Relevant bibliographies by topics / Zebrafish models

Academic literature on the topic 'Zebrafish models'

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Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Zebrafish models"

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Page, L. "Zebrafish as developmental models." Science 250, no. 4986 (December 7, 1990): 1320. http://dx.doi.org/10.1126/science.2255901.

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Daya, Alon, Rajashekar Donaka, and David Karasik. "Zebrafish models of sarcopenia." Disease Models & Mechanisms 13, no. 3 (March 1, 2020): dmm042689. http://dx.doi.org/10.1242/dmm.042689.

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Liu, Shu, and Steven D. Leach. "Zebrafish Models for Cancer." Annual Review of Pathology: Mechanisms of Disease 6, no. 1 (February 28, 2011): 71–93. http://dx.doi.org/10.1146/annurev-pathol-011110-130330.

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Golzio, C. "Zebrafish models of hypogonadisms." Annales d'Endocrinologie 79, no. 4 (September 2018): 197–98. http://dx.doi.org/10.1016/j.ando.2018.06.022.

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Bai, Qing, and Edward A. Burton. "Zebrafish models of Tauopathy." Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1812, no. 3 (March 2011): 353–63. http://dx.doi.org/10.1016/j.bbadis.2010.09.004.

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Rosa, João Gabriel Santos, Carla Lima, and Monica Lopes-Ferreira. "Zebrafish Larvae Behavior Models as a Tool for Drug Screenings and Pre-Clinical Trials: A Review." International Journal of Molecular Sciences 23, no. 12 (June 14, 2022): 6647. http://dx.doi.org/10.3390/ijms23126647.

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To discover new molecules or review the biological activity and toxicity of therapeutic substances, drug development, and research relies on robust biological systems to obtain reliable results. Phenotype-based screenings can transpose the organism’s compensatory pathways by adopting multi-target strategies for treating complex diseases, and zebrafish emerged as an important model for biomedical research and drug screenings. Zebrafish’s clear correlation between neuro-anatomical and physiological features and behavior is very similar to that verified in mammals, enabling the construction of reliable and relevant experimental models for neurological disorders research. Zebrafish presents highly conserved physiological pathways that are found in higher vertebrates, including mammals, along with a robust behavioral repertoire. Moreover, it is very sensitive to pharmacological/environmental manipulations, and these behavioral phenotypes are detected in both larvae and adults. These advantages align with the 3Rs concept and qualify the zebrafish as a powerful tool for drug screenings and pre-clinical trials. This review highlights important behavioral domains studied in zebrafish larvae and their neurotransmitter systems and summarizes currently used techniques to evaluate and quantify zebrafish larvae behavior in laboratory studies.
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Wasel, Ola, and Jennifer L. Freeman. "Chemical and Genetic Zebrafish Models to Define Mechanisms of and Treatments for Dopaminergic Neurodegeneration." International Journal of Molecular Sciences 21, no. 17 (August 20, 2020): 5981. http://dx.doi.org/10.3390/ijms21175981.

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The zebrafish (Danio rerio) is routinely used in biological studies as a vertebrate model system that provides unique strengths allowing applications in studies of neurodevelopmental and neurodegenerative diseases. One specific advantage is that the neurotransmitter systems are highly conserved throughout vertebrate evolution, including between zebrafish and humans. Disruption of the dopaminergic signaling pathway is linked to multiple neurological disorders. One of the most common is Parkinson’s disease, a neurodegenerative disease associated with the loss of dopaminergic neurons, among other neuropathological characteristics. In this review, the development of the zebrafish’s dopaminergic system, focusing on genetic control of the dopaminergic system, is detailed. Second, neurotoxicant models used to study dopaminergic neuronal loss, including 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), the pesticides paraquat and rotenone, and 6-hydroxydopamine (6-OHDA), are described. Next, zebrafish genetic knockdown models of dj1, pink1, and prkn established for investigating mechanisms of Parkinson’s disease are discussed. Chemical modulators of the dopaminergic system are also highlighted to showcase the applicability of the zebrafish to identify mechanisms and treatments for neurodegenerative diseases such as Parkinson’s disease associated with the dopaminergic system.
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Pitchai, Arjun, Rajesh Kannan Rajaretinam, and Jennifer L. Freeman. "Zebrafish as an Emerging Model for Bioassay-Guided Natural Product Drug Discovery for Neurological Disorders." Medicines 6, no. 2 (May 30, 2019): 61. http://dx.doi.org/10.3390/medicines6020061.

