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In this virtual special issue (VSI) we curate and reflect upon 22 articles on formal youth mentoring previously published in the American Journal of Community Psychology (AJCP). First, we provide historical context and highlight AJCP's 2002 special issue on mentoring, which played an important role in establishing youth mentoring as a vibrant area of research. Next, we review and discuss findings from subsequent AJCP studies in three interrelated lines of inquiry: (1) the importance of facilitating high-quality mentoring relationships; (2) associations among youth's presenting needs, relationship quality, and outcomes; and (3) program practices leading to stronger, more impactful relationships. Throughout, we highlight and expand upon critical commentary from AJCP contributors, calling on the field to move away from paternalistic models that overly localize risk with youth and families without interrogating structural oppression. Our recommendations include: (1) centering critical consciousness, racial equity, and social justice in program curricula and mentor trainings; (2) respectfully engaging grassroots programs developed for and by communities of color that are underrepresented in research; (3) making meaningful efforts to recruit mentors from marginalized communities and removing barriers to their participation; and (4) examining youth's racial, ethnic, and other areas of identity development processes during mentoring., (© 2023 Society for Community Research and Action.)

The aim of this study was to examine contextual antecedents and well-being indicators associated with children's and adolescents' access to supportive nonparent adults (SNPAs). We conducted secondary data analysis of the 2016 National Survey of Children's Health, a large-scale caregiver-reported survey. We analyzed separate subsamples of children (ages 6-11, n = 12,849) and adolescents (ages 12-17, n = 17,628). For both children and adolescents, markers of social advantage (e.g., White race, nonimmigrant families, neighborhood/community capital, access to extracurriculars) increased the likelihood of having SNPAs, according to parent or caregiver reports. Familial factors (e.g., parent participation in school and extracurricular activities) were stronger predictors of SNPA presence for children. Access to SNPAs was negatively associated with social difficulties among children and adolescents and positively associated with curiosity and overall health among adolescents. In conclusion, disadvantage across multiple ecological levels impairs children's and adolescents' access to SNPAs. Having an SNPA may be associated with some aspects of youth well-being, although causality cannot be inferred in cross-sectional data., (© 2023 Wiley Periodicals LLC.)

The goal of this study was to identify distinct profiles among first-generation college students' mentoring relationships based on interpersonal characteristics, provision of college-related support, and mentors' educational capital. First-year, first-generation undergraduates (n = 176) identified up to six mentors, rating various relationship characteristics, the types and degrees of college-related support each mentor provided, and each mentor's level of educational attainment. Ratings were used as indicators in a multilevel latent profile analysis among mentoring relationships (n = 254), accounting for clustering of multiple mentors within individual participants. A 3-profile solution best fit the data. Profiles were distinguished by closeness, frequency of contact, degree of college-related support provided, and mentors' educational attainment. Mentors with high educational attainment ("High-Capital Mentors") provided the most support for college-related issues, even with relatively infrequent contact. During their transition to higher education, first-generation college students appear to receive more active mentoring from adults with educational capital, although other adults may serve important functions not captured by the college-specific measures used in this study., (© 2023 Wiley Periodicals LLC.)

Over the past two decades, research and clinical resources on clinical high risk (CHR) for psychosis have both expanded, with goals to better understanding risk and protective factors on the course of illness and inform early intervention efforts. However, some studies have highlighted potential sampling bias among CHR research studies, raising questions about generalizability of findings and inequitable access to early detection and intervention. The current study sought to explore these questions by comparing 94 participants in a CHR longitudinal monitoring study across North America (NAPLS-2) who converted to syndromal psychosis over the course of the study (CHR-CV) to 171 participants who presented for treatment at a localized first-episode psychosis service (FES) after converting. CHR-CV participants were significantly more likely to be White and have a college-educated parent, while FES participants were more likely to be Black and first- or second-generation immigrants. On average, CHR-CV participants were younger at onset of attenuated positive symptoms, had a longer period of attenuated symptoms prior to conversion, and were more likely to be treated with antipsychotics prior to conversion compared to those in FES programs. After controlling for time since conversion, CHR-CV participants had higher global functioning and were less likely to have experienced recent psychiatric hospitalization. Findings suggest that CHR research and FES clinics may be sampling from different populations, although conclusions are limited by inconsistent sampling frames and methods. Integrated early detection that targets defined geographic catchments may deliver more epidemiologically representative samples to both CHR research and FES., Competing Interests: Declaration of competing interest We have no conflicts of interest to declare., (Copyright © 2023 Elsevier B.V. All rights reserved.)

