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1. The human affectome

Author

Schiller, Daniela, Yu, Alessandra N. C, Alia-Klein, Nelly, Becker, Susanne, Cromwell, Howard C., Dolcos, Florin, Eslinger, Paul J., Frewen, Paul, Kemp, Andrew H., Pace-Schott, Edward F., Raber, Jacob, Silton, Rebecca L., Stefanova, Elka, Williams, Justin H. G., Abe, Nobuhito, Aghajani, Moji, Albrecht, Franziska, Alexander, Rebecca, Anders, Silke, Aragón, Oriana R., Arias, Juan A., Arzy, Shahar, Aue, Tatjana, Baez, Sandra, Balconi, Michela, Ballarini, Tommaso, Bannister, Scott, Banta, Marlissa C., Barrett, Karen C., Belzung, Catherine, Bensafi, Moustafa, Booij, Linda, Bookwala, Jamila, Boulanger-Bertolus, Julie, Boutros, Sydney W., Bräscher, Anne-Kathrin, Bruno, Antonio, Busatto, Geraldo, Bylsma, Lauren M., Caldwell-Harris, Catherine, Chan, Raymond C. K., Cherbuin, Nicolas, Chiarella, Julian, Cipresso, Pietro, Critchley, Hugo, Croote, Denise E., Demaree, Heath A., Denson, Thomas F., Depue, Brendan, Derntl, Birgit, Dickson, Joanne M., Dolcos, Sanda, Drach-Zahavy, Anat, Dubljević, Olga, Eerola, Tuomas, Ellingsen, Dan-Mikael, Fairfield, Beth, Ferdenzi, Camille, Friedman, Bruce H., Fu, Cynthia H. Y., Gatt, Justine M., de Gelder, Beatrice, Gendolla, Guido H. E., Gilam, Gadi, Goldblatt, Hadass, Gooding, Anne E. K., Gosseries, Olivia, Hamm, Alfons O., Hanson, Jamie L., Hendler, Talma, Herbert, Cornelia, Hofmann, Stefan G., Ibanez, Agustin, Joffily, Mateus, Jovanovic, Tanja, Kahrilas, Ian J., Kangas, Maria, Katsumi, Yuta, Kensinger, Elizabeth, Kirby, Lauren A. J., Koncz, Rebecca, Koster, Ernst H. W., Kozlowska, Kasia, Krach, Sören, Kret, Mariska E., Krippl, Martin, Kusi-Mensah, Kwabena, Ladouceur, Cecile D., Laureys, Steven, Lawrence, Alistair, Li, Chiang-shan R., Liddell, Belinda J., Lidhar, Navdeep K., Lowry, Christopher A., Magee, Kelsey, Marin, Marie-France, Mariotti, Veronica, Martin, Loren J., Marusak, Hilary A., Mayer, Annalina V., Merner, Amanda R., Minnier, Jessica, Moll, Jorge, Morrison, Robert G., Moore, Matthew, Mouly, Anne-Marie, Mueller, Sven C., Mühlberger, Andreas, Murphy, Nora A., Muscatello, Maria R. A., Musser, Erica D., Newton, Tamara L., Noll-Hussong, Michael, Norrholm, Seth D., Northoff, Georg, Nusslock, Robin, Okon-Singer, Hadas, Olino, Thomas M., Ortner, Catherine, Owolabi, Mayowa, Padulo, Caterina, Palermo, Romina, Palumbo, Rocco, Palumbo, Sara, Papadelis, Christos, Pegna, Alan J., Pellegrini, Silvia, Peltonen, Kirsi, Penninx, Brenda W. J. H., Pietrini, Pietro, Pinna, Graziano, Lobo, Rosario P., Polnaszek, Kelly L., Polyakova, Maryna, Rabinak, Christine, Richter, S. Helene, Richter, Thalia, Riva, Giuseppe, Rizzo, Amelia, Robinson, Jennifer L., Rosa, Pedro, Sachdev, Perminder S., Sato, Wataru, Schroeter, Matthias L., Schweizer, Susanne, Shiban, Youssef, Siddharthan, Advaith, Siedlecka, Ewa, Smith, Robert C., Soreq, Hermona, Spangler, Derek P., Stern, Emily R., Styliadis, Charis, Sullivan, Gavin B., Swain, James E., Urben, Sébastien, Van den Stock, Jan, vander Kooij, Michael A., van Overveld, Mark, Van Rheenen, Tamsyn E., VanElzakker, Michael B., Ventura-Bort, Carlos, Verona, Edelyn, Volk, Tyler, Wang, Yi, Weingast, Leah T., Weymar, Mathias, Williams, Claire, Willis, Megan L., Yamashita, Paula, Zahn, Roland, Zupan, Barbra, Lowe, Leroy, Schiller, Daniela, Yu, Alessandra N. C, Alia-Klein, Nelly, Becker, Susanne, Cromwell, Howard C., Dolcos, Florin, Eslinger, Paul J., Frewen, Paul, Kemp, Andrew H., Pace-Schott, Edward F., Raber, Jacob, Silton, Rebecca L., Stefanova, Elka, Williams, Justin H. G., Abe, Nobuhito, Aghajani, Moji, Albrecht, Franziska, Alexander, Rebecca, Anders, Silke, Aragón, Oriana R., Arias, Juan A., Arzy, Shahar, Aue, Tatjana, Baez, Sandra, Balconi, Michela, Ballarini, Tommaso, Bannister, Scott, Banta, Marlissa C., Barrett, Karen C., Belzung, Catherine, Bensafi, Moustafa, Booij, Linda, Bookwala, Jamila, Boulanger-Bertolus, Julie, Boutros, Sydney W., Bräscher, Anne-Kathrin, Bruno, Antonio, Busatto, Geraldo, Bylsma, Lauren M., Caldwell-Harris, Catherine, Chan, Raymond C. K., Cherbuin, Nicolas, Chiarella, Julian, Cipresso, Pietro, Critchley, Hugo, Croote, Denise E., Demaree, Heath A., Denson, Thomas F., Depue, Brendan, Derntl, Birgit, Dickson, Joanne M., Dolcos, Sanda, Drach-Zahavy, Anat, Dubljević, Olga, Eerola, Tuomas, Ellingsen, Dan-Mikael, Fairfield, Beth, Ferdenzi, Camille, Friedman, Bruce H., Fu, Cynthia H. Y., Gatt, Justine M., de Gelder, Beatrice, Gendolla, Guido H. E., Gilam, Gadi, Goldblatt, Hadass, Gooding, Anne E. K., Gosseries, Olivia, Hamm, Alfons O., Hanson, Jamie L., Hendler, Talma, Herbert, Cornelia, Hofmann, Stefan G., Ibanez, Agustin, Joffily, Mateus, Jovanovic, Tanja, Kahrilas, Ian J., Kangas, Maria, Katsumi, Yuta, Kensinger, Elizabeth, Kirby, Lauren A. J., Koncz, Rebecca, Koster, Ernst H. W., Kozlowska, Kasia, Krach, Sören, Kret, Mariska E., Krippl, Martin, Kusi-Mensah, Kwabena, Ladouceur, Cecile D., Laureys, Steven, Lawrence, Alistair, Li, Chiang-shan R., Liddell, Belinda J., Lidhar, Navdeep K., Lowry, Christopher A., Magee, Kelsey, Marin, Marie-France, Mariotti, Veronica, Martin, Loren J., Marusak, Hilary A., Mayer, Annalina V., Merner, Amanda R., Minnier, Jessica, Moll, Jorge, Morrison, Robert G., Moore, Matthew, Mouly, Anne-Marie, Mueller, Sven C., Mühlberger, Andreas, Murphy, Nora A., Muscatello, Maria R. A., Musser, Erica D., Newton, Tamara L., Noll-Hussong, Michael, Norrholm, Seth D., Northoff, Georg, Nusslock, Robin, Okon-Singer, Hadas, Olino, Thomas M., Ortner, Catherine, Owolabi, Mayowa, Padulo, Caterina, Palermo, Romina, Palumbo, Rocco, Palumbo, Sara, Papadelis, Christos, Pegna, Alan J., Pellegrini, Silvia, Peltonen, Kirsi, Penninx, Brenda W. J. H., Pietrini, Pietro, Pinna, Graziano, Lobo, Rosario P., Polnaszek, Kelly L., Polyakova, Maryna, Rabinak, Christine, Richter, S. Helene, Richter, Thalia, Riva, Giuseppe, Rizzo, Amelia, Robinson, Jennifer L., Rosa, Pedro, Sachdev, Perminder S., Sato, Wataru, Schroeter, Matthias L., Schweizer, Susanne, Shiban, Youssef, Siddharthan, Advaith, Siedlecka, Ewa, Smith, Robert C., Soreq, Hermona, Spangler, Derek P., Stern, Emily R., Styliadis, Charis, Sullivan, Gavin B., Swain, James E., Urben, Sébastien, Van den Stock, Jan, vander Kooij, Michael A., van Overveld, Mark, Van Rheenen, Tamsyn E., VanElzakker, Michael B., Ventura-Bort, Carlos, Verona, Edelyn, Volk, Tyler, Wang, Yi, Weingast, Leah T., Weymar, Mathias, Williams, Claire, Willis, Megan L., Yamashita, Paula, Zahn, Roland, Zupan, Barbra, and Lowe, Leroy

