Techniques for writing and reading data on an optical disk which include formation of holographic optical gratings in plural locations on the optical disk

An optical memory for storing and/or reading data on an optical disk. The optical disk incorporates a material in which holographic gratings can be created, and subsequently detected, at plural locations within the disk by an electro-optical head. Creation and detection of holographic gratings with variable diffraction efficiency is possible with the electro-optical head. Multiple holographic gratings can also be created at each one of the plural locations via a beam of light which has a different wavelength or point of focus. These data elements can be read by the electro-optical head using a beam of light sequentially varied in wavelength or point of focus to correspond to the multiple holographic gratings to be recorded

Large-scale Holographic Memory: Experiment Results

We describe a holographic optical memory capable of storing up to 10^12 bits of information. The stored information is retrieved in blocks or pages, each consisting of 10^3 x 10^3 bits. Each page can be accessed randomly in approximately 100 µsec with an experimentally measured SNR of 816.8, and a projected probability of error of 10^(-28)

Large-scale volume holographic storage in the long interaction length architecture

We describe a page-formatted random-access holographic memory designed to store up to 160,000 holograms. The memory consists of 16 vertically spaced locations, each containing 10,000 holograms, which in turn are organized as 10 fractal-multiplexed rows of 1000 angularly-multiplexed holograms. A segmented mirror array is used to enable random access to any of the stored holograms within the access time of a non-mechanical angle scanner such as an acousto-optic deflector. Using a mechanical scanner with such a mirror array, we demonstrate storage of 10,000 holograms at a single location of the system, as well as simultaneous storage and recall of holograms at 6 locations, including the highest and lowest of the 16 locations

System metric for holographic memory systems

We show that the oxidation state of Fe in LiNbO3 has two competing effects on the diffraction efficiency of multiple holograms in 90 degrees-geometry holographic storage. For crystals with moderate absorption, the saturation space-charge field is larger after high-temperature reduction treatment. However, reduction also increases absorption, which reduces the overall diffraction efficiency. We develop a theoretical model that predicts achievable diffraction efficiency as a function of oxidation state, doping level, photovoltaic field, crystal length, and region of beam overlap. We compare this model with experimental results for achievable diffraction efficiency and erasure-time constant. (C) 1996 Optical Society of Americ

System metric for holographic memory systems

We introduce M/# as a metric for characterizing holographic memory systems. M/# is the constant of proportionality between diffraction efficiency and the number of holograms squared. Although M/# is a function of many variables in a holographic recording system, it can be measured from the recording and erasure of a single hologram. We verify experimentally that the diffraction efficiency of multiple holograms follows the prediction of M/# measured from a single hologram

Sequestration of free cholesterol in cell membranes by prions correlates with cytoplasmic phospholipase A2 activation

<p>Abstract</p> <p>Background</p> <p>The transmissible spongiform encephalopathies (TSEs), otherwise known as the prion diseases, occur following the conversion of the normal cellular prion protein (PrP^C) to an alternatively folded isoform (PrP^Sc). The accumulation of PrP^Scwithin the brain leads to neurodegeneration through an unidentified mechanism. Since many neurodegenerative disorders including prion, Parkinson's and Alzheimer's diseases may be modified by cholesterol synthesis inhibitors, the effects of prion infection on the cholesterol balance within neuronal cells were examined.</p> <p>Results</p> <p>We report the novel observation that prion infection altered the membrane composition and significantly increased total cholesterol levels in two neuronal cell lines (ScGT1 and ScN2a cells). There was a significant correlation between the concentration of free cholesterol in ScGT1 cells and the amounts of PrP^Sc. This increase was entirely a result of increased amounts of free cholesterol, as prion infection reduced the amounts of cholesterol esters in cells. These effects were reproduced in primary cortical neurons by the addition of partially purified PrP^Sc, but not by PrP^C. Crucially, the effects of prion infection were not a result of increased cholesterol synthesis. Stimulating cholesterol synthesis via the addition of mevalonate, or adding exogenous cholesterol, had the opposite effect to prion infection on the cholesterol balance. It did not affect the amounts of free cholesterol within neurons; rather, it significantly increased the amounts of cholesterol esters. Immunoprecipitation studies have shown that cytoplasmic phospholipase A₂(cPLA₂) co-precipitated with PrP^Scin ScGT1 cells. Furthermore, prion infection greatly increased both the phosphorylation of cPLA₂and prostaglandin E₂production.</p> <p>Conclusion</p> <p>Prion infection, or the addition of PrP^Sc, increased the free cholesterol content of cells, a process that could not be replicated by the stimulation of cholesterol synthesis. The presence of PrP^Scincreased solubilisation of free cholesterol in cell membranes and affected their function. It increased activation of the PLA₂pathway, previously implicated in PrP^Scformation and in PrP^Sc-mediated neurotoxicity. These observations suggest that the neuropathogenesis of prion diseases results from PrP^Scaltering cholesterol-sensitive processes. Furthermore, they raise the possibility that disturbances in membrane cholesterol are major triggering events in neurodegenerative diseases.</p