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Most neurodegenerative diseases are currently incurable, with large social and economic impacts. Recently, there has been renewed interest in investigating natural products in the modern drug discovery paradigm as novel, bioactive small molecules. Moreover, the discovery of potential therapies for neurological disorders is challenging and involves developing optimized animal models for drug screening. In contemporary biomedicine, the growing need to develop experimental models to obtain a detailed understanding of malady conditions and to portray pioneering treatments has resulted in the application of zebrafish to close the gap between in vitro and in vivo assays. Zebrafish in pharmacogenetics and neuropharmacology are rapidly becoming a widely used organism. Brain function, dysfunction, genetic, and pharmacological modulation considerations are enhanced by both larval and adult zebrafish. Bioassay-guided identification of natural products using zebrafish presents as an attractive strategy for generating new lead compounds. Here, we see evidence that the zebrafish’s central nervous system is suitable for modeling human neurological disease and we review and evaluate natural product research using zebrafish as a vertebrate model platform to systematically identify bioactive natural products. Finally, we review recently developed zebrafish models of neurological disorders that have the potential to be applied in this field of research.
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Quelle-Regaldie, Ana, Daniel Sobrido-Cameán, Antón Barreiro-Iglesias, María Jesús Sobrido, and Laura Sánchez. "Zebrafish Models of Autosomal Dominant Ataxias." Cells 10, no. 2 (February 17, 2021): 421. http://dx.doi.org/10.3390/cells10020421.

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Hereditary dominant ataxias are a heterogeneous group of neurodegenerative conditions causing cerebellar dysfunction and characterized by progressive motor incoordination. Despite many efforts put into the study of these diseases, there are no effective treatments yet. Zebrafish models are widely used to characterize neuronal disorders due to its conserved vertebrate genetics that easily support genetic edition and their optic transparency that allows observing the intact CNS and its connections. In addition, its small size and external fertilization help to develop high throughput assays of candidate drugs. Here, we discuss the contributions of zebrafish models to the study of dominant ataxias defining phenotypes, genetic function, behavior and possible treatments. In addition, we review the zebrafish models created for X-linked repeat expansion diseases X-fragile/fragile-X tremor ataxia. Most of the models reviewed here presented neuronal damage and locomotor deficits. However, there is a generalized lack of zebrafish adult heterozygous models and there are no knock-in zebrafish models available for these diseases. The models created for dominant ataxias helped to elucidate gene function and mechanisms that cause neuronal damage. In the future, the application of new genetic edition techniques would help to develop more accurate zebrafish models of dominant ataxias.
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Lane, Sarah, Luis Alberto More, and Aarti Asnani. "Zebrafish Models of Cancer Therapy-Induced Cardiovascular Toxicity." Journal of Cardiovascular Development and Disease 8, no. 2 (January 22, 2021): 8. http://dx.doi.org/10.3390/jcdd8020008.

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Purpose of review: Both traditional and novel cancer therapies can cause cardiovascular toxicity in patients. In vivo models integrating both cardiovascular and cancer phenotypes allow for the study of on- and off-target mechanisms of toxicity arising from these agents. The zebrafish is the optimal whole organism model to screen for cardiotoxicity in a high throughput manner, while simultaneously assessing the role of cardiotoxicity pathways on the cancer therapy’s antitumor effect. Here we highlight established zebrafish models of human cardiovascular disease and cancer, the unique advantages of zebrafish to study mechanisms of cancer therapy-associated cardiovascular toxicity, and finally, important limitations to consider when using the zebrafish to study toxicity. Recent findings: Cancer therapy-associated cardiovascular toxicities range from cardiomyopathy with traditional agents to arrhythmias and thrombotic complications associated with newer targeted therapies. The zebrafish can be used to identify novel therapeutic strategies that selectively protect the heart from cancer therapy without affecting antitumor activity. Advances in genome editing technology have enabled the creation of several transgenic zebrafish lines valuable to the study of cardiovascular and cancer pathophysiology. Summary: The high degree of genetic conservation between zebrafish and humans, as well as the ability to recapitulate cardiotoxic phenotypes observed in patients with cancer, make the zebrafish an effective model to study cancer therapy-associated cardiovascular toxicity. Though this model provides several key benefits over existing in vitro and in vivo models, limitations of the zebrafish model include the early developmental stage required for most high-throughput applications.
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Dissertations / Theses on the topic "Zebrafish models"

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Goldsmith, P. "Zebrafish models of retinal degeneration." Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.599478.

