The human brain possesses three predominate phospholipids, phosphatidylcholine (PC), phosphatidylethanolamine (PE) and phosphatidylserine (PS), which account for approximately 35–40%, 35–40%, and 20% of the brain’s phospholipids, respectively. Mitochondrial membranes are relatively diverse, containing the aforementioned PC, PE, and PS, as well as phosphatidylinositol (PI) and phosphatidic acid (PA); however, cardiolipin (CL) and phosphatidylglycerol (PG) are exclusively present in mitochondrial membranes. These phospholipid interactions play an essential role in mitochondrial fusion and fission dynamics, leading to the maintenance of mitochondrial structural and signaling pathways. The essential nature of these phospholipids is demonstrated through the inability of mitochondria to tolerate alteration in these specific phospholipids, with changes leading to mitochondrial damage resulting in neural degeneration. This review will emphasize how the structure of phospholipids relates to their physiologic function, how their metabolism facilitates signaling, and the role of organ- and mitochondria-specific phospholipid compositions. Finally, we will discuss the effects of global ischemia and reperfusion on organ- and mitochondria-specific phospholipids alongside the novel therapeutics that may protect against injury.

Background: Mitochondrial dysfunction, which is triggered by systemic ischemia–reperfusion (IR) injury and affects various organs, is a key factor in the development of post-cardiac arrest syndrome (PCAS). Current research on PCAS primarily addresses generalized mitochondrial responses, resulting in a knowledge gap regarding organ-specific mitochondrial dynamics. This review focuses on the organ-specific mitochondrial responses to IR injury, particularly examining the brain, heart, and kidneys, to highlight potential therapeutic strategies targeting mitochondrial dysfunction to enhance outcomes post-IR injury. Methods and Results: We conducted a narrative review examining recent advancements in mitochondrial research related to IR injury. Mitochondrial responses to IR injury exhibit considerable variation across different organ systems, influenced by unique mitochondrial structures, bioenergetics, and antioxidative capacities. Each organ demonstrates distinct mitochondrial behaviors that have evolved to fulfill specific metabolic and functional needs. For example, cerebral mitochondria display dynamic responses that can be both protective and detrimental to neuronal activity and function during ischemic events. Cardiac mitochondria show vulnerability to IR-induced oxidative stress, while renal mitochondria exhibit a unique pattern of fission and fusion, closely linked to their susceptibility to acute kidney injury. This organ-specific heterogeneity in mitochondrial responses requires the development of tailored interventions. Progress in mitochondrial medicine, especially in the realms of genomics and metabolomics, is paving the way for innovative strategies to combat mitochondrial dysfunction. Emerging techniques such as mitochondrial transplantation hold the potential to revolutionize the management of IR injury in resuscitation science. Conclusions: The investigation into organ-specific mitochondrial responses to IR injury is pivotal in the realm of resuscitation research, particularly within the context of PCAS. This nuanced understanding holds the promise of revolutionizing PCAS management, addressing the unique mitochondrial dysfunctions observed in critical organs affected by IR injury.

Background: Health care systems in the United States are continuously expanding and contracting spaces to treat patients with coronavirus disease 2019 (COVID-19) in intensive care units (ICUs). As a result, hospitals must effectively decontaminate and contain severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in constructed and deconstructed ICUs that care for patients with COVID-19. We assessed decontamination of a COVID-19 ICU and examined the containment efficacy of combined contact and droplet precautions in creating and maintaining a SARS-CoV-2–negative ICU “antechamber”. Methods: To examine the efficacy of chemical decontamination, we used high-density, semi-quantitative environmental sampling to detect SARS-CoV-2 on surfaces in a COVID-19 ICU and COVID-19 ICU antechamber. Quantitative real-time polymerase chain reaction was used to measure viral RNA on surfaces. Viral location mapping revealed the distribution of viral RNA in the COVID-19 ICU and COVID-19 ICU antechamber. Results were further assessed using loop-mediated isothermal amplification. Results: We collected 224 surface samples pre-decontamination and 193 samples post-decontamination from a COVID-19 ICU and adjoining COVID-19 ICU antechamber. We found that 46% of antechamber objects were positive for SARS-CoV-2 pre-decontamination despite the construction of a swinging door barrier system, implementation of contact precautions, and installation of high-efficiency particulate air filters. The object positivity rate reduced to 32.1% and viral particle rate reduced by 95.4% following decontamination. Matched items had an average of 432.2 ± 2729 viral copies/cm² pre-decontamination and 19.2 ± 118 viral copies/cm² post-decontamination, demonstrating significantly reduced viral surface distribution (p < 0.0001). Conclusions: Environmental sampling is an effective method for evaluating decontamination protocols and validating measures used to contain SARS-CoV-2 viral particles. While chemical decontamination effectively removes detectable viral RNA from surfaces, our approach to droplet/contact containment with an antechamber was not highly effective. These data suggest that hospitals should plan for the potential of aerosolized virions when creating strategies to contain SARS-CoV-2.

