Moving-edge detection via heat flow analogy

In this paper, a new and automatic moving-edge detection algorithm is proposed, based on using the heat flow analogy. This algorithm starts with anisotropic heat diffusion in the spatial domain, to remove noise and sharpen region boundaries for the purpose of obtaining high quality edge data. Then, isotropic and linear heat diffusion is applied in the temporal domain to calculate the total amount of heat flow. The moving-edges are represented as the total amount of heat flow out from the reference frame. The overall process is completed by non-maxima suppression and hysteresis thresholding to obtain binary moving edges. Evaluation, on a variety of data, indicates that this approach can handle noise in the temporal domain because of the averaging inherent of isotropic heat flow. Results also show that this technique can detect moving-edges in image sequences, without background image subtraction

Lithospheric controls on melt production during continental breakup at slow rates of extension: Application to the North Atlantic

Rifted margins form from extension and breakup of the continentallithosphere. If this extension is coeval with a region of hotter lithosphere,then it is generally assumed that a volcanic margin would follow. Herewe present the results of numerical simulations of rift margin evolution byextending continental lithosphere above a thermal anomaly. We find that unlessthe lithosphere is thinned prior to the arrival of the thermal anomalyor half spreading rates are more than ? 50mmyr?1, the lithosphere actsas a lid to the hot material. The thermal anomaly cools significantly by conductionbefore having an effect on decompression melt production. If the lithosphereis thinned by the formation of extensional basins then the thermalanomaly advects into the thinned region and leads to enhanced decompressionmelting. In the North Atlantic a series of extensional basins off the coastof northwest Europe and Greenland provide the required thinning. This observationsuggests that volcanic margins that show slow rates of extension,only occur where there is the combination of a thermal anomaly and previousregional thinning of the lithosphere

On using an analogy to heat flow for shape extraction

We introduce a novel evolution-based segmentationalgorithm which uses the heat flow analogy togain practical advantage. The proposed algorithm consistsof two parts. In the first part, we represent a particular heatconduction problem in the image domain to roughly segmentthe region of interest. Then we use geometric heatflow to complete the segmentation, by smoothing extractedboundaries and removing noise inside the prior segmentedregion. The proposed algorithm is compared with activecontour models and is tested on synthetic and medicalimages. Experimental results indicate that our approachworks well in noisy conditions without pre-processing. Itcan detect multiple objects simultaneously. It is alsocomputationally more efficient and easier to control andimplement in comparison with active contour models

Theoretical evaluation of the melting efficiency for the single-screw micro-extrusion process : the case of 3D printing of ABS

One of the challenges for single-screw micro-extrusion or additive manufacturing (AM), thus 3D printing, of polymers is controlling the melting efficiency so that energy and equipment costs can be minimized. Here, a numerical model is presented for AM process design, selecting acrylonitrile-butadiene-styrene (ABS) as viscoelastic reference polymer. It is demonstrated that AM melting is different compared to conventional melting due to variation in extrusion dimensions, leading to a different balance in heating by conduction and viscous heat dissipation as caused by the shearing between the melt layers in the associated film layer near the barrel. The thickness of this melt film layer is variable along the screw length, and it is shown that simplified models assuming an overall average value are too approximate. It is highlighted that the screw frequency, pitch angle and compression ratio are important process parameters to control the point of melt finalization. In addition, the power-law index reflecting the shear thinning nature of the polymer melt is showcased as a key parameter. Moreover, AM process results assuming constant and temperature dependent specific heat capacities and thermal conductivities are compared. The current work opens the door for on-line AM process control, addressing all relevant operating and material parameters

Cellular Monte Carlo Simulation of Coupled Electron and Phonon Dynamics

abstract: A novel Monte Carlo rejection technique for solving the phonon and electron Boltzmann Transport Equation (BTE), including full many-particle interactions, is presented in this work. This technique has been developed to explicitly model population-dependent scattering within the full-band Cellular Monte Carlo (CMC) framework to simulate electro-thermal transport in semiconductors, while ensuring the conservation of energy and momentum for each scattering event. The scattering algorithm directly solves the many-body problem accounting for the instantaneous distribution of the phonons. The general approach presented is capable of simulating any non-equilibrium phase-space distribution of phonons using the full phonon dispersion without the need of the approximations commonly used in previous Monte Carlo simulations. In particular, anharmonic interactions require no assumptions regarding the dominant modes responsible for anharmonic decay, while Normal and Umklapp scattering are treated on the same footing. This work discusses details of the algorithmic implementation of the three particle scattering for the treatment of the anharmonic interactions between phonons, as well as treating isotope and impurity scattering within the same framework. The approach is then extended with a technique based on the multivariable Hawkes point process that has been developed to model the emission and the absorption process of phonons by electrons. The simulation code was validated by comparison with both analytical, numerical, and experimental results; in particular, simulation results show close agreement with a wide range of experimental data such as the thermal conductivity as function of the isotopic composition, the temperature and the thin-film thickness.Dissertation/ThesisDoctoral Dissertation Electrical Engineering 201