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This project has explored whether zebrafish can model human neurological disease, using retinal degeneration as the prototype. The retinal degenerations are a major cause of morbidity, being the commonest cause of blindness in the Western world. Age-related macular degeneration, the commonest retinal degeneration, affects 1 in 20 of the population, and is not treatable. The project began with an F2 mutagenesis screen for candidate blind fish, using an optokinetic assay. Blind fish were characterised using a variety of histological techniques and transplantation studies. Two strains of fish were then selected for more detailed genetic analysis, as they appeared to have a photoreceptor degeneration resembling human retinal degenerations. This involved further mapping of the genes responsible for the phenotype in these two mutants and candidate gene selection.
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Smith, Laura Lindsay. "Zebrafish Models of Congenital Myopathy." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:23845448.

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The congenital myopathies are a diverse group of inherited neuromuscular disorders that manifest as skeletal muscle weakness at birth or in infancy, and are classically defined by the predominant morphological features observed on muscle biopsy. The goals of this dissertation were to better understand the pathophysiology behind these devastating diseases and to identify new therapeutic approaches through the use of faithful vertebrate models. Due to their proliferative capacity, transparency, and well-characterized genome, zebrafish represent a robust vertebrate model system to study muscle development. In the first part of this work, we created and characterized a novel zebrafish model of centronuclear myopathy using antisense morpholinos targeting the bridging integrator 1 (bin1) gene. Bin1 morphant skeletal muscles revealed structural defects reported in human biopsies, and live calcium imaging offered new mechanistic insights linking abnormal triads to impairments in intracellular signaling. Later studies focused on two forms of core myopathy, and utilized stable zebrafish models to guide development of targeted and effective therapies. We began by using TALE nucleases to generate germ line mutations in the zebrafish selenoprotein N (sepn1) gene, and in doing so created the first vertebrate to accurately model human SEPN1-related myopathy (SEPN1-RM). Sepn1 zebrafish mutants exhibited morphological abnormalities, reduced contractile strength, and skeletal muscle “cores” under electron microscopy. We then showed that the sepn1 phenotype could be ameliorated by pharmacological inhibition of a thiol oxidase localized at the sarcoplasmic reticulum. These data served as the first in vivo evidence to indicate that reactive oxygen species significantly contribute to SEPN1-RM, and may do so by impairing calcium re-uptake following muscle contraction. Finally, we performed a medium-throughput chemical screen on the closely related relatively relaxed (ryr1b) zebrafish, and identified JAK-STAT cytokine signaling as a druggable molecular pathway relevant to these pathologies. In summary, these studies increase our knowledge of the affected systems in both centronuclear and core myopathies, and provide strong in vivo support that these conditions arise from defects in skeletal muscle excitation-contraction coupling. This work also further establishes zebrafish-based small molecule screens as a powerful tool for lead compound identification and drug development in human genetic disease.
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Pressley, Meagan E. "Infectious Disease Models for the Zebrafish." Fogler Library, University of Maine, 2004. http://www.library.umaine.edu/theses/pdf/PressleyME2004.pdf.

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Simms, Roslyn Jane. "Zebrafish models of cystic kidney disease related ciliopathies." Thesis, University of Newcastle upon Tyne, 2013. http://hdl.handle.net/10443/2473.

