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Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.

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At least 289 records · Page 16
All sourcesNASA NTRSDOE OSTI
DOE OSTI2016

Arsenic trioxide mediates HAPI microglia inflammatory response and subsequent neuron apoptosis through p38/JNK MAPK/STAT3 pathway

Arsenic is a widely distributed toxic metalloid all over the world. Inorganic arsenic species are supposed to affect astrocytic functions and to cause neuron apoptosis in CNS. Microglias are the key cell type involved in innate immune responses in CNS, and microglia activation has been linked to inflammation and neurotoxicity. In this study, using ELISA, we showed that Arsenic trioxide up-regulated the expression and secretion of IL-1β in a dose-dependent manner and a time-dependent manner in cultured HAPI microglia cells. The secretion of IL-1β caused the apoptosis of SH-SY5Y. These pro-inflammatory responses were inhibited by the STAT3 blocker, AG490 and P38/JNK MAPK blockers SB202190, SP600125. Further, Arsenic trioxide exposure could induce phosphorylation and activation of STAT3, and the translocation of STAT3 from the cytosol to the nucleus in this HAPI microglia cell line. Thus, the STAT3 signaling pathway can be activated after Arsenic trioxide treatment. However, P38/JNK MAPK blockers SB202190, SP600125 also obviously attenuated STAT3 activation and transnuclear transport induced by Arsenic trioxide. In concert with these results, we highlighted that the secretion of IL-1β and STAT3 activation induced by Arsenic trioxide can be mediated by elevation of P38/JNK MAPK in HAPI microglia cells and then induced the toxicity of neurons. - Highlights: • Arsenic trioxide exposure induced expression of IL-β in HAPI microglia. • Arsenic trioxide exposure induced activation of MAPK pathways in HAPI microglia. • Arsenic trioxide exposure induced activation of STAT3 pathways in HAPI microglia. • The expression of IL-β though P38/JNK MAPK/STAT3 pathways in HAPI microglia.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Up-regulation of miR-122 protects against neuronal cell death in ischemic stroke through the heat shock protein 70-dependent NF-κB pathway by targeting FOXO3

Highlights: • miR-122 was decreased in mouse N2A neuroblastoma (N2A) cells after OGD and mouse brain after MCAO. • Gain-of-miR-122 function significantly suppressed OGD- and MCAO-induced injures in vitro and in vivo. • miR-122 was validated to directly bind to the predicted 3′-untranslated region (3′-UTR) of FOXO3. • The inhibitory effects of miR-122 on ischemic injury in vitro and in vivo were overturned by FOXO3 overexpression and miR-122-FOXO3 axis functioned via the heat shock protein 70 (HSP-70)-mediated NF-κB pathway. • miR-122 inhibits ischemic neuronal death through HSP-70-dependent NF-κB pathway by targeting FOXO3. Dysfunction of the microRNA (miRNA) network has been emerging as a main regulator in ischemic stroke. Recently, studies have linked the deregulation of miR-122 to ischemic stroke. However, the specific role and molecular mechanism of miR-122 in ischemic stroke remain to be further investigated. Here, we found that miR-122 was decreased in mouse N2A neuroblastoma (N2A) cells after oxygen-glucose deprivation (OGD) and mouse brain after transient middle cerebral artery occlusion (MCAO). OGD treatment significantly increased N2A cell death and Caspase-3 activity, and decreased Bcl-2 protein expression. In addition, MCAO treatment induced severe mouse brain infarction, mitochondrial reactive oxygen species (ROS) production, and long-term neurological deficit. Gain-of-miR-122 function significantly suppressed OGD- and MCAO-induced injures in vitro and in vivo. Subsequently, miR-122 was validated to directly bind to the predicted 3′-untranslated region (3′-UTR) of FOXO3 gene, and the inhibitory effects of miR-122 on ischemic injury in vitro and in vivo were overturned by FOXO3 overexpression. Moreover, our results further revealed that miR-122-FOXO3 axis functioned via the heat shock protein 70 (HSP-70)-mediated NF-κB pathway. Collectively, our data suggest that miR-122 inhibits ischemic neuronal death through the HSP-70-dependent NF-κB pathway by targeting FOXO3. These findings raise the possibility that this regulatory net may contribute to the pathogenesis of the ischemic brain injury in stroke.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Hippo, Drosophila MST, is a novel modifier of motor neuron degeneration induced by knockdown of Caz, Drosophila FUS

