Engineering topics

Kumar, A.

Publications and source records attributed to Kumar, A..

At least 55 records · Page 3

DOE OSTI2020

Measurement of neutrino-induced neutral-current coherent $π^0$ production in the NOvA near detector

The cross section of neutrino-induced neutral-current coherent $\pi^0$ production on a carbon-dominated target is measured in the NOvA near detector. This measurement uses a narrow-band neutrino beam with the average neutrino energy of 2.7\,GeV, xwhich is of interest to the ongoing and future long-baseline neutrino oscillation experiments. The measured, flux-averaged cross section is $\sigma = 14.0\pm0.9$\,(stat.)$\pm2.1$\,(syst.)$\times 10^{-40}$ $\text{cm}^2/$nucleus, consistent with model prediction. This result is the most precise measurement of neutral-current coherent $\pi^0$ production in the few-GeV neutrino energy region.

72 PHYSICS OF ELEMENTARY PARTICLES AND FIELDS↗

DOE OSTI2020

Search for multimessenger signals in NOvA coincident with LIGO/Virgo detections

Using the NOvA neutrino detectors, a broad search has been performed for any signal coincident with 28 gravitational wave events detected by the LIGO/Virgo Collaboration between September 2015 and July 2019. For all of these events, NOvA is sensitive to possible arrival of neutrinos and cosmic rays of GeV and higher energies. For five (seven) events in the NOvA Far (Near) Detector, timely public alerts from the LIGO/Virgo Collaboration allowed recording of MeV-scale events. No signal candidates were found.

72 PHYSICS OF ELEMENTARY PARTICLES AND FIELDS↗

DOE OSTI2020

Adjusting neutrino interaction models and evaluating uncertainties using NOvA near detector data

The two-detector design of the NOvA neutrino oscillation experiment, in which two functionally identical detectors are exposed to an intense neutrino beam, aids in canceling leading order effects of cross-section uncertainties. However, limited knowledge of neutrino interaction cross sections still gives rise to some of the largest systematic uncertainties in current oscillation measurements. We show contemporary models of neutrino interactions to be discrepant with data from NOvA, consistent with discrepancies seen in other experiments. Adjustments to neutrino interaction models in GENIE are presented, creating an effective model that improves agreement with our data. We also describe systematic uncertainties on these models, including uncertainties on multi-nucleon interactions from a newly developed procedure using NOvA near detector data.

72 PHYSICS OF ELEMENTARY PARTICLES AND FIELDS↗

DOE OSTI2020

Performance of prototype GE1/1 chambers for the CMS muon spectrometer upgrade

The high-luminosity phase of the Large Hadron Collider (HL-LHC) will result in ten times higher particle background than measured during the first phase of LHC operation. In order to fully exploit the highly-demanding operating conditions during HL-LHC, the Compact Muon Solenoid (CMS) Collaboration will use Gas Electron Multiplier (GEM) detector technology. The technology will be integrated into the innermost region of the forward muon spectrometer of CMS as an additional muon station called GE1/1. The primary purpose of this auxiliary station is to help in muon reconstruction and to control level-1 muon trigger rates in the pseudo-rapidity region 1.6 ≤ |η| ≤ 2.2. The new station will contain trapezoidal-shaped GEM detectors called GE1/1 chambers. The design of these chambers is finalized, and the installation is in progress during the Long Shutdown phase two (LS-2) that started in 2019. Several full-size prototypes were built and operated successfully in various test beams at CERN. Here, we describe performance measurements such as gain, efficiency, and time resolution of these prototype chambers, developed after years of R&D, and summarize their behavior in different gas compositions as a function of the applied voltage.

46 INSTRUMENTATION RELATED TO NUCLEAR SCIENCE AND ↗

DOE OSTI2020

Additional Calibration of the Ultraviolet Imaging Telescope on Board AstroSat

Results of the initial calibration of the Ultra-Violet Imaging Telescope (UVIT) were reported earlier by Tandon et al. The results reported earlier were based on the ground calibration as well as the first observations in orbit. Some additional data from the ground calibration and data from more in-orbit observations have been used to improve the results. In particular, extensive new data from in-orbit observations have been used to obtain (a) new photometric calibration that includes (i) zero points, (ii) flat fields, and (iii) saturation; (b) sensitivity variations; (c) spectral calibration for the near ultraviolet (NUV; 2000–3000 Å) and far ultraviolet (FUV; 1300–1800 Å) gratings; (d) point-spread function; and (e) astrometric calibration including distortion. Data acquired over the last three years show continued good performance of UVIT with no reduction in sensitivity in both UV channels.

