Relevant bibliographies by topics / Mammalian models

Academic literature on the topic 'Mammalian models'

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Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Mammalian models"

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Neuweiler, Gerhard. "Bats, models for mammalian ecology?" Trends in Ecology & Evolution 19, no. 1 (January 2004): 10. http://dx.doi.org/10.1016/j.tree.2003.09.019.

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Kundi. "SPINAL CORD INJURY: CURRENT MAMMALIAN MODELS." American Journal of Neuroscience 4, no. 1 (January 1, 2013): 1–12. http://dx.doi.org/10.3844/amjnsp.2013.1.12.

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Fryxell, John M. "Life-history models reconstruct mammalian evolution." Proceedings of the National Academy of Sciences 117, no. 4 (January 8, 2020): 1839–41. http://dx.doi.org/10.1073/pnas.1921256117.

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Ma'ayan, Avi, Robert D. Blitzer, and Ravi Iyengar. "Toward Predictive Models of Mammalian Cells." Annual Review of Biophysics and Biomolecular Structure 34, no. 1 (June 2005): 319–49. http://dx.doi.org/10.1146/annurev.biophys.34.040204.144415.

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Herzel, Hanspeter, and Nils Blüthgen. "Mathematical models in mammalian cell biology." Genome Biology 9, no. 7 (2008): 316. http://dx.doi.org/10.1186/gb-2008-9-7-316.

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Etienne, A. S. "Mammalian Navigation, Neural Models and Biorobotics." Connection Science 10, no. 3-4 (September 1998): 271–89. http://dx.doi.org/10.1080/095400998116440.

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Belser, Jessica A., and Terrence M. Tumpey. "H5N1 pathogenesis studies in mammalian models." Virus Research 178, no. 1 (December 2013): 168–85. http://dx.doi.org/10.1016/j.virusres.2013.02.003.

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Selman, Colin, and Dominic J. Withers. "Mammalian models of extended healthy lifespan." Philosophical Transactions of the Royal Society B: Biological Sciences 366, no. 1561 (January 12, 2011): 99–107. http://dx.doi.org/10.1098/rstb.2010.0243.

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Over the last two centuries, there has been a significant increase in average lifespan expectancy in the developed world. One unambiguous clinical implication of getting older is the risk of experiencing age-related diseases including various cancers, dementia, type-2 diabetes, cataracts and osteoporosis. Historically, the ageing process and its consequences were thought to be intractable. However, over the last two decades or so, a wealth of empirical data has been generated which demonstrates that longevity in model organisms can be extended through the manipulation of individual genes. In particular, many pathological conditions associated with the ageing process in model organisms, and importantly conserved from nematodes to humans, are attenuated in long-lived genetic mutants. For example, several long-lived genetic mouse models show attenuation in age-related cognitive decline, adiposity, cancer and glucose intolerance. Therefore, these long-lived mice enjoy a longer period without suffering the various sequelae of ageing. The greatest challenge in the biology of ageing is to now identify the mechanisms underlying increased healthy lifespan in these model organisms. Given that the elderly are making up an increasingly greater proportion of society, this focused approach in model organisms should help identify tractable interventions that can ultimately be translated to humans.
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Ishikawa, Makoto, Takeshi Yoshitomi, Charles F. Zorumski, and Yukitoshi Izumi. "Experimentally Induced Mammalian Models of Glaucoma." BioMed Research International 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/281214.

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A wide variety of animal models have been used to study glaucoma. Although these models provide valuable information about the disease, there is still no ideal model for studying glaucoma due to its complex pathogenesis. Animal models for glaucoma are pivotal for clarifying glaucoma etiology and for developing novel therapeutic strategies to halt disease progression. In this review paper, we summarize some of the major findings obtained in various glaucoma models and examine the strengths and limitations of these models.
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Cockerell, Alaina, Liam Wright, Anish Dattani, Ge Guo, Austin Smith, Krasimira Tsaneva-Atanasova, and David M. Richards. "Biophysical models of early mammalian embryogenesis." Stem Cell Reports 18, no. 1 (January 2023): 26–46. http://dx.doi.org/10.1016/j.stemcr.2022.11.021.

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Dissertations / Theses on the topic "Mammalian models"

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Weis, Michael Christian. "Computational Models of the Mammalian Cell Cycle." Case Western Reserve University School of Graduate Studies / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=case1323278159.