The demand for child mental health services, including those provided by psychologists, counselors, and social workers, exceeds the supply. This trend is expected to continue or worsen unless there are substantial structural changes in how mental health services are provided. We propose a framework for paraprofessional youth mentors, defined as a subgroup of professionally supervised, non-expert volunteer or paid mentors to whom aspects of professional helping tasks are delegated. Our proposal is aligned with historical and modern solutions to scaling mental health services, and this framework could simultaneously increase the number of youth receiving evidence-based mental health services and reduce the burden on existing systems of care. The framework defines three plausible tasks for paraprofessional mentors: (1) reducing barriers to mental health service, (2) increasing engagement in services, and (3) providing direct services. The safety and effectiveness of these task-shifting efforts will hinge on competency-based training and evaluation, supervision by professionals, and documentation of services rendered, all of which the field of youth mentoring currently lacks. We describe several requisite scientific, institutional, and regulatory advances that will be necessary to realize this variant of youth mentoring for a subgroup of youth who are presenting for assistance with mental health problems., (© 2021 Society for Community Research and Action.)

Background and Aims: The overall goal of this study was to determine the effects of MnSOD-deficiency on vascular structure and function in hypercholesterolemic mice. Previous work suggested that increases in mitochondrial-derived reactive oxygen species (ROS) can exacerbate vascular dysfunction and atherosclerosis. It remains unknown, however, how MnSOD-deficiency and local compensatory mechanisms impact atherosclerotic plaque composition., Methods and Results: We used a hypercholesterolemic mouse model (ldlr -/- /ApoB 100/100 ; LA), either wild-type for MnSOD (LA-MnSOD +/+ ) or MnSOD-haploinsufficient (LA-MnSOD +/- ), that was fed a western diet for either 3 or 6 months. Consistent with previous reports, reductions of MnSOD did not significantly worsen hypercholesterolemia-induced endothelial dysfunction in the aorta. Critically, dramatic impairment of vascular function with Nox2 inhibition or catalase pretreatment suggested the presence of a significant NO-independent vasodilatory mechanism in LA-MnSOD +/- mice (e.g. H 2 O 2 ). Despite remarkably well-preserved overall vascular relaxation, loss of mitochondrial antioxidant capacity in LA-MnSOD +/- mice significantly increased osteogenic signalling and vascular calcification compared to the LA-MnSOD +/+ littermates., Conclusions: Collectively, these data are the first to suggest that loss of mitochondrial antioxidant capacity in hypercholesterolemic mice results in dramatic upregulation of NADPH oxidase-derived H 2 O 2 . While this appears to be adaptive in the context of preserving overall endothelium-dependent relaxation and vascular function, these increases in ROS appear to be remarkably maladaptive and deleterious in the context of vascular calcification., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2021. Published by Elsevier B.V.)

