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Journal articles on the topic 'Mice models'

Author: Grafiati

Published: 4 June 2021

Last updated: 8 March 2025

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1

Tai, Leon M., Katherine L. Youmans, Lisa Jungbauer, Chunjiang Yu, and Mary Jo LaDu. "Introducing HumanAPOEinto AβTransgenic Mouse Models." International Journal of Alzheimer's Disease 2011 (2011): 1–9. http://dx.doi.org/10.4061/2011/810981.

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Apolipoprotein E (apoE) and apoE/amyloid-β(Aβ) transgenic (Tg) mouse models are critical to understanding apoE-isoform effects on Alzheimer's disease risk. Compared to wild type,apoE−/−mice exhibit neuronal deficits, similar to apoE4-Tg compared to apoE3-Tg mice, providing a model for Aβ-independent apoE effects on neurodegeneration. To determine the effects of apoE on Aβ-induced neuropathology,apoE−/−mice were crossed with Aβ-Tg mice, resulting in a significant delay in plaque deposition. Surprisingly, crossing human-apoE-Tg mice withapoE−/−/Aβ-Tg mice further delayed plaque deposition, which eventually developed in apoE4/Aβ-Tg mice prior to apoE3/Aβ-Tg. One approach to address hAPOE-induced temporal delay in Aβpathology is an additional insult, like head injury. Another is crossing human-apoE-Tg mice with Aβ-Tg mice that have rapid-onset Aβpathology. For example, because 5xFAD mice develop plaques by 2 months, the prediction is that human-apoE/5xFAD-Tg mice develop plaques around 6 months and 12 months before other human-apoE/Aβ-Tg mice. Thus, tractable models for human-apoE/Aβ-Tg mice continue to evolve.

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2

Sprigge, T. L. S. "Of Mice, Models and Men." Environmental Ethics 8, no. 1 (1986): 83–87. http://dx.doi.org/10.5840/enviroethics19868115.

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3

McKay, David. "Mice models and weight loss." Trends in Biotechnology 19, no. 6 (June 2001): 203. http://dx.doi.org/10.1016/s0167-7799(01)01679-1.

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4

Macchiarini, Francesca, Markus G. Manz, A. Karolina Palucka, and Leonard D. Shultz. "Humanized mice." Journal of Experimental Medicine 202, no. 10 (November 21, 2005): 1307–11. http://dx.doi.org/10.1084/jem.20051547.

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Animal models have been instrumental in increasing the understanding of human physiology, particularly immunity. However, these animal models have been limited by practical considerations and genetic diversity. The creation of humanized mice that carry partial or complete human physiological systems may help overcome these obstacles. The National Institute of Allergy and Infectious Diseases convened a workshop on humanized mouse models for immunity in Bethesda, MD, on June 13–14, 2005, during which researchers discussed the benefits and limitations of existing animal models and offered insights into the development of future humanized mouse models.

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Sellers, Rani S. "Translating Mouse Models." Toxicologic Pathology 45, no. 1 (November 4, 2016): 134–45. http://dx.doi.org/10.1177/0192623316675767.

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Mice and humans branched from a common ancestor approximately 80 million years ago. Despite this, mice are routinely utilized as animal models of human disease and in drug development because they are inexpensive, easy to handle, and relatively straightforward to genetically manipulate. While this has led to breakthroughs in the understanding of genotype–phenotype relationships and in the identification of therapeutic targets, translation of beneficial responses to therapeutics from mice to humans has not always been successful. In a large part, these differences may be attributed to variations in the alignment of protein expression and signaling in the immune systems between mice and humans. Well-established inbred strains of “The Laboratory Mouse” vary in their immune response patterns as a result of genetic mutations and polymorphisms arising from intentional selection for research relevant traits, and even closely related substrains vary in their immune response patterns as a result of genetic mutations and polymorphisms arising from genetic drift. This article reviews some of the differences between the mouse and human immune system and between inbred mouse strains and shares examples of how these differences can impact the usefulness of mouse models of disease.

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Henry-Smith, Charnae A., and Xianlin Han. "TRANSGENIC MOUSE MODELS OF ALZHEIMER’S DISEASE." Innovation in Aging 3, Supplement_1 (November 2019): S835. http://dx.doi.org/10.1093/geroni/igz038.3077.