79 ASTRONOMY AND ASTROPHYSICS↗

NASA NTRS2018

Late Effects of Heavy-Ion Irradiation on Ex Vivo Osteoblastogenesis and Cancellous Bone Microarchitecture

Prolonged spaceflight causes degeneration of skeletal tissue with incomplete recovery even after return to Earth. We hypothesize that heavy-ion irradiation, a component of Galactic Cosmic Radiation, damages osteoblast progenitors and may contribute to bone loss during long duration space travel beyond the protection of the Earth's magnetosphere. Male, 16 week-old C57BL6/J mice were exposed to high-LET (56-Fe, 600MeV) radiation using either low (5 or 10cGy) or high (50 or 200cGy) doses at the NASA Space Radiation Lab and were euthanized 3-4, 7, or 35 days later. Bone structure was quantified by microcomputed tomography (6.8 μm pixel size) and marrow cell redox assessed using membrane permeable, free radical-sensitive fluorogenic dyes. To assess osteoblastogenesis, adherent marrow cells were cultured ex vivo, then mineralized nodule formation quantified by imaging and gene expression analyzed by RT-PCR. Interestingly, 3-4 days post-exposure, fluorogenic dyes that reflect cytoplasmic generation of reactive nitrogen/oxygen species (DAF-FM Diacetate or CM-H2DCFDA) revealed irradiation (50cGy) reduced free radical generation (20-45%) compared to sham-irradiated controls. Alternatively, use of a dye showing relative specificity for mitochondrial superoxide generation (MitoSOX) revealed an 88% increase compared to controls. One week after exposure, reactive oxygen/nitrogen levels remained lower (24%) relative to sham-irradiated controls. After one month, high dose irradiation (200 cGy) caused an 86% decrement in ex vivo nodule formation and a 16-31% decrement in bone volume to total volume and trabecular number (50, 200cGy) compared to controls. High dose irradiation (200cGy) up-regulated expression of a late osteoblast marker (BGLAP) and select genes related to oxidative metabolism (Catalase) and DNA damage repair (Gadd45). In contrast, lower doses (5, 10cGy) did not affect bone structure or ex vivo nodule formation, but did down-regulate iNOS by 0.54-0.58 fold. Thus, both low- and high-doses of heavy-ion irradiation cause time-dependent, adaptive changes in redox state within marrow cells but only high doses (50, 200cGy) inhibit osteoblastogenesis and cause cancellous bone loss. We conclude space radiation has the potential to cause persistent damage to bone marrow-derived stem and progenitor cells for osteoblasts despite adaptive changes in cellular redox state.

LATE EFFECTS OF HEAVY-ION IRRADIATION↗

NASA NTRS2018

Effects of Mitochondrial-Targeted Human Catalase in Skeletal Tissue of Mice Exposed to Simulated Spaceflight

During prolonged spaceflight, astronauts are exposed to both microgravity and space radiation and are at risk forincreased skeletal fragility due to bone loss, Evidence from rodent experiments has established that bothmicrogravity and ionizing radiation can cause bone loss due to increasd of bone-resorbing osteoclasts and decreasedin bone-forming osteoblasts, although the underlying molecular mechanisms for these changes are not fullyunderstood. We hypothesized that excess reactive oxidative species (ROS) produced by conditions that simulatedspaceflight alters the tight balance between osteoclast and osteoblast activities, leading to accelerated skeletalremodeling and culminating in loss of mineralized tissue. To begin to explore this hypothesis, we used the mCATmouse model [1]; these transgenic mice over-express the human catalase gene targeted to mitochondria, which arethe major organelle responsible for cellular production of free radicals. Catalase is an anti-oxidant that catalyzes theconversion of the reactive species, hydrogen peroxide (H202), into water and oxygen. This animal model wasselected as it displays extended lifespan, reduced cardiovascular disease and reduced central nervous systemradiosensitivity, consistent with elevated anti-oxidant activity conferred by the transgene. We reasoned that miceoverexpressing catalase the mitochondria of osteoblast and osteoclast lineage cells would be protected from the boneloss caused by simulated spaceflight.

