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Готові списки джерел за темами / Identité neuronale

Добірка наукової літератури з теми "Identité neuronale"

Автор: Grafiati

Опубліковано: 10 травня 2022

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Статті в журналах з теми "Identité neuronale":

1

Hobert, Oliver, and Sacha Nelson. "Editorial overview: Neuronal Identity." Current Opinion in Neurobiology 56 (June 2019): iii—iv. http://dx.doi.org/10.1016/j.conb.2019.05.004.

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2

Whalley, Katherine. "Relaying control of neuronal identity." Nature Reviews Neuroscience 18, no. 2 (January 5, 2017): 70. http://dx.doi.org/10.1038/nrn.2016.185.

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3

Sousa, Erick, and Nuria Flames. "Transcriptional regulation of neuronal identity." European Journal of Neuroscience 55, no. 3 (January 18, 2022): 645–60. http://dx.doi.org/10.1111/ejn.15551.

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4

Deneris, Evan S., and Oliver Hobert. "Maintenance of postmitotic neuronal cell identity." Nature Neuroscience 17, no. 7 (June 15, 2014): 899–907. http://dx.doi.org/10.1038/nn.3731.

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5

Tsunemoto, Rachel, Sohyon Lee, Attila Szűcs, Pavel Chubukov, Irina Sokolova, Joel W. Blanchard, Kevin T. Eade, et al. "Diverse reprogramming codes for neuronal identity." Nature 557, no. 7705 (May 2018): 375–80. http://dx.doi.org/10.1038/s41586-018-0103-5.

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6

Mall, Moritz, Michael S. Kareta, Soham Chanda, Henrik Ahlenius, Nicholas Perotti, Bo Zhou, Sarah D. Grieder, et al. "Myt1l safeguards neuronal identity by actively repressing many non-neuronal fates." Nature 544, no. 7649 (April 2017): 245–49. http://dx.doi.org/10.1038/nature21722.

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7

Mesman, Simone, and Marten P. Smidt. "Acquisition of the Midbrain Dopaminergic Neuronal Identity." International Journal of Molecular Sciences 21, no. 13 (June 30, 2020): 4638. http://dx.doi.org/10.3390/ijms21134638.

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The mesodiencephalic dopaminergic (mdDA) group of neurons comprises molecularly distinct subgroups, of which the substantia nigra (SN) and ventral tegmental area (VTA) are the best known, due to the selective degeneration of the SN during Parkinson’s disease. However, although significant research has been conducted on the molecular build-up of these subsets, much is still unknown about how these subsets develop and which factors are involved in this process. In this review, we aim to describe the life of an mdDA neuron, from specification in the floor plate to differentiation into the different subsets. All mdDA neurons are born in the mesodiencephalic floor plate under the influence of both SHH-signaling, important for floor plate patterning, and WNT-signaling, involved in establishing the progenitor pool and the start of the specification of mdDA neurons. Furthermore, transcription factors, like Ngn2, Ascl1, Lmx1a, and En1, and epigenetic factors, like Ezh2, are important in the correct specification of dopamine (DA) progenitors. Later during development, mdDA neurons are further subdivided into different molecular subsets by, amongst others, Otx2, involved in the specification of subsets in the VTA, and En1, Pitx3, Lmx1a, and WNT-signaling, involved in the specification of subsets in the SN. Interestingly, factors involved in early specification in the floor plate can serve a dual function and can also be involved in subset specification. Besides the mdDA group of neurons, other systems in the embryo contain different subsets, like the immune system. Interestingly, many factors involved in the development of mdDA neurons are similarly involved in immune system development and vice versa. This indicates that similar mechanisms are used in the development of these systems, and that knowledge about the development of the immune system may hold clues for the factors involved in the development of mdDA neurons, which may be used in culture protocols for cell replacement therapies.

8

Baker, C. V., and M. Bronner-Fraser. "Establishing neuronal identity in vertebrate neurogenic placodes." Development 127, no. 14 (July 15, 2000): 3045–56. http://dx.doi.org/10.1242/dev.127.14.3045.

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The trigeminal and epibranchial placodes of vertebrate embryos form different types of sensory neurons. The trigeminal placodes form cutaneous sensory neurons that innervate the face and jaws, while the epibranchial placodes (geniculate, petrosal and nodose) form visceral sensory neurons that innervate taste buds and visceral organs. In the chick embryo, the ophthalmic trigeminal (opV) placode expresses the paired homeodomain transcription factor Pax3 from very early stages, while the epibranchial placodes express Pax2. Here, we show that Pax3 expression in explanted opV placode ectoderm correlates at the single cell level with neuronal specification and with commitment to an opV fate. When opV (trigeminal) ectoderm is grafted in place of the nodose (epibranchial) placode, Pax3-expressing cells form Pax3-positive neurons on the same schedule as in the opV placode. In contrast, Pax3-negative cells in the grafted ectoderm are induced to express the epibranchial placode marker Pax2 and form neurons in the nodose ganglion that express the epibranchial neuron marker Phox2a on the same schedule as host nodose neurons. They also project neurites along central and peripheral nodose neurite pathways and survive until well after the main period of cell death in the nodose ganglion. The older the opV ectoderm is at the time of grafting, the more Pax3-positive cells it contains and the more committed it is to an opV fate. Our results suggest that, within the neurogenic placodes, there does not appear to be a two-step induction of ‘generic’ neurons followed by specification of the neuron to a particular fate. Instead, there seems to be a one-step induction in which neuronal subtype identity is coupled to neuronal differentiation.

