To gain insight into willingness and its influencing factors to vaccinate against COVID-19 among health care workers (HCWs), and provide a scientific basis for more reasonable epidemic prevention and control strategies. A comprehensive literature search was conducted in four English databases (PubMed, EMBASE, Web of Science and the Cochrane Library) and four Chinese databases (Chinese National Knowledge Infrastructure (CNKI), the Chongqing VIP Chinese Science (VIP), Wanfang Database and China Biomedical Literature Database (CBM)) to collect the related studies. Quality evaluation was carried out for papers meeting the inclusion criteria using six items from the Downs and Black assessment checklist. The STATA statistical software version 15.1 was hired to perform meta-analysis. Nine records with a total of 24,952 subjects were included in this meta-analysis. The results of this meta-analysis revealed that the pooled effect value of COVID-19 vaccination willingness among HCWs using a random-effects model was 51% (95% confidence interval (CI) 0.41-0.62). Male, aged 30 years or older, having a history of prior influenza vaccination were facilitators for HCWs’ intention to vaccinate against COVID-19 (odds ratio (OR) 1.82, 95% CI 1.37-2.41, P=0.000, I2=59.4%; OR 1.32, 95% CI 1.16-1.51, P=0.000, I2=31.7%; OR 2.97, 95% CI 1.82-4.84, P=0.000, I2=88.1%). The impact of occupation on HCWs’ intention to get vaccinated could not yet be definitively confirmed (OR 0.85, 95% CI 0.69-1.06, P=0.160, I2=85.5%). COVID-19 vaccination acceptance of HCWs was at moderate level. Strengthening awareness of COVID-19 vaccine among HCWs, particularly female HCWs under 30 years who have no history of prior influenza vaccination, is crucial to eliminate concerns about vaccination and promote the application of COVID-19 vaccine in this population.

Idiopathic pulmonary fibrosis (IPF) is a prototype of chronic, progressive, and fibrotic lung disease with high morbidity and high mortality. Menstrual blood-derived stem cells (MenSCs) have proven to be an attractive tool for the treatment of acute lung injury and fibrosis-related diseases through immunosuppression and antifibrosis. However, whether MenSC-derived exosomes have the similar function on pulmonary fibrosis remains unclear. In the present study, exosomes secreted from MenSCs (MenSCs-Exo) were verified by transmission electron microscope (TEM), nanoparticle tracking analyzer (NTA), and western blotting. And MenSC-Exo addition significantly improved BLM-induced lung fibrosis and alveolar epithelial cell damage in mice, mainly reflected in BLM-mediated enhancement of the fibrosis score, blue collagen deposition, dry/wet gravity ratio, hydroxyproline and malondialdehyde levels, and downregulation of glutathione peroxidase, which were all robustly reversed by MenSC-Exo management. Additionally, BLM- and TGF-β1-evoked cellular reactive oxygen species (ROS), mitochondrial DNA (mtDNA) damage, and cell apoptosis were rescued by MenSCs-Exo in vivo and in vitro. Further study indicated that the MenSCs-Exo could transport miRNA Let-7 into recipient alveolar epithelial cells. Let-7 inhibitor administration significantly blocked the exosome-mediated improvement role on lung fibrosis in mice. Mechanistically, Let-7 was able to regulate the expression of lectin-like oxidized low-density lipoprotein receptor-1 (LOX1) through binding to its 3′-UTR region. Forced expression of LOX1 promoted the expression of apoptosis-related protein and mtDNA damage markers via regulating NLRP3 which was also confirmed in BLM model mice under the combination therapy of the exosome and Let-7 inhibitor. Collectively, this study demonstrates that exosomal Let-7 from MenSCs remits pulmonary fibrosis through regulating ROS, mtDNA damage, and NLRP3 inflammasome activation. This provides a new approach of exocytosis on the treatment of fibrotic lung disease.