Highlights: • Mutation in Hippo suppressed aberrant eye morphology induced by Cabeza knockdown. • Mutation in Hippo suppressed neuron-specific defects induced by Cabeza knockdown. • Mutation in Hippo restored Cabeza protein in the nucleus. • Hippo mRNA level increased in Cabeza knockdown. • Cabeza may negatively regulate hippo. Mutations in the Fused in Sarcoma (FUS) gene have been identified in familial ALS in human. Drosophila contains a single ortholog of human FUS called Cabeza (Caz). We previously established Drosophila models of ALS targeted to Caz, which developed the locomotive dysfunction and caused anatomical defects in presynaptic terminals of motoneurons. Accumulating evidence suggests that ALS and cancer share defects in many cellular processes. The Hippo pathway was originally discovered in Drosophila and plays a role as a tumor suppressor in mammals. We aimed to determine whether Hippo pathway genes modify the ALS phenotype using Caz knockdown flies. We found a genetic link between Caz and Hippo (hpo), the Drosophila ortholog of human Mammalian sterile 20-like kinase (MST) 1 and 2. Loss-of-function mutations of hpo rescued Caz knockdown-induced eye- and neuron-specific defects. The decreased Caz levels in nuclei induced by Caz knockdown were also rescued by loss of function mutations of hpo. Moreover, hpo mRNA level was dramatically increased in Caz knockdown larvae, indicating that Caz negatively regulated hpo. Our results demonstrate that hpo, Drosophila MST, is a novel modifier of Drosophila FUS. Therapeutic targets that inhibit the function of MST could modify the pathogenic processes of ALS.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

Wireless Optogenetic Modulation of Cortical Neurons Enabled by Radioluminescent Nanoparticles

While offering high precision control of neural circuits, optogenetics is hampered by the necessity to implant fiber-optic waveguides in order to deliver photons to genetically engineered light-gated neurons in the brain. Unlike laser light, X-rays freely pass biological barriers. In this work, we show that radioluminescent Gd 2 (WO 4 ) 3 :Eu nanoparticles, which absorb an external X-rays energy and then down-converter it into optical photons with wavelengths of ~610 nm, can be used for the transcranial stimulation of cortical neurons expressing red-shifted, ~590-630 nm, channelrhodopsin ReaChR, thereby promoting optogenetic neural control to the practical implementation of minimally-invasive wireless deep brain stimulation.

37 INORGANIC, ORGANIC, PHYSICAL, AND ANALYTICAL CH↗
DOE OSTI2014

Amyloid- β induces NLRP1-dependent neuronal pyroptosis in models of Alzheimer’s disease

Increasing evidence has shown the aberrant expression of inflammasome-related proteins in Alzheimer’s disease (AD) brain; these proteins, including NLRP1 inflammasome, are implicated in the execution of inflammatory response and pyroptotic death. Although current data are associated NLRP1 genetic variants with AD, the involvement of NLRP1 inflammasome in AD pathogenesis is still unknown. Using APPswe/PS1dE9 transgenic mice, we found that cerebral NLRP1 levels were upregulated. Our in vitro studies further showed that increased NLRP1-mediated caspase-1-dependent ‘pyroptosis’ in cultured cortical neurons in response to amyloid-b. Moreover, we employed direct in vivo infusion of non-viral small-interfering RNA to knockdown NLRP1 or caspase-1 in APPswe/PS1dE9 brain, and discovered that these NLRP1 or caspase-1 deficiency mice resulted in significantly reduced neuronal pyroptosis and reversed cognitive impairments. Taken together, our findings indicate an important role for NLRP1/caspase-1 signaling in AD progression, and point to the modulation of NLRP1 inflammasome as a promising strategy for AD therapy.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2015

