111 research outputs found

    Mining sequences in distributed sensors data for energy production.

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    Brief Overview of the Problem: The Environmental Protection Agency (EPA), a government funded agency, provides both legislative and judicial powers for emissions monitoring in the United States. The agency crafts laws based on self-made regulations to enforce companies to operate within the limits of the law resulting in environmentally safe operation. Specifically, power companies operate electric generating facilities under guidelines drawn-up and enforced by the EPA. Acid rain and other harmful factors require that electric generating facilities report hourly emissions recorded via a Supervisory Control and Data Acquisition (SCADA) system. SCADA is a control and reporting system that is present in all power plants consisting of sensors and control mechanisms that monitor all equipment within the plants. The data recorded by a SCADA system is collected by the EPA and allows them to enforce proper plant operation relating to emissions. This data includes a lot of generating unit and power plant specific details, including hourly generation. This hourly generation (termed grossunitload by the EPA) is the actual hourly average output of the generator on a per unit basis. The questions to be answered are do any of these units operate in tandem and do any of the units start, stop, or change operation as a result of another\u27s change in generation? These types of questions will be answered for the years of April 2002 through April 2003 for facilities that operate pipeline natural-gas-fired generating units. Purpose of Research The research conducted has dual uses if fruitful. First, the use of a local modeling between generating units would be highly profitable among energy traders. Betting that a plant will operate a unit based on another\u27s current characteristics would be sensationally profitable to energy traders. This profitability is variable due to fuel type. For instance, if the price of coal is extremely high due to shortages, the value of knowing a semioperating characteristic of two generating units is highly valuable. Second, this known characteristic can also be used in regulation and operational modeling. The second use is of great importance to government agencies. If regulatory committees can be aware of past (or current) similarities between power producers, they may be able to avoid a power struggle in a region caused by greedy traders or companies. Not considering profitable motives, the Department of Energy may use something similar to generate a model of power grid generation availability based on previous data for reliability purposes. Type of Problem: The problem tackled within this Master\u27s thesis is of multiple time series pattern recognition. This field is expansive and well studied, therefore the research performed will benefit from previously known techniques. The author has chosen to experiment with conventional techniques such as correlation, principal component analysis, and kmeans clustering for feature and eventually pattern extraction. For the primary analysis performed, the author chose to use a conventional sequence discovery algorithm. The sequence discovery algorithm has no prior knowledge of space limitations, therefore it searches over the entire space resulting in an expense but complete process. Prior to sequence discovery the author applies a uniform coding schema to the raw data, which is an adaption of a coding schema presented by Keogh. This coding and discovery process is deemed USD, or Uniform Sequence Discovery. The data is highly dimensional along with being extremely dynamic and sporadic with regards to magnitude. The energy market that demands power generation is profit and somewhat reliability driven. The obvious factors are more reliability based, for instance to keep system frequency at 60Hz, units may operate in an idle state resulting in a constant or very low value for a period of time (idle time). Also to avoid large frequency swings on the power grid, companies are require

    Meningitis due to listeria monocytogenes: Case report

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    Due Process and Deeds of Trust—Strange Bedfellows?

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    The authors examine in detail the validity of the private sale provisions of the Washington Deed of Trust Act in light of the recent procedural due process decisions of the United States Supreme Court. In addition to concluding that the present Washington Act appears to be unconstitutional, the authors briefly discuss the policy considerations involved and suggest general guidelines for change

    Expansion of the calcium hypothesis of brain aging and Alzheimer's disease: minding the store

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    Evidence accumulated over more than two decades has implicated Ca2+ dysregulation in brain aging and Alzheimer's disease (AD), giving rise to the Ca2+ hypothesis of brain aging and dementia. Electrophysiological, imaging, and behavioral studies in hippocampal or cortical neurons of rodents and rabbits have revealed aging-related increases in the slow afterhyperpolarization, Ca2+ spikes and currents, Ca2+ transients, and L-type voltage-gated Ca2+ channel (L-VGCC) activity. Several of these changes have been associated with age-related deficits in learning or memory. Consequently, one version of the Ca2+ hypothesis has been that increased L-VGCC activity drives many of the other Ca2+-related biomarkers of hippocampal aging. In addition, other studies have reported aging- or AD model-related alterations in Ca2+ release from ryanodine receptors (RyR) on intracellular stores. The Ca2+-sensitive RyR channels amplify plasmalemmal Ca2+ influx by the mechanism of Ca2+-induced Ca2+ release (CICR). Considerable evidence indicates that a preferred functional link is present between L-VGCCs and RyRs which operate in series in heart and some brain cells. Here, we review studies implicating RyRs in altered Ca2+ regulation in cell toxicity, aging, and AD. A recent study from our laboratory showed that increased CICR plays a necessary role in the emergence of Ca2+-related biomarkers of aging. Consequently, we propose an expanded L-VGCC/Ca2+ hypothesis, in which aging/pathological changes occur in both L-type Ca2+ channels and RyRs, and interact to abnormally amplify Ca2+ transients. In turn, the increased transients result in dysregulation of multiple Ca2+-dependent processes and, through somewhat different pathways, in accelerated functional decline during aging and AD

