Relevant bibliographies by topics / Mice models

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Mice models'

Author: Grafiati
Published: 4 June 2021
Last updated: 8 March 2025

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Journal articles on the topic "Mice models"

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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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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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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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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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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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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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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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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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Dissertations / Theses on the topic "Mice models"

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Gilder, Michael Frederick James. "Molecular investigations in animal models of Huntington's disease." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325046.

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Liu, Chun. "Individual-based models of wood mice in ecotoxicology." Thesis, University of Reading, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.590671.

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The wood mouse (Apodemus sylvaticus) is a common and widespread species in Europe and therefore often used as a focal species in the risk assessments of pesticides. Recent years have seen a growing interest in the use of ecological models in ecological risk assessments. The purpose of this PhD project was to construct and apply population models of the wood mouse to support risk assessment of pesticides. In the thesis I first reviewed the current practice of risk assessment and the weaknesses and the advantages of ecological models, in particular individual-based models. Following a modelling cycle, the PhD project started with a literature review of the basic ecology of the wood mouse and relevant information for modelling purposes. A conceptual model was then constructed, based on which an individual-based model was developed. The model was fully described and its ecological credibility was evaluated by the "pattern-oriented" validation method. The model was then used to link the spatial choice of wood mice and their potential exposure to pesticide application in the field. Analyses of the model showed that when the population density reached a high level in the off-crop hedgerows, which act as the source habitat for wood mice, the surplus were driven to the crop fields and thus have a high risk of exposure if pesticides are applied. The model was further developed by incorporating a sub module of toxicokinetic processes which represented exposure as internal concentration instead of ingested dose. The interactions between the spatial patterns of foraging provided by the individual-based model and the temporal patterns of absorption and elimination provided by the toxicokinetic model were explored. The combined model showed little further reduction of risk than either of the two models respectively alone. It suggested that such a combined approach is most likely to bring added value when the spatio-temporal patterns of feeding are at the intermediate level, i.e. when mice divide their foraging between exposed crop and unexposed areas. I then used the model to explore the population-level sensitivity in terms of both population size and population growth rate, to detrimental effects on individual-level life-history traits. The results showed the two indices had different sensitivities to changes in life-history traits. Thus, endpoint from the models used in risk assessments should take into account whether the protection goal is to ensure that the population remains stable or that it grows. The overall high level of sensitivity to survival also indicated that protection should be more focused on acute effects than chronic effects. Finally I summarised the major findings in the thesis and discussed the need for future research, as well as the lessons learnt about conventional risk assessment approach and the opportunities ecological modelling brings for a more realistic and ecologically relevant risk assessment for pesticides.
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Ho, Wing-lau, and 何穎流. "Investigating neurodegeneration in the retina of tau P301L mice." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B4833392X.

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Neurodegeneration is a collective term for the progressive loss of structure, function or even death of neurons. This includes diseases like Alzheimer’s disease, frontotemporal dementia, Parkinson’s disease and motor neuron disease. Recent researches have shown great interest in the role of tau proteins, which have versatile functions including microtubule stabilization and signal relay in the central nervous system. Retina and optic nerve, being part of the central nervous system, can also be affected by similar processes. In neurodegenerative diseases visual disturbances including difficulties in reading and finding object, depth perception, perceiving structure from motion, color recognition and impairment in spatial contrast sensitivity have all been observed. Some of these defects may be attributed to changes at ocular level. The effect of tau mutation was investigated in this study utilizing a transgenic P301L tau mice model. Morphometric analysis has been utilized to quatify the neurodegenerative changes, including the thickness of inner nuclear layer(INL), density of retinal ganglion cells(RGCs) and size of RGCs. Retinal sections stained by hematoxylin and eosin(H&E) were analyzed. Comparisons were made between the P301L tau mice and the control mice in addition to comparisons between different age groups. The study found that there was a significant decrease of thickness of INL of P301L tau mice when compared with control mice. The effect was more pronounced in the peripheral area and the effect increased with age. Regarding density of RGCs, P301L tau mice showed a similar age-related decline as control mice. And regarding the size of RGCs, the RGCs from P301L tau mice increased in size with age and the RGCs from control mice decreased in size with age.
published_or_final_version
Anatomy
Master
Master of Medical Sciences
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Nguyen, Tam Hong. "Pex13 Mutant Mice as Models for the Peroxisome Biogenesis Disorders." Thesis, Griffith University, 2008. http://hdl.handle.net/10072/366797.

