In postmenopausal never-smoking Korean women, exposure to SHS was positively associated with osteoporosis. This finding further emphasizes a need to identify vulnerable groups exposed to SHS to increase bone health.
Imaging with a novel parallel-plate DOT breast imager that employs highly parallel, high-resolution CCD detection in the frequency-domain was demonstrated.
Background and purpose: p-Coumaryl alcohol-g-O-methyl ether (CAME) was isolated from Alpinia galanga and shown to contain a phenylpropanoid structure similar to p-coumaryl diacetate (CDA). CDA is known to have antioxidant and antiinflammatory activity, but the biochemical activities of CAME are unknown. Inflammation is mediated by inflammatory cytokine production, in particular, by CD4+ T helper cells (Th cells), but it is unclear whether phenylpropanoids affect cytokine production in Th cells. In this study, we decided to investigate the functions of CAME and CDA in CD4+ Th cells. Experimental approach: Mouse CD4+ Th cells were isolated from C57BL6 mice and stimulated with an antibody against T cell receptors in the presence of phenylpropanoids. Cytokine production was measured by ELISA and intracellular cytokine staining. Gene knockout mice and tetracycline-inducible transgenic mice were used to examine the molecular mechanisms of phenylpropanoids on modulation of cytokine production. Key results: CAME potently reduced intracellular reactive oxygen species in Th cells, as does CDA. However, although CDA was cytotoxic, CAME selectively and potently suppresses interferon-g (IFNg) production in CD4+ Th cells, without toxicity. This effect was caused by attenuated expression of the transcription factor, T-box protein expressed in T cells (T-bet), and T-bet was essential for CAME to inhibit IFNg production in CD4+ Th cells. Conclusions and implications: CAME selectively and substantially suppresses IFNg production in CD4+ Th cells by decreasing T-bet expression. As increased IFNg production by CD4+ Th cells can mediate inflammatory immune responses, a selective IFNg suppressor, such as CAME may be an effective, naturally occurring, compound for modulating inflammatory immune disorders.
7646 Background: To investigate whether excision repair cross-complementation group 1 (ERCC1) expression, as determined immunohistochemically, and mutations of epidermal growth factor receptor (EGFR) are related to the prognosis of curatively resected non-small cell lung cancer (NSCLC), and whether these two markers are related. Methods: One-hundred and thirty-three consecutive patients with NSCLC who did not receive adjuvant chemotherapy after curative surgery were included in this study. Representative areas from formalin-fixed paraffin-embedded tumor samples were chosen for tissue microarray analysis. Immunohistochemistry was performed for ERCC1 and the median semiquantitative H-score was used as a cut-off. EGFR mutations (exons 18, 19, and 21) were analyzed by the direct sequencing of tumor samples. Results: ERCC1 expression was evaluable in 130 patients and ERCC1 was found to be positive in 80 patients (61.5%). Moreover, ERCC1 was expressed more frequently in smokers and in squamous cell carcinomas. Patients with positive ERCC1 expression survived longer (median overall survival 2,742 days for ERCC1-positive vs. 1,423 days for ERCC1-negative, P=.0463). EGFR mutations were found in 27 patients (20.3%) but they were not found to affect overall survival. Interestingly, EGFR mutations were more frequent in ERCC1-negative tumors (12.5% in ERCC1-positive vs. 30% in ERCC1-negative tumors, P=0.014). Conclusions: ERCC1 expression was identified as a prognostic marker of longer survival in resected NSCLCs. In addition, EGFR mutations were more frequently found in ERCC1-negative tumors, but were not found to affect survival in our patient group. No significant financial relationships to disclose.
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