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19 results on '"Anderson, Jason G."'

2. Reviewers

Author

Anderson, Jason G., primary, Bednarek, Christopher, additional, Bernstein, Jesse Samuel, additional, Burkard, Gregory, additional, Butler, Sean P., additional, Cuneo, Anthony A., additional, Furman, Aleeza, additional, Gonchikar, Swaroop, additional, Jaffe, Michael J., additional, Jasper, Nicholas R., additional, Overdorf, Paul R., additional, Shapiro, Simon J., additional, Speert, Tory B., additional, and Wahlberg, Brady M., additional

Published
2018
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4. Contributors

Author

Anderson, Jason G., primary, Ante, William A., additional, Baez-Cabrera, Luis D., additional, Batson,, John P., additional, Baxi, Naimish, additional, Bednarek, Christopher, additional, Benjamin, Akil S., additional, Berkwits, Leland, additional, Bodor, Marko, additional, Buttaci, Charles J., additional, Cohen, Isaac, additional, Conly, Jeffrey R., additional, Davidoff, Scott J., additional, Falco, Frank J.E., additional, Fox, Kermit W., additional, Foye, Patrick M., additional, Frey, Michael E., additional, Furman, Michael B., additional, Gilhool, James J., additional, Goodman, Bradly S., additional, Grove, Julie M., additional, Hagerty, Sarah E., additional, Henry, Jimmy M., additional, Johnson, Stephen C., additional, Karkvandeian, Farzad, additional, Kim, Ruby E., additional, Kingsbury, Dallas, additional, Kirschner, Jonathan S., additional, Klein, Michael A., additional, Kothari, Gautam, additional, Lee, Thomas S., additional, Lin, Hwei (Willie), additional, Lin, Paul S., additional, Liu, Jackson, additional, Loveless, Melinda S., additional, Lutz, Gregory, additional, Mallempati, Srinivas, additional, Norton, Denise, additional, Parikh, Tejas N., additional, Patel, Shounuck I., additional, Petrolla, Justin J., additional, Puttlitz, Kirk M., additional, Reeves, Ryan, additional, Rollé, William A., additional, Shapiro, Simon J., additional, Steinmetz, Brian D., additional, Stone, Jonathan B., additional, Tahaei, S. Amir, additional, Tekmyster, Gene, additional, Thakral, Vishal, additional, Torres, Louis, additional, Vallabhaneni, Sridhar, additional, Vo, Alan T., additional, Waltrous, Justin D., additional, Weber, Nicholas H., additional, and White, Brian F., additional

Published
2018
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11. CBRN transformation in the IBCT: too little too late?

Author

Anderson, Jason G.

Subjects
United States. Army -- Powers and duties, Soldiers -- Powers and duties -- Equipment and supplies, Military reconnaissance -- Equipment and supplies, Chemicals, plastics and rubber industries, Military and naval science
Abstract

BCTs [brigade combat teams] are the Army's basic tactical maneuver units, [sic] and the smallest combined arms units that can be committed independently. BCTs are designed to conduct offensive, defensive, [...]

Published
2008

12. SIRT6 Suppresses Cancer Stem-like Capacity in Tumors with PI3K Activation Independently of Its Deacetylase Activity

Author

Ioris, Rafael M., primary, Galié, Mirco, additional, Ramadori, Giorgio, additional, Anderson, Jason G., additional, Charollais, Anne, additional, Konstantinidou, Georgia, additional, Brenachot, Xavier, additional, Aras, Ebru, additional, Goga, Algera, additional, Ceglia, Nicholas, additional, Sebastián, Carlos, additional, Martinvalet, Denis, additional, Mostoslavsky, Raul, additional, Baldi, Pierre, additional, and Coppari, Roberto, additional

Published
2017
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17. A Serotonin and Melanocortin Circuit Mediates D-Fenfluramine Anorexia.

Author

Yong Xu, Jones, Juli E., Lauzon, Danielle A., Anderson, Jason G., Balthasar, Nina, Heisler, Lora K., Zinn, Andrew R., Lowell, Bradford B., and Elmquist, Joel K.

