Academic literature on the topic 'Multifactorial animal model'
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Journal articles on the topic "Multifactorial animal model":
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Pikman, R., S. Kivity, Y. Levy, M.-T. Arango, J. Chapman, H. Yonath, Y. Shoenfeld, and S. G. Gofrit. "Neuropsychiatric SLE: from animal model to human." Lupus 26, no. 5 (April 2017): 470–77. http://dx.doi.org/10.1177/0961203317694261.
Abstract:
Animal models are a key element in disease research and treatment. In the field of neuropsychiatric lupus research, inbred, transgenic and disease-induced mice provide an opportunity to study the pathogenic routes of this multifactorial illness. In addition to achieving a better understanding of the immune mechanisms underlying the disease onset, supplementary metabolic and endocrine influences have been discovered and investigated. The ever-expanding knowledge about the pathologic events that occur at disease inception enables us to explore new drugs and therapeutic approaches further and to test them using the same animal models. Discovery of the molecular targets that constitute the pathogenic basis of the disease along with scientific advancements allow us to target these molecules with monoclonal antibodies and other specific approaches directly. This novel therapy, termed “targeted biological medication” is a promising endeavor towards producing drugs that are more effective and less toxic. Further work to discover additional molecular targets in lupus’ pathogenic mechanism and to produce drugs that neutralize their activity is needed to provide patients with safe and efficient methods of controlling and treating the disease.
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Andersson, Leif. "Fisher’s quantitative genetic model and the molecular genetics of multifactorial traits." Journal of Animal Breeding and Genetics 135, no. 6 (October 2018): 391–92. http://dx.doi.org/10.1111/jbg.12362.
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Von Diemen, Vinicius, Eduardo Neubarth Trindade, and Manoel Roberto Maciel Trindade. "Experimental model to induce obesity in rats." Acta Cirurgica Brasileira 21, no. 6 (December 2006): 425–29. http://dx.doi.org/10.1590/s0102-86502006000600013.
Abstract:
The etiology of obesity is multifactorial and is becoming a problem of public health, due to its increased prevalence and the consequent repercussion of its comorbidities on the health of the population. The great similarity and homology between the genomes of rodents and humans make these animal models a major tool to study conditions affecting humans, which can be simulated in rats. Obesity can be induced in animals by neuroendocrine, dietary or genetic changes. The most widely used models to induce obesity in rats are a lesion of the ventromedial hypothalamic nucleus (VMH) by administering monosodium glutamate or a direct electrical lesion, ovariectomy, feeding on hypercaloric diets and genetic manipulation for obesity.
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Nakhleh-Francis, Yara, Yaseen Awad-Igbaria, Reem Sakas, Sarina Bang, Saher Abu-Ata, Eilam Palzur, Lior Lowenstein, and Jacob Bornstein. "Exploring Localized Provoked Vulvodynia: Insights from Animal Model Research." International Journal of Molecular Sciences 25, no. 8 (April 11, 2024): 4261. http://dx.doi.org/10.3390/ijms25084261.
Abstract:
Provoked vulvodynia represents a challenging chronic pain condition, characterized by its multifactorial origins. The inherent complexities of human-based studies have necessitated the use of animal models to enrich our understanding of vulvodynia’s pathophysiology. This review aims to provide an exhaustive examination of the various animal models employed in this research domain. A comprehensive search was conducted on PubMed, utilizing keywords such as “vulvodynia”, “chronic vulvar pain”, “vulvodynia induction”, and “animal models of vulvodynia” to identify pertinent studies. The search yielded three primary animal models for vulvodynia: inflammation-induced, allergy-induced, and hormone-induced. Additionally, six agents capable of triggering the condition through diverse pathways were identified, including factors contributing to hyperinnervation, mast cell proliferation, involvement of other immune cells, inflammatory cytokines, and neurotransmitters. This review systematically outlines the various animal models developed to study the pathogenesis of provoked vulvodynia. Understanding these models is crucial for the exploration of preventative measures, the development of novel treatments, and the overall advancement of research within the field.
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Olexová, Lucia, Tomáš Senko, Peter Štefánik, Alžbeta Talarovičová, and Lucia Kršková. "Habituation of exploratory behaviour in VPA rats: animal model of autism." Interdisciplinary Toxicology 6, no. 4 (December 1, 2013): 222–27. http://dx.doi.org/10.2478/intox-2013-0033.
