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The purpose of this study was to compare arousal levels and stress response across menstrual cycle phases in women with three perimenstrual symptom patterns. Women with low symptom severity (LS, N = 28), were compared with those with a premenstrual syndrome (PMS, N = 15) and premenstrual magnification (PMM, N = 19) pattern across postmenses and premenses phases. Each woman was assessed during relaxation and in response to mental task and symptom imaging stressors during a postmenses and premenses day. Results of baseline skin conductance (SCL), electromyogram (EMG), and finger temperature (T) demonstrated arousal premenses in women with the PMS pattern, but not in women with the LS pattern. In addition, women with the PMS pattern experienced increased EMG and SCL response to stressors premenses. Women with the PMM pattern experienced a rise in finger temperature premenses, opposite the pattern of the women with LS or PMS. These results support development of symptom management strategies to reduce arousal and modulate stress response for women with PMS who seek help for their symptoms. In addition, the difference in arousal and stress response observed in women with PMS and PMM support development of different symptom management strategies for these two groups of women.

Asbestos exposure leads to malignant mesothelioma (MM), a deadly neoplasm of mesothelial cells of various locations. Although there is no doubt about the role of asbestos in MM tumorigenesis, mechanisms are still not well explored. Recently our group demonstrated that asbestos causes inflammasome priming and activation in mesothelial cells, which in part is dependent on oxidative stress. Our current study sheds light on yet another mechanism of inflammasome activation by asbestos. Here we show the role of actin polymerization in asbestos-induced activation of the nod like receptor pyrin domain containing protein 3 (NLRP3) inflammasome. Using human mesothelial cells we first demonstrate that asbestos and carbon nanotubes induced caspase-1 activation and high mobility group box 1 (HMGB1), interleukin 1 beta (IL-1β) and interleukin 18 (IL-18) secretion was blocked by cytochalasin D (cyto D) an actin polymerization inhibitor. Next, to understand the mechanism, we assessed if phagocytosis of fibers by mesothelial cells is affected by actin polymerization inhibition. Transmission electron microscopy (TEM) showed the inhibition of fiber uptake by mesothelial cells in the presence of cyto D. Furthermore, localization of components of the inflammasome, apoptotic speck-like protein containing a CARD domain (ASC) and NLRP3, to the perinuclear space in mitochondria or endoplasmic reticulum (ER) in response to fiber exposure was also interrupted in the presence of cyto D. Taken together, our studies suggest that actin polymerization plays important roles in inflammasome activation by fibers via regulation of phagocytosis and/or spatial localization of inflammasome components.

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