Subjects
FENFLURAMINE, SEROTONIN, PROOPIOMELANOCORTIN, APPETITE loss, LABORATORY mice, NEUROSCIENCES
Abstract

D-Fenfluramine (D-Fen) increases serotonin (5-HT) content in the synaptic cleft and exerts anorexigenic effects in animals and humans. However, the neural circuits that mediate these effects are not fully identified. To address this issue, we assessed the efficacy of D-Feninduced hypophagia in mouse models with manipulations of several genes in selective populations of neurons. Expectedly, we found that global deletion of 5-HT 2C receptors (5-HT2CRs) significantly attenuated D-Fen-induced anorexia. These anorexigenic effects were restored in mice with 5-HT2CRs expressed only in pro-opiomelanocortin (POMC) neurons. Further, we found that deletion of melanocortin 4 receptors (MC4Rs), a downstream target of POMC neurons, abolished anorexigenic effects of D-Fen. Reexpression of MC4Rs only in SIM1 neurons in the hypothalamic paraventricular nucleus and neurons in the amygdala was sufficient to restore the hypophagic property of D-Fen. Thus, our results identify a neurochemically defined neural circuit through which D-Fen influences appetite and thereby indicate that this 5-HT2CR/POMC-MC4R/SIM1 circuit may yield a more refined target to exploit for weight loss. [ABSTRACT FROM AUTHOR]

Published
2010
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18. Contributors

Author

Anderson, Jason G., Ante, William A., Batson, John P., Benjamin, Akil S., Berkwits, Leland, Buttaci, Charles J., Conly, Jeffrey R., Davidoff, Scott J., Falco, Frank J.E., Fox, Kermit W., Foye, Patrick M., Frey, Michael E., Furman, Michael B., Gilhool, James J., Goodman, Bradly S., Henry, Jimmy M., Kim, Ruby E., Kirschner, Jonathan S., Klein, Michael A., Kothari, Gautam, Lee, Thomas S., Lin, Hwei (Willie), Parikh, Tejas N., Petrolla, Justin J., Puttlitz, Kirk M., Reeves, Ryan, Rollé, William A., Jr., Steinmetz, Brian D., Stone, Jonathan B., Butler, Sean, DePalma, Michael J., Jasper, Nicholas R., O’Neill, Conor, Whitworth, Michael, Yuan, Mike, Consultant, Technical, and Dreyfuss, Paul

Published
2013
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19. 5-HT2CRs Expressed by Pro-Opiomelanocortin Neurons Regulate Energy Homeostasis

Author

Xu, Yong, Jones, Juli E., Kohno, Daisuke, Williams, Kevin W., Lee, Charlotte E., Choi, Michelle J., Anderson, Jason G., Heisler, Lora K., Zigman, Jeffrey M., Lowell, Bradford B., and Elmquist, Joel K.

Subjects
*BIOENERGETICS, *SEROTONIN, *DRUG activation, *APPETITE depressants, *PROOPIOMELANOCORTIN, *HOMEOSTASIS, *NEURONS, *LABORATORY mice
Abstract

Summary: Drugs activating 5-hydroxytryptamine 2C receptors (5-HT2CRs) potently suppress appetite, but the underlying mechanisms for these effects are not fully understood. To tackle this issue, we generated mice with global 5-HT2CR deficiency (2C null) and mice with 5-HT2CRs re-expression only in pro-opiomelanocortin (POMC) neurons (2C/POMC mice). We show that 2C null mice predictably developed hyperphagia, hyperactivity, and obesity and showed attenuated responses to anorexigenic 5-HT drugs. Remarkably, all these deficiencies were normalized in 2C/POMC mice. These results demonstrate that 5-HT2CR expression solely in POMC neurons is sufficient to mediate effects of serotoninergic compounds on food intake. The findings also highlight the physiological relevance of the 5-HT2CR-melanocortin circuitry in the long-term regulation of energy balance. [Copyright &y& Elsevier]

Published
2008
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