Recognition of distinct RNA motifs by the clustered CCCH zinc fingers of neuronal protein Unkempt

Unkempt is an evolutionarily conserved RNA-binding protein that regulates translation of its target genes and is required for the establishment of the early bipolar neuronal morphology. Here we determined the X-ray crystal structure of mouse Unkempt and show that its six CCCH zinc fingers (ZnFs) form two compact clusters, ZnF1–3 and ZnF4–6, that recognize distinct trinucleotide RNA substrates. Both ZnF clusters adopt a similar overall topology and use distinct recognition principles to target specific RNA sequences. Structure-guided point mutations reduce the RNA binding affinity of Unkempt both in vitro and in vivo, ablate Unkempt's translational control and impair the ability of Unkempt to induce a bipolar cellular morphology. Furthermore, our study unravels a new mode of RNA sequence recognition by clusters of CCCH ZnFs that is critical for post-transcriptional control of neuronal morphology.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2020

A NWB-based dataset and processing pipeline of human single-neuron activity during a declarative memory task

A challenge for data sharing in systems neuroscience is the multitude of different data formats used. Neurodata Without Borders: Neurophysiology 2.0 (NWB:N) has emerged as a standardized data format for the storage of cellular-level data together with meta-data, stimulus information, and behavior. A key next step to facilitate NWB:N adoption is to provide easy to use processing pipelines to import/export data from/to NWB:N. Here, we present a NWB-formatted dataset of 1863 single neurons recorded from the medial temporal lobes of 59 human subjects undergoing intracranial monitoring while they performed a recognition memory task. We provide code to analyze and export/import stimuli, behavior, and electrophysiological recordings to/from NWB in both MATLAB and Python. The data files are NWB:N compliant, which affords interoperability between programming languages and operating systems. This combined data and code release is a case study for how to utilize NWB:N for human single-neuron recordings and enables easy re-use of this hard-to-obtain data for both teaching and research on the mechanisms of human memory.

Science & Technology - Other Topics↗
DOE OSTI2021

Neuronally-derived tau is increased in experienced breachers and is associated with neurobehavioral symptoms

Military and law enforcement breachers are exposed to many low-level blasts during their training and occupational experiences in which they detonate explosives to force entry into secured structures. There is a concern that exposure to these repetitive blast events in career breachers could result in cumulative neurological effects. This study aimed to determine concentrations of neurofilament light (NF-L), tau, and amyloid-beta 42 (Aβ42) in serum and in neuronal-derived extracellular vesicles (EVs) in an experienced breacher population, and to examine biomarker associations with neurobehavioral symptoms. Thirty-four participants enrolled in the study: 20 experienced breachers and 14 matched military or civilian law enforcement controls. EV tau concentrations were significantly elevated in experienced breachers (0.3301 ± 0.5225) compared to controls (–0.4279 ± 0.7557; F = 10.43, p = 0.003). No statistically significant changes were observed in EV levels of NF-L or Aβ42 or in serum levels of NF-L, tau, or Aβ42 (p’s > 0.05). Elevated EV tau concentrations correlated with increased Neurobehavioral Symptom Inventory (NSI) score in experienced breachers (r = 0.596, p = 0.015) and predicted higher NSI score (F(1,14) = 7.702, p = 0.015, R 2 = 0.355). These findings show that neuronal-derived EV concentrations of tau are significantly elevated and associated with neurobehavioral symptoms in this sample of experienced breachers who have a history of many low-level blast exposures.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2025

An electro-optical Mott neuron based on niobium dioxide

Various applications—including brain-like computing and on-chip artificial vision—increasingly demand a combination of electronic and photonic techniques. However, integrating both approaches on a single chip is challenging, and solutions typically rely on disparate components with power-hungry signal conversions. Here, in this paper, we report electro-optical Mott neurons that combine visible light emission with electrical threshold switching, as well as neuron-like oscillations. The devices are based on thin films of sputtered niobium dioxide (NbO 2 ), a Mott insulator–metal transition material, operating at room temperature and emitting light that peaks around 810 nm. Operando measurements reveal an electronic origin to the light emission: charge carrier relaxation initiated by high-field transport in the NbO 2 . Our devices combine electrical and optical functions within a single material, thereby expanding the options available for future artificial intelligence hardware.

