39 research outputs found
Invisibility and indistinguishability in structural damage tomography
Structural damage tomography (SDT) uses full-field or distributed measurements collected from sensors or self-sensing materials to reconstruct quantitative images of potential damage in structures, such as civil structures, automobiles, aircraft, etc. In approximately the past ten years, SDT has increased in popularity due to significant gains in computing power, improvements in sensor quality, and increases in measurement device sensitivity. Nonetheless, from a mathematical standpoint, SDT remains challenging because the reconstruction problems are usually nonlinear and ill-posed. Inasmuch, the ability to reliably reconstruct or detect damage using SDT is seldom guaranteed due to factors such as noise, modeling errors, low sensor quality, and more. As such, damage processes may be rendered invisible due to data indistinguishability. In this paper we identify and address key physical, mathematical, and practical factors that may result in invisible structural damage. Demonstrations of damage invisibility and data indistinguishability in SDT are provided using experimental data generated from a damaged reinforced concrete beam
Field Measurements of the Atmospheric Dry Deposition Fluxes and Velocities of Polycyclic Aromatic Hydrocarbons to the Global Oceans
EVALUATION OF BALANCE AND GAIT ABNORMALITIES IN REFRACTORY EPILEPSY: COMPARISON WITH REMISSION EPILEPSY
The effects of balance exercises in Parkinson's disease patients with a home based program
A comparison of the statistical treatment of results using concentrations of elements determined by neutron activation and X-ray fluorescence analysis methods
Effect of lumbosacral corset on position sense of trunk, performance and balance of Parkinson's disease patients
A new magnetic resonance electrical impedance tomography (MREIT) algorithm: the RSM-MREIT algorithm with applications to estimation of human head conductivity
Albuminuria is associated with an increased prostasin in urine while aldosterone has no direct effect on urine and kidney tissue abundance of prostasin
The proteinase prostasin is a candidate mediator for aldosterone-driven proteolytic activation of the epithelial sodium channel (ENaC). It was hypothesized that the aldosterone-mineralocorticoid receptor (MR) pathway stimulates prostasin abundance in kidney and urine. Prostasin was measured in plasma and urine from type 2 diabetic patients with resistant hypertension (n = 112) randomized to spironolactone/placebo in a clinical trial. Prostasin protein level was assessed by immunoblotting in (1) human and rat urines with/without nephrotic syndrome, (2) human nephrectomy tissue, (3) urine and kidney from aldosterone synthase-deficient (AS(-/-)) mice and ANGII- and aldosterone-infused mice, and in (4) kidney from adrenalectomized rats. Serum aldosterone concentration related to prostasin concentration in urine but not in plasma. Plasma prostasin concentration increased significantly after spironolactone compared to control. Urinary prostasin and albumin related directly and were reduced by spironolactone. In patients with nephrotic syndrome, urinary prostasin protein was elevated compared to controls. In rat nephrosis, proteinuria coincided with increased urinary prostasin, unchanged kidney tissue prostasin, and decreased plasma prostasin while plasma aldosterone was suppressed. Prostasin protein abundance in human nephrectomy tissue was similar across gender and ANGII inhibition regimens. Prostasin urine abundance was not different in AS(-/-) and aldosterone-infused mice. Prostasin kidney level was not different from control in adrenalectomized rats and AS(-/-) mice. We found no evidence for a direct relationship between mineralocorticoid receptor signaling and kidney and urine prostasin abundance. The reduction of urinary prostasin in spironolactone-treated patients is most likely the result of an improved glomerular filtration barrier function and generally reduced proteinuria
Pulse inhibition of histone deacetylases induces complete resistance to oxidative death in cortical neurons without toxicity and reveals a role for cytoplasmic p21(waf1/cip1) in cell cycle-independent neuroprotection
Histone deacetylase (HDAC) inhibitors are currently in human clinical trials as antitumor drugs because of their ability to induce cell dysfunction and death in cancer cells. The toxic effects of HDAC inhibitors are also apparent in cortical neurons in vitro, despite the ability of these agents to induce significant protection in the cells they do not kill. Here we demonstrate that pulse exposure of cortical neurons (2 h) in an in vitro model of oxidative stress results in durable neuroprotection without toxicity. Protection was associated with transcriptional upregulation of the cell cycle inhibitor, p21(waf1/cip1), both in this model and in an in vivo model of permanent ischemia. Transgenic overexpression of p21(waf1/cip1) in neurons can mimic the protective effect of HDAC inhibitors against oxidative stress-induced toxicity, including death induced by glutathione depletion or peroxide addition. The protective effect of p21(waf1/cip1) in the context of oxidative stress appears to be unrelated to its ability to act in the nucleus to inhibit cell cycle progression. However, although p21(waf1/cip1) is sufficient for neuroprotection, it is not necessary for HDAC inhibitor neuroprotection, because these agents can completely protect neurons cultured from p21(waf1/cip1)-null mice. Together these findings demonstrate (1) that pulse inhibition of HDACs in cortical neurons can induce neuroprotection without apparent toxicity; (2) that p21(waf1/cip1) is sufficient but not necessary to mimic the protective effects of HDAC inhibition; and (3) that oxidative stress in this model induces neuronal cell death via cell cycle-independent pathways that can be inhibited by a cytosolic, noncanonical action of p21(waf1/cip1)