Journal articles on the topic 'Hyper-plasticity'
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Wilson, J. F., V. Lodhia, D. P. Courtney, I. J. Kirk, and J. P. Hamm. "Evidence of hyper-plasticity in adults with Autism Spectrum Disorder." Research in Autism Spectrum Disorders 43-44 (November 2017): 40–52. http://dx.doi.org/10.1016/j.rasd.2017.09.005.
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Sengupta, Soumya, Gargee Bhattacharya, Subhasmita Mohanty, Shubham K. Shaw, Gajendra M. Jogdand, Rohila Jha, Prakash K. Barik, Jyoti R. Parida, and Satish Devadas. "IL-21, Inflammatory Cytokines and Hyperpolarized CD8+ T Cells Are Central Players in Lupus Immune Pathology." Antioxidants 12, no. 1 (January 12, 2023): 181. http://dx.doi.org/10.3390/antiox12010181.
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Systemic lupus erythematous (SLE) is a chronic autoimmune disorder, broadly characterized by systemic inflammation along with heterogeneous clinical manifestations, severe morbidity, moribund organ failure and eventual mortality. In our study, SLE patients displayed a higher percentage of activated, inflamed and hyper-polarized CD8+ T cells, dysregulated CD8+ T cell differentiation, significantly elevated serum inflammatory cytokines and higher accumulation of cellular ROS when compared to healthy controls. Importantly, these hyper-inflammatory/hyper-polarized CD8+ T cells responded better to an antioxidant than to an oxidant. Terminally differentiated Tc1 cells also showed plasticity upon oxidant/antioxidant treatment, but that was in contrast to the SLE CD8+ T cell response. Our studies suggest that the differential phenotype and redox response of SLE CD8+ T cells and Tc1 cells could be attributed to their cytokine environs during their respective differentiation and eventual activation environs. The polarization of Tc1 cells with IL-21 drove hyper-cytotoxicity without hyper-polarisation suggesting that the SLE inflammatory cytokine environment could drive the extreme aberrancy in SLE CD8+ T cells.
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Stahl, Martin, and Alain Stintzi. "Identification of essential genes in C. jejuni genome highlights hyper-variable plasticity regions." Functional & Integrative Genomics 11, no. 2 (February 23, 2011): 241–57. http://dx.doi.org/10.1007/s10142-011-0214-7.
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Flavahan, William A. "Epigenetic plasticity, selection, and tumorigenesis." Biochemical Society Transactions 48, no. 4 (August 14, 2020): 1609–21. http://dx.doi.org/10.1042/bst20191215.
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Epigenetic processes converge on chromatin in order to direct a cell's gene expression profile. This includes both maintaining a stable cell identity, but also priming the cell for specific controlled transitions, such as differentiation or response to stimuli. In cancer, this normally tight control is often disrupted, leading to a wide scale hyper-plasticity of the epigenome and allowing stochastic gene activation and silencing, cell state transition, and potentiation of the effects of genetic lesions. Many of these epigenetic disruptions will confer a proliferative advantage to cells, allowing for a selection process to occur and leading to tumorigenesis even in the case of reversible or unstable epigenetic states. This review seeks to highlight how the fundamental epigenetic shifts in cancer contribute to tumorigenesis, and how understanding an integrated view of cancer genetics and epigenetics may more effectively guide research and treatment.
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Soldatos, D., and S. P. Triantafyllou. "Logarithmic Spin, Logarithmic Rate and Material Frame-Indifferent Generalized Plasticity." International Journal of Applied Mechanics 08, no. 05 (July 2016): 1650060. http://dx.doi.org/10.1142/s1758825116500605.
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In this work, we present a new rate type formulation of large deformation generalized plasticity which is based on the consistent use of the logarithmic rate concept. For this purpose, the basic constitutive equations are initially established in a local rotationally neutralized configuration which is defined by the logarithmic spin. These are then rephrased in their spatial form, by employing some standard concepts from the tensor analysis on manifolds. Such an approach, besides being compatible with the notion of (hyper)elasticity, offers three basic advantages, namely: (i) The principle of material frame-indifference is trivially satisfied. (ii) The structure of the infinitesimal theory remains essentially unaltered. (iii) The formulation does not preclude anisotropic response. A general integration scheme for the computational implementation of generalized plasticity models which are based on the logarithmic rate is also discussed. The performance of the scheme is tested by two representative numerical examples.
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Biundo, F., C. d'Abramo, M. D. Tambini, H. Zhang, D. Del Prete, F. Vitale, L. Giliberto, O. Arancio, and L. D'Adamio. "Abolishing Tau cleavage by caspases at Aspartate421 causes memory/synaptic plasticity deficits and pre-pathological Tau alterations." Translational Psychiatry 7, no. 8 (August 2017): e1198-e1198. http://dx.doi.org/10.1038/tp.2017.165.
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Abstract TAU mutations are genetically linked to fronto-temporal dementia (FTD) and hyper-phosphorylated aggregates of Tau form neurofibrillary tangles (NFTs) that constitute a pathological hallmark of Alzheimer disease (AD) and FTD. These observations indicate that Tau has a pivotal role in the pathogenesis of neurodegenerative disorders. Tau is cleaved by caspases at Aspartate421, to form a Tau metabolite known as δTau; δTau is increased in AD, due to the hyper-activation of caspases in AD brains. δTau is considered a critical toxic moiety underlying neurodegeneration, which initiates and facilitates NFT formation. As Tau is a therapeutic target in neurodegeneration, it is important to rigorously determine whether δTau is a toxic Tau species that should be pharmacologically attacked. To directly address these questions, we have generated a knock-in (KI) mouse called Tau DN —that expresses a Tau mutant that cannot be cleaved by caspases. Tau DN mice present short-term memory deficits and synaptic plasticity defects. Moreover, mice carrying two mutant Tau alleles show increased total insoluble hyper-phosphorylated Tau in the forebrain. These data are in contrast with the concept that δTau is a critical toxic moiety underlying neurodegeneration, and suggest that cleavage of Tau by caspases represents a negative feedback mechanism aimed to eliminate toxic Tau species. Alternatively, it is possible that either a reduction or an increase in δTau leads to synaptic dysfunction, memory impairments and Tau pathology. Both possibilities will have to be considered when targeting caspase cleavage of Tau in AD therapy.
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Bains, Amarpreet Singh, and Nicolas Schweighofer. "Time-sensitive reorganization of the somatosensory cortex poststroke depends on interaction between Hebbian and homeoplasticity: a simulation study." Journal of Neurophysiology 112, no. 12 (December 15, 2014): 3240–50. http://dx.doi.org/10.1152/jn.00433.2013.
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Together with Hebbian plasticity, homeoplasticity presumably plays a significant, yet unclear, role in recovery postlesion. Here, we undertake a simulation study addressing the role of homeoplasticity and rehabilitation timing poststroke. We first hypothesize that homeoplasticity is essential for recovery and second that rehabilitation training delivered too early, before homeoplasticity has compensated for activity disturbances postlesion, is less effective for recovery than training delivered after a delay. We developed a neural network model of the sensory cortex driven by muscle spindle inputs arising from a six-muscle arm. All synapses underwent Hebbian plasticity, while homeoplasticity adjusted cell excitability to maintain a desired firing distribution. After initial training, the network was lesioned, leading to areas of hyper- and hypoactivity due to the loss of lateral synaptic connections. The network was then retrained through rehabilitative arm movements. We found that network recovery was unsuccessful in the absence of homeoplasticity, as measured by reestablishment of lesion-affected inputs. We also found that a delay preceding rehabilitation led to faster network recovery during the rehabilitation training than no delay. Our simulation results thus suggest that homeoplastic restoration of prelesion activity patterns is essential to functional network recovery via Hebbian plasticity.
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Jiao, Yang, and Jacob Fish. "On the equivalence between the multiplicative hyper-elasto-plasticity and the additive hypo-elasto-plasticity based on the modified kinetic logarithmic stress rate." Computer Methods in Applied Mechanics and Engineering 340 (October 2018): 824–63. http://dx.doi.org/10.1016/j.cma.2018.06.017.
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Albensi, Benedict C., Derek R. Oliver, Justin Toupin, and Gary Odero. "Electrical stimulation protocols for hippocampal synaptic plasticity and neuronal hyper-excitability: Are they effective or relevant?" Experimental Neurology 204, no. 1 (March 2007): 1–13. http://dx.doi.org/10.1016/j.expneurol.2006.12.009.
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van Leeuwe, Tim M., Mark Arentshorst, Gabriel Forn-Cuní, Nicholas Geoffrion, Adrian Tsang, Frank Delvigne, Annemarie H. Meijer, Arthur F. J. Ram, and Peter J. Punt. "Deletion of the Aspergillus niger Pro-Protein Processing Protease Gene kexB Results in a pH-Dependent Morphological Transition during Submerged Cultivations and Increases Cell Wall Chitin Content." Microorganisms 8, no. 12 (December 2, 2020): 1918. http://dx.doi.org/10.3390/microorganisms8121918.