Background: While a small number of studies suggest that oxidative stress has an influential role in fibrocalcific aortic valve disease (FCAVD), the roles of specific antioxidant enzymes in progression of this disease remain poorly understood. Here, we focused on selectively altering mitochondrial-derived oxidative stress-which has been shown to alter progression of a myriad of age-associated diseases-on the progression of molecular and phenotypic drivers of FCAVD. Methods: We generated low-density lipoprotein receptor-deficient, Apolipoprotein B100-only mice (LA) that were either haploinsufficient for MnSOD ( LA-MnSOD +/- ) or genetically overexpressing MnSOD ( LA-MnSOD Tg /0 ). After 6 months of Western diet feeding, mice underwent echocardiography to assess valvular and cardiac function and tissues were harvested. Quantitative-RT PCR, immunohistochemistry, and histopathology were used to measure changes in molecular pathways related to oxidative stress, calcification, and fibrosis. Results: While reductions in MnSOD increased oxidative stress, there was not an overt phenotypic effect of MnSOD deficiency on valvular and cardiac function in LA-MnSOD +/- mice. While markers of canonical bone morphogenetic protein signaling tended to increase in valve tissue from LA-MnSOD +/- (e.g., p-SMAD1/5/8 and osterix), we did not observe statistically significant increases in osteogenic signaling. We did, however, observe highly significant reductions in expression of osteopontin, which were associated with significant increases in calcium burden in LA-MnSOD +/- mice. Reciprocally, genetically increasing MnSOD did not preserve valve function in LA-MnSOD Tg /0 , but we did observe slight reductions in p-SMAD1/5/8 levels compared to their non -transgenic littermates. Interestingly, overexpression of MnSOD dramatically increased expression of osteopontin in valve tissue from LA-MnSOD Tg /0 mice, but was not sufficient to attenuate calcium burden when compared to their LA-MnSOD 0/0 littermates. Conclusions: Collectively, this study demonstrates that maintenance of mitochondrial antioxidant capacity is important in preventing accelerated disease progression in a mouse model of FCAVD, but that effectively altering mitochondrial antioxidant capacity as a monotherapeutic approach to slow key histopathological and molecular drivers of FCAVD remains biologically and therapeutically challenging., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Roos, Zhang, Hagler, Verzosa, Huang, Oehler, Arghami and Miller.)

Social support promotes resilience to adverse childhood events, but little is known about the role of natural mentors-caring, nonparental adults-in the lives of childhood abuse survivors. The current study draws from a large, longitudinal, nationally representative sample (Add Health) to examine the prevalence and characteristics of natural mentoring relationships for adolescents with a history of caregiver childhood abuse, and the extent to which these relationships are associated with psychological and health outcomes in adulthood. Among the sample (n = 12,270), 28.82% and 4.86% reported caregiver childhood physical and sexual abuse, respectively. Youth who reported caregiver childhood physical abuse were more likely than those who did not endorse abuse to report having a natural mentor, but their mentoring relationships were characterized by lower interpersonal closeness, shorter duration, and less frequent contact. Exposure to caregiver childhood abuse was associated with adverse outcomes during adulthood, including antisocial behavior, physical health limitations, and suicidality; the presence of a natural mentor did not buffer the negative impact of trauma on adult outcomes. However, longer mentoring relationships during adolescence buffered the strength of the association between both caregiver physical and sexual abuse during childhood and suicidality during early adulthood., (© 2020 New York Academy of Sciences.)

Despite decades of increased research and funding, youth mentoring programs, overall, yield small effects on youth outcomes. As a result, there are growing calls for programs to utilize the mentoring relationship as context for intentional, targeted skills development, in which mentors employ targeted skills designed to match the presenting concerns of mentees. This targeted approach contrasts with the historically dominant, non-specific friendship model, which holds that a supportive relational bond-alone-promotes positive developmental change. The current study is a follow-up meta-analysis using a comprehensive dataset of all intergenerational, one-on-one mentoring program evaluations published between 1975 and 2018, investigating the comparative impact of targeted, skills-based versus non-specific, relational approaches to mentoring. Analyses of 48 mentoring studies of youth outcomes (average youth age of 12.25 years old) revealed the overall effect size of targeted programs to be more than double that of non-specific relational approaches, with significant moderator effects on academic, psychological, and social functioning. Findings suggest that youth mentoring programs can promote positive outcomes, particularly when mentors employ targeted approaches matched to the needs of their mentees.

Previous research suggests that youth's natural mentoring relationships are associated with better academic, vocational, and psychosocial functioning. However, little is known about the extent to which the impact of mentoring endures beyond adolescence and early adulthood. Furthermore, most natural mentoring research is confounded by selection bias. In this study, we examined the long-term impact of mentoring using the nationally representative, longitudinal Add Health dataset. We conducted counterfactual analysis, a more stringent test of causality than regression-based approaches. Compared to their unmentored counterparts, adults (ages 33-42) who had a natural mentor during adolescence or emerging adulthood reported higher educational attainment, more time spent volunteering, and more close friends, after controlling for a range of confounding factors. However, outcomes differed when mentors were classified as "strong ties" (e.g., grandparents, friends) or "weak ties" (e.g., teachers, coaches, employers). Having a strong-tie mentor was associated with having more close friends and a lower income. In contrast, having a weak-tie mentor was associated with higher educational attainment, higher income, and more time spent volunteering. These findings suggest that natural mentoring relationships can exert lasting influence on young people's developmental trajectories, providing strong rationale for efforts to expand their availability and scope., (© 2018 Society for Community Research and Action.)

