Abstract
Background
Menopausal symptoms are common among middle-aged women. Working women with severe menopausal symptoms are more likely to experience presenteeism—a condition where employees ...continue to work despite feeling unwell. However, it remains unclear as to which specific symptoms women experience during the menopausal transition and postmenopausal periods that primarily contribute to presenteeism.
Aims
To evaluate the associations between types of menopausal symptoms and presenteeism among Japanese women.
Methods
A cross-sectional study of 4000 women aged 40–59 years who were currently working was conducted in Japan in September 2022. We used an online self-administered questionnaire that included items on demographic characteristics, the Menopause Rating Scale for measuring menopausal symptoms and the Work Functioning Impairment Scale for measuring presenteeism. Logistic regression analysis was performed.
Results
Women with severe overall menopausal symptoms had 12.18-fold (95% confidence interval CI 9.09–16.33, P < 0.001) increased odds of presenteeism compared with those without symptoms. Participants with psychological symptoms also had significantly higher presenteeism (severe: odds ratio: 9.18, 95% CI 6.60–12.78, P < 0.001). However, after controlling for psychological symptoms, there were no significant associations between somatic and urogenital symptoms and presenteeism.
Conclusions
The results indicate that menopausal symptoms, especially psychological symptoms, have a significant impact on presenteeism among Japanese women. Organizations need to address menopausal symptoms in the workplace, with an emphasis on reducing work-related stress for women with menopausal symptoms.
Menopausal symptoms are common among middle-aged women. This study revealed that severe menopausal symptoms, especially psychological symptoms, had a significant impact on presenteeism—a condition where employees continue to work despite feeling unwell. The results accentuate the organizations need to address menopausal symptoms in the workplace, with an emphasis on reducing work-related stress for women with menopausal symptoms.
Background and Purpose
Chemotherapeutic agents, including 5‐fluorouracil (5‐FU), frequently cause intestinal mucositis resulting in severe diarrhoea and morphological mucosal damage. 5‐HT3 receptor ...antagonists are clinically effective in the treatment of nausea and emesis during cancer chemotherapy. Therefore we here have examined the effects of 5‐HT3 receptor antagonists on 5‐FU‐induced intestinal mucositis in mice.
Experimental Approach
Intestinal mucositis was induced in male C57BL/6 mice by daily administration of 5‐FU (50 mg·kg−1) for 5 days. Effects of 5‐HT3 receptor antagonists, ramosetron (0.01–0.1 mg·kg−1) and ondansetron (5 mg·kg−1), on the accompanying histology, cytokine production and apoptosis were assessed.
Key Results
Continuous administration of 5‐FU to mice caused severe intestinal mucositis, which was histologically characterized by the shortening of villi and destruction of intestinal crypts, accompanied by body weight loss and diarrhoea. Daily ramosetron administration dose‐dependently reduced the severity of intestinal mucositis, body weight loss and diarrhoea. Similar beneficial effects were observed with ondansetron. The number of apoptotic, caspase‐3‐ and caspase‐8‐activated cells increased 24 h after the first 5‐FU administration, and these responses were reduced by ramosetron. The up‐regulation of TNF‐α, IL‐1β and IL‐6 following 5‐FU treatment was also attenuated by ramosetron.
Conclusions and Implications
5‐HT3 receptor antagonists ameliorated 5‐FU‐induced intestinal mucositis in mice, and this action could result from suppression of apoptotic responses in the intestinal crypt cells via inhibition of cytokine expression. Thus, 5‐HT3 receptor antagonists may be useful for preventing not only nausea and emesis but also intestinal mucositis during 5‐FU chemotherapy.
