Lift Every Voice: Engaging Black Adolescents in Social Justice Service-Learning to Promote Mental Health and Educational Equity.

This study reports on the feasibility and acceptability of a social justice infused service-learning (S-L) program to promote Black adolescent mental health and educational equity. We convened a community advisory board to help adapt and pilot test, via open trial mixed method design, an evidence-based service-learning program for Black middle school adolescents (n = 21) attending summer camp at a faith-based setting. We describe a S-L curriculum, with a focus on the achievement gap, and training for church staff and assess staff and youth reports of feasibility, acceptability, and promise to (a) improve/engage psychological engagement targets, and (b) improve academic motivation, and social-emotional and behavioral outcomes. Mixed method findings revealed high feasibility and acceptability of the S-L intervention as indicated by consistent attendance and enthusiastic engagement by staff and youth, high satisfaction, high completion rates of planned sessions, and emergent qualitative themes from staff interviews and adolescent focus groups highlighting that service-learning (1) facilitated skills (e.g., goal-setting, social-emotional and behavioral regulation, and problem-solving), (2) shaped perspectives and inspired openness, and (3) created a space for all to feel valued and included to address the inequities of education that directly impacted them. There was preliminary evidence for efficacy in that youth report of emotional symptoms, peer problems, and staff report of general internalizing symptoms decreased following the intervention, while youth report of prosocial behaviors increased. Implications suggest that S-L programming demonstrates promise to promote mental health outcomes, raise social awareness, and inspire critical consciousness and lift the voices of Black youth by providing tools for working toward systemic changes to reduce inequities in both education and mental health.

Adamts9 is necessary for ovarian development in zebrafish.

Expression of adamts9 (A disintegrin and metalloprotease with thrombospondin type-1 motif, member 9) increases dramatically in the somatic cells surrounding oocytes during ovulation in vertebrates from zebrafish to human. However, the function of Adamts9 during ovulation has not been determined due to the embryonic lethality of knockouts in mice and Drosophila. To identify the role of Adamts9 during ovulation we generated knockout (adamts9-/-) zebrafish using CRISPR/Cas9 and characterized the effects of the mutation. From 1047 fish generated by crossing adamts9+/- pairs, we found significantly fewer adult adamts9-/- fish (4%) than predicted by Mendelian ratios (25%). Of the mutants found, there was a significant male bias (82%). Only 3 female mutants were identified (7%), and they had small ovaries with few stage III and IV oocytes compared to wildtype (wt) counterparts of comparable size and age. Astoundingly, the remaining mutants (11%) did not appear to have normal testis or ovaries. Instead there was a pair of transparent, ovarian-like membranous shells that filled the abdominal cavity. Histological examination confirmed that shells were largely empty with no internal structure. Surprisingly, seminiferous tubules and various spermatocytes including mature spermatozoa were observed on the periphery of these transparent shells. No female or female like knockouts were observed to release eggs, and no ovulated oocytes were observed in histological sections. To our knowledge, this is the first report of an adamts9 global knockout model in any adult vertebrates and the first description of how gonadal sex and structure are affected- highlighting the importance of Adamts9 during gonadal development and the value of zebrafish as a model organism.

Progestin and Nuclear Progestin Receptor Are Essential for Upregulation of Metalloproteinase in Zebrafish Preovulatory Follicles.

Ovulation requires proteinases to promote the rupture of ovarian follicles. However, the identity of these proteinases remains unclear. In our previous studies using RNA-seq analysis of differential expressed genes, we found significant down-regulation of five metalloproteinases: adam8b (a disintegrin and metalloproteinase domain 8b), adamts8a (a disintegrin and metalloproteinase with thrombospondin motif 8a), adamts9, mmp2 (matrix metalloproteinase 2), and mmp9 in the nuclear progestin receptor knockout (pgr -/-) zebrafish that have failed to ovulate. We hypothesize that these metalloproteinases are responsible for ovulation and are regulated by progestin and Pgr. In this study, we first determined the expression of these five metalloproteinases and adamts1 in preovulatory follicles at different times within the spawning cycle in pgr -/- and wildtype (wt) zebrafish and under varying hormonal treatments. We found that transcripts of adam8b, adamts1, adamts9, and mmp9 increased drastically in the preovulatory follicular cells of wt female zebrafish, while changes of adamts8a and mmp2 were not significant. This increase of adam8b, adamts9, and mmp9 was significantly reduced in pgr -/-, whereas expression of adamts1 was not affected in pgr -/- zebrafish. Among upregulated metalloproteinases, adamts9 mRNA was found to be expressed specifically in follicular cells. Strong immunostaining of Adamts9 protein was observed in the follicular cells of wt fish, and this expression was reduced drastically in pgr -/-. Interestingly, about an hour prior to the increase of metalloproteinases in wt fish, both Pgr transcript and protein increased transiently in preovulatory follicular cells. The results from in vitro experiments showed that adamts9 expression markedly increased in a dose, time and Pgr-dependent manner when preovulatory follicles were exposed to a progestin, 17α,20ß-dihydroxy-4-pregnen-3-one (DHP). Taken together, our results provide the first evidence that upregulation of adamts9 occurs specifically in preovulatory follicular cells of zebrafish prior to ovulation. Progestin and its receptor (Pgr) are essential for the upregulation of metalloproteinases.