217 research outputs found

    A New Linear Inductive Voltage Adder Driver for the Saturn Accelerator

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    Saturn is a dual-purpose accelerator. It can be operated as a large-area flash x-ray source for simulation testing or as a Z-pinch driver especially for K-line x-ray production. In the first mode, the accelerator is fitted with three concentric-ring 2-MV electron diodes, while in the Z-pinch mode the current of all the modules is combined via a post-hole convolute arrangement and driven through a cylindrical array of very fine wires. We present here a point design for a new Saturn class driver based on a number of linear inductive voltage adders connected in parallel. A technology recently implemented at the Institute of High Current Electronics in Tomsk (Russia) is being utilized[1]. In the present design we eliminate Marx generators and pulse-forming networks. Each inductive voltage adder cavity is directly fed by a number of fast 100-kV small-size capacitors arranged in a circular array around each accelerating gap. The number of capacitors connected in parallel to each cavity defines the total maximum current. By selecting low inductance switches, voltage pulses as short as 30-50-ns FWHM can be directly achieved.Comment: 3 pages, 4 figures. This paper is submitted for the 20th Linear Accelerator Conference LINAC2000, Monterey, C

    The Light Ion Pulsed Power Induction Accelerator for ETF

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    The light ion Engineering Test Facility (ETF) driver concept, based on Hermes III and RHEPP technologies, is a scaled-down version of the LMF design incorporating repetition rate capabilities of up to 10 Hz. The preconceptual design presented here provides 250 TW peak power to the ETF target during 8 ns, equal to 2 MJ total ion beam energy. Linear inductive voltage addition driving a self-magnetically insulated transmission line (MITL) is utilized to generate the 36 MV peak voltage needed for lithium ion beams. The ~3 MA ion current is achieved by utilizing many accelerating modules in parallel. Since the current per module is relatively modest (~300 kA), two-stage or one-stage extraction diodes can be utilized for the generation of singly charged lithium ions. The accelerating modules are arranged symmetrically around the fusion chamber in order to provide uniform irradiation onto the ETF target. In addition, the modules are fired in a programmed sequence in order to generate the optimum power pulse shape onto the target. This design utilizes RHEPP accelerator modules as the principal power sourc

    PPARγ-coactivator-1α gene transfer reduces neuronal loss and amyloid-β generation by reducing β-secretase in an Alzheimer’s disease model

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    Current therapies for Alzheimer’s disease (AD) are symptomatic and do not target the underlying Aβ pathology and other important hallmarks including neuronal loss. PPARγ-coactivator-1α (PGC-1α) is a cofactor for transcription factors including the peroxisome proliferator-activated receptor-γ (PPARγ), and it is involved in the regulation of metabolic genes, oxidative phosphorylation, and mitochondrial biogenesis. We previously reported that PGC-1α also regulates the transcription of β-APP cleaving enzyme (BACE1), the main enzyme involved in Aβ generation, and its expression is decreased in AD patients. We aimed to explore the potential therapeutic effect of PGC-1α by generating a lentiviral vector to express human PGC-1α and target it by stereotaxic delivery to hippocampus and cortex of APP23 transgenic mice at the preclinical stage of the disease. Four months after injection, APP23 mice treated with hPGC-1α showed improved spatial and recognition memory concomitant with a significant reduction in Aβ deposition, associated with a decrease in BACE1 expression. hPGC-1α overexpression attenuated the levels of proinflammatory cytokines and microglial activation. This effect was accompanied by a marked preservation of pyramidal neurons in the CA3 area and increased expression of neurotrophic factors. The neuroprotective effects were secondary to a reduction in Aβ pathology and neuroinflammation, because wild-type mice receiving the same treatment were unaffected. These results suggest that the selective induction of PGC-1α gene in specific areas of the brain is effective in targeting AD-related neurodegeneration and holds potential as therapeutic intervention for this disease

    PPAR gamma-coactivator-1 alpha gene transfer reduces neuronal loss and amyloid-beta generation by reducing beta-secretase in an Alzheimer's disease model

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    Current therapies for Alzheimer’s disease (AD) are symptomatic and do not target the underlying Aβ pathology and other important hallmarks including neuronal loss. PPARγ-coactivator-1α (PGC-1α) is a cofactor for transcription factors including the peroxisome proliferator-activated receptor-γ (PPARγ), and it is involved in the regulation of metabolic genes, oxidative phosphorylation, and mitochondrial biogenesis. We previously reported that PGC-1α also regulates the transcription of β-APP cleaving enzyme (BACE1), the main enzyme involved in Aβ generation, and its expression is decreased in AD patients. We aimed to explore the potential therapeutic effect of PGC-1α by generating a lentiviral vector to express human PGC-1α and target it by stereotaxic delivery to hippocampus and cortex of APP23 transgenic mice at the preclinical stage of the disease. Four months after injection, APP23 mice treated with hPGC-1α showed improved spatial and recognition memory concomitant with a significant reduction in Aβ deposition, associated with a decrease in BACE1 expression. hPGC-1α overexpression attenuated the levels of proinflammatory cytokines and microglial activation. This effect was accompanied by a marked preservation of pyramidal neurons in the CA3 area and increased expression of neurotrophic factors. The neuroprotective effects were secondary to a reduction in Aβ pathology and neuroinflammation, because wild-type mice receiving the same treatment were unaffected. These results suggest that the selective induction of PGC-1α gene in specific areas of the brain is effective in targeting AD-related neurodegeneration and holds potential as therapeutic intervention for this disease

    Vertebral artery variations revised: origin, course, branches and embryonic development

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    Background: The vertebral artery originates from the subclavian artery and is divided into four segments. The aim of this study is to investigate the anatomical variations in the course and branches of the vertebral artery. Materials and methods: A research was performed via PubMed database, using the terms: “variations of vertebral artery AND cadaveric study”, “variations of vertebral artery AND cadavers” and “anomalies of vertebral artery AND cadavers”. Results: A total of 24 articles met the inclusion criteria, 13 of them referring to variations of the origin of the vertebral artery, 9 to variations of the course and 3 to variations of its branches. On a total sample of 1192 cadavers of different populations, origin of the left vertebral artery directly from the aortic arch was observed at 6.7%. In addition, among 311 cadavers, 17.4% were found with partially or fully ossified foramen of the atlas for the passage of the vertebral artery, while the bibliographic review also showed variants at the exit site of the artery from the transverse foramen of the axis. Conclusions: Despite the fact that variations of both the course and the branches of vertebral artery are in most cases asymptomatic, good knowledge of anatomy and its variants is of particular importance for the prevention of vascular complications during surgical and radiological procedures in the cervix area
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