Are Screening Tools for Identifying Human Trafficking Victims in Health Care Settings Validated? A Scoping Review.

OBJECTIVE: Although many screening tools, resources, and programs for identifying victims of human trafficking exist, consensus is lacking on which tools are most useful, which have been validated, and whether they are effective. The objectives of this study were to determine what tools exist to identify or screen for victims of human trafficking in health care settings and whether these tools have been validated. METHOD: We conducted a scoping review of the literature on human trafficking identification in health care settings following the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-analyses) protocol for scoping reviews. We searched the MEDLINE, PsycInfo, Embase, and Scopus databases without language or date limitations. Two independent reviewers screened each citation. We included human research studies in English with populations of all ages, all genders, all geographic locations, and using quantitative and/or qualitative research methods. We excluded studies that were not conducted in a health care setting, review articles, and meta-analyses. We summarized additional screening tools available online and identified through hand-searching. RESULTS: Database searches yielded 8730 studies, of which 4806 remained after removing duplicates. We excluded 4720 articles based on title/abstract review, we reviewed 85 full-text studies for eligibility, and we included 8 articles. Hand-searching revealed 9 additional screening tools not found in the literature. Through our search for validated screening tools, only 6 had been studied for validation in health care settings. CONCLUSIONS: Few studies have evaluated screening tools for identifying victims of human trafficking in health care settings. The absence of a gold standard for human trafficking screening and lack of consensus on the definition of human trafficking make screening tool validation difficult. Further research is required for the development of safe, effective approaches to patient screening.

Author Correction: Defining the relative and combined contribution of CTCF and CTCFL to genomic regulation.

An amendment to this paper has been published and can be accessed via the original article.

Defining the relative and combined contribution of CTCF and CTCFL to genomic regulation.

BACKGROUND: Ubiquitously expressed CTCF is involved in numerous cellular functions, such as organizing chromatin into TAD structures. In contrast, its paralog, CTCFL, is normally only present in the testis. However, it is also aberrantly expressed in many cancers. While it is known that shared and unique zinc finger sequences in CTCF and CTCFL enable CTCFL to bind competitively to a subset of CTCF binding sites as well as its own unique locations, the impact of CTCFL on chromosome organization and gene expression has not been comprehensively analyzed in the context of CTCF function. Using an inducible complementation system, we analyze the impact of expressing CTCFL and CTCF-CTCFL chimeric proteins in the presence or absence of endogenous CTCF to clarify the relative and combined contribution of CTCF and CTCFL to chromosome organization and transcription. RESULTS: We demonstrate that the N terminus of CTCF interacts with cohesin which explains the requirement for convergent CTCF binding sites in loop formation. By analyzing CTCF and CTCFL binding in tandem, we identify phenotypically distinct sites with respect to motifs, targeting to promoter/intronic intergenic regions and chromatin folding. Finally, we reveal that the N, C, and zinc finger terminal domains play unique roles in targeting each paralog to distinct binding sites to regulate transcription, chromatin looping, and insulation. CONCLUSION: This study clarifies the unique and combined contribution of CTCF and CTCFL to chromosome organization and transcription, with direct implications for understanding how their co-expression deregulates transcription in cancer.

Hematopoietic Stem and Progenitor Cells Exhibit Stage-Specific Translational Programs via mTOR- and CDK1-Dependent Mechanisms.

Hematopoietic stem cells (HSCs) require highly regulated rates of protein synthesis, but it is unclear if they or lineage-committed progenitors preferentially recruit transcripts to translating ribosomes. We utilized polysome profiling, RNA sequencing, and whole-proteomic approaches to examine the translatome in LSK (Lin-Sca-1+c-Kit+) and myeloid progenitor (MP; Lin-Sca-1-c-Kit+) cells. Our studies show that LSKs exhibit low global translation but high translational efficiencies (TEs) of mRNAs required for HSC maintenance. In contrast, MPs activate translation in an mTOR-independent manner due, at least in part, to proteasomal degradation of mTOR by the E3 ubiquitin ligase c-Cbl. In the near absence of mTOR, CDK1 activates eIF4E-dependent translation in MPs through phosphorylation of 4E-BP1. Aberrant activation of mTOR expression and signaling in c-Cbl-deficient MPs results in increased mature myeloid lineage output. Overall, our data demonstrate that hematopoietic stem and progenitor cells (HSPCs) undergo translational reprogramming mediated by previously uncharacterized mechanisms of translational regulation.