9

Alcalà-Vida, Rafael, Ali Awada, Anne-Laurence Boutillier, and Karine Merienne. "Epigenetic mechanisms underlying enhancer modulation of neuronal identity, neuronal activity and neurodegeneration." Neurobiology of Disease 147 (January 2021): 105155. http://dx.doi.org/10.1016/j.nbd.2020.105155.

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10

Kasthuri, Narayanan, and Jeff W. Lichtman. "The role of neuronal identity in synaptic competition." Nature 424, no. 6947 (July 2003): 426–30. http://dx.doi.org/10.1038/nature01836.

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Більше джерел

Дисертації з теми "Identité neuronale":

1

Zimmer, Céline. "Spécification d'une identité neuronale : implication du gène à homéoboîte Cux2." Aix-Marseille 2, 2004. http://www.theses.fr/2004AIX22017.

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2

Hache, Antoine. "Molecular basis of transcriptional dysregulations in the spinocerebellar ataxia type 7, a neurodegenerative polyglutamine disorder." Thesis, Strasbourg, 2020. http://www.theses.fr/2020STRAJ083.

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SCA7 est une maladie génétique dont l’un des principaux symptômes est une perte progressive d’acuité visuelle pouvant aller jusqu’à la cécité. La mutation responsible de cette pathologie est une expansion instable d’un triplet CAG au sein de l’ATXN7, gene codant une sous-unité du complexe SAGA, un co-activateur de l’ARN polymerase de type II. Des études réalisées sur modèles de souris transgéniques mirent en évidence une perte d’identité des photorécepteurs au niveau morphologique, fonctionnel, et moléculaire. Au cours de ma thèse la caractérisation d’un nouveau modèle knock-in de SCA7 fut réalisée. Ce modèle, qui exprime le gène muté à un niveau endogène récapitule les atteintes rétiniennes observées dans les modèles transgéniques et chez les patients. Une étude transcriptomique (RNA-seq) et épigénomique (ChIP-seq) de ce modèle fut réalisée et mis en évidence des défauts globaux de l’acétylation des lysines 9 et 27 de l’histone H3 (H3K9 et H3K27ac). De plus une étude plus poussée des ARNs non codants mit en évidence l’existance d’ARN enhancer (eRNA) encore non répertoriés au niveau des loci de gènes uniquement exprimés dans les photorécepteurs comme Rho, ces même eRNAs sont retrouvés dérégulés chez les animaux développant la rétinopathie SCA7
SCA7 is a genetic disorder whose one of its main symptoms is a progressive loss of visual acuity which can ultimately lead to blindness. The mutation responsible for this disease is an unstable CAG expansion within ATXN7, a gene encoding a subunit of the SAGA complex, a co-activator of the RNA polymerase II. Previous studies performed on transgenic mouse models highlighted a neuronal identity loss of the photoreceptors at the morphological, functional and molecular levels. During my PhD a characterization of a new SCA7 knock-in mouse model was performed. This model, which expresses the mutated genes at endogenous level recapitulates the retinal impairments observed in transgenic models and in patients. A transcriptomic (RNA-seq) and epigenomic (ChIP-seq) analyses were performed on this model and highlight global acetylation defects on lysine 9 and 27 of histone H3 (H3K9ac and H3K27ac). Moreover, investigations on non-coding RNAs identified the presence of enhancer RNAs (eRNAs) on photoreceptor specific genes such as Rho. These eRNAs, which were never described before, undergo a downregulation in symptomatic SCA7 mice

3

Roque, Anne. "Détermination neurale et neuronale : implication des protéines de la superfamille Snail dans le lignage des soies mécanosensorielles chez la drosophile." Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066559/document.