Abstract:
ABSTRACT Autism is a neurodevelopmental disorder with multifactorial aetiology, represented as impairment in social behaviour, communication and the occurrence of repetitive activities, which can be observed in the early life. The core features are frequently accompanied by other manifestations, including limited environmental exploration. The aim of the presented study, realised on an animal model of autism - VPA rats, i.e. animals prenatally affected with valproic acid on gestation day 12.5, was to investigate the habituation process of exploratory activity (manifested by a gradual decrease in the intensity of locomotor activity), which reflects the stage of the central nervous system. VPA rats were tested in open-field in three developmental periods - weaning (postnatal day 21 - PND 21), puberty (PND 42) and adulthood (PND 72). In each period of ontogenesis, the rapidity of habituation was evaluated by using the method of linear regression. Compared to controls, VPA rats showed a significant decrease in the intensity and an increase in the rapidity of exploratory activity habituation during puberty and adulthood. Our results indicate that the animal model of autism, i.e. VPA rats, showed disabilities in the development of the nervous system. These findings can help confirm not only the validity of this animal model of autism but can also help better understand neuronal changes in humans with autism
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Netto, Cesar de Cesar, Zijun Zhang, Mario Lobao Goncalves, Chris Cychosz, Shuyuan Li, Kyle R. Duchman, Jessica E. Goetz, John E. Femino, Ruth Chimenti, and Lew C. Schon. "Mechanical Overload Followed by Consecutive Collagenase Injections: Developing a Multifactorial and Long-Lasting Animal Model of Induced Achilles Tendinopathy." Foot & Ankle Orthopaedics 5, no. 4 (October 1, 2020): 2473011420S0003. http://dx.doi.org/10.1177/2473011420s00034.
Abstract:
Category: Basic Sciences/Biologics; Hindfoot; Sports Introduction/Purpose: Different animal models of Achilles tendinopathy have been proposed in the literature. They usually involve the induction of tendinopathic findings by either chemical stress (most commonly with one or more injections of collagenase, mimicking intrinsic factors) or mechanical stress (by repetitive exercise-induced stress with treadmill running exercises, simulating extrinsic risk factors). To date, no study has evaluated the combination of a mechanical trigger followed by collagenase injections, replicating the logical and sequential steps involved in the development the human pathology. Our goal was to develop this novel animal model of Achilles tendinopathy and to compare histological and functional findings with animals subjected to isolated mechanical or chemical stress, as well as to controls. Methods: Sixty-four Sprague-Dawley rats were divided into four groups (n=16): isolated treadmill running protocol (15o uphill running, 20meters/minute, 1hour/day, 3 weeks duration, weeks 2-4); isolated injections of collagenase (0.1mg each, 3 injections total, weeks 5-7); treadmill protocol (weeks 2-4) followed by three consecutive collagenase injections (weeks 5-7); and controls, no running and three injections of normal saline (weeks 5-7). Five animals from each group were sacrificed at weeks 8 and 10. Six animals by group were sacrificed at week 12. Gait analysis was performed at weeks one (after acclimation), five (following running protocol), eight (following injection protocol) and twelve (just before latest sacrifice time-point). Histological findings were assessed by the Movin Tendinopathy Score (eight parameters, scored from 0-3, total score 0-24), assessing collagen arrangement, structure, and stainability, cellularity, vascularity, nuclear rounding, hyalinization and presence of glycosaminoglycans. Gait parameters included stand and swing times, stride length, duty cycle and swing length. Results: After 8 weeks, significantly increased tendinopathic scores (p<0.001) were found in animals subjected to collagenase injections (16, CI 13.1-18.9) and to running/collagenase (17.4, CI 14.4-20.3), when compared to controls (1.6, CI -1.3-4.50) and running (3, CI 0.1-5.9). Similarly, after 10 weeks significantly increased scores were found in the same groups, with slight severity regression: controls (1, CI -0.8-2.8), running (2.2, CI 0.4-4.0), collagenase (10, CI 8.2-11.8) and running/collagenase (17.6, CI 15.8- 19.4). After 12 weeks, collagenase group demonstrated reversion of the findings (3.3, CI 1.6-5.1), and wasn’t different than control (2.1, CI 0.4-3.9) and running groups (2.5, CI 0.3-4.7). However, significantly increased pathological findings were noted in the running/collagenase group (20.0, CI 18.2-21.8) consistent with chronic tendinopathic process. Gait analysis results presented in Figure1. Conclusion: When compared to other models of induced Achilles tendinopathy and to controls, the novel animal model induced by a mechanical trigger and sustained by chemical stress demonstrated progressively increased histological tendinopathic scores after 12 weeks. Findings observed after isolated mechanical or chemical stresses were temporary, not maintained at latest follow- up. Steps involved in tendinopathy development, as well as the observed histological results of the combined running/collagenase model, replicate better the findings of human chronic Achilles tendinopathy. Applications for this novel model are promising, potentially supporting a better understanding of early/late findings as well as treatment options for Achilles tendinopathy. [Figure: see text]
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Ureshino, Rodrigo Portes, Angelica Jardim Costa, Adolfo Garcia Erustes, Gustavo José da Silva Pereira, Rita Sinigaglia-Coimbra, and Soraya Soubhi Smaili. "Effects of Aging in the Striatum and Substantia Nigra of a Parkinson’s Disease Animal Model." Toxicologic Pathology 46, no. 3 (April 2018): 348–58. http://dx.doi.org/10.1177/0192623318767065.
