Common Time: Music, Empathy, and a Politics of Care

Frameworks for the application of the arts in community settings tend to focus on the development of individuals’ empathy or social bonds. A commensurate level of consideration tends not to be given to the socio-economic, political, and institutional forces and processes that shape such development and to how the arts might help build capacities to manage the impact of such forces and processes. The recognition of persons as interdependent in systems reliant on mutual care has implications for applications of the arts in many specialised domains as well as in general public life. Especially in clinical or social interventions, unrecognised institutional dynamics may introduce or maintain imbalances of power in community and professional practice. Music, as a participatory and temporal activity facilitating social synchrony, can foster dialogic and reciprocal relations in social life. To systematise and study a participatory music activity on an organisational and community level, I designed and implemented two collaborative songwriting programs in clinical and social service settings carried out through the nonprofit organisation, Humans in Harmony. One activity, music corps¸ was a two-month program in New York City involving participants from colleges and social service organisations serving adults with disabilities, at-risk youth, and nursing home residents. Another activity, implemented through a Humans in Harmony chapter at Columbia University Medical Center, paired health professional students with patients in palliative care support groups. Ethnographic observations and participant interviews revealed that engagement in interpersonal processes aligned with a capabilities-informed approach which emphasised social reciprocity, well-being, and flourishing. Moreover, evaluations of the activities through pre- and post-program measures supported a hypothesis of enhancement of interpersonal closeness and in attitudes about empathy and care. Such participatory approaches may offer new frameworks for the application of the arts in response to current geopolitical and cultural challenges.Gates Cambridge Scholarshi

Kaposi’s Sarcoma-Associated Herpesvirus Reduces Cellular Myeloid Differentiation Primary-Response Gene 88 (MyD88) Expression via Modulation of Its RNA

Kaposi’s sarcoma (KS)-associated herpesvirus (KSHV) is a human gammaherpesvirus associated with several human malignancies. The replication and transcription activator (RTA) is necessary and sufficient for the switch from KSHV latency to lytic replication. Interleukin 1 (IL-1) is a major mediator for inflammation and plays an important role in both innate and adaptive immunity. Myeloid differentiation primary response gene 88 (MyD88) is an essential adaptor molecule for IL-1 as well as most Toll-like receptor signaling. In this study, we identified a novel mechanism by which KSHV interferes with host inflammation and immunity. KSHV RTA specifically reduces the steady-state protein levels of MyD88, and physiological levels of MyD88 are downregulated during KSHV lytic replication when RTA is expressed. The N-terminal region of RTA is required for the reduction of MyD88. Additional studies demonstrated that RTA targets MyD88 expression at the RNA level, inhibits RNA synthesis of MyD88, and may bind MyD88 RNA. Finally, RTA inhibits IL-1-mediated activation of NF-B. Because IL-1 is abundant in the KS microenvironment and inhibits KSHV replication, this work may expand our understanding of how KSHV evades host inflammation and immunity for its survival in vivo

Kaposi’s Sarcoma-Associated Herpesvirus Reduces Cellular Myeloid Differentiation Primary-Response Gene 88 (MyD88) Expression via Modulation of Its RNA

Kaposi’s sarcoma (KS)-associated herpesvirus (KSHV) is a human gammaherpesvirus associated with several human malignancies. The replication and transcription activator (RTA) is necessary and sufficient for the switch from KSHV latency to lytic replication. Interleukin 1 (IL-1) is a major mediator for inflammation and plays an important role in both innate and adaptive immunity. Myeloid differentiation primary response gene 88 (MyD88) is an essential adaptor molecule for IL-1 as well as most Toll-like receptor signaling. In this study, we identified a novel mechanism by which KSHV interferes with host inflammation and immunity. KSHV RTA specifically reduces the steady-state protein levels of MyD88, and physiological levels of MyD88 are downregulated during KSHV lytic replication when RTA is expressed. The N-terminal region of RTA is required for the reduction of MyD88. Additional studies demonstrated that RTA targets MyD88 expression at the RNA level, inhibits RNA synthesis of MyD88, and may bind MyD88 RNA. Finally, RTA inhibits IL-1-mediated activation of NF-B. Because IL-1 is abundant in the KS microenvironment and inhibits KSHV replication, this work may expand our understanding of how KSHV evades host inflammation and immunity for its survival in vivo

