Objective: To systematically evaluate the willingness to receive influenza vaccines among Chinese medical staff, so as to provide the evidence for developing the influenza vaccination strategy and improving the coverage of influenza vaccination among medical staff. Methods: Publications pertaining to the willingness to receive influenza vaccines among Chinese medical staff were retrieved from international and national databases from January 1, 2010 to October 1, 2023, including CNKI, Wanfang Data, VIP, SinoMed, PubMed, Web of Science and Embase. A meta-analysis was performed using the software Stata 17.0, sensitivity analysis was performed using the leave-one-out method, and the publication bias was evaluated using Funnel plot. Results: Totally 674 publications were retrieved, and 17 case-control studies were finally enrolled, with 23 697 participants. Meta-analysis showed that the rate of willingness to receive influenza vaccines among medical staff in China was 52.8% (95%CI: 41.3%-64.4%). The rates of willingness to receive influenza vaccines were 40.2% (95%CI: 28.5%-51.8%) in 2019 and before and 67.2% (95%CI: 56.5%-77.9%) in 2020 and beyond; 54.6% (95%CI: 44.2%-65.0%) in men and 56.8% (95%CI: 49.3%-64.4%) in women; 53.6% (95%CI: 40.9%-66.2%) in doctors, 53.9% (95%CI: 41.0%-66.8%) in nurses, 62.8% (95%CI: 46.2%-79.3%) in technicians and 53.1% (95%CI: 36.1%-70.0%) in administrative and logistical staff; 77.4% (95%CI: 63.7%-91.2%) and 43.3% (95%CI: 30.5%-56.1%) in staff with and without a history of influenza vaccination; 49.8% (95%CI: 27.3%-72.3%) and 58.3% (95%CI: 43.9%-72.6%) in studies with a sample size of <1 000 and ≥1 000, and these differences were statistically significant (all P<0.05). Sensitivity analysis showed robustness of results, and Funnel plot showed publication bias. Conclusion The rates of willingness to receive influenza vaccines among medical staff in China ranged from 41.3% to 64.4%, and were lower in studies in 2019 and before, in men, in administrative and logistical staff and in staff without a history of influenza vaccination.

Objective To explore the expressions of Toll-like receptors (TLRs) 2 and 4 in mouse skin during early immune responses against Sporothrix.Methods A total of 60 BALB/c mice were randomly and equally divided into an experimental group and a control group to be intracutaneously injected with Sporothrix conidium suspensions at a concentration of 1 × 106 cfu/ml and sodium chloride physiological solution respectively.Five mice were sacrificed before the injection,and at 6,12,24,48,and 96 hours after the injection in each group,blood samples were obtained from the mice before sacrifice,and skin tissue specimens were resected from the area around the injection sites after sacrifice.Realtime fluorescence-based quantitative PCR was performed to quantify the mRNA expressions of TLR2 and TLR4,and immunohistochemical staining to observe the protein expressions of TLR2 and TLR4 in mouse skin specimens.Enzymelinked immunosorbent assay (ELISA) was conducted to determine the levels of interleukin 12 (IL-12) and tumor necrosis factor α (TNFα) in serum samples from the mice.Results After injection of Sporothrix conidium suspensions,the mRNA expression level of TLR2 gradually increased and peaked at 24 hours,which was 18.8 times that in the control group at 6 hours and 34 times at 24 hours.In addition,the mRNA expression level of TLR4 in the experiment group reached a peak,and was 56.7 times that in the control group at 6 hours after injection,then gradually decreased and reached the nadir at 96 hours.As immunohistochemical staining revealed,TLR2 and TLR4 were apparently expressed in both keratinocytes and macrophages in skin specimens from the experimental group,but not obviously in those from the control group.No significant differences were observed between the experimental group and control group in serum levels of IL-12 or TNF-α at any of the sampling time points.Conclusion TLR2 and TLR4 may play a favoring role in immunological defense by participating in the recognition of Sporothrix by keratinocytes and macrophages in mouse skin.

Alzheimer's disease (AD) is a leading cause of dementia in the elderly. Mitogen-activated protein kinase phosphatase 1 (MKP-1) plays a neuroprotective role in AD. However, the molecular mechanisms underlying the effects of MKP-1 on AD have not been extensively studied. MicroRNAs (miRNAs) regulate gene expression at the post-transcriptional level, thereby repressing mRNA translation. Here, we reported that the microRNA-429-3p (miR-429-3p) was significantly increased in the brain of APP23/PS45 AD model mice and N2A^APP AD model cells. We further found that miR-429-3p could downregulate MKP-1 expression by directly binding to its 3'-untranslated region (3' UTR). Inhibition of miR-429-3p by its antagomir (A-miR-429) restored the expression of MKP-1 to a control level and consequently reduced the amyloidogenic processing of APP and Aβ accumulation. More importantly, intranasal administration of A-miR-429 successfully ameliorated the deficits of hippocampal CA1 long-term potentiation and spatial learning and memory in AD model mice by suppressing extracellular signal-regulated kinase (ERK1/2)-mediated GluA1 hyperphosphorylation at Ser831 site, thereby increasing the surface expression of GluA1-containing α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs). Together, these results demonstrate that inhibiting miR-429-3p to upregulate MKP-1 effectively improves cognitive and synaptic functions in AD model mice, suggesting that miR-429/MKP-1 pathway may be a novel therapeutic target for AD treatment.