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Zellweger syndrome (ZS) is the most severe form of a spectrum of disorders resulting from mutations in PEX genes, genes that encode proteins necessary for peroxisome biogenesis. Loss of functional peroxiosmes leads to disruption of multiple metabolic pathways involving the peroxisome, including very long chain fatty acid oxidation and plasmalogen and bile acid synthesis. ZS patients exhibit a range of clinical abnormalities, including facial dysmorphism, cataracts, hypotonia, seizures, psychomotor retardation, and hearing impairment. In terms of tissue pathology, there are also wide ranging effects, including neuronal migration defects, hepatomegaly, retinopathy, and renal cysts. Pex13 encodes a peroxisomal membrane protein that is essential for peroxisome biogenesis. Previous work in this laboratory resulted in the generation of a Pex13-null mouse model for the purpose of investigating the pathogenesis of Zellweger syndrome. The work in the first part of this thesis extends these studies and describes the generation and initial characterisation of tissue-specific Pex13 mouse models. These tissue-specific models are expected be useful tools for analysis of the impact of localised, brain- and liver-specific elimination of peroxisomes on the pathogenesis of ZS. In addition, in the second part of the thesis, a separate and novel hypothesis is addressed as an explanation for the molecular pathogenesis of ZS, through investigating the relationship between reduced peroxisome abundance and microtubule-mediated peroxisome trafficking. Pex13 brain mutant mice were generated by mating the previously generated Pex13-floxed mice with mice expressing Cre recombinase under the control of the neuron-specific rat nestin promoter. Pex13 brain mutant mice displayed growth retardation beginning at day 5 postnatal, with gradual deterioration until death at approximately day 22 postnatal. Other clinical features included contracted postures, under-developed lower body mass, abnormal and unsteady gait, and abnormal motor coordination. In terms of brain metabolic function, these mice exhibited significant defects in plasmalogen synthesis, but, surprisingly, VLCFA levels were similar to those of littermate control mice. Significantly, peroxisome elimination in brain resulted in increased levels of plasmalogen levels in liver of Pex13 brain mutant mice. Consistent with the expected pathology resulting from deficiency of brain peroxisomes, brain mutants exhibited defective neuronal migration characterised by increased cellular density in the intermediate zone of the neocortex. Microarray analysis of total brain RNA from Pex13 brain mutants revealed several functionally-linked pathways associated with the differentially expressed genes, including cell-cell signalling, cell compromise/death, lipid metabolism, cell movement, and serotonin synthesis.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Physical Sciences
Science, Environment, Engineering and Technology
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陳醒覺 and Sing-kwok Chan. "Mouse preproendothelin-1 gene: transgenic mouse models to study tissue-specific and developmental expression andregulation." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31236571.

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Chan, Sing-kwok. "Mouse preproendothelin-1 gene : transgenic mouse models to study tissue-specific and developmental expression and regulation /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19737002.

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Lopez-Lastra, Silvia. "Humanized Mice as Models to study Human Innate Immunity and Immunotherapies." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS039/document.

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Les modèles animaux ont largement contribué à notre compréhension de l’immunologie humaine et des mécanismes pathologiques associés au développement des maladies. Cependant, les modèles murins ne permettent pas de reproduire toute la complexité des pathologies humaines. Les souris à système immunitaire humain (HIS), par leur capacité à récapituler l’hématopoïèse humaine et à être infectées par des pathogènes humains, constituent une solution de choix pour combler ce fossé inter-espèce. Après greffe de cellules souches hématopoïétiques humaines, des souris hôtes sévèrement immunodéprimées permettent un haut niveau de développement du système hémato-lymphoïde humain tout au long de leur vie. Cependant, certains types cellulaires, comme les cellules lymphoïdes innées, ne parviennent pas à se différencier et à fonctionner normalement dans les modèles murins HIS actuels. Ici, nous décrivons le développement d’un modèle souris HIS original, nommé BRGSF, montrant une amélioration de la maturation, de la fonction et de l’homéostasie des cellules natural killer (NK) humaines et des autres ILCs. De plus, en récapitulant les différentes étapes du développement des ILCs humaines, ce modèle souris BRGSF nous a permis d’identifier pour la première fois un précurseur d’ILC (ILCP) présent à la fois dans notre modèle HIS ainsi que dans le sang périphérique et plusieurs organes lymphoïdes et non-lymphoïdes humains. Cette population circulante d’ILCPs pourrait constituer un substrat pour la production d’ILCs matures dans les tissus périphériques en réponse à des stress environnementaux, inflammatoires et/ou infectieux. Dans une seconde partie de ce travail de thèse, nous avons utilisé ces souris BRGS afin de tester l’efficacité de deux immunothérapies reposant sur les lymphocytes innés pour le traitement d’un carcinome colorectal exprimant EGFR et muté pour KRAS. La première approche a consisté en la co-administration des cellules NK dérivées de sang de cordon ombilical et d'anticorps monoclonal cetuximab afin de promouvoir le mécanisme de cytotoxicité cellulaire dépendante des anticorps (ADCC) contre la tumeur. La seconde stratégie a reposé sur l’injection de nanobodies VHH combinant l’inhibition de l’EGFR et l’activation spécifique du récepteur Vγ9Vδ2 des cellules T effectrices. Les résultats de cette étude soulignent l’importance des modèles murins HIS pour la compréhension du développement des lymphocytes innés humains et pour mieux les mettre à profit dans les thérapies anti-tumeurs
Animal models have extensively contributed to our understanding of human immunobiology and to uncover the underlying pathological mechanisms occurring in the development of the disease. However, mouse models do not always reproduce the genetic complexity inherent in human disease conditions. Human immune system (HIS) mouse models that are susceptible to human pathogens and can recapitulate human hematopoiesis provide one means to bridge the interspecies gap. Severely immunodeficient host mice support life-long, high level human hematolymphoid development after engraftment with human hematopoietic stem cells (HSC). However, the differentiation and function of some blood cell types, including innate lymphoid cells (ILCs), is poorly characterized in current HIS mice. Here we describe the development of a novel HIS mouse model, named BRGSF, which demonstrate enhanced maturation, function and homeostasis of human natural killer (NK) cells and other ILCs. Furthermore, the BRGSF-based HIS mouse model recapitulated the developmental stages of human ILCs. We could identify for the first time an ILC precursor (ILCP) population that is present both in HIS mice and in human peripheral blood as well as in several lymphoid and non-lymphoid human tissues. This circulating human ILCP population may provide a substrate to generate mature ILCs in tissues in response to environmental stressors, inflammation and infection. In a second part of the thesis we used BRGS immunodeficient mice to assess two innate lymphocyte-based immunotherapeutic approaches for treating EGFR-expressing KRAS-mutated colorectal carcinoma in vivo. The first model used a combination of umbilical cord blood (UCB)-derived NK cells and the monoclonal antibody cetuximab to promote antibody dependent cell cytotoxicity (ADCC) against the tumors. In a second model, we evaluated the therapeutic suitability of novel bispecific VHH constructs that combine inhibition of the EGFR with the target-specific activation of effector Vγ9Vδ2-T cells. These studies highlight the utility for HIS-based mouse models to understand human innate lymphocyte development and to harness these potent effectors for anti-tumor therapies
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Hübner, Roland Karl Peter. "Chromosomal and biochemical variation in wild mice from Switzerland : relevance for models of chromosomal evolution in European house mice." Thesis, University of Oxford, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.316879.