Abstract

Over the last decades, theoretical perspectives in the interdisciplinary field of the affective sciences have proliferated rather than converged due to differing assumptions about what human affective phenomena are and how they work. These metaphysical and mechanistic assumptions, shaped by academic context and values, have dictated affective constructs and operationalizations. However, an assumption about the purpose of affective phenomena can guide us to a common set of metaphysical and mechanistic assumptions. In this capstone paper, we home in on a nested teleological principle for human affective phenomena in order to synthesize metaphysical and mechanistic assumptions. Under this framework, human affective phenomena can collectively be considered algorithms that either adjust based on the human comfort zone (affective concerns) or monitor those adaptive processes (affective features). This teleologically-grounded framework offers a principled agenda and launchpad for both organizing existing perspectives and generating new ones. Ultimately, we hope the Human Affectome brings us a step closer to not only an integrated understanding of human affective phenomena, but an integrated field for affective research.

Published
2024

2. The Human Affectome

Author

Schiller, Daniela, Yu, Alessandra N. C., Alia-Klein, Nelly, Becker, Susanne, Cromwell, Howard C., Dolcos, Florin, Eslinger, Paul J., Frewen, Paul, Kemp, Andrew H., Pace-Schott, Edward F., Raber, Jacob, Silton, Rebecca L., Stefanova, Elka, Williams, Justin H. G., Abe, Nobuhito, Aghajani, Moji, Albrecht, Franziska, Alexander, Rebecca, Anders, Silke, Aragón, Oriana R., Arias, Juan A., Arzy, Shahar, Aue, Tatjana, Baez, Sandra, Balconi, Michela, Ballarini, Tommaso, Bannister, Scott, Banta, Marlissa C., Barrett, Karen Caplovitz, Belzung, Catherine, Bensafi, Moustafa, Booij, Linda, Bookwala, Jamila, Boulanger-Bertolus, Julie, Boutros, Sydney Weber, Bräscher, Anne-Kathrin, Bruno, Antonio, Busatto, Geraldo, Bylsma, Lauren M., Caldwell-Harris, Catherine, Chan, Raymond C. K., Cherbuin, Nicola, Chiarella, Julian, Cipresso, Pietro, Critchley, Hugo, Croote, Denise E., Demaree, Heath A., Denson, Thomas F., Depue, Brendan, Derntl, Birgit, Dickson, Joanne M., Dolcos, Sanda, Drach-Zahavy, Anat, Dubljević, Olga, Eerola, Tuoma, Ellingsen, Dan-Mikael, Fairfield, Beth, Ferdenzi, Camille, Friedman, Bruce H., Fu, Cynthia H. Y., Gatt, Justine M., de Gelder, Beatrice, Gendolla, Guido H. E., Gilam, Gadi, Goldblatt, Hada, Gooding, Anne Elizabeth Kotynski, Gosseries, Olivia, Hamm, Alfons O., Hanson, Jamie L., Hendler, Talma, Herbert, Cornelia, Hofmann, Stefan G., Ibanez, Agustin, Joffily, Mateu, Jovanovic, Tanja, Kahrilas, Ian J., Kangas, Maria, Katsumi, Yuta, Kensinger, Elizabeth, Kirby, Lauren A. J., Koncz, Rebecca, Koster, Ernst H. W., Kozlowska, Kasia, Krach, Sören, Kret, Mariska E., Krippl, Martin, Kusi-Mensah, Kwabena, Ladouceur, Cecile D., Laureys, Steven, Lawrence, Alistair, Li, Chiang-shan R., Liddell, Belinda J., Lidhar, Navdeep K., Lowry, Christopher A., Magee, Kelsey, Marin, Marie-France, Mariotti, Veronica, Martin, Loren J., Marusak, Hilary A., Mayer, Annalina V., Merner, Amanda R., Minnier, Jessica, Moll, Jorge, Morrison, Robert G., Moore, Matthew, Mouly, Anne-Marie, Mueller, Sven C., Mühlberger, Andrea, Murphy, Nora A., Muscatello, Maria Rosaria Anna, Musser, Erica D., Newton, Tamara L., Noll-Hussong, Michael, Norrholm, Seth Davin, Northoff, Georg, Nusslock, Robin, Okon-Singer, Hada, Olino, Thomas M., Ortner, Catherine, Owolabi, Mayowa, Padulo, Caterina, Palermo, Romina, Palumbo, Rocco, Palumbo, Sara, Papadelis, Christo, Pegna, Alan J., Pellegrini, Silvia, Peltonen, Kirsi, Penninx, Brenda W. J. H., Pietrini, Pietro, Pinna, Graziano, Lobo, Rosario Pinto, Polnaszek, Kelly L., Polyakova, Maryna, Rabinak, Christine, Helene Richter, S., Richter, Thalia, Riva, Giuseppe, Rizzo, Amelia, Robinson, Jennifer L., Rosa, Pedro, Sachdev, Perminder S., Sato, Wataru, Schroeter, Matthias L., Schweizer, Susanne, Shiban, Youssef, Siddharthan, Advaith, Siedlecka, Ewa, Smith, Robert C., Soreq, Hermona, Spangler, Derek P., Stern, Emily R., Styliadis, Chari, Sullivan, Gavin B., Swain, James E., Urben, Sébastien, Van den Stock, Jan, vander Kooij, Michael A., van Overveld, Mark, Van Rheenen, Tamsyn E., Vanelzakker, Michael B., Ventura-Bort, Carlo, Verona, Edelyn, Volk, Tyler, Wang, Yi, Weingast, Leah T., Weymar, Mathia, Williams, Claire, Willis, Megan L., Yamashita, Paula, Zahn, Roland, Zupan, Barbra, Lowe, Leroy, Balconi, Michela (ORCID:0000-0002-8634-1951), Cipresso, Pietro (ORCID:0000-0002-0662-7678), Riva, Giuseppe (ORCID:0000-0003-3657-106X), Schiller, Daniela, Yu, Alessandra N. C., Alia-Klein, Nelly, Becker, Susanne, Cromwell, Howard C., Dolcos, Florin, Eslinger, Paul J., Frewen, Paul, Kemp, Andrew H., Pace-Schott, Edward F., Raber, Jacob, Silton, Rebecca L., Stefanova, Elka, Williams, Justin