[Evaluation of quality of life and immune function in cancer patients receiving combined immunotherapy and oral administration of lentinula edodes mycelia extract].

UNLABELLED: Lentinula edodes mycelia extract(LEM) may mitigate the immunosuppression caused by regulatory T cells(Tregs), and it is therefore expected that LEM will be useful with cancer immunotherapy. In this study, we evaluated the quality of life (QOL) and immune function in cancer patients receiving a combination of immunotherapy and oral administration of LEM. METHODS: Ten patients who had received cancer immunotherapy were enrolled. They received cancer immunotherapy alone for the first 4 weeks, and were then administered LEM (1,800 mg/day) with cancer immunotherapy for the next 4 weeks. QOL scores and immune parameters were evaluated at weeks 0, 4, and 8. RESULTS: The total score for QOL was improved during the period with LEM administration compared to the period with immunotherapy alone. Interferon (IFN)-γ secretion from peripheral blood cells was increased during the period with LEM administration. The change in IFN-γ secretion in the LEM administration period possibly correlated with changes in the Treg population. CONCLUSION: Oral administration of LEM may improve QOL and immunity in patients receiving cancer immunotherapy.

Attenuating effect of artemin on herpes-related pain responses in mice infected with herpes simplex.

The influence of artemin (AR) on herpes-related pain responses was examined using mice infected with herpes simplex virus (HSV). BALB/c mice were inoculated with HSV (1x10(6) plaque-forming units) on the right hind paw, while the contralateral hind paw was without inoculation. The changes in nociceptive threshold were examined using an electric Von Fray meter. Intraperitoneal administration of AR prevented a decrease in nociceptive threshold dose-dependently in HSV-inoculated mice, which was first observed at a dose of 1.0 mg/kg and peaked at doses higher than 1.5 mg/kg. This antinociceptive effect of AR attained peaks at 120 min after administration and declined gradually to non-treated levels by 270 min. Intraperitoneal administration of AR at a dose of 1.5 mg/kg scarcely affected beta-endorphin and noradrenaline levels in the central nervous system of HSV-inoculated mice. However, AR caused a significant decrease of the dynorphin levels in spinal cord. These results strongly suggest that AR exerts antinociceptive effects on herpes-related pain through changes of the dynorphin levels in the central nervous system of HSV-inoculated mice. It is also suggested that AR will be a good candidate as an antinociceptive drug for the treatment of acute herpetic pain in humans.

Suppression of matrix metalloproteinase production from synovial fibroblasts by meloxicam in-vitro.

The aim of this study was to evaluate the influence of meloxicam on the production of both matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) from human synovial fibroblasts by TNF-alpha stimulation in-vitro. Synovial fibroblasts (2 x 10(4) cells/mL) derived from patients with osteoarthritis were stimulated with 20.0 ng mL(-1) TNF-alpha in the presence of various concentrations of meloxicam. After 24 h, the culture supernatants were obtained and assayed for MMP-1, MMP-2, MMP-3, MMP-13, TIMP-1 and TIMP-2 by ELISA. mRNA expression for MMPs and TIMPs in 4-h-cultured cells were examined by real-time polymerase chain reaction. Transcriptional factor (NF-kappaB and AP-1) activation in 2-h-cultured cells was also examined by ELISA. Meloxicam could suppress MMP production in a dose-dependent manner. The minimum concentration of the agent that showed significant suppression was 0.6 x 10(-6) M for MMP-1, MMP-2 and MMP-3, and 1.3 x 10(-6) M for MMP-13. The ability of synovial fibroblasts to produce TIMPs was also suppressed by meloxicam as in the case of MMP production. Addition of meloxicam into synovial fibroblast cultures inhibited dose-dependently mRNA expression for MMPs and TIMPs, which were increased by TNF-alpha stimulation, through the suppression of NF-kappaB and AP-1 activation. The suppressive effect of meloxicam on the production of MMPs and TIMPs may partly be involved in attenuation of the clinical conditions of osteoarthritis and rheumatoid arthritis.