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There is a growing interest in the use of post-fermentation mycelial waste to obtain cell wall chitin as an added-value product. In the pursuit to identify suitable production strains that can be used for post-fermentation cell wall harvesting, we turned to an Aspergillus niger strain in which the kexB gene was deleted. Previous work has shown that the deletion of kexB causes hyper-branching and thicker cell walls, traits that may be beneficial for the reduction in fermentation viscosity and lysis. Hyper-branching of ∆kexB was previously found to be pH-dependent on solid medium at pH 6.0, but was absent at pH 5.0. This phenotype was reported to be less pronounced during submerged growth. Here, we show a series of controlled batch cultivations at a pH range of 5, 5.5, and 6 to examine the pellet phenotype of ΔkexB in liquid medium. Morphological analysis showed that ΔkexB formed wild type-like pellets at pH 5.0, whereas the hyper-branching ΔkexB phenotype was found at pH 6.0. The transition of phenotypic plasticity was found in cultivations at pH 5.5, seen as an intermediate phenotype. Analyzing the cell walls of ΔkexB from these controlled pH-conditions showed an increase in chitin content compared to the wild type across all three pH values. Surprisingly, the increase in chitin content was found to be irrespective of the hyper-branching morphology. Evidence for alterations in cell wall make-up are corroborated by transcriptional analysis that showed a significant cell wall stress response in addition to the upregulation of genes encoding other unrelated cell wall biosynthetic genes.
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Javed, Muhammad Afzal, Andrew J. Grant, Mary C. Bagnall, Duncan J. Maskell, Diane G. Newell, and Georgina Manning. "Transposon mutagenesis in a hyper-invasive clinical isolate of Campylobacter jejuni reveals a number of genes with potential roles in invasion." Microbiology 156, no. 4 (April 1, 2010): 1134–43. http://dx.doi.org/10.1099/mic.0.033399-0.
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Transposon mutagenesis has been applied to a hyper-invasive clinical isolate of Campylobacter jejuni, 01/51. A random transposon mutant library was screened in an in vitro assay of invasion and 26 mutants with a significant reduction in invasion were identified. Given that the invasion potential of C. jejuni is relatively poor compared to other enteric pathogens, the use of a hyper-invasive strain was advantageous as it greatly facilitated the identification of mutants with reduced invasion. The location of the transposon insertion in 23 of these mutants has been determined; all but three of the insertions are in genes also present in the genome-sequenced strain NCTC 11168. Eight of the mutants contain transposon insertions in one region of the genome (∼14 kb), which when compared with the genome of NCTC 11168 overlaps with one of the previously reported plasticity regions and is likely to be involved in genomic variation between strains. Further characterization of one of the mutants within this region has identified a gene that might be involved in adhesion to host cells.
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Basshofi Habieb, Ahmad, Tavio Tavio, Gabriele Milani, and Usman Wijaya. "3D-Finite element modeling of lead rubber bearing using high damping material." MATEC Web of Conferences 276 (2019): 01013. http://dx.doi.org/10.1051/matecconf/201927601013.
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Lead Rubber Bearing (LRB) has been widely applied for seismic protection of mid and high-rise buildings around the world. Its excellent energy dissipation becomes the most important aspect of this isolation system thanks to the plasticity and recovery behavior of the lead core. Aiming to develop a deeper knowledge on the behavior of LRB’s, a 3D detailed finite element (FE) modeling is performed in Abaqus FE software. Some important parameters involved in the model are plasticity of the lead core and hyper-elasticity and viscosity of the rubber material. The parameters for rubber material are derived from the results of experimental works in the laboratory, including uniaxial tensile test and relaxation test. The bearing model is then subjected to a cyclic shear-test under constant vertical load. The result of the 3D-FE model is then compared with the analytic-Abaqus model for LRB isolators, developed in the literature. Finally, both 3D-FE model and analytic model result in a good agreement on the shear behaviour of the presented LRB.
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Xu, Wentao, Yang Jiao, and Jacob Fish. "An atomistically-informed multiplicative hyper-elasto-plasticity-damage model for high-pressure induced densification of silica glass." Computational Mechanics 66, no. 1 (May 8, 2020): 155–87. http://dx.doi.org/10.1007/s00466-020-01846-w.
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Guerrero-Rivera, Ruben, Abigail Morrison, Markus Diesmann, and Tim C. Pearce. "Programmable Logic Construction Kits for Hyper-Real-Time Neuronal Modeling." Neural Computation 18, no. 11 (November 2006): 2651–79. http://dx.doi.org/10.1162/neco.2006.18.11.2651.
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Programmable logic designs are presented that achieve exact integration of leaky integrate-and-fire soma and dynamical synapse neuronal models and incorporate spike-time dependent plasticity and axonal delays. Highly accurate numerical performance has been achieved by modifying simpler forward-Euler-based circuitry requiring minimal circuit allocation, which, as we show, behaves equivalently to exact integration. These designs have been implemented and simulated at the behavioral and physical device levels, demonstrating close agreement with both numerical and analytical results. By exploiting finely grained parallelism and single clock cycle numerical iteration, these designs achieve simulation speeds at least five orders of magnitude faster than the nervous system, termed here hyper-real-time operation, when deployed on commercially available field-programmable gate array (FPGA) devices. Taken together, our designs form a programmable logic construction kit of commonly used neuronal model elements that supports the building of large and complex architectures of spiking neuron networks for real-time neuromorphic implementation, neurophysiological interfacing, or efficient parameter space investigations.
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Zamai, Loris. "Unveiling Human Non-Random Genome Editing Mechanisms Activated in Response to Chronic Environmental Changes: I. Where Might These Mechanisms Come from and What Might They Have Led To?" Cells 9, no. 11 (October 27, 2020): 2362. http://dx.doi.org/10.3390/cells9112362.
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This article challenges the notion of the randomness of mutations in eukaryotic cells by unveiling stress-induced human non-random genome editing mechanisms. To account for the existence of such mechanisms, I have developed molecular concepts of the cell environment and cell environmental stressors and, making use of a large quantity of published data, hypothesised the origin of some crucial biological leaps along the evolutionary path of life on Earth under the pressure of natural selection, in particular, (1) virus–cell mating as a primordial form of sexual recombination and symbiosis; (2) Lamarckian CRISPR-Cas systems; (3) eukaryotic gene development; (4) antiviral activity of retrotransposon-guided mutagenic enzymes; and finally, (5) the exaptation of antiviral mutagenic mechanisms to stress-induced genome editing mechanisms directed at “hyper-transcribed” endogenous genes. Genes transcribed at their maximum rate (hyper-transcribed), yet still unable to meet new chronic environmental demands generated by “pollution”, are inadequate and generate more and more intronic retrotransposon transcripts. In this scenario, RNA-guided mutagenic enzymes (e.g., Apolipoprotein B mRNA editing catalytic polypeptide-like enzymes, APOBECs), which have been shown to bind to retrotransposon RNA-repetitive sequences, would be surgically targeted by intronic retrotransposons on opened chromatin regions of the same “hyper-transcribed” genes. RNA-guided mutagenic enzymes may therefore “Lamarkianly” generate single nucleotide polymorphisms (SNP) and gene copy number variations (CNV), as well as transposon transposition and chromosomal translocations in the restricted areas of hyper-functional and inadequate genes, leaving intact the rest of the genome. CNV and SNP of hyper-transcribed genes may allow cells to surgically explore a new fitness scenario, which increases their adaptability to stressful environmental conditions. Like the mechanisms of immunoglobulin somatic hypermutation, non-random genome editing mechanisms may generate several cell mutants, and those codifying for the most environmentally adequate proteins would have a survival advantage and would therefore be Darwinianly selected. Non-random genome editing mechanisms represent tools of evolvability leading to organismal adaptation including transgenerational non-Mendelian gene transmission or to death of environmentally inadequate genomes. They are a link between environmental changes and biological novelty and plasticity, finally providing a molecular basis to reconcile gene-centred and “ecological” views of evolution.
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Brepols, Tim, Ivaylo N. Vladimirov, and Stefanie Reese. "Application and evaluation of hyper- and hypoelastic-based plasticity models in the FE simulation of metal forming processes." PAMM 13, no. 1 (November 29, 2013): 153–54. http://dx.doi.org/10.1002/pamm.201310072.
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Meis, Susanne, Thomas Endres, Thomas Munsch, and Volkmar Lessmann. "Impact of Chronic BDNF Depletion on GABAergic Synaptic Transmission in the Lateral Amygdala." International Journal of Molecular Sciences 20, no. 17 (September 3, 2019): 4310. http://dx.doi.org/10.3390/ijms20174310.
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Brain-derived neurotrophic factor (BDNF) has previously been shown to play an important role in glutamatergic synaptic plasticity in the amygdala, correlating with cued fear learning. While glutamatergic neurotransmission is facilitated by BDNF signaling in the amygdala, its mechanism of action at inhibitory synapses in this nucleus is far less understood. We therefore analyzed the impact of chronic BDNF depletion on GABAA-mediated synaptic transmission in BDNF heterozygous knockout mice (BDNF+/−). Analysis of miniature and evoked inhibitory postsynaptic currents (IPSCs) in the lateral amygdala (LA) revealed neither pre- nor postsynaptic differences in BDNF+/− mice compared to wild-type littermates. In addition, long-term potentiation (LTP) of IPSCs was similar in both genotypes. In contrast, facilitation of spontaneous IPSCs (sIPSCs) by norepinephrine (NE) was significantly reduced in BDNF+/− mice. These results argue against a generally impaired efficacy and plasticity at GABAergic synapses due to a chronic BDNF deficit. Importantly, the increase in GABAergic tone mediated by NE is reduced in BDNF+/− mice. As release of NE is elevated during aversive behavioral states in the amygdala, effects of a chronic BDNF deficit on GABAergic inhibition may become evident in response to states of high arousal, leading to amygdala hyper-excitability and impaired amygdala function.
