Traumatic brain injury (TBI) is still a leading cause of death and disability worldwide, with a disproportionate burden in low- and middle-income countries (LMICs) where access to imaging, invasive intracranial pressure (ICP) monitoring, and neurosurgical care is limited. This review examines recent advances in TBI management in austere environments, where standard high-resource paradigms are frequently impractical, and analyzes the quality of evidence supporting context-adapted approaches. Recent literature highlights the growing role of protocolized care pathways, noninvasive neuromonitoring adjuncts such as optic nerve sheath diameter ultrasonography, quantitative pupillometry, transcranial Doppler, and selected serum biomarkers, as well as alternative surgical strategies including hinge craniectomy. Emerging physiological frameworks, including stage-based models of intracranial decompensation, offer structured decision-making support when numeric ICP thresholds are unavailable. However, most supporting evidence remains observational, heterogeneous, and frequently extrapolated from high-income settings, with major limitations in external validation and implementation science. Enhancing outcomes in austere TBI care will depend less on technological development than on rigorous implementation science, context-specific validation, and sustainable health system strengthening to bridge the gap between evidence and clinical delivery.
Between 10 and 20% of cervical cancers are adenocarcinomas with poorer five-year survival and higher recurrence. To identify somatic alterations driving cervical cancer, we performed whole-exome sequencing of 308 subjects with invasive disease from Guatemala and Venezuela. Consistent with other studies, there is a higher rate of TP53 mutations in adenocarcinomas versus squamous cell carcinomas (SCC), especially in HPV-negative tumors. We identified a higher rate of mutations and deletions (23%) in the STK11 tumor suppressor gene in adenocarcinomas versus SCC. This result was confirmed in the AACR Project Genie and Caris cohorts. Whole-genome sequencing and SNP-array data identified significant numbers of focal deletions on chr19p that disrupt STK11, undetected by exome sequencing. In one tumor, HPV integration disrupts STK11. Chr19p is commonly deleted in cervical cancer, and we document a high rate of independent inversions, chromosomal translocations, and breakage-fusion-bridge events that provide the second hit to STK11. Significantly, STK11 alterations are associated with a younger age of onset and poorer overall survival and survival on immunotherapy. Apart from STK11, PIK3CA mutations and YAP1 amplification are prevalent cervical cancer drivers. STK11 mutations and deletions co-occur significantly with YAP1 amplifications, suggesting an interaction between these pathways. In contrast, STK11 alterations are mutually exclusive to PIK3CA mutation, suggesting redundancy. Cervical adenocarcinomas exhibit significantly lower CD274 (PD-L1) expression and a poorer response to immune checkpoint inhibitors (ICIs). STK11 mutations are associated with poor responses to ICI in other cancers, and elucidating the role of STK11 in cervical cancer may improve targeted and immunotherapies.
Stenotrophomonas maltophilia (SM) is an emerging opportunistic pathogen of increasing clinical relevance due to its intrinsic multidrug resistance and the associated risk of therapeutic failure. Infections caused by SM are frequently observed in intensive care unit (ICU) populations. Its global prevalence has been rising, with reported rates of 32% in Europe and 27.7% in the Americas. Resistance to trimethoprim-sulfamethoxazole (TMP-SMX), the first-line therapy for SM, has been reported in up to 13% of isolates in the Americas. However, data on the prevalence and resistance patterns of SM in hospitalized patients in Guatemala remain unavailable. An ecological analysis of all Stenotrophomonas maltophilia isolates collected between 2022 and 2024 from a Guatemalan national hospital was conducted. The analysis included the site of sample isolation and the hospital unit from which each isolate originated. Resistance to trimethoprim-sulfamethoxazole (TMP-SMX) was determined according to Clinical and Laboratory Standards Institute criteria (≥4/76 mg/L). A total of 349 Stenotrophomonas maltophilia isolates were identified during the study period. An increase in SM isolates was observed in 2023 and 2024 compared to 2022 (84 in 2022, 153 in 2023, and 112 in 2024). The majority of isolates were recovered from endotracheal aspirates (63.32%), followed by blood cultures (10.02%). Nearly half of all isolates originated from patients in the intensive care unit (ICU) (n = 170; 48.71%), followed by the Emergency Department (n = 90; 28.36%). Overall, resistance to trimethoprim-sulfamethoxazole (TMP-SMX) was identified in 65 isolates (18.84%). A higher rate of TMP-SMX resistance was observed in isolates from endotracheal aspirates (19.9%) compared to blood cultures (5.71%) and urine cultures (16.66%). There was no statistically significant difference in resistance rates based on the hospital unit of origin, with ICU samples showing 22.35% resistance, Emergency Department samples 15.15%, and inpatient ward samples 15%. Stenotrophomonas maltophilia shows increasing prevalence and notable resistance to TMP-SMX, particularly in ICU respiratory samples, underscoring the need for targeted surveillance and stewardship in high-risk hospital settings. All Authors: No reported disclosures
