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Objective To investigate the clinical characteristics and influencing factors of insomnia in perimenopausal women based on polysomnography (PSG). Methods A total of 52 perimenopausal women admitted to our psychological clinic due to insomnia were included in this study. According to the results of Pittsburgh sleep quality index (PSQI), they were divided into study group (PSQI≥7) and control group (PSQI < 7). Sleep status was recorded by polysomnography (PSG), and symptoms related to perimenopausal period were measured by menopause rating scale (MRS).The differences of PSG monitoring sleep-related indicators and MRS results were compared between the 2 groups, and the correlations of each sleep indicator with perimenopausal symptoms were analyzed. Results ① The total sleep time and sleep efficiency were significantly decreased in the perimenopausal women from the study group than those from the control group (P < 0.05). The former group had obviously longer sleep latency and wakefulness time when compared with the latter group (P < 0.05). ② These perimenopausal women had the clinical feature of rapid eye movement (REM) sleep behavior, which were characterized by decreased total time of REM sleep, decreased proportion of REM sleep, prolonged latency of REM sleep, and increased frequency of REM to wakefulness in the study group when compared with the control group (P < 0.05). ③The total MRS score, somatic symptom score, psychological symptom score and genitourinary system score were 26.69±5.13, 9.49±2.92, 10.34±2.95 and 6.86±2.89, respectively, in the study group, which were all higher than those of the control group (P < 0.05). ④The proportion of REM sleep and the total time of REM sleep were negatively correlated with depression (P < 0.05), while the latency of REM sleep was positively correlated with anxiety and sexual life quality (P < 0.05). Conclusion Insomnia in perimenopausal women is characterized by REM sleep disorder, and REM sleep is closely related to anxiety, depression and sexual life quality.

Sialic acid (SIA) has been reported to be a risk factor for atherosclerosis (AS) due to its high plasma levels in such patients. However, the effect of increasing SIA in circulation on endothelial function during AS progression remains unclear. In the present study, ApoE−/− mice and endothelial cells line (HUVEC cells) were applied to investigate the effect of SIA on AS progression and its potential molecular mechanism. In vivo, mice were injected intraperitoneally with Neu5Ac (main form of SIA) to keep high‐level SIA in circulation. ORO, H&E, and Masson staining were applied to detect the plaque progression. In vitro, HUVECs were treated with Neu5Ac at different times, CCK‐8, RT‐PCR, western blot, and immunoprecipitation methods were used to analyze its effects on endothelial function and the potential involved mechanism. Results from the present study showed that high plasma levels of Neu5Ac in ApoE−/− mice could aggravate the plaque areas as well as increase necrotic core areas and collagen fiber contents. Remarkably, Neu5Ac levels in circulation displayed a positive correlation with AS plaque areas. Furthermore, results from HUVECs showed that Neu5Ac inhibited cells viability in a time/dose‐dependent manner, by then induced the activation of inflammation makers such as ICAM‐1 and IL‐1β. Mechanism study showed that the activation of excessive autophagy medicated by SQSTM1/p62 displayed an important role in endothelium inflammatory injury. Neu5Ac could modify SQSTM1/p62 as a sialylation protein, and then increase its level with ubiquitin binding, further inducing ubiquitination degradation and being involved in the excessive autophagy pathway. Inhibition of sialylation by P‐3Fax‐Neu5Ac, a sialyltransferase inhibitor, reduced the binding of SQSTM1/p62 to ubiquitin. Together, these findings indicated that Neu5Ac increased SQSTM1/p62‐ubiquitin binding through sialylation modification, thereby inducing excessive autophagy and subsequent endothelial injury. Inhibition of SQSTM1/p62 sialylation might be a potential strategy for preventing such disease with high levels of Neu5Ac in circulation. [ABSTRACT FROM AUTHOR]

Acute pancreatitis is an inflammatory disorder of the pancreas associated with substantial morbidity and mortality, which is characterized by a rapid depletion of glutathione (GSH). Cysthionine- β -synthase (CBS) is a key coenzyme in GSH synthesis, and its deficiency is related to a variety of clinical diseases. However, whether CBS is involved in the pathogenesis of acute pancreatitis remains unclear. First, we found that CBS was downregulated in both in vivo and in vitro AP models. The pancreatic damage and acinar cell necrosis related to CBS deficiency were significantly improved by VB 12, which stimulated clearance of reactive oxygen species (ROS) by conserving GSH. Furthermore, EX-527 (a specific inhibitor of SIRT1) exposure counteracted the protective effect of VB 12 by promoting oxidative stress and aggravating mitochondrial damage without influencing CBS, indicating that vitamin B 12 regulates SIRT1 to improve pancreatical damage by activating CBS. In conclusion, we found that VB 12 protected acute pancreatitis associated with oxidative stress via CBS/SIRT1 pathway., Competing Interests: The authors have declared no conflicts of interest., (Copyright © 2021 Jiyan Yuan et al.)

Triple negative breast cancer (TNBC) is a highly aggressive cancer and lack of targeting therapies. It is believed that the breast cancer stem cells (BCSCs) are responsible for the aggressive characteristics of TNBC. Hence, developing BCSC-targeting agents may provide new therapeutic strategies for the patients. Huaier polysaccharide (HP), an active ingredient extracted from the mushroom Trametes robiniophila Murr, has been widely used in clinical anti-cancer treatments in China. Here we demonstrated that HP could target BCSCs in TNBC cells, resulting in decreased mammosphere formation, downregulated expression of stem-related genes and reduced proportion of aldehyde dehydrogenase positive cells in vitro, and inhibited xenograft tumor formation in vivo . Mechanically, HP markedly reduced the expression of estrogen receptor α-36 (ERα-36), a recently identified subtype of estrogen receptor α, and attenuated ERα-36-mediated activation of AKT/β-catenin signaling in ERα-36 high TNBC cells. This study provides a new insight into the mechanism of HP on BCSC-targeting therapy and new ideas for comprehensive treatment strategies for TNBC., Competing Interests: Competing Interests: The authors have declared that no competing interest exists.