis, Microbiota (Symbiotic organisms) -- Analysis, Scientific equipment industry -- Analysis, T cells -- Analysis, Colitis -- Analysis, Genes, House mouse, Journalists, Health care industry
Abstract

Resident microbiota activates regulatory cells that modulate intestinal inflammation and promote and maintain intestinal homeostasis. IL-10 is a key mediator of immune regulatory function. Our studies describe the functional importance and mechanisms by which gut microbiota and specific microbial components influence the development of intestinal IL10-producing B cells. Using fecal transplant into germ-free (GF) [Il10.sup.+/EGFP] reporter and [Il10.sup.-/-] mice, we demonstrated that microbiota from specific pathogen-free mice primarily stimulated IL-10-producing colon-specific B cells and T regulatory 1 cells in ex-GF mice. IL-10 in turn downregulated microbiota-activated mucosal inflammatory cytokines. TLR2 and -9 ligands and enteric bacterial lysates preferentially induced IL-10 production and the regulatory capacity of intestinal B cells. Analysis of [IL10.sup.+/EGFP] mice crossed with additional gene-deficient strains and B cell cotransfer studies demonstrated that microbiota-induced IL-10-producing intestinal B cells ameliorated chronic T cell-mediated colitis in a TLR2-, MyD88-, and PI3K-dependent fashion. In vitro studies implicated downstream signaling of PI3Kp110[delta] and AKT. These studies demonstrated that resident enteric bacteria activated intestinal IL-10-producing B cells through TLR2, MyD88, and PI3K pathways. These B cells reduced colonic T cell activation and maintained mucosal homeostasis in response to intestinal microbiota., Introduction Inflammatory bowel diseases (IBDs), including Crohn's disease and ulcerative colitis, are T cell-mediated, chronic disorders whose development is influenced in part by dysregulated, aggressive intestinal mucosal immune reactions to [...]

Published
2019
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10. Thermoneutral housing exacerbates nonalcoholic fatty liver disease in mice and allows for sex-independent disease modeling

Author

Giles, Daniel A, Moreno-Fernandez, Maria E, Stankiewicz, Traci E, Graspeuntner, Simon, Cappelletti, Monica, Wu, David, Mukherjee, Rajib, Chan, Calvin C, Lawson, Matthew J, Klarquist, Jared, Sünderhauf, Annika, Softic, Samir, Kahn, C Ronald, Stemmer, Kerstin, Iwakura, Yoichiro, Aronow, Bruce J, Karns, Rebekah, Steinbrecher, Kris A, Karp, Christopher L, Sheridan, Rachel, Shanmukhappa, Shiva K, Reynaud, Damien, Haslam, David B, Sina, Christian, Rupp, Jan, Hogan, Simon P, and Divanovic, Senad

Subjects
Microbiota (Symbiotic organisms) -- Health aspects, Fatty liver -- Care and treatment -- Patient outcomes, Corticosterone -- Dosage and administration, Immune response -- Analysis, Biological sciences, Health
Abstract

Nonalcoholic fatty liver disease (NAFLD), a common prelude to cirrhosis and hepatocellular carcinoma, is the most common chronic liver disease worldwide. Defining the molecular mechanisms underlying the pathogenesis of NAFLD has been hampered by a lack of animal models that closely recapitulate the severe end of the disease spectrum in humans, including bridging hepatic fibrosis. Here we demonstrate that a novel experimental model employing thermoneutral housing, as opposed to standard housing, resulted in lower stress-driven production of corticosterone, augmented mouse proinflammatory immune responses and markedly exacerbated high-fat diet (HFD)-induced NAFLD pathogenesis. Disease exacerbation at thermoneutrality was conserved across multiple mouse strains and was associated with augmented intestinal permeability, an altered microbiome and activation of inflammatory pathways that are associated with the disease in humans. Depletion of Gram-negative microbiota, hematopoietic cell deletion of Toll-like receptor 4 (TLR4) and inactivation of the IL-17 axis resulted in altered immune responsiveness and protection from thermoneutral-housing-driven NAFLD amplification. Finally, female mice, typically resistant to HFD-induced obesity and NAFLD, develop full disease characteristics at thermoneutrality. Thus, thermoneutral housing provides a sex-independent model of exacerbated NAFLD in mice and represents a novel approach for interrogation of the cellular and molecular mechanisms underlying disease pathogenesis., Author(s): Daniel A Giles [1, 2]; Maria E Moreno-Fernandez [1]; Traci E Stankiewicz [1]; Simon Graspeuntner [3]; Monica Cappelletti [1]; David Wu [4]; Rajib Mukherjee [1]; Calvin C Chan [1, [...]