Kaposi’s Sarcoma-Associated Herpesvirus Reduces Cellular Myeloid Differentiation Primary-Response Gene 88 (MyD88) Expression via Modulation of Its RNA

Kaposi’s sarcoma (KS)-associated herpesvirus (KSHV) is a human gammaherpesvirus associated with several human malignancies. The replication and transcription activator (RTA) is necessary and sufficient for the switch from KSHV latency to lytic replication. Interleukin 1 (IL-1) is a major mediator for inflammation and plays an important role in both innate and adaptive immunity. Myeloid differentiation primary response gene 88 (MyD88) is an essential adaptor molecule for IL-1 as well as most Toll-like receptor signaling. In this study, we identified a novel mechanism by which KSHV interferes with host inflammation and immunity. KSHV RTA specifically reduces the steady-state protein levels of MyD88, and physiological levels of MyD88 are downregulated during KSHV lytic replication when RTA is expressed. The N-terminal region of RTA is required for the reduction of MyD88. Additional studies demonstrated that RTA targets MyD88 expression at the RNA level, inhibits RNA synthesis of MyD88, and may bind MyD88 RNA. Finally, RTA inhibits IL-1-mediated activation of NF-B. Because IL-1 is abundant in the KS microenvironment and inhibits KSHV replication, this work may expand our understanding of how KSHV evades host inflammation and immunity for its survival in vivo

Kaposi’s Sarcoma-Associated Herpesvirus Reduces Cellular Myeloid Differentiation Primary-Response Gene 88 (MyD88) Expression via Modulation of Its RNA

Kaposi’s sarcoma (KS)-associated herpesvirus (KSHV) is a human gammaherpesvirus associated with several human malignancies. The replication and transcription activator (RTA) is necessary and sufficient for the switch from KSHV latency to lytic replication. Interleukin 1 (IL-1) is a major mediator for inflammation and plays an important role in both innate and adaptive immunity. Myeloid differentiation primary response gene 88 (MyD88) is an essential adaptor molecule for IL-1 as well as most Toll-like receptor signaling. In this study, we identified a novel mechanism by which KSHV interferes with host inflammation and immunity. KSHV RTA specifically reduces the steady-state protein levels of MyD88, and physiological levels of MyD88 are downregulated during KSHV lytic replication when RTA is expressed. The N-terminal region of RTA is required for the reduction of MyD88. Additional studies demonstrated that RTA targets MyD88 expression at the RNA level, inhibits RNA synthesis of MyD88, and may bind MyD88 RNA. Finally, RTA inhibits IL-1-mediated activation of NF-B. Because IL-1 is abundant in the KS microenvironment and inhibits KSHV replication, this work may expand our understanding of how KSHV evades host inflammation and immunity for its survival in vivo

Kaposi’s Sarcoma-Associated Herpesvirus Reduces Cellular Myeloid Differentiation Primary-Response Gene 88 (MyD88) Expression via Modulation of Its RNA

Kaposi’s sarcoma (KS)-associated herpesvirus (KSHV) is a human gammaherpesvirus associated with several human malignancies. The replication and transcription activator (RTA) is necessary and sufficient for the switch from KSHV latency to lytic replication. Interleukin 1 (IL-1) is a major mediator for inflammation and plays an important role in both innate and adaptive immunity. Myeloid differentiation primary response gene 88 (MyD88) is an essential adaptor molecule for IL-1 as well as most Toll-like receptor signaling. In this study, we identified a novel mechanism by which KSHV interferes with host inflammation and immunity. KSHV RTA specifically reduces the steady-state protein levels of MyD88, and physiological levels of MyD88 are downregulated during KSHV lytic replication when RTA is expressed. The N-terminal region of RTA is required for the reduction of MyD88. Additional studies demonstrated that RTA targets MyD88 expression at the RNA level, inhibits RNA synthesis of MyD88, and may bind MyD88 RNA. Finally, RTA inhibits IL-1-mediated activation of NF-B. Because IL-1 is abundant in the KS microenvironment and inhibits KSHV replication, this work may expand our understanding of how KSHV evades host inflammation and immunity for its survival in vivo

Reconsidering Empathy: An Interpersonal Approach and Participatory Arts in the Medical Humanities.

