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OBJECTIVES: To conduct a meta-analysis of the association between postherpetic neuralgia (PHN), baseline characteristics of patients with herpes zoster (HZ), and early interventions. METHODS: Literature searches were conducted in seven databases, in June 2021 and updated in June 2022. Two investigators independently conducted literature screening and data extraction, and the studies were evaluated according to the Newcastle-Ottawa scale. RESULTS: A total of 53 cohort studies were included. The meta-analyses identified skin lesions, timing of initial treatment (≥3 days), and comorbidities as potential risk factors for PHN. In contrast, female sex (odds ratio [OR] = 1.13, 95% confidence interval [CI]: 0.99-1.29), cervical herpes (OR = 0.80, 95% CI: 0.21-2.99), lumbar herpes (OR = 1.29, 95% CI: 0.61-2.74), and immunosuppressive therapy (OR = 1.96, 95% CI: 0.22-17.12), were not significantly associated with PHN. In addition, glucocorticoid use (OR = 0.61, 95% CI: 0.22-1.70) may be a protective factor for the development of PHN; however, the difference was not statistically significant. CONCLUSION: A series of baseline characteristics were identified among populations at high risk of developing PHN from HZ. Additionally, the timing of initial treatment is associated with PHN occurrence. The preventive effect of glucocorticoids warrants further validation.
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Oxygen therapy is widely used in clinical practice; however, prolonged hyperoxia exposure may result in hyperoxic acute lung injury (HALI). In this study, we investigated the role of FAM134B in hyperoxia-induced apoptosis, cell proliferation, and epithelial-to-mesenchymal transition (EMT) using RLE-6TN cells and rat lungs. We also studied the effect of CeO2-NPs on RLE-6TN cells and lungs following hyperoxia exposure. FAM134B was inhibited in RLE-6TN cells and rat lungs following hyperoxia exposure. Overexpressing FAM134B promoted cell proliferation, and reduced EMT and apoptosis following hyperoxia exposure. FAM134B activation increased ER-phagy, decreased apoptosis, improved lung structure damage, and decreased collagen fiber deposition to limit lung injury. These effects could be reversed by PI3K/AKT pathway inhibitor LY294002. Additionally, CeO2-NPs protected RLE-6TN cells and lung damage following hyperoxia exposure by ameliorating impaired ER-phagy. Therefore, FAM134B restoration is a potential therapeutic target for the HALI. Moreover, CeO2-NPs can be used for the treatment of HALI.