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Thompson, Sally A. "Modulation of glutathione associated with methylmercury exposure in mice /." Thesis, Connect to this title online; UW restricted, 1996. http://hdl.handle.net/1773/8461.

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Buonincontri, Guido. "Advanced MRI for cardiac assessment in mice." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648679.

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Books on the topic "Mice models"

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M, Bader, Offermanns Stefan, and Hein Lutz, eds. Transgenic models in pharmacology. Berlin: Springer, 2004.

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Maria-Grazia, Roncarolo, Péault Bruno, and Namikawa Reiko, eds. Human hematopoiesis in SCID mice. New York: Springer-Verlag, 1995.

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H, Fiebig H., and Berger D. P, eds. Immunodeficient mice in oncology. Basel: Karger, 1992.

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Yanlin, Wang-Fischer, ed. Manual of stroke models in rats. Boca Raton: Taylor & Francis, 2008.

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Lamoreux, M. Lynn. The colors of mice: A model genetic network. Chichester, West Sussex: Wiley-Blackwell, 2010.

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Lynn, Lamoreux M., ed. The colors of mice: A model genetic network. Chichester, West Sussex: Wiley-Blackwell, 2010.

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Shaoguang, Li, ed. Mouse models of human blood cancers: Basic research and pre-clinical applications. New York, NY: Springer, 2008.

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Ried, Thomas, and Jeff Green. Genetically engineered mice for cancer research: Design, analysis, pathways, validation and pre-clinical testing. New York: Springer Verlag, 2012.

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Horst, Bluethmann, and Ohashi Pamela S, eds. Transgenesis and targeted mutagenesis in immunology. San Diego: Academic Press, 1994.

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1931-, Takeda Toshio, ed. The SAM model of senescence: Proceedings of the first International Conference on Senescence, the SAM model, Kyoto, 17-18 March 1994. Amsterdam: Excerpta Medica, 1994.

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Book chapters on the topic "Mice models"

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Ajmone Marsan, Marco, Giovanna Carofiglio, Michele Garetto, Paolo Giaccone, Emilio Leonardi, Enrico Schiattarella, and Alessandro Tarello. "Of Mice and Models." In Quality of Service in Multiservice IP Networks, 15–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/978-3-540-30573-6_2.

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Waterhouse, Dawn. "Oncology Models in Mice." In Encyclopedia of Cancer, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_7168-3.

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Waterhouse, Dawn. "Oncology Models in Mice." In Encyclopedia of Cancer, 3214–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_7168.

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Wess, J., W. Zhang, A. Duttaroy, T. Miyakawa, J. Gomeza, Y. Cui, A. S. Basile, et al. "Muscarinic Acetylcholine Receptor Knockout Mice." In Transgenic Models in Pharmacology, 65–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18934-0_3.

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Rosales, Cecilia, and Manel Esteller. "Epigenetic Mouse Models." In Genetically Engineered Mice for Cancer Research, 375–96. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-69805-2_18.

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Heljasvaara, Ritva, and Taina Pihlajaniemi. "Experimental Tumour Models in Mice." In Mouse as a Model Organism, 89–104. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-0750-4_5.

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Lorenz, Julia, and Susanne Grässel. "Experimental Osteoarthritis Models in Mice." In Methods in Molecular Biology, 401–19. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1215-5_23.

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Allen, Irving C. "Contact Hypersensitivity Models in Mice." In Methods in Molecular Biology, 139–44. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-496-8_11.

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Thomas, S., A. D. Pearse, and R. Marks. "Transplantation Studies on Solar Keratoses in Nude Mice." In Skin Models, 73–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-70387-4_9.

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McKenzie, I. F. C., Y. Q. Li, and M. S. Sandrin. "Transgenic Mouse Models and Knockout Mouse Models to Manipulate the Xenograft Response." In Organtransplantation in Rats and Mice, 595–604. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-72140-3_61.