electrical engineering↗
DOE OSTI2016

Simulation of a spiking neuron circuit using carbon nanotube transistors

Neuromorphic engineering is related to the existing analogies between the physical semiconductor VLSI (Very Large Scale Integration) and biophysics. Neuromorphic systems propose to reproduce the structure and function of biological neural systems for transferring their calculation capacity on silicon. Since the innovative research of Carver Mead, the neuromorphic engineering continues to emerge remarkable implementation of biological system. This work presents a simulation of an elementary neuron cell with a carbon nanotube transistor (CNTFET) based technology. The model of the cell neuron which was simulated is called integrate and fire (I&F) model firstly introduced by G. Indiveri in 2009. This circuit has been simulated with CNTFET technology using ADS environment to verify the neuromorphic activities in terms of membrane potential. This work has demonstrated the efficiency of this emergent device; i.e CNTFET on the design of such architecture in terms of power consumption and technology integration density.

77 NANOSCIENCE AND NANOTECHNOLOGY↗
DOE OSTI2026

Viability of perturbative expansion for quantum field theories on neurons

Neural Network (NN) architectures that break statistical independence of parameters have been proposed as a new approach for simulating local quantum field theories (QFTs) [1]. In the infinite neuron number limit, single-layer NNs can exactly reproduce QFT results. This paper examines the viability of this architecture for perturbative calculations of local QFTs for finite neuron number N using scalar ϕ 4 theory in d Euclidean dimensions as an example. We find that the renormalized O(1/N ) corrections to two-and four-point correlators yield perturbative series which are sensitive to the UV cut-off and therefore have a weak convergence. We propose a modification to the architecture to improve this convergence and discuss constraints on the parameters of the theory and the scaling of N which allow us to extract accurate field theory results.

Sen, Srimoyee [Iowa State University, Ames, IA (Un↗
DOE OSTI2014

Identification of the first small-molecule ligand of the neuronal receptor sortilin and structure determination of the receptor–ligand complex

The identification of the first small-molecule ligand of the neuronal receptor sortilin and structure determination of the receptor–ligand complex are reported. Sortilin is a type I membrane glycoprotein belonging to the vacuolar protein sorting 10 protein (Vps10p) family of sorting receptors and is most abundantly expressed in the central nervous system. Sortilin has emerged as a key player in the regulation of neuronal viability and has been implicated as a possible therapeutic target in a range of disorders. Here, the identification of AF40431, the first reported small-molecule ligand of sortilin, is reported. Crystals of the sortilin–AF40431 complex were obtained by co-crystallization and the structure of the complex was solved to 2.7 Å resolution. AF40431 is bound in the neurotensin-binding site of sortilin, with the leucine moiety of AF40431 mimicking the binding mode of the C-terminal leucine of neurotensin and the 4-methylumbelliferone moiety of AF40431 forming π-stacking with a phenylalanine.

75 CONDENSED MATTER PHYSICS, SUPERCONDUCTIVITY AND↗
DOE OSTI2024

Modeling the Impacts of Material Properties on Oscillatory Neuron Behavior

In this study, neuromorphic computing, which mimics the functions of biological brains, offers improvements in both latency and energy efficiency over typical von Neumann computing architectures. Spiking neural networks can be especially power-efficient because they encode information temporally and can use more sparse electrical inputs. Here, we study the design of volatile memristors (variable resistors with memory) for neuronal devices, with particular consideration toward the feasibility of all-on-chip oscillation using built-in capacitance. We use circuit simulations to model the behavior of oscillator neurons with a range of realistic material properties. We find that energy inputs increase with insulating-phase resistivity, thermal conductivity, and device aspect ratio. However, we also find that the minimum capacitance needed for oscillation decreases with increasing insulating-phase resistivity, which opposes the constraints for power efficiency. Based on published data on NbO 2 , VO 2 , and EuNiO 3 , we find that existing materials can be engineered for all-on-chip spiking using their parasitic capacitance.