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Cystic kidney diseases are a fascinating cluster of discrete conditions and an important, common cause of established renal failure. Both isolated and syndromic inherited cystic kidney diseases are known to be linked by their pathogenesis involving ciliary dysfunction. Interestingly to date, all mutated genes which have been related to cystic kidney disease, encode proteins which are located on cilia, the basal body or centrosomes and are required for ciliary function. To date, over 50 causal genes have been identified and are capable of causing additional disease phenotypes, such as neurological disorders and blindness, often of variable severity. Understanding this clinical heterogeneity may considerably guide appropriate genetic counselling and screening of patients for relevant complications. Zebrafish are a well-recognised animal model, their advantages of: transparency; conserved genome; representative kidney and rapid external development; make them useful for studying organogenesis in the context of disease. Furthermore the ability to perform combined gene knockdown in zebrafish, to study the effect of oliogenicity, which was proposed to influence clinical phenotypes in cystic kidney disease related ciliopathies, was of interest. Using zebrafish models, this work studied the impact of four key genes, independently and in combination: ahi1, cc2d2a, nphp6 and mks3 on the development of cystic kidney disease and ciliopathy phenotypes, to resemble the human diseases nephronophthisis (NPHP), Joubert syndrome (JBTS) and Meckel Gruber syndrome, (MKS). A frequent finding in zebrafish morphants was a reduction in the number of cilia, which was usually associated with abnormal development of left-right body patterning and cystic kidney disease. Additionally, combined gene knockdown of: nphp6 and cc2d2a; ahi1 and cc2d2a; ahi1 and nphp6 was associated with a synergistic increase in disease phenotypes, suggesting an interaction between these genes. In conclusion, zebrafish are a powerful developmental model to study and ideally improve understanding of cystic kidney disease related ciliopathies.
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Novorol, Claire. "Microcephaly models in the developing zebrafish retinal neuroepithelium." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648860.

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Daggett, Jenny. "Evaluation and characterisation of two zebrafish models of schizophrenia." Thesis, University of St Andrews, 2016. http://hdl.handle.net/10023/9603.

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Cognitive deficits are the single strongest predictor of the functional outcome in patients with schizophrenia. Current treatments are largely ineffective in improving cognitive impairments and promising pre-clinical research has mostly failed to translate clinically. Despite the advances provided by rodent models, the neurobiological basis of cognitive deficits in schizophrenia is poorly understood. Therefore, this thesis proposes a zebrafish model for studying cognitive impairments of schizophrenia. Although more evolutionarily distant to humans compared to the rat, the zebrafish has emerged as a popular vertebrate model of human disorders due to its genetic tractability, complex nervous system and elaborate behavioural repertoire. We investigated the effects of genetic alterations and neurodevelopmental disruption on behaviour and learning in zebrafish. Using both disc1 mutant lines and sub-chronic phencyclidine (PCP) on larvae from 6-10 dpf, we were able to assess behavioural changes as a function of developmental age. In particular, this thesis aimed to develop appropriate behavioural assays to assess zebrafish learning and executive function relevant to disorders seen in human patients with schizophrenia. It was possible to demonstrate robust learning across several domains, namely, reversal, classical avoidance and non-associative learning, alongside locomotor and anxiety-related behaviours. There were varied deficits associated with each of the two – genetic (disc1 gene mutation) and environmental (sub-chronic PCP) – manipulations, consistent with observations in rat research. Together, the research in this thesis demonstrates that a zebrafish model exhibits behaviour resembling that of mammalian models of schizophrenia and provides a foundation for the utility of zebrafish in examining cognitive impairments associated with schizophrenia.
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Ganis, Jared Jason. "Regulators of hemoglobin switching in zebrafish and human models." Thesis, Harvard University, 2014. http://dissertations.umi.com/gsas.harvard:11391.

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Hemoglobin switching is a developmental process involving the dynamic transcriptional regulation of multiple globin genes. This molecular process involves multiple layer of complexity, and elucidating new mechanisms in this process will result in a more complete understanding of general gene regulation and will likely have direct clinical implications for hemoglobinopathies, such as sickle cell anemia. In this dissertation, I develop and characterize a new model for hemoglobin switching, the zebrafish. I defined and fully annotated the two zebrafish globin loci, termed major and minor loci. Both loci contain α– and β–genes oriented in a head–to–head fashion. Characterization of the globin expression pattern precisely defined the timing of normal switching and demonstrated that zebrafish, like humans, have two globin switches. The locus control region for the major locus was identified and in conjunction with a proximal promoter was able to generate robust, erythroid–specific expression in a transgenic line.
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Albacker, Colleen Elizabeth. "Chromatin-Modifying Factors in Zebrafish Models of Rhabdomyosarcoma and Hematopoiesis." Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10098.

