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BackgroundFor 15 months in 1981-1982, the commercial milk supply on the Hawaiian island of Oahu was contaminated with heptachlor epoxide, a metabolite of the insecticide heptachlor, resulting in gestational and/or lactational exposure to offspring of women who drank cow milk during that period.ObjectiveTo determine whether gestational and lactational exposure to heptachlor epoxide alters reproductive function and age at puberty in men or women.Methods457 participants were recruited from a prior high school enrollment sampling frame of 20,000 adults born during 1981-1982 who lived on Oahu since at least first grade. Number of glasses of cow milk consumed weekly by the mother during the participant's gestation was used as a surrogate measure of heptachlor epoxide exposure. Reproductive function measures included semen analyses; reproductive hormones or their metabolites in daily urine specimens for one menstrual cycle; serum reproductive hormone levels in both sexes; and reported ages of onset for pubertal milestones.ResultsWe observed no strong associations of heptachlor epoxide exposure during gestation and lactation with reproductive endpoints. In females, heptachlor epoxide exposure was associated with longer luteal phase length and slower drop in the ratio of estradiol to progesterone metabolites after ovulation. In males, heptachlor epoxide exposure was weakly associated with higher serum follicle stimulating hormone and luteinizing hormone concentrations, but no dose-response relationship was apparent.ConclusionsThe results provide limited evidence that gestational and lactational exposure to heptachlor epoxide, due to milk contamination on Oahu in 1981-1982, resulted in clinically significant disturbances of reproductive function in men or women.

Animal-vehicle collisions affect human safety, property and wildlife, and the number of animal-vehicle collisions has substantially increased across much of North America over the last decades. Systematically collected animal-vehicle collision data help estimate the magnitude of the problem and help record potential changes in animal-vehicle collisions over time. Such data also allow for the identification and prioritization of locations that may require mitigation. Furthermore, systematically collected animal-vehicle collision data allow for the evaluation of the effectiveness of mitigation measures in reducing the number of animal-vehicle collisions. In the United States and Canada, animal-vehicle collision data are typically collected and managed by transportation agencies, law enforcement agencies and/or natural resource management agencies. These activities result in two types of data: data from accident reports (AR data) and data based on animal carcass counts (AC data). Here we report on a survey that examined the extent to which AR and AC data are collected across the United States and Canada. While a substantial percentage of the DOTs and DNRs collect and manage AR and/or AC data, many of them do not. Furthermore, DOTs and DNRs that do collect or manage AR or AC data typically do this for different or only partly overlapping reasons. In addition, DOTs and DNRs use different reporting thresholds, have varying search and reporting effort, and only have partial overlap in the parameters recorded. These differences also occur between DOTs and between DNRs, and oftentimes one and the same organization collects inconsistent data as certain parameters may only be recorded ‘sometimes’. These differences and inconsistencies affect the comparability and ultimately the usefulness of the data. Before an AR or AC program is initiated or improved, it is important to illustrate the needs and benefits of such data collection. We list the most important needs and benefits and provide considerations for the initiation or improvement of AR and AC data collection programs.

Objective: This study was undertaken to identify blood markers of juvenile dermatomyositis (DM) disease activity (DA), which are needed to improve disease management. Methods: The study comprised a total of 123 juvenile DM patients and 53 healthy controls. Results of laboratory tests (aldolase, creatinine kinase, lactate dehydrogenase [LDH], aspartate aminotransferase) and clinical measures of DA in patients with juvenile DM, including the Manual Muscle Testing in 8 muscles (MMT‐8), Childhood Myositis Assessment Scale (CMAS), and disease activity scores (DAS) (total DAS for juvenile DM, the muscle DAS, and the skin DAS), were recorded when available. Surface phenotype of peripheral blood mononuclear cells was assessed using flow cytometry. Whole blood transcriptional profiles were studied using either RNA‐sequencing or microarrays. Differential gene expression was determined using DESeq and compared by pathway and gene ontology analyses. Results: Conventional memory (CD27+IgD–) B cells expressing low CXCR5 levels (CXCR5low/– CM B cells) were significantly increased in frequency and absolute numbers in 2 independent cohorts of juvenile DM patients compared with healthy controls. The frequency of CD4+ Th2 memory cells (CD45RA–CXCR5–CCR6–CXCR3–) was also increased in juvenile DM, especially in patients who were within <1 year from diagnosis. The frequency of CXCR5low/– CM B cells correlated with serum aldolase levels and with a blood interferon‐stimulated gene transcriptional signature. Furthermore, both the frequency and absolute numbers of CXCR5low/– CM B cells correlated with clinical and laboratory measures of muscle DA (MMT‐8, CMAS, aldolase, and LDH). Conclusion: These findings suggest that both CM B cells lacking the CXCR5 follicular marker and CXCR5– Th2 cells represent potential biomarkers of DA in juvenile DM and may contribute to its pathogenesis. [ABSTRACT FROM AUTHOR]

The survival, reproduction and birth rates of bison in Yellowstone National Park to study their overabundance in the park are examined. It is suggested that eradication of brucellosis by vaccination would result in an increase in their population, thus facilitating their movement outside the park.

The density-dependent changes in population growth rates for bison during 1970 to 2000 were detected as numbers increased from to more than 3000 animals. Results concluded that pulses of climate-induced dispersal of bison from the central herd to the northern range during winter could create a source-sink dynamic that worsens the current controversy about management of bison.

A 16-year-old boy presents with a massive acute pulmonary embolism requiring emergent surgical embolectomy and extracorporeal membrane oxygenation for right ventricular failure. Subsequently he was diagnosed with catastrophic antiphospholipid syndrome requiring immunosuppression, and then pneumatoceles causing tension pneumothoraxes. The rarity of presentation in a child required collaboration across pediatric and adult disciplines., Competing Interests: The authors have reported that they have no relationships relevant to the contents of this paper to disclose., (© 2025 The Authors.)

Systemic Lupus Erythematosus (SLE) is characterized by autoreactive B cell activation, upregulation of Type I Interferon (IFN) and widespread inflammation. Mitochondrial nucleic acids (NAs) are increasingly recognized as triggers of IFN 1 . Thus, defective removal of mitochondria from mature red blood cells (Mito + RBCs), a feature of SLE, contributes to IFN production by myeloid cells 2 . Here we identify blood monocytes (Mo) that have internalized RBCs and co-express IFN-stimulated genes (ISGs) and interleukin-1β (IL-1β) in SLE patients with active disease. We show that ISG expression requires the interaction between Mito + RBC-derived mitochondrial DNA (mtDNA) and cGAS, while IL-1β production entails Mito + RBC-derived mitochondrial RNA (mtRNA) triggering of RIG-I-like receptors (RLRs). This leads to the cytosolic release of Mo-derived mtDNA that activates the NLRP3 inflammasome. Importantly, IL-1β release depends on the IFN-inducible myxovirus resistant protein 1 (MxA), which enables the translocation of this cytokine into a trans-Golgi network (TGN)-mediated unconventional secretory pathway. Our study highlights a novel and synergistic pathway involving IFN and the NLRP3 inflammasome in SLE.