Laboratory Animal Research最新文献

{"title":"Faster immobilization and recovery with remimazolam compared to midazolam in medetomidine-butorphanol balanced anesthesia in male Sprague-Dawley rats: a randomized crossover study.","authors":"Takeru Sasaki, Masaki Watanabe, Ryuya Nakagawa, Riyu Inoue, Nobuya Sasaki","doi":"10.1186/s42826-026-00300-x","DOIUrl":"10.1186/s42826-026-00300-x","url":null,"abstract":"<p><strong>Background: </strong>Balanced injectable anesthesia combining an α2-adrenoceptor agonist, a benzodiazepine, and an opioid is widely used in laboratory rodents because it provides sedation, muscle relaxation, and analgesia through complementary pharmacological mechanisms. In Japan, a mixture of medetomidine, midazolam, and butorphanol (MMB) is commonly used as an injectable anesthetic regimen in mice and rats. Remimazolam is an ultra-short-acting benzodiazepine that is rapidly metabolized by tissue esterases and produces no active metabolites. Because of its rapid metabolism and predictable pharmacokinetic profile, remimazolam has attracted attention as a sedative agent in clinical anesthesia and procedural sedation. Replacing midazolam with remimazolam generates a novel balanced anesthetic combination consisting of medetomidine, remimazolam, and butorphanol (MRB). Although this regimen has been investigated in mice, its anesthetic characteristics in rats have not yet been fully evaluated. The present study aimed to compare the anesthetic and physiological effects of MMB and MRB anesthesia in Sprague-Dawley (SD) rats.</p><p><strong>Results: </strong>Both mixtures induced anesthesia in all animals. The MRB regimen produced faster immobilization than the MMB regimen, whereas the time to loss of righting reflex did not differ significantly between regimens. Reflex-based anesthetic depth during the observation period was comparable between the two regimens. Physiological monitoring revealed regimen-dependent differences in time-course dynamics, particularly for oxygen saturation and respiratory rate. For oxygen saturation, pointwise comparisons showed no significant difference after Holm correction, whereas the area under the curve (AUC) analysis did show a significant difference. Linear mixed-effects modeling (LMM) further demonstrated significant group, time, and group × time interaction effects for oxygen saturation, and significant time and group × time interaction effects for respiratory rate. Recovery after atipamezole (ATI) administration was faster in the MRB group, as shown by both return of righting reflex and behavioral recovery score analyses.</p><p><strong>Conclusions: </strong>MRB produced a reflex-score profile comparable to that of MMB while accelerating early immobilization and antagonist-assisted recovery. Substitution of midazolam with remimazolam also altered SpO₂ and respiratory-rate trajectories. MRB may therefore be useful when rapid recovery is desired. However, comparability was limited to the reflex-based scoring system; these findings do not establish equivalence for painful or invasive surgical procedures.</p>","PeriodicalId":17993,"journal":{"name":"Laboratory Animal Research","volume":"42 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13663112/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149182883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intraluminal micro-stenting improves urinary tract reconstruction in murine kidney transplant model.","authors":"Zi-Jie Xu, Long He, Zheng Tang, Ren-Jie Wang, Yin Yang, Kai-Ying Chen, Ze-Tao Ding, Jun-Ru Lu, Hao-Dong Chi, Ji-Fu Ge, Zhi-Hong Liu","doi":"10.1186/s42826-026-00301-w","DOIUrl":"10.1186/s42826-026-00301-w","url":null,"abstract":"<p><strong>Background: </strong>Urinary tract reconstruction is a key technical barrier in murine kidney transplantation due to the tiny ureteral caliber. Conventional methods are technically demanding with high morbidity. This study assesses a refined intraluminal stenting approach for better surgical stability, fewer complications, and preserved anti-reflux structural anatomy of the ureterovesical junction. We performed 88 orthotopic mouse kidney transplantations using three distinct reconstruction modalities: bladder patch (n = 31), ureter implantation (n = 28), and intraluminal stenting (n = 29). The stenting protocol utilized a micro-polyethylene (PE) stent to achieve end-to-end ureteral alignment. Outcomes included operative efficiency, learning curve trajectories, postoperative survival, and urinary-related morbidity.</p><p><strong>Results: </strong>The stenting cohort achieved a 14-day survival rate of 96.6% (28/29), significantly higher than the bladder patch group (67.7%, 21/31; p = 0.006), while the difference compared with the ureter implantation group (82.1%, 23/28) did not reach statistical significance (p = 0.102). Intraluminal stenting markedly reduced reconstruction time (8'22''±0'41'', p < 0.05 vs. both control groups) and was associated with an accelerated proficiency acquisition curve. The overall urological morbidity in the stenting group was 10.3% (3/29), consisting of 1 case of mild urinary leakage and 2 cases of mild hydronephrosis, which was significantly lower than in the bladder patch (58.1%, 18/31) and ureter implantation (42.9%, 12/28) cohorts (p < 0.05 for morbidity comparison). Notably, this approach effectively precluded severe complications including ischemic necrosis, ureteral dislodgement, and obstruction, with no urinary tract reconstruction-related deaths observed.