Memories are stored in synapses that consist of axon terminals and dendritic spines. Dendritic spines are postsynaptic structures of synapses and are essential for synaptic plasticity and cognition. ...Therefore, extensive investigations concerning the functions and structures of spines have been performed. Sex steroids and stress steroids have been shown to modulate hippocampal synapses. Although the rapid modulatory action of sex steroids on synapses has been studied in hippocampal neurones over several decades, the essential molecular mechanisms have not been fully understood. Here, a description of kinase‐dependent signalling mechanisms is provided that can explain the rapid nongenomic modulation of dendritic spinogenesis in rat and mouse hippocampal slices by the application of sex steroids, including dihydrotestosterone, testosterone, oestradiol and progesterone. We also indicate the role of synaptic (classic) sex steroid receptors that trigger these rapid synaptic modulations. Moreover, we describe rapid nongenomic spine modulation by applying corticosterone, which is an acute stress model of the hippocampus. The explanations for the results obtained are mainly based on the optical imaging of dendritic spines. Comparisons are also performed with results obtained from other types of imaging, including electron microscopic imaging. Relationships between spine modulation and modulation of cognition are discussed. We recognise that most of rapid effects of exogenously applied oestrogen and androgen were observed in steroid‐depleted conditions, including acute slices of the hippocampus, castrated male animals and ovariectomised female animals. Therefore, the previously observed effects can be considered as a type of recovery event, which may be essentially similar to hormone replacement therapy under hormone‐decreased conditions. On the other hand, in gonadally intact young animals with high levels of endogenous sex hormones, further supplementation of sex hormones might not be effective, whereas the infusion of blockers for steroid receptors or kinases may be effective, with respect to suppressing sex hormone functions, thus providing useful information regarding molecular mechanisms.
Abstract In the gut, transient receptor potential vanilloid (TRPV) 1 activation leads to release of neurotransmitters such as neuropeptides and nitric oxide. However, the distribution of TRPV1 nerve ...fibers and neurotransmitters released form sensory nerve endings in the enteric nervous system are currently not well understood. The present study investigated the immunohistochemical distribution of TRPV1 channels, sensory neuropeptides, and nitric oxide and their co-localization in mouse large intestine. Numerous TRPV1 and calcitonin gene-related peptide (CGRP) immunoreactivities were detected, mainly in the mucosa, submucosal layer, and myenteric plexus. Abundant substance P (SP), neurokinin A (NKA), and neuronal nitric oxide synthase (nNOS)-immunoreactivity were revealed in muscle layers. Motor function studies of circular and longitudinal muscles found that contractile responses to capsaicin in the rectum were most sensitive among the rectum, and distal, transverse, and proximal colon. Double labeling studies were carried out in horizontal sections of mouse rectum. TRPV1/protein gene product (PGP)9.5 double labeled axons were observed, but PGP9.5 and neuronal nuclear protein immunopositive cell bodies did not express TRPV1 immunoreactivity in the myenteric plexus. In the mucosa, submucosal layer, deep muscular plexus, circular muscle, myenteric plexus and longitudinal muscle layer, TRPV1 nerve fibers were found to contain CGRP, SP and nNOS. SP and NKA were almost entirely colocalized at the axons and cell bodies in all layers. Double labeling with c-Kit revealed that TRPV1 nerve fibers localized adjacent to the interstitial cells of Cajal (ICC). These results suggest that the TRPV1-expressing nerve and its neurotransmitters regulate various functions of the large intestine.
Background
Transient receptor potential channel melastatin 8 (TRPM8) is activated by cold temperatures and cooling agents (menthol and icilin). Recent studies showed TRPM8 is expressed in visceral ...organs and peripheral sensory pathways. However, the role of TRPM8 in visceral hyperalgesia is poorly understood in pathological states such as inflammatory bowel disease. Hence, we investigated the distribution of TRPM8 and its involvement in visceral hyperalgesia in experimental colitis mice.
Methods
TRPM8 immunoreactivity was detected using immunohistochemical staining with fluorescein‐conjugated tyramide amplification. Visceral hyperalgesia was measured by the intracolonic administration of TRPM8 agonist, WS‐12, in control and dextran sodium sulfate (DSS)‐induced colitis mice.
Key Results
TRPM8 immunoreactivity in the distal colon was much higher than in the transverse and proximal colon under physiological conditions. TRPM8 immunoreactivity markedly increased in the distal colon mucosa of DSS‐induced colitis mice compared with control mice. The number of TRPM8 nerve fibers in mucosa of DSS‐ or 2,4,6‐trinitrobenzene sulfonic acid‐induced colitis model mice drastically increased compared with control mice. TRPM8 immunoreactivities colocalized with the calcitonin gene‐related peptide‐ and substance P‐immunoreactive nerve fibers in the mucosa. Intracolonic administration of WS‐12 induced behavioral visceral pain‐like responses. The numbers of these responses in the colitis model mice were 3 times higher than in control mice, and were decreased by pretreatment with the TRPM8 channel blocker AMTB.
Conclusions & Inferences
Increased expression of TRPM8 may contribute to the visceral hyperalgesia of experimental colitis.