Abstract:
Aging is a multifactorial process associated with functional deficits, and the brain is more prone to developing chronic degenerative diseases such as Parkinson’s disease. Several groups have tried to correlate the age-related ultrastructural alterations to the neurodegeneration process using in vivo pharmacological models, but due to the limitations of the animal models, particularly in aged animals, the results are difficult to interpret. In this work, we investigated neurodegeneration induced by rotenone, as a pharmacological model of Parkinson’s disease, in both young and aged Wistar rats. We assessed animal mobility, tyrosine hydroxylase staining in the substantia nigra pars compacta (SNpc), and TdT-mediated dUTP-biotin nick end labeling-positive nuclei and reactive oxygen species production in the striatum. Interestingly, the mobility impairment, dopaminergic neuron loss, and elevated number of apoptotic nuclei in the striatum of aged control rats were similar to young rotenone-treated animals. Moreover, we observed many ultrastructural alterations, such as swollen mitochondria in the striatum, and massive lipofuscin deposits in the SNpc of the aged rotenone-treated animals. We conclude that the rotenone model can be employed to explore age-related alterations in the ontogeny that can increase vulnerability in the striatum and SNpc, which may contribute to Parkinson’s disease pathogenesis.
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Sauer, Sven W., Silvana Opp, Shoko Komatsuzaki, Anna-Eva Blank, Michel Mittelbronn, Peter Burgard, D. M. Koeller, Jürgen G. Okun, and Stefan Kölker. "Multifactorial modulation of susceptibility to l-lysine in an animal model of glutaric aciduria type I." Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1852, no. 5 (May 2015): 768–77. http://dx.doi.org/10.1016/j.bbadis.2014.12.022.
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Perše, Martina, and Anton Cerar. "Dextran Sodium Sulphate Colitis Mouse Model: Traps and Tricks." Journal of Biomedicine and Biotechnology 2012 (2012): 1–13. http://dx.doi.org/10.1155/2012/718617.
Abstract:
Inflammatory bowel disease (IBD) is a complex multifactorial disease of unknown etiology. Thus, dozens of different animal models of IBD have been developed in past decades. Animal models of IBD are valuable and indispensable tools that provide a wide range of options for investigating involvement of various factors into the pathogenesis of IBD and to evaluate different therapeutic options. However, the dextran sulphate sodium (DSS-) induced colitis model has some advantages when compared to other animal models of colitis. It is well appreciated and widely used model of inflammatory bowel disease because of its simplicity. It has many similarities to human IBD, which are mentioned in the paper. In spite of its simplicity and wide applicability, there are also traps that need to be taken into account when using DSS model. As demonstrated in the present paper, various factors may affect susceptibility to DSS-induced lesions and modify results.
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Zerani, Massimo, Angela Polisca, Cristiano Boiti, and Margherita Maranesi. "Current Knowledge on the Multifactorial Regulation of Corpora Lutea Lifespan: The Rabbit Model." Animals 11, no. 2 (January 25, 2021): 296. http://dx.doi.org/10.3390/ani11020296.
Abstract:
Our research group studied the biological regulatory mechanisms of the corpora lutea (CL), paying particular attention to the pseudopregnant rabbit model, which has the advantage that the relative luteal age following ovulation is induced by the gonadotrophin-releasing hormone (GnRH). CL are temporary endocrine structures that secrete progesterone, which is essential for maintaining a healthy pregnancy. It is now clear that, besides the classical regulatory mechanism exerted by prostaglandin E2 (luteotropic) and prostaglandin F2 (luteolytic), a considerable number of other effectors assist in the regulation of CL. The aim of this paper is to summarize our current knowledge of the multifactorial mechanisms regulating CL lifespan in rabbits. Given the essential role of CL in reproductive success, a deeper understanding of the regulatory mechanisms will provide us with valuable insights on various reproductive issues that hinder fertility in this and other mammalian species, allowing to overcome the challenges for new and more efficient breeding strategies.