CATALASE IN SKELETAL TISSUE↗

NASA NTRS2016

Mitochondrial Oxidative Stress: Importance for Skeletal Structure and Responses to Simulated Spaceflight

Spaceflight environment poses challenges to the human body. Both microgravity and radiation may lead to excess production of reactive oxygen species (ROS) and resulting oxidative stress and tissue damage. Specifically in bone, elevated ROS can contribute to excess bone resorption by osteoclasts over bone formation by osteoblasts, reduced viability of osteocytes, and ultimately, osteoporosis. Thus, we hypothesized that suppression of mitochondrial ROS in bone cells improves overall bone structure in the adult skeleton and skeletal defenses from spaceflight. To begin to test our hypothesis, we (1) modified ROS levels in bone cells using mCAT (Malonyl CoA-acyl carrier protein transacylase) mice, which overexpress the human anti-oxidant catalase gene targeted to the mitochondria. We also increased ROS and stimulated skeletal remodeling by exposing mice to simulated spaceflight (hindlimb-unloading and total body-irradiation) or sham treatment. When challenged with treatment, bones from wildtype mice showed elevated levels of oxidative damage whereas mCAT mice did not. Treatment caused expected bone loss in wildtype mice. Treatment caused deficits in microarchitecture of mCAT mice, although lower in magnitude than wildtype. In conclusion, our results indicate mitochondrial ROS generation in osteoblast and osteoclast lineage cells of skeletal tissue contributes to skeletal remodeling and quenching oxidative damage may improve the skeletal responses to spaceflight.

Radiation↗

NASA NTRS2016

Effects of Simulated Spaceflight on Mitochondrial Oxidative Stress in Bone Remodelling

Microgravity and ionizing radiation may contribute to cellular stress; resulting in increased generation of reactive oxygen species (ROS), DNA damage, cell cycle arrest, and cell death. We hypothesized that suppression of excess ROS in osteoblasts and osteoclasts will improve bone microarchitecture. To test our hypothesis, we used irradiated transgenic mCAT mice overexpressing human anti-oxidant catalase gene targeted to the mitochondria (main site for ROS production). mCAT mice expressed the transgene and displayed elevated catalase activity in bone and ex vivo osteoblast and osteoclast cultures. Treated bone from wildtype mice showed elevated levels of oxidative damage whereas mCAT mice did not. Also, increased catalase activity correlated with decreased MDA levels and that increased oxidative damage correlated with decreased % bone volume. Ex-vivo osteoblast colony growth positively correlated with osteoblast catalase activity. mCAT mice displayed reduced % bone volume. Treatment caused significant bone loss in wildtype mice. Treatment also caused slight deficits in microarchitecture of mCAT mice. In conclusion, ROS signaling in both osteoblast and osteoclast lineage cells contribute to skeletal development and remodeling and quenching oxidative damage could play a role in bone loss prevention.

bone loss↗

NASA NTRS2016

Transgenic Mouse Model for Reducing Oxidative Damage in Bone

Bone loss can occur due to many challenges such age, radiation, microgravity, and Reactive Oxygen Species (ROS) play a critical role in bone resorption by osteoclasts (Bartell et al. 2014). We hypothesize that suppression of excess ROS in skeletal cells, both osteoblasts and osteoclasts, regulates skeletal growth and remodeling. To test our hypothesis, we used transgenic mCAT mice which overexpress the human anti-oxidant catalase gene targeted to the mitochondria, the main site for endogenous ROS production. mCAT mice have a longer life-span than wildtype controls and have been used to study various age-related disorders. To stimulate remodeling, 16 week old mCAT mice or wildtype mice were exposed to treatment (hindlimb-unloading and total body-irradiation) or sham treatment conditions (control). Tissues were harvested 2 weeks later for skeletal analysis (microcomputed tomography), biochemical analysis (gene expression and oxidative damage measurements), and ex vivo bone marrow derived cell culture (osteoblastogenesis and osteoclastogenesis). mCAT mice expressed the transgene and displayed elevated catalase activity in skeletal tissue and marrow-derived osteoblasts and osteoclasts grown ex vivo. In addition, when challenged with treatment, bone tissues from wildtype mice showed elevated levels of malondialdehyde (MDA), indicating oxidative damage) whereas mCAT mice did not. Correlation analysis revealed that increased catalase activity significantly correlated with decreased MDA levels and that increased oxidative damage correlated with decreased percent bone volume (BVTV). In addition, ex-vivo cultured osteoblast colony growth correlated with catalase activity in the osteoblasts. Thus, we showed that these transgenic mice can be used as a model to study the relationship between markers of oxidative damage and skeletal properties. mCAT mice displayed reduced BVTV and trabecular number relative to wildtype mice, as well as increased structural model index in the cancellous tibia. Treatment caused bone loss in wildtype mice, as expected. Treatment also caused deficits in microarchitecture of mCAT mice, although less severe than wildtype mice in some parameters (percent bone volume, structural model index and cortical area). In conclusion, our results indicate that endogenous ROS signaling in both osteoblast and osteoclast lineage cells contributes to skeletal growth and remodeling, and quenching oxidative damage could play a role in bone loss prevention.