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Epigenetics, or the reversible and heritable marks of gene regulation not including DNA sequence, encompasses modifications on both the DNA and histones and is as important as the DNA sequence itself. Gene transcription, DNA repair, DNA replication, and the cell cycle are each impacted by the chromatin structure. A variety of enzymes modulate these modifications, and a suite of factors interacts with them to aid in promoting or inhibiting cellular functions. Many of these chromatin-modifying factors are deregulated in cancer, making them novel therapeutic targets. This dissertation describes the identification of an H3K9 histone methyltransferase, SUV39H1, as a suppressor of rhabdomyosarcoma formation in zebrafish. This suppressor is dependent on the methyltransferase domain of the enzyme, ruling out any scaffold effects since this enzyme is a part of a multiprotein complex. SUV39H1-overexpressing and control tumors share many of the same characteristics, including proliferation rate, muscle differentiation state, and tumor growth rate. The tumor suppressive phenotype cannot be rescued by alterations in the downstream muscle program alone. However, SUV39H1-overexpressing fish initiate fewer tumors, which results in the observed suppressive phenotype. This initiation defect occurs between 5 and 7 days of life in the zebrafish, likely by impacting cyclin B1 expression. This dissertation also describes the development of a novel F1 transgenic screening strategy in the zebrafish. This approach was utilized to screen a variety of chromatin-modifying factors for their effects on hematopoietic development. The developed strategy will have future applications as a zebrafish screening tool. Our data suggest that chromatin-modifying factors play an important role in rhabdomyosarcoma and illustrate the use of the zebrafish in discovering genes involved in tumorigenesis and hematopoiesis.
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Dong, Bo. "High-throughput image analysis of zebrafish models of Parkinson's disease." Thesis, University of Sheffield, 2017. http://etheses.whiterose.ac.uk/18090/.

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Light microscopy can be used to advance our understanding of the molecular and cellular biology related to human health and diseases. As a powerful new vertebrate model, zebrafish have been used in various research areas, particularly in cancer and Parkinson's disease research. Large-scale data extraction from microscopy is highly attractive because it enables unbiased multivariate analysis that could lead to systems medicine approaches. To obtain useful information from large-scale data, high-throughput image analysis methods and applications are desperately required. In this thesis, we have explored methods and developed applications for highthroughput light microscopy zebrafish image analysis, including addressing the key problems related to three-dimensional (3D) deconvolution/deblurring, robust feature detection and description, and object counting. In biological image analysis, dealing with out-of-focus light noise, low image quality, large-scale dataset, illumination, overlapping, occlusion and insufficient prior knowledge remains challenging. Methods to address the following problems have been presented in this thesis. The low image quality of fluorescence microscopy images is addressed in Chapter 3. Owing to the limitations of light microscopes, the whole imaging process can be considered as a convolution between the object and the point spread function. Out-of-focus light and noise cause loss of detail in captured images. Deconvolution is an ill-posed inverse problem; thus, regularization methods are required to obtain better results. A maximum a posterior approach with a novel regularisation strategy to remove out-of-focus blur in 3D fluorescence microscopy images is introduced in Chapter 3. The second problem is dyed dopaminergic neurone detection in zebrafish RGB optical sections (Chapter 4). Owing to the large-scale of the image, low image quality, irregular appearance of neurones and touching situations, manually counting individual neurones via the microscope can be labour-intensive, time-consuming, subjective, and error-prone. To solve this problem, this thesis explores different methods to detect individual neurones in 3D zebrafish RGB images, including using detectors with many different handcrafted features and features learned automatically from deep learning architectures. An additional class-imbalanced problem is discovered during the experiments involving the training of patch-based deep learning techniques using a large-scale dataset that contains a limited number of positive samples. To solve this problem, a dynamic cascade framework with deep learning architectures is designed. The last problem is cell counting in fluorescent microscopy images (Chapter 5). Detecting individual cells in two-dimensional (2D) fluorescence microscopy images is difficult owing to overlap. Rather than counting-by-detection methods, a countingby- regression method with an interactive interface for cell counting in a fluorescent image is proposed. Sparse Bayesian Poisson regression based on a Relevance Vector Machine framework is also proposed. The proposed framework enables accurate counting of a discrete number of cells and leads to much sparser models, which results in faster performance and maintains a comparable generalisation error.
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Metzner, Aylin. "A study of ADPKD pathogenesis and treatment in zebrafish models." Thesis, University of Sheffield, 2016. http://etheses.whiterose.ac.uk/16020/.

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Books on the topic "Zebrafish models"

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Zebrafish models in neurobehavioral research. New York: Humana Press, 2011.

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Kalueff, Allan V., and Jonathan M. Cachat, eds. Zebrafish Models in Neurobehavioral Research. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-60761-922-2.

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Zebrafish neurobehavioral protocols. New York: Humana Press, 2011.