Dissertations / Theses on the topic "Multifactorial animal model":
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Lahogue, Caroline. "Stratégie de traitement visant les récepteurs 5-HT6 dans un modèle animal de schizophrénie innovant." Electronic Thesis or Diss., Normandie, 2023. http://www.theses.fr/2023NORMC433.
Abstract:
La schizophrénie (SCZ) est une maladie mentale multifactorielle qui entraîne des répercussions souvent dramatiques sur la vie personnelle et professionnelle des patients. Si au moins un tiers des patients atteints de SCZ connaît une rémission des symptômes, d’autres les voient persister, voire s’aggraver au fil du temps. Afin d’améliorer les traitements actuels et de tester de nouvelles cibles thérapeutiques de la maladie, une amélioration des modèles animaux est primordiale et doit se rapprocher de son étiologie complexe. Nous avons ici développé un nouveau modèle animal multifactoriel qui associe chez la souris un facteur génétique (1er hit, délétion du gène de la sérine racémase) avec un stress environnemental précoce (2ème hit, séparation maternelle de 24h au 9ème jour de vie). Notre étude comportementale montre que l’interaction des deux facteurs permet de générer des symptômes de type productif ainsi que des déficits cognitifs, présents dans la SCZ. Une étude électrophysiologique ex-vivo parallèle ne révèle pas en revanche de physiopathologie spécifique de l’activité fonctionnelle du champ CA1 de l’hippocampe dans ce modèle. Nous avons ensuite testé l’efficacité du blocage des récepteurs à la sérotonine de type 6 (5-HT6R) par un antagoniste sélectif, le SB-271046. Ce blocage induit des effets bénéfiques sur les déficits cognitifs, notamment mnésiques, et améliore les déficits de mémoire de travail et de sociabilité chez les souris 2-hit. L’étude électrophysiologique montre que l’antagonisme des 5-HT6R facilite la neurotransmission glutamatergique par deux mécanismes distincts selon le sexe : une activation indirecte des neurones pyramidaux chez les individus mâles par un mécanisme de désinhibition GABAergique et une activation directe des neurones pyramidaux chez les sujets femelles. Chez les souris 2-hit, seul le mécanisme de désinhibition des neurones pyramidaux induit chez les mâles par le blocage des 5-HT6R est altéré.Ce travail de thèse montre l’intérêt de développer des modèles multifactoriels de SCZ pour mieux cerner les interactions pouvant exister entre différents facteurs de risque de la maladie. Il montre également des limites pour considérer les 5-HT6R comme une cible thérapeutique dans le traitement de certains déficits associés à la SCZ, mais suggère plutôt son utilité comme traitement complémentaire associé aux neuroleptiquesSchizophrenia (SCZ) is a multifactorial mental disease which has repercussions on patients' personal and professional lives. While at least 1/3 of patients with SCZ present a remission of symptoms, other patients display persistent or even an aggravation of symptoms over time. To improve current treatments by testing new therapeutic targets, animal models need to be improved to get closer to the etiology of SCZ. We have developed a new multifactorial model which combines in mouse a genetic factor (1st hit, deletion of the serine racemase gene) with an early environmental stress (2nd hit, maternal separation for 24h on postnatal day 9). Our behavioral study showed that the interaction between the two factors in 2-hit mice leads to productive-like symptoms and cognitive deficits, observed in SCZ. However, the ex-vivo electrophysiological study reveals no specific pathophysiology of the functional activity of the hippocampal CA1 field in this model. Then, we tested the efficacy of blockade of serotonin subtype 6 receptors (5-HT6R) with a selective antagonist, SB-271046. This blockade induces beneficial effects on cognitive deficits, particularly memory, by improving working memory and sociability deficits in 2-hit mice. Electrophysiological studies show that 5-HT6R antagonism facilitates glutamatergic neurotransmission by two distinct sex-dependent mechanisms: an indirect activation of pyramidal neurons in males via a blockade of GABAergic inhibition, and a direct activation of pyramidal neurons in females. In 2-hit mice, only the disinhibition mechanism of pyramidal neurons induced in males by 5-HT6R blockade is altered.This thesis shows the interest of developing multifactorial models to get closer to the complex etiology of SCZ. It also shows the potential of 5-HT6R to treat several SCZ-related deficits, which are currently untreated, and suggests that it could be a useful adjunct treatment to neuroleptics
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Percelay, Solenn. "Validation d'un modèle murin de schizophrénie pour améliorer la recherche de nouveaux traitements : approche psychopharmacologique, en imagerie et en électrophysiologie A new 3-hit mouse model of schizophrenia built on genetic, early and late factors Functional dysregulations in CA1 hippocampal networks of a 3-hit mouse model of schizophrenia Olfactory laterality is valence-dependent in mice Assessing olfactory laterality in mice: new tool in preclinical psychiatric study Combination of MAP6 deficit, maternal separation and MK801 in female mice: a 3-hit animal model of neurodevelopmental disorder with cognitive deficits Antipsychotic lurasidone: Behavioural and pharmacokinetic data in C57BL/6 mice." Thesis, Normandie, 2021. http://www.theses.fr/2021NORMC403.