H. G., Abe, Nobuhito, Aghajani, Moji, Albrecht, Franziska, Alexander, Rebecca, Anders, Silke, Aragón, Oriana R., Arias, Juan A., Arzy, Shahar, Aue, Tatjana, Baez, Sandra, Balconi, Michela, Ballarini, Tommaso, Bannister, Scott, Banta, Marlissa C., Barrett, Karen Caplovitz, Belzung, Catherine, Bensafi, Moustafa, Booij, Linda, Bookwala, Jamila, Boulanger-Bertolus, Julie, Boutros, Sydney Weber, Bräscher, Anne-Kathrin, Bruno, Antonio, Busatto, Geraldo, Bylsma, Lauren M., Caldwell-Harris, Catherine, Chan, Raymond C. K., Cherbuin, Nicola, Chiarella, Julian, Cipresso, Pietro, Critchley, Hugo, Croote, Denise E., Demaree, Heath A., Denson, Thomas F., Depue, Brendan, Derntl, Birgit, Dickson, Joanne M., Dolcos, Sanda, Drach-Zahavy, Anat, Dubljević, Olga, Eerola, Tuoma, Ellingsen, Dan-Mikael, Fairfield, Beth, Ferdenzi, Camille, Friedman, Bruce H., Fu, Cynthia H. Y., Gatt, Justine M., de Gelder, Beatrice, Gendolla, Guido H. E., Gilam, Gadi, Goldblatt, Hada, Gooding, Anne Elizabeth Kotynski, Gosseries, Olivia, Hamm, Alfons O., Hanson, Jamie L., Hendler, Talma, Herbert, Cornelia, Hofmann, Stefan G., Ibanez, Agustin, Joffily, Mateu, Jovanovic, Tanja, Kahrilas, Ian J., Kangas, Maria, Katsumi, Yuta, Kensinger, Elizabeth, Kirby, Lauren A. J., Koncz, Rebecca, Koster, Ernst H. W., Kozlowska, Kasia, Krach, Sören, Kret, Mariska E., Krippl, Martin, Kusi-Mensah, Kwabena, Ladouceur, Cecile D., Laureys, Steven, Lawrence, Alistair, Li, Chiang-shan R., Liddell, Belinda J., Lidhar, Navdeep K., Lowry, Christopher A., Magee, Kelsey, Marin, Marie-France, Mariotti, Veronica, Martin, Loren J., Marusak, Hilary A., Mayer, Annalina V., Merner, Amanda R., Minnier, Jessica, Moll, Jorge, Morrison, Robert G., Moore, Matthew, Mouly, Anne-Marie, Mueller, Sven C., Mühlberger, Andrea, Murphy, Nora A., Muscatello, Maria Rosaria Anna, Musser, Erica D., Newton, Tamara L., Noll-Hussong, Michael, Norrholm, Seth Davin, Northoff, Georg, Nusslock, Robin, Okon-Singer, Hada, Olino, Thomas M., Ortner, Catherine, Owolabi, Mayowa, Padulo, Caterina, Palermo, Romina, Palumbo, Rocco, Palumbo, Sara, Papadelis, Christo, Pegna, Alan J., Pellegrini, Silvia, Peltonen, Kirsi, Penninx, Brenda W. J. H., Pietrini, Pietro, Pinna, Graziano, Lobo, Rosario Pinto, Polnaszek, Kelly L., Polyakova, Maryna, Rabinak, Christine, Helene Richter, S., Richter, Thalia, Riva, Giuseppe, Rizzo, Amelia, Robinson, Jennifer L., Rosa, Pedro, Sachdev, Perminder S., Sato, Wataru, Schroeter, Matthias L., Schweizer, Susanne, Shiban, Youssef, Siddharthan, Advaith, Siedlecka, Ewa, Smith, Robert C., Soreq, Hermona, Spangler, Derek P., Stern, Emily R., Styliadis, Chari, Sullivan, Gavin B., Swain, James E., Urben, Sébastien, Van den Stock, Jan, vander Kooij, Michael A., van Overveld, Mark, Van Rheenen, Tamsyn E., Vanelzakker, Michael B., Ventura-Bort, Carlo, Verona, Edelyn, Volk, Tyler, Wang, Yi, Weingast, Leah T., Weymar, Mathia, Williams, Claire, Willis, Megan L., Yamashita, Paula, Zahn, Roland, Zupan, Barbra, Lowe, Leroy, Balconi, Michela (ORCID:0000-0002-8634-1951), Cipresso, Pietro (ORCID:0000-0002-0662-7678), and Riva, Giuseppe (ORCID:0000-0003-3657-106X)

Abstract

Over the last decades, theoretical perspectives in the interdisciplinary field of the affective sciences have proliferated rather than converged due to differing assumptions about what human affective phenomena are and how they work. These metaphysical and mechanistic assumptions, shaped by academic context and values, have dictated affective constructs and operationalizations. However, an assumption about the purpose of affective phenomena can guide us to a common set of metaphysical and mechanistic assumptions. In this capstone paper, we home in on a nested teleological principle for human affective phenomena in order to synthesize metaphysical and mechanistic assumptions. Under this framework, human affective phenomena can collectively be considered algorithms that either adjust based on the human comfort zone (affective concerns) or monitor those adaptive processes (affective features). This teleologically-grounded framework offers a principled agenda and launchpad for both organizing existing perspectives and generating new ones. Ultimately, we hope the Human Affectome brings us a step closer to not only an integrated understanding of human affective phenomena, but an integrated field for affective research.

Published
2024

3. Experiences of child welfare social workers in addressing substance use among maltreated young mothers to prevent child maltreatment

Author

Doig, Amara Channell, Doig, Amara Channell, Jasczynski, Michelle, Phillips, Danielle R., Robinson, Jennifer L., Aden, Faduma, Huq, Maisha, Lee, Kaitlyn, Jones, Gary, Bernardi, Chloe, Aparicio, Elizabeth M., Doig, Amara Channell, Doig, Amara Channell, Jasczynski, Michelle, Phillips, Danielle R., Robinson, Jennifer L., Aden, Faduma, Huq, Maisha, Lee, Kaitlyn, Jones, Gary, Bernardi, Chloe, and Aparicio, Elizabeth M.

