Integrating Both Parallax and Latency Compensation into Video See-through Head-mounted Display.

This work introduces a perspective-corrected video see-through mixed-reality head-mounted display with edge-preserving occlusion and low-latency capabilities. To realize the consistent spatial and temporal composition of a captured real world containing virtual objects, we perform three essential tasks: 1) to reconstruct captured images so as to match the user's view; 2) to occlude virtual objects with nearer real objects, to provide users with correct depth cues; and 3) to reproject the virtual and captured scenes to be matched and to keep up with users' head motions. Captured image reconstruction and occlusion-mask generation require dense and accurate depth maps. However, estimating these maps is computationally difficult, which results in longer latencies. To obtain an acceptable balance between spatial consistency and low latency, we rapidly generated depth maps by focusing on edge smoothness and disocclusion (instead of fully accurate maps), to shorten the processing time. Our algorithm refines edges via a hybrid method involving infrared masks and color-guided filters, and it fills disocclusions using temporally cached depth maps. Our system combines these algorithms in a two-phase temporal warping architecture based upon synchronized camera pairs and displays. The first phase of warping is to reduce registration errors between the virtual and captured scenes. The second is to present virtual and captured scenes that correspond with the user's head motion. We implemented these methods on our wearable prototype and performed end-to-end measurements of its accuracy and latency. We achieved an acceptable latency due to head motion (less than 4 ms) and spatial accuracy (less than 0.1° in size and less than 0.3° in position) in our test environment. We anticipate that this work will help improve the realism of mixed reality systems.

High-throughput deterministic plasma etching using array-type plasma generator system.

A deterministic processing method is a high-precision finishing method, where the to-be-removed amount of material at each point of the work surface is calculated based on an accurately measured present surface shape and is removed precisely using a numerically controlled (NC) processing system. Although this method has achieved nanometer-scale accuracy, the method requires considerable time to scan the work surface, leading to low productivity. Therefore, using an individual on-off controllable array-type plasma generator covering the entire work surface, enabling simultaneous NC plasma processing is proposed herein. A novel intermittent gas flow system was constructed using cyclic on-off control of the gas supply and exhaust valves instead of the commonly used continuous gas flow to achieve uniform in-plane plasma etching. It was found that uniform removal could be achieved by combining it with a pulse-modulated high-frequency power supply and setting the plasma generation time in one cycle to be sufficiently short. Furthermore, a power control approach was developed for maintaining a constant plasma state, even while varying the plasma-generating array elements, which resulted in a demonstration experiment of NC plasma etching that successfully reduced the thickness variation of a silicon substrate.

Highly polarized single-c-domain single-crystal Pb(Mn,Nb)O(3)-PZT thin films.

In-plane unstrained single-c-domain/single-crystal thin films of PZT-based ternary ferroelectric perovskite, ξPb(Mn,Nb)O3-(1 - ξ)PZT, were grown on SrRuO(3)/Pt/MgO substrates using magnetron sputtering followed by quenching. The sputtered unstrained thin films exhibit unique ferroelectric properties: high coercive field, Ec > 180 kV/cm, large remanent polarization, P(r) = 100 µC/cm(2), small relative dielectric constants, ε* = 100 to 150, high Curie temperature, Tc = ~600 °C, and bulk-like large transverse piezoelectric constants, e31,f = -12.0 C/m(2) for PZT(48/52) at ξ = 0.06. The unstrained thin films are an ideal structure to extract the bulk ferroelectric properties. Their micro-structures and ferroelectric properties are discussed in relation to the potential applications for piezoelectric MEMS.

Influence of Pb and La contents on the lattice configuration of La-substituted Pb(Zr,Ti)O3 films fabricated by CSD method.

The influence of Pb and La contents on the lattice configuration in La-substituted Pb(Zr0(.65),Ti0(.35))O3 (La- PZT) films was systematically investigated. La-PZT films with various La and Pb contents were fabricated on Pt/Ti/SiO(2)/Si substrates by chemical solution deposition (CSD). In the La- PZT films with a Pb content ratio of 125% relative to a stoichiometric value, La ions were substituted for not only A-site ions but also B-site ions at La contents greater than 3 mol%. La substitution for B-site seems to cause larger reduction of the unit cell size. In addition, we found that in the La-PZT films with a La content of 3 mol%, the Pb content of 116 mol% (120% relative to a stoichiometric value) was optimum from the viewpoint of site occupancy. This indicates that excess Pb prevented the A-site substitution of La ions.

Monocyte chemoattractant protein-1 is an essential inflammatory mediator in angiotensin II-induced progression of established atherosclerosis in hypercholesterolemic mice.

OBJECTIVE: Chronic inflammatory processes might be involved in the progression and destabilization of atherosclerotic plaques. Therefore, identification of the mechanism underlying arterial inflammatory function might lead to the development of novel therapeutic strategies. Angiotensin II (AngII) is implicated in atherogenesis by activating the vascular inflammation system, mainly through monocyte chemotaxis. Therefore, we hypothesized that AngII increases plaque size and promotes destabilization of established atheromas by activating the monocyte chemoattractant protein-1 (MCP-1) pathway. METHODS AND RESULTS: We report here that 4-week infusion of AngII not only increased plaque size but also induced a destabilization phenotype (ie, increased macrophages and lipids and decreased collagen and smooth muscle cells) of pre-existing atherosclerotic lesions of hypercholesterolemic mice. AngII also enhanced the gene expression of inflammatory cytokines (TNFalpha, IL-6, etc.) and chemokines (MCP-1, CCR2, etc). Blockade of MCP-1, by transfecting the deletion mutant of the human MCP-1 gene into the skeletal muscles, limited AngII-induced progression and destabilization of established atherosclerotic lesions and suppressed the induction of proinflammatory genes. CONCLUSIONS: These data suggest that MCP-1 functions as a central inflammatory mediator in the AngII-induced progression and changes in plaque composition of established atheroma.

