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Background: To investigate the effects of benzodiazepine receptor agonists on cognitive function in patients with chronic insomnia. Method: According to the history of taking hypnotic drugs, they were divided into no medication group (n = 62), benzodiazepines group (n = 57) and non‐benzodiazepines group (n = 53); all subjects The Pittsburgh Sleep Quality Scale, the Epworth Scale, and the Insomnia Severity Index were used to evaluate their sleep quality, and the Hamilton Anxiety and Depression Scale to evaluate their anxiety and depression. The conversion test, the auditory word learning test was used to evaluate the memory function, and the Stroop color word test and the connection function test were used to evaluate the executive function. Result: Compared with no medication, the non‐benzodiazepine group and the benzodiazepine group had longer sleep time throughout the night (P<0.05), and the non‐benzodiazepine group and the benzodiazepine group. The anxiety and depression scores of the drug group were lower than those of the non‐drug group (P<0.05), and the immediate memory and delayed memory scores of the benzodiazepine group and the non‐drug group were lower than those of the non‐benzodiazepine group (P<0.05). 0.05), the dose and duration of medication in the benzodiazepine group were negatively correlated with immediate memory (P<0.05), and the duration of medication in the benzodiazepine group was negatively correlated with prolonged memory (P<0.05). Regression analysis showed that the immediate memory score of taking benzodiazepines was 2.612 times lower than that of the non‐drug group, and the delayed memory score of taking non‐benzodiazepines was 1.439 times higher Regression analysis showed that the immediate memory score of taking benzodiazepines was 2.612 times lower than that of the non‐drug group, and the delayed memory score of taking non‐benzodiazepines was 1.439 times higher than that of the non‐drug group (P<0.05). The difference is statistically significant. Conclusion: Benzodiazepines increase the risk of impaired immediate memory function in patients with chronic insomnia, and non‐benzodiazepines can improve their delayed memory function. [ABSTRACT FROM AUTHOR]

Objective: To describe the changes in sleep pattern throughout pregnancy and to evaluate the relationship between sleep and adverse perinatal outcomes., Methods: Pregnant women at Qianfoshan Hospital completed questionnaires regarding their sleep during each of the three trimesters. Additionally, a subset of participants engaged in objective sleep monitoring using actigraphy devices. In the perinatal period, the following data were collected: pregnancy complications; gestational age; mode of delivery; Apgar scores for the neonate; and birth weight., Results: The total night sleep time in the second trimester was about 15 minutes shorter than that in the first trimester (P=0.024), and about 31 minutes shorter in the third trimester than in the second trimester (P<0.001). The sleep efficiency in the second trimester was about 10.23% lower than in the first trimester (P<0.001), and the efficiency in the third trimester was about 5.16% lower than in the second trimester (P<0.001). The occurrence of pregnancy-induced hypertension (PIH) was associated with sleep duration (P=0.019), sleep efficiency (P<0.001) and PSQI scores (P<0.001) in the first trimester. Furthermore, the mode of delivery was also found to be associated with sleep duration (P=0.011), sleep efficiency (P<0.001) and PSQI scores (P<0.001) in the first trimester., Conclusion: With the development of the pregnancy process, the sleep situation gets worse. Pregnant women's sleep situation in the first trimester of pregnancy is associated with the occurrence of PIH and delivery mode., Competing Interests: None., (AJTR Copyright © 2024.)

