Modeling GATA2 deficiency in mice: the R396Q mutation disrupts normal hematopoiesis.

GATA2 deficiency is an autosomal dominant germline disorder of immune dysfunction and bone marrow failure with a high propensity for leukemic transformation. While sequencing studies have identified several secondary mutations thought to contribute to malignancy, the mechanisms of disease progression have been difficult to identify due to a lack of disease-specific experimental models. Here, we describe a murine model of one of the most common GATA2 mutations associated with leukemic progression in GATA2 deficiency, Gata2.

ReXamine-Global: A Framework for Uncovering Inconsistencies in Radiology Report Generation Metrics.

Given the rapidly expanding capabilities of generative AI models for radiology, there is a need for robust metrics that can accurately measure the quality of AI-generated radiology reports across diverse hospitals. We develop ReXamine-Global, a LLM-powered, multi-site framework that tests metrics across different writing styles and patient populations, exposing gaps in their generalization. First, our method tests whether a metric is undesirably sensitive to reporting style, providing different scores depending on whether AI-generated reports are stylistically similar to ground-truth reports or not.

NR4A1 and NR4A2 orphan nuclear receptors regulate endothelial-to-hematopoietic transition in mouse hematopoietic stem cell specification.

Hematopoietic stem cells (HSCs) sustain life-long hematopoiesis and emerge during mid-gestation from hemogenic endothelial progenitors via an endothelial-to-hematopoietic transition (EHT). The full scope of molecular mechanisms governing this process remains unclear. The NR4A subfamily of orphan nuclear receptors act as tumor suppressors in myeloid leukemogenesis and have never been implicated in HSC specification.