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Abstract Alzheimer’s disease is a progressive brain disease that slowly destroys memory and thinking skills. Alzheimer’s is characterized by an increase in Aβ plaques , and tau tangles. Neurons in the brain have axons covered in myelin sheath that connect microglia and astrocytes. The myelin sheath is composed of about 70% lipid composition; Sulfatide contributing to 30% overall. Sulfatide changes the morphology of primary microglia to their activated form. To study the role of microglia activation and sulfatide levels, three different mouse models were created: APP KI mice, CST Whole Body Ko mice, and cCST (conditional) KO. In order to create the genotype of the APP KI mice, a breeding mouse line was created. The APP KI gene had to be introduced in Plp1-Cre and cCST KO crossed mice to receive a working mouse model. During the duration of breeding for the APP KI mice, a preliminary experiment was performed on the CST KO mice. These mice were given the PLX3397 diet with the aim to remove the microglia and to see the effect of Aβ plaques. The PLX3397 will reduce the microglia targeting the CSF1R. After consuming the diet, the mice were harvested to collect tissues from the brain and spinal cord. Lipidomics and immunohistology were performed. In conclusion, we will continue the breeding of the CST flox/flox / Plp1-Cre / APP KI mice, and the drug dosage and treatment to be used in our APP KI mice will be based on preliminary data from our CST mice.

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7

Merlino, Glenn. "Transgenic Mice as Models for Tumorigenesis." Cancer Investigation 12, no. 2 (January 1994): 203–13. http://dx.doi.org/10.3109/07357909409024875.

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8

Rink, L., and B. E. Wenzel. "Transgenic mice models in autoimmunity – discussion." Experimental and Clinical Endocrinology & Diabetes 104, S 03 (July 15, 2009): 46–48. http://dx.doi.org/10.1055/s-0029-1211684.

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9

Li, Y., and J. T. Dudman. "Mice infer probabilistic models for timing." Proceedings of the National Academy of Sciences 110, no. 42 (September 30, 2013): 17154–59. http://dx.doi.org/10.1073/pnas.1310666110.

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10

Johns, Conrado, Irene Gavras, Diane E. Handy, Abrahao Salomao, and Haralambos Gavras. "Models of Experimental Hypertension in Mice." Hypertension 28, no. 6 (December 1996): 1064–69. http://dx.doi.org/10.1161/01.hyp.28.6.1064.

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11

Buer, Jan, and Rudi Balling. "Mice, microbes and models of infection." Nature Reviews Genetics 4, no. 3 (March 2003): 195–205. http://dx.doi.org/10.1038/nrg1019.

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12

Bourin, Michel, Benoit Petit-Demoulière, Brid Nic Dhonnchadha, and Martine Hascöet. "Animal models of anxiety in mice." Fundamental & Clinical Pharmacology 21, no. 6 (December 2007): 567–74. http://dx.doi.org/10.1111/j.1472-8206.2007.00526.x.

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13

Graham, Dustin M. "Dirty mice might make better models." Lab Animal 45, no. 6 (May 20, 2016): 198. http://dx.doi.org/10.1038/laban.1035.

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14

Kerekov, Nikola, Nikolina Mihaylova, Jozsef Prechl, and Andrey Tchorbanov. "Humanized SCID Mice Models of SLE." Current Pharmaceutical Design 17, no. 13 (May 1, 2011): 1261–66. http://dx.doi.org/10.2174/138161211795703780.

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15

Coll, Jean-Luc, and Véronique Josserand. "Imaging lung cancer in mice models." Drug Discovery Today: Disease Models 3, no. 3 (September 2006): 219–24. http://dx.doi.org/10.1016/j.ddmod.2006.09.005.

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16

Morahan, Grant. "Transgenic mice as immune system models." Current Opinion in Immunology 3, no. 2 (January 1991): 219–23. http://dx.doi.org/10.1016/0952-7915(91)90054-5.

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McCune, Joseph M. "SCID mice as immune system models." Current Opinion in Immunology 3, no. 2 (January 1991): 224–28. http://dx.doi.org/10.1016/0952-7915(91)90055-6.

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18

Metcalf, Donald. "Transgenic mice as models of hemopoiesis." Cancer 67, S10 (May 15, 1991): 2695–99. http://dx.doi.org/10.1002/1097-0142(19910515)67:10+<2695::aid-cncr2820671704>3.0.co;2-m.

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19

Vrana, Paul B., Kimberly R. Shorter, Gabor Szalai, Michael R. Felder, Janet P. Crossland, Monika Veres, Jasmine E. Allen, et al. "Peromyscus(deer mice) as developmental models." Wiley Interdisciplinary Reviews: Developmental Biology 3, no. 3 (December 3, 2013): 211–30. http://dx.doi.org/10.1002/wdev.132.