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Conference papers on the topic "Mice models"

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Ólafsdóttir, Hildur, Tron A. Darvann, Bjarne K. Ersbøll, Nuno V. Hermann, Estanislao Oubel, Rasmus Larsen, Alejandro F. Frangi, et al. "Craniofacial statistical deformation models of wild-type mice and Crouzon mice." In Medical Imaging, edited by Josien P. W. Pluim and Joseph M. Reinhardt. SPIE, 2007. http://dx.doi.org/10.1117/12.697406.

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Ross, Alexis, Ana Marasović, and Matthew Peters. "Explaining NLP Models via Minimal Contrastive Editing (MiCE)." In Findings of the Association for Computational Linguistics: ACL-IJCNLP 2021. Stroudsburg, PA, USA: Association for Computational Linguistics, 2021. http://dx.doi.org/10.18653/v1/2021.findings-acl.336.

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Wan, William, Hiromi Yanagisawa, and Rudolph L. Gleason. "Biomechanical and Microstructural Properties of Fibulin-5 Null Mice." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206435.

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Fibulin-5 is an extracellular matrix (ECM) protein that interacts with integrins and plays a critical role in organizing elastic fibers. Gross observation and histological examination reveal that carotid arteries from fibulin-5 knockout (fib5-/-) mice have disrupted elastic lamellae and are more tortuous [1]. The properties of fibulin-5 null mice provide a unique platform for developing constituent based models for vascular mechanics. While numerous models for blood vessels exist, there is a need to relate measurable microstructural metrics of structurally-based constitutive relations. We performed mechanical tests on carotid arteries from wildtype (WT) and fib5-/-mice and imaged live vessels under multiple loading scenarios to quantify microstructure during deformation. We also fit experimental results to a constitutive relation based on Holzapfel’s model [2]. These results provide a basis for further model development.
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YU, YONG A., and ALADAR A. SZALAY. "EXAMINATIONS OF BACTERIUM-MEDIATED DETECTION OF TUMORS IN MICE MODELS." In Chemistry, Biology and Applications. WORLD SCIENTIFIC, 2007. http://dx.doi.org/10.1142/9789812770196_0051.

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Ortega, M. P., C. Sunkel, and J. G. Priego. "PROTECTIVE EFFECT OF A NEW SYNTHETIC COMPOUND: PCA-4230, ON SEVERAL In vivo THROMBOSIS MODELS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643430.

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PCA-4230 is a new anti-thrombotic compound which inhibits pla. telet aggregation In vltn.0 and ex. vivo in several species, including man, prolongs the bleeding time and has potent protective ac tivity in several thrombosis models. Phase I trials with different dosage schedules have recently been initiated.In the present study, the effects of PCA-4230 on bleeding time and on several In vivo thrombosis models were studied in mice. Mice were treated with one single oral dose of PCA-4230 (1-10 mg/ kg). One hour after treatment, mice were injected intravenously with four thrombotic challengers {arachidonic acid (AA), thromboxane agonist (U46619), Platelet Activating Factor (PAF) or collagen/epinephrine combination (C/E)} at a dose which induced 80-90% of mortality. The thrombotic agents were prepared in saline. The appropiate doses were dissolved in a volume of 100 μl/mouse. Bleeding time was measured in non-anesthetized mice by the tail transection technique.Effects of compound were recorded from1 to 4 hours after dosage. Acute pre-treatment with PCA-4230 showed a significant dose-depen dent protective effect.Results of each series of experiments are given in the next table.The compound inhibited thrombotic sudden death induced by U46619, PAF or C/E combination, reduced the duration of respiratory distress induced by AA and prolonged bleeding time. Thus, PCA-4230 is protective against a variety of thrombotic stimuli.These results suggest that PCA-4230 may be a promising anti-throm botic drug.
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Nguyen, Ngoc, Mera Delimayanti, Bedy Purnama, Kunti Mahmudah, Mamoru Kubo, Makiko Kakikawa, Yoichi Yamada, and Kenji Satou. "Applying Deep Learning Models to Action Recognition of Swimming Mice with the Scarcity of Training Data." In 10th International Conference on Bioinformatics Models, Methods and Algorithms. SCITEPRESS - Science and Technology Publications, 2019. http://dx.doi.org/10.5220/0007567602700275.

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Sakai, Mizu, Tetsuya Kubota, Takashi Yamane, Naoki Shiota, Hiroshi Ohnishi, and Akihito Yokoyama. "Analysis Of Lung Injury Models By Using Human MUC1 Transgenic Mice." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a6305.

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Yang, Shu. "Dependence of neurons mortality on synaptogenesis in conditional mutant mice models." In ISAIMS 2021: 2nd International Symposium on Artificial Intelligence for Medicine Sciences. New York, NY, USA: ACM, 2021. http://dx.doi.org/10.1145/3500931.3501028.

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Vengrenyuk, Yuliya, Theodore J. Kaplan, Luis Cardoso, Gwendalyn J. Randolph, and Sheldon Weinbaum. "Biomechanical Modeling of Atherosclerotic Lesions in ApoE Deficient Mice." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206571.