Abstract:
La schizophrénie est une maladie psychiatrique très invalidante qui concerne près de 1% de la population. Bien que son étiologie soit toujours inconnue, elle est certainement multifactorielle et comprend une interaction entre prédisposition génétique et facteurs environnementaux. Il existe des traitements médicamenteux mais ils ne sont pas totalement efficaces, particulièrement pour la prise en charge des symptômes négatifs et des déficits cognitifs. Le développement de nouveaux traitements plus efficaces passe par l’amélioration des modèles animaux prenant en compte le caractère multifactoriel de l’étiologie de cette pathologie.Nous avons développé un modèle murin multifactoriel de schizophrénie innovant (modèle 3-hit) présentant une forte validité de construction. Pour cela, nous avons combiné une modification génétique (1er hit : délétion partielle du gène MAP6) avec un stress environnemental précoce (2nd hit : séparation maternelle de 24h au 9ème jour de vie) et une exposition tardive au THC durant l’adolescence (3ème hit : administration quotidienne de tétrahydrocannabinol à 8mg/kg du 32ème au 52ème jour).Dans un premier temps, nous avons montré une bonne validité d’apparence de ce modèle à travers des études comportementale, en imagerie et en électrophysiologie. En effet, au niveau comportemental les souris 3-hit présentent des symptômes de type négatif, des déficits cognitifs et une altération de la latéralité olfactive. Nous avons aussi montré un déficit d’inhibition du réflexe de sursaut, qui est un élément comportemental clef dans les modèles animaux de schizophrénie, car il est également utilisé en recherche clinique. Nous avons également observé certaines altérations morphologiques et fonctionnelles cérébrales caractéristiques de la schizophrénie comme une réduction du volume de l’hippocampe, une altération des fibres du corps calleux et un dysfonctionnement des systèmes de neurotransmission glutamatergique et GABAergique. Certains dimorphismes sexuels ont été également montrés dans nos études.Dans un deuxième temps, nous avons comparé les déficits des animaux 3-hit avec ceux d’autres modèles de schizophrénie développés au laboratoire. La caractérisation des effets de chaque facteur, indépendamment et en association, nous a permis de mettre en évidence un phénomène de synergie entre les facteurs et non une simple addition des déficits induits par chacun d’entre eux.Le modèle de schizophrénie 3-hit présente de bonnes validités de construction et d’apparence, il est maintenant nécessaire afin de parfaire sa caractérisation de tester sa validité pharmacologiqueAffecting 1% of worldwide population, schizophrenia is a debilitating pathology. Whether the aetiology of schizophrenia remains unknown, its multifactorial aspect is conversely now well admitted, and certainly gathers genetic vulnerability and environmental factors. Actual treatments are still unmet, particularly for negative and cognitive symptoms. For a better translation from treatments design of schizophrenia to clinical efficiency, there is a crucial need to refine preclinical animal models that considers the multifactorial aspects of this disease.We developed a new murine multifactorial model of schizophrenia (3-hit), that possesses a strong construct validity. To this, we combined a genetic predisposition (1st hit: partial deletion of MAP-6) with an early postnatal stress (2nd hit: 24 h maternal separation at postnatal day 9), and a late cannabinoid exposure during adolescence (3rd hit: tetrahydrocannabinol THC from post-natal day 32 to 52; 8 mg/kg/day).First, we characterised a promising face validity through behavioural, imaging and electrophysiological studies. At behavioural level, we demonstrated that 3-hit mice displayed negative-like symptoms, cognitive deficits and altered olfactory laterality. Moreover, we showed a sensory motor gating deficit, that is a major translational clue for animal models of schizophrenia. Additionally, 3-hit mice displayed some characteristic morphological and functional impairments of the disease: reduced hippocampal volume, altered callosal fibres, glutamatergic and GABAergic neurotransmission dysfunctions. We moreover highlighted some sexual dimorphisms.Second, we compared deficits of 3-hit mice to those of others models of schizophrenia developed in our laboratory. Deficits induced by one factor, or combination of several factors, evidenced a synergistic effect, and not a simple addition between each of them.The 3-hit model therefore presents strong construct validity and promising face validity, encouraging to assess the pharmacological validity
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Jiao, Hong. "Genetic dissection of multifactorial disease models in the rat /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-287-6.
