Diabetic ketoacidosis (DKA) is a serious and potentially life-threatening complication of diabetes mellitus, responsible for up to 40 % of diabetes-related morbidity and mortality. Despite its use in severe cases of pediatric DKA, bicarbonate therapy remains controversial due to potential associations with adverse outcomes such as cerebral edema. Prior studies evaluating bicarbonate therapy in pediatric DKA have been limited by confounding variables, small sample sizes, and short follow-up periods. This study aims to evaluate the association between bicarbonate therapy and adverse outcomes using a large clinical dataset, extended follow-up, and propensity score (PS) matching to control for baseline differences. We conducted a retrospective cohort study using TriNetX, a global research network of deidentified electronic health records. Pediatric DKA patients (<12 years) were stratified by bicarbonate therapy status and matched using PS to reduce confounders. Risk analysis was conducted to assess clinical outcomes. After PS matching, each cohort included 211 patients. No significant difference in cerebral edema was observed between groups (RD = 0.002; 95 % CI: -0.039 to 0.044; p = 0.911). However, bicarbonate use was associated with higher risks of coma (RD = 0.047; p = 0.001), pulmonary edema (RD = 0.048; p = 0.001), and acute respiratory failure (RD = 0.071; p = 0.008). Although bicarbonate therapy was not linked to increased cerebral edema, it was associated with significant respiratory and neurologic complications. These findings suggest that clinicians should use bicarbonate cautiously and that current treatment guidelines may warrant reevaluation.

Background: Many researchers believe that cardia (CGC) and non-cardia (NCGC) are two different types of tumors, having different features like incidence rate, risk factors, geographical location, and socioeconomic status. This study aims to investigate the causes of death (COD) survival rates among early gastric cancer patients with a focus on differences between CGC and NCGC. Methods: This retrospective study employed SEER*stat software (version 8.3.92) to analyze the SEER 17 plus dataset (2000–2019). Standardized mortality ratios (SMR) were computed. Relative survival and conditional survival post-diagnosis were calculated using R software (version 4.1.0) among the different subgroups. Results: Within the follow-up period, 55.4% (5381) died, predominantly within the initial year post-diagnosis. Esophageal cancer was the leading non-gastric cancer cause in CGC, while miscellaneous tumors dominated in NCGC. The 1-year and 5-year relative survival for CGC patients were 76.4% and 48.9% respectively, while for NCGC were 80.4% and 63.9%. The 3-year conditional survival after 1 year and 5e years of survival for CGC were 68.7% and 88.8%, respectively, while for NCGC were 82.2% and 93.5%, respectively. This means that the longer a person has survived after diagnosis with cancer, the greater the likelihood that person will survive for another 3 years. Conclusions: This study sheds light on the substantial impact of non-cancer COD in GC patients, underscoring the necessity of considering comorbidities in their comprehensive management and follow-up. Impact: This study contributes valuable insights for clinical decision-making and informs future research directions regarding CGC and NCGC.

Background: Mild traumatic brain injury (mTBI) may rapidly alter neurocognitive function and has been associated with an increased risk for post-traumatic stress disorder (PTSD). However, neuroimaging investigations during the acute post-trauma phase remain sparse. We previously reported greater left anterior insular cortex (aIC) activation during the cognitive appraisal of fearful versus neutral emotional faces in survivors who did and did not exhibit probable PTSD at 3 months, but not at 2 weeks, after a motor vehicle collision (MVC). Given previous studies suggesting that mTBI may lead to increased cortical activation in the early post-trauma period, we hypothesize that aIC activation within 2 weeks post-MVC may be elevated among probable PTSD survivors who sustained an mTBI compared to those who did not sustain mTBI. Methods: In this secondary hypothesis-driven analysis, previously reported task-related activation at both 2 weeks and 3 months after trauma was extracted from the aIC region of interest and compared among groups of survivors diagnosed with probable PTSD at 3 months with (n = 5) and without (n = 11) mTBI in the emergency department. An exploratory analysis of change over time included two time points and additional groups of survivors without probable PTSD with (n = 10) and without (n = 12) mTBI. Results: At 2 weeks, aIC activation was significantly greater in the probable PTSD with mTBI group than in the probable PTSD without mTBI group (mean = 0.125, SD = 0.053 vs. 0.014, SD = 0.111) (Welch’s t (13.86) = 2.71, two-sided p = 0.017). aIC activation in probable PTSD survivors with and without mTBI was not significantly different at 3 months after MVC. The time and time × group interactions were not significant in brain activation and post-traumatic stress symptoms, but within-group tests suggest that decreases in post-traumatic stress symptoms over time were significant in groups without mTBI. Conclusions: These preliminary results are consistent with the hypothesized association between mTBI and greater aIC activation to negative emotional stimuli in the early post-trauma period among survivors with probable PTSD, but do not support post-trauma brain changes in survivors with mTBI, probable PTSD, both conditions, or neither condition. These preliminary findings warrant further investigation into the relationship between mTBI and probable PTSD-related cortical alterations during the acute post-trauma period.

Our study sought to evaluate the association between Glucagon-like peptide-1 receptor agonist use and the development of hypersomnolence at 1 and 5-year timepoints. A retrospective cohort study was done using TriNetX’s research network. Patients aged 18–50 with type-2 diabetes mellitus or obesity who underwent polysomnography were included. Patients were excluded if they had any prior use of antidepressants. Patients who used Glucagon-like peptide-1 receptor agonists were 1:1 propensity matched to patients without Glucagon-like peptide-1 receptor agonist exposure. The primary outcome was new onset hypersomnolence with secondary outcomes including parasomnia, narcolepsy/cataplexy, disturbed sleep, restless legs syndrome, iron deficiency, and Parkinsonism. Hazard ratios and risk ratios were calculated at 1- and 5-years. Kaplan-Meier analyses and log-rank tests were performed for time to event comparisons. After matching, there were two equal cohorts of 118,993 patients. The Glucagon-like peptide-1 receptor agonist cohort was associated with increased hypersomnolence at 1-year (HR 1.21, 95% CI 1.10–1.32; p < 0.001) and 5-years (HR 1.23, 95% CI 1.14–1.32; p < 0.001). The absolute risk increase was approximately 0.4% at 1 year and 0.7% at 5 years. Iron deficiency was significantly increased at 5-years (HR 1.11, 95% CI 1.06–1.16; p < 0.001). A decreased hazard of Parkinsonism was observed at 5-years (HR 0.26, 95% CI 0.08–0.80; p = 0.012), although event counts were low. Time to event analyses did not demonstrate statistically significant associations for parasomnia, disturbed sleep, restless legs syndrome, or narcolepsy/cataplexy. These findings highlight the need for further studies to evaluate the effects of Glucagon-like peptide-1 receptor agonists on sleep regulation and the neurophysiological consequences of these agents.