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Cardiovascular disease remains the principal killer in the western world despite major advances in treatment of its patients [1]. It is generally accepted that sudden rupture of vulnerable plaque followed by thrombus formation underlies most cases of myocardial infarction and is responsible for more than a half of 500,000 coronary heart disease deaths every year. Although histopathological analysis of postmortem specimens have provided important data on histological features of ruptured human plaques, there is an urgent need for good representative animal models of plaque rupture. Over the last decade and a half, genetically engineered mice have been widely used to study the pathogenesis and potential treatment of atherosclerotic lesions, as well as genetic, hormonal and environmental influences on development of atherosclerosis. Though many of the features of plaque development and progression that occur in human plaques are similarly observed in murine plaques, these mouse models have long been regarded as poor models to study plaque rupture because the aortic sinus lesions seldom show any signs of fibrous cap disruption. Several recent studies reported potentially unstable atherosclerotic lesions in older apoE-deficient mice in another anatomic site, the proximal part of the brachiocephalic artery (BCA) [2, 3]. The unusual stability of aortic lesions compared to the BCA lesions in ApoE knockout mice is an unexplained paradox in developing a mouse model of plaque rupture. In this paper, we use histology based finite element analysis to evaluate peak circumferential stresses in aortic and BCA lesions from high fat fed ApoE KO mice.
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Ajmal, Ajmal, JunZhu Pei, Amanda Sanchez, and Jessica C. Ramella-Roman. "Depth Resolved Mueller Matrix Analysis of Cervical Remodeling in Murine Models." In Clinical and Translational Biophotonics. Washington, D.C.: Optica Publishing Group, 2024. http://dx.doi.org/10.1364/translational.2024.ttu3b.6.

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Early softening of the uterine cervix leads to Preterm Birth. Mueller matrix of mice ecto-cervix to endo-cervix at different pregnancy time points were assessed. Changes in the micro-structural organization of the cervical ECM are quantified.
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Reports on the topic "Mice models"

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Deng, Yingjun, ShengJing Liu, Ming Zhao, Feng Zhao, Jun Guo, and Bin Yan. Diet-induced male infertility in mice models: a systematic review and network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0116.

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Review question / Objective: In order to compare the different high energy diet such as high-fat diet and high sugar diet how to damage the male mice model in metabolize and fertility,and explore a reliable mice model method in the study of obesity with male infertility. P：obesity mice model with male infertility. I: High energy diet such as High-fat or High-sugar diet. C:High-fat diet,High-sugar diet, compared with normal diet in mice model. O:High energy diet induce male mice obesity model and damage their fertility. S: Use network meta-analysis. Condition being studied: The relationship between obesity and male infertility attacth more and more attention at present.So many animal expriments are carried out on this problem,there are enough exprimental article to support this meta analysis.
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Rice, Aaron. Effects of dietary ω-3 Polyunsaturated Fatty Acids (n-3 PUFA) in light sensitivity of retinas of mice models to prevent retinal damage. University of Tennessee Health Science Center, August 2022. http://dx.doi.org/10.21007/com.lsp.2022.0013.

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Rice, Aaron. Effects of dietary ω-3 Polyunsaturated Fatty Acids (n-3 PUFA) in light sensitivity of retinas of mice models to prevent retinal damage. University of Tennessee Health Science Center, August 2022. http://dx.doi.org/10.21007/com.lsp.2022.0014.

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Schwartz, Bertha, Vaclav Vetvicka, Ofer Danai, and Yitzhak Hadar. Increasing the value of mushrooms as functional foods: induction of alpha and beta glucan content via novel cultivation methods. United States Department of Agriculture, January 2015. http://dx.doi.org/10.32747/2015.7600033.bard.

