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With the growing worldwide refugee crisis, there is a need for evidence-based interventions that specifically deal with the consequences of cumulative trauma-exposure in refugee youth. Refugee children have unique service needs and differ from their non-refugee peers in terms of sociocultural trauma, language, culture, and educational barriers. This article explains the complexities associated with understanding refugee youth and presents a proposal for studying the possible benefits of Tree of Life therapy. At the present time, Tree of Life therapy has no evidence-base because the published studies of Tree of Life with refugee and/or immigrant youth have sample sizes of one, six, eight, and twenty-nine. As a culturally-grounded, strength-based group counseling approach, Tree of Life therapy addresses traumatic experiences, recognizes participants' cultural differences, highlights individual skills, and aids in instilling both confidence and hope for the future. Ncazelo Ncube, the co-founder and main developer of Tree of Life, describes this therapy as a collective narrative practice that considers cultural beliefs and values (2006, 2010, 2018, 2019). The proposed research design is to study the effectiveness of the Tree of Life in Canada, the United States, the United Kingdom, and South Africa. The research plan is to use pragmatic, group-randomized controlled trials in the "real world" settings of schools and agencies in each of the four countries. In addition, the article describes the development of the Roots and Wings Questionnaire for Children and Youth, a culturally relevant, child-friendly questionnaire. The Tree of Life is a readily available therapy with great potential for helping traumatized refugee youth as well as other trauma-impacted young people worldwide., Competing Interests: Conflict of InterestThe authors declare they have no conflict of interest., (© Springer Nature Switzerland AG 2019.)

Background: The 1000 Genomes Project provides a database of genomic variants from whole genome sequencing of 2504 individuals across five continental superpopulations. This database can enrich our background knowledge of worldwide blood group variant geographic distribution and identify novel variants of potential clinical significance., Study Design and Methods: The 1000 Genomes database was analyzed to 1) expand knowledge about continental distributions of known blood group variants, 2) identify novel variants with antigenic potential and their geographic association, and 3) establish a baseline scaffold of chromosomal coordinates to translate next-generation sequencing output files into a predicted red blood cell (RBC) phenotype., Results: Forty-two genes were investigated. A total of 604 known variants were mapped to the GRCh37 assembly; 120 of these were reported by 1000 Genomes in at least one superpopulation. All queried variants, including the ACKR1 promoter silencing mutation, are located within exon pull-down boundaries. The analysis yielded 41 novel population distributions for 34 known variants, as well as 12 novel blood group variants that warrant further validation and study. Four prediction algorithms collectively flagged 79 of 109 (72%) known antigenic or enzymatically detrimental blood group variants, while 4 of 12 variants that do not result in an altered RBC phenotype were flagged as deleterious., Conclusion: Next-generation sequencing has known potential for high-throughput and extended RBC phenotype prediction; a database of GRCh37 and GRCh38 chromosomal coordinates for 120 worldwide blood group variants is provided as a basis for this clinical application., (© 2018 AABB.)

The authors of the above paper noticed an error in publication. In Results section, under sub-section RHD genetic variations, the deletion nomenclature for Sample 1 was incorrectly given as [NC_000001.11(NG_007494.1):c.(1-15149_1-15153)_(148+3154_148+3158)del].

Only two partial deletions longer than 655 nucleotides had been reported for the RHD gene, constrained within the gene and causing DEL phenotypes. Using a combination of quantitative PCR and long-range PCR, we examined three distinct deletions affecting parts of the RHD gene in three blood donors. Their RHD nucleotide sequences and exact boundaries of the breakpoint regions were determined. DEL phenotypes were caused by a novel 18.4 kb deletion and a previously published 5.4 kb deletion of the RHD gene; a D-negative phenotype was caused by a novel 7.6 kb deletion. Examination of the deletion-flanking regions suggested microhomology-mediated end-joining, replication slippage, and non-homologous end-joining, respectively, as the most likely mechanisms for the three distinct deletions. We described two new deletions affecting parts of the RHD gene, much longer than any previously reported partial deletion: one was the first deletion observed at the 5' end of the RHD gene extending into the intergenic region, and the other the second deletion observed at its 3' end. Large deletions present at either end are a mechanism for a much reduced RhD protein expression or its complete loss. Exact molecular characterization of such deletions is instrumental for accurate RHD genotyping.