Financial support policies as a mechanism to reduce child welfare involvement.

None.

Kinship Care and Foster Care: A Comparison of Out-of-Home Placement From the Perspective of Child Abuse Experts in North Carolina.

BACKGROUND Children may be placed in either kinship or foster care, forms of out-of-home placement (OHP), if maltreatment is suspected. The American Academy of Pediatrics has identified them as children with special health needs requiring elevated care. While North Carolina has increased support for foster care, it is unclear whether similar support exists for kinship care. Child abuse medical providers (CAMPs) were interviewed regarding their understanding and assessment of the state of the kinship care system in North Carolina, and how it can be improved.METHODS CAMPs were individually interviewed using a semi-structured, open-ended question guide to assess their perspectives on kinship versus foster care in North Carolina. Data were coded, and the analysis was conducted in an inductive manner, allowing themes and then recommendations to emerge from interviews.RESULTS The following three themes were identified: 1) providers have a foundational understanding of the kinship care system, marked by knowledge gaps; 2) children in kinship care and foster care have equivalent, elevated health needs, but children in kinship care do not receive the same level of care; 3) individual and structural changes have to be made to the interprofessional teams working within the OHP system.LIMITATIONS The study sample was small, including eight CAMPs who had relatively homogenous demographic characteristics. CAMPs typically see the worst cases of maltreatment, which may bias responses. Additionally, the majority of children in kinship care are unknown to CAMPs and may not be fully represented in responses.CONCLUSION CAMPs' responses were summarized into a set of recommendations targeting four different components of the OHP team: the general interprofessional team, policymakers and state leaders, medical providers, and social workers.

Sex-induced silencing operates during opposite-sex and unisexual reproduction in Cryptococcus neoformans.

Cryptococcus neoformans is a human fungal pathogen that undergoes a dimorphic transition from yeast to hyphae during a-α opposite-sex mating and α-α unisexual reproduction (same-sex mating). Infectious spores are generated during both processes. We previously identified a sex-induced silencing (SIS) pathway in the C. neoformans serotype A var. grubii lineage, in which tandem transgene arrays trigger RNAi-dependent gene silencing at a high frequency during a-α opposite-sex mating, but at an ∼250-fold lower frequency during asexual mitotic vegetative growth. Here we report that SIS also operates during α-α unisexual reproduction. A self-fertile strain containing either SXI2a-URA5 or NEO-URA5 transgene arrays exhibited an elevated silencing frequency during solo and unisexual mating compared with mitotic vegetative growth. We also found that SIS operates at a similar efficiency on transgene arrays of the same copy number during either α-α unisexual reproduction or a-α opposite-sex mating. URA5-derived small RNAs were detected in the silenced progeny of α-α unisexual reproduction and RNAi core components were required, providing evidence that SIS induced by same-sex mating is also mediated by RNAi via sequence-specific small RNAs. In addition, our data show that the SIS RNAi pathway also operates to defend the genome via squelching transposon activity during same-sex mating as it does during opposite-sex mating. Taken together, our results confirm that SIS is conserved between the divergent C. neoformans serotype A and serotype D cryptic sibling species.

Transgene induced co-suppression during vegetative growth in Cryptococcus neoformans.

Introduction of DNA sequences into the genome often results in homology-dependent gene silencing in organisms as diverse as plants, fungi, flies, nematodes, and mammals. We previously showed in Cryptococcus neoformans that a repeat transgene array can induce gene silencing at a high frequency during mating (∼50%), but at a much lower frequency during vegetative growth (∼0.2%). Here we report a robust asexual co-suppression phenomenon triggered by the introduction of a cpa1::ADE2 transgene. Multiple copies of the cpa1::ADE2 transgene were ectopically integrated into the genome, leading to silencing of the endogenous CPA1 and CPA2 genes encoding the cyclosporine A target protein cyclophilin A. Given that CPA1-derived antisense siRNAs were detected in the silenced isolates, and that RNAi components (Rdp1, Ago1, and Dcr2) are required for silencing, we hypothesize that an RNAi pathway is involved, in which siRNAs function as trans factors to silence both the CPA1 and the CPA2 genes. The silencing efficiency of the CPA1 and CPA2 genes is correlated with the transgene copy number and reached ∼90% in the presence of >25 copies of the transgene. We term this transgene silencing phenomenon asexual co-suppression to distinguish it from the related sex-induced silencing (SIS) process. We further show that replication protein A (RPA), a single-stranded DNA binding complex, is required for transgene silencing, suggesting that RPA might play a similar role in aberrant RNA production as observed for quelling in Neurospora crassa. Interestingly, we also observed that silencing of the ADE2 gene occurred at a much lower frequency than the CPA1/2 genes even though it is present in the same transgene array, suggesting that factors in addition to copy number influence silencing. Taken together, our results illustrate that a transgene induced co-suppression process operates during C. neoformans vegetative growth that shares mechanistic features with quelling.