A Comparative Gender Analysis of Injury Characteristics, Treatments and Outcomes among Persons Seeking Emergency Care in Kigali, Rwanda

In high-income nations, gender has been associated with injury characteristics. This study evaluated injury epidemiology and care based on gender at the Centre Hospitalier Universitaire de Kigali in Rwanda. Patients presenting to the emergency department with acute injuries were prospectively enrolled from 27 January–28 June 2020, and descriptive statistics were performed with comparisons between males and females. Of 601 patients, 25.6% were female and 74.4% were male. There were gender differences in the mechanism of injury, with females more likely to be injured in falls (43.5% versus 23.0%, p = 0.001); meanwhile, males were more likely to suffer road traffic accidents (52.6% versus 39.6%, p = 0.006). The severity of injury was similar between genders based on the mean Kampala Trauma Score (14.4 versus 14.7, p = 0.09). Females were more likely to have been transported by prehospital services (87.7% versus 72.9%, p = 0.001), and less likely to receive acute treatment during the first six hours of care (67.5% versus 78.1%, p = 0.009). There was no significant difference in mortality between females and males (2.0% versus 1.3%, p = 0.568). This study highlights differences in the epidemiology and care between males and females presenting for emergency injury care in Rwanda. These findings can inform future research and developments in gender-centered healthcare delivery

PPM1D mutations are oncogenic drivers of de novo diffuse midline glioma formation

Abstract The role of PPM1D mutations in de novo gliomagenesis has not been systematically explored. Here we analyze whole genome sequences of 170 pediatric high-grade gliomas and find that truncating mutations in PPM1D that increase the stability of its phosphatase are clonal driver events in 11% of Diffuse Midline Gliomas (DMGs) and are enriched in primary pontine tumors. Through the development of DMG mouse models, we show that PPM1D mutations potentiate gliomagenesis and that PPM1D phosphatase activity is required for in vivo oncogenesis. Finally, we apply integrative phosphoproteomic and functional genomics assays and find that oncogenic effects of PPM1D truncation converge on regulators of cell cycle, DNA damage response, and p53 pathways, revealing therapeutic vulnerabilities including MDM2 inhibition