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- Moslehi, S., et al.
(author)
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Fractal Electronics for Stimulating and Sensing Neural Networks : Enhanced Electrical, Optical, and Cell Interaction Properties
- 2024
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In: The Fractal Geometry of the Brain. - 2190-5223 .- 2190-5215. - 9783031476068 - 9783031476051 ; 36, s. 849-875
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Book chapter (peer-reviewed)abstract
- Imagine a world in which damaged parts of the body – an arm, an eye, and ultimately a region of the brain – can be replaced by artificial implants capable of restoring or even enhancing human performance. The associated improvements in the quality of human life would revolutionize the medical world and produce sweeping changes across society. In this chapter, we discuss several approaches to the fabrication of fractal electronics designed to interface with neural networks. We consider two fundamental functions – stimulating electrical signals in the neural networks and sensing the location of the signals as they pass through the network. Using experiments and simulations, we discuss the favorable electrical performances that arise from adopting fractal rather than traditional Euclidean architectures. We also demonstrate how the fractal architecture induces favorable physical interactions with the cells they interact with, including the ability to direct the growth of neurons and glia to specific regions of the neural–electronic interface.
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| 2. |
- Leke, Renata, 1979, et al.
(author)
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The glutamine transporters and their role in the glutamate/GABA-glutamine cycle
- 2016
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In: The Glutamate/GABA-Glutamine Cycle. - Cham : Springer. - 2190-5215. - 9783319450940 ; , s. 223-257
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Book chapter (other academic/artistic)abstract
- Glutamine is a key amino acid in the CNS, playing an important role in the glutamate/GABA-glutamine cycle (GGC). In the GGC, glutamine is transferred from astrocytes to neurons, where it will replenish the inhibitory and excitatory neurotransmitter pools. Different transporters participate in this neural communication, i.e., the transporters responsible for glutamine efflux from astrocytes and influx into the neurons, such as the members of the SNAT, LAT, y+LAT, and ASC families of transporters. The SNAT family consists of the transporter isoforms SNAT3 and SNAT5 that are related to efflux from the astrocytic compartment, and SNAT1 and SNAT2 that are associated with glutamine uptake into the neuronal compartment. The isoforms SNAT7 and SNAT8 do not have their role completely understood, but they likely also participate in the GGC. The isoforms LAT2 and y+LAT2 facilitate the exchange of neutral amino acids and cationic amino acids (y+LAT2 isoform) and have been associated with glutamine efflux from astrocytes. ASCT2 is a Na+-dependent antiporter, the participation of which in the GGC also remains to be better characterized. All these isoforms are tightly regulated by transcriptional and translational mechanisms, which are induced by several determinants such as amino acid deprivation, hormones, pH, and the activity of different signaling pathways. Dysfunctional glutamine transporter activity has been associated with the pathophysiological mechanisms of certain neurologic diseases, such as Hepatic Encephalopathy and Manganism. However, there might also be other neuropathological conditions associated with an altered GGC, in which glutamine transporters are dysfunctional. Hence, it appears to be of critical importance that the physiological and pathological aspects of glutamine transporters are thoroughly investigated. © Springer International Publishing Switzerland 2016.
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| 3. |
- Uygar, Batuhan, et al.
(author)
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Brain o-glcnacylation : from molecular mechanisms to clinical phenotype
- 2023
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In: Advances in neurobiology. - Cham : Springer Nature. - 2190-5215. ; 29, s. 255-280
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Journal article (peer-reviewed)abstract
- O-GlcNAc is the attachment of β-N-acetylglucosamine to the hydroxyl group of serine and threonine in nuclear and cytoplasmic proteins. It is generally not further elongated but exists as a monosaccharide that can be rapidly added or removed. Thousands of proteins involved in gene transcription, protein translation and degradation as well as the regulation of signal transduction contain O-GlcNAc. Brain is one of the tissues where O-GlcNAc is the most highly expressed and deletion of neuronal O-GlcNAc leads to death early in development. O-GlcNAc is also important for normal adult brain function, where dynamic processes like learning and memory at least in part depend on the modification of specific proteins by O-GlcNAc. Conversely, too much or too little O-GlcNAc in the brain contributes to several disorders including obesity, intellectual disability and Alzheimer's disease. In this chapter, we describe the expression and regulation of O-GlcNAc in the nervous system.
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