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Rabani, Michal. "Models of dynamic RNA regulation in mammalian cells." Thesis, Massachusetts Institute of Technology, 2013. http://hdl.handle.net/1721.1/84894.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Department of Electrical Engineering and Computer Science, 2013.
Cataloged from PDF version of thesis.
Includes bibliographical references (pages 135-142).
Complex molecular circuits, consisting of multiple intertwined feedback loops and non-linear interactions, are a hallmark of every living cell, and a model of a dynamic complex network. Here, I systematically study the dynamic changes in the cellular circuits that control RNA levels in mammalian cells, focusing on the model response of immune dendritic cells to pathogens, through an integration of comprehensive computational models and innovative empirical approaches. I establish a computational framework to follow the dynamics of processes for RNA birth (production, by transcription), maturation (processing), and death (degradation), and their integration in the dynamic RNA life cycle. I study the kinetics of a gene's RNA population with a model of its production and degradation, and generalize the system as an ensemble of genes. I further model genes as composite particles and study the regulation and kinetics of altering their internal structure. To allow robust statistical inference from these models, I develop innovative laboratory assays and collect extensive experimental data on the system. I directly measure RNA production rates by coupling short RNA metabolic labeling with advanced RNA quantification. I leverage recent improvements in RNA quantification by next-generation sequencing technology, to significantly increase the resolution of metabolic labeling in both time and gene-structure. Finally, I collect perturbation data, by monitoring RNA levels when specific elements of the network are disabled. In this way, I formulated several general principles of RNA regulation and its temporal evolution in mammalian cells. I find that temporal changes in production provide a dominant input in computing RNA levels by the cell over time. Yet, dynamic degradation changes contribute to shaping expression peaks, and dynamic processing changes allow a fast accumulation of mature transcripts. Static degradation and processing rates vary between genes and between individual splicing junctions, consistently with their function and expression dynamics. This study is broadly applicable to many normal as well as diseases misregulated cellular networks, and is also relevant for a more general analysis of complex systems dynamics.
by Michal Rabani.
Ph.D.
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Shaw, Alexander George. "Developing models of the mammalian cell S phase." Thesis, University of Manchester, 2011. https://www.research.manchester.ac.uk/portal/en/theses/developing-models-of-the-mammalian-cell-s-phase(3df7caaf-fd64-4bd2-b500-802f1a2c8ce2).html.

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The accurate replication of the mammalian genome is a complex and logistically challenging process. The entirety of the genome must undergo a single duplication with as little error as possible. This must occur in a coordinated fashion and over suitably short time scale so as to allow timely cellular division within a cell cycle that is typically around 24 hours in a human cell. A great wealth of knowledge already exists describing various aspects of the S phase, during which this replication of the genome occurs. This data has been gathered over a variety of model systems, ranging from inferences from the replicative mechanics of SV40 through to direct observations of replication in mammalian cells.In order integrate this data and determine the value of inferences from different data sources, quantitative models of the mammalian cell S phase are required. This study documents the development of several such models and the exploration of the influences that experimentally determined parameters and different mechanistic theories can have on the behaviour of a simulated S phase. Of particular exploratory interest were the modes of activating replication of replicon clusters, with the aim of simulating experimentally observed dynamics. Additionally, the study also aimed to investigate the variation of replication fork rates and the density of origins of replication, along with the relationship that occurs between the two during both replicational stress and during a normal S phase. Through an iterative series of models, relevant parameters and key theories are sequentially explored so as to better understand the S phase. Particularly influential parameters were identified and studied in detail, with experimental determination where necessary in order to more accurately inform the model system. Conclusions concerning the behaviour of the system and the potential impact of the results were drawn upon the completion of each level of modelling and experimental work.To conclude the study, a linear model simulating the genome of the MRC5 cell line was used to estimate the modes activation of DNA replication along chromosomes in order to recreate experimentally observed replication dynamics. Experimentally determined profiles of replication fork rates and the density of origin firing were also determined for the MRC5 cell line, and were used to populate the model with accurate and appropriate data. Using the model to simulate S phase through a variety of behavioural parameters, realistic S phase dynamics were found to occur through a combination of de novo activation of replicon clusters and a specific probability of neighbour activation by completed clusters. These derived mechanics, when performed on a system correctly parameterised with suitable data, can simulate experimentally observed phenomena. The development of the model highlighted the requirements of data fit for purpose, and the study also stresses the need for critical consideration of inferences made between different model systems.
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Patel, Nirmal Praful School of Medicine UNSW. "Olfactory progenitor cell transplantation into the mammalian inner ear." Awarded by:University of New South Wales. School of Medicine, 2006. http://handle.unsw.edu.au/1959.4/26180.