TRPM8 immunoreactivity markedly increased in the distal colon mucosa of DSS‐induced colitis mice compared with control mice. The numbers of TRPM8 agonist WS‐12 induced visceral pain‐like responses in the colitis model mice were three times higher than in control mice, and were decreased by pretreatment with the TRPM8 channel blocker AMTB. Increased expression of TRPM8 may contribute to the visceral hyperalgesia of experimental colitis.
Background
Although opioids induce intestinal muscle contraction and provoke constipation, the intestinal region(s) that contribute to the constipation have remained unclear. We report here a ...region‐specific response of intestinal muscle contraction to morphine and its correlation with in vivo constipation.
Methods
Regions of mice small and large intestines were dissected histologically and circular muscle contractile responses were measured using isometric transducers. Bead expulsion assays were performed to assess in vivo constipation.
Key Results
The strongest contraction in response to morphine was detected in the rectum. The distal and transverse colon also showed strong contractions, whereas weak responses were detected in the proximal colon, jejunum, and ileum. Regarding the sustainability of muscle contractions during morphine exposure, prolonged waves were detected only in the rectum, while the waves diminished gradually in other regions. To identify the mechanism(s) underlying this difference, we focused on nitric oxide synthase (NOS). In the distal colon, decreased contraction during morphine exposure was recovered by application of a NOS inhibitor (L‐NAME), while a NOS substrate (L‐arginine) enhanced contractile degradation. In contrast L‐NAME and L‐arginine modestly affected the sustained contraction in the rectum. To confirm the correlation with constipation, beads were inserted into the transverse colon, distal colon, or rectum after morphine administration and expulsion times were examined. Beads tended to stop at the rectum even when inserted in the deeper colonic regions.
Conclusions & Inferences
The rectum showed the greatest response to morphine in both in vitro and in vivo analyses, therefore it may play a key role for opioid‐induced constipation.
Although opioids induce intestinal muscle contraction and provoke constipation, the intestinal region(s) that contribute to the constipation have remained unclear. To identify the key region involved in opioid‐induced constipation, we compared morphine‐induced circular muscle contractile potency and sustainability in histologically known regions of the mouse intestine. Using isometric recording and bead expulsion assay, we suggest that rectum plays a key role for opioid‐induced constipation.
The present study aimed to investigate current sexuality education in Japanese medical schools and the impact of position title in the Japanese Society for Sexual Medicine (JSSM). Questionnaires were ...mailed to urology departments in all Japanese medical schools. The responses were evaluated according to four factors: the number of lecture components, curriculum hours, degree of satisfaction with the components and degree of satisfaction with the curriculum hours. We also investigated differences in these four factors among three groups: Directors, Council members and non-members of the JSSM. The medians of curriculum hours and the number of the lecture components were 90.0 min and 7.0, respectively. The curriculum hours of the Directors (140.0 min) were significantly longer than those of the non-members (90.0 min; P<0.05). The number of lecture components taught by Directors (9.5) was significantly higher than that of the Council (4.0; P<0.01) and non-members (7.0; P<0.05). More than half of the faculties were not satisfied with the lecture components and curriculum hours. This is the first study on sexuality education in Japanese medical schools. It showed the inadequacy of both curriculum hours and lecture components, and that the position title of department chair affects sexuality education in medical schools.
Vasohibin-1 (VASH1) was isolated as a negative-feedback regulator of angiogenesis expressed in endothelial cells (ECs). There are two transcripts of VASH1, that is, the full-length VASH1A consisting ...of seven exons and the splicing variant VASH1B consisting of four exons. Here, we compared the effects of VASH1A and VASH1B on tumor angiogenesis. When ECs were transfected with VASH1A or VASH1B cDNAs, VASH1B transfectants, but not VASH1A ones, induced autophagic cell death of ECs. With sonoporation, the VASH1A or VASH1B gene were transfected specifically in ECs of tumor vessels in mice. Both VASH1A and VASH1B decreased tumor vessel density and inhibited tumor growth. VASH1A normalized the remaining tumor vessels, increased their rate of perfusion, decreased tumor hypoxia and enhanced the efficacy of anticancer chemotherapy, whereas VASH1B pruned tumor vessels without causing normalization, increased tumor hypoxia and tumor necrosis and did not enhance the efficacy of anticancer chemotherapy. The alternate transfection of mice with the VASH1A and VASH1B gene showed the highest effects on antitumor activity and normalization of tumor vessels. Our present findings on VASH1A and VASH1B should provide an innovative approach that would improve the efficacy of antiangiogenic cancer therapy by balancing vascular normalization and pruning.
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