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L'engagement des cellules vers un destin donné, ou détermination cellulaire, est un processus clé du développement. Quels sont les mécanismes qui sous-tendent la détermination cellulaire ? Pour aborder cette question, nous utilisons le lignage des soies mécanosensorielles de la drosophile. Dans ce lignage, la diversité des cellules résulte de l'activation différentielle de la voie Notch ainsi que la ségrégation asymétrique de déterminants cellulaire à chaque division. Cependant, comment la répétition d’un même mécanisme peut-elle être à l’origine des destins cellulaires différents ? D'autres facteurs doivent être impliqués dans ce processus. Afin des les identifier, mon intérêt s’est porté sur les facteurs de transcription de la superfamille Snail, connus pour être impliqués dans la détermination cellulaire au cours du développement de la drosophile.Deux membres de cette superfamille, Escargot (Esg) et Scratch (Scrt) sont exprimés dans le lignage des soies, en particulier dans les cellules neurales et leurs précurseurs. Des analyses de perte et de gain de fonction indiquent qu’Esg et Scrt, agissant de manière redondante, sont nécessaires pour le maintien de l'identité du précurseur secondaire neural. Des tests d’interaction génétique ont montré que ces facteurs agissent en interaction avec la voie Notch, probablement via la répression de l’expression des gènes cibles de la voie. De plus, Esg, mais pas Scrt, a un rôle supplémentaire lors de la formation du lignage des soies. La perte de fonction de ce facteur provoque un défaut de l’arborisation et de la croissance axonales. En outre, l'expression des gènes impliqués dans la différenciation neuronale, tels que Elav et Prospero, est altérée dans ce contexte, suggérant qu’Esg contrôle la différenciation neuronale en régulant l'expression de gènes clés de l’identité neuronale.Ensemble, mes résultats ont montré qu’Esg et Scrt participent à la mise en place de la diversité cellulaire dans le lignage des soies de la drosophile
The commitment of cells to a given fate, or cell fate determination, is a key process in development. Cell type diversity arises from variations in this process. What are the mechanisms underlying cell determination and how is cell diversity achieved? In order to approach these questions, we use the Drosophila mechanosensory bristle lineage. In this lineage, cell diversity arises from the differential activation of the Notch pathway as well as the asymmetric segregation of cell fate determinants at each division. However, how does the repetition of the same mechanism trigger different cell fates? Other factors might be involved in cell fate commitment. In order to identify such factors, I focused my interest on the transcription factor of the Snail superfamily, known to be involved in cell determination during Drosophila development.Two members of this superfamily, escargot (esg) and scratch (scrt) are expressed in the bristle lineage, specifically in the inner neural cells and their precursor cells. Loss and gain of function analysis indicate that Esg and Scrt, acting redundantly, are necessary for the maintenance of the neural secondary precursor cell identity. A genetics interaction test showed that this role is achieved in interaction with the Notch pathway, probably through the repression of Notch target genes expression. Moreover, Esg, but not Scrt, has an additional role during the inner bristle cell formation. Loss of function of this factor induces a defect in neuronal differentiation, specifically axon growth and patterning. Moreover, the expression of genes involved in neuronal differentiation, such as elav and prospero, is impaired in this context. Altogether, these data suggests that Esg is involved in neuronal differentiation by regulating the expression of key neuronal genes.Together, my results showed that Esg and Scrt participate to the establishment of cell diversity in Drosophila bristle cell lineage

4

Stamataki, Despina. "Shh signalling and the specification of neuronal identity." Thesis, Open University, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.409850.

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5

Carney, Travis. "Stem Cell Self-renewal and Neuronal Differentiation in the Drosophila Central Nervous System." Thesis, University of Oregon, 2013. http://hdl.handle.net/1794/13336.

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The adoption and subsequent retention of distinct cellular fates upon cell division is a critical phenomenon in the development of multicellular organisms. A well-studied example of this process is stem cell divisions; stem cells must possess the capacity to self-renew in order to maintain a stem cell population, as well as to generate differentiated daughters for tissue growth and repair. Drosophila neuroblasts are the neural stem cells of the central nervous system and have emerged as an important model for stem cell divisions and the genetic control of daughter cell identities. Neuroblasts divide asymmetrically to generate daughters with distinct fates; one retains a neuroblast identity and the other, a ganglion mother cell, divides only once more to generate differentiated neurons and glia. Perturbing the asymmetry of neuroblast divisions can result in the failure to self-renew and the loss of the neural stem cell population; alternatively, ectopic self-renewal can occur, resulting in excessive neuroblast proliferation and tumorigenesis. Several genetic lesions have been characterized which cause extensive ectopic self-renewal, resulting in brains composed of neuroblasts at the expense of differentiated cells. This contrasts with wild type brains, which are composed mostly of differentiated cells and only a small pool of neuroblasts. We made use of these mutants by performing a series of microarray experiments comparing mutant brains (consisting mostly of neuroblasts) to wild type brains (which are mostly neurons). Using this approach, we generated lists of over 1000 putatively neuroblast-expressed genes and over 1000 neuronal genes; in addition, we were able to compare the transcriptional output of different mutants to infer the neuroblast subtype specificity of some of the transcripts. Finally, we verified the self-renewal function of a subset of the neuroblast genes using an RNAi-based screen, resulting in the identification of 84 putative self-renewal regulators. We went on to show that one of these genes, midlife crisis (mammals: RNF113a), is a well-conserved RNA splicing regulator which is required in postmitotic neurons for the maintenance of their differentiated state. Our data suggest that the mammalian ortholog performs the same function, implicating RNF113a as an important regulator of neuronal differentiation in humans.

