Browsing by Author "Yang, W"

Now showing 1 - 7 of 7
  • Thumbnail Image
    ItemOpen Access
    A wearable hydraulic shock absorber with efficient energy dissipation
    (International Journal of Mechanical Sciences, 2024-05-15) Cecchi, NJ; Liu, Y; Vegesna, RV; Zhan, X; Yang, W; Espinoza Campomanes, LA; Grant, GA; Camarillo, DB
    Advances in shock absorber technology are often translated to wearable personal protective equipment (PPE) to protect humans from impact-related injuries. However, the effectiveness of PPE is limited by factors such as the tolerable size and weight of the PPE device and the environmental conditions in which the PPE will be used. In this study, we leveraged the energy dissipation of fluid flow using soft structures to prototype a novel, wearable hydraulic shock absorber — the Soft Hydraulic Shock. The Soft Hydraulic Shock achieved an efficient energy absorption ratio of 100 % across a range of impact loading conditions due to its fluid-based mechanism of energy absorption. In comparison, five state-of-the-art shock-absorbing technologies with similar dimensions and weights used in American football helmets were found to have average energy absorption ratios ranging from 74.0 % to 90.0 %, on average. Furthermore, the Soft Hydraulic Shock maintained a stable energy dissipation across a wide range of temperatures (-18 °C, 19.5 °C, 50 °C), while the energy dissipation of other shock absorbing technologies varied up to 20 % across these temperatures. Analyses of the behavior of the Soft Hydraulic Shock with different design parameters and impact loadings were further explored with a validated finite element model of the device. Finally, the Soft Hydraulic Shock demonstrated the ability to significantly mitigate brain injury risk (average 23.9 % reduction in Head Acceleration Response Metric) when implemented into a full helmet system. The results of this study demonstrate the promise of wearable hydraulic shock absorbers and provide a platform for further optimizing their performance.
  • Thumbnail Image
    ItemOpen Access
    Analysis of oxygen/glucose-deprivation-induced changes in SUMO3 conjugation using SILAC-based quantitative proteomics.
    (Journal of proteome research, 2012-02) Yang, W; Thompson, JW; Wang, Z; Wang, L; Sheng, H; Foster, MW; Moseley, MA; Paschen, W
    Transient cerebral ischemia dramatically activates small ubiquitin-like modifier (SUMO2/3) conjugation. In cells exposed to 6 h of transient oxygen/glucose deprivation (OGD), a model of ischemia, SUMOylation increases profoundly between 0 and 30 min following re-oxygenation. To elucidate the effect of transient OGD on SUMO conjugation of target proteins, we exposed neuroblastoma B35 cells expressing HA-SUMO3 to transient OGD and used stable isotope labeling with amino acids in cell culture (SILAC) to quantify OGD-induced changes in levels of specific SUMOylated proteins. Lysates from control and OGD-treated cells were mixed equally, and HA-tagged proteins were immunoprecipitated and analyzed by 1D-SDS-PAGE-LC-MS/MS. We identified 188 putative SUMO3-conjugated proteins, including numerous transcription factors and coregulators, and PIAS2 and PIAS4 SUMO ligases, of which 22 were increased or decreased more than ±2-fold. In addition to SUMO3, the levels of protein-conjugated SUMO1 and SUMO2, as well as ubiquitin, were all increased. Importantly, protein ubiquitination induced by OGD was completely blocked by gene silencing of SUMO2/3. Collectively, these results suggest several mechanisms for OGD-modulated SUMOylation, point to a number of signaling pathways that may be targets of SUMO-based signaling and recovery from ischemic stress, and demonstrate a tightly controlled crosstalk between the SUMO and ubiquitin conjugation pathways.
  • Thumbnail Image
    ItemOpen Access
    Development of a simplified spinal cord ischemia model in mice.
    (Journal of neuroscience methods, 2010-06) Wang, Z; Yang, W; Britz, GW; Lombard, FW; Warner, DS; Sheng, H
    Use of genetically manipulated mice facilitates understanding pathological mechanisms in many diseases and contributes to therapy development. However, there is no practical and clinically relevant mouse model available for spinal cord ischemia. This report introduces a simplified long-term outcome mouse model of spinal cord ischemia. Male C57Bl/6J mice were anesthetized with isoflurane and endotracheally intubated. The middle segment of the thoracic aorta was clamped for 0, 8, 10 or 12 min via left lateral thoracotomy. Rectal temperature was maintained at 37.0+/-0.5 degrees C. A laser Doppler probe was used to measure lumbar spinal cord blood flow during thoracic aorta cross-clamping. Open field locomotor function and rotarod performance were evaluated at 1h and 1, 3, 5, and 7 days post-injury. Surviving neurons in the lumbar ventral horn were counted at 7 days post-injury. Cross-clamping the middle segment of the thoracic aorta resulted in approximately 90% blood flow reduction in the lumbar spinal cord. Neurological deficit and neuronal cell death were associated with ischemia duration. Another set of mice were subjected to 10 min aortic clamping or sham surgery and neurological function was examined at 1h and 1, 3, 5, 7, 14, and 28 days. Four of 5 mice (80%) in the injured group survived 28 days and had significant neurological deficit. This study indicates that cross-clamping of the aorta via left thoracotomy is a simple and reliable method to induce spinal cord ischemia in mice allowing definition of long-term outcome.
  • Thumbnail Image
    ItemOpen Access
    Predicting the frequency dispersion of electronic hyperpolarizabilities on the basis of absorption data and thomas-kuhn sum rules
    (Journal of Physical Chemistry C, 2010-02-11) Hu, X; Xiao, D; Keinan, S; Asselberghs, I; Therien, MJ; Clays, K; Yang, W; Beratan, DN
    Successfully predicting the frequency dispersion of electronic hyperpolarizabilities is an unresolved challenge in materials science and electronic structure theory. We show that the generalized Thomas-Kuhn sum rules, combined with linear absorption data and measured hyperpolarizability at one or two frequencies, may be used to predict the entire frequency-dependent electronic hyperpolarizability spectrum. This treatment includes two- and three-level contributions that arise from the lowest two or three excited electronic state manifolds, enabling us to describe the unusual observed frequency dispersion of the dynamic hyperpolarizability in high oscillator strength M-PZn chromophores, where (porphinato)zinc(II) (PZn) and metal(II)polypyridyl (M) units are connected via an ethyne unit that aligns the high oscillator strength transition dipoles of these components in a head-to-tail arrangement. We show that some of these structures can possess very similar linear absorption spectra yet manifest dramatically different frequency dependent hyperpolarizabilities, because of three-level contributions that result from excited state-to excited state transition dipoles among charge polarized states. Importantly, this approach provides a quantitative scheme to use linear optical absorption spectra and very limited individual hyperpolarizability measurements to predict the entire frequency-dependent nonlinear optical response. Copyright © 2010 American Chemical Society.
  • Thumbnail Image
    ItemOpen Access
    Product selectivity in plasmonic photocatalysis for carbon dioxide hydrogenation
    (Nature Communications, 2017-02-23) Zhang, X; Li, X; Zhang, D; Su, NQ; Yang, W; Everitt, HO; Liu, J
  • Thumbnail Image
    ItemOpen Access
    Time-dependent transport through molecular junctions.
    (J Chem Phys, 2010-06-21) Ke, SH; Liu, R; Yang, W; Baranger, HU
    We investigate transport properties of molecular junctions under two types of bias--a short time pulse or an ac bias--by combining a solution for Green's functions in the time domain with electronic structure information coming from ab initio density functional calculations. We find that the short time response depends on lead structure, bias voltage, and barrier heights both at the molecule-lead contacts and within molecules. Under a low frequency ac bias, the electron flow either tracks or leads the bias signal (resistive or capacitive response) depending on whether the junction is perfectly conducting or not. For high frequency, the current lags the bias signal due to the kinetic inductance. The transition frequency is an intrinsic property of the junctions.
  • Thumbnail Image
    ItemOpen Access
    Transient ischemia induces massive nuclear accumulation of SUMO2/3-conjugated proteins in spinal cord neurons.
    (Spinal cord, 2013-02) Wang, Z; Wang, R; Sheng, H; Sheng, SP; Paschen, W; Yang, W