Background: Pathological processes underlying myxomatous mitral valve degeneration (MMVD) remain poorly understood. We sought to identify novel mechanisms contributing to the development of this condition., Methods and Results: Microarrays were used to measure gene expression in 11 myxomatous and 11 nonmyxomatous human mitral valves. Differential gene expression (thresholds P<0.05; fold-change >1.5) and pathway activation (Ingenuity) were confirmed using quantitative reverse transcriptase polymerase chain reaction and immunohistochemistry. Contributions of bone morphogenetic protein 4 and transforming growth factor (TGF)-β2 to differential gene expression were evaluated in vitro. Contributions of angiotensin II to differential pathway activation were examined in mice in vivo. A total of 2602 genes were differentially expressed between myxomatous and nonmyxomatous valves. Canonical TGF-β signaling was increased in MMVD because of increased ligand expression and derepression of SMA mothers against decapentaplegic 2/3 signaling and was confirmed with quantitative reverse transcriptase polymerase chain reaction and immunohistochemistry. Myxomatous valves demonstrated activation of canonical bone morphogenetic protein and Wnt/β-catenin signaling and upregulation of their common target runt-related transcription factor 2. Our data set provided transcriptional and immunohistochemical evidence for activated immune cell infiltration. In vitro treatment of mitral valve interstitial cells with TGF-β2 increased β-catenin signaling at mRNA and protein levels, suggesting interactions between TGF-β2 and Wnt signaling. In vivo infusion of mice with angiotensin II recaptured several changes in signaling pathways characteristic of human MMVD., Conclusions: These data support a new disease framework whereby activation of TGF-β2, bone morphogenetic protein 4, Wnt/β-catenin, or immune signaling plays major roles in the pathogenesis of MMVD. We propose these pathways act in a context-dependent manner to drive phenotypic changes that fundamentally differ from those observed in aortic valve disease and open novel avenues guiding future research into the pathogenesis of MMVD., (© 2015 American Heart Association, Inc.)

Aims: Myxomatous mitral valve disease (MMVD) is associated with leaflet thickening, fibrosis, matrix remodelling, and leaflet prolapse. Molecular mechanisms contributing to MMVD, however, remain poorly understood. We tested the hypothesis that increased transforming growth factor-β (TGF-β) signalling and reactive oxygen species (ROS) are major contributors to pro-fibrotic gene expression in human and mouse mitral valves., Methods and Results: Using qRT-PCR, we found that increased expression of TGF-β1 in mitral valves from humans with MMVD (n = 24) was associated with increased expression of connective tissue growth factor (CTGF) and matrix metalloproteinase 2 (MMP2). Increased levels of phospho-SMAD2/3 (western blotting) and expression of SMAD-specific E3 ubiquitin-protein ligases (SMURF) 1 and 2 (qRT-PCR) suggested that TGF-β1 signalling occurred through canonical signalling cascades. Oxidative stress (dihydroethidium staining) was increased in human MMVD tissue and associated with increases in NAD(P)H oxidase catalytic subunits (Nox) 2 and 4, occurring despite increases in superoxide dismutase 1 (SOD1). In mitral valves from SOD1-deficient mice, expression of CTGF, MMP2, Nox2, and Nox4 was significantly increased, suggesting that ROS can independently activate pro-fibrotic and matrix remodelling gene expression patterns. Furthermore, treatment of mouse mitral valve interstitial cells with cell permeable antioxidants attenuated TGF-β1-induced pro-fibrotic and matrix remodelling gene expression in vitro., Conclusion: Activation of canonical TGF-β signalling is a major contributor to fibrosis and matrix remodelling in MMVD, and is amplified by increases in oxidative stress. Treatments aimed at reducing TGF-β activation and oxidative stress in early MMVD may slow progression of MMVD.