Real-time fault diagnosis for propulsion systems

Current research toward real time fault diagnosis for propulsion systems at NASA-Lewis is described. The research is being applied to both air breathing and rocket propulsion systems. Topics include fault detection methods including neural networks, system modeling, and real time implementations

Modulation of Neurally Mediated Vasodepression and Bradycardia by Electroacupuncture through Opioids in Nucleus Tractus Solitarius.

Stimulation of vagal afferent endings with intravenous phenylbiguanide (PBG) causes both bradycardia and vasodepression, simulating neurally mediated syncope. Activation of µ-opioid receptors in the nucleus tractus solitarius (NTS) increases blood pressure. Electroacupuncture (EA) stimulation of somatosensory nerves underneath acupoints P5-6, ST36-37, LI6-7 or G37-39 selectively but differentially modulates sympathoexcitatory responses. We therefore hypothesized that EA-stimulation at P5-6 or ST36-37, but not LI6-7 or G37-39 acupoints, inhibits the bradycardia and vasodepression through a µ-opioid receptor mechanism in the NTS. We observed that stimulation at acupoints P5-6 and ST36-37 overlying the deep somatosensory nerves and LI6-7 and G37-39 overlying cutaneous nerves differentially evoked NTS neural activity in anesthetized and ventilated animals. Thirty-min of EA-stimulation at P5-6 or ST36-37 reduced the depressor and bradycardia responses to PBG while EA at LI6-7 or G37-39 did not. Congruent with the hemodynamic responses, EA at P5-6 and ST36-37, but not at LI6-7 and G37-39, reduced vagally evoked activity of cardiovascular NTS cells. Finally, opioid receptor blockade in the NTS with naloxone or a specific μ-receptor antagonist reversed P5-6 EA-inhibition of the depressor, bradycardia and vagally evoked NTS activity. These data suggest that point specific EA stimulation inhibits PBG-induced vasodepression and bradycardia responses through a μ-opioid mechanism in the NTS

Paraventricular Nucleus Modulates Excitatory Cardiovascular Reflexes during Electroacupuncture.

The paraventricular nucleus (PVN) regulates sympathetic outflow and blood pressure. Somatic afferent stimulation activates neurons in the hypothalamic PVN. Parvocellular PVN neurons project to sympathoexcitatory cardiovascular regions of the rostral ventrolateral medulla (rVLM). Electroacupuncture (EA) stimulates the median nerve (P5-P6) to modulate sympathoexcitatory responses. We hypothesized that the PVN and its projections to the rVLM participate in the EA-modulation of sympathoexcitatory cardiovascular responses. Cats were anesthetized and ventilated. Heart rate and mean blood pressure were monitored. Application of bradykinin every 10-min on the gallbladder induced consistent pressor reflex responses. Thirty-min of bilateral EA stimulation at acupoints P5-P6 reduced the pressor responses for at least 60-min. Inhibition of the PVN with naloxone reversed the EA-inhibition. Responses of cardiovascular barosensitive rVLM neurons evoked by splanchnic nerve stimulation were reduced by EA and then restored with opioid receptor blockade in the PVN. EA at P5-P6 decreased splanchnic evoked activity of cardiovascular barosensitive PVN neurons that also project directly to the rVLM. PVN neurons labeled with retrograde tracer from rVLM were co-labeled with μ-opioid receptors and juxtaposed to endorphinergic fibers. Thus, the PVN and its projection to rVLM are important in processing acupuncture modulation of elevated blood pressure responses through a PVN opioid mechanism

elPBN neurons regulate rVLM activity through elPBN-rVLM projections during activation of cardiac sympathetic afferent nerves.

