Human papillomavirus (HPV) infection remains a critical public health challenge in China, particularly in Guangdong Province, where HPV-52, 16, and 58 genotypes predominate, and male infection rates exceed 40%. Despite the successful implementation of a government-funded school-based program that has achieved 88% HPV vaccine coverage among adolescent girls, several persistent barriers, including genotype mismatch (the free HPV vaccine covers < 50% of high-risk local strains), regional disparities (80% vs. 60% for first-dose coverage), and exclusion of males, thwart progress toward herd immunity. Financial sustainability risks pose an even more significant threat to the expansion of HPV vaccination programs, especially in Guangdong province where annual expenditures exceed CNY 200 million. This review delves into Guangdong’s pioneering efforts and proposes practical solutions: accelerating domestic multivalent HPV vaccine development, adopting gender-neutral vaccination policies, and leveraging mobile clinics for remote populations. These strategies not only provide a roadmap for China but also serve as valuable insight for other LMICs striving to overcome HPV-related inequalities.

Background: The present study aimed to evaluate the association between the cumulative dose of glucocorticoids (GCs) and case fatality in hospitalized patients who developed pneumonia while receiving glucocorticoid therapy.Methods: This retrospective cohort study included 625 patients receiving long-term GC treatment who were hospitalized with pneumonia (322 male and 303 female). Data were obtained from the Dryad Digital Repository and were used to perform secondary analysis. Multivariable Cox proportional hazard regression model and restricted cubic splines (RCS) were used to evaluate the association between the cumulative dose of GCs and case fatality. Sensitivity analyses and subgroup analyses were performed.Results: The 30-day and 90-day death rates were 22.9 and 26.2%, respectively. After adjusting for potential confounders, compared with those in the lowest quintile (≤ 1.5 g), the Cox proportional hazard regression model analysis showed that patients with different cumulative doses of GCs (1.5 to 2.95, 2.95 to 5, 5 to 11.5, and > 11.5 g) had lower risks for 30-day death, with respective hazard ratios of 0.86 (95% CI, 0.52 to 1.42), 0.81 (0.49 to 1.33), 0.29 (0.15 to 0.55), and 0.42 (0.22 to 0.79). The multivariable-adjusted RCS analysis suggested a statistically significant N-shaped association between the cumulative dose of GCs and 30-day death. A higher cumulative dose of GC tended to first lead to an increase in 30-day death within 1.8 g, then to a statistically significant decrease until around 8 g [HR for 1 g = 0.82 (0.69 to 0.97)], and again to an increase afterward. Similar results were found in the subgroup analyses and sensitivity analyses.Conclusion: N-shaped association between the cumulative dose of GCs and case fatality was observed in patients receiving long-term GC treatment who were hospitalized with pneumonia. Our findings may help physicians manage these patients.

Metabolic syndrome (MetS) is a cluster of risk factors for cardiovascular diseases and type 2 diabetes. Gut microbiota dysbiosis has been implicated in the pathogenesis of MetS, but the mechanisms remain poorly understood. This study investigates gut microbiota interaction networks in MetS and explores their potential role in host metabolic regulation. In this population-based cross-sectional study, 221 MetS patients and 382 healthy controls were analyzed. Co-abundance network analysis was used to examine microbial interactions across the study. Significant differences in microbial co-abundance patterns were observed between MetS and healthy participants. In MetS, the gut microbiota displayed fewer and generally weaker co-abundance correlations compared with healthy controls. These changes appear to be more strongly associated with the synergistic effects of microbial interactions than solely with the abundance of individual taxa investigated here. Specific microbiota combinations were found to influence key metabolic functions, contributing to MetS development. The findings suggest that microbial interactions, rather than the abundance of individual bacteria, are associated with MetS. This study provides new insights into the role of disrupted gut microbiota networks in MetS pathogenesis.