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McCart, Amy E., Nicola K. Vickaryous, and Andrew Silver. "Apc mice: Models, modifiers and mutants." Pathology - Research and Practice 204, no. 7 (July 2008): 479–90. http://dx.doi.org/10.1016/j.prp.2008.03.004.

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21

Rodriguez‐Lozano, Francisco J., Fernando León‐García, Juan C. Gámez‐Granados, Jose M. Palomares, and J. Olivares. "Benefits of ensemble models in road pavement cracking classification." Computer-Aided Civil and Infrastructure Engineering 35, no. 11 (February 24, 2020): 1194–208. http://dx.doi.org/10.1111/mice.12543.

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22

Bockamp, Ernesto, Marko Maringer, Christian Spangenberg, Stephan Fees, Stuart Fraser, Leonid Eshkind, Franz Oesch, and Bernhard Zabel. "Of mice and models: improved animal models for biomedical research." Physiological Genomics 11, no. 3 (December 3, 2002): 115–32. http://dx.doi.org/10.1152/physiolgenomics.00067.2002.

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The ability to engineer the mouse genome has profoundly transformed biomedical research. During the last decade, conventional transgenic and gene knockout technologies have become invaluable experimental tools for modeling genetic disorders, assigning functions to genes, evaluating drugs and toxins, and by and large helping to answer fundamental questions in basic and applied research. In addition, the growing demand for more sophisticated murine models has also become increasingly evident. Good state-of-principle knowledge about the enormous potential of second-generation conditional mouse technology will be beneficial for any researcher interested in using these experimental tools. In this review we will focus on practice, pivotal principles, and progress in the rapidly expanding area of conditional mouse technology. The review will also present an internet compilation of available tetracycline-inducible mouse models as tools for biomedical research ( http://www.zmg.uni-mainz.de/tetmouse/ ).

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23

Bešinović, Nikola, Rob M. P. Goverde, and Egidio Quaglietta. "Microscopic Models and Network Transformations for Automated Railway Traffic Planning." Computer-Aided Civil and Infrastructure Engineering 32, no. 2 (June 7, 2016): 89–106. http://dx.doi.org/10.1111/mice.12207.

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24

Drevet, Sabine, Bertrand Favier, Emmanuel Brun, Gaëtan Gavazzi, and Bernard Lardy. "Mouse Models of Osteoarthritis: A Summary of Models and Outcomes Assessment." Comparative Medicine 72, no. 1 (February 1, 2022): 3–13. http://dx.doi.org/10.30802/aalas-cm-21-000043.

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Osteoarthritis (OA) is a multidimensional health problem and a common chronic disease. It has a substantial impact on patient quality of life and is a common cause of pain and mobility issues in older adults. The functional limitations, lack of curative treatments, and cost to society all demonstrate the need for translational and clinical research. The use of OA models in mice is important for achieving a better understanding of the disease. Models with clinical relevance are needed to achieve 2 main goals: to assess the impact of the OA disease (pain and function) and to study the efficacy of potential treatments. However, few OA models include practical strategies for functional assessment of the mice. OA signs in mice incorporate complex interrelations between pain and dysfunction. The current review provides a comprehensive compilation of mouse models of OA and animal evaluations that include static and dynamic clinical assessment of the mice, merging evaluation of pain and function by using automatic and noninvasive techniques. These new techniques allow simultaneous recording of spontaneous activity from thousands of home cages and also monitor environment conditions. Technologies such as videography and computational approaches can also be used to improve pain assessment in rodents but these new tools must first be validated experimentally. An example of a new tool is the digital ventilated cage, which is an automated home-cage monitor that records spontaneous activity in the cages.

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25

Hasan, Syed Rehan, Manish Sinha, and Nitin Bansal. "Anxiolytic activity of Angiotensin-Receptor-Blocker in Experimental Models of Anxiety in Mice." Journal of Pharmaceutical Technology, Research and Management 2, no. 2 (November 4, 2014): 189–202. http://dx.doi.org/10.15415/jptrm.2014.22013.

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Grande, Zacarías, Enrique Castillo, Elena Mora, and Hong K. Lo. "Highway and Road Probabilistic Safety Assessment Based on Bayesian Network Models." Computer-Aided Civil and Infrastructure Engineering 32, no. 5 (March 23, 2017): 379–96. http://dx.doi.org/10.1111/mice.12248.

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Castillo, Enrique, Zacarías Grande, Elena Mora, Xiangdong Xu, and Hong K. Lo. "Proactive, Backward Analysis and Learning in Road Probabilistic Bayesian Network Models." Computer-Aided Civil and Infrastructure Engineering 32, no. 10 (August 4, 2017): 820–35. http://dx.doi.org/10.1111/mice.12294.