    Expansion of the Calcium Hypothesis of Brain Aging and Alzheimer\u27s Disease: Minding the Store

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    Evidence accumulated over more than two decades has implicated Ca2+ dysregulation in brain aging and Alzheimer\u27s disease (AD), giving rise to the Ca2+ hypothesis of brain aging and dementia. Electrophysiological, imaging, and behavioral studies in hippocampal or cortical neurons of rodents and rabbits have revealed aging-related increases in the slow afterhyperpolarization, Ca2+ spikes and currents, Ca2+transients, and L-type voltage-gated Ca2+ channel (L-VGCC) activity. Several of these changes have been associated with age-related deficits in learning or memory. Consequently, one version of the Ca2+ hypothesis has been that increased L-VGCC activity drives many of the other Ca2+-related biomarkers of hippocampal aging. In addition, other studies have reported aging- or AD model-related alterations in Ca2+ release from ryanodine receptors (RyR) on intracellular stores. The Ca2+-sensitive RyR channels amplify plasmalemmal Ca2+ influx by the mechanism of Ca2+-induced Ca2+ release (CICR). Considerable evidence indicates that a preferred functional link is present between L-VGCCs and RyRs which operate in series in heart and some brain cells. Here, we review studies implicating RyRs in altered Ca+ regulation in cell toxicity, aging, and AD. A recent study from our laboratory showed that increased CICR plays a necessary role in the emergence of Ca2+-related biomarkers of aging. Consequently, we propose an expanded L-VGCC/Ca2+ hypothesis, in which aging/pathological changes occur in both L-type Ca2+ channels and RyRs, and interact to abnormally amplify Ca2+ transients. In turn, the increased transients result in dysregulation of multiple Ca2+-dependent processes and, through somewhat different pathways, in accelerated functional decline during aging and AD

    Apparatus for Leak Testing Pressurized Hoses

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    A hose-attaching apparatus for leak-testing a pressurized hose may include a hose-attaching member. A bore may extend through the hose-attaching member. An internal annular cavity may extend coaxially around the bore. At least one of a detector probe hole and a detector probe may be connected to the internal annular cavity. At least a portion of the bore may have a diameter which is at least one of substantially equal to and less than a diameter of a hose to be leak-tested

    Methods for Diagnosing and Treating Alzheimer\u27s Disease (AD) Using the Molecules that Stabilize Intracellular Calcium (CA\u3csub\u3e2+\u3c/sub\u3e) Release

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    The subject technology relates, in part, to a method of treating Alzheimer\u27s Disease (AD), early-stage AD, elevated risk of AD, mild cognitive impairment (MCI), or other forms of age-related cognitive decline in a subject in need thereof by administering to the subject a molecule that promotes calcium-release stabilization in ryanodine receptors (RyRs) and/or inosital triphosphate receptors (InsP3Rs) in brain cells. Diagnostic methods using calcium-release stabilizing immunophilins, junctophilins or calmodulin are also disclosed

    Neuronal Calcium Imaging, Excitability, and Plasticity Changes in the \u3cem\u3eAldh2\u3c/em\u3e\u3csup\u3e-/-\u3c/sup\u3e Mouse Model of Sporadic Alzheimer\u27s Disease

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    BACKGROUND: Dysregulated signaling in neurons and astrocytes participates in pathophysiological alterations seen in the Alzheimer\u27s disease brain, including increases in amyloid-β, hyperphosphorylated tau, inflammation, calcium dysregulation, and oxidative stress. These are often noted prior to the development of behavioral, cognitive, and non-cognitive deficits. However, the extent to which these pathological changes function together or independently is unclear. OBJECTIVE: Little is known about the temporal relationship between calcium dysregulation and oxidative stress, as some reports suggest that dysregulated calcium promotes increased formation of reactive oxygen species, while others support the opposite. Prior work has quantified several key outcome measures associated with oxidative stress in aldehyde dehydrogenase 2 knockout (Aldh2-/-) mice, a non-transgenic model of sporadic Alzheimer\u27s disease. METHODS: Here, we tested the hypothesis that early oxidative stress can promote calcium dysregulation across aging by measuring calcium-dependent processes using electrophysiological and imaging methods and focusing on the afterhyperpolarization (AHP), synaptic activation, somatic calcium, and long-term potentiation in the Aldh2-/- mouse. RESULTS: Our results show a significant age-related decrease in the AHP along with an increase in the slow AHP amplitude in Aldh2-/- animals. Measures of synaptic excitability were unaltered, although significant reductions in long-term potentiation maintenance were noted in the Aldh2-/- animals compared to wild-type. CONCLUSION: With so few changes in calcium and calcium-dependent processes in an animal model that shows significant increases in HNE adducts, Aβ, p-tau, and activated caspases across age, the current findings do not support a direct link between neuronal calcium dysregulation and uncontrolled oxidative stress

