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2.
Acute Med Surg ; 10(1): e824, 2023.
Article in English | MEDLINE | ID: mdl-36844677

ABSTRACT

Background: Elsberg syndrome (ES) is an acute-onset lumbosacral radiculitis with myelitis caused by a herpes virus infection. Case Presentation: We present a case of a 77-year-old woman who was admitted with urinary retention prior to genital rash. The patient was diagnosed with ES and treated with intravenous acyclovir 250 mg every 8 h for 1 week. Conclusion: Physicians should consider ES in patients with voiding dysfunction, as preceding neurological symptoms may lead to a misdiagnosis. Considering the adverse effects of the antiviral drug, its dosage should be according to the causative virus of the ES as well as the patient's age and medical history.

3.
JID Innov ; 1(3): 100026, 2021 Sep.
Article in English | MEDLINE | ID: mdl-34909725

ABSTRACT

TRIAL DESIGN: Human papillomavirus infection causes verruca vulgaris. CDK9 inhibitor FIT039 inhibits DNA virus proliferation in animal models. We conducted a multicenter, single-blind, placebo-controlled, randomized phase I/II clinical trial evaluating the safety and efficacy of FIT039 against verruca vulgaris. METHODS: Target lesions were treated with liquid nitrogen once, and a FIT039 patch or placebo patch was applied for 14 days. The primary endpoint was lesion disappearance. The secondary endpoints were safety and changes in dimension, cross-sectional area, and the number of petechial lesions. RESULTS: A total of 24 participants were randomly allocated to the FIT039 (n = 13, median age, 54 years) and placebo (n = 11, median age, 62 years) groups. Verruca vulgaris did not disappear. FIT039 decreased the dimension to 76% of the initial value on day 29, followed by an increase to 98% on day 57. Placebo showed a monotonic increase to 107% on day 57. Changes in the cross-sectional area and petechiae number were comparable between the groups. CONCLUSIONS: No drug-related adverse reactions occurred. FIT039 efficacy was not determined in this study.

6.
J Invest Dermatol ; 134(11): 2709-2718, 2014 Nov.
Article in English | MEDLINE | ID: mdl-24756110

ABSTRACT

Contact hypersensitivity (CHS) has been widely used to study cutaneous immune responses, as a prototype of delayed-type hypersensitivity. Although natural killer T (NKT) cells have been assumed to have an important role in CHS, their role is controversial. Here, we report the role of NKT cells in the sensitization phase of CHS, by promoting the survival and maturation of dendritic cells (DCs) in the draining lymph nodes (LNs). The CHS response was attenuated with Cd1d1(-/-) and Traj18(-/-) BALB/c mice in which NKT cells were absent. In the draining LNs, the number of effector T cells and cytokine production were significantly reduced with NKT cell-deficient mice. NKT cells activated and colocalized with DCs in the draining LNs after sensitization. The number of migrated and mature DCs was reduced in NKT cell-deficient mice 72 hours after FITC application. In in vitro experiments, activated NKT cells enhanced bone marrow-derived DC (BMDC) survivability via tumor necrosis factor (TNF) production from BMDCs. In addition, TNF production from BMDCs was partially suppressed by the neutralizing anti-CD54 or CD154 antibodies. Our data demonstrate that DC-NKT interaction has a pivotal role in the sensitization phase of CHS.


Subject(s)
Dermatitis, Contact/immunology , Natural Killer T-Cells/cytology , Animals , Apoptosis , Bone Marrow Cells/cytology , Cell Movement , Cell Proliferation , Cell Survival , Coculture Techniques , Cytokines/metabolism , Dendritic Cells/cytology , Female , Mice , Mice, Inbred BALB C , Tumor Necrosis Factor-alpha/metabolism
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