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28

Wandersee, Nancy J., Anne C. Frei, Sandra L. Holzhauer, J. Paul Scott, Kirkwood A. Pritchard, Karen A. Fagan, Neil Hogg, and Cheryl A. Hillery. "Vascular Dysfunction in Murine Models of Hemolytic Anemia." Blood 110, no. 11 (November 16, 2007): 846. http://dx.doi.org/10.1182/blood.v110.11.846.846.

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Abstract Pulmonary hypertension affects approximately 30% of young adults with sickle cell disease (SCD) and is a risk factor for early death. There is increasing evidence that intravascular hemolysis contributes to the pathophysiology of pulmonary hypertension in SCD as well as other hemolytic disorders. In this study, we compare measures of vascular dysfunction in Berkeley sickle cell mice (SCD mice) with a murine model of hereditary spherocytosis (sph/sph mice) that exhibit severe hemolytic anemia due to alpha spectrin deficiency, but without HbS-induced RBC sickling. We assessed right ventricular systolic pressure in vivo as a measure of pulmonary arterial function and endothelial-dependent vasodilation of facialis arteries ex vivo as a measure of systemic arterial function. Right ventricular systolic pressures and right ventricle to body weight ratios were increased to similar levels in both SCD and sph/sph mice as compared to control mice (p <0.025), consistent with pulmonary hypertension in both SCD and sph/sph mice. Acetylcholine-induced vasodilation of facialis arteries (a branch of the carotid artery) was severely impaired in both SCD and sph/sph mice compared to control mice (p<0.02). We also found increased plasma levels of soluble VCAM-1, E-selectin, and P-selectin in SCD and sph/sph mice compared to control mice (p<0.005 for all groups), providing further evidence for increased endothelial injury in both murine models. Interestingly, sVCAM-1 and E-selectin were more elevated in SCD mice compared to sph/sph mice (p<0.0001), suggesting hemolysis combined with HbS induces further endothelial injury. We hypothesized that plasma free hemoglobin released by intravascular hemolysis initiates endothelial impairment and injury due to scavenging of nitric oxide (NO) and generation of oxidative damage. Plasma methemoglobin levels were determined by helium electron paramagnetic resonance (EPR) spectroscopy before and after the addition of the NO donor molecule PROLI/NO. The difference between these two signals represents the total NO scavenging capacity of plasma. We found that both the plasma free Hb and NO scavenging capacity in plasma from SCD and sph/sph mice was much greater than that of healthy control mice (p<0.05). In addition, we developed an oxygen electrode assay to assess the oxidizing potential of plasma. The initiation of lipid peroxidation by oxidants present in the plasma results in the consumption of oxygen. We found that plasma from SCD and sph/sph mice has a significantly higher oxidizing potential than plasma from control mice (p<0.05). We obtained similar results (increased plasma free Hb, NO scavenging capacity, and oxidizing potential) comparing plasma from individuals with SCD to plasma from healthy control individuals. Consistent with the higher levels of hemolysis in the sph/sph mice, plasma free Hb, NO scavenging and oxidizing capacity were greater in sph/sph mice compared SCD mice (p<0.05). These results indicate that both pulmonary and systemic vascular function is impaired in these two different murine models of hemolysis, and suggest that nitric oxide-based vasoregulatory mechanisms are particularly affected. These data, combined with previous pathologic reports, suggest that while hemolysis importantly contributes to aberrant vasoregulation and initiating pathways of oxidative damage, sickle hemoglobin may uniquely provoke additional vascular and organ injury.

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Kutle, Ivana, Anne Dittrich, and Dagmar Wirth. "Mouse Models for Human Herpesviruses." Pathogens 12, no. 7 (July 19, 2023): 953. http://dx.doi.org/10.3390/pathogens12070953.

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More than one hundred herpesviruses have been isolated from different species so far, with nine infecting humans. Infections with herpesviruses are characterized by life-long latency and represent a significant challenge for human health. To investigate the consequences of infections and identify novel treatment options, in vivo models are of particular relevance. The mouse has emerged as an economical small animal model to investigate herpesvirus infections. However, except for herpes simplex viruses (HSV-1, HSV-2), human herpesviruses cannot infect mice. Three natural herpesviruses have been identified in mice: mouse-derived cytomegalovirus (MCMV), mouse herpesvirus 68 (MHV-68), and mouse roseolovirus (MRV). These orthologues are broadly used to investigate herpesvirus infections within the natural host. In the last few decades, immunocompromised mouse models have been developed, allowing the functional engraftment of various human cells and tissues. These xenograft mice represent valuable model systems to investigate human-restricted viruses, making them particularly relevant for herpesvirus research. In this review, we describe the various mouse models used to study human herpesviruses, thereby highlighting their potential and limitations. Emphasis is laid on xenograft mouse models, covering the development and refinement of immune-compromised mice and their application in herpesvirus research.

