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Primary amebic meningoencephalitis (PAM) is a necrotizing and hemorrhagic inflammation of the brain and meninges caused by Naegleria fowleri, a free-living thermophilic ameba of freshwater systems. PAM remains a neglected disease that disproportionately affects children in tropical and subtropical climates, with an estimated mortality rate of 95–98%. Due to anthropogenic climate change, the average temperature in the USA has increased by 0.72 to 1.06 °C in the last century, promoting the poleward spread of N. fowleri. PAM is often misdiagnosed as bacterial meningitis or viral encephalitis, which shortens the window for potentially life-saving treatment. Diagnosis relies on the patient’s history of freshwater exposure and the physician’s high index of suspicion, supported by cerebrospinal fluid studies. While no experimental trials have been conducted to assess the relative efficacy of treatment regimens, anti-amebic therapy with adjunctive neuroprotection is standard treatment in the USA. We performed a literature review and identified five patients from North America between 1962 and 2022 who survived PAM with various degrees of sequelae. [ABSTRACT FROM AUTHOR]

This article discusses the illness and death of President William Henry Harrison in 1841. After taking office, Harrison fell ill with a severe chill and was treated for what was believed to be pneumonia. However, his condition worsened, and he eventually passed away. The exact cause of his illness has been a subject of debate, with some suggesting that he may have had enteric (typhoid) fever. Regardless of the diagnosis, Harrison's death led to a constitutional crisis. [Extracted from the article]

Dr. Thomas E. Starzl, known as the "Father of Transplantation," was a renowned surgeon whose career spanned four decades. He achieved the first successful human liver transplant and made significant contributions to the understanding of immunosuppressants. Despite facing criticism and doubt, Dr. Starzl persevered and performed groundbreaking surgeries, including the first successful pediatric liver transplant and the world's first heart-liver transplant. He authored numerous publications and books throughout his career. Dr. Starzl's work has had a profound impact on the field of transplantation, and his legacy continues to influence transplant surgeons worldwide. [Extracted from the article]

Background: New or worsened mitral regurgitation (MR) is an uncommon yet serious complication after surgical aortic valve replacement (SAVR). While there have been numerous reports of its occurrence, there is little consensus regarding its presentation and management. This systematic review summarizes the evidence in the current literature surrounding new or worsened MR after SAVR and analyzes its potential implications. Methods: Databases were examined for all articles and abstracts reporting on new or worsened MR after SAVR. Data collected included number of patients studied; patient characteristics; incidences of new or worsened MR; timing of diagnosis; and treatment. Results: Thirty-six full-text citations were included in this review. The prevalence of new or worsened MR after SAVR was 8.4%. Sixteen percent of new MR occurrences were from an organic etiology, and 83% of new MR occurrences were that of a functional etiology. Most diagnoses were made in the late or unspecified postoperative period using echocardiography (range: 0 minutes to 18 years postoperatively). While no patients died from this complication, 7.7% of patients (16 out of 207) required emergent procedural re-intervention. Conclusions: This systematic review underscores the importance of identifying new or worsened MR following SAVR and accurate scoring of MR severity to guide treatment. It also outlines the associated clinical measures commonly documented following this complication, and the usefulness of transesophageal echocardiography for the detection of significant MR. These results reflect the current, limited state of the literature on this topic and warrant further investigation into MR detection and management strategies in SAVR patients. [ABSTRACT FROM AUTHOR]

Traumatic brain injury (TBI) alters stress responses, which may influence neuroinflammation and behavioral outcome. Sleep disruption (SD) is an understudied post-injury environmental stressor that directly engages stress-immune pathways. Thus, we predicted that maladaptive changes in the hypothalamic-pituitary-adrenal (HPA) axis after TBI compromise the neuroendocrine response to SD and exacerbate neuroinflammation. To test this, we induced lateral fluid percussion TBI or sham injury in female and male C57BL/6 mice aged 8–10 weeks that were then left undisturbed or exposed to 3 days of transient SD. At 3 days post-injury (DPI) plasma corticosterone (CORT) was reduced in TBI compared with sham mice, indicating altered HPA-mediated stress response to SD. This response was associated with approach-avoid conflict behavior and exaggerated cortical neuroinflammation. Post-injury SD specifically enhanced neutrophil trafficking to the injured brain in conjunction with dysregulated aquaporin-4 (AQP4) polarization. Delayed and persistent effects of post-injury SD were determined 4 days after SD concluded at 7 DPI. SD prolonged anxiety-like behavior regardless of injury and was associated with increased cortical Iba1 labeling in both sham and TBI mice. Strikingly, TBI SD mice displayed an increased number of CD45+ cells near the site of injury, enhanced cortical glial fibrillary acidic protein (GFAP) immunolabeling, and persistent expression of Trem2 and Tlr4 7 DPI compared with TBI mice. These results support the hypothesis that post-injury SD alters stress-immune pathways and inflammatory outcomes after TBI. These data provide new insight to the dynamic interplay between TBI, stress, and inflammation. [ABSTRACT FROM AUTHOR]

Traumatic brain injury (TBI) impairs the ability to restore homeostasis in response to stress, indicating hypothalamic-pituitary-adrenal (HPA)-axis dysfunction. Many stressors result in sleep disturbances, thus mechanical sleep fragmentation (SF) provides a physiologically relevant approach to study the effects of stress after injury. We hypothesize SF stress engages the dysregulated HPA-axis after TBI to exacerbate post-injury neuroinflammation and compromise recovery. To test this, male and female mice were given moderate lateral fluid percussion TBI or sham-injury and left undisturbed or exposed to daily, transient SF for 7- or 30-days post-injury (DPI). Post-TBI SF increases cortical expression of interferon- and stress-associated genes characterized by inhibition of the upstream regulator NR3C1 that encodes glucocorticoid receptor (GR). Moreover, post-TBI SF increases neuronal activity in the hippocampus, a key intersection of the stress-immune axes. By 30 DPI, TBI SF enhances cortical microgliosis and increases expression of pro-inflammatory glial signaling genes characterized by persistent inhibition of the NR3C1 upstream regulator. Within the hippocampus, post-TBI SF exaggerates microgliosis and decreases CA1 neuronal activity. Downstream of the hippocampus, post-injury SF suppresses neuronal activity in the hypothalamic paraventricular nucleus indicating decreased HPA-axis reactivity. Direct application of GR agonist, dexamethasone, to the CA1 at 30 DPI increases GR activity in TBI animals, but not sham animals, indicating differential GR-mediated hippocampal action. Electrophysiological assessment revealed TBI and SF induces deficits in Schaffer collateral long-term potentiation associated with impaired acquisition of trace fear conditioning, reflecting dorsal hippocampal-dependent cognitive deficits. Together these data demonstrate that post-injury SF engages the dysfunctional post-injury HPA-axis, enhances inflammation, and compromises hippocampal function. Therefore, external stressors that disrupt sleep have an integral role in mediating outcome after brain injury. • Traumatic brain injury (TBI) compromises stress responses to mechanical sleep fragmentation. • Post-TBI sleep fragmentation enhances inflammation associated with inhibition of NR3C1. • TBI alters agonist-induced glucocorticoid receptor activity in the hippocampus. • Sleep fragmentation impairs long-term potentiation after brain injury. • Post-TBI sleep fragmentation compromises hippocampal-dependent cognition. [ABSTRACT FROM AUTHOR]