Published
2017
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17. Differential colonization with segmented filamentous bacteria and Lactobacillus murinus do not drive divergent development of diet-induced obesity in C57BL/6 mice

Author

Harley, Isaac T.W., Giles, Daniel A., Pfluger, Paul T., Burgess, Stacey L., Walters, Stephanie, Hembree, Jazzminn, Raver, Christine, Rewerts, Cheryl L., Downey, Jordan, Flick, Leah M., Stankiewicz, Traci E., McAlees, Jaclyn W., Wills-Karp, Marsha, Balfour Sartor, R., Divanovic, Senad, Tschöp, Matthias H., and Karp, Christopher L.

Published
2013
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22. Reply to Schroecksnadel, et al.

Author

Divanovic, Senad, Sawtell, Nancy M., Trompette, Aurelien, Warning, Jamie I., Dias, Alexandra, Cooper, Andrea M., Yap, George S., Arditi, Moshe, Shimada, Kenichi, DuHadaway, James B., Prendergast, George C., Basaraba, Randall J., Mellor, Andrew L., Munn, David H., Aliberti, Julio, and Karp, Christopher L.

Published
2012
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24. Innovative vaccine approaches—a Keystone Symposia report

Author

Cable, Jennifer, primary, Rappuoli, Rino, additional, Klemm, Elizabeth J., additional, Kang, Gagandeep, additional, Mutreja, Ankur, additional, Wright, Gavin J., additional, Pizza, Mariagrazia, additional, Castro, Sowmya Ajay, additional, Hoffmann, Joseph P., additional, Alter, Galit, additional, Carfi, Andrea, additional, Pollard, Andrew J., additional, Krammer, Florian, additional, Gupta, Ravindra K., additional, Wagner, Caroline E., additional, Machado, Viviane, additional, Modjarrad, Kayvon, additional, Corey, Lawrence, additional, B. Gilbert, Peter, additional, Dougan, Gordon, additional, Lurie, Nicole, additional, Bjorkman, Pamela J., additional, Chiu, Christopher, additional, Nemes, Elisa, additional, Gordon, Stephen B., additional, Steer, Andrew C., additional, Rudel, Thomas, additional, Blish, Catherine A., additional, Sandberg, John Tyler, additional, Brennan, Kiva, additional, Klugman, Keith P., additional, Stuart, Lynda M., additional, Madhi, Shabir A., additional, and Karp, Christopher L., additional

Published
2022
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29. Interferon-dependent IL-10 production by Tregs limits tumor Th17 inflammation

Author

Stewart, C. Andrew, Metheny, Hannah, Iida, Noriho, Smith, Loretta, Hanson, Miranda, Steinhagen, Folkert, Leighty, Robert M., Karp, Christopher L., Muller, Werner, and Trinchieri, Giorgio

Subjects
Inflammation -- Physiological aspects -- Genetic aspects -- Research, Interleukin-10 -- Physiological aspects -- Genetic aspects -- Research, Macrophages -- Physiological aspects -- Genetic aspects -- Research, Health care industry
Abstract

IL-10 is a cytokine with broad antiinflammatory properties. It acts primarily on APCs, including dendritic cells, monocytes, and macrophages, by inhibiting production of proinflammatory cytokines such as TNF and IL-12 [...]

Published
2013

30. The TLR4 antagonist Eritoran protects mice from lethal influenza infection

Author

Shirey, Kari Ann, Lai, Wendy, Scott, Alison J., Lipsky, Michael, Mistry, Pragnesh, Pletneva, Lioubov M., and Karp, Christopher L.

