Obstructive sleep apnea syndrome (OSAS) is characterized by chronic nocturnal intermittent hypoxia and sleep fragmentations. Neurocognitive dysfunction, a significant and extraordinary complication of OSAS, influences patients’ career, family, and social life and reduces quality of life to some extent. Previous researches revealed that repetitive hypoxia and reoxygenation caused mitochondria and endoplasmic reticulum dysfunction, overactivated NADPH oxidase, xanthine oxidase, and uncoupling nitric oxide synthase, induced an imbalance between prooxidants and antioxidants, and then got rise to a series of oxidative stress (OS) responses, such as protein oxidation, lipid peroxidation, and DNA oxidation along with inflammatory reaction. OS in brain could trigger neuron injury especially in the hippocampus and cerebral cortex regions. Those two regions are fairly susceptible to hypoxia and oxidative stress production which could consequently result in cognitive dysfunction. Apart from continuous positive airway pressure (CPAP), antioxidant may be a promising therapeutic method to improve partially reversible neurocognitive function. Understanding the role that OS played in the cognitive deficits is crucial for future research and therapeutic strategy development. In this paper, recent important literature concerning the relationship between oxidative stress and cognitive impairment in OSAS will be summarized and the results can provide a rewarding overview for future breakthrough in this field.

The present study investigated the nuclear factor erythroid 2‐related factor 2‐ (Nrf2‐) antioxidant response element (ARE) signaling pathway in patients with moderate to severe obstructive sleep apnea‐hypopnea syndrome (OSAHS). Their correlation with neurocognitive impairment metrics was investigated to explore potential pathogenesis in OSAHS. Forty‐eight patients with OSAHS and 28 controls underwent testing with the Epworth Sleep Scale (ESS), MATRICS Consensus Cognitive Battery (MCCB), Stroop Color and Word Test, polysomnography (PSG), and measurements of the concentration of plasma superoxide dismutase (SOD) and thioredoxin (Trx). Further, 20 pairs of matched patients with OSAHS and controls were selected for measurement of the expression (protein and mRNA) of Nrf2 and of its downstream antioxidase, heme oxygenase‐1 (HO‐1), in peripheral mononuclear cells (PBMCs). Finally, correlations between neurocognitive impairment and the above metrics were analyzed. Expression of Nrf2 and HO‐1 mRNA and protein in the PBMCs, as well as plasma SOD and Trx levels, were significantly reduced in patients with OSAHS. After adjusting for education, sex, age, and smoking index, the expression of Nrf2‐ARE signaling pathway proteins (or mRNA) was closely correlated with sleep respiratory parameters. An inverse relationship was demonstrated between the expression of nuclear Nrf2 in PBMCs, concentration of plasma SOD and Trx, and apnea‐hypopnea index (AHI) in patients with OSAHS. Trx, nuclear Nrf2 protein, and HO‐1 protein were also negatively correlated with the percent of time that SaO₂ was less than 90% (TSat90). Total Nrf2 protein level was positively correlated with AHI and TSat90 and negatively correlated with minimum SaO₂ (LSaO₂), while nuclear Nrf2 protein and HO‐1 protein were positively correlated with LSaO₂. Moreover, significant positive correlations were found between maze scores and expression of nuclear Nrf2 protein, HO‐1 protein, and SOD and Trx levels. Furthermore, inverse relationships between total Nrf2 protein in PBMCs and HVLT‐R and maze scores were found. Multiple linear regression showed plasma Trx concentration as a potential predictor of maze and BVMT‐R scores. In conclusion, the expression of Nrf2‐ARE molecules and related antioxidases is significantly decreased in patients with OSAHS and is correlated with neurocognitive dysfunction. The Nrf2‐ARE signaling pathway may play a crucial role in neurocognitive impairment in patients with moderate to severe OSAHS. Further studies are needed to explore the exact mechanisms and potential treatment interventions.

Background: Bone marrow mesenchymal stem cells (BMSCs)-derived exosomes are rich in a variety of active substances, including microRNA (miR) and have shown powerful therapeutic effects to ameliorate cell injury and diseases. However, the role of BMSCs-derived exosomes on chronic obstructive pulmonary disease (COPD) has been poorly studied. In addition, pulmonary microvascular endothelial cells (PMVECs) apoptosis contributes to the onset of COPD. Inhibition of PMVECs apoptosis can reverse COPD changes. Therefore, the aim of this study was to explore the role of BMSCs-derived exosomes in the apoptosis of PMVECs in COPD and to investigate the potential mechanisms. Methods: We isolated and characterized normal mouse BMSCs-derived exosomes and PMVECs. We performed miR sequencing of BMSCs-derived exosomes. We transfected PMVECs with the miR-30b mimic and Wnt5a overexpression plasmid to assess the underlying mechanisms. Cigarette smoke extract (CSE)-induced COPD mice were treated with exosomes and HBLV-mmu-miR-30b via intratracheal instillation. Finally, we determined the expression of miR-30b and Wnt5a in tissues from patients with COPD. Results: BMSCs-derived exosomes could significantly reduce apoptosis of CSE-induced PMVECs and increase the expression of miR-30b (p< 0.05). Based on miR sequencing, miR-30b was highly enriched in BMSCs-derived exosomes. The knockdown of miR-30b in BMSCs-derived exosomes could increase the apoptosis of CSE-induced PMVECs (p< 0.05). miR-30b overexpression significantly reduced apoptosis and repressed Wnt5a protein expression in CSE-induced PMVECs (p< 0.05). Furthermore, Wnt5a overexpression reversed the anti-apoptotic effect of miR-30b on CSE-induced PMVECs (p< 0.05). In addition, compared with the COPD group, treatment with BMSCs-derived exosomes and miR-30b overexpression could alleviate emphysema changes, decrease the mean linear intercept and alveolar destructive index, reduce apoptosis, increase the expression of miR-30b, and decrease the expression of Wnt5a in lung tissue (p< 0.05). Finally, miR-30b expression was decreased in patients with COPD, while Wnt5a expression was increased in these patients (p< 0.05). Conclusion: BMSCs-derived exosomes could improve the damage of COPD perhaps by delivering miR-30b. miR-30b could reduce apoptosis of CSE-induced PMVECs by targeting Wnt5a.