transgenic mice↗

NASA NTRS2014

Transgenic Mouse Model for Reducing Oxidative Damage in Bone

Exposure to musculoskeletal disuse and radiation result in bone loss; we hypothesized that these catabolic treatments cause excess reactive oxygen species (ROS), and thereby alter the tight balance between bone resorption by osteoclasts and bone formation by osteoblasts, culminating in bone loss. To test this, we used transgenic mice which over-express the human gene for catalase, targeted to mitochondria (MCAT). Catalase is an anti-oxidant that converts the ROS hydrogen peroxide into water and oxygen. MCAT mice were shown previously to display reduced mitochondrial oxidative stress and radiosensitivity of the CNS compared to wild type controls (WT). As expected, MCAT mice expressed the transgene in skeletal tissue, and in marrow-derived osteoblasts and osteoclast precursors cultured ex vivo, and also showed greater catalase activity compared to wildtype (WT) mice (3-6 fold). Colony expansion in marrow cells cultured under osteoblastogenic conditions was 2-fold greater in the MCAT mice compared to WT mice, while the extent of mineralization was unaffected. MCAT mice had slightly longer tibiae than WT mice (2%, P less than 0.01), although cortical bone area was slightly lower in MCAT mice than WT mice (10%, p=0.09). To challenge the skeletal system, mice were treated by exposure to combined disuse (2 wk Hindlimb Unloading) and total body irradiation Cs(137) (2 Gy, 0.8 Gy/min), then bone parameters were analyzed by 2-factor ANOVA to detect possible interaction effects. Treatment caused a 2-fold increase (p=0.015) in malondialdehyde levels of bone tissue (ELISA) in WT mice, but had no effect in MCAT mice. These findings indicate that the transgene conferred protection from oxidative damage caused by treatment. Unexpected differences between WT and MCAT mice emerged in skeletal responses to treatment.. In WT mice, treatment did not alter osteoblastogenesis, cortical bone area, moment of inertia, or bone perimeter, whereas in MCAT mice, treatment increased these parameters. Taken together, this typically catabolic treatment (disuse and irradiation) appeared to stimulate cortical expansion in MCAT mice but not WT mice. In conclusion, these results reveal the importance of mitochondrial ROS generation in skeletal remodeling and show that MCAT mice provide a useful animal model for bone studies.

trandgenic↗

NASA NTRS2013

Causes and Predictability of the 2012 Great Plains Drought

Central Great Plains precipitation deficits during May-August 2012 were the most severe since at least 1895, eclipsing the Dust Bowl summers of 1934 and 1936. Drought developed suddenly in May, following near-normal precipitation during winter and early spring. Its proximate causes were a reduction in atmospheric moisture transport into the Great Plains from the Gulf of Mexico. Processes that generally provide air mass lift and condensation were mostly absent, including a lack of frontal cyclones in late spring followed by suppressed deep convection in summer owing to large-scale subsidence and atmospheric stabilization. Seasonal forecasts did not predict the summer 2012 central Great Plains drought development, which therefore arrived without early warning. Climate simulations and empirical analysis suggest that ocean surface temperatures together with changes in greenhouse gases did not induce a substantial reduction in summertime precipitation over the central Great Plains during 2012. Yet, diagnosis of the retrospective climate simulations also reveals a regime shift toward warmer and drier summertime Great Plains conditions during the recent decade, most probably due to natural decadal variability. As a consequence, the probability for severe summer Great Plains drought may have increased in the last decade compared to the 1980s and 1990s, and the so-called tail-risk for severe drought may have been heightened in summer 2012. Such an extreme drought event was nonetheless still found to be a rare occurrence within the spread of 2012 climate model simulations. Implications of this study's findings for U.S. seasonal drought forecasting are discussed.

Forecasts↗

NASA NTRS2010

Quantifying the Negative Feedback of Vegetation to Greenhouse Warming: A Modeling Approach

Several climate models indicate that in a 2 x CO2 environment, temperature and precipitation would increase and runoff would increase faster than precipitation. These models, however, did not allow the vegetation to increase its leaf density as a response to the physiological effects of increased CO2 and consequent changes in climate. Other assessments included these interactions but did not account for the vegetation down-regulation to reduce plant's photosynthetic activity and as such resulted in a weak vegetation negative response. When we combine these interactions in climate simulations with 2 x CO2, the associated increase in precipitation contributes primarily to increase evapotranspiration rather than surface runoff, consistent with observations, and results in an additional cooling effect not fully accounted for in previous simulations with elevated CO2. By accelerating the water cycle, this feedback slows but does not alleviate the projected warming, reducing the land surface warming by 0.6 C. Compared to previous studies, these results imply that long term negative feedback from CO2-induced increases in vegetation density could reduce temperature following a stabilization of CO2 concentration.