Subjects
Prevention, Physiological aspects, TLR4 -- Physiological aspects, Antagonists (Biochemistry) -- Physiological aspects, Influenza -- Prevention
Abstract

Author(s): Kari Ann Shirey [sup.1] , Wendy Lai [sup.1] , Alison J. Scott [sup.2] , Michael Lipsky [sup.3] , Pragnesh Mistry [sup.1] , Lioubov M. Pletneva [sup.4] , Christopher L. [...], TLR4 stimulation is known to contribute to acute lung injury after administration of inactivated influenza virus; here, the synthetic TLR4 antagonist Eritoran is shown to protect mice from death after infection with a lethal dose of the virus. Protective action of TLR4 antagonists in influenza With the influenza virus continually evolving, and resistance to existing antiviral therapies spreading, there is a pressing need for new anti-influenza therapies. Previous work has shown that TLR4 signalling mediates influenza-induced acute lung injury, cytokine production and systemic effects in mice. Stefanie Vogel and colleagues now report that Eritoran, a synthetic TLR4 antagonist, can protect mice from death when administered up to six days after infection with the influenza virus. Existing antivirals must be administered within three days of infection to be effective. This work suggests that TLR4 antagonists may be effective against influenza and could usefully extend the period during which the infection can be effectively treated. There is a pressing need to develop alternatives to annual influenza vaccines and antiviral agents licensed for mitigating influenza infection. Previous studies reported that acute lung injury caused by chemical or microbial insults is secondary to the generation of host-derived, oxidized phospholipid that potently stimulates Toll-like receptor 4 (TLR4)-dependent inflammation.sup.1. Subsequently, we reported that Tlr4.sup.-/- mice are highly refractory to influenza-induced lethality.sup.2, and proposed that therapeutic antagonism of TLR4 signalling would protect against influenza-induced acute lung injury. Here we report that therapeutic administration of Eritoran (also known as E5564)--a potent, well-tolerated, synthetic TLR4 antagonist.sup.3,4--blocks influenza-induced lethality in mice, as well as lung pathology, clinical symptoms, cytokine and oxidized phospholipid expression, and decreases viral titres. CD14 and TLR2 are also required for Eritoran-mediated protection, and CD14 directly binds Eritoran and inhibits ligand binding to MD2. Thus, Eritoran blockade of TLR signalling represents a novel therapeutic approach for inflammation associated with influenza, and possibly other infections.

Published
2013
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32. A BAFF/APRIL axis regulates obesogenic diet-driven weight gain

Author

Chan, Calvin C, Harley, Isaac T W, Pfluger, Paul T, Trompette, Aurelien, Stankiewicz, Traci E, Allen, Jessica L, Moreno-Fernandez, Maria E, Damen, Michelle S M A, Oates, Jarren R, Alarcon, Pablo C, Doll, Jessica R, Flick, Matthew J, Flick, Leah M, Sanchez-Gurmaches, Joan, Mukherjee, Rajib, Karns, Rebekah, Helmrath, Michael, Inge, Thomas H, Weisberg, Stuart P, Pamp, Sünje J, Relman, David A, Seeley, Randy J, Tschöp, Matthias H, Karp, Christopher L, Divanovic, Senad, Chan, Calvin C, Harley, Isaac T W, Pfluger, Paul T, Trompette, Aurelien, Stankiewicz, Traci E, Allen, Jessica L, Moreno-Fernandez, Maria E, Damen, Michelle S M A, Oates, Jarren R, Alarcon, Pablo C, Doll, Jessica R, Flick, Matthew J, Flick, Leah M, Sanchez-Gurmaches, Joan, Mukherjee, Rajib, Karns, Rebekah, Helmrath, Michael, Inge, Thomas H, Weisberg, Stuart P, Pamp, Sünje J, Relman, David A, Seeley, Randy J, Tschöp, Matthias H, Karp, Christopher L, and Divanovic, Senad

Abstract

The impact of immune mediators on weight homeostasis remains underdefined. Interrogation of resistance to diet-induced obesity in mice lacking a negative regulator of Toll-like receptor signaling serendipitously uncovered a role for B cell activating factor (BAFF). Here we show that overexpression of BAFF in multiple mouse models associates with protection from weight gain, approximating a log-linear dose response relation to BAFF concentrations. Gene expression analysis of BAFF-stimulated subcutaneous white adipocytes unveils upregulation of lipid metabolism pathways, with BAFF inducing white adipose tissue (WAT) lipolysis. Brown adipose tissue (BAT) from BAFF-overexpressing mice exhibits increased Ucp1 expression and BAFF promotes brown adipocyte respiration and in vivo energy expenditure. A proliferation-inducing ligand (APRIL), a BAFF homolog, similarly modulates WAT and BAT lipid handling. Genetic deletion of both BAFF and APRIL augments diet-induced obesity. Lastly, BAFF/APRIL effects are conserved in human adipocytes and higher BAFF/APRIL levels correlate with greater BMI decrease after bariatric surgery. Together, the BAFF/APRIL axis is a multifaceted immune regulator of weight gain and adipose tissue function.