Abstract

Substance use during the perinatal period and while parenting can pose a significant risk to children's safety and well-being. Mothers who have experienced child maltreatment are more likely to use substances than mothers without a history of maltreatment. This study explores how child welfare social workers experience supporting young, maltreated mothers struggling with substance use to prevent the intergenerational transmission of child maltreatment. Semi-structured in-depth interviews were conducted with four social workers working with young mothers with a history of maltreatment and substance use. Interpretative Phenomenological Analysis revealed two themes: (1) grappling with system challenges and (2) supporting strategies for disrupting intergenerational transmission of child maltreatment. The results highlight the need for systemic changes around support for social workers who work with young mothers who use substances and have a history of maltreatment, and substance use treatment and mental health programs themselves. Mothers need access to prenatal programs that are trauma-informed, non-judgemental and that support participants' basic needs and parenting skills.

Published
2023

4. Physiological feelings

Author

Pace-Schott, Edward F., Amole, Marlissa C., Aue, Tatjana, Balconi, Michela, Bylsma, Lauren M., Critchley, Hugo, Demaree, Heath A., Friedman, Bruce H., Gooding, Anne Elizabeth Kotynski, Gosseries, Olivia, Jovanovic, Tanja, Kirby, Lauren A.J., Kozlowksa, Kasia, Laureys, Steven, Lowe, Leroy, Magee, Kelsey, Marin, Marie-France, Merner, Amanda R., Robinson, Jennifer L., Smith, Robert C., Spangler, Derek P., Van Overveld, Mark, VanElzakker, Michael B., Pace-Schott, Edward F., Amole, Marlissa C., Aue, Tatjana, Balconi, Michela, Bylsma, Lauren M., Critchley, Hugo, Demaree, Heath A., Friedman, Bruce H., Gooding, Anne Elizabeth Kotynski, Gosseries, Olivia, Jovanovic, Tanja, Kirby, Lauren A.J., Kozlowksa, Kasia, Laureys, Steven, Lowe, Leroy, Magee, Kelsey, Marin, Marie-France, Merner, Amanda R., Robinson, Jennifer L., Smith, Robert C., Spangler, Derek P., Van Overveld, Mark, and VanElzakker, Michael B.

Abstract

The role of peripheral physiology in the experience of emotion has been debated since the 19th century following the seminal proposal by William James that somatic responses to stimuli determine subjective emotion. Subsequent views have integrated the forebrain's ability to initiate, represent and simulate such physiological events. Modern affective neuroscience envisions an interacting network of “bottom-up” and “top-down” signaling in which the peripheral (PNS) and central nervous systems both receive and generate the experience of emotion. “Feelings” serves as a term for the perception of these physical changes whether emanating from actual somatic events or from the brain's representation of such. “Interoception” has come to represent the brain's receipt and representation of these actual and “virtual” somatic changes that may or may not enter conscious awareness but, nonetheless, influence feelings. Such information can originate from diverse sources including endocrine, immune and gastrointestinal systems as well as the PNS. We here examine physiological feelings from diverse perspectives including current and historical theories, evolution, neuroanatomy and physiology, development, regulatory processes, pathology and linguistics.

Published
2019
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5. Physiological feelings

Author

Pace-Schott, Edward F., Amole, Marlissa C., Aue, Tatjana, Balconi, Michela, Bylsma, Lauren M., Critchley, Hugo, Demaree, Heath A., Friedman, Bruce H., Gooding, Anne Elizabeth Kotynski, Gosseries, Olivia, Jovanovic, Tanja, Kirby, Lauren A.J., Kozlowksa, Kasia, Laureys, Steven, Lowe, Leroy, Magee, Kelsey, Marin, Marie-France, Merner, Amanda R., Robinson, Jennifer L., Smith, Robert C., Spangler, Derek P., Van Overveld, Mark, VanElzakker, Michael B., Pace-Schott, Edward F., Amole, Marlissa C., Aue, Tatjana, Balconi, Michela, Bylsma, Lauren M., Critchley, Hugo, Demaree, Heath A., Friedman, Bruce H., Gooding, Anne Elizabeth Kotynski, Gosseries, Olivia, Jovanovic, Tanja, Kirby, Lauren A.J., Kozlowksa, Kasia, Laureys, Steven, Lowe, Leroy, Magee, Kelsey, Marin, Marie-France, Merner, Amanda R., Robinson, Jennifer L., Smith, Robert C., Spangler, Derek P., Van Overveld, Mark, and VanElzakker, Michael B.

Abstract

The role of peripheral physiology in the experience of emotion has been debated since the 19th century following the seminal proposal by William James that somatic responses to stimuli determine subjective emotion. Subsequent views have integrated the forebrain's ability to initiate, represent and simulate such physiological events. Modern affective neuroscience envisions an interacting network of “bottom-up” and “top-down” signaling in which the peripheral (PNS) and central nervous systems both receive and generate the experience of emotion. “Feelings” serves as a term for the perception of these physical changes whether emanating from actual somatic events or from the brain's representation of such. “Interoception” has come to represent the brain's receipt and representation of these actual and “virtual” somatic changes that may or may not enter conscious awareness but, nonetheless, influence feelings. Such information can originate from diverse sources including endocrine, immune and gastrointestinal systems as well as the PNS. We here examine physiological feelings from diverse perspectives including current and historical theories, evolution, neuroanatomy and physiology, development, regulatory processes, pathology and linguistics.

Published
2019

6. Clinical Aspects of Type 3 Long-QT Syndrome:An International Multicenter Study

Author

Wilde, Arthur A M, Moss, Arthur J, Kaufman, Elizabeth S, Shimizu, Wataru, Peterson, Derick R, Benhorin, Jesaia, Lopes, Coeli, Towbin, Jeffrey A, Spazzolini, Carla, Crotti, Lia, Zareba, Wojciech, Goldenberg, Ilan, Kanters, Jørgen K, Robinson, Jennifer L, Qi, Ming, Hofman, Nynke, Tester, David J, Bezzina, Connie R, Alders, Mariëlle, Aiba, Takeshi, Kamakura, Shiro, Miyamoto, Yoshihiro, Andrews, Mark L, McNitt, Scott, Polonsky, Bronislava, Schwartz, Peter J, Ackerman, Michael J, Wilde, Arthur A M, Moss, Arthur J, Kaufman, Elizabeth S, Shimizu, Wataru, Peterson, Derick R, Benhorin, Jesaia, Lopes, Coeli, Towbin, Jeffrey A, Spazzolini, Carla, Crotti, Lia, Zareba, Wojciech, Goldenberg, Ilan, Kanters, Jørgen K, Robinson, Jennifer L, Qi, Ming, Hofman, Nynke, Tester, David J, Bezzina, Connie R, Alders, Mariëlle, Aiba, Takeshi, Kamakura, Shiro, Miyamoto, Yoshihiro, Andrews, Mark L, McNitt, Scott, Polonsky, Bronislava, Schwartz, Peter J, and Ackerman, Michael J

Abstract

BACKGROUND: -Risk stratification in patients with type 3 long QT syndrome (LQT3) by clinical and genetic characteristics and effectiveness of ß-blocker therapy have not been studied previously in a large LQT3 population.METHODS: -The study population included 406 LQT3 patients with 51 different sodium-channel mutations; 391 patients were known to be event free during the first year of life and were the focus of our study. Clinical, electrocardiographic, and genetic parameters were acquired on patients from 7 participating LQT3 registries. Cox regression analysis was used to evaluate the independent contribution of clinical, genetic, and therapeutic factors to the first occurrence of time-dependent cardiac events (CE) from age 1 to 41 years.RESULTS: -118 (30%) patients (41 males) experienced at least one CE (syncope, aborted cardiac arrest [ACA] or LQTS-related sudden death [SD]), and 20% suffered from LQT3-related ACA/SD. The risk of a first CE was directly related to the degree of QTc prolongation. Cox regression analysis revealed that time-dependent ß-blocker therapy was associated with an 83% reduction in CE's in females (p=0.015) but not in males (who had much fewer events), with a significant gender x ß-blocker interaction (p=0.04). Each 10ms increase in QTc duration up to 500ms was associated with a 19% increase in CE's. Prior syncope doubled the risk for life-threatening events (p<0.02).CONCLUSIONS: -Prolonged QTc and syncope predispose patients with LQT3 to life-threatening CE's. ß-blocker therapy reduces this risk in females, but efficacy in males could not be conclusively determined due to low number of events.