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BIBI, SAFURA, MUHAMMAD SAJID AQEEL AHMAD, MANSOOR HAMEED, and AMBREEN KHADIJA ALVI. "Modulation of physiological plasticity through structural and functional modifications in Stipagrostis plumosa L. for adaptability to hyper-arid environments." Turkish Journal of Botany 46, no. 5 (January 1, 2022): 435–58. http://dx.doi.org/10.55730/1300-008x.2721.
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Ito, Hiroshi, Masatoshi Nagano, Hidenori Suzuki, and Takayuki Murakoshi. "Chronic stress enhances synaptic plasticity due to disinhibition in the anterior cingulate cortex and induces hyper-locomotion in mice." Neuropharmacology 58, no. 4-5 (March 2010): 746–57. http://dx.doi.org/10.1016/j.neuropharm.2009.12.011.
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Wangpraseurt, Daniel, Camilla Wentzel, Steven L. Jacques, Michael Wagner, and Michael Kühl. "In vivo imaging of coral tissue and skeleton with optical coherence tomography." Journal of The Royal Society Interface 14, no. 128 (March 2017): 20161003. http://dx.doi.org/10.1098/rsif.2016.1003.
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Application of optical coherence tomography (OCT) for in vivo imaging of tissue and skeleton structure of intact living corals enabled the non-invasive visualization of coral tissue layers (endoderm versus ectoderm), skeletal cavities and special structures such as mesenterial filaments and mucus release from intact living corals. Coral host chromatophores containing green fluorescent protein-like pigment granules appeared hyper-reflective to near-infrared radiation allowing for excellent optical contrast in OCT and a rapid characterization of chromatophore size, distribution and abundance. In vivo tissue plasticity could be quantified by the linear contraction velocity of coral tissues upon illumination resulting in dynamic changes in the live coral tissue surface area, which varied by a factor of 2 between the contracted and expanded state of a coral. Our study provides a novel view on the in vivo organization of coral tissue and skeleton and highlights the importance of microstructural dynamics for coral ecophysiology.
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Bastian, J. "Plasticity in an Electrosensory System. III. Contrasting Properties of Spatially Segregated Dendritic Inputs." Journal of Neurophysiology 79, no. 4 (April 1, 1998): 1839–57. http://dx.doi.org/10.1152/jn.1998.79.4.1839.
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Bastian, J. Plasticity in an electrosensory system. III. Contrasting properties of spatially segregated dendritic inputs. J. Neurophysiol. 79: 1839–1857, 1998. Efferent neurons of the first-order electrosensory processing center of the brain, the electrosensory lateral line lobe (ELL), receive electroreceptor afferent input as well as feedback inputs descending from higher centers. These ELL efferents, pyramidal cells, adaptively filter predictable patterns of sensory input while preserving sensitivity to novel stimuli. The filter mechanism involves integration of centrally generated predictive inputs with the afferent inputs being canceled. The predictive inputs, referred to as “negative image” inputs, terminate on pyramidal cell apical dendrites and generate responses that are opposite those resulting from the predictable afference, hence integration of these signals results in attenuation of pyramidal cell responses. The system also shows a robust form of plasticity; the pyramidal cells learn, with a time course of a few minutes, to cancel new patterns of repetitive inputs. This is accomplished by adjusting the strength of excitatory and inhibitory apical dendritic inputs according to an anti-Hebbian learning rule. This study focuses on the properties of two separate pathways that convey descending information to pyramidal cell apical dendrites. One pathway terminates proximally, nearer to the pyramidal cell body, whereas the other terminates distally. Recordings of ELL evoked potentials, extracellular pyramidal cell spike responses, and intracellularly recorded synaptic potentials show that the pyramidal cells respond oppositely to moderate-frequency (> ∼8 Hz) single pulse stimulation or repeated (1/s) tetanic activation of these two pathways. Repetitive activation of the proximally terminating pathway results in highly facilitating responses due to potentiation of pyramidal cell excitatory postsynaptic potentials (EPSPs). These same stimuli applied to the distally terminating pathway result in a reduction of pyramidal cell responses due to depression of EPSPs and potentiation of inhibitatory postsynaptic potentials (IPSPs). Anti-Hebbian plasticity was demonstrated by pairing tetanic stimulation of either pathway with changes in the postsynaptic cell's membrane potential. After stabilization of the response potentiation due to tetanic stimulation of the proximally terminating pathway, paired postsynaptic hyperpolarization resulted in further increases in spike responses and additional potentiation of pyramidal cell EPSPs. Paired postsynaptic depolarization reduced subsequent responses to the tetanus, depressed EPSP amplitudes, and, in many cases, potentiated IPSPs. The same pattern of plasticity was observed when postsynaptic hyper- or depolarization was paired with tetanic stimulation of the distally terminating pathway except that the plasticity was superimposed on the depressed pyramidal cell responses resulting from stimulating this pathway alone. Modulation of a postsynaptic form of synaptic depression is proposed to account for the anti-Hebbian plasticity associated with both pathways.
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Breton, Jocelyn M., Kimberly L. P. Long, Matthew K. Barraza, Olga S. Perloff, and Daniela Kaufer. "Hormonal Regulation of Oligodendrogenesis II: Implications for Myelin Repair." Biomolecules 11, no. 2 (February 16, 2021): 290. http://dx.doi.org/10.3390/biom11020290.
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Alterations in myelin, the protective and insulating sheath surrounding axons, affect brain function, as is evident in demyelinating diseases where the loss of myelin leads to cognitive and motor dysfunction. Recent evidence suggests that changes in myelination, including both hyper- and hypo-myelination, may also play a role in numerous neurological and psychiatric diseases. Protecting myelin and promoting remyelination is thus crucial for a wide range of disorders. Oligodendrocytes (OLs) are the cells that generate myelin, and oligodendrogenesis, the creation of new OLs, continues throughout life and is necessary for myelin plasticity and remyelination. Understanding the regulation of oligodendrogenesis and myelin plasticity within disease contexts is, therefore, critical for the development of novel therapeutic targets. In our companion manuscript, we review literature demonstrating that multiple hormone classes are involved in the regulation of oligodendrogenesis under physiological conditions. The majority of hormones enhance oligodendrogenesis, increasing oligodendrocyte precursor cell differentiation and inducing maturation and myelin production in OLs. Thus, hormonal treatments present a promising route to promote remyelination. Here, we review the literature on hormonal regulation of oligodendrogenesis within the context of disorders. We focus on steroid hormones, including glucocorticoids and sex hormones, peptide hormones such as insulin-like growth factor 1, and thyroid hormones. For each hormone, we describe whether they aid in OL survival, differentiation, or remyelination, and we discuss their mechanisms of action, if known. Several of these hormones have yielded promising results in both animal models and in human conditions; however, a better understanding of hormonal effects, interactions, and their mechanisms will ultimately lead to more targeted therapeutics for myelin repair.
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Mancini, Monica, Margherita Grasso, Livio Muccillo, Federica Babbio, Francesca Precazzini, Ilaria Castiglioni, Valentina Zanetti, et al. "DNMT3A epigenetically regulates key microRNAs involved in epithelial-to-mesenchymal transition in prostate cancer." Carcinogenesis 42, no. 12 (October 23, 2021): 1449–60. http://dx.doi.org/10.1093/carcin/bgab101.
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Abstract Epithelial-to-mesenchymal transition (EMT) is involved in prostate cancer (PCa) metastatic progression, and its plasticity suggests epigenetic implications. Deregulation of DNA methyltransferases (DNMTs) and several microRNAs (miRNAs) plays a relevant role in EMT, but their interplay has not been clarified yet. In this study, we provide evidence that DNMT3A interaction with several miRNAs has a central role in an ex vivo EMT PCa model obtained via exposure of PC3 cells to conditioned media from cancer-associated fibroblasts. The analysis of the alterations of the miRNA profile shows that miR-200 family (miR-200a/200b/429, miR-200c/141), miR-205 and miR-203, known to modulate key EMT factors, are down-regulated and hyper-methylated at their promoters. DNMT3A (mainly isoform a) is recruited onto these miRNA promoters, coupled with the increase of H3K27me3/H3K9me3 and/or the decrease of H3K4me3/H3K36me3. Most interestingly, our results reveal the differential expression of two DNMT3A isoforms (a and b) during ex vivo EMT and a regulatory feedback loop between miR-429 and DNMT3A that can promote and sustain the transition towards a more mesenchymal phenotype. We demonstrate the ability of miR-429 to target DNMT3A 3′UTR and modulate the expression of EMT factors, in particular ZEB1. Survey of the PRAD-TCGA dataset shows that patients expressing an EMT-like signature are indeed characterized by down-regulation of the same miRNAs with a diffused hyper-methylation at miR-200c/141 and miR-200a/200b/429 promoters. Finally, we show that miR-1260a also targets DNMT3A, although it does not seem to be involved in EMT in PCa.
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Natale, Francesca, Matteo Spinelli, Saviana Antonella Barbati, Lucia Leone, Salvatore Fusco, and Claudio Grassi. "High Fat Diet Multigenerationally Affects Hippocampal Neural Stem Cell Proliferation via Epigenetic Mechanisms." Cells 11, no. 17 (August 27, 2022): 2661. http://dx.doi.org/10.3390/cells11172661.
