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Background: Racial bias in medical care is a significant public health issue, with increased focus on microaggressions and the quality of patient-provider interactions. Innovations in training interventions are needed to decrease microaggressions and improve provider communication and rapport with patients of color during medical encounters., Methods: This paper presents a pilot randomized trial of an innovative clinical workshop that employed a theoretical model from social and contextual behavioral sciences. The intervention specifically aimed to decrease providers' likelihood of expressing biases and negative stereotypes when interacting with patients of color in racially charged moments, such as when patients discuss past incidents of discrimination. Workshop exercises were informed by research on the importance of mindfulness and interracial contact involving reciprocal exchanges of vulnerability and responsiveness. Twenty-five medical student and recent graduate participants were randomized to a workshop intervention or no intervention. Outcomes were measured via provider self-report and observed changes in targeted provider behaviors. Specifically, two independent, blind teams of coders assessed provider emotional rapport and responsiveness during simulated interracial patient encounters with standardized Black patients who presented specific racial challenges to participants., Results: Greater improvements in observed emotional rapport and responsiveness (indexing fewer microaggressions), improved self-reported explicit attitudes toward minoritized groups, and improved self-reported working alliance and closeness with the Black standardized patients were observed and reported by intervention participants., Conclusions: Medical providers may be more likely to exhibit bias with patients of color in specific racially charged moments during medical encounters. This small-sample pilot study suggests that interventions that directly intervene to help providers improve responding in these moments by incorporating mindfulness and interracial contact may be beneficial in reducing racial health disparities.

Functional Analytic Psychotherapy (FAP; Kohlenberg & Tsai, 1991) is a transdiagnostic approach to outpatient psychotherapy that presented guidelines to instantiate the behavioral principle of natural, social reinforcement applied to idiographic behavioral targets within a genuine and authentic psychotherapy relationship. We present the first comprehensive review of research on FAP, including qualitative studies, uncontrolled and controlled single-case designs, group designs, and studies on training therapists in FAP. We conclude that current research support for FAP is promising but not sufficient to justify claims that FAP is research-supported for specific psychiatric disorders. There is stronger support for FAP's mechanism of therapist-as-social reinforcer: FAP techniques, when appropriately applied to idiographically defined behavioral problems-primarily in the realm of social functioning-produce positive change in those behaviors., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Background and Objectives: Our understanding of how Behavioral Activation (BA) for depression works is limited. BA is theorized to lead to changes in depression through changes in activation. While distal support for activation as a mechanism has been obtained, more research is needed before definitive conclusions can be drawn. Research on mechanism should consider the appropriate time-frame for examining changes in the theorized mechanism variable and whether the proposed mechanism is expected to exert causal influence in all BA cases. These issues were considered in the current study in which a post-hoc analysis was conducted to explore BA's mechanism using single-subject data obtained at each session during the course of treatment., Methods: Activation and depression data were obtained from a randomized-controlled trial of BA for Latinos (BAL) compared to treatment-as-usual (TAU). Cross-lagged correlations were computed to test whether activation changes preceded, co-occurred with, or lagged behind changes in depression in a sample of 21 clients (BAL n = 14; TAU n = 7). Differences among participants based on activation-depression patterns were examined., Results: For 79% of the BAL sample, changes in activation preceded or co-occurred with changes in depression, while no clients in the TAU sample evidenced this pattern., Limitations: Use of more proximal and objective measures of the constructs of interest and a higher dosage of BA may have served as a stronger test of the treatment's mechanism., Conclusions: More time-sensitive measurement of changes in variables of interest is needed., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