Published
2016

7. States Taking Charge: Examining the Role of Race, Party Affiliation, and Preemption in the Development of In-State Tuition Laws for Undocumented Immigrant Students

Author

Nelson, Stephen L., Robinson, Jennifer L., Glaubitz, Kara Hetrick, Nelson, Stephen L., Robinson, Jennifer L., and Glaubitz, Kara Hetrick

Abstract

Immigration policy “continues to command significant attention in state legislatures” across the United States, and in-state tuition benefits for undocumented immigrant students remain near the center of this ongoing debate. Given the controversy and passion surrounding the issue, in-state tuition benefits for undocumented students can be described as the intersection of immigration policy and education policy in legislatures across the United States. This Article does not seek to advance any particular position in this policy controversy; rather, it aims to examine more deeply the development and future viability of such laws in the instance of a preemption challenge in state or federal court. The purpose of this Article, in other words, is twofold: (1) to understand the development of laws regarding tuition benefits for undocumented immigrant students throughout the country, in the context of race and party affiliation; and (2) to examine the federal preemption implications for state legislation regarding tuition benefits for undocumented immigrant students.

Published
2014

8. States Taking Charge: Examining the Role of Race, Party Affiliation, and Preemption in the Development of In-State Tuition Laws for Undocumented Immigrant Students

Author

Nelson, Stephen L., Robinson, Jennifer L., Glaubitz, Kara Hetrick, Nelson, Stephen L., Robinson, Jennifer L., and Glaubitz, Kara Hetrick

Abstract

Immigration policy “continues to command significant attention in state legislatures” across the United States, and in-state tuition benefits for undocumented immigrant students remain near the center of this ongoing debate. Given the controversy and passion surrounding the issue, in-state tuition benefits for undocumented students can be described as the intersection of immigration policy and education policy in legislatures across the United States. This Article does not seek to advance any particular position in this policy controversy; rather, it aims to examine more deeply the development and future viability of such laws in the instance of a preemption challenge in state or federal court. The purpose of this Article, in other words, is twofold: (1) to understand the development of laws regarding tuition benefits for undocumented immigrant students throughout the country, in the context of race and party affiliation; and (2) to examine the federal preemption implications for state legislation regarding tuition benefits for undocumented immigrant students.

Published
2014

9. Use of mutant-specific ion channel characteristics for risk stratification of long QT syndrome patients

Author

Jons, Christian, O-Uchi, Jin, Moss, Arthur J, Reumann, Matthias, Rice, John J, Goldenberg, Ilan, Zareba, Wojciech, Wilde, Arthur A M, Shimizu, Wataru, Kanters, Jørgen K., McNitt, Scott, Hofman, Nynke, Robinson, Jennifer L, Lopes, Coeli M B, Jons, Christian, O-Uchi, Jin, Moss, Arthur J, Reumann, Matthias, Rice, John J, Goldenberg, Ilan, Zareba, Wojciech, Wilde, Arthur A M, Shimizu, Wataru, Kanters, Jørgen K., McNitt, Scott, Hofman, Nynke, Robinson, Jennifer L, and Lopes, Coeli M B

Abstract

Inherited long QT syndrome (LQTS) is caused by mutations in ion channels that delay cardiac repolarization, increasing the risk of sudden death from ventricular arrhythmias. Currently, the risk of sudden death in individuals with LQTS is estimated from clinical parameters such as age, gender, and the QT interval, measured from the electrocardiogram. Even though a number of different mutations can cause LQTS, mutation-specific information is rarely used clinically. LQTS type 1 (LQT1), one of the most common forms of LQTS, is caused by mutations in the slow potassium current (I(Ks)) channel a subunit KCNQ1. We investigated whether mutation-specific changes in I(Ks) function can predict cardiac risk in LQT1. By correlating the clinical phenotype of 387 LQT1 patients with the cellular electrophysiological characteristics caused by an array of mutations in KCNQ1, we found that channels with a decreased rate of current activation are associated with increased risk of cardiac events (hazard ratio=2.02), independent of the clinical parameters usually used for risk stratification. In patients with moderate QT prolongation (a QT interval less than 500 ms), slower activation was an independent predictor for cardiac events (syncope, aborted cardiac arrest, and sudden death) (hazard ratio = 2.10), whereas the length of the QT interval itself was not. Our results indicate that genotype and biophysical phenotype analysis may be useful for risk stratification of LQT1 patients and suggest that slow channel activation is associated with an increased risk of cardiac events.

Published
2011

10. Use of mutant-specific ion channel characteristics for risk stratification of long QT syndrome patients

Author

Jons, Christian, O-Uchi, Jin, Moss, Arthur J, Reumann, Matthias, Rice, John J, Goldenberg, Ilan, Zareba, Wojciech, Wilde, Arthur A M, Shimizu, Wataru, Kanters, Jørgen K., McNitt, Scott, Hofman, Nynke, Robinson, Jennifer L, Lopes, Coeli M B, Jons, Christian, O-Uchi, Jin, Moss, Arthur J, Reumann, Matthias, Rice, John J, Goldenberg, Ilan, Zareba, Wojciech, Wilde, Arthur A M, Shimizu, Wataru, Kanters, Jørgen K., McNitt, Scott, Hofman, Nynke, Robinson, Jennifer L, and Lopes, Coeli M B

Abstract

Inherited long QT syndrome (LQTS) is caused by mutations in ion channels that delay cardiac repolarization, increasing the risk of sudden death from ventricular arrhythmias. Currently, the risk of sudden death in individuals with LQTS is estimated from clinical parameters such as age, gender, and the QT interval, measured from the electrocardiogram. Even though a number of different mutations can cause LQTS, mutation-specific information is rarely used clinically. LQTS type 1 (LQT1), one of the most common forms of LQTS, is caused by mutations in the slow potassium current (I(Ks)) channel a subunit KCNQ1. We investigated whether mutation-specific changes in I(Ks) function can predict cardiac risk in LQT1. By correlating the clinical phenotype of 387 LQT1 patients with the cellular electrophysiological characteristics caused by an array of mutations in KCNQ1, we found that channels with a decreased rate of current activation are associated with increased risk of cardiac events (hazard ratio=2.02), independent of the clinical parameters usually used for risk stratification. In patients with moderate QT prolongation (a QT interval less than 500 ms), slower activation was an independent predictor for cardiac events (syncope, aborted cardiac arrest, and sudden death) (hazard ratio = 2.10), whereas the length of the QT interval itself was not. Our results indicate that genotype and biophysical phenotype analysis may be useful for risk stratification of LQT1 patients and suggest that slow channel activation is associated with an increased risk of cardiac events.

