Short-term exposure to noise on stroke volume and left ventricular contractility: A repeated-measure study.

Prolonged exposure to noise has been associated with cardiovascular disease, but the possible mechanism for its influence on cardiac activity is unknown. This study investigated the acute effects of noise exposure on 24-h ambulatory cardiac parameters among male workers. We recruited 75 volunteers in an aviation-industry cohort in 2009. Personal noise-exposure levels and individual cardiac parameters, including stroke volume (SV) and left ventricular contractility (LVC), were measured simultaneously over 24 h on working and nonworking days. Linear mixed-effects regression models were used to estimate transient and sustained effects on ambulatory SV and LVC among high-noise-exposure (≥80 A-weighted decibels [dBA]), low-noise-exposure (<80 dBA) and office workers. Every 1-dBA increase in noise exposure was significantly associated with transient changes of -1.50 (95% confidence interval [CI]: -2.18, -1.03) ml/beat in SV and -1.76 (-2.99, -1.03) L/sec in LVC at work on working days only among high-exposure workers. The 1-dBA increase in nocturnal noise exposure was also significantly associated with transiently decreased SV among high-exposure (-1.62 [-2.15, -1.22] ml/beat), low-exposure (-1.27 [-1.57, -1.03] ml/beat) and office workers (-1.09 [-1.18, -1.00] ml/beat), but only the high-exposure group had the transiently reduced LVC (-1.70, [-2.37, -1.22] L/sec) after the current noise exposure on nonworking days. Such decreasing effects persisted to become sustained decreases in 24-h ambulatory SV in high-exposure (-1.10 [-1.20, -1.01] ml/beat) and office workers (-1.13 [-1.22, -1.05] ml/beat) on working days and in all three groups (-1.19 [-1.36, -1.04]; -1.15 [-1.31, -1.02]; -1.08 [-1.13, -1.02] ml/beat, respectively) on nonworking days. No significant effect on 24-h ambulatory LVC was found in any group on working or nonworking days. Occupational and nocturnal noise exposure may have acute effects on 24-h ambulatory SV among male workers, directly influencing the cardiac function related to cardiovascular disease.

Androgen receptor increases CD133 expression and progenitor-like population that associate with cisplatin resistance in endometrial cancer cell line.

Endometrial cancer (EMC) is a sex steroid hormone-related female malignancy. Androgen and androgen receptor (androgen/AR) signals have been implicated in EMC progression. Cancer stem/progenitor cells (CSPCs) are suspected to link to chemoresistance in patients with EMC. In this study, we examined the androgen/AR roles in cisplatin resistance and CSPC population. We found AR expression increased naive EMC side population, CSPC population, cell migration, and epithelial-mesenchymal transition. Meanwhile, it decreased cisplatin cytotoxic effect on EMC cells. Collaterally, endogenous AR expressions in EMC cells were upregulated in the cisplatin-resisting state. Moreover, AR expression could further enhance CD133 expression, CSPC-related markers, and drug-resistance gene messenger RNA expression in EMC cells. Finally, the AR-associated gene expression might go through indirect regulation. This is the first report revealing AR function on EMC cells' CSPC and cisplatin resistance.

Docetaxel-induced growth inhibition and apoptosis in androgen independent prostate cancer cells are enhanced by 1alpha,25-dihydroxyvitamin D3.

Pre-treatment with high-dose 1alpha,25-dihydroxyvitamin D(3) (1,25-VD) enhanced the antitumor activity of docetaxel in the androgen-independent prostate cancer cell line, PC-3. The effect manifested as an increasing population of apoptotic cells and amount of pro-apoptotic protein, Bax, under combined treatment compared with single treatment of either 1,25-VD or docetaxel alone. We further demonstrated that pre-treatment with 1,25-VD reduced the expression of multidrug resistance-associated protein-1 at both the mRNA and protein levels. This suggests pre-treatment with 1,25-VD can potentiate cytotoxicity of docetaxel in PC-3 due to 1,25-VD reducing multidrug resistance-associated protein-1 expression.