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During the granting period, we performed the following projects: Firstly, we differentially measured glucan content in several pleurotus mushroom strains. Mushroom polysaccharides are edible polymers that have numerous reported biological functions; the most common effects are attributed to β-glucans. In recent years, it became apparent that the less abundant α-glucans also possess potent effects in various health conditions. In our first study, we explored several Pleurotus species for their total, β and α-glucan content. Pleurotuseryngii was found to have the highest total glucan concentrations and the highest α-glucans proportion. We also found that the stalks (stipe) of the fruit body contained higher glucan content then the caps (pileus). Since mushrooms respond markedly to changes in environmental and growth conditions, we developed cultivation methods aiming to increase the levels of α and β-glucans. Using olive mill solid waste (OMSW) from three-phase olive mills in the cultivation substrate. We were able to enrich the levels mainly of α-glucans. Maximal total glucan concentrations were enhanced up to twice when the growth substrate contained 80% of OMSW compared to no OMSW. Taking together this study demonstrate that Pleurotuseryngii can serve as a potential rich source of glucans for nutritional and medicinal applications and that glucan content in mushroom fruiting bodies can be further enriched by applying OMSW into the cultivation substrate. We then compared the immune-modulating activity of glucans extracted from P. ostreatus and P. eryngii on phagocytosis of peripheral blood neutrophils, and superoxide release from HL-60 cells. The results suggest that the anti-inflammatory properties of these glucans are partially mediated through modulation of neutrophileffector functions (P. eryngiiwas more effective). Additionally, both glucans dose-dependently competed for the anti-Dectin-1 and anti-CR3 antibody binding. We then tested the putative anti-inflammatory effects of the extracted glucans in inflammatory bowel disease (IBD) using the dextran sulfate sodium (DSS)–induced model in mice. The clinical symptoms of IBD were efficiently relieved by the treatment with two different doses of the glucan from both fungi. Glucan fractions, from either P. ostreatus or P. eryngii, markedly prevented TNF-α mediated inflammation in the DSS–induced inflamed intestine. These results suggest that there are variations in glucan preparations from different fungi in their anti-inflammatory ability. In our next study, we tested the effect of glucans on lipopolysaccharide (LPS)-induced production of TNF-α. We demonstrated that glucan extracts are more effective than mill mushroom preparations. Additionally, the effectiveness of stalk-derived glucans were slightly more pronounced than of caps. Cap and stalk glucans from mill or isolated glucan competed dose-dependently with anti-Dectin-and anti-CR-3 antibodies, indicating that they contain β-glucans recognized by these receptors. Using the dextran sulfate sodium (DSS)-inflammatory bowel disease mice model, intestinal inflammatory response to the mill preparations was measured and compared to extracted glucan fractions from caps and stalks. We found that mill and glucan extracts were very effective in downregulatingIFN-γ and MIP-2 levels and that stalk-derived preparations were more effective than from caps. The tested glucans were equally effective in regulating the number of CD14/CD16 monocytes and upregulating the levels of fecal-released IgA to almost normal levels. In conclusion, the most effective glucans in ameliorating some IBD-inflammatory associated symptoms induced by DSS treatment in mice were glucan extracts prepared from the stalk of P. eryngii. These spatial distinctions may be helpful in selecting more effective specific anti-inflammatory mushrooms-derived glucans. We additionally tested the effect of glucans on lipopolysaccharide-induced production of TNF-α, which demonstrated stalk-derived glucans were more effective than of caps-derived glucans. Isolated glucans competed with anti-Dectin-1 and anti-CR3 antibodies, indicating that they contain β-glucans recognized by these receptors. In conclusion, the most effective glucans in ameliorating IBD-associated symptoms induced by DSS treatment in mice were glucan extracts prepared from the stalk of P. eryngii grown at higher concentrations of OMSW. We conclude that these stress-induced growing conditions may be helpful in selecting more effective glucans derived from edible mushrooms. Based on the findings that we could enhance glucan content in Pleurotuseryngii following cultivation of the mushrooms on a substrate containing different concentrations of olive mill solid waste (OMSW) and that these changes are directly related to the content of OMSW in the growing substrate we tested the extracted glucans in several models. Using dextran sulfate sodium (DSS)–inflammatory bowel disease (IBD) mice model, we measured the colonic inflammatory response to the different glucan preparations. We found that the histology damaging score (HDS) resulting from DSS treatment reach a value of 11.8 ± 2.3 were efficiently downregulated by treatment with the fungal extracted glucans, glucans extracted from stalks cultivated at 20% OMSWdownregulated to a HDS value of 6.4 ± 0.5 and at 80% OMSW showed the strongest effects (5.5 ± 0.6). Similar downregulatory effects were obtained for expression of various intestinal cytokines. All tested glucans were equally effective in regulating the number of CD14/CD16 monocytes from 18.2 ± 2.7 % for DSS to 6.4 ± 2.0 for DSS +glucans extracted from stalks cultivated at 50% OMSW. We finally tested glucans extracted from Pleurotuseryngii grown on a substrate containing increasing concentrations of olive mill solid waste (OMSW) contain greater glucan concentrations as a function of OMSW content. Treatment of rat Intestinal epithelial cells (IEC-6) transiently transfected with Nf-κB fused to luciferase demonstrated that glucans extracted from P. eryngii stalks grown on 80% OMSWdownregulatedTNF-α activation. Glucans from mushrooms grown on 80% OMSW exerted the most significant reducing activity of nitric oxide production in lipopolysaccharide (LPS) treated J774A.1 murine macrophages. The isolated glucans were tested in vivo using the Dextran Sodium Sulfate (DSS) induced colitis in C57Bl/6 mice and found to reduce the histology damaging score resulting from DSS treatment. Expression of various intestinal cytokines were efficiently downregulated by treatment with the fungal extracted glucans. We conclude that the stress-induced growing conditions exerted by OMSW induces production of more effective anti-inflammatory glucans in P. eryngii stalks.
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Rodier, Caroline, Andrea Broaddus, Miguel Jaller, Jeffery Song, Joschka Bischoff, and Yunwan Zhang. Cost-Benefit Analysis of Novel Access Modes: A Case Study in the San Francisco Bay Area. Mineta Transportation Institute, November 2020. http://dx.doi.org/10.31979/mti.2020.1816.

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The first-mile, last-mile problem is a significant deterrent for potential transit riders, especially in suburban neighborhoods with low density. Transit agencies have typically sought to solve this problem by adding parking spaces near transit stations and adding stops to connect riders to fixed-route transit. However, these measures are often only short-term solutions. In the last few years, transit agencies have tested whether new mobility services, such as ridehailing, ridesharing, and microtransit, can offer fast, reliable connections to and from transit stations. However, there is limited research that evaluates the potential impacts of these projects. Concurrently, there is growing interest in the future of automated vehicles (AVs) and the potential of AVs to solve this first-mile problem by reducing the cost of providing these new mobility services to promote access to transit. This paper expands upon existing research to model the simulate the travel and revenue impacts of a fleet of automated vehicles that provide transit access services in the San Francisco Bay Area offered over a range of fares. The model simulates a fleet of AVs for first-mile transit access at different price points for three different service models (door-to-door ridehailing and ridesharing and meeting point ridesharing services). These service models include home-based drop-off and pick-up for single passenger service (e.g., Uber and Lyft), home-based drop-off and pick-up for multi-passenger service (e.g., microtransit), and meeting point multi-passenger service (e.g., Via).
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Yu, Y. S. Capabilities, limitations and the use of the GEOROC computer package. Natural Resources Canada/CMSS/Information Management, 1987. http://dx.doi.org/10.4095/325534.