Funder: Gates Cambridge Trust; doi: http://dx.doi.org/10.13039/501100005370The decline of empathy among health professional students, highlighted in the literature on health education, is a concern for medical educators. The evidence suggests that empathy decline is likely to stem more from structural problems in the healthcare system rather than from individual deficits of empathy. In this paper, we argue that a focus on direct empathy development is not effective and possibly detrimental to justice-oriented aims. Drawing on critical and narrative theory, we propose an interpersonal approach to enhance empathic capacities that is centered on constructive and transformative interactions which integrates the participatory arts and involves both patients and health professional students. We describe and evaluate a program where patients and students create collaborative, original songs. Interviews and a focus group revealed interactional processes summarized in four themes: reciprocal relationships, interactions in the community, joint goal, and varied collaboration. There was a significant enhancement of positive attitudes about care post-program amongst health professional students. The interpersonal approach may be a preliminary framework for the medical humanities to shift away from a focus on direct empathy development and further towards participatory, co-creative, and justice-oriented approaches to enhance health and thereby empathic capabilities

Reconsidering Empathy: An Interpersonal Approach and Participatory Arts in the Medical Humanities.

Funder: Gates Cambridge Trust; doi: http://dx.doi.org/10.13039/501100005370The decline of empathy among health professional students, highlighted in the literature on health education, is a concern for medical educators. The evidence suggests that empathy decline is likely to stem more from structural problems in the healthcare system rather than from individual deficits of empathy. In this paper, we argue that a focus on direct empathy development is not effective and possibly detrimental to justice-oriented aims. Drawing on critical and narrative theory, we propose an interpersonal approach to enhance empathic capacities that is centered on constructive and transformative interactions which integrates the participatory arts and involves both patients and health professional students. We describe and evaluate a program where patients and students create collaborative, original songs. Interviews and a focus group revealed interactional processes summarized in four themes: reciprocal relationships, interactions in the community, joint goal, and varied collaboration. There was a significant enhancement of positive attitudes about care post-program amongst health professional students. The interpersonal approach may be a preliminary framework for the medical humanities to shift away from a focus on direct empathy development and further towards participatory, co-creative, and justice-oriented approaches to enhance health and thereby empathic capabilities

Sleep-promoting neurons remodel their response properties to calibrate sleep drive with environmental demands

Falling asleep at the wrong time can place an individual at risk of immediate physical harm. However, not sleeping degrades cognition and adaptive behavior. To understand how animals match sleep need with environmental demands, we used live-brain imaging to examine the physiological response properties of the dorsal fan-shaped body (dFB) following interventions that modify sleep (sleep deprivation, starvation, time-restricted feeding, memory consolidation) in Drosophila. We report that dFB neurons change their physiological response-properties to dopamine (DA) and allatostatin-A (AstA) in response to different types of waking. That is, dFB neurons are not simply passive components of a hard-wired circuit. Rather, the dFB neurons intrinsically regulate their response to the activity from upstream circuits. Finally, we show that the dFB appears to contain a memory trace of prior exposure to metabolic challenges induced by starvation or time-restricted feeding. Together, these data highlight that the sleep homeostat is plastic and suggests an underlying mechanism

TLR-TRIF Pathway Enhances the Expression of KSHV Replication and Transcription Activator

Background: Host innate immunity is against virus infection and replication. Results: Toll-like receptor 3 activation leads to enhanced expression of a key Kaposi’s sarcoma-associated herpesvirus (KSHV) protein. Conclusion: KSHV uses host Toll-like receptor pathway to augment its critical gene expression. Significance: A virus may usurp host innate immunity for its own benefits