Objective: The aim of this study was to compare serum leptin, apolipoprotein A1 (ApoA1), apolipoprotein J (ApoJ) and apolipoprotein H (ApoH) levels in males with obstructive sleep apnea and hypopnea syndrome (OSAHS) to those in healthy control subjects and to examine the possible relation between neurocognitive performance and these factors/serum markers in the subjects. Methods: In this observational, cross-sectional study, a full-night polysomnography and sensitive neuropsychological assessment were performed on 50 newly diagnosed Chinese male patients and 30 healthy subjects. Fasting blood samples were used to measure leptin and ApoA1, ApoH and ApoJ levels using ELISA. Results: Compared with normal control subjects, OSAHS patients have significantly lower levels of ApoA1 and higher levels of leptin, ApoH and ApoJ. After adjustment for age, years of education, body mass index (BMI) and apnea–hypopnea index, leptin and ApoA1 were associated with global cognitive function, and leptin level was positively correlated with inhibition reaction time. ApoJ was negatively correlated with visual reproduction and logical memory performance. Multiple regression analysis shows that from age, BMI, education year, biomarker levels and the parameters of PSG, only the variables of leptin and education year added to the prediction of the Montreal cognitive assessment score in a statistically significant way. Conclusions: Abnormal expression of leptin and apolipoproteins and poor performance on neuropsychological tests were observed in patients with OSAHS. There is also an association between serum leptin, ApoA1, and ApoJ levels and cognitive performance in the patients.

Background: Since most internal medicine nurses work with chronic obstructive pulmonary disease (COPD) patients daily, their ability to meet the needs of COPD patients is an important issue. Our study aimed to assess COPD-related knowledge in internal medicine nurses. Methods: A descriptive cross-sectional study including 175 participants was conducted to investigate COPD-related knowledge levels among internal medicine nurses in a large top-ranked tertiary hospital in China. The Bristol COPD Knowledge Questionnaire (BCKQ) was used to test COPD-related knowledge levels in the participants. Results: Overall BCKQ score for all nurses in this study was 35.76 ± 5.49. In comparison with non-respiratory nurses, the overall score among respiratory nurses was significantly higher (39.01 ± 3.95 vs 33.32 ± 5.23, p < 0.001). The mean scores for four topics (epidemiology, breathlessness, oral steroids, and inhaled steroids) were less than 3 among both respiratory and non-respiratory nurses. Subgroup analysis of specialist respiratory wards showed that nurses in the chronic airway disease ward had the highest overall knowledge score (40.47 ± 4.03). Linear regression analysis demonstrated that the overall BCKQ score was significantly related to the population of nurses (β coefficient = 3.016, 95% confidence interval [CI]: 0.953–5.079, p < 0.01), education (β coefficient = 4.710, 95% CI: 1.979-7.440, p < 0.01) and previous rotation in respiratory wards (β coefficient = 3.871, 95% CI: 1.776-5.967, p < 0.001). Conclusion: Internal medicine nurses at this tertiary hospital showed deficits in COPD-related knowledge. Appropriate and systematic education about COPD knowledge and strengthening rotation among different wards are necessary for improving COPD-related knowledge levels among internal medicine nurses.

Background: The revised Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2023 group ABE classification has undergone major modifications, which can simplify clinical assessment and optimize treatment recommendations for Chronic Obstructive Pulmonary Disease (COPD). However, the predictive value of the new grouping classification for prognosis is worth further exploration. We aimed to compare the prediction of hospitalization and mortality between this new GOLD group 2023 ABE classification and the earlier 2017 ABCD classification in a Chinese COPD cohort. Methods: Data from 2,499 outpatients with COPD, who first registered in the RealDTC study of Second Xiangya Hospital from December 2016 to December 2019, were collected prospectively and assessed retrospectively. Patients were followed up on all-cause mortality until October 2022 or death. Results: : Of the 2,499 patients with COPD, the risk of hospitalization during the first-year follow-up was higher in group E than in groups A and B. The mortality was higher in group E than in groups A and B, and group B was higher than group A. No differences were seen in the area under the curve (AUC) of 2017 vs 2023 GOLD grouping to predict hospitalization. The time-dependent AUC and concordance index for predicting mortality is slightly higher in the GOLD 2017 ABCD than in the 2023 ABE groups. The new GOLD 12-subgroup (1A– 4E) classification combining the GOLD 1– 4 staging and grouping performed similarly discriminate predictive power for mortality to the GOLD 2017 16-subgroup (A1– 4D) classification. Conclusion: The risk of hospitalization during the first-year follow-up was higher in group E than in groups A and B. The all-cause mortality increased gradually from GOLD group A to E. The GOLD 2023 classification based on ABE groups did not predict mortality better than the earlier 2017 ABCD classifications.