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Miao, Miao, Henry Masengere, Guang Yu, and Fengping Shan. "Reevaluation of NOD/SCID Mice as NK Cell-Deficient Models." BioMed Research International 2021 (November 10, 2021): 1–11. http://dx.doi.org/10.1155/2021/8851986.

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Objective. Natural killer (NK) cell-deficient mice are useful models in biomedical research. NOD/SCID mice have been used as a model of this type in research. However, the actual status of NK cells in NOD/SCID mice and CB17/SCID mice in comparison with that in BALB/c mice has not been sufficiently evaluated. Methods. Splenocytes from naïve or poly(I:C)-treated mice were isolated for phenotyping and analysis of cytotoxicity-related molecules and inhibitory receptors; for cytotoxicity assay, purified NK cells were also used. Results. The proportion of splenic NK cells did not differ significantly between NOD/SCID and CB17/SCID mice. The perforin levels in NK cells were similar between the poly(I:C)-treated CB17/SCID and NOD/SCID mice, while the granzyme B and NKG2A/C/E levels in NK cells from NOD/SCID mice were significantly lower than those from CB17/SCID mice. Moreover, the NKG2D and Ly49A levels in NK cells from NOD/SCID mice were higher than those from CB17/SCID. The splenocytes from CB17/SCID mice showed higher cytotoxicity than those from NOD/SCID mice, while the cytotoxicity of purified NK cells basically did not differ between the two strains. After in vitro stimulation with cytokines, the splenocytes from CB17/SCID mice showed higher IFN-γ production than those from NOD/SCID mice; however, NK cells did not. Conclusion. There was no significant difference in the proportion of splenic NK cells between CB17/SCID and NOD/SCID mice, and the function of NK cells was only partially compromised in NOD/SCID mice. Caution should be taken when considering the use of NOD/SCID mice as an NK-deficient model.

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Kim, Tae Hoon, Nayoung Bae, Taeho Kim, Albert L. Hsu, Mark I. Hunter, Jung-Ho Shin, and Jae-Wook Jeong. "Leptin Stimulates Endometriosis Development in Mouse Models." Biomedicines 10, no. 9 (September 1, 2022): 2160. http://dx.doi.org/10.3390/biomedicines10092160.

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Endometriosis is a chronic inflammatory condition in women, and obesity leads to an inflammatory condition that is directly involved in the etiology of endometriosis. However, observational studies have shown an inverse correlation between endometriosis and a low body mass index (BMI). Obesity does not protect against endometriosis, and on the contrary, an increased BMI may lead to more severe forms of the disease. To determine the effect of obesity on endometriosis, diet-induced and genetically engineered obese mouse models were integrated with endometriosis mouse models with fluorescence-tagged ectopic lesions. High-fat diet-induced obese mice revealed a significant increase in endometriosis development compared with regular-diet control mice. However, obese recipient mice with leptin deficiency and leptin receptor deficiency showed suppressed endometriosis development compared with control mice. Furthermore, donor uterine tissues with leptin deficiency and leptin receptor deficiency suppressed endometriosis development compared with control donor in control recipient mice. Importantly, we revealed that aberrant high levels of leptin concentration significantly increased endometriosis development compared with vehicle treatment group in control mice with normal body weight. Our results suggest that leptin and its receptor are critical for endometriosis development.

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Feinstein, Sheldon. "Mouse Models of Genetically Altered Peroxiredoxin 6." Antioxidants 8, no. 4 (March 27, 2019): 77. http://dx.doi.org/10.3390/antiox8040077.