6

Lischinsky, Julieta E. "Embryonic Transcription Factor Expression Predicts Neuronal Identity and Innate Behavioral Activation Patterns in the Limbic System." Thesis, The George Washington University, 2017. http://pqdtopen.proquest.com/#viewpdf?dispub=10263849.

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Instinctive behaviors such as mating and aggression are key for the survival and propagation of species. As innate behaviors manifest without prior training, there must be embryonic genetic mechanisms that specify these innate behavioral circuits. Focusing on the MeA and hypothalamus, both major integration centers of olfactory inputs, first, we sought to elucidate the link between embryonic transcription factor expression, neuronal identity and innate behavioral activation patterns in the MeA, and second, the link between embryonic transcription factor expression and instinctive behavioral activation patterns in hypothalamic subnuclei. Using mice as a model organism, we observed that the MeA progenitor niche in the preoptic area (POA) is comprised of distinct progenitor populations differentially marked by the transcription factors Dbx1 and Foxp2. Both embryonically and postnatally, Dbx1-derived and Foxp2+ subpopulations remain spatially segregated. We also observed that Dbx1-derived and Foxp2+ neurons differentially express sets of sex-steroid pathway proteins. Furthermore, both subpopulations differed in their intrinsic and extrinsic electrophysiological properties. Additionally, behavioral activation patterns were investigated in both subpopulations by determining the co-expression of the immediate early gene c-fos, an indirect marker of neuronal activity. During aggressive encounters, both Dbx1-derived and Foxp2+ neurons were activated in male and female mice; however, during mating cues, Dbx1-derived neurons in male and female mice were activated while only Foxp2+ neurons in male mice were activated and not in female mice. This denotes sex-specific differences in behavioral activation patterns in the MeA. Thus, parcellation of MeA neuronal subpopulations based on developmental genetics predicts molecular, electrophysiological, and behavioral specificity. Secondly, we were interested in determining whether embryonic transcription factor expression would be predictive of innate behavioral activation patterns in other limbic system structures implicated in the generation of innate behaviors such as the hypothalamus. Interestingly, we observed the presence of Dbx1-derived neurons in the lateral (LH), arcuate (Arc) and ventromedial (VMH) hypothalamic subnuclei. As Foxp2+ neurons are not present in the hypothalamus, we only analyzed Dbx1-derived neurons in these three hypothalamic regions. We show that Dbx1-derived neurons are activated in these structures during mating and aggression in both male and female mice. Thus, embryonic transcription factor expression in the hypothalamus is also linked to postnatal behavioral activation patterns. Taken together our findings indicate that embryonic transcription factor expression is predictive of behavioral activation patterns in the limbic system. We found that progenitor populations present in the same region but expressing distinct transcription factors, can generate MeA postnatal diversity based on molecular, electrophysiological and behavioral activation patterns. Furthermore, this can be generalized to other limbic system structures such as the hypothalamus, in which embryonic transcription factor expression of Dbx1 is also predictive of activation patterns during instinctive behavioral cues.

7

Etheredge, Jack. "Transcriptional profiling of Drosophila larval ventral nervous system hemilineages." Thesis, University of Cambridge, 2017. https://www.repository.cam.ac.uk/handle/1810/270548.

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Over 90% of neurons in the adult CNS of Drosophila are born from neuronal stem cells (neuroblasts) during the post-embryonic phase of neurogenesis. Most of the post-embryonic neurons derive from type I neuroblasts, which undergo repeated asymmetric divisions to produce a series of ganglion mother cells (GMCs). Each GMC then divides once resulting in two neurons, the “A” (Notch-on) and “B” (Notch-off) daughters. The respective daughter neurons of each type then constitute the A and B hemilineages for that neuroblast. 33 postembryonic hemilineages contribute neurons to each thoracic hemisegment, and these immature neurons arrest their development at a similar stage until metamorphosis. These arrested neuroblast lineages are uniquely identifiable by morphology. Access to a large pool of clonally-related and morphologically similar neurons makes this system tractable to RNA-seq analysis, since one can genetically label and isolate many cells per animal, which are predicted to share similar gene expression profiles. Our primary focus is to examine hemilineages with similar targets (e.g. leg neuropil) to identify genes that are required to establish and maintain hemilineage identity early in development. Given that activating these hemilineage neurons as a group drives distinct behaviors and that they form morphologically coherent structural units during development, we hypothesized that these hemilineages should express patterns of genes that are: 1) distinct from other hemilineages and 2) characteristic of individual hemilineages. We have used hemilineage-specific GAL4 lines to isolate hemilineages for RNA-seq analysis, ultimately gathering data for 11 of the 33 hemilineages as well as for some larger populations of neurons. We found that, in addition to combinatorial patterns of genes specifying the hemilineage neurons, there are some genes that are expressed by only a single hemilineage within the ventral nervous system (VNS). Most hemilineages display unique expression of certain transcription factors (TFs) and axon guidance genes. We collected data for two pairs of sibling hemilineages (lineage 1 and lineage 12) in order to identify differences between the A and B hemilineages derived from a common neuroblast. While A neurons display greater overall transcriptional diversity than B neurons, sibling hemilineages share very similar expression profiles. Comparing the gene expression between immature and mature larval neurons revealed that mature neurons express many genes not expressed in immature neurons, such as neuropeptide signaling genes and many neurotransmitter and ion channel genes associated with mature neuron function. Birth order also appears to dictate many differences in expression profile. Late-born immature neurons are typified by a period of transient Notch-related gene expression that is absent from early-born neurons. We are characterizing the function of many differentially expressed genes in particular hemilineages.