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Early-life metabolic stress has been demonstrated to affect brain development, persistently influence brain plasticity and to exert multigenerational effects on cognitive functions. However, the impact of an ancestor’s diet on the adult neurogenesis of their descendants has not yet been investigated. Here, we studied the effects of maternal high fat diet (HFD) on hippocampal adult neurogenesis and the proliferation of neural stem and progenitor cells (NSPCs) derived from the hippocampus of both the second and the third generations of progeny (F2HFD and F3HFD). Maternal HFD caused a multigenerational depletion of neurogenic niche in F2HFD and F3HFD mice. Moreover, NSPCs derived from HFD descendants showed altered expression of genes regulating stem cell proliferation and neurodifferentiation (i.e., Hes1, NeuroD1, Bdnf). Finally, ancestor HFD-related hyper-activation of both STAT3 and STAT5 induced enhancement of their binding on the regulatory sequences of Gfap gene and an epigenetic switch from permissive to repressive chromatin on the promoter of the NeuroD1 gene. Collectively, our data indicate that maternal HFD multigenerationally affects hippocampal adult neurogenesis via an epigenetic derangement of pro-neurogenic gene expression in NSPCs.
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Jia, Fei, Martine Ben Amar, Bernard Billoud, and Bénédicte Charrier. "Morphoelasticity in the development of brown alga Ectocarpus siliculosus : from cell rounding to branching." Journal of The Royal Society Interface 14, no. 127 (February 2017): 20160596. http://dx.doi.org/10.1098/rsif.2016.0596.
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A biomechanical model is proposed for the growth of the brown alga Ectocarpus siliculosus . Featuring ramified uniseriate filaments, this alga has two modes of growth: apical growth and intercalary growth with branching. Apical growth occurs upon the mitosis of a young cell at one extremity and leads to a new tip cell followed by a cylindrical cell, whereas branching mainly occurs when a cylindrical cell becomes rounded and swells, forming a spherical cell. Given the continuous interplay between cell growth and swelling, a poroelastic model combining osmotic pressure and volumetric growth is considered for the whole cell, cytoplasm and cell wall. The model recovers the morphogenetic transformations of mature cells: transformation of a cylindrical shape into spherical shape with a volumetric increase, and then lateral branching. Our simulations show that the poro-elastic model, including the Mooney–Rivlin approach for hyper-elastic materials, can correctly reproduce the observations. In particular, branching appears to be a plasticity effect due to the high level of tension created after the increase in volume of mature cells.
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Fujikawa, Yoshiko, Kazunari Tominaga, Fumio Tanaka, Mitsue Sogawa, Hirokazu Yamagami, Tetsuya Tanigawa, Masatsugu Shiba, et al. "Sa2059 Structural Plasticity of Colonic Glial Cells Enhanced by Acute Stress in Adulthood Was Associated With Colonic Hyper-Contraction in Maternally Separated Rats." Gastroenterology 144, no. 5 (May 2013): S—371. http://dx.doi.org/10.1016/s0016-5085(13)61368-2.
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Armijo, Enrique, George Edwards, Andrea Flores, Jorge Vera, Mohammad Shahnawaz, Fabio Moda, Cesar Gonzalez, Magdalena Sanhueza, and Claudio Soto. "Induced Pluripotent Stem Cell-Derived Neural Precursors Improve Memory, Synaptic and Pathological Abnormalities in a Mouse Model of Alzheimer’s Disease." Cells 10, no. 7 (July 16, 2021): 1802. http://dx.doi.org/10.3390/cells10071802.
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Alzheimer’s disease (AD) is the most common type of dementia in the elderly population. The disease is characterized by progressive memory loss, cerebral atrophy, extensive neuronal loss, synaptic alterations, brain inflammation, extracellular accumulation of amyloid-β (Aβ) plaques, and intracellular accumulation of hyper-phosphorylated tau (p-tau) protein. Many recent clinical trials have failed to show therapeutic benefit, likely because at the time in which patients exhibit clinical symptoms the brain is irreversibly damaged. In recent years, induced pluripotent stem cells (iPSCs) have been suggested as a promising cell therapy to recover brain functionality in neurodegenerative diseases such as AD. To evaluate the potential benefits of iPSCs on AD progression, we stereotaxically injected mouse iPSC-derived neural precursors (iPSC-NPCs) into the hippocampus of aged triple transgenic (3xTg-AD) mice harboring extensive pathological abnormalities typical of AD. Interestingly, iPSC-NPCs transplanted mice showed improved memory, synaptic plasticity, and reduced AD brain pathology, including a reduction of amyloid and tangles deposits. Our findings suggest that iPSC-NPCs might be a useful therapy that could produce benefit at the advanced clinical and pathological stages of AD.
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Tumminia, Andrea, Federica Vinciguerra, Miriam Parisi, and Lucia Frittitta. "Type 2 Diabetes Mellitus and Alzheimer’s Disease: Role of Insulin Signalling and Therapeutic Implications." International Journal of Molecular Sciences 19, no. 11 (October 24, 2018): 3306. http://dx.doi.org/10.3390/ijms19113306.
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In the last two decades, numerous in vitro studies demonstrated that insulin receptors and theirs downstream pathways are widely distributed throughout the brain. This evidence has proven that; at variance with previous believes; insulin/insulin-like-growth-factor (IGF) signalling plays a crucial role in the regulation of different central nervous system (CNS) tasks. The most important of these functions include: synaptic formation; neuronal plasticity; learning; memory; neuronal stem cell activation; neurite growth and repair. Therefore; dysfunction at different levels of insulin signalling and metabolism can contribute to the development of a number of brain disorders. Growing evidences demonstrate a close relationship between Type 2 Diabetes Mellitus (T2DM) and neurodegenerative disorders such as Alzheimer’s disease. They, in fact, share many pathophysiological characteristics comprising impaired insulin sensitivity, amyloid β accumulation, tau hyper-phosphorylation, brain vasculopathy, inflammation and oxidative stress. In this article, we will review the clinical and experimental evidences linking insulin resistance, T2DM and neurodegeneration, with the objective to specifically focus on insulin signalling-related mechanisms. We will also evaluate the pharmacological strategies targeting T2DM as potential therapeutic tools in patients with cognitive impairment.
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Hussain, M. Iftikhar, François Mitterand tsombou, and Ali El-Keblawy. "Surface Canopy Position Determines the Photosystem II Photochemistry in Invasive and Native Prosopis Congeners at Sharjah Desert, UAE." Forests 11, no. 7 (July 8, 2020): 740. http://dx.doi.org/10.3390/f11070740.
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Plants have evolved photoprotective mechanisms in order to counteract the damaging effects of excess light in hyper-arid desert environments. We evaluated the impact of surface canopy positions on the photosynthetic adjustments and chlorophyll fluorescence attributes (photosystem II photochemistry, quantum yield, fluorescence quenching, and photon energy dissipation), leaf biomass and nutrient content of sun-exposed leaves at the south east (SE canopy position) and shaded-leaves at the north west (NW canopy position) in the invasive Prosopis juliflora and native Prosopis cineraria in the extreme environment (hyper-arid desert area, United Arab Emirates (UAE)). The main aim of this research was to study the photoprotection mechanism in invasive and native Prosopis congeners via the safe removal—as thermal energy—of excess solar energy absorbed by the light collecting system, which counteracts the formation of reactive oxygen species. Maximum photosynthetic efficiency (Fv/Fm) from dark-adapted leaves in P. juliflora and P. cineraria was higher on NW than SE canopy position while insignificant difference was observed within the two Prosopis congeners. Greater quantum yield was observed in P. juliflora than P. cineraria on the NW canopy position than SE. With the change of canopy positions from NW to SE, the reduction of the PSII reaction center activity in the leaves of both Prosopis congeners was accelerated. On the SE canopy position, a significant decline in the electron transport rate (ETR) of in the leaves of both Prosopis congeners occurred, which might be due to the blockage of electron transfer from QA to QB on the PSII acceptor side. On the SE canopy position; Prosopis leaves dissipated excess light energy by increasing non-photochemical quenching (NPQ). However, in P. cineraria, the protective ability of NPQ decreased, which led to the accumulation of excess excitation energy (1 − qP)/NPQ and the aggravation of photoinhibition. The results also explain the role of different physiological attributes contributing to invasiveness of P. juliflora and to evaluate its liaison between plasticity of these characters and invasiveness.
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Flores, Fernando G. "A Two-Dimensional Linear Assumed Strain Triangular Element for Finite Deformation Analysis." Journal of Applied Mechanics 73, no. 6 (December 19, 2005): 970–76. http://dx.doi.org/10.1115/1.2173674.
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An assumed strain approach for a linear triangular element able to handle finite deformation problems is presented in this paper. The element is based on a total Lagrangian formulation and its geometry is defined by three nodes with only translational degrees of freedom. The strains are computed from the metric tensor, which is interpolated linearly from the values obtained at the mid-side points of the element. The evaluation of the gradient at each side of the triangle is made resorting to the geometry of the adjacent elements, leading to a four element patch. The approach is then nonconforming, nevertheless the element passes the patch test. To deal with plasticity at finite deformations a logarithmic stress-strain pair is used where an additive decomposition of elastic and plastic strains is adopted. A hyper-elastic model for the elastic linear stress-strain relation and an isotropic quadratic yield function (Mises) for the plastic part are considered. The element has been implemented in two finite element codes: an implicit static/dynamic program for moderately non-linear problems and an explicit dynamic code for problems with strong nonlinearities. Several examples are shown to assess the behavior of the present element in linear plane stress states and non-linear plane strain states as well as in axi-symmetric problems.
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Bottjer, Sarah W. "Silent Synapses in a Thalamo-Cortical Circuit Necessary for Song Learning in Zebra Finches." Journal of Neurophysiology 94, no. 6 (December 2005): 3698–707. http://dx.doi.org/10.1152/jn.00282.2005.
