Shifting the discourse on disability: Moving to an inclusive, intersectional focus.

Individuals with disabilities comprise one of the largest marginalized groups in the United States and experience systemic barriers in health care. In Westernized communities, disability has historically been conceptualized via the medical model, which considers disability an individual-level deficit in need of correction. Although other models of disability (e.g., social model) have been developed to address the medical model's ableist shortcomings, these fail to consistently acknowledge intersectionality. Specifically, these models fail to consider that (a) a disabled individual may hold other marginalized or oppressed identities and (b) these intersecting oppressions may exacerbate health inequities. Intersectionality, which originates from Black feminist literature, describes the ways that systems of power and oppression (e.g., racism, sexism) interact to form an individual's unique experience. To date, the intersection of disability and other marginalized identities has been neglected in psychology and related fields, leaving little guidance for how scholars, clinicians, and other stakeholders can address disability via an intersectional lens. The present article discusses how a disability-affirmative, intersectional approach can serve as a strategy for challenging and reforming oppressive systems across the field of psychology. We assert that, ultimately, this approach has the potential to optimize and expand access to equitable, inclusive mental health care, and we propose actionable steps psychologists can take in research, practice, training, and policy in pursuit of this aim. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

The Relation of Parental Expressed Emotion, Parental Affiliate Stigma, and Typically-developing Sibling Internalizing Behavior in Families with a Child with ASD.

Caregivers of children with autism spectrum disorder (ASD) experience greater stress, expressed emotion (EE), and affiliate stigma than caregivers of children without ASD. Siblings of children with ASD often experience greater negative functioning than siblings of individuals without ASD. The current study found significant interrelations among symptom severity and externalizing behavior in children with ASD; parental stress, affiliate stigma, and EE; and TD sibling internalizing behavior. In addition, certain subcomponents of affiliate stigma predicted unique variance in EE and TD sibling internalizing behavior. Findings may increase understanding of psychosocial functioning in families with children with ASD and allow clinicians to improve outcomes for all family members. Limitations of the study included self-report data, limited sample diversity, and a cross-sectional design.

A prospective study of the incidence and open-label treatment of interferon-induced major depressive disorder in patients with hepatitis C.

Interferon (IFN) therapy has been associated with the development of Major Depressive Disorder (MDD) when given to patients with hepatitis C (HCV). The incidence, time course, risk factors, and treatment of IFN-induced MDD are poorly understood. The objectives of the present study were to determine the incidence of IFN-induced MDD, as well as to determine the efficacy of open-label antidepressant treatment, in particular selective serotonin reuptake inhibitors (SSRIs) for IFN-induced MDD. Thirty-nine HCV patients on IFN therapy were monitored weekly using the Beck Depression Inventory (BDI). Those who became depressed were treated with citalopram, a SSRI antidepressant. Main outcome measures included the incidence of IFN-induced MDD, as well as response rates to antidepressants in those patients who developed IFN-induced MDD. Our results showed that 13 of 39 patients (33%) developed IFN-induced MDD. There were no differences in age, gender, past history of MDD, or substance use between those who became depressed and those who did not. However, there were significantly fewer African American patients in the depressed group. Patients who developed IFN-induced MDD were on IFN therapy for an average of 12.1 weeks prior to the development of MDD. Eleven of 13 patients (85%) were responsive to antidepressant treatment. We conclude that IFN-induced MDD is common in HCV patients. Health care providers should follow IFN-treated HCV patients for the development of MDD, particularly between the 2nd and 5th months of IFN therapy. SSRIs, in particular citalopram, are an effective treatment for IFN-induced depression in HCV patients.

Effect of short-term treatment with a monoclonal antibody to P-selectin on balloon catheter-induced: intimal hyperplasia, re-endothelialization, and attenuation of endothelial-dependent relaxation.

The effects of an anti-P-selectin monoclonal antibody (MAb, PB1.3; Cytel Corporation) on neoendothelialization; neoendothelial function, as evidenced by acetylcholine-induced relaxation (nitric oxide formation); and intimal hyperplasia following embolectomy catheter-induced injury to the rabbit thoracic aorta were investigated. Catheter injury was induced in two groups of New Zealand White rabbits. One group received no treatment, while the second group received short-term treatment with the MAb (i.p., immediately before and 12 h after induction of catheter injury). A third group underwent a sham operation and served as uninjured controls. Following sacrifice at 2 weeks after injury, aortic rings were assessed for degree of intimal hyperplasia, neoendothelial morphology (scanning electron microscopy), and acetylcholine-induced relaxation. Aortic tissue from catheter-injured animals that received treatment exhibited improved neoendothelial morphology, as compared with tissue from untreated but catheterized animals; however, no statistically significant attenuation of the hyperplastic response or improvement in the attenuated neoendothelial-dependent acetylcholine-induced relaxant response that is characteristic of neoendothelium that forms after catheter denudation was observed. These data suggest that short-term attenuation of P-selectin-mediated polymorphonuclear leukocyte (PMN)/endothelium, PMN/platelet interactions, and/or thrombin formation beneficially affects neoendothelialization of the vascular wall following balloon catheter-induced injury.

L-arginine inhibits balloon catheter-induced intimal hyperplasia.

Intimal hyperplasia that results from therapeutic revascularization is an important etiologic factor in the failure of these procedures (i.e., restenosis). Drugs which donate nitric oxide have been shown to inhibit the proliferation of vascular smooth muscle cells in vitro. We tested the hypothesis that administration of L-arginine (0.5 g/kg/day), the precursor of nitric oxide, would inhibit development of intimal hyperplasia following balloon catheter-induced injury. L-arginine administration from 2 days prior to and 2 weeks following catheter-induced injury to the rabbit thoracic aorta attenuated the development of intimal hyperplasia by 39% as compared with untreated controls. This effect was due to decreased intimal area. The effect of L-arginine was inhibited by co-administration of an inhibitor of nitric oxide synthase, NG-nitro-L-arginine methyl ester (0.5 g/kg/day). These data demonstrate that L-arginine attenuates intimal hyperplasia and suggest that the mechanism for this effect is the conversion of L-arginine to nitric oxide.