Human Resources Analytics for Public Personnel Management: Concepts, Cases, and Caveats

The advancement of data technology such as machine learning and artificial intelligence has broadened the scope of human resources (HR) analytics, commonly referred to as “people analytics.” This field has seen significant growth in recent years as organizations increasingly rely on algorithm-based predictive tools for HR-related decision making. However, its application in the public sector is not yet fully understood. This study examined the concepts and practices of HR analytics through a thematic review, and proposed a five-step process (define, collect, analyze, share, and reflect) for implementation in the public sector—the process aims to assist with the integration of HR analytics in public personnel management practices. By analyzing cases in both the public and private sectors, this study identified key lessons for functional areas such as workforce planning, recruitment, HR development, and performance management. This research also identified the necessary conditions for introducing HR analytics in public organizations, including data management, staff capabilities, and acceptance, and discussed the potential challenges of privacy, integrity, algorithmic bias, and publicness

Ldb1 is required for Lmo2 oncogene–induced thymocyte self-renewal and T-cell acute lymphoblastic leukemia

Prolonged or enhanced expression of the proto-oncogene Lmo2 is associated with a severe form of T-cell acute lymphoblastic leukemia (T-ALL), designated early T-cell precursor ALL, which is characterized by the aberrant self-renewal and subsequent oncogenic transformation of immature thymocytes. It has been suggested that Lmo2 exerts these effects by functioning as component of a multi-subunit transcription complex that includes the ubiquitous adapter Ldb1 along with b-HLH and/or GATA family transcription factors; however, direct experimental evidence for this mechanism is lacking. In this study, we investigated the importance of Ldb1 for Lmo2-induced T-ALL by conditional deletion of Ldb1 in thymocytes in an Lmo2 transgenic mouse model of T-ALL. Our results identify a critical requirement for Ldb1 in Lmo2-induced thymocyte self-renewal and thymocyte radiation resistance and for the transition of preleukemic thymocytes to overt T-ALL. Moreover, Ldb1 was also required for acquisition of the aberrant preleukemic ETP gene expression signature in immature Lmo2 transgenic thymocytes. Co-binding of Ldb1 and Lmo2 was detected at the promoters of key upregulated T-ALL driver genes (Hhex, Lyl1, and Nfe2) in preleukemic Lmo2 transgenic thymocytes, and binding of both Ldb1 and Lmo2 at these sites was reduced following Cre-mediated deletion of Ldb1. Together, these results identify a key role for Ldb1, a nonproto-oncogene, in T-ALL and support a model in which Lmo2-induced T-ALL results from failure to downregulate Ldb1/Lmo2-nucleated transcription complexes which normally function to enforce self-renewal in bone marrow hematopoietic progenitors