Published
2021

39. Identification of IFRD1 as a modifier gene for cystic fibrosis lung disease

Author

Gu, YuanYuan, Harleys, Isaac T.W., Henderson, Lindsay B., Aronow, Bruce J., Vietor, Ilja, Huber, Lukas A., Harley, John B., Kilpatrick, Jeffrey R., Langefeld, Carl D., Williams, Adrienne H., Jegga, Anil G., Chen, Jing, Wills-Karp, Marsha, Arshads, S. Hasan, Ewart, Susan L., Thio, Chloe L., Flick, Leah M., Filippi, Marie-Dominique, Grimes, H. Leighton, Drumm, Mitchell L., Cutting, Garry R., Knowles, Michael R., and Karp, Christopher L.

Subjects
Cystic fibrosis -- Genetic aspects -- Research, Single nucleotide polymorphisms -- Health aspects -- Research -- Physiological aspects -- Genetic aspects, Membrane proteins -- Physiological aspects -- Genetic aspects -- Research -- Health aspects, Environmental issues, Science and technology, Zoology and wildlife conservation, Physiological aspects, Research, Genetic aspects, Health aspects
Abstract

Lung disease is the major cause of morbidity and mortality in cystic fibrosis, an autosomal recessive disease caused by mutations in CFTR. In cystic fibrosis, chronic infection and dysregulated neutrophilic inflammation lead to progressive airway destruction. The severity of cystic fibrosis lung disease has considerable heritability, independent of CFTR genotype (1). To identify genetic modifiers, here we performed a genome-wide single nucleotide polymorphism scan in one cohort of cystic fibrosis patients, replicating top candidates in an independent cohort. This approach identified IFRD1 as a modifier of cystic fibrosis lung disease severity. IFRD1 is a histone-deacetylase-dependent transcriptional co-regulator expressed during terminal neutrophil differentiation. Neutrophil, but not macrophages, from Ifrd1-deficient mice showed blunted effector function, associated with decreased NF-κB p65 transactivation. In vivo, IFRD1 deficiency caused delayed bacterial clearance from the airway, but also less inflammation and disease--a phenotype primarily dependent on haematopoietic cell expression, or lack of expression, of IFRD1. In humans, IFRD1 polymorphisms were significantly associated with variation in neutrophil effector function. These data indicate that IFRD1 modulates the pathogenesis of cystic fibrosis lung disease through the regulation of neutrophil effector function., Attention to the role of CFTR in regulating epithelial ion transport has failed to illuminate the path from gene to pathogenesis in cystic fibrosis (CF) lung disease. In CF, colonization [...]

Published
2009

40. Allergenicity resulting from functional mimicry of a Toll-like receptor complex protein

Author

Trompette, Aurelien, Divanovic, Senad, Visintins, Alberto, Blanchard, Carine, Hegde, Rashmi S., Madan, Rajat, Thorne, Peter S., Wills-Karp, Marsha, Gioannini, Theresa L., Weiss, Jerry P., and Karp, Christopher L.

Subjects
Immune system -- Evaluation -- Research -- Health aspects -- Chemical properties, Aerobiology -- Research -- Health aspects -- Chemical properties, Proteins -- Health aspects -- Properties -- Chemical properties -- Research, Allergens -- Chemical properties -- Health aspects -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation, Evaluation, Chemical properties, Research, Properties, Health aspects
Abstract

Aeroallergy results from maladaptive immune responses to ubiquitous, otherwise innocuous environmental proteins (1). Although the proteins targeted by aeroallergic responses represent a tiny fraction of the airborne proteins humans are [...]

