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Objective To explore the impact of macrophage-to-myofibroblast transition (MMT) on pulmonary fibrosis induced by acute lung injury by LPS. Methods Totally 21 male mice were randomly classified into 7 groups: control group, model group (LPS-PF) at different time points and intervention group of clodronate-liposomes (CL-LIP)treatement at different time points(n=3). Pulmonary fibrosis was identified by HE and Masson staining microscopy. The immuno-fluorescence technology was used for the evaluation of numbers of macrophage- to- myofibroblast transition cells (MMT cell which co-expressed CD68 and α-SMA). Bone marrow-derived macrophages (BMDMs) were randomly classified into two group: control (Ctrl) group and TGF-β1-treated group induced by transforming growthfactor-β1. α-SMA, FN and Col1 were detected by RT-qPCR. The expression of α-SMA, Smad3 and p-Smad3 protein was evaluated by Western blot. Results At day 7, the Ashcroft score of lung tissue in LPS-PF mouse model was significantly increased when compared with the Ctrl group (P＜0.01); While the score significantly declined when the model was pretreated with CL-LIP (P＜0.05). As detected by immuno-fluorescence staining, in CL-LIP group the number of CD68-positive cells co-labeled with α-SMA was obviously less then that of LPS-PF group of the corresponding time point(P＜0.01). When the BMDMs were stimulated by TGF-β1 at 24 h, 48 h and 96 h respectively, a higher expression of α-SMA,FN,Col1, were found in TGF-β1-treated group than that in Ctrl group at the corresponding time point (P＜0.01). The expression of Smad3, p-Smad3 significantly higher in LPS-PF group (at both day 7 and day 10) and TGF-β1-treated group (at both 48 h and 96 h) as compared to corresponding control group (P＜0.01). Conclusions MMT promotes pulmonary fibrosis induced by ALI via LPS. Smad3 is proved to be involved in the MMT process.

Summary: In a prospective, randomized, controlled crossover study, we explored the effects of acute intermittent hypoxia and acute continuous hypoxia on patients with mild–moderate obstructive sleep apnea. Over three single‐night sessions, subjects were alternately exposed to normoxia, acute continuous hypoxia and acute intermittent hypoxia before sleep. The apnea–hypopnea index and oxygen desaturation index were used to diagnose obstructive sleep apnea and evaluate efficacy. A responder was defined as a participant with a ≥ 50% reduction in apnea–hypopnea index between normoxia and hypoxia exposure. Sixteen participants with mild–moderate obstructive sleep apnea completed the study. Compared with normoxia, the mean apnea–hypopnea index decreased by 8.9 events per hr (95% confidence interval, 4.2–13.6, p = 0.001) with acute intermittent hypoxia and by 4.1 events per hr (95% confidence interval, 0.5–8.8, p = 0.082) with acute continuous hypoxia, equating to a mean decrease in apnea–hypopnea index of 4.8 events per hr (95% confidence interval, 0.1–9.5, p = 0.046) with acute intermittent hypoxia compared with acute continuous hypoxia. Compared with normoxia, the mean oxygen desaturation index decreased by 9.8 events per hr (95% confidence interval, 4.4–15.1, p = 0.001) with acute intermittent hypoxia but did not significantly decrease with acute continuous hypoxia; the mean oxygen desaturation index decreased by 7.2 events per hr (95% confidence interval, 1.8–12.6, p = 0.010) with acute intermittent hypoxia compared with acute continuous hypoxia. Of the 16 participants, 11 responded to acute intermittent hypoxia and four responded to acute continuous hypoxia (p = 0.032), of whom eight of 11 cases and all four cases had oxygen desaturation indexes <5 events per hr, respectively (p = 0.273). All participants tolerated acute intermittent hypoxia and there were no obvious adverse events during acute intermittent hypoxia exposure. In conclusion, acute intermittent hypoxia exposure improved apnea–hypopnea index and oxygen desaturation index in patients with mild–moderate obstructive sleep apnea, suggesting that further prospective validation of intermittent hypoxia exposure in patients with obstructive sleep apnea is needed to establish its clinical feasibility as a therapeutic modality. [ABSTRACT FROM AUTHOR]

Summary: The present study was conducted to systematically evaluate the acute effect of morphine on obstructive sleep apnea (OSA). The PubMed, Embase, Cochrane Library, Clinicaltrials.gov, China National Knowledge Infrastructure (CNKI), and Wan‐Fang databases were searched for randomised controlled trials studying the influence of morphine on OSA published up to May 24, 2021. The Cochrane risk of bias tool was used to assess study quality and meta‐analysis was performed on the included clinical trial results to quantify the impact of morphine on various sleep and respiratory parameters. Three studies (n = 132 patients) were ultimately examined. There were no significant differences between patients with OSA taking morphine and placebo/non‐opioids with respect to the sleep Apnea–Hypopnea Index (mean difference [MD] 1.78, 95% confidence interval [CI] −2.41, 5.98; p > 0.05); Oxygen Desaturation Index (MD 1.49, 95% CI −3.21, 6.19; p > 0.05); Obstructive Sleep Apnea Index (MD 0.83, 95% CI −2.08, 3.75; p > 0.05); Hypopnea Index (MD –0.01, 95% CI −2.64, 2.63; p > 0.05); lowest oxygen saturation (MD 0.68, 95% CI –4.50, 5.86; p > 0.05); or sleep oxygen saturation >90% (MD 0.10, 95% CI –1.14, 1.34; p > 0.05). In conclusion, a single dose of 30 or 40 mg morphine does not have a significant effect on sleep or respiratory outcomes compared to placebo in patients with OSA, challenging the orthodoxy that opioids worsen OSA. [ABSTRACT FROM AUTHOR]

Purpose: SARS-CoV-2 can invade the thyroid gland. This study was to delineate the risk of thyroid dysfunction amidst the prevalence of the Omicron variant, and to investigate the correlation between thyroid function and Coronavirus disease 2019 (COVID-19) outcomes. The study also aimed to ascertain whether thyroid dysfunction persisted during COVID-19 recovery phase., Methods: This was a retrospective cohort study. COVID-19 patients from the Renmin Hospital of Wuhan University, China during the epidemic of Omicron variants were included, and their thyroid function were analyzed in groups., Results: A history of thyroid disease was not associated with COVID-19 outcomes. COVID-19 can lead to a bimodal distribution of thyroid dysfunction. The severity of COVID-19 was inversely proportional to the levels of thyroid- stimulating hormone (TSH), free triiodothyronine (FT3) and free thyroxine (FT4), leading to a higher prevalence of thyroid dysfunction. Severe COVID-19 was a risk factor for euthyroid sick syndrome (ESS) (OR=22.5, 95% CI, 12.1 - 45.6). Neutrophil to lymphocyte ratio mediated the association between severe COVID-19 and ESS (mediation effect ratio = 41.3%, p < 0.001). ESS and decreased indicators of thyroid function were associated with COVID-19 mortality, while high levels of FT3 and FT4 exhibited a protective effect against death. This effect was more significant in women (p < 0.05). During the recovery period, hyperthyroidism was quite uncommon, while a small percentage of individuals (7.7%) continued to exhibit hypothyroidism., Conclusion: COVID-19 severity was linked to thyroid dysfunction. Severe COVID-19 increased the risk of ESS, which was associated with COVID-19 mortality. Post-recovery, hyperthyroidism was rare, but some individuals continued to have hypothyroidism., 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 Zhang, Zhang, Liu, Wang, Chen, Hao, Zha, Zhang, He, Zhou and Hu.)