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An affective approach to culture and cognition may hold the key to uniting findings across experimental psychology and, eventually, the human sciences. Many accounts of the human mind concentrate on the brain’s computational power, yet for nearly 200 million years before humans developed a capacity to reason the emotional centers of the brain were running the show. To attain a clearer picture of the evolution of mind, we challenge the cognitivist and behaviorist paradigms in psychology by exploring how the emotional capacities that we share with other animals saturate every thought and perception. Many of the distinctive social and cultural behaviors of our species, including, bonding, social learning, hierarchy, decision-making, self-identity, can be integrated if we use an affective approach.

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Drawing from empirical literature on ecological psychology, affective neuroscience, and philosophy of mind, this article describes a model of affect-as-motivation in the intentional bond between organism and environment. An epistemological justification for the motivating role of emotions is provided through articulating the perceptual context of emotions as embodied, situated, and functional, and positing perceptual salience as a biasing signal in an affordance competition model. The motivational role of affect is pragmatically integrated into discussions of action selection in the neurosciences.

The cultural project is a therapeutic melding of emotion, symbols, and knowledge. In this paper, I describe how spiritual emotions engendered through encounters in imaginative culture enable fixation of metaphysical beliefs. Evolved affective systems are domesticated through the social practices of imaginative culture so as to adapt people to live in culturally defined cooperative groups. Conditioning, as well as tertiary-level cognitive capacities such as symbols and language are enlisted to bond groups through the imaginative formats of myth and participatory ritual. These cultural materializations can be shared by communities both synchronically and diachronically in works of art. Art is thus a form of self-knowledge that equips us with a motivated understanding of ourselves in the world. In the sacred state produced through the arts and in religious acts, the sense of meaning becomes noetically distinct because affect infuses the experience of immanence, and one's memory of it, with salience. The quality imbued thereby makes humans attentive to subtle signs and broad “truths.” Saturated by emotions and the experience of alterity in the immanent encounter of imaginative culture, information made salient in the sacred experience can become the basis for belief fixation. Using examples drawn from mimetic arts and arts of immanence, I put forward a theory about how sensible affective knowledge is mediated through affective systems, direct perception, and the imagination.

Metaphors of mind and their elaboration into models serve a crucial explanatory role in psychology. In this article, an attempt is made to describe how biology and engineering provide the predominant metaphors for contemporary psychology. A contrast between the discursive and descriptive functions of metaphor use in theory construction serves as a platform for deliberation upon the pragmatic consequences of models derived therefrom. The conclusion contains reflections upon the possibility of an integrative interdisciplinary psychology.

BACKGROUND AND OBJECTIVE: To evaluate whether brimonidine can prevent cytotoxicity in human retinal pigment epithelial (RPE) and Müller (MIO) cells after exposure to amyloid-beta 1–42 (Aβ42). MATERIALS AND METHODS: An in vitro model of geographic atrophy (GA), which is an end-stage complication of age-related macular degeneration (AMD), simulated with the application of Aβ42 in cell culture. RPE and MIO cells were pretreated with brimonidine for 6 hours, then exposed to 10μM Aβ42 for 24 hours. Several concentrations (one time [1×], two times [2×], and five times [5×]) of brimonidine were used to assess for a dose-related effect. Assays were immediately run following the treatment period. 2′,7′-Dichlorofluorescein diacetate was used to assess reactive oxygen species production, the MTT assay was used to assess cell viability, and the JC-1 dye assay was used to assess mitochondrial membrane potential. The main outcome measures were reactive oxygen species (ROS) production, cell viability, and mitochondrial membrane potential (ΔΨm) of RPE and MIO cells following the treatment phase. RESULTS: High-dose (5×) brimonidine was capable of reducing ROS production in RPE and MIO cells with exposure to Aβ42. The application of Aβ42 alone did not trigger a rise in ROS production. Brimonidine was unable to rescue cell viability and ΔΨm after exposure to Aβ42 in both cell cultures. Instead, high-dose (5×) brimonidine appeared to increase the toxicity to cell viability and ΔΨm in cultures exposed to Aβ42. However, this was not due to medication toxicity alone, because high-dose (5×) brimonidine without exposure to Aβ42 did not affect the cell viability in both cell types. CONCLUSION: Brimonidine may have a role in preventing oxidative cellular injury in AMD. However, this role does not appear to translate into protection against some of the cytotoxic effects observed from this in vitro model of GA. In this cellular model of GA, brimonidine is able to reduce oxidative stress but is unable to rescue cell viability or prevent mitochondrial dysfunction. [ Ophthalmic Surg Lasers Imaging Retina . 2018;49:S23–S28.]

Haloperidol is a first-generation antipsychotic butyrophenone that is lipophilic, readily absorbed, and extensively metabolized in the liver. The occurrence of elevated liver enzymes with haloperidol is reported to be 2.4% with cases generally occurring in the setting of chronic use. In this case, we present a patient who developed elevated liver enzymes 1-2 days after starting haloperidol treatment on two separate occasions and in the context of negative hepatic viral and autoimmune serology. Liver enzymes consistently had alanine transaminase > aspartate transaminase and peaked at 288 U/L prior to discontinuation of the medication. The patient was taken off haloperidol after serology resulted and clozapine regimen started. He was able to tolerate clozapine well with recovery of his transaminitis and psychiatric stabilization.