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Zon, Leonard I., H. William Detrich, and Monte Westerfield. The zebrafish: Disease models and chemical screens. 3rd ed. Amsterdam [Netherlands]: Elsevier/Academic Press, 2011.

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C, Nüsslein-Volhard, and Dahm Ralf, eds. Zebrafish: A practical approach. Oxford: Oxford University Press, 2002.

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Zebrafish protocols for neurobehavioral research. New York: Humana Press, 2012.

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McGrath, Patricia. Zebrafish: Methods for assessing drug safety and toxicity. Hoboken, N.J: John Wiley & Sons, 2011.

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Bhandari, Prasan R., Kala Kumar Bharani, and Amit Khurana, eds. Zebrafish Model for Biomedical Research. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-5217-2.

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Ramachandran, Saravanan, and Senthilkumar Rajagopal. Zebrafish: A Model for Marine Peptide Based Drug Screening. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-7844-7.

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Kalueff, Allan V., and Jonathan M. Cachat. Zebrafish Models in Neurobehavioral Research. Humana Press, 2016.

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Book chapters on the topic "Zebrafish models"

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Sakai, Catalina, and Ellen J. Hoffman. "Zebrafish Models." In Encyclopedia of Autism Spectrum Disorders, 1–6. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6435-8_102152-1.

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Sakai, Catalina, and Ellen J. Hoffman. "Zebrafish Models." In Encyclopedia of Autism Spectrum Disorders, 5247–52. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-319-91280-6_102152.

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McGrath, Patricia. "Use of Emerging Models for Developmental Toxicity Testing." In Zebrafish, 27–44. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118102138.ch3.

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Beuerle, Florian, Patrick Witte, Uwe Hartnagel, Russell Lebovitz, Chuenlei Parng, and Andreas Hirsch. "Cytoprotective Activities of Water-Soluble Fullerenes in Zebrafish Models." In Zebrafish, 257–81. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118102138.ch19.

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Pittman, Julian. "Zebrafish Neurotoxicity Models." In The rights and wrongs of zebrafish: Behavioral phenotyping of zebrafish, 207–19. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-33774-6_9.

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Schartl, Manfred, and Ronald B. Walter. "Xiphophorus and Medaka Cancer Models." In Cancer and Zebrafish, 531–52. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-30654-4_23.

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Mayrhofer, Marie, and Marina Mione. "The Toolbox for Conditional Zebrafish Cancer Models." In Cancer and Zebrafish, 21–59. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-30654-4_2.

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Brock, Alistair J., Ari Sudwarts, Matthew O. Parker, and Caroline H. Brennan. "Zebrafish Behavioral Models of Ageing." In The rights and wrongs of zebrafish: Behavioral phenotyping of zebrafish, 241–58. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-33774-6_11.

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Pittman, Julian, and Angelo Piato. "Developing Zebrafish Depression-Related Models." In The rights and wrongs of zebrafish: Behavioral phenotyping of zebrafish, 33–43. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-33774-6_2.

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Harrison, Nicholas R., Fabrice J. F. Laroche, Alejandro Gutierrez, and Hui Feng. "Zebrafish Models of Human Leukemia: Technological Advances and Mechanistic Insights." In Cancer and Zebrafish, 335–69. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-30654-4_15.

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Conference papers on the topic "Zebrafish models"

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Ellis, L., E. Samarut, J. Nixon, and P. Drapeau. "Assessing the efficacy of Zebrafish seizure models for testing cannabinoids." In Abstracts of the NHPRS – The 15th Annual Meeting of the Natural Health Products Research Society of Canada (NHPRS). Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1644918.

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"NUMERICAL ANALYSIS OF IMAGE BASED HIGH THROUGHPUT ZEBRAFISH INFECTION SCREENS - Matching Meaning with Data." In International Conference on Bioinformatics Models, Methods and Algorithms. SciTePress - Science and and Technology Publications, 2012. http://dx.doi.org/10.5220/0003872902570262.

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Schmitz, Rebecca, Alex J. Walsh, Kelsey Tweed, Steven Trier, Anna Huttenlocher, and Melissa Skala. "Zebrafish xenograft breast cancer models for high-throughput drug response screening." In Biophysics, Biology and Biophotonics IV: the Crossroads, edited by Adam Wax and Vadim Backman. SPIE, 2019. http://dx.doi.org/10.1117/12.2513688.