Background. Podocyte migration is actively involved in the process of podocyte loss and proteinuria production, which is closely associated with the development of diabetic nephropathy (DN). Exosomes from adipose‐derived stem cells (ADSCs‐Exos) effectively inhibit podocyte apoptosis in the treatment of DN. However, how ADSCs‐Exos affect the migration of podocytes is obscure. This study is aimed at exploring the regulatory role of ADSCs‐Exos on cell migration and the underlying mechanism. Methods. ADSCs‐Exo was authenticated by transmission electron microscopy (TEM), western blotting, and flow cytometry. Cell viability and migration ability of podocytes were measured by CCK8 and Transwell assays, respectively. Relative expressions of miRNAs and mRNAs were determined by qRT‐PCR. The transmitting between PKH26‐labeled exosome and podocytes was evaluated by IF assay. Dual luciferase reporter assay was employed to detect the relationship between miR‐215‐5p and ZEB2. Results. The exposure to serum from DN patient (hDN‐serum) significantly inhibited cell viability of podocytes, but ADSCs‐Exo addition notably blunts cytotoxicity induced by the transient stimulus of hDN‐serum. Besides, ADSCs‐Exo administration powerfully impeded high glucose‐ (HG‐) induced migration and injury of podocyte. With the podocyte dysfunction, several miRNAs presented a significant decline under the treatment of HG including miR‐251‐5p, miR‐879‐5p, miR‐3066‐5p, and miR‐7a‐5p, all of which were rescued by the addition of ADSCs‐Exo. However, only miR‐251‐5p was a key determinant in the process of ADSCs‐Exo‐mediated protective role on podocyte damage. The miR‐251‐5p inhibitor counteracted the improvement from the ADSCs‐Exo preparation on HG‐induced proliferation inhibition and migration promotion. Additionally, miR‐215‐5p mimics alone remarkably reversed HG‐induced EMT process of podocyte. Mechanistically, we confirmed that ADSCs‐Exos mediated the shuttling of miR‐215‐5p to podocyte, thereby protecting against HG‐induced metastasis, possibly through inhibiting the transcription of ZEB2. Conclusion. ADSCs‐Exo has the protective effect on HG‐evoked EMT progression of podocytes thru a mechanism involving ZEB2. Potentially, the ADSCs‐Exo preparation is a useful therapeutic strategy for improving podocyte dysfunction and DN symptoms clinically.

Background: Immunoglobulin A nephropathy (IgAN), a globally common primary chronic glomerulopathy, is one of the leading causes of end-stage renal disease. However, the underlying mechanisms of IgAN have yet to be demonstrated. There were no adequate and reliable plasma biomarkers for clinical diagnosis, especially at the early stage. In the present study, integrative proteomics and metabolomics were aimed at exploring the mechanism of IgAN and identifying potential biomarkers. Methods: Plasma from IgAN and healthy individuals were collected and analyzed in a randomized controlled manner. Data-independent acquisition quantification proteomics and mass spectrometry based untargeted metabolomics techniques were used to profile the differentially expressed proteins (DEPs) and differentially abundant metabolites (DAMs) between two groups and identify potential biomarkers for IgAN from health at the early stage. Disease-related pathways were screened out by clustering and function enrichment analyses of DEPs and DAMs. And the potential biomarkers for IgAN were identified through the machine learning approach. Additionally, an independent cohort was used to validate the priority candidates by enzyme-linked immunosorbent assay (ELISA). Results: Proteomic and metabolomic analyses of IgAN plasma showed that the complement and the immune system were activated, while the energy and amino acid metabolism were disordered in the IgAN patients. PRKAR2A, IL6ST, SOS1, and palmitoleic acid have been identified as potential biomarkers. Based on the AUC value for the training and test sets, the classification performance was 0.994 and 0.977, respectively. The AUC of the external validation of the four biomarkers was 0.91. Conclusion: In this study, we combined proteomics and metabolomics techniques to analyze the plasma of IgAN patients and healthy individuals, constructing a biomarker panel, which could provide new insights and provide potential novel molecular diagnoses for IgAN.

Diabetic kidney disease (DKD) is the most common microvascular complication of diabetes, and there is an urgent need to discover reliable biomarkers for early diagnosis. Here, we established an effective urine multi-omics platform and integrated metabolomics and peptidomics to investigate the biological changes during DKD pathogenesis.

The comorbidity of diabetes mellitus (DM) significantly increases the risk of tuberculosis infection and adverse tuberculosis treatment outcomes. Most previous studies have focused on the relationship between the effect of blood glucose control and the outcome of antituberculosis treatment in pulmonary tuberculosis (PTB) with DM (PTB_DM); however, early prediction and the underlying molecular mechanism of susceptibility to PTB infection in patients with DM remain unclear.