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Peroxiredoxin 6 (Prdx6) has been shown to have three enzymatic activities: peroxidase, phospholipase A2 (PLA2) and acyl transferase. The peroxidase activity is unusual, as it is capable of reducing phospholipid hydroperoxides (as well as hydrogen peroxide and short chain organic peroxides). Knockout and overexpressing mice have been produced that demonstrate the effect that eliminating or overproducing Prdx6 has on the animals’ physiology. In addition, mutations in various amino acids of Prdx6 have been identified that interfere with different enzymatic functions as well as protein transport. These mutations were originally characterized biochemically; subsequently, several knock-in mouse strains have been produced, each containing one mutation. These mice include the S32T knock-in that affects protein transport, the C47S knock-in that inactivates the peroxidase enzymatic activity, the D140A knock-in that inactivates the PLA2 enzymatic activity and the H26A knock-in that inactivates the peroxidase and blocks binding to phospholipids. This review summarizes the properties of these mice based upon studies conducted with the knockout, overexpressing and knock-in mice and the effect of the genetic changes on the biochemistry and physiology of these mice. The availability of these mice is also briefly discussed.

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Hadrian, Krzysztof, and Adam Przybyłkowski. "Toxic milk mice models of Wilson’s disease." Molecular Biology Reports 48, no. 2 (February 2021): 1903–14. http://dx.doi.org/10.1007/s11033-021-06192-5.

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AbstractWilson’s disease (WD) is a rare genetic disorder inherited as an autosomal recessive trait. The signs and symptoms of this disease are related to dysfunctional ATP7B protein which leads to copper accumulation and cellular damage. The organs that are most commonly affected by WD are the liver and brain. The dysfunctional ATP7B homolog has previously been identified in many different species, including two naturally occurring murine models called toxic milk mice. The aim of this paper was to compare the toxic milk mouse described by Rauch (tx) to that from Jackson Laboratory (txJ) through a review of studies on these two groups of mice. The two mice strains differ in the type of carried mutation and the phenotype of the disease. The data of the studies showed that the tx mice developed mild chronic hepatitis but suffered severe organ destruction with faster progression to full-liver cirrhosis. No changes were noted in the neurological and behavioral status of this strain despite the described toxic accumulation of copper and neuronal destruction in their brain. On the other hand, though the Jackson toxic milk mice (txJ) also presented chronic hepatitis, the condition was a bit milder with slower progression to end-stage disease. Moreover, hepatocyte suitable to perform neurobehavioral research as their phenotype characterized by tremors and locomotor disabilities better corresponds with the cliniconeurological picture of the humans.

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Hanna, Zaher, and Paul Jolicoeur. "Mice as animal models for human disease." Qatar Foundation Annual Research Forum Proceedings, no. 2012 (October 2012): AESNP10. http://dx.doi.org/10.5339/qfarf.2012.aesnp10.

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35

Sankaranarayanan, Sethu. "Genetically Modified Mice Models for Alzheimers Disease." Current Topics in Medicinal Chemistry 6, no. 6 (March 1, 2006): 609–27. http://dx.doi.org/10.2174/156802606776743020.

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36

Jr, G. S. Deepe, L. Romani, V. L. G. Calich, G. Huffnagle, C. Arruda, E. E. I. W. Molinari-Madlum, and J. R. Perfect. "Knockout mice as experimental models of virulence." Medical Mycology 38, no. 1 (January 2000): 87–98. http://dx.doi.org/10.1080/mmy.38.1.87.98.

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Jr, G. S. Deepe, L. Romani, V. L. G. Calich, G. Huffnagle, C. Arruda, E. E. I. W. Molinari-Madlum, and J. R. Perfect. "Knockout mice as experimental models of virulence." Medical Mycology 38, s1 (January 2000): 87–98. http://dx.doi.org/10.1080/mmy.38.s1.87.98.

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Deepe, G. S., L. Romani, V. L. G. Calich, G. Huffnagle, C. Arruda, E. E. I. W. Molinari-Madlum, and J. R. Perfect. "Knockout mice as experimental models of virulence." Medical Mycology 38, no. 1 (December 30, 2000): 87–98. http://dx.doi.org/10.1080/744118735.

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McKinnon, Ross A., and Daniel W. Nebert. "CYTOCHROME P450 KNOCKOUT MICE: NEW TOXICOLOGICAL MODELS." Clinical and Experimental Pharmacology and Physiology 25, no. 10 (October 1998): 783–87. http://dx.doi.org/10.1111/j.1440-1681.1998.tb02153.x.

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Sage, R. D., W. R. Atchley, and E. Capanna. "House Mice as Models in Systematic Biology." Systematic Biology 42, no. 4 (December 1, 1993): 523–61. http://dx.doi.org/10.1093/sysbio/42.4.523.

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Metsäranta, Marjo, and Eero Vuorio. "Transgenic Mice as Models for Heritable Diseases." Annals of Medicine 24, no. 2 (January 1992): 117–20. http://dx.doi.org/10.3109/07853899209148338.