Ice formation on a smooth or rough cold surface due to the impact of a supercooled water droplet

Ice accretion is considered in the impact of a supercooled water droplet on a smooth or rough solid surface, the roughness accounting for earlier icing. In this theoretical investigation the emphasis and novelty lie in the full nonlinear interplay of the droplet motion and the growth of the ice surface being addressed for relatively small times, over a realistic range of Reynolds numbers, Froude numbers, Weber numbers, Stefan numbers and capillary underheating parameters. The Prandtl number and the kinetic under-heating parameter are taken to be order unity. The ice accretion brings inner layers into play forcibly, affecting the outer flow. (The work includes viscous effects in an isothermal impact without phase change, as a special case, and the differences between impact with and without freezing.) There are four main findings. First, the icing dynamically can accelerate or decelerate the spreading of the droplet whereas roughness on its own tends to decelerate spreading. The interaction between the two and the implications for successive freezings are found to be subtle. Second, a focus on the dominant physical effects reveals a multi-structure within which restricted regions of turbulence are implied. The third main finding is an essentially parabolic shape for a single droplet freezing under certain conditions. Fourth is a connection with a body of experimental and engineering work and with practical findings to the extent that the explicit predictions here for ice-accretion rates are found to agree with the experimental range.

Caveolin-1 and Altered Neuregulin Signaling Contribute to the Pathophysiological Progression of Diabetic Peripheral Neuropathy

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.OBJECTIVE Evaluate if Erb B2 activation and the loss of caveolin-1 (Cav1) contribute to the pathophysiological progression of diabetic peripheral neuropathy (DPN). RESEARCH DESIGN AND METHODS Cav1 knockout and wild-type C57BL/6 mice were rendered diabetic with streptozotocin, and changes in motor nerve conduction velocity (MNCV), mechanical and thermal hypoalgesia, Erb B2 phosphorylation (pErb B2), and epidermal nerve fiber density were assessed. The contribution of Erb B2 to DPN was assessed using the Erb B2 inhibitors PKI 166 and erlotinib and a conditional bitransgenic mouse that expressed a constitutively active form of Erb B2 in myelinated Schwann cells (SCs). RESULTS Diabetic mice exhibited decreased MNCV and mechanical and thermal sensitivity, but the extent of these deficits was more severe in diabetic Cav1 knockout mice. Diabetes increased pErb B2 levels in both genotypes, but the absence of Cav1 correlated with a greater increase in pErb B2. Erb B2 activation contributed to the mechanical hypoalgesia and MNCV deficits in both diabetic genotypes because treatment with erlotinib or PKI 166 improved these indexes of DPN. Similarly, induction of a constitutively active Erb B2 in myelinated SCs was sufficient to decrease MNCV and induce a mechanical hypoalgesia in the absence of diabetes. CONCLUSIONS Increased Erb B2 activity contributes to specific indexes of DPN, and Cav1 may be an endogenous regulator of Erb B2 signaling. Altered Erb B2 signaling is a novel mechanism that contributes to SC dysfunction in diabetes, and inhibiting Erb B2 may ameliorate deficits of tactile sensitivity in DPN. Diabetic peripheral neuropathy (DPN) is a common complication of diabetes (1). Although hyperglycemia is the definitive cause of DPN (2), the vascular, glial, and neuronal damage that underlies the progressive axonopathy in DPN has a complex biochemical etiology involving oxidative stress (3,4), protein glycation (5), protein kinase C activation (6), polyol synthesis (7), and the hexosamine pathway (8). Altered neurotrophic support also contributes to sensory neuron dysfunction in DPN (9), but whether diabetes may alter growth factor signaling in Schwann cells (SCs), which also undergo substantial degeneration in diabetes, is poorly defined. Neuregulins are growth factors that control SC growth, survival, and differentiation via their interaction with Erb B receptors (10). Although Erb B2 signaling promotes developmental myelination and is clearly trophic for SCs, pharmacological evidence supports that pathologic activation of Erb B2 after axotomy (11) or infection with leprosy bacilli (12) is sufficient to induce SC dedifferentiation and demyelination. Additionally, genetic evidence supports that Erb B2 can promote the development of sensory neuropathies independent of diabetes because expression of a dominant-negative Erb B4 in nonmyelinating (13) or myelinating (14) SCs induced a temperature or mechanical sensory neuropathy, respectively. Given the contribution of Erb B2 to the degeneration of SCs, endogenous proteins that regulate Erb B2 activity may influence the development of certain aspects of sensory neuropathies. The interaction of Erb B2 with the protein caveolin-1 (Cav1) inhibits the intrinsic tyrosine kinase activity of the receptor (15). Cav1 is highly expressed in mature, myelinated SCs (16), and we have shown that prolonged hyperglycemia promoted the downregulation of Cav1 in SCs of sciatic nerve (17). Cav1 may regulate Erb B2 signaling in SCs because its forced downregulation was sufficient to enhance neuregulin-induced demyelination of SC–dorsal root ganglion (DRG) neuron cocultures (18). However, it is unknown whether an increase in Erb B2 activity may contribute to the pathophysiological development of DPN and if changes in Cav1 expression may alter Erb B2 activation in diabetic nerve. In the current study, we demonstrate that diabetic Cav1 knockout mice showed an increased activation of Erb B2 and developed greater motor nerve conduction velocity (MNCV) deficits relative to their wild-type counterparts. Inhibition of Erb B2 with two structurally diverse inhibitors corrected the MNCV deficits and mechanical hypoalgesia evident after 6 or 15 weeks of diabetes. Also, induction of a constitutively active Erb B2 in myelinated SCs of adult mice was sufficient to recapitulate the MNCV and mechanical sensitivity deficits observed in the diabetic mice. These studies provide the first evidence that activation of Erb B2 contributes to deficits associated with myelinated fiber function in diabetic nerve and suggest that Cav1 may serve as an endogenous regulator of Erb B2.This work was supported by grants from the Juvenile Diabetes Research Foundation and the National Institutes of Health (NS-054847 and DK-073594)