Books on the topic "Multifactorial animal model":
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DRAGANI. Human Polygenic Diseases: Animal Models. Taylor & Francis, 1998.
Book chapters on the topic "Multifactorial animal model":
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Karalis, Katia P. "Multifactorial regulation of the corticotroph axis: animal models." In The Acth Axis: Pathogenesis, Diagnosis and Treatment, 47–64. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0501-3_3.
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Bortolato, Marco, and Roberto Cadeddu. "Animal Models of Tic Disorders." In Tourette Syndrome, edited by Liana Fasching, Melanie Brady, and Flora M. Vaccarino, 277–98. 2nd ed. Oxford University Press, 2022. http://dx.doi.org/10.1093/med/9780197543214.003.0017.
Abstract:
Abstract Animal models of Tourette syndrome (TS) and other tic disorders are powerful research tools to advance our knowledge of the neurodevelopmental and molecular foundations of these disorders. Assessing the reliability and translational validity of an animal model of TS is a particularly intricate task due to the heterogeneous presentation, multifactorial ontogeny, and neurobiological complexity of this disorder. Even with these limits, recent advances in understanding the semiology and ontogeny of tics and their accompanying phenotypes are paving the way for new refinements in the characterization and validation of animal models. In addition, the development of novel models reflecting the impact of genetic and environmental vulnerability factors is greatly expanding knowledge on the causes of TS and providing a rich source of molecular mechanisms to account for the neurobiological dysregulations associated with this disorder. This chapter recapitulates the current state of the art in animal modeling of tic disorders and highlights how each model allows for the analysis of complementary aspects of phenomenology, pathophysiology, etiology, and therapy of TS. The chapter also outlines several methodological and conceptual directions for the future development of new animal models and the refinement of available ones. The implementation of these translational strategies will be critical to further improve knowledge of the biological foundation of TS and expand the therapeutic arsenal for tic disorders and comorbid symptoms.
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Rasche, Axel. "Approaching Type 2 Diabetes Mellitus by Systems Biology." In Handbook of Research on Systems Biology Applications in Medicine, 361–76. IGI Global, 2009. http://dx.doi.org/10.4018/978-1-60566-076-9.ch022.
Abstract:
We acquired new computational and experimental prospects to seek insight and cure for millions of afflicted persons with an ancient malady. Type 2 diabetes mellitus (T2DM) is a complex disease with a network of interactions among several tissues and a multifactorial pathogenesis. Research conducted in human and multiple animal models has strongly focused on genetics so far. High-throughput experimentation technics like microarrays provide new tools at hand to amend current knowledge. By integrating those results the aim is to develop a systems biology model assisting the diagnosis and treatment. Beside experimentation techniques and platforms or rather general concepts for a new term in biology and medicine this chapter joins the conceptions with a rather actual medical challenge. It outlines current results and envisions a possible alley to the comprehension of T2DM.
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Rho, Jonathan, Paul Percelay, Sophie Pilkinton, T. J. Hollingsworth, Ilyse Kornblau, and Monica Jablonski. "An Overview of Age-Related Macular Degeneration: Clinical, Pre-Clinical Animal Models and Bidirectional Translation." In Animal Models in Medicine and Biology [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96601.
Abstract:
Age-related macular degeneration (AMD) is a multifactorial disease that results from a complex and unknown interplay among environmental, genetic, and epidemiologic factors. Risk factors include aging, family history, obesity, hypercholesterolemia, and hypertension, along with cigarette smoking, which is the most influential modifiable risk factor. Single nucleotide polymorphisms (SNPs) in numerous genes such as complement factor H (CFH) pose some of the known genetic risks. The pathophysiology in AMD is incompletely understood, but is known to involve oxidative stress, inflammation, dysregulated antioxidants, lipid metabolism, and angiogenesis. Animal models have been integral in expanding our knowledge of AMD pathology. AMD is classified as non-exudative or exudative. Because there is no perfect animal model that recapitulates all aspects of the human disease, rodents, rabbits, and non-human primates offer different advantages and disadvantages to serve as models for various aspects of the disease. Scientific advances have also allowed for the creation of polygenic pre-clinical models that may better represent the complexity of AMD, which will likely expand our knowledge of disease mechanisms and serve as platforms for testing new therapeutics. There have been, and there continues to be, many drugs in the pipeline to treat both exudative and non-exudative AMD. However, Food and Drug Administration (FDA)-approved therapies for exudative AMD that mainly target angiogenic growth factors are the only therapeutics currently being used in the clinics. There remains no FDA-approved therapy for the non-exudative form of this disease. This chapter contains a basic overview and classification of AMD and multiple animal models of AMD are highlighted. We include an overview of both current FDA-approved treatments and those in development. Lastly, we conclude with a summary of the important role of pre-clinical studies in the development of therapeutics for this highly prevalent disease.