    Objectives

    The objective of this study is to determine whether transient spinal cord ischemia activates small ubiquitin-like modifier (SUMO1-3) conjugation, a post-translational protein modification that protects neurons from ischemia-like conditions.

    Methods

    Mice were subjected to 8-12 min of spinal cord ischemia and 3-24 h of recovery using a newly developed experimental model. To characterize the model, activation of stress response pathways induced after spinal cord ischemia, previously observed in other experimental models, was verified by western blot analysis. Levels and subcellular localization of SUMO-conjugated proteins in spinal cords were evaluated by western blot analysis and immunohistochemistry, respectively.

    Results

    Following transient spinal cord ischemia, stress responses were activated as indicated by increased phosphorylation of eukaryotic initiation factor 2 (eIF2α), extracellular signal-regulated kinases (ERK1/2) and Akt. SUMO1 conjugation was not altered, but a selective rise in levels of SUMO2/3-conjugated proteins occurred, peaking at 6 h reperfusion. The marked activation of SUMO2/3 conjugation was a neuronal response to ischemia, as indicated by co-localization with the neuronal marker NeuN, and was associated with nuclear accumulation of SUMO2/3-conjugated proteins.

    Conclusion

    Our study suggests that spinal cord neurons respond to ischemic stress by activation of SUMO2/3 conjugation. Many of the identified SUMO target proteins are transcription factors and other nuclear proteins involved in gene expression and genome stability. It is therefore concluded that the post-ischemic activation of SUMO2/3 conjugation may define the fate of neurons exposed to a transient interruption of blood supply, and that this pathway could be a therapeutic target to increase the resistance of spinal cord neurons to transient ischemia.