Published
2011

11. Use of mutant-specific ion channel characteristics for risk stratification of long QT syndrome patients

Author

Jons, Christian, O-Uchi, Jin, Moss, Arthur J, Reumann, Matthias, Rice, John J, Goldenberg, Ilan, Zareba, Wojciech, Wilde, Arthur A M, Shimizu, Wataru, Kanters, Jørgen K., McNitt, Scott, Hofman, Nynke, Robinson, Jennifer L, Lopes, Coeli M B, Jons, Christian, O-Uchi, Jin, Moss, Arthur J, Reumann, Matthias, Rice, John J, Goldenberg, Ilan, Zareba, Wojciech, Wilde, Arthur A M, Shimizu, Wataru, Kanters, Jørgen K., McNitt, Scott, Hofman, Nynke, Robinson, Jennifer L, and Lopes, Coeli M B

Abstract

Inherited long QT syndrome (LQTS) is caused by mutations in ion channels that delay cardiac repolarization, increasing the risk of sudden death from ventricular arrhythmias. Currently, the risk of sudden death in individuals with LQTS is estimated from clinical parameters such as age, gender, and the QT interval, measured from the electrocardiogram. Even though a number of different mutations can cause LQTS, mutation-specific information is rarely used clinically. LQTS type 1 (LQT1), one of the most common forms of LQTS, is caused by mutations in the slow potassium current (I(Ks)) channel a subunit KCNQ1. We investigated whether mutation-specific changes in I(Ks) function can predict cardiac risk in LQT1. By correlating the clinical phenotype of 387 LQT1 patients with the cellular electrophysiological characteristics caused by an array of mutations in KCNQ1, we found that channels with a decreased rate of current activation are associated with increased risk of cardiac events (hazard ratio=2.02), independent of the clinical parameters usually used for risk stratification. In patients with moderate QT prolongation (a QT interval less than 500 ms), slower activation was an independent predictor for cardiac events (syncope, aborted cardiac arrest, and sudden death) (hazard ratio = 2.10), whereas the length of the QT interval itself was not. Our results indicate that genotype and biophysical phenotype analysis may be useful for risk stratification of LQT1 patients and suggest that slow channel activation is associated with an increased risk of cardiac events.

Published
2011

12. Risk for Life-Threatening Cardiac Events in Patients With Genotype-Confirmed Long-QT Syndrome and Normal-Range Corrected QT Intervals

Author

Goldenberg, Ilan, Horr, Samuel, Moss, Arthur J., Lopes, Coeli M., Barsheshet, Alon, McNitt, Scott, Zareba, Wojciech, Andrews, Mark L., Robinson, Jennifer L., Locati, Emanuela H., Ackerman, Michael J., Benhorin, Jesaia, Kaufman, Elizabeth S., Napolitano, Carlo, Platonov, Pyotr, Priori, Silvia G., Qi, Ming, Schwartz, Peter J., Shimizu, Wataru, Towbin, Jeffrey A., Vincent, G. Michael, Wilde, Arthur A. M., Zhang, Li, Goldenberg, Ilan, Horr, Samuel, Moss, Arthur J., Lopes, Coeli M., Barsheshet, Alon, McNitt, Scott, Zareba, Wojciech, Andrews, Mark L., Robinson, Jennifer L., Locati, Emanuela H., Ackerman, Michael J., Benhorin, Jesaia, Kaufman, Elizabeth S., Napolitano, Carlo, Platonov, Pyotr, Priori, Silvia G., Qi, Ming, Schwartz, Peter J., Shimizu, Wataru, Towbin, Jeffrey A., Vincent, G. Michael, Wilde, Arthur A. M., and Zhang, Li

Abstract

Objectives This study was designed to assess the clinical course and to identify risk factors for life-threatening events in patients with long-QT syndrome (LQTS) with normal corrected QT (QTc) intervals. Background Current data regarding the outcome of patients with concealed LQTS are limited. Methods Clinical and genetic risk factors for aborted cardiac arrest (ACA) or sudden cardiac death (SCD) from birth through age 40 years were examined in 3,386 genotyped subjects from 7 multinational LQTS registries, categorized as LQTS with normal-range QTc (<= 440 ms [n = 469]), LQTS with prolonged QTc interval (>440 ms [ n = 1,392]), and unaffected family members (genotyped negative with <= 440 ms [ n = 1,525]). Results The cumulative probability of ACA or SCD in patients with LQTS with normal-range QTc intervals (4%) was significantly lower than in those with prolonged QTc intervals (15%) (p < 0.001) but higher than in unaffected family members (0.4%) (p < 0.001). Risk factors ACA or SCD in patients with normal-range QTc intervals included mutation characteristics (transmembrane-missense vs. nontransmembrane or nonmissense mutations: hazard ratio: 6.32; p = 0.006) and the LQTS genotypes (LQTS type 1: LQTS type 2, hazard ratio: 9.88; p = 0.03; LQTS type 3: LQTS type 2, hazard ratio: 8.04; p = 0.07), whereas clinical factors, including sex and QTc duration, were associated with a significant increase in the risk for ACA or SCD only in patients with prolonged QTc intervals (female age >13 years, hazard ratio: 1.90; p = 0.002; QTc duration, 8% risk increase per 10-ms increment; p = 0.002). Conclusions Genotype-confirmed patients with concealed LQTS make up about 25% of the at-risk LQTS population. Genetic data, including information regarding mutation characteristics and the LQTS genotype, identify increased risk for ACA or SCD in this overall lower risk LQTS subgroup. (J Am Coll Cardiol 2011;57:51-9) (C) 2011 by the American College of Cardiology Foundation

Published
2010

13. Mutations in conserved amino acids in the KCNQ1 channel and risk of cardiac events in type-1 long-QT syndrome

Author

Jons, Christian, Moss, Arthur J, Lopes, Coeli M, McNitt, Scott, Zareba, Wojciech, Goldenberg, Ilan, Qi, Ming, Wilde, Arthur A M, Shimizu, Wataru, Kanters, Jørgen K., Towbin, Jeffrey A, Ackerman, Michael J, Robinson, Jennifer L, Jons, Christian, Moss, Arthur J, Lopes, Coeli M, McNitt, Scott, Zareba, Wojciech, Goldenberg, Ilan, Qi, Ming, Wilde, Arthur A M, Shimizu, Wataru, Kanters, Jørgen K., Towbin, Jeffrey A, Ackerman, Michael J, and Robinson, Jennifer L

Abstract

BACKGROUND: Type-1 long-QT syndrome (LQT1) is caused by mutations in the KCNQ1 gene. The purpose of this study was to investigate whether KCNQ1 mutations in highly conserved amino acid residues within the voltage-gated potassium channel family are associated with an increased risk of cardiac events. METHODS AND RESULTS: The study population involved 492 LQT1 patients with 54 missense mutations in the transmembrane region of the KCNQ1 channel. The amino acid sequences of the transmembrane region of 38 human voltage-gated potassium channels were aligned. An adjusted Shannon entropy score for each amino acid residue was calculated ranging from 0 (no conservation) to 1.0 (full conservation). Cox analysis was used to identify independent factors associated with the first cardiac event (syncope, aborted cardiac arrest, or death). Patients were subcategorized into tertiles by their adjusted Shannon entropy scores. The lowest tertile (score 0-0.469; n = 146) was used as a reference group; patients with intermediate tertile scores (0.470-0.665; n = 150) had no increased risk of cardiac events (HR = 1.19, P = 0.42) or aborted cardiac arrest/sudden cardiac death (HR = 1.58, P = 0.26), and those with the highest tertile scores (>0.665; n = 196) showed significantly increased risk of cardiac events (HR = 3.32, P <0.001) and aborted cardiac arrest/sudden cardiac death (HR = 2.62, P = 0.04). The increased risk in patients with the highest conservation scores was independent of QTc, gender, age, and beta-blocker therapy. CONCLUSIONS: Mutations in highly conserved amino acid residues in the KCNQ1 gene are associated with a significant risk of cardiac events independent of QTc, gender, and beta-blocker therapy Udgivelsesdato: 2009/8