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Computer codes have been used by various researchers in modelling viscoelastic formations, with a good degree of success. Serata used a complex rheological model, REM (Rheological Element Model) code, to simulate mine openings [2]. Others, in the U.S. Nuclear Waste Isolation Programme, have evaluated the capability of various codes for the design of nuclear waste repository [3]. Because of the proprietary nature of the above codes, they are not available to mine operators in Canada. Consequently, in 1984, CANMET initiated a research project to develop a numerical modelling package for use in the design of underground potash mine openings. GEOROC is the resultant computer program; it was developed by RE/SPEC Ltd., of Calgary under contract to CANMET. In recent years, computer simulation is playing an increasingly important role in evaluating the short and long term structural stability of underground mine openings, and in ground control studies related to mine design and layout. Such simulations are increasingly being used in the design of underground salt and potash mines. Because of the viscoelastic nature of salt rock formations, simulation models must take into consideration their time dependent properties if they are to correctly predict opening closures, ground stresses, and ground stability based on prescribed failure criteria. This presentation describes the capabilities, limitations and the use of computer code - GEOROC. A case history in which GEOROC is used to simulate a typical room and pillar mining section of a Western Canadian potash mine is provided. Predicted ground behaviour using the code is compared with actual behaviour as determined through field measurements. Results indicate that good correlation exits between predicted and measured ground behaviour, and is an encouragement to greater use of modelling in mine stability studies related to mine design.
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Briggs, Kevin, and Daniel F. Lott. Using an Instrumented Mine to Validate Models Predicting Mine Burial. Fort Belvoir, VA: Defense Technical Information Center, September 1999. http://dx.doi.org/10.21236/ada630761.

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Nasr, Elhami, Tariq Shehab, Nigel Blampied, and Vinit Kanani. Estimating Models for Engineering Costs on the State Highway Operation and Protection Program (SHOPP) Portfolio of Projects. Mineta Transportation Institute, November 2024. http://dx.doi.org/10.31979/mti.2024.2365.

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The State Highway Operation and Protection Program (SHOPP) is crucial for maintaining California’s 15,000-mile state highway system, which includes projects like pavement rehabilitation, bridge repair, safety enhancements, and traffic management systems. Administered by Caltrans, SHOPP aims to preserve highway efficiency and safety, supporting economic growth and public safety. This research aimed to develop robust cost-estimating models to improve budgeting and financial planning, aiding Caltrans, the California Transportation Commission (CTC), and the Legislature. The research team collected and refined comprehensive data from Caltrans project expenditures from 1983 to 2021, ensuring a high-quality dataset. Subject matter experts validated the data, enhancing its reliability. Two models were developed: a statistical model using exponential regression to account for non-linear cost growth, and an AI model employing neural networks to handle complex relationships in the data. Model performance was evaluated based on accuracy and reliability through repeated testing and validation. Key findings indicated that the new models significantly improved the precision of cost forecasts, reducing the variance between predicted and actual project costs. This advancement minimizes budget overruns and enhances resource allocation efficiency. Additionally, leveraging historical data with current market trends refined the models’ predictive power, boosting stakeholder confidence in project budgeting and financial planning. The study’s innovative approach, integrating machine learning and big data analytics, transforms traditional estimation practices and serves as a reference for other state highway programs. Continuous improvement and broader application of these models are recommended to further enhance cost estimation accuracy and support informed decision-making in transportation infrastructure management.
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Roa, Julio, Joseph Oldham, and Marina Lima. Recognizing the Potential to Reduce GHG Emissions Through Air Transportation Electrification. Mineta Transportation Institute, July 2023. http://dx.doi.org/10.31979/mti.2023.2223.

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California is aggressively moving forward with efforts to deploy zero-emission transportation technology to fight climate change, especially the Greenhouse Gas (GHG) emissions from the high-impact transportation sector. However, to date, the investments California has made with Cap-and-Trade funding have focused on ground transportation and some marine sources and not the aircraft at the over 140 airports in the state. Through a California-focused comprehensive GHG emissions analysis, this research project seeks to determine how RAM using electric/hybrid electric aircraft can provide new high-speed transportation for high-priority passenger and cargo movement within Fresno County and connections to coastal urban centers. Using VISION, a model developed by the Argonne National Laboratory Transportation Systems Assessment Group, the research team identified and compared the emission per mile and emission per passenger mile between different modes of transportation using traditional petroleum fuel and other sustainable alternatives at an individual level and within the context of the transportation sector, by comparing different modes of transportation. With this estimation on hand, it becomes more viable for the state of California and other states, as well as the federal government, to establish guidelines and goals for transportation policies and investments.
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Ficht, Thomas, Gary Splitter, Menachem Banai, and Menachem Davidson. Characterization of B. Melinensis REV 1 Attenuated Mutants. United States Department of Agriculture, December 2000. http://dx.doi.org/10.32747/2000.7580667.bard.