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Developmental changes in synaptic properties may act to limit neural and behavioral plasticity associated with sensitive periods. This study characterized synaptic maturation in a glutamatergic thalamo-cortical pathway that is necessary for vocal learning in songbirds. Lesions of the projection from medial dorsolateral nucleus of the thalamus (DLM) to the cortical nucleus lateral magnocellular nucleus of the anterior nidopallium (LMAN) greatly disrupt song behavior in juvenile birds during early stages of vocal learning. However, such lesions lose the ability to disrupt vocal behavior in normal birds at 60–70 days of age, around the time that selective auditory tuning for each bird’s own song (BOS) emerges in LMAN neurons. This pattern has suggested that LMAN is involved in processing song-related information and evaluating the degree to which vocal motor output matches the tutor song to be learned. Analysis of reversed excitatory postsynaptic currents at DLM→LMAN synapses in in vitro slice preparations revealed a pronounced N-methyl-d-aspartate receptor (NMDAR)-mediated component in both juvenile and adult cells with no developmental decrease in the relative contribution of NMDARs to synaptic transmission. However, the synaptic failure rate at DLM→LMAN synapses in juvenile males during the sensitive period for song learning was significantly lower at depolarized potentials than at hyperpolarized potentials. In contrast, the failure rate at DLM→LMAN synapses did not differ at hyper- versus depolarized holding potentials in adult males that had completed the acquisition of a stereotyped song. This pattern indicates that juvenile cells have a higher incidence of silent (NMDAR-only) synapses, which are postsynaptically silent at hyperpolarized potentials due to the voltage-dependent gating of NMDARs. Thus the decreased involvement of the LMAN pathway in vocal behavior is mirrored by a decline in the incidence of silent synapses but not by changes in the relative number of NMDA and AMPA receptors at DLM→LMAN synapses. These findings suggest that a developmental decrease in silent synapses within LMAN may represent a neural correlate of behavioral plasticity during song learning.
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Xie, Qiang, Xiaoxuan Tian, Yan Qin, and Wenjun Bu. "Phylogenetic comparison of local length plasticity of the small subunit of nuclear rDNAs among all Hexapoda orders and the impact of hyper-length-variation on alignment." Molecular Phylogenetics and Evolution 50, no. 2 (February 2009): 310–16. http://dx.doi.org/10.1016/j.ympev.2008.10.025.
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Fedi, Marco, Shi Hong Shen, Bruce Campbell, Mathias Dutschmann, Terrence O’brien, James Anstey, and Christopher MacIsaac. "101 Dispelling the curse: improvement of ventilatory drive in central alveolar hypoventilation syndrome after medullary infarction." Journal of Neurology, Neurosurgery & Psychiatry 89, no. 6 (May 24, 2018): A40.1—A40. http://dx.doi.org/10.1136/jnnp-2018-anzan.100.
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IntroductionCentral alveolar hypoventilation syndrome (CAHS) is a rare complication of stroke affecting the medullary respiratory centre. CAHS is characterised by impaired ventilatory response to CO2 leading to hypoventilation, hyper-capnoea and coma. Experimental studies have linked this syndrome to areas in the dorsal and ventrolateral medulla. CAHS is associated with long-term invasive ventilatory support, high mortality and morbidity. It is unclear whether sensitivity to CO2 can improve after the initial ischaemic medullary insult.CaseA 78 year old woman presenting with CAHS secondary to a unilateral left posterior inferior cerebellar artery infarction. MRI images confirmed that dorsal and ventrolateral medullary areas were affected. The patient was intubated initially for hyper-capnoeic respiratory failure and required a tracheostomy for ongoing respiratory support. To assess progress of respiratory recovery, we measured the patient’s ventilatory response to PaCO2 at 5, 7, and 14 days of admission. Parameters recorded included PaO2, ETCO2, PaCO2, pH, respiratory rate, and minute ventilation. During this time the patient underwent progressive periods of unsupported ventilation with close monitoring. Statistical correlation between respiratory rate and CO2 was measured by Pearson’s correlation coefficient (R). Her RR initially did not increase with PaCO2 during spontaneous ventilation (R=0.2604 p=0.077). Apnoeic episodes were frequent up to 41 episodes per 30 min of observation lasting up to 30 s. On day 7(R=0.7203 p<0.05) and up to day 14 (R=0.6295 p<0.05), there was a progressive statistically significant improvement in positive correlation between PCO2 and respiratory rate. This was associated with a reduction in apnoeic episodes possibly reflecting a recovery in ventilatory drive.ConclusionThis is the first detailed report demonstrating spontaneous recovery in CO2 responsiveness in the setting of CAHS secondary to unilateral medullary stroke. Plasticity of structures such as the retro-trapezoid nucleus are likely to play a role in recovery of CO2 sensitivity.References. Harper, et al. Functional neuroanatomy and sleep-disordered breathing: implications for autonomic regulation. Anatomical record2012;295(9):1385–95.. Mishina, et al. Efficacy of tracheostomy for central alveolar hypoventilation syndrome caused by lateral medullary infarction. Journal of Nippon Medical School2014;81(4):276–84.
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denDekker, Aaron, Frank Davis, Andrew Kimball, Matthew Schaller, Amrita Joshi, Ronald Allen, and Katherine Gallagher. "55270 The Histone Methyltransferase SETDB2 Regulates Inflammation in Normal and Diabetic Wound Repair." Journal of Clinical and Translational Science 5, s1 (March 2021): 15. http://dx.doi.org/10.1017/cts.2021.441.
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ABSTRACT IMPACT: Our data reveal a histone modifying enzyme involved in regulating inflammation that may be a novel target for treating non-healing diabetic wounds. OBJECTIVES/GOALS: We investigate molecular mechanisms that regulate the inflammatory phenotype of macrophages in normal and diabetic wound healing. Our goal is to identify novel pathways that may be used to better treat diabetic patients with non-healing wounds. METHODS/STUDY POPULATION: We utilize normal and transgenic murine models on standard chow or high-diet to identify chromatin modifying enzymes involved in regulating macrophage function during wound healing. We validate our murine studies with human blood monocytes or wound macrophages from diabetic patients undergoing limb amputation surgery. RESULTS/ANTICIPATED RESULTS: We have identified the histone methyltransferase SETDB2 as a regulator inflammation in normal and diabetic wound macrophages. We found that SETDB2 was dependent on IFNβ singaling and that both IFNβ and Setdb2 expression were impaired in diabetic wound macrophages. Further, we show that SETDB2 regulates inflammatory response and immune cell trafficking pathways. We also show that SETDB2 genomic localization is dependent on *NFκΒ deposition of the promoter. DISCUSSION/SIGNIFICANCE OF FINDINGS: Our results indicate that SETDB2 is a regulator of macrophage plasticity and that SETDB2 expression is impaired in diabetic wound macrophages leading to hyper-inflammatory response and delayed wound healing. These data provide a novel potential therapeutic pathway for treating non-healing diabetic wounds.
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Mititelu, A. "Sleep-memory-plasticity:A circuit closed by Gaba?" European Psychiatry 26, S2 (March 2011): 1262. http://dx.doi.org/10.1016/s0924-9338(11)72967-4.
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It is already widely known that benzodiazepines, the most prolific compound for pharma industry, are the most used psychotropic medication used at moment. It is striking that even now, after more than 50 yrs from first use of Diazepam, still exerts such a massive interest. Both mechanism, of dependence and withdrawn are not still unknown. Benzodiazepines by their structure and sites of action upon GABA receptors realise a huge effect in majority of neuronal circuits.ObjectivesThe effect of BDZ in mood and affective disorders and also in major psychotic sdr-Schizophrenia realise an reduction of hyper GABA influence. acting on specific neuronal populations which posses particularly alpha 5 GABAa receptors they produce sedative but non anxiolytic effect. Also is still an “mistery” how only retrograde amnesia is produced and why plasticiticity occurs after a longtime use of BDZ facilitating the development of tolerance.AimsBy a better intimate description of mechanisms by which GABAa receptors realise the sedative action and development of less side effects comparing with actual BDZ in use, even from different classes.MethodsIn this communication we had realised a thematical analysis of all studies (randomised clinical trials, clinical case study) but also various experimental research with this subjects-sleep, memory, plasticity. All had been indexed in PubMed, EMBASE, www.ionchannels.com and Science Direct.ResultsThe conclusion of our tematical study and also, our previous research suggests antagonists of GABA a or agonists of beta carbolines could be proven solid point of start for more efficient therapeutic substances.
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Gaiti, Federico, Ronan Chaligne, Dana Silverbush, Joshua Schiffman, Hannah Weisman, lloyd Kluegel, Simon Gritsch, et al. "EPCO-14. DECIPHERING DIFFERENTIATION HIERARCHIES, HERITABILITY AND PLASTICITY IN HUMAN GLIOMAS VIA SINGLE-CELL MULTI-OMICS." Neuro-Oncology 22, Supplement_2 (November 2020): ii72. http://dx.doi.org/10.1093/neuonc/noaa215.293.