    FK506-Binding Protein 12.6/1b, a Negative Regulator of [Ca\u3csup\u3e2+\u3c/sup\u3e], Rescues Memory and Restores Genomic Regulation in the Hippocampus of Aging Rats

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    Hippocampal overexpression of FK506-binding protein 12.6/1b (FKBP1b), a negative regulator of ryanodine receptor Ca2+ release, reverses aging-induced memory impairment and neuronal Ca2+ dysregulation. Here, we tested the hypothesis that FKBP1b also can protect downstream transcriptional networks from aging-induced dysregulation. We gave hippocampal microinjections of FKBP1b-expressing viral vector to male rats at either 13 months of age (long-term, LT) or 19 months of age (short-term, ST) and tested memory performance in the Morris water maze at 21 months of age. Aged rats treated ST or LT with FKBP1b substantially outperformed age-matched vector controls and performed similarly to each other and young controls (YCs). Transcriptional profiling in the same animals identified 2342 genes with hippocampal expression that was upregulated/downregulated in aged controls (ACs) compared with YCs (the aging effect). Of these aging-dependent genes, 876 (37%) also showed altered expression in aged FKBP1b-treated rats compared with ACs, with FKBP1b restoring expression of essentially all such genes (872/876, 99.5%) in the direction opposite the aging effect and closer to levels in YCs. This inverse relationship between the aging and FKBP1b effects suggests that the aging effects arise from FKBP1b deficiency. Functional category analysis revealed that genes downregulated with aging and restored by FKBP1b were associated predominantly with diverse brain structure categories, including cytoskeleton, membrane channels, and extracellular region. Conversely, genes upregulated with aging but not restored by FKBP1b associated primarily with glial–neuroinflammatory, ribosomal, and lysosomal categories. Immunohistochemistry confirmed aging-induced rarefaction and FKBP1b-mediated restoration of neuronal microtubular structure. Therefore, a previously unrecognized genomic network modulating diverse brain structural processes is dysregulated by aging and restored by FKBP1b overexpression

    Reversal of Aging-Related Neuronal Ca\u3csup\u3e2+\u3c/sup\u3e Dysregulation and Cognitive Impairment by Delivery of a Transgene Encoding FK506-Binding Protein 12.6/1b to the Hippocampus

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    Brain Ca(2+) regulatory processes are altered during aging, disrupting neuronal, and cognitive functions. In hippocampal pyramidal neurons, the Ca(2+)-dependent slow afterhyperpolarization (sAHP) exhibits an increase with aging, which correlates with memory impairment. The increased sAHP results from elevated L-type Ca(2+) channel activity and ryanodine receptor (RyR)-mediated Ca(2+) release, but underlying molecular mechanisms are poorly understood. Previously, we found that expression of the gene encoding FK506-binding protein 12.6/1b (FKBP1b), a small immunophilin that stabilizes RyR-mediated Ca(2+) release in cardiomyocytes, declines in hippocampus of aged rats and Alzheimer\u27s disease subjects. Additionally, knockdown/disruption of hippocampal FKBP1b in young rats augments neuronal Ca(2+) responses. Here, we test the hypothesis that declining FKBP1b underlies aging-related hippocampal Ca(2+) dysregulation. Using microinjection of adeno-associated viral vector bearing a transgene encoding FKBP1b into the hippocampus of aged male rats, we assessed the critical prediction that overexpressing FKBP1b should reverse Ca(2+)-mediated manifestations of brain aging. Immunohistochemistry and qRT-PCR confirmed hippocampal FKBP1b overexpression 4-6 weeks after injection. Compared to aged vector controls, aged rats overexpressing FKBP1b showed dramatic enhancement of spatial memory, which correlated with marked reduction of sAHP magnitude. Furthermore, simultaneous electrophysiological recording and Ca(2+) imaging in hippocampal neurons revealed that the sAHP reduction was associated with a decrease in parallel RyR-mediated Ca(2+) transients. Thus, hippocampal FKBP1b overexpression reversed key aspects of Ca(2+) dysregulation and cognitive impairment in aging rats, supporting the novel hypothesis that declining FKBP1b is a molecular mechanism underlying aging-related Ca(2+) dysregulation and unhealthy brain aging and pointing to FKBP1b as a potential therapeutic target. Significance Statement This paper reports critical tests of a novel hypothesis that proposes a molecular mechanism of unhealthy brain aging and possibly, Alzheimer\u27s disease. For more than 30 years, evidence has been accumulating that brain aging is associated with dysregulation of calcium in neurons. Recently, we found that FK506-binding protein 12.6/1b (FKBP1b), a small protein that regulates calcium, declines with aging in the hippocampus, a brain region important for memory. Here we used gene therapy approaches and found that raising FKBP1b reversed calcium dysregulation and memory impairment in aging rats, allowing them to perform a memory task as well as young rats. These studies identify a potential molecular mechanism of brain aging and may also have implications for treatment of Alzheimer\u27s disease
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