36 MATERIALS SCIENCE↗
DOE OSTI2022

Association of AK4 Protein From Stem Cell–Derived Neurons With Cognitive Reserve

Background and Objectives: Identifying protein targets that provide cognitive reserve is a strategy to prevent and treat Alzheimer disease and Alzheimer disease related dementias (AD/ADRD). Previous studies using bulk human brain tissue reported 12 proteins associated with cognitive reserve. This study examined whether the same proteins from induced neurons (iNs) are associated with cognitive reserve of their human donors. Methods: Here, induced pluripotent stem cell (iPSC) lines were generated from cryopreserved peripheral blood mononuclear cells of older adults who were autopsied as part of the Religious Orders Study or Rush Memory and Aging Project. Neurons were induced from iPSCs using a standard neurogenin2 protocol. Tandem mass tag proteomics analyses were conducted on iNs day 21. Cognitive reserve of their human donors was measured as person-specific slopes of cognitive change not accounted for by common neuropathologies. Results: The 53 human donors died at a mean age of 91 years, all were non-Latino White, and 36 (67.9%) were female. Eighteen were diagnosed with Alzheimer dementia proximate to death, and 34 had pathologic AD diagnosis at autopsy. Approximately 60% of the donors had above-average cognitive reserve such that their cognition declined slower than an average person with comparable burdens of neuropathologies. Eight of the 12 candidate proteins were quantified in iNs proteomics analyses. Higher adenylate kinase 4 (AK4) expression in iNs was associated with lower cognitive reserve, consistent with the previous report for brain AK4 expression. Discussion: By replicating cortical protein associations with cognitive reserve in human iNs, these data provide a valuable molecular readout for studying complex clinical phenotypes such as cognitive reserve in a dish.

59 BASIC BIOLOGICAL SCIENCES↗
NASA NTRS1987

Cat vestibular neurons that exhibit different responses to active and passive yaw head rotations

Neurons in the vestibular nuclei were recorded in alert cats during voluntary yaw rotations of the head and during the same rotations delivered with a turntable driven from a record of previous voluntary movements. During both voluntary and passive rotations, 35 percent (6/17) of neurons tested responded at higher rates or for a larger part of the movement during voluntary movements than during the same rotations delivered with the turntable. Neck sensory input was evaluated separately in many of these cells and can account qualitatively for the extra firing present during active movement.

Robinson, F. R.↗
NASA NTRS1987

Expiratory muscle control during vomiting - Role of brain stem expiratory neurons

The neural mechanisms controlling the muscles involved during vomiting were examined using decerebrated cats. In one experiment, the activity of the ventral respiratory group (VRG) expiratory (E) neurons was recorded during induced 'fictive vomiting' (i.e., a series of bursts of coactivation of abdominal and phrenic nerves that would be expected to produce expulsion in unparalyzed animals) and vomiting. In a second, abdominal muscle electromyographic and nerve activity were compared before and after sectioning the axons of descending VRG E neurons as they cross the midline between C1 and the obex (the procedure that is known to abolish expiratory modulation of internal intercostal muscle activity). The results of the study indicate that the abdominal muscles are controlled differently during respiration and vomiting.

Miller, A. D.↗
NASA NTRS1990

Adaptive Neurons For Artificial Neural Networks

Training time decreases dramatically. In improved mathematical model of neural-network processor, temperature of neurons (in addition to connection strengths, also called weights, of synapses) varied during supervised-learning phase of operation according to mathematical formalism and not heuristic rule. Evidence that biological neural networks also process information at neuronal level.

Tawel, Raoul↗
NASA NTRS1993

Numbers And Gains Of Neurons In Winner-Take-All Networks

Report presents theoretical study of gains required in neurons to implement winner-take-all electronic neural network of given size and related question of maximum size of winner-take-all network in which neurons have specified sigmoid transfer or response function with specified gain.

Brown, Timothy X.↗