8

Natinsky, Ari Simon. "Psychotherapy and the Embodiment of the Neuronal Identity: A Hermeneutic Study of Louis Cozolino's (2010) The Neuroscience of Psychotherapy: Healing the Social Brain." Antioch University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=antioch1399924216.

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9

Atlan, Henri. "Spinoza et la biologie actuelle." Thesis, Paris 1, 2017. http://www.theses.fr/2017PA01H232.

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Les avancées de la biologie contemporaine, posent de façon nouvelle des problèmes philosophiques anciens. Ceux des rapports entre le vivant et l'inanimé, entre le corps et l'esprit, l'erreur et la vérité, sont les plus évidents. La philosophie de Spinoza, bien que datant du 17e siècle, apporte à ces problèmes des solutions plus pertinentes que la plupart des philosophies plus récentes, développées dans les siècles qui l'ont suivie. En retour, les acquis actuels des sciences physiques et biologiques, notamment des neurosciences cognitives, permettent de porter un nouveau regard sur certaines notions propres à la philosophie de Spinoza, telles que sa «petite physique», la nature cause de soi, la notion de matière, l'essence des choses, les genres de connaissance, qui acquièrent de ce fait un surcroît d'actualité
Old philosophical problems are raised in renewed ways by advances in biology of today. Most obvious are the problems of relationship between living and non-living, mind and body, error en truth. Spinoza's philosophy, although from 17th century, offers solutions to these problems more relevant than most more recent philosophies. In return, present knowledge from physical and biological sciences, especially cognitive neurosciences, can provide a new look at some specifically Spinozist notions such as his "little physics", Nature as cause of itself, the notion of matter, the essence of a thing, kinds of knowledge, which gain all the more interest from a present day point of view

10

Pagliaro, Sarah Beatriz De Oliveira. "Transcriptional control induced by bcr-abl and its role in leukemic stem cell heterogeneity. Single-Cell Transcriptome in Chronic Myeloid Leukemia: Pseudotime Analysis Reveals Evidence of Embryonic and Transitional Stem Cell States Single Cell Transcriptome in Chronic Myeloid Leukemia (CML): Pseudotime Analysis Reveals a Rare Population with Embryonic Stem Cell Features and Druggable Intricated Transitional Stem Cell States A novel neuronal organoid model mimicking glioblastoma (GBM) features from induced pluripotent stem cells (iPSC) Experimental and integrative analyses identify an ETS1 network downstream of BCR-ABL in chronic myeloid leukemia (CML)." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASQ032.