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"The Biology of Cytokines: General Principles, Properties, and Lessons from Animal Models." In Cytokine Gene Polymorphisms in Multifactorial Conditions, 31–62. CRC Press, 2006. http://dx.doi.org/10.1201/9781420005325-9.
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Alonazi, Fahad N., Yousef M. Hawsaw, Helal G. Alanazi, Adel M. Alqarni, Suad A. Alghamdi, and Rakan J. Alanazi. "Animal Models for Cancer." In Animal Models In Experimental Medicine, 1–19. BENTHAM SCIENCE PUBLISHERS, 2024. http://dx.doi.org/10.2174/9789815196382124010004.
Abstract:
Cancer is a complex multifactorial disease that affects many people worldwide. Animal models play an important role in deciphering cancer biology and developing new therapies. The animal models widely used in cancer research include tumor xenografts, genetically engineered mice, chemically induced models, and spontaneous tumor models. These models provide a controlled environment to study cancer progression, the interaction of cancer and the immune system, and the effectiveness of new therapies. Although animal models have several advantages, it is important to identify their limitations and use them in conjunction with other preclinical models, such as in-vitro cell culture and patient-derived xenografts, to ensure that results are transferable to humans. In this chapter, we discuss the importance of animal models in cancer research, the different types of animal models, and their advantages and disadvantages. We also provide some examples of animal models used in cancer research. Collectively, animal models have been invaluable in advancing our understanding of cancer and will continue to be important tools in the development of new therapies.
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Cachuba, Roberta Mello, Elaine Carlos Scherrer, Karla Antunes Ramos, Alessandra Paula Carli, Sandra Bertelli Ribeiro Castro, and Caio César Souza Alves. "Multiple sclerosis and experimental autoimmune encephalomyelitis: A review." In UNITING KNOWLEDGE INTEGRATED SCIENTIFIC RESEARCH FOR GLOBAL DEVELOPMENT. Seven Editora, 2023. http://dx.doi.org/10.56238/uniknowindevolp-045.
Abstract:
Multiple sclerosis is a chronic inflammatory autoimmune disease of the central nervous system, characterized by mononuclear cell infiltration, axon demyelination and gliosis in the myelin sheath, with formation of multiple plaques. It affects individuals aged between 25 and 50 years old, female and residents of higher latitudes. The etiology of multiple sclerosis is multifactorial and not fully understood; however, the influence of genetic predisposition and environmental factors on immune dysregulation is recognized. The pathophysiology of the disease is mediated by self-reactive T lymphocytes that respond to autoantigens from the central nervous system. The emergence of multifocal regions of demyelination, axonal loss, loss of oligodendrocytes and astroglial scarring result in impaired neurological function, leading to neurodegeneration. Although there is still no cure for multiple sclerosis, scientific research has provided great advances in therapeutic strategies. Currently there are approaches to attenuate specific signs and symptoms, drugs to control disease relapses and treatments designed to modify or delay the course of multiple sclerosis. Although these drugs show promising effects, they are ineffective in curing the patient. In addition, they present a fundamental problem, which is the non-selective action on the cells of the immune system, which triggers serious side effects. Considering the limitations of studies in humans due to the difficulty of accessing the affected tissues, the use of experimental models that simulate the singularities of multiple sclerosis is a key element for the study of the pathogenesis of inflammation and therapeutic alternatives. Experimental autoimmune encephalomyelitis, an animal model that presents several similarities with pathophysiological, histological and clinical aspects of multiple sclerosis, is the most used model for these studies. Therefore, in this chapter, the aim was to review the historical context, definition, etiology, pathophysiology, clinical manifestations, diagnosis and treatment of multiple sclerosis and, at the same time, address aspects of the timeline, induction, the evolutionary course and the immunopathogenesis of the most studied model for the investigation of the nuances of multiple sclerosis, correlating the similarities and differences between both.