Mitochondrial transplantation (MTx) has emerged as a potential therapeutic approach for diseases associated with mitochondrial dysfunction, yet its scalability and cross-species feasibility remain underexplored. This study aimed to evaluate the dose-dependent uptake and molecular effects of xenogeneic mitochondrial transplantation (xeno-MTx) using rat-derived mitochondria in mouse neuronal systems. HT-22 hippocampal neuronal cells and a murine model of cardiac arrest-induced global cerebral ischemia were used to assess mitochondrial uptake, gene expression, and mitochondrial DNA presence. Donor mitochondria were isolated from rat pectoralis muscle and labeled with MitoTracker dyes. Flow cytometry and confocal microscopy revealed a dose-dependent increase in donor mitochondrial uptake in vitro. Quantitative PCR demonstrated a corresponding increase in rat-specific mitochondrial DNA and upregulation of Mfn2 and Bak1, with no changes in other fusion, fission, or apoptotic genes. Inhibitor studies indicated that mitochondrial internalization may involve actin-dependent macropinocytosis and cholesterol-sensitive endocytic pathways. In vivo, rat mitochondrial DNA was detected in mouse brains post–xeno-MTx, confirming donor mitochondrial delivery to ischemic tissue. These findings support the feasibility of xeno-MTx and its dose-responsive biological effects in neuronal systems while underscoring the need for further research to determine long-term functional outcomes and clinical applicability.

Background: Bupropion is a common cause of drug-induced seizures, but evidence guiding prophylactic therapy is limited. No prospective head-to-head comparison of phenobarbital and benzodiazepines for symptomatic bupropion overdose has been reported. Methods: We performed a 6-month prospective observational cohort study of patients with symptomatic bupropion overdose. Patients were grouped by receipt of seizure prophylaxis versus no prophylaxis, with agent-specific exploratory analyses for phenobarbital and lorazepam. Baseline characteristics and clinical outcomes were summarized using descriptive statistics. Continuous variables were assessed for normality using Shapiro-Wilk testing and summarized as median and interquartile range (IQR) when non-normally distributed. Categorical outcomes were compared using two-tailed Fisher exact tests with statistical significance defined as p < 0.05. Exploratory logistic regression evaluated seizure odds by prophylaxis group with and without adjustment for initial heart rate. Results: Fifty-five patients were enrolled: 39 received prophylaxis and 16 who did not receive recommended prophylaxis and served as controls. The prophylaxis agents used were phenobarbital in 20 patients, lorazepam in 12, other benzodiazepines in 6, and combined phenobarbital plus lorazepam in 1. Initial heart rate was 114 bpm (IQR 97–133.5) in the prophylaxis group versus 109 bpm (IQR 103.5–117.8) in controls. Reported ingestion dose was 2.70 g (IQR 1.39–5.18) versus 1.80 g (IQR 0.98–7.13), respectively. Three patients had a documented seizure history and were in the prophylaxis group, none of which experienced a seizure. Overall seizure incidence was lower with prophylaxis but did not reach statistical significance (1/39 [2.6%] vs 3/16 [18.8%]; p = 0.069). Proconvulsant co-ingestions were similar between groups (12/39 [30.8%] vs 7/16 [43.8%]; p = 0.370). Among patients with known ingestion ≥3 g, seizures occurred in 0/10 phenobarbital-treated patients, 1/4 lorazepam-treated patients, and 3/5 controls; phenobarbital differed from control (p = 0.022), whereas lorazepam did not (p = 0.524), and phenobarbital did not differ significantly from lorazepam (p = 0.286). Among patients with initial heart rate ≥120 bpm, seizures occurred in 0/7 phenobarbital-treated patients, 1/6 lorazepam-treated patients, and 3/4 controls; phenobarbital differed from control (p = 0.024), whereas lorazepam did not (p = 0.190) and phenobarbital did not differ significantly from lorazepam (p = 0.462). Exploratory logistic regression adjusted for initial heart rate found