</p><p><strong>Conclusions: </strong>This retrospective study shows that the intraluminal stenting technique offers a reliable and highly reproducible approach for urinary tract reconstruction in murine kidney transplantation. This modality significantly minimizes technical complexity and postoperative morbidity, and maintains the intact ureterovesical anatomy that provides the structural foundation for physiological anti-reflux function. It provides an optimized surgical platform for short-term experimental protocols, particularly in acute rejection research.</p>","PeriodicalId":17993,"journal":{"name":"Laboratory Animal Research","volume":"42 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13663044/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149182904","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rethinking non-human primate models for emerging viral infections after COVID-19.","authors":"Dong-Yeon Kim, Jung Joo Hong","doi":"10.1186/s42826-026-00299-1","DOIUrl":"10.1186/s42826-026-00299-1","url":null,"abstract":"<p><p>Non-human primates (NHPs) retain particular value in emerging viral infection research when questions require integrated analysis of systemic viral kinetics, protective immunity, tissue pathology, or longitudinal outcomes. However, their cost, limited availability, specialized husbandry, and ethical constraints preclude their routine use as default screening platforms. Using severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) as a case study, we compare how rhesus macaques, cynomolgus macaques, African green monkeys, baboons, and marmosets have contributed to studies of pathogenesis, vaccine protection, therapeutic efficacy, immune memory, and post-acute outcomes. We emphasize that these species-question relationships cannot be transferred uncritically to future pathogens; model suitability must be re-established according to receptor usage, tissue tropism, disease phenotype, and experimental objective. AI-guided prediction, human organoids, and organ-on-chip systems can support this process by prioritizing variants and candidates, identifying tissue-specific mechanisms, and refining endpoints before NHP studies begin. We therefore propose a question-driven workflow in which computational and human-relevant platforms narrow the evidence gap before fit-for-purpose NHP validation. This strategy can improve interpretability, reproducibility, and alignment with the 3Rs while preserving NHP use for questions that require intact organism-level biology.</p>","PeriodicalId":17993,"journal":{"name":"Laboratory Animal Research","volume":"42 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13602516/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149039742","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel mouse calvarial defect model of osteomyelitis induced by Staphylococcus aureus (ATCC 6538).","authors":"Seongju Ko, Heung Myong Woo, Kihoon Kim, Junhyung Kim","doi":"10.1186/s42826-026-00289-3","DOIUrl":"10.1186/s42826-026-00289-3","url":null,"abstract":"<p><strong>Background: </strong>Osteomyelitis is a severe bone infection that causes chronic inflammation, tissue necrosis, and vascular compromise. The infection often requires surgical debridement and prolonged high-dose antibiotic therapy. Despite numerous osteomyelitis models in different species and skeletal sites, a standardized mouse calvarial defect model that reflects cranial intramembranous ossification and enables research on craniofacial infection is unavailable. Therefore, this study aimed to establish a reproducible mouse calvarial defect osteomyelitis model and to define an inoculum threshold that reliably induces infection while preserving experimental feasibility for downstream mechanistic and therapeutic studies.</p><p><strong>Results: </strong>Bilateral calvarial defects (diameter = 4 mm) were created in C57BL/6J mice, and the defects were inoculated with graded doses of Staphylococcus aureus (ATCC 6538). Four weeks postoperatively, micro-computed tomography (micro-CT), bacteriological culture, and histopathological scoring for inflammation, necrosis, and bacterial presence were performed. Mice receiving 5 µL of 10⁸ colony-forming units (CFU)/mL showed clear osteomyelitis, with significantly lower bone volume/total volume and defect union scores, together with higher CFU counts and histologic scores, compared with the controls (all p < 0.05). Bone mineral density showed no significant pairwise difference between groups, but a significant linear decreasing trend was detected across the ordered groups (p for trend = 0.0031). The lower inoculum groups exhibited only mild or no significant changes upon micro-CT imaging and histological evaluation, indicating incomplete or absent infection. Consequently, 10⁸ CFU/mL was identified as a practical cutoff for consistently inducing destructive cranial osteomyelitis in this model.