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Tannock, Lisa R., and Victoria L. King. "Animal models of atherosclerosis: More than mice." Atherosclerosis 212, no. 1 (September 2010): 32–33. http://dx.doi.org/10.1016/j.atherosclerosis.2010.06.013.

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Stanley, S. L., and H. W. Virgin. "SCID mice as models for parasitic infections." Parasitology Today 9, no. 11 (November 1993): 406–11. http://dx.doi.org/10.1016/0169-4758(93)90047-j.

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Crawley, Jacqueline N. "Exploratory behavior models of anxiety in mice." Neuroscience & Biobehavioral Reviews 9, no. 1 (March 1985): 37–44. http://dx.doi.org/10.1016/0149-7634(85)90030-2.

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Seldin, David C. "New models of lymphoma in transgenic mice." Current Opinion in Immunology 7, no. 5 (October 1995): 665–73. http://dx.doi.org/10.1016/0952-7915(95)80075-1.

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Kiouptsi, Klytaimnistra, Martina Casari, Jonathan Mandel, Zhenling Gao, and Carsten Deppermann. "Intravital Imaging of Thrombosis Models in Mice." Hämostaseologie 43, no. 05 (October 2023): 348–59. http://dx.doi.org/10.1055/a-2118-2932.

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AbstractIntravital microscopy is a powerful tool to study thrombosis in real time. The kinetics of thrombus formation and progression in vivo is studied after inflicting damage to the endothelium through mechanical, chemical, or laser injury. Mouse models of atherosclerosis are also used to induce thrombus formation. Vessels of different sizes and from different vascular beds such as carotid artery or vena cava, mesenteric or cremaster arterioles, can be targeted. Using fluorescent dyes, antibodies, or reporter mouse strains allows to visualize key cells and factors mediating the thrombotic processes. Here, we review the latest literature on using intravital microscopy to study thrombosis as well as thromboinflammation following transient middle cerebral artery occlusion, infection-induced immunothrombosis, and liver ischemia reperfusion.

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Castillo, Enrique, Aida Calviño, María Nogal, and Hong K. Lo. "On the Probabilistic and Physical Consistency of Traffic Random Variables and Models." Computer-Aided Civil and Infrastructure Engineering 29, no. 7 (March 12, 2014): 496–517. http://dx.doi.org/10.1111/mice.12061.

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Tu, Xiaolong, Xinhe Feng, Weifang Wang, Xunhua Ding, Dong Huang, Ludo Bourre, and Xiaobo Chen. "Abstract 7174: Pharmacokinetics and immunogenicity of anti-PD-1 antibody in humanized FcRn mouse models compared to immunocompetent mouse models." Cancer Research 84, no. 6_Supplement (March 22, 2024): 7174. http://dx.doi.org/10.1158/1538-7445.am2024-7174.

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Abstract Introduction: The development and use of therapeutic antibodies in cancer therapy has increased significantly in recent years, led by the success of approved immune checkpoint blockade antibodies targeting PD-1 and PD-L1 axis. However, obtaining more clinically relevant pharmacokinetics (PK), safety and efficacy data for antibodies is still challenging in preclinical phase. Humanized FcRn (hFcRn) transgenic mouse model has a more faithful catabolism compared to WT mice, providing more accurate and predictable PK data of innovative antibody-based therapeutics at discovery stage[1]. In this study, we sought to investigate pharmacokinetics and immunogenicity characteristics of anti-PD-1 antibody in hFcRn transgenic mice and provide guidance for its differentiation of prediction value for drug PK and safety by comparing to WT mice. Methods: Non-tumor bearing hFcRn mice and wild type C57BL/6 mice were divided into 2 groups, 5 mice were enrolled into each group. Mice were administered anti-PD-1(Nivolumab) at 10 mg/kg single dose after grouping by intravenous (IV) injection. Blood samples at 12 timepoints (15min, 6h, 1, 2, 4, 7, 10, 14, 21, 28, 35, 42 days) post-dosing were collected for PK and Anti-Drug Antibody (ADA) analysis by MSD and ELISA. Results: Nivolumab clearance in hFcRn mice followed a typical linear profile with rapid distribution phase and slow elimination phase (t1/2 = 350 to 400 h). While the PK profile in C57BL/6 mice displayed non-linear clearance and very short elimination phase (t1/2 = 45 to 50 h). This data demonstrated that hFcRn mice have better correlated half-life with human (Nivolumab single dose by IV with 10mg/kg, t1/2 = 595 h) [2]. ADA analysis revealed that it was produced starting from Day 10 in wild type C57BL/6 mice and the frequency of ADA induced by Nivolumab in wild type mice (2/5) was higher than hFcRn mice (0/5). The variation of Nivolumab level was correlated with ADA production in wild type mice. This suggested hFcRn shows lower immunogenicity than wild type mice for human IgG drug and can potentially improve negative effect of ADA interference on PK evaluation. Conclusion: The result of this study demonstrated that the PK data in hFcRn mouse model was more predictive of human PK profile compared to wild type C57BL/6 mice. This advances innovation in antibody-based therapeutics and translational applications, with improved PK, safety and efficacy evaluation for preclinical human IgG drug development in cancer therapy. References: 1. Enhanced half-life of genetically engineered human IgG1 antibodies in a humanized FcRn mouse model: potential application in humorally mediated autoimmune disease. Int Immunol. 18(12):1759-69. 2. Centre for drug evaluation and research. Clinical pharmacology and biopharmaceutics reviews of pembrolizumab: application number:125514Orig1s000. Accessed 04 April 2016. Citation Format: Xiaolong Tu, Xinhe Feng, Weifang Wang, Xunhua Ding, Dong Huang, Ludo Bourre, Xiaobo Chen. Pharmacokinetics and immunogenicity of anti-PD-1 antibody in humanized FcRn mouse models compared to immunocompetent mouse models [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 7174.