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La leucémie myéloïde chronique est une hématopoïèse maligne clonale, caractérisée par l'acquisition de la translocation t (9;22) conduisant au chromosome Ph1 et à son homologue l'oncogène BCR-ABL, dans une cellule souche hématopoïétique très primitive. La LMC est un modèle de thérapies ciblées, car il a été démontré que la preuve de la faisabilité du ciblage de l'activité tyrosine kinase (TK) BCR-ABL à l'aide d'inhibiteurs de TK (TKI) entraîne des réponses et des rémissions majeures. Cependant, les problèmes actuels rencontrés dans ces thérapies sont la résistance des cellules souches leucémiques primitives et leur persistance qui serait liée à l'hétérogénéité des cellules souches au moment du diagnostic, ce qui conduit à la sélection clonale de cellules résistant aux thérapies TKI. J'ai appliqué la technologie de l'analyse du transcriptome des cellule uniques aux cellules de la LMC en utilisant un panel de gènes impliqués dans différentes voies, combinée à l'analyse d'inférence de trajectoire au modèle d'expression des gènes. Les résultats ont montré un état transitoire des cellules souches comprenant des gènes embryonnaires identifiés dans les cellules de la LMC au moment du diagnostic, ce qui pourrait contribuer à la résistance et à la persistance de la LSC. En outre, l'oncoprotéine Bcr-Abl est la tyrosine kinase constitutivement active produite par le gène chimérique BCR-ABL dans la leucémie myéloïde chronique (LMC). Les cibles transcriptionnelles de Bcr-Abl dans les cellules leucémiques n'ont pas été étudiées de manière approfondie. Une expérience de transcriptome utilisant la lignée cellulaire UT7 hématopoïétique exprimant BCR-ABL, a identifié la surexpression du facteur d'élongation eucaryote kinase 2 (eEF2K) qui joue un rôle majeur dans la survie des cellules en cas de privation de nutriments. Dans l'ensemble, les données suggèrent que la surexpression de eEF2K dans la LMC est associée à une sensibilité accrue à la privation de nutriments
Chronic myeloid leukemia is a clonal hematopoietic malignancy, characterized by the acquisition of the t (9;22) translocation leading to Ph1 chromosome and its counterpart BCR-ABL oncogene, in a very primitive hematopoietic stem cell. CML is a model of targeted therapies as the proof of concept of the feasibility of targeting the tyrosine kinase (TK) activity BCR-ABL using TK inhibitors (TKI) has been shown to lead to major responses and remissions. However, the current problems encountered in these therapies are primitive leukemic stem cells resistance and their persistence which is thought to be related to the heterogeneity of the stem cells at diagnosis leading to clonal selection of cells resisting to TKI therapies. I have applied the technology of single cell transcriptome analysis to CML cells using a panel of genes involved in different pathways combined with trajectory inference analysis to the gene expression pattern. The results showed a transitional stem cell states including embryonic genes identified in CML cells at diagnosis which could contribute to LSC resistance and persistence. Furthermore, the oncoprotein Bcr-Abl is the constitutively active tyrosine kinase produced by the chimeric BCR-ABL gene in chronic myeloid leukemia (CML). The transcriptional targets of Bcr-Abl in leukemic cells have not been extensively studied. A transcriptome experiment using the hematopoietic UT7 cell line expressing BCR-ABL, has identified the overexpression of eukaryotic elongation factor kinase 2 (eEF2K) which plays a major role in the survival of cells upon nutrient deprivation. Overall, the data suggest that overexpression of eEF2K in CML is associated with an increased sensitivity to nutrient-deprivation

Книги з теми "Identité neuronale":

1

Marty, Shankland, and Macagno Eduardo R, eds. Determinants of neuronal identity. San Diego: Academic Press, 1992.

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2

Determinants of Neuronal Identity. Elsevier, 1992. http://dx.doi.org/10.1016/b978-0-12-638280-8.x5001-2.

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3

Rager, Günter, Josef Quitterer, and Edmund Runggaldier. Unser Selbst. Identität im Wandel der neuronalen Prozesse. Schöningh, 2003.

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4

Cohen, Marlene R., and John H. R. Maunsell. Neuronal Mechanisms of Spatial Attention in Visual Cerebral Cortex. Edited by Anna C. (Kia) Nobre and Sabine Kastner. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199675111.013.007.

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Attention is associated with improved performance on perceptual tasks and changes in the way that neurons in the visual system respond to sensory stimuli. While we now have a greater understanding of the way different behavioural and stimulus conditions modulate the responses of neurons in different cortical areas, it has proven difficult to identify the neuronal mechanisms responsible for these changes and establish a strong link between attention-related modulation of sensory responses and changes in perception. Recent conceptual and technological advances have enabled progress and hold promise for the future. This chapter focuses on newly established links between attention-related modulation of visual responses and bottom-up sensory processing, how attention relates to interactions between neurons, insights from simultaneous recordings from groups of cells, and how this knowledge might lead to greater understanding of the link between the effects of attention on sensory neurons and perception.

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Martin, Rebecca E., and Ross D. MacPherson. Pathophysiology and assessment of pain. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0356.

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From a clinical viewpoint, pain can generally be classified as nociceptive, visceral, or neuropathic. This distinction is important, as it will help guide pain management strategies. In this section the authors discuss the current state of the art with regard to pain mechanisms at a neuronal and neurotransmitter level. Much has been clarified in recent years to help identify neurotransmitters involved in pain pathways, and target new drugs and treatments. The second part of the chapter discusses assessment of pain in the critical care setting. Assessment of pain severity and of response to treatment is clearly a difficult process in the patient who is unable to communicate verbally. This section discusses the various strategies and assessment protocols that have been formulated to try and assist in this difficult task.

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Sprigings, David. Coma. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0040.

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Coma is a pathological state of unconsciousness from which a patient cannot be roused to wakefulness by stimuli, and reflects dysfunction of the brainstem reticular system and its thalamic projections (the neuronal basis of wakefulness), or diffuse injury of both cerebral hemispheres. A unilateral lesion of a cerebral hemisphere (e.g. haemorrhagic stroke) will not cause coma unless there is secondary compression of the contralateral hemisphere or brainstem. Coma is a medical emergency, because a comatose patient is at high risk of permanent brain injury or death, caused either by the underlying disorder or the secondary effects of coma. Stabilization of the airway, breathing, and circulation, and exclusion of hypoglycaemia are the first priorities, before diagnosis is explored further. Clinical assessment together with neuroimaging will usually identify the likely cause or causes. The clinical approach to diagnosis and management of the comatose patient is described in this chapter.