A Systematic Molecular Pathology Study of a Laboratory Confirmed H5N1 Human Case

Autopsy studies have shown that human highly pathogenic avian influenza virus (H5N1) can infect multiple human organs other than just the lungs, and that possible causes of organ damage are either viral replication and/or dysregulation of cytokines and chemokines. Uncertainty still exists, partly because of the limited number of cases analysed. In this study, a full autopsy including 5 organ systems was conducted on a confirmed H5N1 human fatal case (male, 42 years old) within 18 hours of death. In addition to the respiratory system (lungs, bronchus and trachea), virus was isolated from cerebral cortex, cerebral medullary substance, cerebellum, brain stem, hippocampus ileum, colon, rectum, ureter, aortopulmonary vessel and lymph-node. Real time RT-PCR evidence showed that matrix and hemagglutinin genes were positive in liver and spleen in addition to positive tissues with virus isolation. Immunohistochemistry and in-situ hybridization stains showed accordant evidence of viral infection with real time RT-PCR except bronchus. Quantitative RT-PCR suggested that a high viral load was associated with increased host responses, though the viral load was significantly different in various organs. Cells of the immunologic system could also be a target for virus infection. Overall, the pathogenesis of HPAI H5N1 virus was associated both with virus replication and with immunopathologic lesions. In addition, immune cells cannot be excluded from playing a role in dissemination of the virus in vivo

Multi-ancestry genome-wide association meta-analysis of Parkinson?s disease

Although over 90 independent risk variants have been identified for Parkinson’s disease using genome-wide association studies, most studies have been performed in just one population at a time. Here we performed a large-scale multi-ancestry meta-analysis of Parkinson’s disease with 49,049 cases, 18,785 proxy cases and 2,458,063 controls including individuals of European, East Asian, Latin American and African ancestry. In a meta-analysis, we identified 78 independent genome-wide significant loci, including 12 potentially novel loci (MTF2, PIK3CA, ADD1, SYBU, IRS2, USP8, PIGL, FASN, MYLK2, USP25, EP300 and PPP6R2) and fine-mapped 6 putative causal variants at 6 known PD loci. By combining our results with publicly available eQTL data, we identified 25 putative risk genes in these novel loci whose expression is associated with PD risk. This work lays the groundwork for future efforts aimed at identifying PD loci in non-European populations

The LRRK2 p.L1795F variant causes Parkinson's disease in the European population

LRRK2-PD represents the most common form of autosomal dominant Parkinson’s disease. We identified the LRRK2 p.L1795F variant in three families and six additional unrelated cases using genetic data from over 50,000 individuals. Carriers with available genotyping data shared a common haplotype. The clinical presentation resembles other LRRK2-PD forms. Combined with published functional evidence showing strongly enhanced LRRK2 kinase activity, we provide evidence that LRRK2 p.L1795F is pathogenic