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A practical consideration in the development of cellular therapy technology for the inner ear is the development of an in vitro model for assessing the optimal conditions for successful application of cells. The first part of this thesis describes the adaptation of the cochleovestibular structure harvested from P1 mouse pups for analysis of factors critical for the optimal implantation of stem cells in the inner ear. Results of these studies establish that the c17.2 neural stem cell line can be introduced into the cochleovestibular structure in vitro. Using this model, c17.2 cells demonstrated survival predominantly within the vestibule and basal spiral ganglion regions. Furthermore, the addition of the ototoxin, cisplatin and the neurotrophin, Brain Derived Neurotrophic Growth Factor (BDNF) enhanced the survival and migration/dispersion of c17.2 cells within the cochleovestibular explant. The second part of this thesis examines the hypothesis that olfactory neurosphere (ONS) and progenitor cells harvested from the olfactory epithelium represent a viable source of graft material for potential therapeutic applications in the inner ear. Olfactory epithelium represents a unique source of pluripotent cells that may serve as either homografts or autografts. The feasibility of ONSs to survive and integrate into a mammalian cochlea in vivo was assessed. The ONSs were isolated as a crude fraction from the olfactory epithelium of P1 to P3 day old swiss webster mouse pups, ubiquitously expressing the Green Fluorescent Protein (GFP) marker. The ONSs were microinjected into the cochleae of adult CD1 male mice. Four weeks following their implantation, ONS cells expressing the GFP marker and stained by Nestin were identified in all areas of the cochlea and vestibule, including the spiral ganglion. Robust survival and growth of the implanted ONS and ONS derived cells in the cochlea also included the development of ???tumor-like??? clusters, a phenomenon not observed in control animals implanted with c17.2 neural stem cells. Collectively, the results of this thesis illustrate the potential of olfactory neurosphere and progenitor cells to survive in the inner ear and expose a potential harmful effect of their transplantation.
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Nel, Maria Elizabeth. "Mammalian cell cultures as models for metabolomic studies / Nel Z." Thesis, North-West University, 2012. http://hdl.handle.net/10394/8205.

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The use of cultured cells in metabolomic studies is receiving more and more attention. There are many advantages when using cultured cells in metabolomic studies, for example cultured cells can easily be manipulated for the purpose of the experiment. This creates many opportunities for metabolomics studies, for example cell cultures can offer an alternative manner of drug testing. Even though the use of cultured cells in metabolomic studies is very promising and they create many opportunities for metabolomic research, there are still challenges that create obstacles in this research. One of the challenges is that present analytical technologies do not always fully meet the requirements for metabolomics. There is, however, much effort going into optimising the methods concerning cultured cells and metabolomics, but there is a lack of attention when it comes to the sample preparation which is initiated by quenching. The aim of this study was to investigate cultured cells as models for metabolomics investigations and to standardise a proper quenching method for a metabolomics analysis of mammalian cultured cells. A quenching method adapted from the literature was evaluated for the cell line used in this study, namely HeLa. Metabolites of the central carbon metabolism were targeted, using a published list. This method was tested for its effectiveness by introducing the samples to waiting periods (0, 3, 6 and 24 hours) before extraction after immediate quenching. Results indicated that the entire metabolism under study was not effectively quenched. The optimum composition and temperature for this quenching method were also investigated by comparing three different quenching methods derived from the literature. The results were contradicting. Cell cultures were exposed to two perturbations (environmental and genetic) to investigate if these perturbations can be captured and measured by using metabolomics as an instrument. There was a significant difference between control groups and the groups exposed to the different perturbations. The results gained from this study indicate that it is definitely possible to use cultured cells in metabolomics studies.
Thesis (MSc (Biochemistry))--North-West University, Potchefstroom Campus, 2012.
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Hayes, Chris. "Genetic and functional analysis of mammalian limb development." Thesis, University of Oxford, 1998. http://ora.ox.ac.uk/objects/uuid:1443b218-fb63-4ced-9b15-e81947448ced.

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Siepel, Adam C. "Comparative mammalian genomics : models of evolution and detection of functional elements /." Diss., Digital Dissertations Database. Restricted to UC campuses, 2005. http://uclibs.org/PID/11984.

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Dalle, Pezze Piero. "Dynamical models of the mammalian target of rapamycin network in ageing." Thesis, University of Newcastle upon Tyne, 2013. http://hdl.handle.net/10443/2183.

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The mammalian Target of Rapamycin (mTOR)kinase is a central regulator of cellular growth and metabolism and plays an important role in ageing and age- related diseases. The increase of invitro data collected to extend our knowledge on its regulation, and consequently improve drug intervention,has highlighted the complexity of the mTOR network. This complexity is also aggravated by the intrinsic time-dependent nature of cellular regulatory network cross-talks and feedbacks. Systems biology constitutes a powerful tool for mathematically for- malising biological networks and investigating such dynamical properties. The present work discusses the development of three dynamical models of the mTOR network. The first aimed at the analysis of the current literature-based hypotheses of mTOR Complex2(mTORC2)regulation. For each hypothesis, the model predicted specific differential dynamics which were systematically tested by invitro experiments. Surprisingly, nocurrent hypothesis could explain the data and a new hypothesis of mTORC2 activation was proposed. The second model extended the previous one with an AMPK module. In this study AMPK was reported to be activated by insulin. Using a hypothesis ranking approach based on model goodness-of-fit, AMPK activity was insilico predicted and in vitro tested to be activated by the insulin receptor substrate(IRS).Finally,the last model linked mTOR with the oxidative stress response, mitochondrial reg- ulation, DNA damage and FoxO transcription factors. This work provided the characterisation of a dynamical mechanism to explain the state transition from normal to senescent cells and their reversibility of the senescentphenotype.
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Roopra, Avtar. "Transcriptional control of the m4 muscarinic receptor gene : mammalian and yeast models." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.313823.