Caveolin-1 and Altered Neuregulin Signaling Contribute to the Pathophysiological Progression of Diabetic Peripheral Neuropathy

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.OBJECTIVE Evaluate if Erb B2 activation and the loss of caveolin-1 (Cav1) contribute to the pathophysiological progression of diabetic peripheral neuropathy (DPN). RESEARCH DESIGN AND METHODS Cav1 knockout and wild-type C57BL/6 mice were rendered diabetic with streptozotocin, and changes in motor nerve conduction velocity (MNCV), mechanical and thermal hypoalgesia, Erb B2 phosphorylation (pErb B2), and epidermal nerve fiber density were assessed. The contribution of Erb B2 to DPN was assessed using the Erb B2 inhibitors PKI 166 and erlotinib and a conditional bitransgenic mouse that expressed a constitutively active form of Erb B2 in myelinated Schwann cells (SCs). RESULTS Diabetic mice exhibited decreased MNCV and mechanical and thermal sensitivity, but the extent of these deficits was more severe in diabetic Cav1 knockout mice. Diabetes increased pErb B2 levels in both genotypes, but the absence of Cav1 correlated with a greater increase in pErb B2. Erb B2 activation contributed to the mechanical hypoalgesia and MNCV deficits in both diabetic genotypes because treatment with erlotinib or PKI 166 improved these indexes of DPN. Similarly, induction of a constitutively active Erb B2 in myelinated SCs was sufficient to decrease MNCV and induce a mechanical hypoalgesia in the absence of diabetes. CONCLUSIONS Increased Erb B2 activity contributes to specific indexes of DPN, and Cav1 may be an endogenous regulator of Erb B2 signaling. Altered Erb B2 signaling is a novel mechanism that contributes to SC dysfunction in diabetes, and inhibiting Erb B2 may ameliorate deficits of tactile sensitivity in DPN. Diabetic peripheral neuropathy (DPN) is a common complication of diabetes (1). Although hyperglycemia is the definitive cause of DPN (2), the vascular, glial, and neuronal damage that underlies the progressive axonopathy in DPN has a complex biochemical etiology involving oxidative stress (3,4), protein glycation (5), protein kinase C activation (6), polyol synthesis (7), and the hexosamine pathway (8). Altered neurotrophic support also contributes to sensory neuron dysfunction in DPN (9), but whether diabetes may alter growth factor signaling in Schwann cells (SCs), which also undergo substantial degeneration in diabetes, is poorly defined. Neuregulins are growth factors that control SC growth, survival, and differentiation via their interaction with Erb B receptors (10). Although Erb B2 signaling promotes developmental myelination and is clearly trophic for SCs, pharmacological evidence supports that pathologic activation of Erb B2 after axotomy (11) or infection with leprosy bacilli (12) is sufficient to induce SC dedifferentiation and demyelination. Additionally, genetic evidence supports that Erb B2 can promote the development of sensory neuropathies independent of diabetes because expression of a dominant-negative Erb B4 in nonmyelinating (13) or myelinating (14) SCs induced a temperature or mechanical sensory neuropathy, respectively. Given the contribution of Erb B2 to the degeneration of SCs, endogenous proteins that regulate Erb B2 activity may influence the development of certain aspects of sensory neuropathies. The interaction of Erb B2 with the protein caveolin-1 (Cav1) inhibits the intrinsic tyrosine kinase activity of the receptor (15). Cav1 is highly expressed in mature, myelinated SCs (16), and we have shown that prolonged hyperglycemia promoted the downregulation of Cav1 in SCs of sciatic nerve (17). Cav1 may regulate Erb B2 signaling in SCs because its forced downregulation was sufficient to