7

McShane, Tony, Peter Clayton, Michael Donaghy, and Robert Surtees. Neurometabolic disorders. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0213.

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Various disorders result from genetically determined abnormalities of enzymes, the metabolic consequences of which affect the development or functioning of the nervous system. The range of metabolic disturbances is wide, as is the resultant range of clinical syndromes. Although most occur in children, some can present in adult life, and increasing numbers of affected children survive into adult life. In some, specific treatments are possible or are being developed. The last 20 years has seen a considerable expansion in our understanding of the genetic and metabolic basis for many neurological conditions. Particular clinical presentations of neurometabolic disorders include ataxias, movement disorders, childhood epilepsies, or peripheral neuropathy. Detailed coverage of the entire range of inherited metabolic diseases of the nervous system is available in other texts (Brett 1997; Scriver et al. 2001; Menkes et al. 2005).Treatment is possible for some metabolic diseases. For instance, the devastating neurological effects of phenylketonuria have been recognized for many years. Neonatal screening for this disorder and dietary modification in the developed world has removed phenylketonuria from the list of important causes of serious neurological disability in children. This success has led to new challenges in the management of the adult with phenylketonuria and unexpected and devastating effect of the disorder on the unborn child of an untreated Phenylketonuria mother. More recently Biotinidase deficiency has been recognized as an important and easily treatable cause of serious neurological disease usually presenting with early onset drug resistant seizures. This and some other neurometabolic diseases can be identified on neonatal blood screening although a full range of screening is not yet routine in the United Kingdom. More disorders are likely to be picked up at an earlier asymptomatic stage as the sophistication of screening tests increases (Wilcken et al. 2003; Bodamer et al. 2007).Although individual metabolic disorders are rare, collectively such disorders are relatively common. In reality most clinicians will see an individual condition only rarely in a career. Furthermore, patients with certain rare conditions are often concentrated in specialist referral centres, further reducing the exposure of general and paediatric neurologists to these disorders. A recent study into progressive intellectual and neurological deterioration, PIND, gives some information about the relative frequency and distribution of some childhood neurodegenerative diseases in the United Kingdom (Verity et al. 2000; Devereux et al. 2004). Although primarily designed to identify any childhood cases of variant Creutzfeldt- Jakob disease, the study also provided much information about the distribution of neurometabolic disease in children in the United Kingdom. The commonest five causes of progressive intellectual and neurological deterioration over 5 years were Sanfilippo syndrome, 41 cases, adrenoleukodystrophy, 32 cases, late infantile neuronal ceroid lipofuschinosis, 32 cases, mitochondrial cytopathy, 30 cases, and Rett syndrome, 29 cases. Notably, geographical foci of these disorders were also found and correlate with high rate of consanguinity in some local populations.

Частини книг з теми "Identité neuronale":

1

Appel, Bruce, and Ajay Chitnis. "Neurogenesis and Specification of Neuronal Identity." In Results and Problems in Cell Differentiation, 237–51. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-540-46041-1_12.

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2

Marcus, Donald M. "The Use of Antibodies to Identify Glycosphingolipids and to Localize Them in Tissues." In Gangliosides and Neuronal Plasticity, 77–82. New York, NY: Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4757-5309-7_6.

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3

Xavier, André Machado, and Isaias Glezer. "CD36 Neuronal Identity in the Olfactory Epithelium." In Methods in Molecular Biology, 1–19. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8609-5_1.

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4

Natinsky, Ari. "Psychotherapy and the Embodiment of Neuronal Identity." In Hermeneutic Approaches to Interpretive Research, 48–62. New York: Routledge, 2021. http://dx.doi.org/10.4324/9781003140177-4.

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5

Kim, Chiho, and Young J. Oh. "A Novel 2-DE-Based Proteomic Analysis to Identify Multiple Substrates for Specific Protease in Neuronal Cells." In Methods in Molecular Biology, 229–45. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6952-4_10.

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6

Pecchinenda, Gianfranco. "The neuronal identity." In Postmortal Society, 138–55. Routledge, 2017. http://dx.doi.org/10.4324/9781315601700-8.

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7

"Front Matter." In Determinants of Neuronal Identity, iii. Elsevier, 1992. http://dx.doi.org/10.1016/b978-0-12-638280-8.50001-1.

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8

"Copyright." In Determinants of Neuronal Identity, iv. Elsevier, 1992. http://dx.doi.org/10.1016/b978-0-12-638280-8.50002-3.

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9

Shankland, Marty, and Eduardo R. Macagno. "Preface." In Determinants of Neuronal Identity, xv—xvi. Elsevier, 1992. http://dx.doi.org/10.1016/b978-0-12-638280-8.50004-7.