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Zaksauskaite, Ringaile. "Analysis of chromosomal protein-linked break repair in zebrafish and mammalian models." Thesis, University of Sheffield, 2018. http://etheses.whiterose.ac.uk/20765/.

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Books on the topic "Mammalian models"

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Janigro, Damir. Mammalian Brain Development. Totowa, NJ: Humana Press, 2009.

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Mammalian cardiovascular system simulation: A catastrophe theoretic approach with the matching simulation method. Winnipeg: Wuerz Publishing, 1993.

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Addie, Siobhan, Meredith Hackmann, Anna Nicholson, and Sarah H. Beachy, eds. Examining the State of the Science of Mammalian Embryo Model Systems. Washington, D.C.: National Academies Press, 2020. http://dx.doi.org/10.17226/25779.

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Sketches of the natural history of Ceylon with narratives and anecdotes illustrative of the habits and instincts of the mammalia, birds, reptiles, fishes, insects, including a monograph of the elephant and a description of the modes of capturing and training it with engravings from original drawings. New Delhi: Asian Educational Services, 1999.

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Mammalian Models for Biomedical Research. Diane Pub, 1994.

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Janigro, Damir. Mammalian Brain Development. Humana Press, 2009.

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Vincan, Elizabeth. Wnt Signaling : Volume 1: Pathway Methods and Mammalian Models. Humana Press, 2011.

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Handbook of Mammalian Models in Biomedical Research (Pharmacology & Toxicology). CRC, 2001.

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National Center for Research Resources (U.S.), ed. Mammalian models for biomedical research: A research resources directory. [Bethesda, Md.]: National Institutes of Health, 1994.

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MAMMALIAN CARDIOVASCULAR SYSTEM SIMULATION. Wuerg Publishing Ltd., 1993.

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Book chapters on the topic "Mammalian models"

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Usherwood, James R. "Reductionist Models of Walking and Running." In Understanding Mammalian Locomotion, 143–72. Hoboken, NJ: John Wiley & Sons, Inc, 2016. http://dx.doi.org/10.1002/9781119113713.ch6.

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Anzar, Muhammad. "Cryopreservation of Mammalian Oocytes." In Animal Models and Human Reproduction, 519–56. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2017. http://dx.doi.org/10.1002/9781118881286.ch21.

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Velíšková, Jana, Annamaria Vezzani, and Astrid Nehlig. "Seizure Propensity and Brain Development: A Lesson from Animal Models." In Mammalian Brain Development, 77–104. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-287-2_5.

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Britton, Robert S., Bruce R. Bacon, and Robert E. Fleming. "Mammalian Models of Iron Homeostasis." In Iron Physiology and Pathophysiology in Humans, 631–52. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-60327-485-2_29.

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Galanopoulou, Aristea S., Libor Velíšek, and Solomon L. Moshé. "Seizures and Antiepileptic Drugs: Does Exposure Alter Normal Brain Development in Animal Models?" In Mammalian Brain Development, 105–32. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-287-2_6.

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Medina, Leonel E., and Warren M. Grill. "Mammalian Motor Nerve Fibers, Models of." In Encyclopedia of Computational Neuroscience, 1645–48. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-6675-8_369.

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Smith, Jeffrey C. "Computational Models of Mammalian Respiratory CPG." In Encyclopedia of Computational Neuroscience, 733–51. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-6675-8_41.

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Medina, Leonel E., and Warren M. Grill. "Mammalian Motor Nerve Fibers, Models of." In Encyclopedia of Computational Neuroscience, 1–4. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-7320-6_369-2.

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Smith, Jeffrey C. "Computational Models of Mammalian Respiratory CPG." In Encyclopedia of Computational Neuroscience, 1–20. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-7320-6_41-1.

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Wircer, Einav, Shifra Ben-Dor, and Gil Levkowitz. "Non-Mammalian Models for Neurohypophysial Peptides." In Molecular Neuroendocrinology, 301–28. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781118760369.ch14.

