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Abstract Objective Left hippocampal sclerosis (HS) is associated with verbal‐specific memory impairment. This association is well established for word list learning tasks, and there is some evidence that this may also be relevant to verbal paired associates learning (PAL), though the evidence is limited. We aimed to evaluate the utility of verbal PAL as a marker for left HS, compare this with word list learning, and derive cutoff scores to facilitate clinical application. Methods Retrospective analysis of Rey Auditory Verbal Learning Test (RAVLT) and PAL scores obtained from 116 surgically naïve temporal lobe epilepsy patients with HS (14 bilateral, 57 left, 45 right; range of N across test indices: 77–110). Results Relative to right HS, left HS and bilateral HS were associated with poorer performance on PAL Hard Pairs (p 0.05). PAL Hard Pairs and all RAVLT indices displayed acceptable discriminatory ability (AUC > 0.70) in classifying left‐sided HS (unilateral left or bilateral HS), with RAVLT delayed recall the strongest predictor (AUC = 0.87; PAL Hard Pairs Learning and Delay = 0.80 and 0.83, respectively). Optimal cutoff scores for left‐sided HS classification were generated. Significance Although the RAVLT delayed recall was the strongest predictor of left‐sided HS, PAL Hard Pairs also demonstrated excellent discriminatory capacity, offering an additional cognitive marker of left hippocampal integrity to complement word list learning in clinical assessments. Plain Language Statement The results of the study show that the ability to learn unrelated pairs of words (e.g., “silver”–“run”) is compromised in the setting of epilepsy with left‐sided hippocampal sclerosis (HS), be it unilateral left HS or bilateral HS. The ability of unrelated word pair learning to discriminate left vs. right HS was comparable to word list learning, a task with demonstrated sensitivity to left HS. Our results suggest that the ability to learn unrelated pairs of words provides another useful marker of left‐sided hippocampal compromise in epilepsy. We provide cutoff scores to facilitate clinical interpretation.

Introduction: Although an increasing number of headlines have highlighted the problem of employee burnout, an employer may not be aware of how specifically disengagement and burnout may be affecting their employees' health and their bottom line., Methods: To quantify the burden of disengagement and burnout among different employee types, in 2024, the authors developed a computational model representing different engagement/burnout states they could be in and different stressors within and outside the workplace on the basis of the work-life framework, which impact movement among these states and subsequent productivity losses (i.e., missed workdays and reduced productivity at work) and health effects in each state., Results: Employee disengagement, overextension, ineffectiveness, and burnout over the course of 1 year costs an employer an average of $3,999 (95% range=$3,958-$4,299) for an average U.S. nonmanagerial hourly employee; an average of $4,257 (95% range=$4,215-$4,299) for an average nonmanagerial salaried employee; $10,824 (95% range=$10,700-$10,948) for an average manager; and $20,683 (95% range=$20,451-$20,915) for an average executive. At an average U.S. 1,000-person company (assuming average wages by employee type and an employee distribution of 59.7% nonmanagerial hourly, 28.6% nonmanagerial salaried, 10% managers, and 1.7% executives), employee disengagement/burnout resulted in $5.04 million (95% range=$5.03-$5.05 million) in costs and 801.7 (95% range=801.5-801.9) quality-adjusted life years lost annually., Conclusions: Employee disengagement/burnout can cost employers 0.2-2.9 times the average cost of health insurance and 3.3-17.1 times the cost of training per employee., (Copyright © 2025 Elsevier Inc. All rights reserved.)

Background: Long COVID, which affects an estimated 44.69-48.04 million people in the U.S., is an ongoing public health concern that will continue to grow as SARS-CoV-2 continues to spread., Methods: We developed a computational simulation model representing the clinical course, the health effects, and the associated costs of a person with Long COVID., Results: Simulations show that the average total cost of a Long COVID case can range from $5,084-$11,646 (assuming symptoms only last 1 year) with 92.5%-95.2% of these costs being productivity losses. Therefore, the current number of Long COVID cases could end up costing society at least $2.01-$6.56 billion, employers at least $1.99-$6.49 billion in productivity losses, and third-party payers $21-68.5 million annually (6%-20% probability of developing Long COVID). These cases would accrue 35,808-121,259 QALYs lost and 13,484-45,468 DALYs. Moreover, each year, there may be an additional $698.5 million in total costs, 14,685 QALYs lost, and 5,628 DALYs, if the incidence of COVID is 100 per 10,000 persons (similar to that seen in 2023). Every 10-point increase in COVID incidence results in an additional $365 million in total costs, 5,070 QALYs lost, and 1,900 DALYs each year., Conclusion: The current health and economic burden of Long COVID may already exceed that of a number of other chronic disease and will continue to grow each year as there are more and more COVID-19 cases. This could be a significant drain on businesses, third party payers, the healthcare system, and all of society., (© The Author(s) 2025. Published by Oxford University Press on behalf of Infectious Diseases Society of America. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)