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Saré, Rachel Michelle, Abigail Lemons, Alex Song, and Carolyn Beebe Smith. "Sleep Duration in Mouse Models of Neurodevelopmental Disorders." Brain Sciences 11, no. 1 (December 30, 2020): 31. http://dx.doi.org/10.3390/brainsci11010031.

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Sleep abnormalities are common in patients with neurodevelopmental disorders, and it is thought that deficits in sleep may contribute to the unfolding of symptoms in these disorders. Appreciating sleep abnormalities in neurodevelopmental disorders could be important for designing a treatment for these disorders. We studied sleep duration in three mouse models by means of home-cage monitoring: Tsc2+/− (tuberous sclerosis complex), oxytocin receptor (Oxtr) knockout (KO) (autism spectrum disorders), and Shank3 e4-9 KO (Phelan–McDermid syndrome). We studied both male and female mice, and data were analyzed to examine effects of both genotype and sex. In general, we found that female mice slept less than males regardless of genotype or phase. We did not find any differences in sleep duration in either Tsc2+/− or Oxtr KO mice, compared to controls. In Shank3 e4-9 KO mice, we found a statistically significant genotype x phase interaction (p = 0.002) with a trend that Shank3e4-9 KO mice regardless of sex slept more than control mice in the active phase. Our results have implications for the management of patients with Phelan–McDermid syndrome.

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Roberts, Rachael R., Joel C. Bornstein, Annette J. Bergner, and Heather M. Young. "Disturbances of colonic motility in mouse models of Hirschsprung's disease." American Journal of Physiology-Gastrointestinal and Liver Physiology 294, no. 4 (April 2008): G996—G1008. http://dx.doi.org/10.1152/ajpgi.00558.2007.

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Mutations in genes encoding members of the GDNF and endothelin-3 (Et-3) signaling pathways can cause Hirschsprung's disease, a congenital condition associated with an absence of enteric neurons in the distal gut. GDNF signals through Ret, a receptor tyrosine kinase, and Et-3 signals through endothelin receptor B (Ednrb). The effects of Gdnf, Ret, and ET- 3 haploinsufficiency and a null mutation in ET- 3 on spontaneous motility patterns in adult and developing mice were investigated. Video recordings were used to construct spatiotemporal maps of spontaneous contractile patterns in colon from postnatal and adult mice in vitro. In Ret+/− and ET- 3+/− mice, which have normal numbers of enteric neurons, colonic migrating motor complexes (CMMCs) displayed similar properties under control conditions and following inhibition of nitric oxide synthase (NOS) activity to wild-type mice. In the colon of Gdnf+/− mice and in the ganglionic region of ET- 3−/− mice, there was a 50–60% reduction in myenteric neuron number. In Gdnf+/− mice, CMMCs were present, but abnormal, and the proportion of myenteric neurons containing NOS was not different from that of wild-type mice. In the ganglionic region of postnatal ET- 3−/− mice, CMMCs were absent, and the proportion of myenteric neurons containing NOS was over 100% higher than in wild-type mice. Thus impairments in spontaneous motility patterns in the colon of Gdnf+/− mice and in the ganglionic region of ET- 3−/− mice are correlated with a reduction in myenteric neuron density.

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