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Conference papers on the topic "Mammalian models"

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Lace, Lelde, Karlis Cerans, Karlis Freivalds, Gatis Melkus, and Juris Viksna. "Hybrid Gene Regulation Models of Mammalian Circadian Cycles." In 13th International Conference on Bioinformatics Models, Methods and Algorithms. SCITEPRESS - Science and Technology Publications, 2022. http://dx.doi.org/10.5220/0010834400003123.

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Walter, Marcelo, Alain Fournier, and Daniel Menevaux. "Integrating shape and pattern in mammalian models." In the 28th annual conference. New York, New York, USA: ACM Press, 2001. http://dx.doi.org/10.1145/383259.383294.

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"A review of computational models of mammalian cell cycle." In 21st International Congress on Modelling and Simulation (MODSIM2015). Modelling and Simulation Society of Australia and New Zealand, 2015. http://dx.doi.org/10.36334/modsim.2015.c2.abroudi2.

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"Towards a Large Integrated Model of Signal Transduction and Gene Regulation Events in Mammalian Cells." In International Conference on Bioinformatics Models, Methods and Algorithms. SCITEPRESS - Science and and Technology Publications, 2014. http://dx.doi.org/10.5220/0004739601170122.

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Duifhuis, Hendrikus, Christopher A. Shera, and Elizabeth S. Olson. "Hopf-Bifurcations and Van der Pol Oscillator Models of the Mammalian Cochlea." In WHAT FIRE IS IN MINE EARS: PROGRESS IN AUDITORY BIOMECHANICS: Proceedings of the 11th International Mechanics of Hearing Workshop. AIP, 2011. http://dx.doi.org/10.1063/1.3658086.

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Lattenkamp, Ella, Sonja Vernes, and Lutz Wiegrebe. "Mammalian models for the study of vocal learning: A new paradigm in bats." In The Evolution of Language. Proceedings of the 12th International Conference on the Evolution of Language (Evolang12). Wydawnictwo Naukowe Uniwersytetu Mikołaja Kopernika, 2018. http://dx.doi.org/10.12775/3991-1.056.

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Meyer, G. F., and William A. Ainsworth. "Vowel pitch period extraction by models of neurones in the mammalian brain-stem." In 3rd European Conference on Speech Communication and Technology (Eurospeech 1993). ISCA: ISCA, 1993. http://dx.doi.org/10.21437/eurospeech.1993-459.

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Winslow, Raimond L., Dongming Cai, and Ying Cheng Lai. "Factors controlling generation and propagation of pacemaker potentials in network models of mammalian SA node." In the 1994 ACM/IEEE conference. New York, New York, USA: ACM Press, 1994. http://dx.doi.org/10.1145/602770.602865.

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Grosh, Karl, and John M. Dodson. "Cochlear-Based Transducer Designs." In ASME 1999 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1999. http://dx.doi.org/10.1115/imece1999-0219.

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Showalter, Brent L., Jesse C. Beckstein, John T. Martin, Elizabeth E. Beattie, Alejandro A. Espinoza Orías, Thomas P. Schaer, Edward J. Vresilovic, and Dawn M. Elliott. "Disc Torsion Mechanics: Comparison of Animal Models to Human." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53607.

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The intervertebral disc plays a critical role in providing structural support to the spine while permitting extensive flexibility in a number of orientations. Axial rotation is a key parameter in spine function and torsional instability is related to spinal degeneration [1]. Animal models are integral components in many in vivo disc studies, however each animal varies in availability, size, cost, and scientific criteria such as cell phenotype and biomechanics. Selection of an appropriate animal model requires knowledge of the similarities and differences in biomechanical and biochemical factors between the model and human discs. Previous studies have often compared the characteristics of a single animal model with the human disc [2, 3]. However, variations in animal models and testing protocols between groups hinder comparisons and interpretations between different studies. This is especially relevant in torsion mechanics, where the magnitude of an applied compressive load and other testing parameters significantly affect the apparent torsional stiffness of the disc [4]. The objective of this study was to measure and compare the torsion mechanical properties of the human disc and 11 disc types from 8 mammalian species.
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Reports on the topic "Mammalian models"

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Ehrlich, Marcelo, John S. Parker, and Terence S. Dermody. Development of a Plasmid-Based Reverse Genetics System for the Bluetongue and Epizootic Hemorrhagic Disease Viruses to Allow a Comparative Characterization of the Function of the NS3 Viroporin in Viral Egress. United States Department of Agriculture, September 2013. http://dx.doi.org/10.32747/2013.7699840.bard.