Published
2009

43. Contributors

Author

Abdalla, Saad H., primary, Acrani, Gustavo Olszanski, additional, Aggarwal, Rakesh, additional, Allos, Ban Mishu, additional, Alter, Miriam J., additional, Andrus, Jon K., additional, Angel, Juana, additional, Anstead, Gregory M., additional, Arathoon, Eduardo, additional, Arruda, Eurico, additional, Arthur, Ray R., additional, Atmar, Robert L., additional, Banura, Patrick, additional, Barbour, Alan G., additional, Barrett, Alan D.T., additional, Bausch, Dan, additional, Berk, Steven L., additional, Bessong, Pascal O., additional, Bia, Frank J., additional, Bicanic, Tihana, additional, Black, Robert E., additional, Bleck, Thomas P., additional, Boggild, Andrea K., additional, Bonnez, William, additional, Bresee, Joseph S., additional, Brown, Corrie, additional, Brown, Lillian B., additional, Brunetti, Enrico, additional, Bruschi, Fabrizio, additional, Bryant, Amy E., additional, Campbell, Carlos C. (Kent), additional, Castillo-Solorzano, Carlos, additional, Cetron, Martin S., additional, Chen, Ding-Shinn, additional, Chen, Pei-Jer, additional, Chen, Xiang-Sheng, additional, Cherian, Thomas, additional, Chua, K.B., additional, Cohen, Myron S., additional, Cooke, Graham S., additional, Cooper, Chester R., additional, Cooper, Edward S., additional, Coyle, Christina M., additional, Cross†, John H., additional, Dance, David A.B., additional, Danesi, Mustapha A., additional, Dawson, Chandler R., additional, de Martel, Catherine, additional, De Quadros, Ciro A., additional, de Queiroz Sousa, Anastacio, additional, de Silva, Nilanthi R., additional, de Souza, Alexandre Leite, additional, Dehio, Christoph, additional, Diemert, David J., additional, Dillingham, Rebecca, additional, Donelson, John E., additional, Dumler, J. Stephen, additional, Duncan, Joseph A., additional, DuPont, Herbert L., additional, Durand, Marlene L., additional, Eberhard, Mark L., additional, Eby, Joshua C., additional, Edwards, Charles, additional, Eidex, Rachel B., additional, Ellner, Jerrold J., additional, Enría, Delia A., additional, Ergonul, Onder, additional, Estes, Mary K., additional, Fahal, Ahmed Hassan, additional, Farmer, Paul E., additional, Faruque, A.S.G., additional, Feldman, Charles, additional, Feldmann, Heinz, additional, Fox, Kimberley K., additional, Franceschi, Silvia, additional, Franco, Manuel A., additional, Fulhorst, Charles F., additional, Garcia, Hector H., additional, Genta, Robert M., additional, Gilman, Robert H., additional, Glass, Roger I., additional, Goddard, Jerome, additional, Gotuzzo, Eduardo, additional, Graybill, John R., additional, Greenberg, Harry B., additional, Griffiths, Paul D., additional, Gubler, Duane J., additional, Guerrant, Richard L., additional, Gutierrez, Yezid, additional, Hewlett, Erik L., additional, Heymann, David L., additional, Hill, David R., additional, Ho, Mei-Shang, additional, Hoerauf, Achim M., additional, Hoffman, Paul S., additional, Hoffman, Stephen L., additional, Holbrook, Michael R., additional, Holland, Thomas L., additional, Hopkins, Donald R., additional, Hospenthal, Duane R., additional, Hotez, Peter J., additional, Hudnall, S. David, additional, Hughes, James M., additional, Hwang, Kao-Pin, additional, Isturiz, Raul E., additional, Jahrling, Peter B., additional, Jameel, Shahid, additional, Jeronimo, Selma M.B., additional, Jones-Lopez, Edward C., additional, Kabanova, Anna, additional, Kang, Gagandeep, additional, Karp, Christopher L., additional, Kazura, James W., additional, Kern, Peter, additional, Keusch, Gerald T., additional, Keystone, Jay S., additional, Khuroo, Mehnaaz S., additional, Khuroo, Mohammad S., additional, Kim, Ik-Sang, additional, King, Charles H., additional, Kirchhoff, Louis V., additional, Klion, Amy D., additional, Klugman, Keith P., additional, Kopecko, Dennis J., additional, Kosek, Margaret, additional, Koster, Frederick T., additional, Kozarsky, Phyllis E., additional, Ksiazek, Thomas G., additional, Kuhn, Jens H., additional, Lastovica, Albert J., additional, LeDuc, James W., additional, Leone, Peter A., additional, Levett, Paul N., additional, Levin, Michael, additional, Levine, Myron M., additional, Lima, Aldo