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"INTERACTIVE VISUALIZATION OF COMPLEX THREE-DIMENSIONAL MODELS: CASE STUDY IN ZEBRAFISH." In 14 th International Conference on Interfaces and Human Computer Interaction 2020 and 13 th International Conference on Game and Entertainment Technologies 2020. IADIS Press, 2020. http://dx.doi.org/10.33965/ihci_get2020_202010c026.

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Wu, Chia-Chou, and Bor-Sen Chen. "Essential Proteins and Functional Modules in the Host-Pathogen Interactions from Innate to Adaptive Immunity - C. albicans-zebrafish Infection Model." In International Conference on Bioinformatics Models, Methods and Algorithms. SCITEPRESS - Science and and Technology Publications, 2015. http://dx.doi.org/10.5220/0005201700170025.

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Kendall, Genevieve, Sarah Watson, Lin Xu, Franck Tirode, Olivier Delattre, and James Amatruda. "Abstract NG03: Zebrafish models of PAX3-FOXO1 pathogenesis reveal novel targets in human rhabdomyosarcoma." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-ng03.

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Oppel, Felix, Ting Tao, Shuning He, Mark W. Zimmerman, Dong H. Ki, Nina Weichert, and A. Thomas Look. "Abstract 1540: Creating faithful genetic zebrafish models of pediatric high grade gliomas and MPNSTs." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1540.

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Gjini, Evisa, Marc Mansour, Jeffry Sander, Shuning He, Myunggon Ko, Yi Zhou, Scott Rodig, et al. "Abstract 5152: Zebrafish models of myeloid malignancies produced through tet2 and asxl1 genomic editing." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-5152.

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Gao, Weijian, Mengyu Zhou, Jing Huang, Shuqi Gan, Yao Xu, Ting Lu, Yiqing Zhang, and Jian Zhang. "In-vivo characterization of zebrafish bone degradation and regeneration models by optical coherence tomography." In Sixteenth National Conference on Laser Technology and Optoelectronics, edited by Jianqiang Zhu, Weibiao Chen, Pu Wang, Zhenxi Zhang, and Jianrong Qiu. SPIE, 2021. http://dx.doi.org/10.1117/12.2603248.

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Li, Gen, Hao Liu, Ulrike K. Mu¨ller, and Johan L. van Leeuwen. "Swimming Hydrodynamics and Maneuverability in C-Start of Zebrafish Larvae: An Integrated Computational Study." In ASME-JSME-KSME 2011 Joint Fluids Engineering Conference. ASMEDC, 2011. http://dx.doi.org/10.1115/ajk2011-19020.

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Fishes often exhibit stable body undulating in body and caudal fin (BCF) mode during cyclic swimming, but can perform remarkable maneuverability with significantly different swimming modes in case of C-start. Aiming at unveiling the mechanisms of swimming hydrodynamics and maneuverability of C-start, we have developed an integrated computational framework to model a free-swimming larval zebrafish (Danio rerio) by coupling the equations of 3DoF (Degrees of Freedom) motion and Navier-Stokes (NS) equations. Unsteady hydrodynamics is resolved by integrating models of realistic fin-body morphology and body-undulatory kinematics with an in-house NS solver. The instantaneous forces and moments on the body provided by the NS-solutions serve as input for 3DoF equations of motion. In this study, with a specific focus on a C- start as well as a subsequent transient phase till the cyclic swimming phase, we construct a larval zebrafish model, which can mimics realistic body motions and deformations based on measurements. Validation of the simulation is discussed by comparing model predictions with experimental measurements, which indicates that the present integrated model is capable to accurately predict free-swimming dynamics and hydrodynamics. The model successfully simulated a swimming bout of C-start and cyclic swimming: a wake topology of double row vortex ring structures is observed behind the fish; and a strong jet is visible at the center of the vortex ring, pushing water backward as the fish accelerates.
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Reports on the topic "Zebrafish models"

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Epstein, Jonathan A. Developing a Zebrafish Model of NF1 for Structure-Function Analysis and Identification of Modifier Genes. Fort Belvoir, VA: Defense Technical Information Center, April 2008. http://dx.doi.org/10.21236/ada485806.

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Epstein, Jonathan A. Developing a Zebrafish Model of NF1 for Structure-Function Analysis and Identification of Modifier Genes. Fort Belvoir, VA: Defense Technical Information Center, April 2009. http://dx.doi.org/10.21236/ada502775.