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Abstract Human diffuse gliomas are incurable malignancies, where cellular state diversity fuels tumor progression and resistance to therapy. Single-cell RNA-sequencing (scRNAseq) studies recently charted the cellular states of the two major categories of human gliomas, IDH-mutant gliomas (IDH-MUT) and IDH-wildtype glioblastoma (GBM), showing that malignant cells partly recapitulate neurodevelopmental trajectories. This raises the central questions of how cell states are encoded epigenetically and whether unidirectional hierarchies or more plastic state transitions govern glioma cellular architectures. To address these questions, we generated multi-omics single-cell profiling, integrating DNA methylation (DNAme), transcriptome and genotyping of 1,728 cells from 11 GBM and IDH-MUT primary patient samples. Direct comparison of the methylomes of distinct glioma cell states revealed Polycomb repressive complex 2 (PRC2) targets DNAme as a key switch in the differentiation of malignant GBM cells. In contrast, dissecting aberrant circuits of hyper-methylation and gene expression in IDH-MUT gliomas, we observed a decoupling of the promoter methylation-expression relationship, with disruption of CTCF insulation and enhancer vulnerability which increases with cellular differentiation. To define cell state transition dynamics directly in patient samples, we generated high-resolution lineage histories of glioma cells using heritable DNAme changes, and projected the scRNAseq-derived cell states onto the lineage trees. This analysis demonstrated that cell states are heritable across malignant gliomas and, while in IDH-MUT differentiation far outpaces de-differentiation, GBM harbors a higher degree of cell state plasticity allowing reversion of GBM cells from a differentiated to a stem-like state. Overall, our work provides detailed insights into gliomagenesis, dissecting the epigenetic encoding, regulatory programs, and dynamics of the cellular states that drive human gliomas. Importantly, it also carries significant translational implication, as the high degree of de-differentiation in GBM challenges the paradigm of therapeutically targeting glioma stem-like cells to deprive tumors of their ability to regenerate.
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Dehghani, Reihaneh, Farzaneh Rahmani, and Nima Rezaei. "MicroRNA in Alzheimer’s disease revisited: implications for major neuropathological mechanisms." Reviews in the Neurosciences 29, no. 2 (February 23, 2018): 161–82. http://dx.doi.org/10.1515/revneuro-2017-0042.
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AbstractPathology of Alzheimer’s disease (AD) goes far beyond neurotoxicity resulting from extracellular deposition of amyloid β (Aβ) plaques. Aberrant cleavage of amyloid precursor protein and accumulation of Aβ in the form of the plaque or neurofibrillary tangles are the known primary culprits of AD pathogenesis and target for various regulatory mechanisms. Hyper-phosphorylation of tau, a major component of neurofibrillary tangles, precipitates its aggregation and prevents its clearance. Lipid particles, apolipoproteins and lipoprotein receptors can act in favor or against Aβ and tau accumulation by altering neural membrane characteristics or dynamics of transport across the blood-brain barrier. Lipids also alter the oxidative/anti-oxidative milieu of the central nervous system (CNS). Irregular cell cycle regulation, mitochondrial stress and apoptosis, which follow both, are also implicated in AD-related neuronal loss. Dysfunction in synaptic transmission and loss of neural plasticity contribute to AD. Neuroinflammation is a final trail for many of the pathologic mechanisms while playing an active role in initiation of AD pathology. Alterations in the expression of microRNAs (miRNAs) in AD and their relevance to AD pathology have long been a focus of interest. Herein we focused on the precise pathomechanisms of AD in which miRNAs were implicated. We performed literature search through PubMed and Scopus using the search term: (‘Alzheimer Disease’) OR (‘Alzheimer’s Disease’) AND (‘microRNAs’ OR ‘miRNA’ OR ‘MiR’) to reach for relevant articles. We show how a limited number of common dysregulated pathways and abnormal mechanisms are affected by various types of miRNAs in AD brain.
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Akkawi, Paula, Nacho Villar, Calebe P. Mendes, and Mauro Galetti. "Dominance hierarchy on palm resource partitioning among Neotropical frugivorous mammals." Journal of Mammalogy 101, no. 3 (May 18, 2020): 697–709. http://dx.doi.org/10.1093/jmammal/gyaa052.
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Abstract In tropical forests, the diets of many frugivorous mammals overlap, yet how hyper-diverse assemblages of consumers exploit resources and coexist remains poorly understood. We evaluated competitive interactions among three species of terrestrial frugivorous mammals, the ungulate Tayassu pecari (white-lipped peccary), its close relative Pecari tajacu (collared peccary), and a large rodent (Dasyprocta azarae, agouti), in their exploitation strategies of palm resources of different quality. We conducted the study in a large isolated fragment at the tropical Atlantic Forest of Brazil, where these mammal species show high spatial and temporal overlap. We evaluated if body mass and foraging group size define a hierarchy in exploitation of preferentially richer palm resources. We used camera traps and two-species occupancy models to examine patterns of co-occurrence and variable interaction strength between these consumers and three species of palms. Our analyses supported the hypothesis of partial resource overlap but no competition among frugivores, and a body mass dominance hierarchical exploitation of resources. The larger frugivore (white-lipped peccary) dominated patches of the lipid-rich palm Euterpe edulis, where the smallest frugivore (agouti) was absent. Instead, the smallest frugivore concentrated its foraging in areas with the poorest palm resource, Syagrus oleracea. Collared peccaries preferred areas of high abundance of Syagrus romanzoffiana when the other two mammal species were rarely detected or absent, strongly avoided patches of E. edulis, and showed higher average detection probabilities when agoutis were present. Our study highlights the important role of behavioral plasticity in promoting coexistence and indicates that through context-dependent interactions and hierarchical partitioning of resources, consumers can avoid strong competition, even under conditions of high spatial and temporal overlap and high levels of habitat fragmentation and isolation.
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Ruan, Hang, Jian Peng, Ye Chen, Silu He, Zhenshi Zhang, and Haifeng Li. "A Class-Incremental Detection Method of Remote Sensing Images Based on Selective Distillation." Symmetry 14, no. 10 (October 9, 2022): 2100. http://dx.doi.org/10.3390/sym14102100.
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With the rapid development of remote sensing technology and the growing demand for applications, the classical deep learning-based object detection model is bottlenecked in processing incremental data, especially in the increasing classes of detected objects. It requires models to sequentially learn new classes of objects based on the current model, while preserving old categories-related knowledge. Existing class-incremental detection methods achieve this goal mainly by constraining the optimization trajectory in the feature of output space. However, these works neglect the case where the previously learned background is a new category to learn, resulting in performance degradation in the new category because of the conflict between remaining the background-related knowledge or updating the background-related knowledge. This paper proposes a novel class-incremental detection method incorporated with the teacher-student architecture and the selective distillation (SDCID) strategy. Specifically, it is the asymmetry architecture, i.e., the teacher network temporarily stores historical knowledge of previously learned objects, and the student network integrates historical knowledge from the teacher network with the newly learned object-related knowledge, respectively. This asymmetry architecture reveals the significance of the distinct representation of history knowledge and new knowledge in incremental detection. Furthermore, SDCID selectively masks the shared subobject of new images to learn and previously learned background, while learning new categories of images and then transfers the classification results of the student model to the background class following the judgment model of the teacher model. This manner avoids interferences between the background category-related knowledge from a teacher model and the learning of other new classes of objects. In addition, we proposed a new incremental learning evaluation metric, C-SP, to comprehensively evaluate the incremental learning stability and plasticity performance. We verified the proposed method on two object detection datasets of remote sensing images, i.e., DIOR and DOTA. The experience results in accuracy and C-SP suggest that the proposed method surpasses existing class-incremental detection methods. We further analyzed the influence of the mask component in our method and the hyper-parameters sensitive to our method.
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Meier, Sarah K., Kimberly L. Ray, Noah C. Waller, Barry C. Gendron, Semra A. Aytur, and Donald A. Robin. "Network Analysis of Induced Neural Plasticity Post-Acceptance and Commitment Therapy for Chronic Pain." Brain Sciences 11, no. 1 (December 23, 2020): 10. http://dx.doi.org/10.3390/brainsci11010010.
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Chronic musculoskeletal pain is a costly and prevalent condition that affects the lives of over 50 million individuals in the United States. Chronic pain leads to functional brain changes in those suffering from the condition. Not only does the primary pain network transform as the condition changes from acute to persistent pain, a state of hyper-connectivity also exists between the default mode, frontoparietal, and salience networks. Graph theory analysis has recently been used to investigate treatment-driven brain network changes. For example, current research suggests that Acceptance and Commitment Therapy (ACT) may reduce the chronic pain associated hyper-connectivity between the default mode, frontoparietal, and salience networks, as well as within the salience network. This study extended previous work by examining the associations between the three networks above and a meta-analytically derived pain network. Results indicate decreased connectivity within the pain network (including left putamen, right insula, left insula, and right thalamus) in addition to triple network connectivity changes after the four-week Acceptance and Commitment Therapy intervention.
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Chretien, Marie-Lorraine, Romain Aucagne, Nathalie Droin, Arlette Hammann, Eric Solary, Jean-Noël Bastie, and Laurent Delva. "Tif1gamma Is Essential for Macrophage Differentiation." Blood 118, no. 21 (November 18, 2011): 2370. http://dx.doi.org/10.1182/blood.v118.21.2370.2370.