A.M., additional, Lindeque, Gerhard, additional, Longworth, David L., additional, Mabey, David, additional, Maclean†, J. Dick, additional, Magill, Alan J., additional, Maguilnik, Ismael, additional, Maguiña, Ciro, additional, Maguire, James H., additional, Mahanty, Siddhartha, additional, Makino, Shinji, additional, Mandl, Christian W., additional, Marrie, Thomas J., additional, Marshall, Barry J., additional, Martin, Gregory J., additional, Matsumoto, Tadahiko, additional, Mawhorter, Steven D., additional, McCarthy, James S., additional, McGinnis, Michael R., additional, Mead, Paul S., additional, Meyers, Wayne M., additional, Miller, Robert F., additional, Miller, Samuel I., additional, Mills, James N., additional, Monath, Thomas P., additional, Moore, Christopher C., additional, Moore, Thomas A., additional, Morrill, J.C., additional, Morris, J. Glenn, additional, Murray, Megan, additional, Murrell, K. Darwin, additional, Nair, G. Balakrish, additional, Nash, Theodore E., additional, Nathan, Barnett R., additional, Negroni, Ricardo, additional, Nicholson-Weller, Anne, additional, Nucci, Marcio, additional, Nutman, Thomas B., additional, O’Farrell, Nigel, additional, Olano, Juan P., additional, Ooi, Eng Eong, additional, Ortega, Luis S., additional, Ortega, Ynés R., additional, Pallansch, Mark A., additional, Pape, Jean W., additional, Pappas, Georgios, additional, Parsonnet, Julie, additional, Pasvol, Geoffrey, additional, Peacock, Sharon J., additional, Pearson, Richard D., additional, Peeling, Rosanna W., additional, Pegues, David A., additional, Pépin, Jacques, additional, Peters, C.J., additional, Peterson, Kristine M., additional, Petri, William A., additional, Portaels, Françoise, additional, Proença-Módena, José Luiz, additional, Quinn, Thomas C., additional, Rao, G. Raghurama, additional, Raoult, Didier, additional, Rappuoli, Rino, additional, Rex, John H., additional, Reynolds, Steven J., additional, Ribeiro, José M.C., additional, Roilides, Emmanuel, additional, Rollin, Pierre E., additional, Ronald, Allan R., additional, Rota, Paul A., additional, Roy, Sharon L., additional, Ruiz-Tiben, Ernesto, additional, Ryan, Edward T., additional, Saha, Debasish, additional, Salam, Mohammed A., additional, Samie, Amidou, additional, Schachter, Julius, additional, Schantz, Peter M., additional, Scheld, W. Michael, additional, Schlaudecker, Elizabeth P., additional, Schwartz, David A., additional, Schwartzman, Joseph D., additional, Seña, Arlene C., additional, Sexton, Daniel J., additional, Sharp, Truman W., additional, Shieh, Wun-Ju, additional, Shoham, Shmuel, additional, Siddiqui, Afzal A., additional, Singh, Upinder, additional, Smith, David W., additional, Smith, Michael B., additional, Smoak, Bonnie L., additional, Smulian, A. George, additional, Snider, Cynthia B., additional, Solomon, Tom, additional, Sow, Samba O., additional, Sparling, P. Frederick, additional, Spencer, Lisa A., additional, Stanberry, Lawrence R., additional, Staples, J. Erin, additional, Steffen, Robert, additional, Steiner, Theodore S., additional, Steinhoff, Mark C., additional, Stevens, Dennis L., additional, Suh, Kathryn N., additional, Supparatpinyo, Khuanchai, additional, Szaniszlo, Paul J., additional, Tapia, Milagritos D., additional, Tanowitz, Herbert B., additional, Telford, Sam R., additional, Tesh, Robert B., additional, Thielman, Nathan M., additional, Torres-Vélez, Fernando J., additional, Tucker, Joseph D., additional, Valdez, Luis M., additional, Valenzuela, Jesus G., additional, van de Beek, Diederik, additional, Vasconcelos, Pedro F.C., additional, Visvesvara, Govinda S., additional, Wahl-Jensen, Victoria, additional, Walker, David H., additional, Walsh, Douglas S., additional, Walsh, Thomas J., additional, Walton, David A., additional, Walzer, Peter D., additional, Warren, Cirle A., additional, Weaver, Scott C., additional, Weiss, Louis M., additional, Weller, Peter F., additional, White, A. Clinton, additional, White, Nicholas J., additional, Wilkinson, Robert J., additional, Wilson, Mary E., additional, Wittner, Murray, additional, Zaidi, Anita K.M., additional, and Zaki, Sherif R., additional

Published
2011
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