higher seizure odds in controls than in prophylaxis patients (OR 26.86, 95% CI 1.21–598.08; p = 0.038); initial heart rate showed a nonsignificant trend (OR 1.08 per bpm; p = 0.070). Conclusions: In this interim cohort, phenobarbital was associated with fewer seizures than no prophylaxis in higher-risk subgroups. However, direct phenobarbital-lorazepam comparisons were not statistically different. Findings remain hypothesis-generating given the small sample, observational design, statistical fragility, sparse seizure events, wide regression confidence intervals, and potential reporting bias. Background: Bromadiolone is a long-acting anticoagulant rodenticide that can cause severe and prolonged coagulopathy in humans, while clinical data from low- and middle-income countries remain limited. This study aimed to describe the clinical characteristics, laboratory findings, management strategies, and outcomes of patients with bromadiolone poisoning treated at an emergency center in Vietnam, and to identify factors associated with severe outcomes. We conducted a retrospective observational study of adult patients with confirmed bromadiolone poisoning admitted to the Emergency Center of Thai Nguyen Medical University Hospital, Vietnam, between February 2021 and August 2024. Demographic data, exposure characteristics, clinical manifestations, laboratory parameters, treatment details, and outcomes were extracted from medical records. Severe outcome was defined as major bleeding, international normalized ratio (INR) ≥ 5, requirement for blood product transfusion, or death. A total of 33 patients were included, with a median age of 46 years; 60.6% were male, and suicidal ingestion accounted for 66.7% of cases. Severe outcomes occurred in 7 patients (21.2%). Patients with severe outcomes presented significantly later after exposure (median 48 vs. 5.5 h, p = 0.001) and had markedly higher admission INR values. Bleeding manifestations and blood product transfusion were observed exclusively in the severe outcome group, and no in-hospital deaths occurred. In conclusion, bromadiolone poisoning is associated with substantial morbidity due to prolonged coagulopathy. Delayed hospital presentation and severe coagulopathy at admission are strongly associated with adverse outcomes, highlighting the importance of early recognition and appropriate vitamin K therapy in resource-limited settings. Methods: This retrospective observational study was conducted at the Emergency Center of Thai Nguyen Medical University Hospital, Thai Nguyen, Vietnam. Study population: All consecutive adult patients diagnosed with bromadiolone poisoning and admitted between February 2021 and August 2024 were eligible. Inclusion criteria: Exclusion criteria: Data collection Data extracted from medical records included: Results: Baseline characteristics: Thirty-three patients with bromadiolone poisoning were included. The median age was 46 years (IQR 27), and 20 patients (60.6%) were male. Suicidal ingestion was the most common exposure intent, accounting for 22 cases (66.7%). The median time from exposure to hospital presentation was 7 h (IQR 20), and the median estimated ingestion dose was 1 mg (IQR 4). Conclusions: Bromadiolone poisoning is a serious clinical condition associated with prolonged coagulopathy and a substantial risk of severe bleeding. Delayed hospital presentation and severe coagulopathy at admission are strongly associated with adverse outcomes. Early diagnosis, close monitoring of coagulation parameters, and appropriate vitamin K therapy are essential to improve outcomes, particularly in low- and middle-income countries. Background: Amiodarone is an antiarrhythmic drug used to treat life-threatening cardiac dysrhythmias, but its use is limited by multiorgan toxicity. Large-scale age-stratified data on clinical outcomes remain limited. The National Poison Data System (NPDS) is a national database of over 81 million de-identified case records from all 53 U.S. poison centers. The objective of this study was to describe amiodarone exposures reported to U.S. poison centers.