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Project Title: "Development of a plasmid-based reverse genetics system for the Bluetongue and Epizootic Hemorrhagic Disease viruses to allow comparative characterization of the function of the NS3 viroporin in viral egress". Project details: No - IS-4192-09; Participants – Ehrlich M. (Tel Aviv University), Parker J.S. (Cornell University), DermodyT.S. (Vanderbilt University); Period - 2009-2013. Orbiviruses are insect-borne infectious agents of ruminants that cause diseases with considerable economical impact in Israel and the United States. The recent outbreaks of BTV in Europe and of Epizootic Hemorrhagic Disease Virus (EHDV) in Israel, underscore the need for: (i) a better comprehension of the infection process of orbiviruses, (ii) the identification of unique vs. common traits among different orbiviruses, (iii) the development of novel diagnosis and treatment techniques and approaches; all aimed at the achievement of more effective control and treatment measures. It is the context of these broad goals that the present project was carried out. To fulfill our long-term goal of identifying specific viral determinants of virulence, growth, and transmission of the orbiviruses, we proposed to: (i) develop reverse genetics systems for BTV and EHDV2-Ibaraki; and (ii) identify the molecular determinants of the NS3 nonstructural protein related to viroporin/viral egress activities. The first objective was pursued with a two-pronged approach: (i) development of a plasmid-based reverse genetics system for BTV-17, and (ii) development of an "in-vitro" transcription-based reverse genetics system for EHDV2-Ibaraki. Both approaches encountered technical problems that hampered their achievement. However, dissection of the possible causes of the failure to achieve viral spread of EHDV2-Ibaraki, following the transfection of in-vitro transcribed genomic segments of the virus, revealed a novel characteristic of EHDV2-Ibaraki infection: an uncharacteristically low fold increase in titer upon infection of different cell models. To address the function and regulation of NS3 we employed the following approaches: (i) development (together with Anima Cell Metrology) of a novel technique (based on the transfection of fluorescently-labeledtRNAs) that allows for the detection of the levels of synthesis of individual viral proteins (i.e. NS3) in single cells; (ii) development of a siRNA-mediated knockdown approach for the reduction in levels of expression of NS3 in EHDV2-Ibaraki infected cells; (iii) biochemical and microscopy-based analysis of the localization, levels and post-translational modifications of NS3 in infected cells. In addition, we identified the altered regulation and spatial compartmentalization of protein synthesis in cells infected with EHDV2-Ibaraki or the mammalian reovirus. In EHDV2-Ibaraki-infected cells such altered regulation in protein synthesis occurs in the context of a cell stress reponse that includes the induction of apoptosis, autophagy and activation of the stressrelated kinase c-Jun N-terminal Kinase (JNK). Interestingly, inhibition of such stress-related cellular processes diminishes the production of infectious virions, suggesting that EHDV usurps these responses for the benefit of efficient infection. Taken together, while the present project fell short of the generation of novel reverse genetics systems for orbiviruses, the development of novel experimental approaches and techniques, and their employment in the analysis of EHDV-infected cells, yielded novel insights in the interactions of orbiviruses with mammalian cells.
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2

Gurevitz, Michael, William A. Catterall, and Dalia Gordon. Learning from Nature How to Design Anti-insect Selective Pesticides - Clarification of the Interacting Face between Insecticidal Toxins and their Na-channel Receptors. United States Department of Agriculture, January 2010. http://dx.doi.org/10.32747/2010.7697101.bard.

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Structural details on the interacting faces of toxins and sodium channels (Navs), and particularly identification of elements that confer specificity for insects, are difficult to approach and require suitable experimental systems. Therefore, natural toxins capable of differential recognition of insect and mammalian Navs are valuable leads for design of selective compounds in insect control. We have characterized several scorpion toxins that vary in preference for insect and mammalian Navs, and identified residues important for their action. However, despite many efforts worldwide, only little is known about the receptor sites of these toxins, and particularly on differences between these sites on insect and mammalian Navs. Another problem arises from the massive overuse of chemical insecticides, which increases resistance buildup among various insect pests. A possible solution to this problem is to combine different insecticidal compounds, especially those that provide synergic effects. Our recent finding that combinations of insecticidal receptor site-3 toxins (sea anemone and scorpion alpha) with scorpion beta toxins or their truncated derivatives are synergic in toxicity to insects is therefore timely and strongly supports this approach. Our ability to produce toxins and various Navs in recombinant forms, enable thorough analysis and structural manipulations of both toxins and receptors. On this basis we propose to (1) restrict by mutagenesis the activity of insecticidal scorpion -toxins and sea anemone toxins to insects, and clarify the molecular basis of their synergic toxicity with antiinsect selective -toxins; (2) identify Nav elements that interact with scorpion alpha and sea anemone toxins and those that determine toxin selectivity to insects; (3) determine toxin-channel pairwise side-chain interactions by thermodynamic mutant cycle analysis using our large collection of mutant -toxins and Nav mutants identified in aim 2; (4) clarify the mode of interaction of truncated -toxins with insect Navs, and elucidate how they enhance the activity of insecticidal site-3 toxins. This research may lead to rational design of novel anti-insect peptidomimetics with minimal impact on human health and the environment, and will establish the grounds for a new strategy in insect pest control, whereby a combination of allosterically interacting compounds increase insecticidal action and reduce risks of resistance buildup.
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Rosenberg, Avi Z. In-Vivo Characterization of Mammalian Polarity Genes as Novel Tumor Suppressors Involved in Breast Cancer Development and Progression in a Mouse Model. Fort Belvoir, VA: Defense Technical Information Center, March 2006. http://dx.doi.org/10.21236/ada462385.