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Abstract Abstract 2370 TIF1gamma (or TRIM33) is an ubiquitous nuclear protein that belongs to the transcriptional intermediary factor 1 family. Human and mouse TIF1gamma are closely related to zebrafish moonshine (mon), a gene whose mutations disrupt embryonic and adult hematopoiesis with severe red blood cell aplasia. Targeted deletion of Tif1gamma is embryonic lethal in mice. In zebrafish and human CD34+ cells, TIF1gamma functionally links positive elongation factors such as p-TEFb and FACT to blood specific transcription complexes (e.g. the SCL/TAL1 complex) to regulate elongation of genes by antagonizing Pol II pausing. TIF1gamma also affects the human hematopoietic progenitor cell response to the cytokines of the transforming growth factor-beta superfamily through various mechanisms. Recently, we showed that the loss of Tif1gamma in mouse hematopoietic stem cells (cFES-Cre-Tif1gamma) favors the expansion of the granulo-monocytic progenitor compartment. The gene deletion induces the age-dependent appearance of a cell-autonomous myeloproliferative disorder with myelodysplastic features, monocytosis, and hepatosplenomegaly that recapitulates essential features of human chronic myelomonocytic leukemia (CMML). Interestingly, TIF1gamma is almost undetectable in leukemic cells of 35% of patients with CMML. This down-regulation is related to the hyper-methylation of CpG sequences in the gene promoter. Our results demonstrated that TIF1gamma is an epigenetically regulated tumor suppressor gene in hematopoietic cells. In addition, an altered production of peritoneal macrophages was observed in our mouse model. These macrophages did not adhere to the plastic and were morphologically abnormal in vitro. In bone marrow and in Lin- progenitor cells, Tif1gamma deletion leads to a significant decrease of cfms (Csf-1r) expression, required for the differentiation, proliferation, and survival of monocytic phagocytes. We also identified in CMML patients the association between low levels of TIF1gamma and cFMS (Aucagne et al., J. Clin. Invest., 121, 2361–2370, 2011). To gain insight into the possible mechanism accounting for diminished accumulation of macrophages, we examined the expression of c-Fms. We show that level of its expression is reduced significantly in blood monocytes isolated from Tif1gamma-deleted mice. When Tif1gamma-deleted sorted myeloid cells were induced to differentiate into macrophages in presence of CSF-1, a delayed production of few abnormal large macrophages was observed. Apoptosis was associated with this alteration of differentiation. This phenomenon was also characterized in young mice not developing the disease yet. The morphological abnormalities were correlated with very important alterations of specific macrophage differentiation markers. Expression of specific transcription factors involved in macrophage differentiation was deeply deregulated. Moreover, macrophage function such as migration, cytokine or chemokine secretion in response to LPS was altered. Likewise, in vitro differentiation of monocytes into dendritic cells was also abnormal. Altogether, our results suggest that monocyte plasticity is at least partially orchestrated by Tif1gamma. Disclosures: No relevant conflicts of interest to declare.
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Khasanov, Bakhridin, Alisher Tillaev, and Timur Mirzaev. "Compressive strength properties of hyper-compacted concrete." E3S Web of Conferences 264 (2021): 02060. http://dx.doi.org/10.1051/e3sconf/202126402060.
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The most important property of a concrete mix is concrete workability, i.e., the ability of the mixture to spread and take a given form while maintaining solidity and uniformity. The main influence on the workability of the concrete mixture is exerted by water consumption and, in part, cement consumption. Workability is determined by the mobility of the concrete mixture at the time of filling the mold and plasticity, i.e., the ability to deform without breaking the continuity. In the process of vibrating and pressing the concrete mixture placed in the mold, the total volume of the mixture changes until the pressure is balanced by the resistance forces. Deformation of concrete mix or, more precisely, freshly laid concrete with any compaction methods, including vibration compaction, is divided into elastic (reversible) and residual (irreversible). Residual deformations during vibration compaction occur as a result of water squeezing out and redistribution of aggregate fractions. Permanent deformation is part of the total. Its value at the same composition of the concrete mixture depends on the shape and size of the pressed sample. At the same time, it is noteworthy that after reaching a certain pressure, only elastic deformations will be characteristic of the freshly laid concrete mixture. So, A.D. Nikitin, in the course of the experiments, found that at a pressure of 2.2 MPa, the elastic moduli of the components of the concrete mixture have the following values: for cement paste - 0.16 · 104 MPa, aggregate - 4.5 · 104 MPa and air - 3 MPa ... After reaching a static pressure of 2.2 MPa, the compressible mixture showed only elastic deformation. This indicates that by the time the specified pressure was reached, the relative movement of the aggregates had ended, i.e., they are located most compactly.
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Гундарова, O. Gundarova, Федоров, V. Fedorov, Сгибнева, N. Sgibneva, Маслов, and N. Maslov. "The Neuronal Plasticity of Sensorimotor Cortex in the Conditions of Increased Background Radiation." Medical Radiology and radiation safety 62, no. 1 (February 26, 2017): 20–26. http://dx.doi.org/10.12737/25044.
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Purpose: Observe the changes in the structural and functional organization of the sensomotor cortex neurons throughout the post-radiation period. Material and methods: White male rats (120 animals) were irradiated on the “Hizatron» γ-rays 60Co single dose of 0.5 Gy with a dose rate of 0.5 Gy/h. Material taken away by 100 min; 5 hr; 1, 3, 7 and 14 days, 1, 6, 12 and 18 months after irradiation. Counted the number of neurons with different tinctorial properties, was calculated the nerve cell index, morphometric characteristics of nerve cells and content of nucleic acids. The obtained data were statistically processed, followed by mathematical modeling. Results: By the end of the post-radiation period the number of normochromic neurons decreased due to increasing the number of hyper- and hypochromic cells, as well as their destructive forms. In animals as the control and exposed groups values nerve-cell index decrease with age. In control and exposed groups of rats values nerve-cell index decrease with age. The dynamics of the cytoplasm shows a negative correlation with an index of the contents of cytoplasmic RNA. By the end of the experiment the content of RNA in the cytoplasm of neurons corresponded to the age control. Profile index of nuclear DNA in all periods of post-radiation is negatively correlated with cross-sectional area of the nuclei. The amplitude of fluctuations in the size of nucleoli of neurons was significantly greater than the corresponding figure in the cytoplasm and nuclei. In the period from 6 to 18 months post-radiation period RNA content in the nucleolus had a positive correlation with the index size. Immediately after the exposure indicator nucleocytoplasmic index exceeded the reference values, subsequently decreased, and by the end of postradiation period – almost matched up to it. Nucleolus-nuclear index immediately after irradiation not changed, in subsequent periods had a phase-change, but at 18 months matched to age-control. Conclusion: Research has shown that neuromorphological effects were nonlinear stochastic nature, and exposure to these parameters had no significant effect on neurons. However, some indicators are not always consistent with the age-control, which could affect their functional activity.
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Chatterjee, Shankha Subhra, Mayukh Biswas, Liberalis Debraj Boila, Sayan Chakraborty, Sayantani Sinha, Debasis Banerjee, and Amitava Sengupta. "UTX and MBD3 Epistasis Regulates Rac Gtpase Activation and Sensitizes Human Acute Myeloid Leukemia Cells to Dock Inhibition." Blood 132, Supplement 1 (November 29, 2018): 3880. http://dx.doi.org/10.1182/blood-2018-99-113843.
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Abstract Transcriptional plasticity is an evolving phenomenon in cancer biology. Mutational profiling alone may not suffice to dissect transcriptional dependency and underlying epigenetic vulnerabilities in tumorigenesis. Histone 3 lysine 27 (H3K27) demethylases (UTX, UTY and JMJD3) critically regulate transcriptional architecture. Recently it has been demonstrated that Utx (Kdm6a) plays tumor suppressor role in myeloid leukemogenesis through noncatalytic activity (Gozdecka M, et al., Nat Genet, 2018). Conditional (Mx1-Cre) deletion of Utx caused development of acute myeloid leukemia (AML) in ~ 60% of the mice; wherein, only Utx-/-, but not Utx+/-, aged (22 months) mice presented with AML. Paradoxically, previous report suggested that Utx conditional (Vav1-Cre) knock out male/female mice did not develop leukemia over 18 months (Tian, L., et al., Blood, 2015). In our recent report we have identified that expression of UTX is significantly increased in human primary AML, and pharmacological inhibition of H3K27 demethylase catalytic activity attenuated survival of AML cells (Boila L.D. et al,. Exp Hematol, 2017). Therefore the contribution of UTX in AML pathogenesis remains context dependent, and probably contentious, and warrants further investigations. ATP-dependent chromatin remodelers have been implicated in AML pathobiology (Chatterjee S.S., et al., Mol Cancer Res, 2018). We reported that loss of MBD3, a scaffold of NuRD chromatin remodeler, in human primary AML cells associates with nucleation of leukemic NuRD (Biswas M et al., Blood, 2017). Loss of Mbd3(Vav1-Cre) has been shown to disrupt NuRD complex integrity and causes T-cell lymphoma, suggesting tissue-specific function of NuRD (Loughran, S.J., et al., J Exp Med, 2017). Interestingly, in our present study we have identified for the first time that endogenous UTX, but not JMJD3, reversibly co-immunoprecipitates with NuRD in AML cells. These findings led us to test the hypothesis whether UTX would participate with NuRD in AML. ChIP-seq analysis in AML blasts using antibodies against UTX and CHD4 (intact ATPase component of leukemic NuRD) along with H3K27ac identified the co-localized genes. ChIP-qPCR, transcriptome, pathway analysis (P<0.001) performed in paired AML, and MBD3loss of function experiments suggested an enrichment of Dedicator of Cytokinesis (DOCK) transcripts as bona fide effectors of UTX and NuRD in AML. DOCK proteins are conserved atypical guanine nucleotide exchange factors (GEFs) for Rho GTPase activation, regulating cell motility and invasion. Earlier we had shown that small GTPases regulate myeloid leukemia cell engraftment, survival in vivo (Sengupta A et al., Blood, 2010). DOCK1 upregulation is associated with a poor prognosis in AML (Hwei, L.S., Blood, 2016). TCGA cross-cancer analysis showed that UTX is maximally expressed, whereas MBD3 is downregulated in AML among all cancer types. Consistent with this observation, DOCK expression was significantly (P<0.001) increased in MBD3loUTXhi AML cohort compared to MBD3hiUTXlo AML. Importantly, MBD3loUTXhi patients have relatively poor survival compared to MBD3hiUTXhi individuals, indicating that a combination of high UTX and low MBD3 expression could be a marker of poor prognosis in AML. Mechanistically, MBD3 deficiency caused loss of HDAC1 occupancy with a corresponding increase in UTX, CBP and H3K27ac on target DOCK loci leading to de-repression of gene expression. In agreement with this finding, loss of MBD3 resulted in ~ 2-fold increase in active Rac GTP and promoted AML cell migration to CXCL12. Interestingly, UTX silencing opposed DOCK expression, Rac activation and reversed hyper-migratory phenotype of MBD3-deficient AML cells. Together, these data account for UTX and MBD3 epistasis in regulating DOCK-Rac signalling in AML. Finally, treatment with DOCK inhibitor CPYPP dramatically inhibited survival of AML cells while having minimal effect on the survival of normal CD34+ cells. In unison, our findings highlight UTX as a putative oncogene in conjunction with leukemic NuRDand posit DOCK proteins as an important target of UTX-NuRD axis in human AML cells. To conclude, we provide evidence for MBD3-deficient NuRD in leukemia pathobiology, and inform a novel epistasis between UTX and NuRD towards maintenance of oncogenic gene expression in AML, and rationalize DOCK inhibition as a novel therapeutic modality for precision medicine in AML. Disclosures No relevant conflicts of interest to declare.