Published
2009

14. Mutations in conserved amino acids in the KCNQ1 channel and risk of cardiac events in type-1 long-QT syndrome

Author

Jons, Christian, Moss, Arthur J, Lopes, Coeli M, McNitt, Scott, Zareba, Wojciech, Goldenberg, Ilan, Qi, Ming, Wilde, Arthur A M, Shimizu, Wataru, Kanters, Jørgen K., Towbin, Jeffrey A, Ackerman, Michael J, Robinson, Jennifer L, Jons, Christian, Moss, Arthur J, Lopes, Coeli M, McNitt, Scott, Zareba, Wojciech, Goldenberg, Ilan, Qi, Ming, Wilde, Arthur A M, Shimizu, Wataru, Kanters, Jørgen K., Towbin, Jeffrey A, Ackerman, Michael J, and Robinson, Jennifer L

Abstract

BACKGROUND: Type-1 long-QT syndrome (LQT1) is caused by mutations in the KCNQ1 gene. The purpose of this study was to investigate whether KCNQ1 mutations in highly conserved amino acid residues within the voltage-gated potassium channel family are associated with an increased risk of cardiac events. METHODS AND RESULTS: The study population involved 492 LQT1 patients with 54 missense mutations in the transmembrane region of the KCNQ1 channel. The amino acid sequences of the transmembrane region of 38 human voltage-gated potassium channels were aligned. An adjusted Shannon entropy score for each amino acid residue was calculated ranging from 0 (no conservation) to 1.0 (full conservation). Cox analysis was used to identify independent factors associated with the first cardiac event (syncope, aborted cardiac arrest, or death). Patients were subcategorized into tertiles by their adjusted Shannon entropy scores. The lowest tertile (score 0-0.469; n = 146) was used as a reference group; patients with intermediate tertile scores (0.470-0.665; n = 150) had no increased risk of cardiac events (HR = 1.19, P = 0.42) or aborted cardiac arrest/sudden cardiac death (HR = 1.58, P = 0.26), and those with the highest tertile scores (>0.665; n = 196) showed significantly increased risk of cardiac events (HR = 3.32, P <0.001) and aborted cardiac arrest/sudden cardiac death (HR = 2.62, P = 0.04). The increased risk in patients with the highest conservation scores was independent of QTc, gender, age, and beta-blocker therapy. CONCLUSIONS: Mutations in highly conserved amino acid residues in the KCNQ1 gene are associated with a significant risk of cardiac events independent of QTc, gender, and beta-blocker therapy Udgivelsesdato: 2009/8

Published
2009

15. In-State Tuition for Undocumented Students in Utah

Author

Robinson, Jennifer L. and Robinson, Jennifer L.

Abstract

Utah is one of the states that allows undocumented students to pay in-state tuition at state colleges and universities. However, there is significant disagreement over whether undocumented students can legally attend a public institution of higher education and pay in-state tuition. This report illustrates two cases have developed in recent years challenging such laws, including lawsuits in Kansas and California. Although both cases were unsuccessful challenges to tuition benefit laws for undocumented students, the debate continues in many state legislatures (Morse 2007).

Published
2007

16. In-State Tuition for Undocumented Students in Utah

Author

Robinson, Jennifer L. and Robinson, Jennifer L.

Abstract

Utah is one of the states that allows undocumented students to pay in-state tuition at state colleges and universities. However, there is significant disagreement over whether undocumented students can legally attend a public institution of higher education and pay in-state tuition. This report illustrates two cases have developed in recent years challenging such laws, including lawsuits in Kansas and California. Although both cases were unsuccessful challenges to tuition benefit laws for undocumented students, the debate continues in many state legislatures (Morse 2007).

