Ying Zhao

Objectives: To examine the impacts of two consecutive rounds of the National Volume-Based Procurement (NVBP) programme for insulin on medication utilisation and structure in Hubei province, China. Design: Insulin procurement records were extracted from the Hubei Provincial Drug Procurement Trading Platform from May 2020 to December 2025. Descriptive statistics and interrupted time series analysis with segmented regression were employed. Setting: All medical institutions on the Hubei Provincial Drug Procurement Trading Platform. Primary outcome measures: Defined daily doses (DDDs), defined daily dose cost (DDDc) and procurement amount. Results: After two consecutive rounds of NVBP for insulin, average monthly DDDs increased by 2.33 million and 1.80 million DDD (first and second NVBP, respectively), with growth rates of 65.47% and 30.51% (both p0.05) and a significant increase after the second (trend: 78 280 DDD per month, p<0.01). DDDc declined immediately at both intervention points (¥−4.818 and ¥−0.174, respectively; both p<0.01), with no further monthly trend thereafter. Further subgroup analysis revealed that the growth rate of consumption for insulin analogues was faster than human insulin; the growth rate of consumption for domestic enterprises was faster than imported enterprises. Tertiary, secondary and primary medical institutions all achieved significant increases in procurement volume over two consecutive procurement periods. Conclusions: This study suggests that two consecutive rounds of the NVBP for insulin have achieved sustained price reductions accompanied by steady growth in overall procurement volume. The policy has significantly improved insulin medication utilisation patterns, sustained optimisation of the market structure and balanced development of the pharmaceutical supply.

Objectives: Seasonal influenza leads to substantial global morbidity and mortality, especially in adults aged 65 years and older, who present poor immune responses to standard-dose influenza vaccines. This study aimed to systematically evaluate the preclinical safety and immunogenicity of a high-dose quadrivalent seasonal influenza split vaccine (HD-QIV), providing preclinical evidence for its clinical application in the elderly. Methods: Following GLP guidelines, we performed single-dose and repeated-dose toxicity tests in Sprague–Dawley rats, active systemic anaphylaxis assays in guinea pigs, and immunogenicity assessments in young and aged BALB/c mice. Safety indicators included general clinical signs, hematology, blood biochemistry, histopathology and allergic reactions; immunogenicity was evaluated via hemagglutination inhibition (HI) antibody titers and antigen-specific cellular immune responses. Results: HD-QIV only caused mild and reversible local irritation in rats without obvious systemic toxicity, and no dose-related systemic anaphylaxis was observed in guinea pigs. HD-QIV induced robust and dose-dependent humoral immune responses, and showed significantly higher HI antibody titers, earlier seroconversion and longer antibody persistence than standard quadrivalent influenza vaccine in aged mice. Cellular immunity was slightly enhanced but not the dominant protective response. Conclusions: The HD-QIV demonstrates favorable preclinical safety and superior immunogenicity, supporting its further clinical development and use as a priority vaccine for the elderly population.

Background: Hydrogen sulfide (H₂S) acts as a neuromodulator in the brain and is shown to be associated with cognitive impairments in schizophrenia. Atypical antipsychotics can provide cognitive benefits for schizophrenia patients. This prospective observational study aims to investigate whether H ₂ S signaling is involved in the cognitive improvement effects of atypical antipsychotics in patients with schizophrenia. Methods: A total of 25 schizophrenia patients with acute exacerbation who completed follow-up and 28 healthy controls were included in this study. Psychopathological symptoms and cognitive function were assessed using the Positive and Negative Syndrome Scale (PANSS) and a neuropsychological test battery, respectively. Plasma H ₂ S levels were determined using high-performance liquid chromatography (HPLC). Results: We found that compared with normal controls, schizophrenia patients exhibited poorer cognitive function and lower plasma H ₂ S levels at baseline ( p < 0.05). After two months of atypical antipsychotic treatment, the patients showed significant improvements in processing speed, working memory, visuospatial memory, attention, and executive function (all p < 0.01). At the same time, plasma H ₂ S levels in patients after treatment were significantly elevated compared to baseline (0.918 ± 0.036 vs. 0.712 ± 0.023 µmol/L; t = 6.807, p < 0.001). Correlation analysis revealed that the increase in H ₂ S was significantly associated with improvements in working memory (r = 0.291, p = 0.005) and visuospatial memory (r = 0.227, p = 0.016). Conclusion: Our findings demonstrated that cognitive improvement in patients with schizophrenia after treatment with atypical antipsychotics is correlated with an increase of plasma H₂S levels, suggesting that H ₂ S signaling is involved in the pathophysiological process of cognitive impairment in schizophrenia.

Hematological and neurological expressed 1 (HN1) is upregulated in many tumors, but the role of HN1 in breast cancer progression and its regulatory mechanism have not been well understood. To study the role of HN1 in the initiation and progression of breast cancer, we examined HN1 levels in breast cancer cells and tissues and analyzed the relationship between HN1 levels and patient survival. We used mammosphere formation assay, side population analysis, wound healing assay, transwell assay, soft agar formation assay, and xenografted tumor model to determine the effect of HN1 on the expansion of breast cancer stem cells, and the migration, invasion and tumorigenesis of breast cancer. To determine whether HN1 regulates MYC, we used quantitative real-time PCR and Western blot analysis to assess the expression of MYC and their targeted genes to determine the phenotype caused by knockdown of MYC in breast cancer cell with HN1 overexpression. In this study, we found that HN1 was upregulated in breast cancer tissues. Patients with high levels of HN1 expression had significantly shorter survival than those with low HN1 expression. In breast cancer cell line, ectopic overexpression of HN1 not only promoted the expansion of breast cancer stem cells, but also promoted cell migration, invasion, and tumorigenesis, while knockdown of HN1 reduced these effects. Furthermore, there was a positive correlation between MYC (also known as c-MYC) level and HN1 level, mechanism analysis suggested HN1 promoted the expression of MYC and its targeted genes like CDK4, CCND1, p21, CAV1, and SFRP1. Downregulation of MYC abrogated the effect of HN1 overexpression in breast cancer cell lines. Taken together, these data reveal that HN1 promotes the progression of breast cancer by upregulating MYC expression, and might be a therapeutic target for breast cancer.