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Brucella Mutagenesis (TAMU) The working hypothesis for this study was that survival of Brucella vaccines was directly related to their persistence in the host. This premise is based on previously published work detailing the survival of the currently employed vaccine strains S19 and Rev 1. The approach employed signature-tagged mutagenesis to construct mutants interrupted in individual genes, and the mouse model to identify mutants with attenuated virulence/survival. Intracellular survival in macrophages is the key to both reproductive disease in ruminants and reticuloendothelial disease observed in most other species. Therefore, the mouse model permitted selection of mutants of reduced intracellular survival that would limit their ability to cause reproductive disease in ruminants. Several classes of mutants were expected. Colonization/invasion requires gene products that enhance host-agent interaction or increase resistance to antibacterial activity in macrophages. The establishment of chronic infection requires gene products necessary for intracellular bacterial growth. Maintenance of chronic infection requires gene products that sustain a low-level metabolism during periods characterized little or no growth (1, 2). Of these mutants, the latter group was of greatest interest with regard to our originally stated premise. However, the results obtained do not necessarily support a simplistic model of vaccine efficacy, i.e., long-survival of vaccine strains provides better immunity. Our conclusion can only be that optimal vaccines will only be developed with a thorough understanding of host agent interaction, and will be preferable to the use of fortuitous isolates of unknown genetic background. Each mutant could be distinguished from among a group of mutants by PCR amplification of the signature tag (5). This approach permitted infection of mice with pools of different mutants (including the parental wild-type as a control) and identified 40 mutants with apparently defective survival characteristics that were tentatively assigned to three distinct classes or groups. Group I (n=13) contained organisms that exhibited reduced survival at two weeks post-infection. Organisms in this group were recovered at normal levels by eight weeks and were not studied further, since they may persist in the host. Group II (n=11) contained organisms that were reduced by 2 weeks post infection and remained at reduced levels at eight weeks post-infection. Group III (n=16) contained mutants that were normal at two weeks, but recovered at reduced levels at eight weeks. A subset of these mutants (n= 15) was confirmed to be attenuated in mixed infections (1:1) with the parental wild-type. One of these mutants was eliminated from consideration due to a reduced growth rate in vitro that may account for its apparent growth defect in the mouse model. Although the original plan involved construction of the mutant bank in B. melitensis Rev 1 the low transformability of this strain, prevented accumulation of the necessary number of mutants. In addition, the probability that Rev 1 already carries one genetic defect increases the likelihood that a second defect will severely compromise the survival of this organism. Once key genes have been identified, it is relatively easy to prepare the appropriate genetic constructs (knockouts) lacking these genes in B. melitensis Rev 1 or any other genetic background. The construction of "designer" vaccines is expected to improve immune protection resulting from minor sequence variation corresponding to geographically distinct isolates or to design vaccines for use in specific hosts. A.2 Mouse Model of Brucella Infection (UWISC) Interferon regulatory factor-1-deficient (IRF-1-/- mice have diverse immunodeficient phenotypes that are necessary for conferring proper immune protection to intracellular bacterial infection, such as a 90% reduction of CD8+ T cells, functionally impaired NK cells, as well as a deficiency in iNOS and IL-12p40 induction. Interestingly, IRF-1-/- mice infected with diverse Brucella abortus strains reacted differently in a death and survival manner depending on the dose of injection and the level of virulence. Notably, 50% of IRF-1-/- mice intraperitoneally infected with a sublethal dose in C57BL/6 mice, i.e., 5 x 105 CFU of virulent S2308 or the attenuated vaccine S19, died at 10 and 20 days post-infection, respectively. Interestingly, the same dose of RB51, an attenuated new vaccine strain, did not induce the death of IRF-1-/- mice for the 4 weeks of infection. IRF-1-/- mice infected with four more other genetically manipulated S2308 mutants at 5 x 105 CFU also reacted in a death or survival manner depending on the level of virulence. Splenic CFU from C57BL/6 mice infected with 5 x 105 CFU of S2308, S19, or RB51, as well as four different S2308 mutants supports the finding that reduced virulence correlates with survival Of IRF-1-/- mice. Therefore, these results suggest that IRF-1 regulation of multi-gene transcription plays a crucial role in controlling B. abortus infection, and IRF-1 mice could be used as an animal model to determine the degree of B. abortus virulence by examining death or survival. A3 Diagnostic Tests for Detection of B. melitensis Rev 1 (Kimron) In this project we developed an effective PCR tool that can distinguish between Rev1 field isolates and B. melitensis virulent field strains. This has allowed, for the first time, to monitor epidemiological outbreaks of Rev1 infection in vaccinated flocks and to clearly demonstrate horizontal transfer of the strain from vaccinated ewes to unvaccinated ones. Moreover, two human isolates were characterized as Rev1 isolates implying the risk of use of improperly controlled lots of the vaccine in the national campaign. Since atypical B. melitensis biotype 1 strains have been characterized in Israel, the PCR technique has unequivocally demonstrated that strain Rev1 has not diverted into a virulent mutant. In addition, we could demonstrate that very likely a new prototype biotype 1 strain has evolved in the Middle East compared to the classical strain 16M. All the Israeli field strains have been shown to differ from strain 16M in the PstI digestion profile of the omp2a gene sequence suggesting that the local strains were possibly developed as a separate branch of B. melitensis. Should this be confirmed these data suggest that the Rev1 vaccine may not be an optimal vaccine strain for the Israeli flocks as it shares the same omp2 PstI digestion profile as strain 16M.
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