Published
2007

17. The Human Affectome

Author

Schiller, Daniela, Yu, Alessandra N.C., Alia-Klein, Nelly, Becker, Susanne, Cromwell, Howard C., Dolcos, Florin, Eslinger, Paul J., Frewen, Paul, Kemp, Andrew H., Pace-Schott, Edward F., Raber, Jacob, Silton, Rebecca L., Stefanova, Elka, Williams, Justin H.G., Abe, Nobuhito, Aghajani, Moji, Albrecht, Franziska, Alexander, Rebecca, Anders, Silke, Aragón, Oriana R., Arias, Juan A., Arzy, Shahar, Aue, Tatjana, Baez, Sandra, Balconi, Michela, Ballarini, Tommaso, Bannister, Scott, Banta, Marlissa C., Barrett, Karen Caplovitz, Belzung, Catherine, Bensafi, Moustafa, Booij, Linda, Bookwala, Jamila, Boulanger-Bertolus, Julie, Boutros, Sydney Weber, Bräscher, Anne-Kathrin, Bruno, Antonio, Busatto, Geraldo, Bylsma, Lauren M., Caldwell-Harris, Catherine, Chan, Raymond C.K., Cherbuin, Nicolas, Chiarella, Julian, Cipresso, Pietro, Critchley, Hugo, Croote, Denise E., Demaree, Heath A., Denson, Thomas F., Depue, Brendan, Derntl, Birgit, Dickson, Joanne M., Dolcos, Sanda, Drach-Zahavy, Anat, Dubljević, Olga, Eerola, Tuomas, Ellingsen, Dan-Mikael, Fairfield, Beth, Ferdenzi, Camille, Friedman, Bruce H., Fu, Cynthia H.Y., Gatt, Justine M., deGelder, Beatrice, Gendolla, Guido H.E., Gilam, Gadi, Goldblatt, Hadass, Gooding, Anne Elizabeth Kotynski, Gosseries, Olivia, Hamm, Alfons O., Hanson, Jamie L., Hendler, Talma, Herbert, Cornelia, Hofmann, Stefan G., Ibanez, Agustin, Joffily, Mateus, Jovanovic, Tanja, Kahrilas, Ian J., Kangas, Maria, Katsumi, Yuta, Kensinger, Elizabeth, Kirby, Lauren A.J., Koncz, Rebecca, Koster, Ernst H.W., Kozlowska, Kasia, Krach, Sören, Kret, Mariska E., Krippl, Martin, Kusi-Mensah, Kwabena, Ladouceur, Cecile D., Laureys, Steven, Lawrence, Alistair, Li, Chiang-shan R., Liddell, Belinda J., Lidhar, Navdeep K., Lowry, Christopher A., Magee, Kelsey, Marin, Marie-France, Mariotti, Veronica, Martin, Loren J., Marusak, Hilary A., Mayer, Annalina V., Merner, Amanda R., Minnier, Jessica, Moll, Jorge, Morrison, Robert G., Moore, Matthew, Mouly, Anne-Marie, Mueller, Sven C., Mühlberger, Andreas, Murphy, Nora A., Muscatello, Maria Rosaria Anna, Musser, Erica D., Newton, Tamara L., Noll-Hussong, Michael, Norrholm, Seth Davin, Northoff, Georg, Nusslock, Robin, Okon-Singer, Hadas, Olino, Thomas M., Ortner, Catherine, Owolabi, Mayowa, Padulo, Caterina, Palermo, Romina, Palumbo, Rocco, Palumbo, Sara, Papadelis, Christos, Pegna, Alan J., Pellegrini, Silvia, Peltonen, Kirsi, Penninx, Brenda W.J.H., Pietrini, Pietro, Pinna, Graziano, Lobo, Rosario Pintos, Polnaszek, Kelly L., Polyakova, Maryna, Rabinak, Christine, HeleneRichter, S., Richter, Thalia, Riva, Giuseppe, Rizzo, Amelia, Robinson, Jennifer L., Rosa, Pedro, Sachdev, Perminder S., Sato, Wataru, Schroeter, Matthias L., Schweizer, Susanne, Shiban, Youssef, Siddharthan, Advaith, Siedlecka, Ewa, Smith, Robert C., Soreq, Hermona, Spangler, Derek P., Stern, Emily R., Styliadis, Charis, Sullivan, Gavin B., Swain, James E., Urben, Sébastien, Van den Stock, Jan, vander Kooij, Michael A., van Overveld, Mark, Van Rheenen, Tamsyn E., VanElzakker, Michael B., Ventura-Bort, Carlos, Verona, Edelyn, Volk, Tyler, Wang, Yi, Weingast, Leah T., Weymar, Mathias, Williams, Claire, Willis, Megan L., Yamashita, Paula, Zahn, Roland, Zupan, Barbra, Lowe, Leroy, Gabriela, Gan, Charlotte F, Huggins, Leonie, Loeffler, Schiller, Daniela, Yu, Alessandra N.C., Alia-Klein, Nelly, Becker, Susanne, Cromwell, Howard C., Dolcos, Florin, Eslinger, Paul J., Frewen, Paul, Kemp, Andrew H., Pace-Schott, Edward F., Raber, Jacob, Silton, Rebecca L., Stefanova, Elka, Williams, Justin H.G., Abe, Nobuhito, Aghajani, Moji, Albrecht, Franziska, Alexander, Rebecca, Anders, Silke, Aragón, Oriana R., Arias, Juan A., Arzy, Shahar, Aue, Tatjana, Baez, Sandra, Balconi, Michela, Ballarini, Tommaso, Bannister, Scott, Banta, Marlissa C., Barrett, Karen Caplovitz, Belzung, Catherine, Bensafi, Moustafa, Booij, Linda, Bookwala, Jamila, Boulanger-Bertolus, Julie, Boutros, Sydney Weber, Bräscher, Anne-Kathrin, Bruno, Antonio, Busatto, Geraldo, Bylsma, Lauren M., Caldwell-Harris, Catherine, Chan, Raymond C.K., Cherbuin, Nicolas, Chiarella, Julian, Cipresso, Pietro, Critchley, Hugo, Croote, Denise E., Demaree, Heath A., Denson, Thomas F., Depue, Brendan, Derntl, Birgit, Dickson, Joanne M., Dolcos, Sanda, Drach-Zahavy, Anat, Dubljević, Olga, Eerola, Tuomas, Ellingsen, Dan-Mikael, Fairfield, Beth, Ferdenzi, Camille, Friedman, Bruce H., Fu, Cynthia H.Y., Gatt, Justine M., deGelder, Beatrice, Gendolla, Guido H.E., Gilam, Gadi, Goldblatt, Hadass, Gooding, Anne Elizabeth Kotynski, Gosseries, Olivia, Hamm, Alfons O., Hanson, Jamie L., Hendler, Talma, Herbert, Cornelia, Hofmann, Stefan G., Ibanez, Agustin, Joffily, Mateus, Jovanovic, Tanja, Kahrilas, Ian J., Kangas, Maria, Katsumi, Yuta, Kensinger, Elizabeth, Kirby, Lauren A.J., Koncz, Rebecca, Koster, Ernst H.W., Kozlowska, Kasia, Krach, Sören, Kret, Mariska E., Krippl, Martin, Kusi-Mensah, Kwabena, Ladouceur, Cecile D., Laureys, Steven, Lawrence, Alistair, Li, Chiang-shan R., Liddell, Belinda J., Lidhar, Navdeep K., Lowry, Christopher A., Magee, Kelsey, Marin, Marie-France, Mariotti, Veronica, Martin, Loren J., Marusak, Hilary A., Mayer, Annalina V., Merner, Amanda R., Minnier, Jessica, Moll, Jorge, Morrison, Robert G., Moore, Matthew, Mouly, Anne-Marie, Mueller, Sven C., Mühlberger, Andreas, Murphy, Nora A., Muscatello, Maria Rosaria Anna, Musser, Erica D., Newton, Tamara L., Noll-Hussong, Michael, Norrholm, Seth Davin, Northoff, Georg, Nusslock, Robin, Okon-Singer, Hadas, Olino, Thomas M., Ortner, Catherine, Owolabi, Mayowa, Padulo, Caterina, Palermo, Romina, Palumbo, Rocco, Palumbo, Sara, Papadelis, Christos, Pegna, Alan J., Pellegrini, Silvia, Peltonen, Kirsi, Penninx, Brenda W.J.H., Pietrini, Pietro, Pinna, Graziano, Lobo, Rosario Pintos, Polnaszek, Kelly L., Polyakova, Maryna, Rabinak, Christine, HeleneRichter, S., Richter, Thalia, Riva, Giuseppe, Rizzo, Amelia, Robinson, Jennifer L., Rosa, Pedro, Sachdev, Perminder S., Sato, Wataru, Schroeter, Matthias L., Schweizer, Susanne, Shiban, Youssef, Siddharthan, Advaith, Siedlecka, Ewa, Smith, Robert C., Soreq, Hermona, Spangler, Derek P., Stern, Emily R., Styliadis, Charis, Sullivan, Gavin B., Swain, James E., Urben, Sébastien, Van den Stock, Jan, vander Kooij, Michael A., van Overveld, Mark, Van Rheenen, Tamsyn E., VanElzakker, Michael B., Ventura-Bort, Carlos, Verona, Edelyn, Volk, Tyler, Wang, Yi, Weingast, Leah T., Weymar, Mathias, Williams, Claire, Willis, Megan L., Yamashita, Paula, Zahn, Roland, Zupan, Barbra, Lowe, Leroy, Gabriela, Gan, Charlotte F, Huggins, and Leonie, Loeffler

Abstract

Over the last decades, the interdisciplinary field of the affective sciences has seen proliferation rather than integration of theoretical perspectives. This is due to differences in metaphysical and mechanistic assumptions about human affective phenomena (what they are and how they work) which, shaped by academic motivations and values, have determined the affective constructs and operationalizations. An assumption on the purpose of affective phenomena can be used as a teleological principle to guide the construction of a common set of metaphysical and mechanistic assumptions—a framework for human affective research. In this capstone paper for the special issue “Towards an Integrated Understanding of the Human Affectome”, we gather the tiered purpose of human affective phenomena to synthesize assumptions that account for human affective phenomena collectively. This teleologically-grounded framework offers a principled agenda and launchpad for both organizing existing perspectives and generating new ones. Ultimately, we hope Human Affectome brings us a step closer to not only an integrated understanding of human affective phenomena, but an integrated field for affective research.

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