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Look, A. T. Zebrafish Model of NF1 for Structure-Function Analysis, Mechanisms of Glial Tumorigenesis, and Chemical Biology. Fort Belvoir, VA: Defense Technical Information Center, May 2014. http://dx.doi.org/10.21236/ada609199.

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Epstein, Jonathan A., and A. T. Look. Developing a Zebrafish Model of NF1 for Structure-Function Analysis and Identification of Modifier Genes. Fort Belvoir, VA: Defense Technical Information Center, April 2012. http://dx.doi.org/10.21236/ada570844.

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Look, A. T. Zebrafish Model of NF1 for Structure-Function Analysis, Mechanisms of Glial Tumorigenesis, and Chemical Biology. Fort Belvoir, VA: Defense Technical Information Center, May 2013. http://dx.doi.org/10.21236/ada581661.

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Kokkotou, Efi. Investigation of the Role of Stress in Inflammatory Bowel Disease Using Zebrafish as an Experimental Model. Fort Belvoir, VA: Defense Technical Information Center, August 2012. http://dx.doi.org/10.21236/ada566781.

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Gothilf, Yoav, Yonathan Zohar, Susan Wray, and Hanna Rosenfeld. Inducing sterility in farmed fish by disrupting the development of the GnRH System. United States Department of Agriculture, October 2007. http://dx.doi.org/10.32747/2007.7696512.bard.

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Hypothalamic gonadotropinreleasing hormone (GnRH1) is the key hormone in the control of gametogenesis and gonadal growth in vertebrates. Developmentally, hypothalamic GnRHproducing neurons originate from the olfactory placode, migrate along olfactory axons into the forebrain, and continue to the preoptic area and hypothalamus where they function to stimulate gonadotropin secretion from the pituitary gland. An appropriate location of GnRH neurons within the hypothalamus is necessary for normal reproductive function in the adult; abnormal migration and targeting of GnRH neurons during embryogenesis results in hypogonadism and infertility. The developmental migration of GnRH neurons and axonal pathfinding in mammals are modulated by a plethora of factors, including receptors, secreted molecules, adhesion molecules, etc. Yet the exact mechanism that controls these developmental events is still unknown. We investigated these developmental events and the underlying mechanisms using a transgenic zebrafish model, Tg(gnrh1: EGFP), in which GnRH1 neurons and axons are fluorescently labeled. The role of factors that potentially affect the development of this system was investigated by testing the effect of their knockdown and mutation on the development of the GnRH1 system. In addition, their localization in relation to GnRH1 was described during development. These studies are expected to generate the scientific foundation that will lead to developing innovative technologies, based on the disruption of the early establishment of the GnRH system, for inducing sterility in farmed fish, which is highly desirable for economical and environmental reasons.
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Ori, Naomi, and Sarah Hake. Similarities and differences in KNOX function. United States Department of Agriculture, March 2008. http://dx.doi.org/10.32747/2008.7696516.bard.

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Hypothalamic gonadotropinreleasing hormone (GnRH1) is the key hormone in the control of gametogenesis and gonadal growth in vertebrates. Developmentally, hypothalamic GnRHproducing neurons originate from the olfactory placode, migrate along olfactory axons into the forebrain, and continue to the preoptic area and hypothalamus where they function to stimulate gonadotropin secretion from the pituitary gland. An appropriate location of GnRH neurons within the hypothalamus is necessary for normal reproductive function in the adult; abnormal migration and targeting of GnRH neurons during embryogenesis results in hypogonadism and infertility. The developmental migration of GnRH neurons and axonal pathfinding in mammals are modulated by a plethora of factors, including receptors, secreted molecules, adhesion molecules, etc. Yet the exact mechanism that controls these developmental events is still unknown. We investigated these developmental events and the underlying mechanisms using a transgenic zebrafish model, Tg(gnrh1: EGFP), in which GnRH1 neurons and axons are fluorescently labeled. The role of factors that potentially affect the development of this system was investigated by testing the effect of their knockdown and mutation on the development of the GnRH1 system. In addition, their localization in relation to GnRH1 was described during development. These studies are expected to generate the scientific foundation that will lead to developing innovative technologies, based on the disruption of the early establishment of the GnRH system, for inducing sterility in farmed fish, which is highly desirable for economical and environmental reasons.
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