High doses of the nicotinic acetylcholine receptor (nAChR) antagonist mecamylamine can elicit somatic signs resembling those associated with nicotine withdrawal in nicotine-naïve adult rats. Understanding this phenomenon, and its possible modulation by acute nicotine and age, could inform the use of mecamylamine as both an experimental tool and potential pharmacotherapy for tobacco dependence and other disorders. This study evaluated the ability of high-dose mecamylamine to elicit somatic signs in adolescent rats, and the potential for acute nicotine pretreatment to potentiate this effect as previously reported in adults. Single or repeated injections of mecamylamine (1.5 or 3.0 mg/kg, s.c.) elicited somatic signs in nicotine-naïve adolescents, but this effect was not influenced by 2 h pretreatment with acute nicotine (0.5 mg/kg, s.c.). In an initial evaluation of the effects of age in this model, mecamylamine (2.25 mg/kg, s.c.) elicited somatic signs in nicotine-naïve adolescents and adults. This effect was modestly enhanced following acute nicotine injections in adults but not in adolescents, even when a higher nicotine dose (1.0 rather than 0.5 mg/kg, s.c.) was used in adolescents to account for age differences in nicotine pharmacokinetics. These studies are the first to show that mecamylamine elicits somatic signs in nicotine-naïve adolescent rats, an effect that should be considered when designing and interpreting studies examining effects of high doses of mecamylamine in adolescents. Our findings also provide preliminary evidence that these signs may be differentially modulated by acute nicotine pretreatment in adolescents versus adults.

Development of medications that attenuate symptoms of nicotine withdrawal may be useful for facilitating smoking cessation. The neuropeptide oxytocin (OXY) decreases withdrawal signs and other addiction-related effects of several drugs of abuse in animals, but has not been examined in a preclinical model of nicotine addiction. The goal of this study was to examine the effects of OXY on nicotine withdrawal in rats, measured as increases in somatic signs and elevations in intracranial self-stimulation (ICSS) thresholds (anhedonia-like behavior) during antagonist-precipitated withdrawal from a chronic nicotine infusion. Effects of OXY on baseline ICSS thresholds in non-dependent rats were also evaluated. OXY (0.06 - 1.0mg/kg, i.p.) blocked withdrawal-induced elevations in somatic signs in nicotine-dependent rats without affecting somatic signs in non-dependent rats. In contrast, OXY did not affect nicotine withdrawal-induced elevations in ICSS thresholds. Relatively high doses of OXY (0.75 or 2.0mg/kg) elevated baseline ICSS thresholds in non-dependent rats. These findings demonstrate that OXY blocks somatic signs but not elevations in ICSS thresholds during antagonist-precipitated nicotine withdrawal. The ability of higher OXY doses to elevate baseline ICSS thresholds in non-dependent rats may reflect an aversive and/or motoric effect. These data suggest that OXY-based medications may be useful for treating the somatic component of the nicotine withdrawal syndrome, but may not be effective in attenuating withdrawal-induced anhedonia., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Rationale: The ability of nicotine to induce dependence (result in a withdrawal syndrome) is typically thought to require long-term, daily smoking. Emerging evidence suggests that symptoms of nicotine withdrawal may occur following only a few cigarettes. Whether acute exposure to nicotine can induce dependence in animals has not been well established., Objective: The objective of this paper is to examine whether the nicotinic acetylcholine receptor antagonist mecamylamine elicits withdrawal-like signs in rats following acute nicotine exposure., Methods and Results: Mecamylamine (3.0 mg/kg, s.c.) administered ≈2 h after a single dose of nicotine (0.5 mg/kg, s.c.) elicited increases in intracranial self-stimulation (ICSS) thresholds and somatic signs, two well-established effects of withdrawal from long-term (chronic) nicotine exposure. The magnitude of these effects remained constant across five daily test sessions. A lower dose of mecamylamine (1.5 mg/kg, s.c.) had little or no effect on ICSS thresholds or somatic signs following acute nicotine exposure, but precipitated robust increases in these measures during a chronic nicotine infusion. Finally, rats exhibited a small increase in ICSS thresholds over time following a single nicotine injection (0.5 mg/kg, s.c.), possibly reflecting a modest spontaneous withdrawal-like effect., Conclusions: Mecamylamine elicited withdrawal-like signs in rats following a single dose of nicotine. The different effects of mecamylamine 1.5 mg/kg following acute versus chronic nicotine exposure supports the notion that these models simulate the early and more advanced stages of nicotine dependence, respectively. While further optimization and validation of these models is necessary, they may provide a novel approach for studying the earliest stages of nicotine dependence.