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Background and aims: Lung cancer patients suffer from deterioration in their physical and psychological function, which exerts a negative influence on their quality of life (QOL). Telemedicine has been proven to be an effective intervention for patients with several chronic diseases. The aim of this systematic review and meta-analysis was to investigate the efficacy of telemedicine in improving QOL in lung cancer patients. Methods: PubMed, Cochrane Library, EMBASE, Web of Science and Scopus databases were searched for randomized controlled trials that investigated the effectiveness of telemedicine in lung cancer patients. Review Manager 5.3 and Stata 15.1 were used to perform data analysis. Results: Our meta-analysis included eight clinical trials with a total of 635 lung cancer patients. The results showed that the telemedicine group had significantly higher QOL than the usual care group [standard mean difference (SMD) 0.96, 95% confidence interval (CI) 0.29–1.63, I2 = 91%]. In addition, the telemedicine group had lower anxiety (SMD −0.44, 95% CI −0.66 to −0.23, I2 = 3%) and depression scores (SMD −0.48, 95% CI −0.91 to −0.05, I2 = 66%) than the usual care group. However, no significant differences were found in fatigue and pain outcomes between the two groups. Conclusion: Telemedicine may be an effective method of improving QOL in lung cancer patients and the further development and use of telemedicine care is recommended.

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Infectious diseases caused by bacteria, viruses, and fungi and their global spread pose a great threat to human health.

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The intervertebral disc (IVD) acts as a fibrocartilaginous joint to anchor adjacent vertebrae. Although several studies have demonstrated the cellular heterogeneity of adult mature IVDs, a single‐cell transcriptomic atlas mapping early IVD formation is still lacking. Here, the authors generate a spatiotemporal and single cell‐based transcriptomic atlas of human IVD formation at the embryonic stage and a comparative mouse transcript landscape. They identify two novel human notochord (NC)/nucleus pulposus (NP) clusters, SRY‐box transcription factor 10 (SOX10)+ and cathepsin K (CTSK)+, that are distributed in the early and late stages of IVD formation and they are validated by lineage tracing experiments in mice. Matrisome NC/NP clusters, T‐box transcription factor T (TBXT)+ and CTSK+, are responsible for the extracellular matrix homeostasis. The IVD atlas suggests that a subcluster of the vertebral chondrocyte subcluster might give rise to an inner annulus fibrosus of chondrogenic origin, while the fibroblastic outer annulus fibrosus preferentially expresseds transgelin and fibromodulin . Through analyzing intercellular crosstalk, the authors further find that notochordal secreted phosphoprotein 1 (SPP1) is a novel cue in the IVD microenvironment, and it is associated with IVD development and degeneration. In conclusion, the single‐cell transcriptomic atlas will be leveraged to develop preventative and regenerative strategies for IVD degeneration.

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Background: Acute respiratory distress syndrome (ARDS) is characterized by severe local and systemic inflammation. Ac2-26, an Annexin A1 Peptide, can reduce the lung injury induced by reperfusion via the inhibition of inflammation. The present study aims to evaluate the effect and mechanism of Ac2-26 in ARDS. Methods: Thirty-two rats were anaesthetized and randomized into four groups: sham (S), ARDS (A), ARDS/Ac2-26 (AA), and ARDS/Ac2-26/BOC-2 (AAB) groups. Rats in the S group received saline for intratracheal instillation, while rats in the other three groups received endotoxin for intratracheal instillation, in order to prepare the ARDS and inject the saline, Ac2-26, and Ac2-26 combined with BOC-2. After 24 h, the PaO 2 /FiO 2 ratio was calculated. The lung tissue wet-to-dry weight ratio and the protein level in bronchoalveolar lavage fluid (BALF) were tested. Then, the cytokines in BALF and serum, and the inflammatory cells in BALF were investigated. Afterwards, the oxidative stress response and histological injury was evaluated. Subsequently, the epithelium was cultured and analyzed to estimate the effect of Ac2-26 on apoptosis. Results: Compared to the S group, all indexes worsened in the A, AA, and AAB groups. Furthermore, compared to the S group, Ac2-26 significantly improved the lung injury and alveolar-capillary permeability, and inhibited the oxidative stress response. In addition, Ac2-26 reduced the local and systemic inflammation through the regulation of pro-and anti-inflammatory cytokines, and the decrease in inflammatory cells in BALF. Moreover, Ac2-26 inhibited the epithelium apoptosis induced by LPS through the modulation of apoptosis-regulated proteins. The protective effect of Ac2-26 on ARDS was partially reversed by the FPR inhibitor, BOC-2. Conclusion: Ac2-26 reduced the lung injury induced by LPS, promoted alveolar-capillary permeability, ameliorated the local and systemic inflammation, and inhibited the oxidative stress response and apoptosis. The protection of Ac2-26 on ARDS was mainly dependent on the FPR pathway.