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Macrì, Simone, Martina Proietti Onori, Veit Roessner, and Giovanni Laviola. "Animal Models Recapitulating the Multifactorial Origin of Tourette Syndrome." In International Review of Neurobiology, 211–37. Elsevier, 2013. http://dx.doi.org/10.1016/b978-0-12-411546-0.00008-1.
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Rubattu, Speranza, Bruna Gigante, Rosita Stanzione, and Massimo Volpe. "Animal models of stroke: implications for genetic studies of human stroke." In Stroke Genetics, 115–26. Oxford University PressOxford, 2003. http://dx.doi.org/10.1093/oso/9780198515869.003.0005.
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Juriloff, Diana M. "Mapping Studies in Animal Models." In Cleft Lip And Palate, 265–82. Oxford University PressNew York, NY, 2002. http://dx.doi.org/10.1093/oso/9780195139068.003.0022.
Abstract:
Abstract Orofacial clefting has been observed sporadically in a variety of vertebrates, including monkeys (Stills and Bullock, 1981), gorillas (Siebert et al., 1998), cattle (Swartz et al., 1982), cats (Loevy and Feynes, 1968), dogs (Dreyer and Preston, 1974), and chickens (Juriloff and Roberts, 1975), but genetic studies have usually been limited. The most advanced animal models for genetic analysis and linkage mapping of orofacial defects are laboratory mice, where the extensive resources of specialized strains and crosses, spontaneous and targeted mutations, polymorphic markers, and welldeveloped linkage and physical maps can be used to identify genes and their effects on orofacial development. Conservation of genes and linkage relationships between mice and humans is well documented, and the chromosomal location of a gene in humans can often be predicted from its genetic map position in mice. Development of the orofacial complex is very similar between mouse and human embryos, and much of the understanding of developmental mechanisms in humans has been inferred from mice (Diewert and Wang, 1992). Highly penetrant Mendelian defects of craniofacial development are relatively easily mapped in both mice and humans. The most common orofacial clefting in humans does not follow Mendelian transmission ratios, however, and is clearly genetically complex and not well understood (Mitchell and Risch, 1992; Schutte and Murray, 1999). Mapping and identification of mouse genes that participate in genetically complex (“multifactorial”) causes of orofacial clefting will lead to knowledge of the gene-regulatory pathways important to nonsyndromic orofacial clefting and will identify candidate pathways, as well as candidate genes, for examination in studies of human genetic risk factors.
Conference papers on the topic "Multifactorial animal model":
1
Miquel Bartual, Mijo. "Modificaciones del concepto de lo salvaje en el antropoceno." In III Congreso Internacional de Investigación en Artes Visuales :: ANIAV 2017 :: GLOCAL. Valencia: Universitat Politècnica València, 2017. http://dx.doi.org/10.4995/aniav.2017.6345.
Abstract:
En un momento de crisis sistémica como en el que nos encontramos, la lucha contra el cambio climático es una de las prioridades a las que debemos hacer frente, incluso por delante del anunciado agotamiento de los combustibles fósiles y la consecuente transición hacia el consumo de energías renovables. Desde un análisis multifactorial, todas las disciplinas coinciden en la urgencia del cambio y a escala municipal, esta convicción debería transformar igualmente la planificación urbana integrando criterios ecosistémicos en cualquier nuevo plan. En algunas de nuestras ciudades, están empezando a aplicarse estas modificaciones para fomentar un cambio de paradigma casi civilizatorio estableciendo alianzas que agrupan a instituciones públicas, iniciativas privadas y universidades en el diseño de planes conjuntos que atiendan a este nuevo panorama cada vez más urgente. La creación de redes internacionales que buscan el desarrollo de proyectos piloto en donde la introducción de la naturaleza en el ambito urbano se plantea como una opción deseable de recuperación de espacios degradados, permite asimismo ampliar el alcance de la investigación y agiliza el procesamiento de resultados. Esta oportunidad de transformación supone una ventana para la modificación de los espacios de juego, de relación, de tránsito en el espacio úrbano ; para la ideación de ciudades ya no para el tránsito sino para la transición en un modelo que incluya educación, participación, permeabilidad. En este espacio de oportunidad, el arte puede trabajar buscando sinergias con otras disciplinas para hacer una ciudad más sostenible, inclusiva, ecológica, en donde se diseñen espacios para las nuevas relaciones, creativos, constructivos, lábiles y bellos, dotando de sentido la idea inicial del Land Art de conquistar espacios pero haciéndolo para la vida.http://dx.doi.org/10.4995/ANIAV.2017.6345