The external lateral parabrachial nucleus (elPBN) within the pons and rostral ventrolateral medulla (rVLM) contributes to central processing of excitatory cardiovascular reflexes during stimulation of cardiac sympathetic afferent nerves (CSAN). However, the importance of elPBN cardiovascular neurons in regulation of rVLM activity during CSAN activation remains unclear. We hypothesized that CSAN stimulation excites the elPBN cardiovascular neurons and, in turn, increases rVLM activity through elPBN-rVLM projections. Compared with controls, in rats subjected to microinjection of retrograde tracer into the rVLM, the numbers of elPBN neurons double-labeled with c-Fos (an immediate early gene) and the tracer were increased after CSAN stimulation (P < 0.05). The majority of these elPBN neurons contain vesicular glutamate transporter 3. In cats, epicardial bradykinin and electrical stimulation of CSAN increased the activity of elPBN cardiovascular neurons, which was attenuated (n = 6, P < 0.05) after blockade of glutamate receptors with iontophoresis of kynurenic acid (Kyn, 25 mM). In separate cats, microinjection of Kyn (1.25 nmol/50 nl) into the elPBN reduced rVLM activity evoked by both bradykinin and electrical stimulation (n = 5, P < 0.05). Excitation of the elPBN with microinjection of dl-homocysteic acid (2 nmol/50 nl) significantly increased basal and CSAN-evoked rVLM activity. However, the enhanced rVLM activity induced by dl-homocysteic acid injected into the elPBN was reversed following iontophoresis of Kyn into the rVLM (n = 7, P < 0.05). These data suggest that cardiac sympathetic afferent stimulation activates cardiovascular neurons in the elPBN and rVLM sequentially through a monosynaptic (glutamatergic) excitatory elPBN-rVLM pathway

The Neon Gap: Probing Ionization with Dwarf Galaxies at z~1

We present measurements of [NeIII]{\lambda}3869 emission in z~1 low-mass galaxies taken from the Keck/DEIMOS spectroscopic surveys HALO7D and DEEPWinds. We identify 167 individual galaxies with significant [NeIII] emission lines, including 112 "dwarf" galaxies with log(M_{\star}/M_{\odot}) < 9.5, with 0.3 < z < 1.4. We also measure [NeIII] emission from composite spectra derived from all [OII]{\lambda}{\lambda}3727,3729 line emitters in this range. This provides a unique sample of [NeIII]-emitters in the gap between well-studied emitters at z = 0 and 2 < z < 3. To study evolution in ionization conditions in the ISM over this time, we analyze the log([NeIII]{\lambda}3869/[OII]{\lambda}{\lambda}3727,3729) ratio (Ne3O2) as a function of the stellar mass and of the log([OIII]{\lambda}{\lambda}4959,5007/[OII]{\lambda}{\lambda}3727,3729) ratio (O32). We find that the typical star-forming dwarf galaxy at this redshift, as measured from the composite spectra, shares the Ne3O2-M_{\star} relation with local galaxies, but have higher O32 at given Ne3O2. This finding implies that the ionization and metallicity characteristics of the z~1 dwarf population do not evolve substantially from z~1 to z=0, suggesting that the known evolution in those parameter from z~2 has largely taken place by z~1. Individual [NeIII]-detected galaxies have emission characteristics situated between local and z~2 galaxies, with elevated Ne3O2 and O32 emission potentially explained by variations in stellar and nebular metallicity. We also compare our dwarf sample to similarly low-mass z > 7 galaxies identified in JWST Early Release Observations, finding four HALO7D dwarfs with similar size, metallicity, and star formation properties.Comment: Accepted to ApJL, 16.01.202

Mode specific electronic friction in dissociative chemisorption on metal surfaces : H2 on Ag(111)

Electronic friction and the ensuing nonadiabatic energy loss play an important role in chemical reaction dynamics at metal surfaces. Using molecular dynamics with electronic friction evaluated on the fly from density functional theory, we find strong mode dependence and a dominance of nonadiabatic energy loss along the bond stretch coordinate for scattering and dissociative chemisorption of H2 on the Ag(111) surface. Exemplary trajectories with varying initial conditions indicate that this mode specificity translates into modulated energy loss during a dissociative chemisorption event. Despite minor nonadiabatic energy loss of about 5%, the directionality of friction forces induces dynamical steering that affects individual reaction outcomes, specifically for low-incidence energies and vibrationally excited molecules. Mode-specific friction induces enhanced loss of rovibrational rather than translational energy and will be most visible in its effect on final energy distributions in molecular scattering experiments

Bring Your Own Device (BYOD): Current Status, Issues, and Future Directions

The smart mobile device has emerged as an extension of the self, closely tied to the personal behaviors and preferences. This panel discussion covers the current status, real world cases, adoption, pros/cons, issues (security, privacy), and future direction of the use and adoption of Bring-Your-Own-Device (BYOD). The panel also covers BYOS (Bring-Your-Own-Service) and BYOA (Bring-Your-Own-Apps)