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4

Gurevitz, Michael, William A. Catterall, and Dalia Gordon. face of interaction of anti-insect selective toxins with receptor site-3 on voltage-gated sodium channels as a platform for design of novel selective insecticides. United States Department of Agriculture, December 2013. http://dx.doi.org/10.32747/2013.7699857.bard.

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Voltage-gated sodium channels (Navs) play a pivotal role in excitability and are a prime target of insecticides like pyrethroids. Yet, these insecticides are non-specific due to conservation of Navs in animals, raising risks to the environment and humans. Moreover, insecticide overuse leads to resistance buildup among insect pests, which increases misuse and risks. This sad reality demands novel, more selective, insect killers whose alternative use would avoid or reduce this pressure. As highly selective insect toxins exist in venomous animals, why not exploit this gift of nature and harness them in insect pest control? Many of these peptide toxins target Navs, and since their direct use via transformed crop plants or mediator microorganisms is problematic in public opinion, we focus on the elucidation of their receptor binding sites with the incentive of raising knowledge for design of toxin peptide mimetics. This approach is preferred nowadays by agro-industries in terms of future production expenses and public concern. However, characterization of a non-continuous epitope, that is the channel receptor binding site for such toxins, requires a suitable experimental system. We have established such a system within more than a decade and reached the stage where we employ a number of different insect-selective toxins for the identification of their receptor sites on Navs. Among these toxins we wish to focus on those that bind at receptor site-3 and inhibit Nav inactivation because: (1) We established efficient experimental systems for production and manipulation of site-3 toxins from scorpions and sea anemones. These peptides vary in size and structure but compete for site-3 on insect Navs. Moreover, these toxins exhibit synergism with pyrethroids and with other channel ligands; (2) We determined their bioactive surfaces towards insect and mammalian receptors (see list of publications); (3) We found that despite the similar mode of action on channel inactivation, the preference of the toxins for insect and mammalian channel subtypes varies greatly, which can direct us to structural features in the basis of selectivity; (4) We have identified by channel loop swapping and point mutagenesis extracellular segments of the Navinvolved with receptor site-3. On this basis and using channel scanning mutagenesis, neurotoxin binding, electrophysiological analyses, and structural data we offer: (i) To identify the residues that form receptor site-3 at insect and mammalian Navs; (ii) To identify by comparative analysis differences at site-3 that dictate selectivity toward various Navs; (iii) To exploit the known toxin structures and bioactive surfaces for modeling their docking at the insect and mammalian channel receptors. The results of this study will enable rational design of novel anti-insect peptide mimetics with minimized risks to human health and to the environment. We anticipate that the release of receptor site-3 molecular details would initiate a worldwide effort to design peptide mimetics for that site. This will establish new strategies in insect pest control using alternative insecticides and the combined use of compounds that interact allosterically leading to increased efficiency and reduced risks to humans or resistance buildup among insect pests.
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5

Gordon, Dalia, Ke Dong, and Michael Gurevitz. Unexpected Specificity of a Sea Anemone Small Toxin for Insect Na-channels and its Synergic Effects with Various Insecticidal Ligands: A New Model to Mimic. United States Department of Agriculture, November 2010. http://dx.doi.org/10.32747/2010.7697114.bard.

