Mpox, known before now as monkeypox, is a novel zoonotic disease that may infect both humans and animals. It usually spreads by direct contact with bodily fluids, lesion material, or fomites (such as contaminated linens) and prolonged face-to-face contact. Mpox can spread to laboratory animals in a research laboratory through either a general outbreak or during procedures. Animal models are essential as we learn more about how infections occur and how to treat illnesses in both humans and animals which require laboratory procedures with mpox virus. As drug-resistant organisms proliferate, bioterrorism becomes a greater danger, international trade and travel expand, and the number of newly developing infectious illnesses grows, the use of animals in infectious disease research has increased. Animal research offers a solid basis for clinical trials used in standard medication development.Animal studies must be planned to produce conclusive effectiveness evidence that is robust, rigorous, and repeatable per the animal rule so that the agency may depend on the results when making regulatory decisions.There is a need to understand the transmission risk and biosafety protocol to be in place in laboratory settings to prevent an outbreak and probably contain an outbreak. Hence, this review discussed the overview of mpox in animal research, biosafety protocols in mpox research, laboratory waste management methods, legal and ethical considerations in mpox research, challenges in carrying out mpox research and future directions.

Background: Despite advancements in laboratory animal facility management, pinworm infections remain a persistent issue in immunodeficient mouse colonies. Rapid diagnosis and treatment are crucial to mitigating potential scientific and economic consequences. Effective control requires both the administration of anthelmintic agents and rigorous environmental decontamination. However, the safety and efficacy of these treatments in genetically modified mouse models remains uncertain.Case presentation Aspiculuris tetraptera infestation was identified in multiple immunodeficient mouse models housed in a laboratory facility. Diagnosis was confirmed through fecal flotation for egg detection and necropsy for adult worm examination in the large intestines. Mice received three subcutaneous ivermectin injections at two-week intervals, coupled with environmental decontamination using ivermectin spray for four consecutive weeks. Following treatment, all colonies tested negative for A. tetraptera without any mortality. Conclusions A combination of subcutaneous ivermectin injection and environmental spray application effectively eradicated A. tetraptera infestation in immunodeficient mouse colonies. The treatment protocol led to the complete elimination of eggs and adult worms, offering a practical strategy for managing pinworm infections in genetically modified mouse models. Limitations include the small sample size, and the lack of a comprehensive evaluation of physiological and metabolic safety in immunodeficient mice. Further validation will be required to confirm the broader applicability of this approach.

Background: The taxonomic status of house mice (Mus musculus) on the Korean Peninsula has long been debated due to conflicting morphological classifications and limited genetic evidence. Historically, three subspecies (M. m.molossinus, M. m. utsuryonis, and M. m. yamashinai) have been proposed based on external traits, although the validity of these proposals remains uncertain. Thus, this study aimed to integrate genetic and morphological analyses to clarify the phylogenetic relationships of Korean mice relative to the well-known primary M. musculus subspecies and evaluate the taxonomic distinctiveness. Results: Genetic analysis of mitochondrial DNA (cytb gene) from mice across Korea, including islands, mountains, and agricultural fields, confirmed that these mice belong to the Eurasian M. m. musculus lineage. Morphologically, Korean mice exhibited tail ratios consistent with previously assigned subspecies, suggesting these traits represent intraspecific variation within M. m. musculus. Craniometric analyses revealed distinctive features, such as a shorter, narrower premaxillary tooth-patch width and a longer maxillary tooth-row length, thereby distinguishing these mice from laboratory strains derived from M. m. domesticus. These cranial configurations, visualized via three-dimensional micro-computed tomography scans, further supported the morphological divergence of these mice from other subspecies. Conclusions Our findings indicate that Korean house mice belong to a single subspecific group within M. m.musculus, with observed morphological variations reflecting local adaptation rather than distinct taxonomic divisions.The Korean Peninsula likely served as an ecological bridge, facilitating the spatiotemporal diversification of M. m.musculus across East Eurasia. This study resolves longstanding taxonomic ambiguities and underscores the subspecific status of Korean house mice within M. m. musculus. These insights provide a foundation for understanding the biogeographic history of human commensal species and future biomedical research utilizing wild-derived mouse models.