Nonrequirement of continuous stimulation with MCP-1 for cell migration and determination of directional migration by initial stimulation with chemokine.

Monocyte chemoattractant protein-1 (MCP-1) induces monocyte migration through interaction with the MCP-1 receptor CCR2. In this report we have examined the length of chemokine stimulation necessary for induction of cell migration and whether continuous stimulation is required for active migration. Monocytic THP-1 cells prestimulated with MCP-1 for 15 to 30 min exhibited a migration response after the chemokine was removed from the culture medium, indicating that a short exposure to chemokine stimulation is sufficient for migration of THP-1 cells and continuous stimulation is not required for active migration. A reverse gradient of MCP-1 had no effect on migration after prestimulation with MCP-1. This implies that cells are determined to directionally migrate by initial stimulation with MCP-1. Furthermore, cell migration after prestimulation with MCP-1 was inhibited by a p38 inhibitor, but not by a phosphatidylinositol 3-kinase (PI3-kinase) inhibitor, indicating that p38, but not PI3-kinase, is involved in the migration response after the determination of direction by initial chemokine stimulation.

Anti-monocyte chemoattractant protein-1 gene therapy limits progression and destabilization of established atherosclerosis in apolipoprotein E-knockout mice.

BACKGROUND: Monocyte infiltration into the arterial wall and its activation is the central event in atherogenesis. Thus, monocyte chemoattractant protein-1 (MCP-1) might be a novel therapeutic target against atherogenesis. We and others recently reported that blockade or abrogation of the MCP-1 pathway attenuates the initiation of atheroma formation in hypercholesterolemic mice. It remains unclear, however, whether blockade of MCP-1 can limit progression or destabilization of established lesions. METHODS AND RESULTS: We report here that blockade of MCP-1 by transfecting an N-terminal deletion mutant of the MCP-1 gene limited progression of preexisting atherosclerotic lesions in the aortic root in hypercholesterolemic mice. In addition, blockade of MCP-1 changed the lesion composition into a more stable phenotype, ie, containing fewer macrophages and lymphocytes, less lipid, and more smooth muscle cells and collagen. This strategy decreased expression of CD40 and the CD40 ligand in the atherosclerotic plaque and normalized the increased chemokine (RANTES and MCP-1) and cytokine (tumor necrosis factor alpha, interleukin-6, interleukin-1beta, and transforming growth factor beta(1)) gene expression. These data suggest that MCP-1 is a central mediator in the progression and destabilization of established atheroma. CONCLUSIONS: The results of the present study suggest that the inflammatory responses mediated by MCP-1 are important in atherosclerosis and its complications.

Anti-monocyte chemoattractant protein-1 gene therapy attenuates pulmonary hypertension in rats.

Monocyte/macrophage chemoattractant protein-1 (MCP-1), a potent chemoattractant chemokine and an activator for mononuclear cells, may play a role in the initiation and/or progression of pulmonary hypertension (PH). To determine whether blockade of a systemic MCP-1 signal pathway in vivo may prevent PH, we intramuscularly transduced a naked plasmid encoding a 7-NH(2) terminus-deleted dominant negative inhibitor of the MCP-1 (7ND MCP-1) gene in monocrotaline-induced PH. We also simultaneously gave a duplicate transfection at 2-wk intervals or skeletal muscle-directed in vivo electroporation (EP) to evaluate whether a longer or higher expression might be more effective. The intramuscular reporter gene expression was enhanced 10 times over that by EP than by simple injection, and a significant 7ND MCP-1 protein in plasma was detected only in the EP group. 7ND MCP-1 gene transfer significantly inhibited the progression of MCT-induced PH as evaluated by right ventricular systolic pressure, right ventricular hypertrophy, medial hypertrophy of pulmonary arterioles, and mononuclear cell infiltration into the lung. Differential effects of longer or higher transgene expression were not apparent. Although the in vivo kinetics of 7ND MCP-1 gene therapy should be studied further, these encouraging results suggest that an anti-inflammatory strategy via blockade of the MCP-1 signal pathway may be an alternative approach to treat subjects with PH.

Importance of monocyte chemoattractant protein-1 pathway in neointimal hyperplasia after periarterial injury in mice and monkeys.

Neointimal hyperplasia is a major cause of restenosis after coronary intervention. Because vascular injury is now recognized to involve an inflammatory response, monocyte chemoattractant protein-1 (MCP-1) might be involved in underlying mechanisms of restenosis. In the present study, we demonstrate the important role of MCP-1 in neointimal hyperplasia after cuff-induced arterial injury. In the first set of experiments, placement of a nonconstricting cuff around the femoral artery of intact mice and monkeys resulted in inflammation in the early stages and subsequent neointimal hyperplasia at the late stages. We transfected with an N-terminal deletion mutant of the human MCP-1 gene into skeletal muscles to block MCP-1 activity in vivo. This mutant MCP-1 works as a dominant-negative inhibitor of MCP-1. This strategy inhibited early vascular inflammation (monocyte infiltration, increased expression of MCP-1, and inflammatory cytokines) and late neointimal hyperplasia. In the second set of experiments, the cuff-induced neointimal hyperplasia was found to be less in CCR2-deficient mice than in control CCR2(+/+) mice. The MCP-1/CCR2 pathway plays a central role in the pathogenesis of neointimal hyperplasia in cuffed femoral artery of mice and monkeys. Therefore, the MCP-1/CCR2 pathway can be a therapeutic target for human restenosis after coronary intervention.