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    <title>DSpace community: 附設醫院雲林分院</title>
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    <title>Temporal Changes in Cytokine/Chemokine Profiles and Pulmonary Involvement in Severe Acute Respiratory Syndrome</title>
    <link>http://140.112.114.62/handle/246246/169113</link>
    <description>title: Temporal Changes in Cytokine/Chemokine Profiles and Pulmonary Involvement in Severe Acute Respiratory Syndrome abstract: Objective and background: Pathological changes in severe acute respiratory syndrome (SARS) suggest that SARS sequelae are associated with dysregulation of cytokine and chemokine production. To improve understanding of the immuno- pathological processes involved in lung injury associated with SARS, the temporal changes in cytokine/chemokine profiles in the sera of SARS patients were compared with those of patients with community-acquired pneumonia (CAP), according to the degree of lung involvement. Methods: Serum levels of 11 cytokines and chemokines, in 14 patients with SARS and 24 patients with CAP, were serially checked using a bead-based multiassay system. Sera from 12 healthy subjects were used as normal controls. Results: The serum levels of interferon-gamma-inducible protein-10 (IP-10), IL-2 and IL-6 were significantly elevated during SARS infection. In patients with CAP, but not in those with SARS, the levels of interferon-gamma, IL-10, IL-8 and monokine induced by interferon-gamma ( MIG) were significantly elevated compared with the levels in healthy controls. Among the chemokines/ cytokines, IL-6 levels correlated most strongly with radiographic scores (r = 0.62). The elevation of IP-10 and IL-2 antedated the development of chest involvement and reached peak levels earlier than the radiographic scores. In contrast, the dynamic changes in IL-6, C-reactive protein and neutrophils occurred synchronously with the changes in radiographic scores. The mean ratio of IL-6 to IL-10 in SARS patients (4.84; range 0.41-21) was significantly higher than that in CAP patients (2.95; range 0.02-10.57) (P = 0.04 ). Conclusions: The early induction of IP-10 and IL-2, as well as the subsequent over- production of IL-6 and lack of IL-10 production, probably contribute to the main immuno- pathological processes involved in lung injury in SARS. These changes in cytokine/chemokine profile are remarkably different from those observed in CAP patients.
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    <title>Relapse of Sars Upon Tapering Corticosteroid</title>
    <link>http://140.112.114.62/handle/246246/169111</link>
    <description>title: Relapse of Sars Upon Tapering Corticosteroid</description>
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  <item rdf:about="http://140.112.114.62/handle/246246/169109">
    <title>Vibrio Alginolyticus as the Cause of Pleural Empyema and Bacteremia in an Immunocompromised Patient</title>
    <link>http://140.112.114.62/handle/246246/169109</link>
    <description>title: Vibrio Alginolyticus as the Cause of Pleural Empyema and Bacteremia in an Immunocompromised Patient</description>
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  <item rdf:about="http://140.112.114.62/handle/246246/169107">
    <title>Bilateral Rapidly Progressive Hearing Loss Followed by Loss of Vestibular Function- Case Report</title>
    <link>http://140.112.114.62/handle/246246/169107</link>
    <description>title: Bilateral Rapidly Progressive Hearing Loss Followed by Loss of Vestibular Function- Case Report abstract: Rapidly progressive sensorineural hearing loss is a specific type of sudden deafness characterized by a progressive stepwise process over a period of few hours to months with the mechanism attributable to autoimmune reactivity. The hearing organs are always involved and usually the vestibular organs as well. Recently, we have encountered a 33-year-old woman with rapidly progressive sensorineural hearing loss bilaterally. A battery of audiovestibular function tests e.g. audiometry, distortion product otoacoustic emission (DPOAE), auditory brainstem response ( ABR), caloric test, and vestibular evoked myogenic potential (VEMP) test were conducted throughout the course. The sequence of audiovestibular dysfunction was absent DPOAE initially, followed by total deafness and absent ABR, and finally absent VEMPs and caloric areflexia, indicating that the cochlea is vulnerable earlier than the vestibule. Hence, this case demonstrates the sequence of degeneration in the inner ear, that is, rapid progressive hearing loss followed by vestibular loss, similar to that seen in the aging process (degeneration) in the inner ear.
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