Group housing is highly important for social animals. However, it can also give rise to aggression, one of the most serious welfare concerns in laboratory mouse husbandry. Severe fighting can lead to pain, injury and even death. In addition, working with animals that are severely socially stressed, wounded or singly-housed as a result of aggression may compromise scientific validity. Some general recommendations on how to minimize aggression exist, but the problem persists. Thus far, studies attempting to find solutions have mainly focused on social dominance and territorial behavior, but many other aspects of routine housing and husbandry that might influence aggressive behavior have been overlooked. The present way of housing laboratory mice is highly unnatural: mice are prevented from performing many species-typical behaviors and are routinely subjected to painful and aversive stimuli. Giving animals control over their environment is an important aspect of improving animal welfare and has been well-studied in the field of animal welfare science. How control over the environment influences aggression in laboratory mice, however, has not been closely examined. In this article, we challenge current ways of thinking and propose alternative perspectives that we hope will lead to an enhanced understanding of aggression in laboratory mice.
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http://dx.doi.org/10.1038/laban.1219 | DOI Listing |
Allergol Immunopathol (Madr)
January 2025
Department of Neurofunction, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei Province, China;
Acanthoside B (Aca.B), a principal bioactive compound extracted from , exhibits superior anti-inflammatory capacity. Ulcerative colitis is a nonspecific inflammatory bowel disease with unknown etiology.
View Article and Find Full Text PDFAllergol Immunopathol (Madr)
January 2025
Department of Geriatric Medicine, Qinghai University Affiliated Hospital, Xining, Qinghai, China.
The main goal of this investigation is to find out how solute carrier family 27 member 3 (SLC27A3) is expressed in the lung tissue of mice with chronic obstructive pulmonary disease (COPD), and how it relates to lung function. A model of COPD was established by exposing organisms to cigarette smoke, followed by investigating the role of SLC27A3 in COPD through experiments conducted both in living organisms and in laboratory settings. Knockout mice lacking SLC27A3 were produced through siRNA transfection to investigate lung function and inflammatory response, using methods such as hematoxylin-eosin staining and enzyme-linked immunosorbent assay.
View Article and Find Full Text PDFAllergol Immunopathol (Madr)
January 2025
Department of Pediatrics, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zheiiang, China.
To illustrate the potential of mesenchymal stem cell-derived exosomes (MSC-Exos) in mitigating septic lung injury by reducing the excessive formation of neutrophil extracellular traps (NETs), a mouse model of septic lung injury was induced through cecal ligation and puncture (CLP). The mice received intraperitoneal injections of MSC-Exos. Post injection, pathological alterations of the lung tissue were evaluated through HE staining, and the levels of inflammatory markers in each mouse group at various time points were assessed using ELISA kits.
View Article and Find Full Text PDFInvest Ophthalmol Vis Sci
January 2025
State Key Laboratory of Ophthalmology, Optometry and Visual Science, Eye Hospital, Wenzhou Medical University, Wenzhou, China.
Purpose: Protein arginine methyltransferase 1 (PRMT1) is an integral constituent of numerous cellular processes. However, its role in corneal epithelial wound healing (CEWH) remains unclear. This study investigates the impact of PRMT1 on cellular mechanisms underlying corneal epithelial repair and its potential to improve wound healing outcomes.
View Article and Find Full Text PDFJ Endocrinol Invest
January 2025
Department of Endocrinology, Nanshi Hospital of Nanyang, No. 130, West Zhongzhou Road, Nanyang, 473065, China.
Background: Diabetic nephropathy (DN) is a severe complication of diabetes mellitus and has the complex pathogenesis. The previous study reported that protein kinase Bγ (AKT3) was involved in DN progression. Our aim was to explore the detailed mechanisms of AKT3 in DN development.
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