</p><p><strong>Conclusions: </strong>This study established a mouse model of calvarial defect osteomyelitis that recapitulates the key features of cranial bone infection, including bone loss, impaired union, and robust inflammatory and bacterial burdens. This model provides a platform for studying the mechanisms of cranial osteomyelitis by incorporating genetically modified mice and testing local and systemic therapeutic strategies. Although only a single S. aureus strain and limited ancillary staining were used, the study data lay the groundwork for future investigations that incorporate diverse clinical isolates, comorbid conditions, and advanced regenerative or anti-infective interventions targeting craniofacial bone infections.</p>","PeriodicalId":17993,"journal":{"name":"Laboratory Animal Research","volume":"42 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13591727/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149012697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advancing neurofibromatosis research: a comparative review of animal models and their utility in dissecting the tumor microenvironment.","authors":"Ai-Lun Li, Ya-Mei Chen","doi":"10.1186/s42826-026-00298-2","DOIUrl":"10.1186/s42826-026-00298-2","url":null,"abstract":"<p><p>Neurofibromatosis is a genetic disorder characterized by nervous system tumors arising primarily from NF1 or NF2 mutations. Given the complexity of the genetic background and heterogeneity of associated tumor phenotypes in neurofibromatosis, mechanistic investigations rely heavily on experimental animal models. Human tissue-based studies alone cannot fully elucidate causal relationships, temporal dynamics, modifier gene effects, or cell type-specific contributions to tumor development, progression, and microenvironmental regulation. Consequently, various animal models have been developed, including genetically engineered mouse models, large-animal systems, alternative vertebrate models, and transplantation-based approaches. These experimental platforms enable the controlled manipulation of gene dosage, lineage-specific gene deletion, immune modulation, targeted disruption of stromal and extracellular matrix components, and evaluation of therapeutic response and drug resistance mechanisms. Animal models have helped demonstrate the cell-autonomous and non-cell-autonomous mechanisms underlying neurofibromatosis tumorigenesis. Furthermore, sustained tumor maintenance and progression require coordinated interactions between neoplastic cells and their surrounding microenvironment. Notably, these experimental systems offer a temporal resolution not achievable in clinical specimens, demonstrating that microenvironmental alterations may precede overt tumor formation. Such findings depict the tumor microenvironment (TME) as an active contributor to disease rather than merely as a consequence of tumor growth. In this review, we evaluate the experimental scope, methodological strengths, and inherent limitations of current animal models used in neurofibromatosis research, with emphasis on their utility in elucidating interactions within the TME and non-neoplastic disease manifestations. This work characterizes model-specific advantages and constraints to emphasize the continued importance of animal models as essential tools for hypothesis-driven investigation and translational development in elucidating the various attributes of neurofibromatosis.</p>","PeriodicalId":17993,"journal":{"name":"Laboratory Animal Research","volume":"42 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13589872/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149012706","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reframing emergency preparedness from facility survival to laboratory animal welfare.","authors":"Seung Yeon Kim, Ji Min Lee, Seung Hyeok Seok","doi":"10.1186/s42826-026-00295-5","DOIUrl":"10.1186/s42826-026-00295-5","url":null,"abstract":"<p><strong>Background: </strong>Natural disasters, infrastructure failures, and infectious disease outbreaks can disrupt the operations of laboratory animal facilities and threaten both research continuity and animal welfare. Previous events, including Tropical Storm Allison and the Great East Japan Earthquake, demonstrated the vulnerability of laboratory animal populations during emergencies and highlighted the need to incorporate animal welfare considerations into emergency preparedness planning. The aim of this study was to identify key elements of emergency preparedness programs for laboratory animal facilities and to propose a framework to support the development of practical Standard Operating Procedures (SOPs) in which animal welfare considerations are integrated into facility operations and decision-making processes during emergencies.