Bounous, L.↗

NASA NTRS2008

To What Extent Can Vegetation Mitigate Greenhouse Warming? A Modeling Approach

Climate models participating in the IPCC Fourth Assessment Report indicate that under a 2xCO2 environment, runoff would increase faster than precipitation overland. However, observations over large U.S watersheds indicate otherwise. This inconsistency suggests that there may be important feedbacks between climate and land surface unaccounted for in the present generation of models. We postulate that the increase in precipitation associated with the increase in CO2 is also increasing vegetation density, which may already be feeding back onto climate. Including this feedback in a climate model simulation resulted in precipitation and runoff trends consistent with observations and reduced the warming by 0.6OC overland. This unaccounted for missing water may be linked to about 10% of the missing land carbon sink. A recent compilation of outputs from 19 coupled atmosphere-ocean general circulation models used in the IPCC Fourth Assessment Report (AR4) shows projected increases in air temperature, precipitation and river discharge for 24 major rivers in the world in response to doubling CO2 by the end of the century (1). The ensemble mean from these models also indicates that, compared to their respective baselines overland, the global mean of the runoff change would increase faster (8.9% per year) than that of the precipitation (5% per year). We analyze century-scale observed annual runoff time-series (1901-2002) over 9 hydrological units covering large regions of the Eastern United States (Fig.1) compiled by the United States Geological Survey (USGS)(2). These regions were selected because they are the most forested; the least water-limited and are not under extensive irrigation. We compare these time-series to similar time-series of observed annual precipitation anomalies spanning the period 1900-1995 (3). Both time-series exhibit a positive longterm trend (Fig. 2); however, in contrast to the analysis of (I), these historic data records show that the rate of precipitation increase is 5.5 % per year, roughly double the rate of runoff increase of 3.1 % per year.

Bounoua, L.↗

NASA NTRS2003

Solid Inflammability Boundary At Low-Speed (SIBAL)

This research program is concerned with the effect of low-speed flow on the spreading and extinction processes over solid fuels. The project has passed the Science Concept Review and the experiment is currently scheduled to be performed in the ISS Combustion Integrated Rack. We present an overview of recent and ongoing experimental and theoretical efforts.

T'ien, J.↗

NASA NTRS1995

Magnetic clouds, helicity conservation, and intrinsic scale flux ropes

An intrinsic-scale flux-rope model for interplanetary magnetic clouds, incorporating conservation of magnetic helicity, flux and mass is found to adequately explain clouds' average thermodynamic and magnetic properties. In spite their continuous expansion as they balloon into interplanetary space, magnetic clouds maintain high temperatures. This is shown to be due to magnetic energy dissipation. The temperature of an expanding cloud is shown to pass through a maximum above its starting temperature if the initial plasma beta in the cloud is less than 2/3. Excess magnetic pressure inside the cloud is not an important driver of the expansion as it is almost balanced by the tension in the helical field lines. It is conservation of magnetic helicity and flux that requires that clouds expand radially as they move away from the Sun. Comparison with published data shows good agreement between measured cloud properties and theory. Parameters determined from theoretical fits to the data, when extended back to the Sun, are consistent with the origin of interplanetary magnetic clouds in solar filament eruptions. A possible extension of the heating mechanism discussed here to heating of the solar corona is discussed.

Kumar, A.↗

NASA NTRS1994

Helicity charging and eruption of magnetic flux from the Sun

The ejection of helical toroidal fields from the solar atmosphere and their detection in interplanetary space are described. The discovery that solar magnetic fields are twisted and that they are segregated by hemisphere according to their chirality has important implications for the escape process. The roles played by erupting prominences, coronal mass ejections (CME's) and active region (AR) loops in expressing the escape of magnetic flux and helicity are discussed. Sporadic flux escape associated with filament eruptions accounts for less than one-tenth the flux loss. Azimuthal flux loss by CME's could account for more, but the major contributor to flux escape may be AR loop expansion. It is shown how the transfer of magnetic helicity from the sun's interior into emerged loops ('helicity charging') could be the effective driver of solar eruptions and of flux loss from the sun.

Rust, David M.↗

NASA NTRS1994

Comparison of Gap Elements and Contact Algorithm for 3D Contact Analysis of Spiral Bevel Gears

Three dimensional stress analysis of spiral bevel gears in mesh using the finite element method is presented. A finite element model is generated by solving equations that identify tooth surface coordinates. Contact is simulated by the automatic generation of nonpenetration constraints. This method is compared to a finite element contact analysis conducted with gap elements.

Bibel, G. D.↗