Code Crimson: A Postpartum Hemorrhage Bundled Intervention Quality Improvement Project.

BACKGROUND: Postpartum hemorrhage (PPH) is a leading cause of maternity mortality in the United States. The Code Crimson project aimed to enhance PPH management by implementing a standardized intervention bundle to mitigate morbidity and mortality associated with PPH. LOCAL PROBLEM: At a large Philadelphia tertiary hospital, health disparities existed for severe maternal morbidity and mortality, and PPH was a significant factor. METHODS: A quality improvement design, using Plan-Do-Study-Act cycles and interrupted time series analysis, was undertaken. INTERVENTIONS: The Code Crimson project implemented a standardized bundle to manage PPH, including blood product administration and massive transfusion protocol activation. RESULTS: After implementing the Code Crimson bundle, there was a significant decrease in blood product use ( P < .001), with minor reductions in packed red blood cell administration over 4 units and mean blood loss. CONCLUSIONS: The Code Crimson bundle effectively reduced blood product utilization for PPH treatment.

Diabetes and cardiometabolic risk in South Asian youth: A review.

South Asians are at increased risk for developing type 2 diabetes and cardiovascular disease at lower body mass index compared to other ancestral groups. Many factors contribute to this increased risk, including genetics, maternal-fetal factors, diet, fitness, body composition, and unique pathophysiology. Increased cardiometabolic risk is also seen at younger ages in South Asian individuals as compared to their White counterparts. This risk persists in migrant communities outside of South Asia. With the growing prevalence of obesity, diabetes, and cardiovascular disease in the South Asian population, it is imperative that we had better understand the mechanisms underlying this increased risk and implement strategies to address this growing public health problem during childhood and adolescence.

In vivo epigenetic editing of Sema6a promoter reverses transcallosal dysconnectivity caused by C11orf46/Arl14ep risk gene.

Many neuropsychiatric risk genes contribute to epigenetic regulation but little is known about specific chromatin-associated mechanisms governing the formation of neuronal connectivity. Here we show that transcallosal connectivity is critically dependent on C11orf46, a nuclear protein encoded in the chromosome 11p13 WAGR risk locus. C11orf46 haploinsufficiency was associated with hypoplasia of the corpus callosum. C11orf46 knockdown disrupted transcallosal projections and was rescued by wild type C11orf46 but not the C11orf46R236H mutant associated with intellectual disability. Multiple genes encoding key regulators of axonal development, including Sema6a, were hyperexpressed in C11orf46-knockdown neurons. RNA-guided epigenetic editing of Sema6a gene promoters via a dCas9-SunTag system with C11orf46 binding normalized SEMA6A expression and rescued transcallosal dysconnectivity via repressive chromatin remodeling by the SETDB1 repressor complex. Our study demonstrates that interhemispheric communication is sensitive to locus-specific remodeling of neuronal chromatin, revealing the therapeutic potential for shaping the brain's connectome via gene-targeted designer activators and repressor proteins.