</p><p><strong>Results: </strong>Regulatory frameworks and guidance documents from the United States, Europe, Canada, and Korea were reviewed and compared to identify approaches applicable to laboratory animal facility management. The analysis included definitions of emergencies, core program components, veterinary oversight systems, and decision-making structures across these four regulatory contexts. Despite differences in regulatory approaches and institutional contexts, common elements were identified and organized into three functional domains: continuity of facility operations, protection of animal welfare, and institutional response capacity. Based on these findings, we propose an integrated emergency preparedness framework and a stepwise operational checklist intended to facilitate the integration of welfare priorities into emergency planning and response.</p><p><strong>Conclusions: </strong>Emergency preparedness should not be regarded solely as an operational requirement. In laboratory animal facilities, it should be understood as an extension of the animal welfare program that, while prioritizing personnel safety and institutional resilience, also seeks to minimize animal suffering and preserve the value of ongoing research when normal operating conditions cannot be maintained.</p>","PeriodicalId":17993,"journal":{"name":"Laboratory Animal Research","volume":"42 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13551745/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148912014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adipocyte-specific MC2R overexpression exerts minimal metabolic effects in mice.","authors":"Sangyi Lim, Edzel Evallo, Dong-Il Kim, Min-Jung Park","doi":"10.1186/s42826-026-00296-4","DOIUrl":"10.1186/s42826-026-00296-4","url":null,"abstract":"<p><strong>Background: </strong>Obesity is often associated with elevated glucocorticoid (GC) levels mediated by melanocortin 2 receptor (MC2R), the adrenocorticotropic hormone (ACTH) receptor expressed in the adrenal gland. Meanwhile, previous in vitro studies in non-adrenal cells suggest a potential role for MC2R in lipid metabolism in murine primary adipocytes; however, the functional relevance of MC2R in vivo remains poorly understood. Here, we assessed the metabolic effects and therapeutic potential of MC2R in obesity and GC regulation in vivo by generating mice with adipocyte-specific MC2R overexpression using the adeno-associated virus doublef-floxed inverse orientation (AAV-DIO) system.</p><p><strong>Results: </strong>Our findings show that under basal, high-fat diet (HFD), and stress-induced conditions, MC2R overexpression in adipocytes has minimal effects on thermogenic and lipolytic markers and is insufficient to promote weight reduction in mice. Moreover, adipocyte-specific overexpression of MC2R failed to sequester the ACTH and decrease elevated serum corticosterone levels after exogenous ACTH administration.</p><p><strong>Conclusions: </strong>These findings demonstrate that adipocyte-specific MC2R overexpression does not induce strong metabolic benefits, suggesting that MC2R-directed gene therapy may not be an effective treatment strategy for obesity.</p>","PeriodicalId":17993,"journal":{"name":"Laboratory Animal Research","volume":"42 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13543462/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148891902","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rabbit models of hip dysplasia: a narrative review.","authors":"Jessica E Goetz, Joshua Hockman, Michael C Willey","doi":"10.1186/s42826-026-00291-9","DOIUrl":"10.1186/s42826-026-00291-9","url":null,"abstract":"<p><p>The natural history of osteoarthritis development in individuals with hip dysplasia diagnosed after skeletal maturity is difficult to predict. While reorienting acetabular osteotomy improves pain and function for those with pre-arthritic hip dysplasia, the impact of dysplastic deformity correction on cartilage health and future cartilage degeneration remains unknown. The rabbit has been used as a preclinical model of hip dysplasia for investigation of joint degeneration and surgical treatment, but there is variability among protocols used to induce and characterize dysplastic deformity. The aim of this narrative review was to summarize techniques for inducing hip dysplasia, the associated morphologic and histopathologic changes, and the ability of surgical correction to mitigate joint degeneration in order to guide future research using the rabbit as a model of hip dysplasia. We identified 21 studies that induced dysplastic deformity in the rabbit hip. The most common method to induce dysplastic deformity was immobilization of the knee in extension in skeletally immature rabbits. Immobilization initiated at a younger age and for longer duration resulted in more severe dysplasia. In the few studies that assessed surgical treatment of the dysplastic hip, cartilage degeneration was reduced with correction of dysplastic deformity. We concluded that immobilizing skeletally immature rabbit knees in extension reliably causes dysplastic deformity of the hip, replicating a shallow and abnormally oriented acetabulum, which can progress to full dislocation more characteristic of hip dysplasia in infants and children, or be present without complete femoral head dislocation more characteristic of human hip dysplasia that presents in young adults. This model thereby offers the opportunity to assess the tissue level effects of hip dysplasia and the effects of surgical correction across the age spectrum.Clinical trials number : Not applicable.