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Neri, Paola, Ines Tagoug, Ranjan Maity, Jacquelyn Babich, Lindsay Lockwood, Jonathan J. Keats, Larry H. Boise, Leif Bergsagel, and Nizar J. Bahlis. "IKZF1 Regulates BRD4 Retention and Recruitement at Enhancer in Myeloma Cells: Role of BRD4 in IMiDs Resistance." Blood 128, no. 22 (December 2, 2016): 358. http://dx.doi.org/10.1182/blood.v128.22.358.358.
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Abstract Background: MYC rearrangement is a recurrent somatic event in MM and results in super-enhancers repositioning within 3Kb (centromeric or telomeric) of the MYC locus. BRD4, a member of the bromodomain family, binds H3K27Ac and regulates enhancers activity, RNA polymerase II transcription initiation and elongation and in particular it regulates MYC transcription in MM cells. Immunomodulatory drugs (IMiDs) promote the proteasomal degradation of IKZF1/3 and the transcriptional repression of MYC and IRF4. However the exact mechanisms through which IMiDs downregulate MYC are not well understood. Methods and Results: Using a extended panel of 12 MM cell lines we have first confirmed our previous observartion that IMIDs universally degraded IKZF1/3, however unlike in IMiDs-sensitive cell lines it failed to downregulate MYC in resistant cells. Therefore, this finding suggests that MYC transcriptional regulation rather than IKF1/3 degradation is the "bottleneck" in IMiDs anti-myeloma activity or resistance. In addition, RNA-seq of paired and serially collected primary myeloma cells with acquired resistance to IMIDsconfirmed the enrichment of genes signatures associated with MYC at the time of acquired resistance. Of note, in a library of t(4;14) MM cell lines lenalidomide significantly downregulates FGFR3 while the expression of WHSC1 was not affected. As in t(4;14) cells FGFR3 is driven by the 3' IGH enhancer while WHSC1 is under the control of the intronic Em enhancer, and in view of the known role of IKZF1 in CSR, we posit that IKZF1 regulates plasma cells enhancer activity and hence MYC expression. To validate this hypothesis we first established the genome-wide distribution of IKZF1 in MM1S, RPMI8226 and OPM2 cells by ChIP-Seq. This analysis revealed the distribution of IKZF1 across the genome, predominantly to intronic an intragenic loci with only ~ 8% or reads mapping within +/- 5 kb of genes TSS. Importantly IKZF1 was also enriched at known myeloma cells enhancers or super-enhancers such as IGLL5, TXNDC5, BCL2L1, and DUSP22. We also mapped BRD4 binding to the genome in 8226 and MM1S cell lines and confirmed previously described mapping to known B-cell enhancers. Of note IKZF1 nearly universally overlapped with all BRD4 enhancers and superenhancers loci. These findings lead us to propose that IKZF1 depletion in response to IMiDs treatment will result in enhancer destabilization and displacement of BRD4 from enhancer loci. Indeed, Chip-Seq analysis of IKZF1 and BRD4 genomic distribution pre- and post- treatment with lenalidomide (10 uM for 4 or 8h) in IMiDs sensitive cell lines significantly depleted IKZF1 and BRD4 at superenhancer loci. In contrast, in IMiDs resistant cell lines (RPMI8226) and despite IKZF1 depletion, BRD4 was largely retained at these loci. These findings suggest that in IMiDs sensitive cells, IKZF1 is the major transcription factor mediating BRD4 recruitment to enhancer and superenhancer loci. In contrast, in IMiDs resistant cells and similar to BET-bromodomain inhibitor (JQ1) resistance, transcriptional plasticity or hyper-phosphorylation of BRD4 attributable to the phosphatase PP2A inactivation may also be mediating IMiDs resistance. Indeed the levels of p-BRD4 determined by western blotting were significantly higher in IMiDs resistant INA6 and RPMI8226 cells compared to MM1S cells. Furthermore, treatment of INA6 cells with the PP2A activator phenothiazine significantly sensitized INA6 cells to lenalidomide. Lastly, in order to investigate whether IMiDs resistance was associated with acquired new MYC rearrangements with an "IKZF1_resisant enhancer," we performed mate-pair sequencing of IMiDs resistance patients (18 post acquisition of IMIDs resistance and 7 pairs of pre- and post- acquisition of IMIDs resistance). MYC structural rearrangements (indels, translocations, inversions) were detected using DELLY and MANTA. Of note several MYC rearrangement were identified including MYC duplication in 1 patient, MYC structural rearrangement (±3Kb of TSS) in 9 patients (enhancer partner: TXNDC5, IGHa2, NSMCE2, IGLL5) and a newly acquired IRF4-IGH a2 rearrangement in 1 patient with pre-existing MYC-IGLL5 rearrangement. Conclusion:We have demonstrated that IMIDs alter enhancer activity in myeloma cells by depleting IKZF1 / IKZF3 and disrupting BRD4 binding to enhancers and super-enhancers, stalling of RNA polymerase II and MYC transcription. Disclosures Neri: Celgene and Jannsen: Consultancy, Honoraria. Bergsagel:Amgen, BMS, Novartis, Incyte: Consultancy; Novartis: Research Funding. Bahlis:Onyx: Consultancy, Honoraria; Amgen: Consultancy, Honoraria; Janssen: Consultancy, Honoraria, Other: Travel Expenses, Research Funding, Speakers Bureau; BMS: Honoraria; Celgene: Consultancy, Honoraria, Other: Travel Expenses, Research Funding, Speakers Bureau.
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Morin, Jean-Pascal, Luis F. Rodríguez-Durán, Kioko Guzmán-Ramos, Claudia Perez-Cruz, Guillaume Ferreira, Sofia Diaz-Cintra, and Gustavo Pacheco-López. "Palatable Hyper-Caloric Foods Impact on Neuronal Plasticity." Frontiers in Behavioral Neuroscience 11 (February 14, 2017). http://dx.doi.org/10.3389/fnbeh.2017.00019.
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Ryckelynck, David, and Djamel Missoum Benziane. "Hyper-reduction framework for model calibration in plasticity-induced fatigue." Advanced Modeling and Simulation in Engineering Sciences 3, no. 1 (May 4, 2016). http://dx.doi.org/10.1186/s40323-016-0068-6.
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Chakraborty, Biswadeep, and Saibal Mukhopadhyay. "Characterization of Generalizability of Spike Timing Dependent Plasticity Trained Spiking Neural Networks." Frontiers in Neuroscience 15 (October 29, 2021). http://dx.doi.org/10.3389/fnins.2021.695357.
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A Spiking Neural Network (SNN) is trained with Spike Timing Dependent Plasticity (STDP), which is a neuro-inspired unsupervised learning method for various machine learning applications. This paper studies the generalizability properties of the STDP learning processes using the Hausdorff dimension of the trajectories of the learning algorithm. The paper analyzes the effects of STDP learning models and associated hyper-parameters on the generalizability properties of an SNN. The analysis is used to develop a Bayesian optimization approach to optimize the hyper-parameters for an STDP model for improving the generalizability properties of an SNN.
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Soda, Teresa, Lisa Mapelli, Francesca Locatelli, Laura Botta, Mitchell Goldfarb, Francesca Prestori, and Egidio D'Angelo. "Hyper-excitability and hyper-plasticity disrupt cerebellar signal transfer in the IB2 KO mouse model of autism." Journal of Neuroscience, January 29, 2019, 1985–18. http://dx.doi.org/10.1523/jneurosci.1985-18.2019.
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Rinaldi, Tania. "Hyper-connectivity and hyper-plasticity in the medial prefrontal cortex in the valproic acid animal model of autism." Frontiers in Neural Circuits 2 (October 29, 2008). http://dx.doi.org/10.3389/neuro.04.004.2008.
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