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The text reviews Drew Leder's book "The Healing Body: Creative Responses to Illness, Aging, and Affliction," which explores the intersection of philosophy and the care of the body. Leder's work, rooted in critical phenomenology, delves into various healing strategies drawn from philosophical sources like Husserl and Merleau-Ponty, as well as personal experiences and medical training. The book presents a range of strategies, from objectification to interoception, and concludes with a speculative chapter on non-Western inspirations for understanding the body as a channel for transpersonal awareness. Leder's approach aims to promote engagement and reflection on healing practices beyond the text, embodying the essence of philosophical inquiry. [Extracted from the article]

Phenomenology's return to lived experience and "to the things themselves" is often contrasted with the synthesized perspective of science and its "view from nowhere." The extensive use of neuropsychological case reports in Merleau-Ponty's Phenomenology of Perception, however, suggests that the relationship between phenomenology and science is more complex than a sheer opposition, and a fruitful one for the praxis of medicine. Here, I propose a new reading of how Merleau-Ponty justifies his use of Adhémar Gelb and Kurt Goldstein's reports on Johann Schneider for his phenomenology of embodied perception. I argue that for Merleau-Ponty these neuropsychological case reports represent a coherent deformation of the intercorporeally expressed existence of Schneider that through speech fall again onto the common ground of perception, thereby allowing Merleau-Ponty to understand, in the equivalent sense delivered by language, Schneider's total being and fundamental illness. I then discuss what Merleau-Ponty's method implies for a phenomenological praxis of medicine, and for the role of science in this praxis. [ABSTRACT FROM AUTHOR]

Older organs represent an untapped potential to close the gap between demand and supply in organ transplantation but are associated with age-specific responses to injury and increased immunogenicity, thereby aggravating transplant outcomes. Here we show that cell-free mitochondrial DNA (cf-mt-DNA) released by senescent cells accumulates with aging and augments immunogenicity. Ischemia reperfusion injury induces a systemic increase of cf-mt-DNA that promotes dendritic cell-mediated, age-specific inflammatory responses. Comparable events are observed clinically, with the levels of cf-mt-DNA elevated in older deceased organ donors, and with the isolated cf-mt-DNA capable of activating human dendritic cells. In experimental models, treatment of old donor animals with senolytics clear senescent cells and diminish cf-mt-DNA release, thereby dampening age-specific immune responses and prolonging the survival of old cardiac allografts comparable to young donor organs. Collectively, we identify accumulating cf-mt-DNA as a key factor in inflamm-aging and present senolytics as a potential approach to improve transplant outcomes and availability. Organ transplantation involving aged donors is often confounded by reduced post-transplantation organ survival. By studying both human organs and mouse transplantation models, here the authors show that pretreating the donors with senolytics to reduce mitochondria DNA and pro-inflammatory dendritic cells may help promote survival of aged organs. [ABSTRACT FROM AUTHOR]