</p>","PeriodicalId":17993,"journal":{"name":"Laboratory Animal Research","volume":"42 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13527900/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148865931","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Optimised murine model of influenza-induced respiratory sepsis for studying acute kidney injury.","authors":"Yaqing Jiao, Will Lung Chan, Yuee Cai, Arthur Chuxi Liu, Yilin Zhang, John M Nicholls, Timothy H Rainer","doi":"10.1186/s42826-026-00294-6","DOIUrl":"10.1186/s42826-026-00294-6","url":null,"abstract":"<p><strong>Background: </strong>Viral respiratory sepsis, driven by influenza and COVID-19, is increasingly prominent clinically. However, there is a lack of preclinical models that reliably replicate its associated acute kidney injury (AKI), a major contributor to morbidity and mortality. To address this gap, we refined an established model of influenza-induced respiratory sepsis by administering graded intranasal H1N1 A/PR/8/34 doses (3.7 × 10¹, 3.7 × 10³, and 3.7 × 10⁴ TCID₅₀) in male BALB/c mice. We defined humane endpoints at ≥ 30% body weight loss, monitored clinical severity, weight, and glycaemia daily for 14 days, and assessed multi-organ dysfunction via serum biochemistry, histopathology, renal qPCR, and longitudinal serum neutrophil gelatinase-associated lipocalin (NGAL) ELISA.</p><p><strong>Results: </strong>The 3.7 × 10⁴ TCID₅₀ dose yielded 66.7% mortality by day 8, with a peak clinical score (MSS) of 10, > 30% weight loss, and hypoglycaemia (blood glucose < 70 mg/dL). Infected mice exhibited dose-dependent multi-organ dysfunction, with substantial elevations in serum creatinine (median: 204 [IQR: 142-600] µmol/L), bilirubin (40.62 [IQR: 29.3-124.9] µmol/L), and creatine phosphokinase (CPK) (9822 [IQR: 1,272-11,352] U/L). Renal NGAL expression increased up to 7-fold, aligning with rising serum creatinine levels and histopathological evidence of glomerular enlargement and tubular degeneration. Serum NGAL showed early elevation (up to 4,990 ng/mL on day 2) in severely affected mice, with levels remaining 5.7-7.6-fold higher than sham controls through days 4-8.</p><p><strong>Conclusions: </strong>This exploratory study describes an optimised murine model of influenza-induced respiratory sepsis that develops biochemical and histopathological evidence of AKI. Early elevation of serum NGAL was observed in severely affected animals, supporting its potential as a candidate early biomarker. The model provides a useful platform for further mechanistic and therapeutic investigation in viral respiratory infection-associated AKI.</p>","PeriodicalId":17993,"journal":{"name":"Laboratory Animal Research","volume":"42 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13508304/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148829785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Considerations for selecting immunodeficient mouse strains for cancer xenograft models.","authors":"Jiwon Lee, Joohee Jung","doi":"10.1186/s42826-026-00292-8","DOIUrl":"10.1186/s42826-026-00292-8","url":null,"abstract":"<p><p>Preclinical (in vivo) experiments for efficacy and toxicity are predominantly conducted in mice. Nevertheless, human-derived cells, tissues, and organoids are generally rejected by the immune system of mice. Thus, immunodeficient mice are used as xenograft models to overcome immune rejection in cancer research. Xenograft mouse models are divided into ectopic, orthotopic, and metastatic models based on the transplant sites. Xenograft mouse models are established by transplanting cancer cells, tissues, or organoids derived from patients. These models show diverse success rates and production times depending on the transplant materials and recipient mice. In this review, mouse strains for the establishment of xenograft models in cancer research are introduced. Genetic engineering of immune cells, such as T cells, B cells, and natural killer cells, shows specific properties. To select an immunodeficient mouse strain, the differences in the characteristics of the models must be understood. Optimized mouse models can provide information to investigate cancer progression and evaluate anticancer drugs.</p>","PeriodicalId":17993,"journal":{"name":"Laboratory Animal Research","volume":"42 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13505039/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148818821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}