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Motivated by the high risks to the environment and human health imposed by the current overuse of chemical insecticides we offer an alternative approach for the design of highly active insect-selective compounds that will be based on the ability of natural toxins to differentiate between insect and mammalian targets. We wish to unravel the interacting surfaces of insect selective toxins with their receptor sites on voltage-gated sodium channels. In this proposal we put forward two recent observations that may expedite the development of a new generation of insect killers that mimic the highly selective insecticidal toxins: (i) A small (27aa) highly insecticidal sea anemone toxin, Av3, whose toxicity to mammals is negligible; (ii) The prominent positive cooperativity between distinct channel ligands, such as the strong enhancement of pyrethroids effects by anti-insect selective scorpion depressant toxins. We possess a repertoire of insecticidal toxins and sodium channel subtypes all available in recombinant form for mutagenesis followed by analysis of various pharmacological, electrophysiological, and structural methods. Our recent success to express Av3 provides for the first time a selective toxin for receptor site-3 on insect sodium channels. In parallel, our recent success to determine the structures and bioactive surfaces of insecticidal site-3 and site-4 toxins establishes a suitable system for elucidation of toxin-receptor interacting faces. This is corroborated by our recent identification of channel residues involved with these two receptor sites. Our specific aims in this proposal are to (i) Determine the bioactive surface of Av3 toward insect Na-channels; (ii) Identify channel residues involved in binding or activity of the insecticidal toxins Av3 and LqhaIT, which differ substantially in their potency on mammals; (iii) Illuminate channel residues involved in recognition by the anti-insect depressant toxins; (iv) Determine the face of interaction of both site-3 (Av3) and site-4 (LqhIT2) toxins with insect sodium channels using thermodynamic mutant cycle analysis; and, (v) Examine whether Av3, LqhIT2, pyrethroids, and indoxacarb (belongs to a new generation of insecticides), enhance allosterically the action of one another on the fruit fly and cockroach paraNa-channels and on their kdr and super-kdr mutants. This research establishes the grounds for rational design of novel anti-insect peptidomimetics with minimal impact on human health, and offers a new approach in insect pest control, whereby a combination of allosterically interacting compounds increases insecticidal action and reduces risks of resistance buildup.
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Malkinson, Mertyn, Irit Davidson, Moshe Kotler, and Richard L. Witter. Epidemiology of Avian Leukosis Virus-subtype J Infection in Broiler Breeder Flocks of Poultry and its Eradication from Pedigree Breeding Stock. United States Department of Agriculture, March 2003. http://dx.doi.org/10.32747/2003.7586459.bard.

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Objectives 1. Establish diagnostic procedures to identify tolerant carrier birds based on a) Isolation of ALV-J from blood, b) Detection of group-specific antigen in cloacal swabs and egg albumen. Application of these procedures to broiler breeder flocks with the purpose of removing virus positive birds from the breeding program. 2. Survey the AL V-J infection status of foundation lines to estimate the feasibility of the eradication program 3. Investigate virus transmission through the embryonated egg (vertical) and between chicks in the early post-hatch period (horizontal). Establish a model for limiting horizontal spread by analyzing parameters operative in the hatchery and brooder house. 4. Compare the pathogenicity of AL V-J isolates for broiler chickens. 5. Determine whether AL V-J poses a human health hazard by examining its replication in mammalian and human cells. Revisions. The: eradication objective had to be terminated in the second year following the closing down of the Poultry Breeders Union (PBU) in Israel. This meant that their foundation flocks ceased to be available for selection. Instead, the following topics were investigated: a) Comparison of commercial breeding flocks with and without myeloid leukosis (matched controls) for viremia and serum antibody levels. b) Pathogenicity of Israeli isolates for turkey poults. c) Improvement of a diagnostic ELISA kit for measuring ALV-J antibodies Background. ALV-J, a novel subgroup of the avian leukosis virus family, was first isolated in 1988 from broiler breeders presenting myeloid leukosis (ML). The extent of its spread among commercial breeding flocks was not appreciated until the disease appeared in the USA in 1994 when it affected several major breeding companies almost simultaneously. In Israel, ML was diagnosed in 1996 and was traced to grandparent flocks imported in 1994-5, and by 1997-8, ML was present in one third of the commercial breeding flocks It was then realized that ALV-J transmission was following a similar pattern to that of other exogenous ALVs but because of its unusual genetic composition, the virus was able to establish an extended tolerant state in infected birds. Although losses from ML in affected flocks were somewhat higher than normal, both immunosuppression and depressed growth rates were encountered in affected broiler flocks and affected their profitability. Conclusions. As a result of the contraction in the number of international primary broiler breeders and exchange of male and female lines among them, ALV-J contamination of broiler breeder flocks affected the broiler industry worldwide within a short time span. The Israeli national breeding company (PBU) played out this scenario and presented us with an opportunity to apply existing information to contain the virus. This BARD project, based on the Israeli experience and with the aid of the ADOL collaborative effort, has managed to offer solutions for identifying and eliminating infected birds based on exhaustive virological and serological tests. The analysis of factors that determine the efficiency of horizontal transmission of virus in the hatchery resulted in the workable solution of raising young chicks in small groups through the brooder period. These results were made available to primary breeders as a strategy for reducing viral transmission. Based on phylogenetic analysis of selected Israeli ALV-J isolates, these could be divided into two groups that reflected the countries of origin of the grandparent stock. Implications. The availability of a simple and reliable means of screening day old chicks for vertical transmission is highly desirable in countries that rely on imported breeding stock for their broiler industry. The possibility that AL V-J may be transmitted to human consumers of broiler meat was discounted experimentally.
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