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10

Sternberg, Paul W., Katharine Liu, and Helen M. Chamberlin. "Specification of Neuronal Identity in Caenorhabditis elegans." In Determinants of Neuronal Identity, 1–43. Elsevier, 1992. http://dx.doi.org/10.1016/b978-0-12-638280-8.50005-9.

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Тези доповідей конференцій з теми "Identité neuronale":

1

Jabalameli, Amirhossein, and Aman Behal. "A constrained linear approach to identify a multi-timescale adaptive threshold neuronal model." In 2015 IEEE 5th International Conference on Computational Advances in Bio and Medical Sciences (ICCABS). IEEE, 2015. http://dx.doi.org/10.1109/iccabs.2015.7344704.

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2

Zhang, H., N. Ye, J. He, A. Roontiva, and J. Aguayo. "Two-way ANOVA to identify impacts of multiple interactive behavioral factors on the neuronal population dependency during the reaching motion." In 2008 30th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2008. http://dx.doi.org/10.1109/iembs.2008.4649411.

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3

Shukla, Amit, Ashutosh Mani, Amit Bhattacharya, and Fredy Revilla. "Classification of Postural Response in Parkinson’s Patients Using Support Vector Machines." In ASME 2013 Dynamic Systems and Control Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/dscc2013-3888.

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Parkinson’s disease (PD) is a neurodegenerative condition with neuronal cell death in the substantia nigra and striatal dopamine deficiency that produces slowness, stiffness, tremor, shuffling gait and postural instability. More than 1 million people in North America are affected by PD resulting in balance problems and falls. It is observed that postural instability and gait problems become resistant to pharmacologic therapy as the disease progresses. Furthermore, studies suggest that postural sway abnormalities are worsened by levodopa, the mainstay of therapy for PD. This paper presents a classification of postural balance test data using Support Vector Machines (SVM) to identify the effect of medicine (levodopa) as well as dyskinesia. It is demonstrated that SVM is a useful tool and can complement the widely accepted (but very resource intensive) Unified Parkinson’s Disease Rating Scale (UPDRS).

4

Morales, Juan, Jorge G. Pen˜a, Jaime Ferna´ndez, and Angel Rodri´guez. "Towards a Scalable ESPINA for Neuroscience Data Analysis." In ASME 2011 World Conference on Innovative Virtual Reality. ASMEDC, 2011. http://dx.doi.org/10.1115/winvr2011-5553.

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ESPINA is an image segmentation tool designed to analyse microscopy images in order to identify neuronal structures and to produce 3D models of these structures. This tool allows to display three-dimensional volumes using auto-stereoscopic monitors. It was initially designed for workstations, but when data volume management or its processing complexity makes unfeasible the implementation of the new tools on these computers, it is necessary to resort to computing servers that delimit response times or by means of scalable solutions and algorithmic optimizations. This paper analyses the migration of this tool from the original implementation to a scalable solution and describes the experience achieved during the development of the workstation version. The proposed alternative is a distributed version of the tool that delegate heavy-computational processes to a cluster, improving the performance of the system in a master/slave architecture.

5

Rizzi, Liara, and Marcio Balthazar. "THE SUSPECTED NON-ALZHEIMER’S DISEASE PATHOPHYSIOLOGY." In XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda070.

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Background: Individuals that are negative for amyloid biomarkers and positive for p-Tau and/or neurodegeneration ones are known as with the suspected non-Alzheimer’s disease pathophysiology (SNAP). It is a biomarker-based concept that underlying etiology has not been completely understood. Objective: To report the main characteristics of the SNAP group. Methods: PubMed was searched to identify articles about the SNAP for inclusion. Results: The prevalence of SNAP varies from 18% to 35% among cognitively normal individuals, from 16,6% to 35% among mild cognitive impairment (MCI), and from 7% to 39% among clinical probable Alzheimer’s Disease (AD). SNAP subjects have a lower risk of clinical progression to MCI or AD dementia than those with positive amyloid biomarkers, but higher than those whose biomarkers for amyloid and neurodegeneration are negative. SNAP predominate in older men and have a lower incidence of the APOE ε4 allele than in individuals with AD. Cognitive decline in SNAP subjects is related to neuronal damage. They present greater hippocampal atrophy than AD, but a similar pattern of hypometabolism. Hippocampus-specific pathologies and cerebrovascular diseases may underlie neurodegeneration and cognitive impairments. Conclusion: The construct of SNAP has been challenging, therefore, a deeper understanding of the main pathways that underlie SNAP can allow substrates for disease prevention and/or remission in the future.

Звіти організацій з теми "Identité neuronale":

1

Library, Spring. The Cycle of Learning, Memorizing, and Forgetting. Spring Library, December 2020. http://dx.doi.org/10.47496/sl.blog.17.

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