68 research outputs found

    High Power Gamma-Ray Flash Generation in Ultra Intense Laser-Plasma Interaction

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    When high-intensity laser interaction with matter enters the regime of dominated radiation reaction, the radiation losses open the way for producing short pulse high power gamma ray flashes. The gamma-ray pulse duration and divergence are determined by the laser pulse amplitude and by the plasma target density scale length. On the basis of theoretical analysis and particle-in-cell simulations with the radiation friction force incorporated, optimal conditions for generating a gamma-ray flash with a tailored overcritical density target are found.Comment: 12 pages, 5 figures Accepted for publication in Physical Review Letters (this http://prl.aps.org/

    Therapeutic strategies in HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP)

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    Human T lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is chronic progressive myelopathy characterized by bilateral pyramidal tracts involvement with sphincteric disturbances. HTLV-I infects approximately 10-20 million people worldwide. There are large endemic areas in southern Japan, the Caribbean, Central and South America, the Middle East, Melanesia, and equatorial regions of Africa. Since the primary neuropathological feature of HAM/TSP is chronic inflammation caused by HTLV-I infection in the spinal cord, various treatments focusing on immunomodulatory or anti-viral effects were performed for HAM/TSP patients until now. However, there are still many of problems, such as insufficient effects, side effects and expensive costs in long-term treatments, etc., in these treatments. Therefore, an ideal therapeutic strategy against HAM/TSP is still not established yet. Although only a small proportion of HTLV-I-infected individuals develops HAM/TSP, neurological symptoms are certainly progressive once myelopathy develops, leading to deterioration of the quality of life. Therefore, we now need the therapeutic regimens to protect the development, or be able to commence the treatments as soon as possible after the development safely and inexpensively even in long-term course or lifelong course of treatment. As HTLV-I-infected CD4+ T cells are the first responders in the immunopathogenesis of HAM/TSP, the ideal treatment is the elimination of HTLV-I-infected cells from the peripheral blood. In this article, we will review the therapeutic strategies against HAM/TSP up to now and will introduce our new therapeutic approach focusing on the targeting of HTLV-I-infected cells in HAM/TSP patients

    On extreme field limits in high power laser matter interactions: radiation dominant regimes in high intensity electromagnetic wave interaction with electrons

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    We discuss the key important regimes of electromagnetic field interaction with charged particles. Main attention is paid to the nonlinear Thomson/Compton scattering regime with the radiation friction and quantum electrodynamics effects taken into account. This process opens a channel of high efficiency electromagnetic energy conversion into hard electromagnetic radiation in the form of ultra short high power gamma ray flashes.Comment: 15 pages, 10 figures, invited talk presented at the SPIE-2013 conference, Prague, Czech Republic, Apr. 15, 201

    Acute Polyradiculoneuropathy Associated With Salmonella Gastroenteritis

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    We reported a case of acute polyradiculoneuropathy associated with Salmonella gastroenteritis. A68-year-oldman developed progressive motor weakness and areflexia following the febrile illness and diarrhea caused by a strain of Salmonella species O8 group. He showed a rapid and complete recovery from the illness. This is the first report in which Salmonella gastroenteritis might be etiologically related to an acute polyradiculoneuropathy

    Reevaluation for clinical manifestations of HTLV-I-seropositive patients with Sjogren’s syndrome

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    Background: The aim of the study was to reassess the prevalence and characteristics of human T lymphotropic virus type I (HTLV-I)-associated Sjogren\u27s syndrome (SS) and SS in HTLV-I-associated myelopathy (HAM) based on the American European Consensus Group (AECG) criteria in HTLV-I endemic area, Nagasaki prefecture. Methods: The 349 patients who underwent a minor salivary gland biopsy (MSGB) for suspected SS were retrospectively classified by AECG classification criteria and divided with or without anti-HTLV-I antibody. Results: The HTLV-I data-available 294 patients were investigated. One hundred-seventy patients were classified as SS and 26.5 % were HTLV-I-seropositive. We have included 26 patients with HTLV-I-associated myelopathy (HAM) and 38.5 % were classified as having SS. The prevalences of ANA and anti-SS-A/Ro antibody of HAM + SS were significantly low compared to the HTLV-I asymptomatic carriers (AC) with SS and the HTLV-I-seronegative SS patients, although lacrimal dysfunction tended to be high in HAM + SS and significantly high in AC + SS patients compared with the patients with HTLV-I-seronegative SS. The focus scores of MSGB in the HAM + SS patients were similar to those of the AC + SS patients and the HTLV-I-seronegative patients with SS. Among the MSGB-positive patients, there was a low prevalence of ANA in the HAM + SS patients. Similar results were obtained in case of anti-SS-A/Ro or SS-B/La antibody. Conclusion: In HTLV-I endemic area, high prevalence of anti-HTLV-I antibody among SS as well as the characteristics of HAM + SS and AC + SS was still determined by AECG classification criteria

    Development of sensory neuropathy in streptozotocin-induced diabetic mice.

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    Diabetic polyneuropathy is a major complication of diabetes and the most common cause of peripheral neuropathy. Sensory-dominant neuropathy is the most common type. We previously used streptozotocin (STZ)-induced diabetic ddY mice with sensory neuropathy to evaluate the therapeutic effects of vascular endothelial growth factor and placental growth factor isoforms. In this study, to characterize the development of diabetic sensory neuropathy, electrophysiological, behavioral, and histopathological studies were performed in these diabetic mice. A significant difference in sensory conduction velocity in the tail nerve was observed between healthy and diabetic mice at 1 week after STZ injection. Diabetic mice developed hypoalgesia at 5 weeks after STZ injection. Axon area and myelin thickness of the myelinated fibers were increased in 17-week-old healthy mice compared with those in 8-week-old healthy mice. However, these increases were retarded in 17-week-old diabetic mice. In unmyelinated fibers, axon area was significantly reduced in 17-week-old diabetic mice compared with 8- and 17-week-old healthy mice. These findings suggest that both impaired maturation of myelinated fibers and atrophy of unmyelinated fibers simultaneously occur in the early stage of diabetes in these mice. Our mouse model may be useful for studying the pathogenesis of and therapies for diabetic sensory neuropathy.Diabetic polyneuropathy is a major complication of diabetes and the most common cause of peripheral neuropathy. Sensory-dominant neuropathy is the most common type. We previously used streptozotocin (STZ)-induced diabetic ddY mice with sensory neuropathy to evaluate the therapeutic effects of vascular endothelial growth factor and placental growth factor isoforms. In this study, to characterize the development of diabetic sensory neuropathy, electrophysiological, behavioral, and histopathological studies were performed in these diabetic mice. A significant difference in sensory conduction velocity in the tail nerve was observed between healthy and diabetic mice at 1 week after STZ injection. Diabetic mice developed hypoalgesia at 5 weeks after STZ injection. Axon area and myelin thickness of the myelinated fibers were increased in 17-week-old healthy mice compared with those in 8-week-old healthy mice. However, these increases were retarded in 17-week-old diabetic mice. In unmyelinated fibers, axon area was significantly reduced in 17-week-old diabetic mice compared with 8- and 17-week-old healthy mice. These findings suggest that both impaired maturation of myelinated fibers and atrophy of unmyelinated fibers simultaneously occur in the early stage of diabetes in these mice. Our mouse model may be useful for studying the pathogenesis of and therapies for diabetic sensory neuropathy
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