Background and Objective: At present, the etiology of narcolepsy is not fully understood, and it is generally believed to be an autoimmune reaction caused by interactions between environmental and genetic factors. Human leukocyte antigen (HLA) class II genes are strongly associated with this gene, especially HLA-DQB1*0602/DQA1*0102. In this study, we mainly analyzed the correlation between different genotypes of HLA-DQB1*0602/DQA1*0102 and clinical manifestations in Chinese patients with narcolepsy., Experimental Method: Narcolepsy patients who were treated at the Department of Neurology, The First Affiliated Hospital of Shandong First Medical University from January 2021 to September 2023 were selected. General information, sleep monitoring data, cerebrospinal fluid (CSF) orexin levels, and human leukocyte antigen gene typing data were collected. The statistical analysis was performed using SPSS 26.0, and the graphs were drawn using GraphPad Prism 9.5., Main Results: A total of 78 patients were included in this study. The DQA1 and DQB1 gene loci were detected in 54 patients, and only the DQB1 gene locus was detected in 24 narcoleptic patients. The most common allele at the HLA-DQB1 locus was *0602 (89.7%), and the most common genotype at this locus was *0602*0301 (19.2%), followed by *0602*0602 (17.9%). The most common phenotype of the HLA-DQA1 locus is *0102 (92.6%), and the most common genotype of this locus is *0102*0102 (27.8%), followed by *0102*0505 (14.8%). There were significant differences ( p  < 0.05) between HLA-DQB1*0602-positive and HLA-DQB1*0602-negative patients in terms of orexin-A levels, presence or absence of cataplexy, UNS, PSG sleep latency, REM sleep latency, N1 sleep percentage, oxygen depletion index, and average REM latency on the MSLT. The HLA-DQA1*0102-positive and HLA-DQA1*0102-negative patients showed significant differences ( p  < 0.05) in disease course, presence or absence of sudden onset, PSG REM sleep latency, N1 sleep percentage, and average REM latency on the MSLT. There were significant differences in the average REM latency of the MSLT between HLA-DQB1*0602/DQA1*0102 homozygous and heterozygous patients p  < 0.05, and no differences were found in the baseline data, orexin-A levels, scale scores, or other sleep parameters., Conclusion: Different genotypes of HLA-DQA1*0102/DQB1*0602 are associated with symptoms of cataplexy in Chinese narcoleptic patients. Homozygous individuals have a shorter mean REM latency in the MSLT, greater genetic susceptibility, and relatively more severe sleepiness., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Zhao, Zhang, Yan, Zhao, Zhang, Zhang, Liu and Tang.)

Objective: To explore the effects of N-butylphthalide on the expressions of ZO-1 and claudin-5 in blood-brain barrier (BBB) in rats with acute carbon monoxide (CO) poisoning., Methods: A total of 144 adult healthy male Sprague-Dawley (SD) rats were randomly divided into normal control group, CO poisoning group, and NBP treatment group, with 48 rats in each group. The acute CO poisoning model was reproduced in hyperbaric oxygen chamber, and all model rats were given hyperbaric oxygen therapy once daily. The rats in the normal control group were free to breathe fresh air. The rats in NBP treatment group were administered orally NBP 60 mg/kg twice a day at 2 hours after poisoning until death. The rats in normal control group and CO poisoning group were treated with equal amount of pure olive oil. Four rats were sacrificed from each group at 1, 3, 7, 14 days after model reproducing, respectively. The changes in ultrastructure of BBB were observed under transmission electron microscope. The expressions of ZO-1 and claudin-5 proteins were determined by immunofluorescence staining and Western Blot. The localization of the two target proteins was observed by immunofluorescence double staining. The correlation between the two proteins was analyzed by linear regression., Results: The ultrastructure of BBB was normal in normal control group, some ZO-1 and a large number of claudin-5 positive cells were observed. The ultrastructure of BBB was seriously injured, ZO-1 and claudin-5 positive cells in brain tissue were significantly decreased, and the expressions of ZO-1 and claudin-5 proteins in brain tissue at 1 day after poisoning in CO poisoning group were significantly lower than those of normal control group (ZO-1 protein: 3.38±0.30 vs. 24.50±5.62, claudin-5 protein: 11.38±0.93 vs. 46.35±6.88, both P < 0.05), and although gradually restored, they were maintained at relatively lower levels until 14 days as compared with those in normal control group (ZO-1 protein: 10.35±0.80 vs. 24.63±3.57, claudin-5 protein: 32.35±3.11 vs. 46.43±7.20, both P < 0.05). NBP treatment could significantly alleviate the ultrastructure injury of BBB induced by acute CO poisoning, the amount of ZO-1 and claudin-5 positive cells in brain tissue were significantly increased, as well as the expressions of ZO-1 and claudin-5 proteins were significantly increased, which were significantly higher than those of CO poisoning group from 1 day and 3 days on, respectively (1-day ZO-1 protein: 7.57±0.69 vs. 3.38±0.30, 3-day claudin-5 protein: 20.46±1.42 vs. 11.43±0.86, both P < 0.05), and which showed an increase tendency with time prolongation. The results of immunofluorescence double staining showed that ZO-1 and claudin-5 proteins could not only coexist in the same cell, but also could be expressed separately in different cells. Linear regression analysis showed the positive correlation between the expressions of ZO-1 and claudin-5 proteins in brain tissue of rats with acute CO poisoning (R 2 = 0.917, P = 0.022)., Conclusions: NBP could markedly improve the ultrastructure and functional integrity of BBB through up-regulating the expressions of ZO-1 and claudin-5 proteins, and then reduce brain damage caused by CO poisoning.