enhance neuregulin-induced demyelination of SC–dorsal root ganglion (DRG) neuron cocultures (18). However, it is unknown whether an increase in Erb B2 activity may contribute to the pathophysiological development of DPN and if changes in Cav1 expression may alter Erb B2 activation in diabetic nerve. In the current study, we demonstrate that diabetic Cav1 knockout mice showed an increased activation of Erb B2 and developed greater motor nerve conduction velocity (MNCV) deficits relative to their wild-type counterparts. Inhibition of Erb B2 with two structurally diverse inhibitors corrected the MNCV deficits and mechanical hypoalgesia evident after 6 or 15 weeks of diabetes. Also, induction of a constitutively active Erb B2 in myelinated SCs of adult mice was sufficient to recapitulate the MNCV and mechanical sensitivity deficits observed in the diabetic mice. These studies provide the first evidence that activation of Erb B2 contributes to deficits associated with myelinated fiber function in diabetic nerve and suggest that Cav1 may serve as an endogenous regulator of Erb B2.This work was supported by grants from the Juvenile Diabetes Research Foundation and the National Institutes of Health (NS-054847 and DK-073594)

Development of Cd1-xMgxTe thin films for application as an electron reflector in CdS/CdTe solar cells

2014 Summer.Efficiencies of CdS/CdTe photovoltaic cells significantly lag behind their theoretical limit, primarily because open-circuit voltage (VOC) of record efficiency cells (872 mV) is well below what is expected for the CdTe band gap (1.5 eV). A substantial VOC improvement can be achieved through addition of an electron reflector (ER) layer to CdTe devices. The ER layer forms a conduction-band barrier that reflects minority-charge carriers (i.e. electrons in p-type CdTe) away from the back surface. Similar to back-surface fields in c-Si, III-V, and CIGS solar cells, the ER strategy is expected to reduce back-surface recombination and is estimated to increase CdTe VOC by about 200 mV based on numerical simulation. The presented research investigates the addition of a thin layer of wider band gap Cd1-xMgxTe (CMT) to achieve a CdTe ER structure. First, a novel co-sublimation process was developed for deposition of Cd1-xMgxTe thin films that demonstrates excellent experimental capabilities, commercial viability, and improved alloy control over other techniques. Next, the effects of processing on material properties of CMT deposition onto CdS/CdTe structures were investigated. It was discovered that substrate temperature during CMT deposition is a critical parameter for achieving uniform CMT film coverage on polycrystalline CdTe. Furthermore, CMT film growth was found to be epitaxial on CdTe where the CMT films retain the same microstructural features as the underlying CdTe grains. Despite film uniformity, significant Mg loss from the CMT film, oxide formation, and a reduction of the optical band gap was found after CdCl2-based passivation treatments. Preliminary process optimization found that band gap degradation can be minimized by utilizing MgCl2 in addition to CdCl2 as a treatment source material. Finally, development of CdS/CdTe/Cd1-xMgxTe electron reflector devices demonstrated a barrier behavior at high voltage bias and improved voltage when CdTe thickness is held below 1 μm. Additional electro-optical characterization and device modeling was used to understand the source of this device behavior. The results suggest the CdTe/Cd1-xMgxTe interface is likely free of detrimental electronic defects and the barrier behavior comes from a larger than expected valence band offset for the material system. Finally, future work to improve ER device performance is suggested