Background: Mice are useful small animal models to study the pathogenesis of SARS-CoV-2 infection. As the ancestral SARS-CoV-2 strains did not utilize murine Ace2 as a receptor, wild-type mice were not susceptible to the SARS-CoV-2 infection. Infection of human ACE2-expressing transgenic mice with SARS-CoV-2 induces fatal encephalitis, which is not commonly observed in humans. We and others have previously demonstrated the ability of the SARS-CoV-2 Beta variant to productively infect wild-type mice. Herein, we employed RNA-seq to investigate the transcriptomic landscapes in the lungs after the infection of wild-type mice with SARS-CoV-2 Beta variant. Methods: We intranasally infected 6-week-old wild-type C57BL/6J mice with the SARS-CoV-2 (B.1.351 strain) and collected lungs at 3- and 6-days post-infection for RNA-sequencing. We used the Limma-Voom package to identify differentially expressed genes (DEGs) and the fgsea package for pathway enrichment analysis. We used Cytoscape to identify hub genes and gene networks. Lastly, we employed RT-qPCR and multiplex assay to validate the RNA-seq data. Results: Using a cutoff of an adjusted p-value below 0.05 and an absolute log2 fold change value greater than 0.75, we identified 285 DEGs on day 3 and 46 DEGs on day 6. The canonical pathways analysis showed that several key pathways such as apoptosis and cytokine response were upregulated in the infected lungs. Protein-protein interaction analyses identified innovative target genes such as if11, Ccna2, and Aurkb. We also identified the top 10 hub genes that included Prc1, Ube2c, Ccnb2, Ncapg, Aurkb, Cep55, Mki67, Dlgap5, Ccna2, and Kif11. RT-qPCR analysis for Tnfa, Il6, Ccl2, and Ccl3 further validated the RNA-seq analysis. Consistent with gene expression results, we detected significantly increased protein levels of various inflammatory mediators such as IL-6, CCL2, CXCL2, and CXCL10 in the infected lungs. Conclusions This is the first transcriptomic analysis of the lungs of wild-type mice infected with a clinical isolate of SARS-CoV-2. Our findings provide a further understanding of the pathogenic events that occur in this mouse model of SARS-CoV-2 infection.

Hypertension is a prevalent condition that significantly raises the incidence of cerebrovascular and cognitive disorders. This review focuses on the factors most closely linked to stroke, cognitive impairment, and Alzheimer’s disease. Research into pathophysiology and treatment of hypertensive brain damage has greatly benefited from rodent models, which have been crucial in uncovering the underlying mechanisms and developing effective therapeutic strategies. Rodent models, particularly spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHR-SP), have been essential in elucidating the pathophysiological mechanisms connecting hypertension to brain damage. These models exhibit structural and functional cerebrovascular alterations, including blood-brain barrier disruption, microvascular rarefaction, and neuroinflammation. Interventions targeting the renin-angiotensin system have shown promise in mitigating these adverse effects. This review synthesizes current findings from rodent studies, underscoring the pivotal impact of hypertension in brain pathology and the potential therapeutic benefits of antihypertensive treatments.

Background: Malignant pleural effusion (MPE), a common complication of advanced cancers, is associated with poor prognosis and reduced quality of life. Although host–tumor interactions are known to drive MPE development, the associated immune dynamics during disease progression remain unclear. Using a Lewis lung carcinoma-induced MPE model in C57BL/6JNidfc mice, we systematically evaluated general parameters and immune cell changes at two-day intervals throughout disease progression. Results: The day of Lewis lung carcinoma cell injection into the pleural space was designated as day 0. By day 10 post-injection (p.i.), MPE-bearing mice exhibited ~ 10% body weight loss, marking the experimental endpoint. Pleural tumor mass and pleural effusion volume were minimal up to day 4 p.i. but increased sharply from day 6 onward.CD45⁺ immune cell counts rose over time, and days 6, 8, and 10 p.i. marked key stages of MPE progression. On day 6, B cells, T cells, and natural killer cells, but not macrophages and neutrophils, increased significantly compared to earlier timepoints. By day 8, all immune cell subsets except T cells exceeded day 6 levels, and at day 10, natural killer cell numbers declined while others continued to increase. Besides, the numbers of CD8⁺ T cells, Th1 cells, regulatory T cells, and M2 macrophages progressively increased from day 6 to 10. Based on these data, days 6 and 10 were defined as early and advanced MPE stages, respectively, with distinct immune phenotypes. In advanced MPE, CD8⁺ T cells displayed reduced IFN-γ, TNF-α, Granzyme B, Perforin, FasL, and Ki-67, but upregulated PD-1 and CTLA-4 relative to early stage. Similarly, Th1 cells showed decreased IFN-γ, TNF-α, and IL-2 production along with reduced Ki-67 expression. Advanced-stage M2 macrophages exhibited lower MHC-II levels and impaired phagocytosis, but higher PD-L1 and IL-10 production, while neutrophils showed reduced TNF-α release and phagocytic activity. Conclusions Our findings characterize the temporal immune dynamics associated with MPE progression in a mouse model, revealing a transition from an early immunostimulatory state to a late immunosuppressive state. This study enhances our understanding of MPE immunopathogenesis and provides a foundation for developing precise, stagespecific therapeutic strategies.