Background: Lymphocytic choriomeningitis virus (LCMV) infection in immunocompromised hosts can result in disseminated disease, meningoencephalitis, and death. Published cases in transplant recipients have been traced to transmission from infected donors. We report 2 cases of serious, non-donor-derived LCMV infection in solid organ transplant recipients., Methods: Initial identification of LCMV infection was done by using metagenomic next-generation sequencing (mNGS). Subsequent evaluations and confirmatory testing involved molecular diagnostics, serology, and phylogenetic analysis. A detailed epidemiologic investigation was conducted., Results: LCMV was detected by mNGS in 2 solid organ transplant recipients from distinct donors. A heart transplant recipient (from donor 1) died of progressive, disseminated LCMV infection, while a kidney transplant recipient (from donor 2) with LCMV meningoencephalitis survived. A multistate laboratory and epidemiologic investigation of both donors and all their organ recipients was initiated. Postmortem samples were obtained from both donors, and pretransplant and/or posttransplant samples were obtained from 5 of the 6 organ recipients. mNGS, serologic, and real-time reverse-transcription polymerase chain reaction testing confirmed LCMV infection in both solid organ transplant recipients. Epidemiologic investigation revealed significant pretransplant rodent exposures for both LCMV-infected recipients. Laboratory studies for the other organ recipients from both donors were negative for LCMV infection., Conclusions: Our investigations suggest that LCMV infection in 2 solid organ transplant recipients originated from rodent exposure preceding transplantation and were not donor derived. Although uncommon, healthcare providers should be aware of LCMV-associated serious and life-threatening illness in immunocompromised hosts. Diagnostic modalities are limited to reference laboratories., Competing Interests: Potential conflicts of interest. C. Y. C. receives research funding from Abbott Laboratories and Delve Bio for pathogen detection and discovery projects using mNGS and is a cofounder of and owns equity in Delve Bio. C. Y. C. is also a coinventor on US patent 11380421, Pathogen Detection Using Next Generation Sequencing, under which algorithms for taxonomic classification, filtering, and pathogen detection are used by SURPI+ software. All other authors report no potential conflicts., (Published by Oxford University Press on behalf of Infectious Diseases Society of America 2025.)

Aims: Thyroid hormones (TH) are major regulators of cell differentiation, growth, and metabolic rate. TH synthesis in the thyroid gland requires high amounts of H 2 O 2 to oxidize iodide for the iodination of thyroglobulin (TG). Retinol Saturase (RetSat) is an oxidoreductase implicated in dihydroretinol formation and cellular sensitivity toward peroxides and ferroptosis. RetSat is highly expressed in metabolically active organs where it regulates lipid metabolism and the production of reactive oxygen species. Due to the high expression of RetSat in the thyroid gland and its role in peroxide sensitivity, we investigated the regulation and function of RetSat in the thyroid gland in appropriate mouse models. Results: RetSat is strongly expressed in thyrocytes, induced by hypothyroidism, and decreased by iodide overload in mice. Thyrocyte-specific deletion of RetSat increased circulating thyroid-stimulating hormone levels, altered thyroid morphology, and disturbed metabolic homeostasis in a diet- and sex-dependent manner without major effects on the concentrations of circulating TH. Moreover, deletion of RetSat increased TG protein levels but lowered TG iodination upon iodide overload. In cultured thyrocytes, acute RetSat depletion altered the expression of genes involved in TH biosynthesis and the response to endoplasmic reticulum stress. Innovation: This is the first report that specifically dissects the regulation and function of the oxidoreductase RetSat in the thyroid gland. Conclusion: Deletion of RetSat in thyrocytes induces compensatory feedback mechanisms to maintain TH homeostasis in mice. We conclude that RetSat in the thyroid gland is required for TH biosynthesis and secretion and metabolic homeostasis in mice. Antioxid. Redox Signal. 00, 000-000.

Objective: To describe a combined transdiaphragmatic and caudal median sternotomy (TDCM) approach to the accessory lung lobe and to compare its accessibility with intercostal thoracotomy (ICT) and median sternotomy (MS)., Study Design: Cadaveric study., Animals: Twelve canine cadavers., Methods: Cadavers underwent an accessory lung lobectomy using an articulating EndoGIA stapler via randomly assigned approach: ICT (n = 4), MS (n = 4) or TDCM (n = 4). The percentage of accessory lung tissue removed was measured in surface area and weight. Exposure was measured as area of cavitary or bicavitary exposure at maximal retraction, by tracing a line around the circumference of the exposed cavity using an imaging software. Staple line leak pressures were evaluated to 40 cmH 2 O., Results: The average area of exposure was larger in the TDCM approach (TDCM = 193.5 cm 2 , MS = 106.5 cm 2 , ICT = 73.5 cm 2 ); (p = .01). Two of four ICT staple lines leaked at 40 cmH 2 O or lower, and 1/4 MS resulted in iatrogenic damage to an adjacent lobe. There was no difference in the percentage of the lobe excised by weight or surface area between groups., Conclusion: The transdiaphragmatic and caudal median sternotomy approach provided greater exposure, although the percentage of the lobe excised and the surgical time did not differ between approaches., Clinical Significance: All three approaches allowed for adequate excision of the accessory lung lobe (ALL) with similar surgical times; however, the TDCM approach provided a greater area of exposure, which could increase accessibility to the ALL., (© 2024 American College of Veterinary Surgeons.)