Background: Lapsi (Choerospondias axillaris), a plant native to Nepal, has been traditionally used in Asian countries to treat cardiovascular conditions. However, its effects on immune regulatory function remain largely unexplored.This study aimed to in vivo evaluate the immunoregulatory properties of Lapsi fruit extract in mice on immunotoxic responses with analysis on in vitro mechanism for immune suppression, oxidative stress, and inflammatory response.Male Balb/c mice were intragastrically administered various doses of the extract for 21 days. In some mice, immune suppression was induced with cyclophosphamide, and subsequent immune recovery was assessed. In addition, RAW264.7 cells and THP-1-derived macrophages were treated in vitro with lipopolysaccharide and different concentrations of the extract. Results: Administration of extract increased the IgG2a/IgG1 ratio while reducing serum IgE and IgG1 level compared with control mice. Tumor necrosis factor (TNF)-α and interleukin (IL)-17 levels were lower in splenic culture supernatants of mice administered extract. Lapsi extract also effectively reversed cyclophosphamide (CP)-induced immunosuppression by enhancing serum levels of IgA and IgG2a, of interferon-γ and interleukin (IL)-4 secreted by splenic T cells, and of IgG1 and IgG2a secreted by B cells, as well as by increasing immune cell counts. In cell cultures, the extract decreased the levels of inflammation markers, including nitric oxide, reactive oxygen species, prostaglandin E2, and pro-inflammatory cytokines (IL-6, TNF-α, and IL-1β). Mechanistic analysis showed that Lapsi extract modulated the NF-κB p65, MAPK, and inflammasome pathways. Conclusions Lapsi extract may act as both an immunostimulatory and anti-inflammatory agent, indicating its potential as a candidate immunomodulatory activity under polyclonal and CP-suppressed conditions; however, further disease-specific studies, along with isolation and characterization of active phytochemicals, are warranted to evaluate its therapeutic applicability.

Background: Farnesoid X receptor (FXR) is known to play important roles in glucose and lipid metabolism. We aimed to evaluate effects of FXR agonist on metabolic disorders in db/db mice. Seven week-old db/db mice were injected FXR agonist GW4064 (30 mg/kg/day) or carrier solution (dimethyl sulfoxide) intraperitoneally for 4 weeks. Body weight, food intake, and blood glucose levels were measured weekly. Glucose tolerance test and insulin tolerance test were performed at the end of study. Hepatic genes involed in lipogenesis and gluconeogenesis were analyzed by real time polymerase chain reaction. Endoplasmic reticulum stress markers were analyzed by western blot. Results: GW4064 treatment significantly attenuated weight gain, and improved glucose intolerance and insulin resistance in db/db mice. In addition, GW4064 treatment significantly repressed hepatic steatosis. GW4064 treatment significantly lowered hepatic gene expression of phosphoenolpyruvate carboxykinase 1, glucose 6-phosphatase, and sterol regulatory element binding protein 1c. GW4064 treatment significantly lowered the protein levels of ATF6, CHOP, Caspase3, and Cleaved Caspase3 in liver. FXR agonist GW4064 showed beneficial effects on weight gain, glucose intolerance, insulin resistance, hepatic steatosis, and hepatic ER stress. Conclusions These findings suggest that FXR agonists are promising therapeutic agents for treatment of various metabolic disorders.

Hemorrhage is a prevalent side effect of various injuries and can be life-threatening in certain instances. It is categorized into compressible and non-compressible types, each necessitating distinct modeling, laboratory assessments, and hemostatic approaches. This study utilized the keywords Hemorrhage, Bleeding, Animal Modeling, and Hemostat in reputable databases. The findings indicate that femoral artery hemorrhage and hepatic parenchymal hemorrhage are the predominant modeling techniques for compressible and noncompressible bleeding, respectively. Furthermore, it is noted that animal models of compressible hemorrhages are primarily situated in superficial body areas to investigate dressing or additive hemostats, while non-compressible hemorrhage models, typically located in visceral organs, are employed to examine adhesive or surgical instrumentbased hemostats.