Objective This study aims to establish a transnational evaluation framework for academic competitiveness in obstetrics and gynecology,precisely positioning West China Second Hospital(WCSH)globally,identifying development bottle-necks and proposing strategic improvements.Methods Based on Elsevier's SciVal platform,bibliometric data from 12 top global institutions(7 Chinese,5 international)during 2020-2024 were analyzed.A three-dimensional indicator system was construc-ted:research output(publication volume,Q1 publications),academic impact(citations,citations per paper,FWCI),and col-laboration(international collaboration rate).Entropy weight method was employed to assign objective weights to calculate com-posite competitiveness scores.Results WCSH led in total publications(n=541)but underperformed in Q1 publication rate(34.57％vs domestic average 43.01％)and FWCI(0.67＜global baseline 1.0).Its international collaboration rate(2.8％)lagged significantly behind global peers(e.g.,NUH Singapore:53.5％).Entropy weighting identified Q1 publications(31.8％)and FWCI(28.5％)as core drivers.WCSH ranked 9th among 12 global institutions(4th domestically).Conclusion WCSH exhibits"scale advantage with quality gaps and collaboration deficit".Strategic recommendations include quality-fo-cused incentive reform,enhanced international networks,and dynamic monitoring.The study provides a data-driven transnational evaluation paradigm for the disciplinary development of obstetrics and gynecology.

Objective This study aims to establish a transnational evaluation framework for academic competitiveness in obstetrics and gynecology,precisely positioning West China Second Hospital(WCSH)globally,identifying development bottle-necks and proposing strategic improvements.Methods Based on Elsevier's SciVal platform,bibliometric data from 12 top global institutions(7 Chinese,5 international)during 2020-2024 were analyzed.A three-dimensional indicator system was construc-ted:research output(publication volume,Q1 publications),academic impact(citations,citations per paper,FWCI),and col-laboration(international collaboration rate).Entropy weight method was employed to assign objective weights to calculate com-posite competitiveness scores.Results WCSH led in total publications(n=541)but underperformed in Q1 publication rate(34.57％vs domestic average 43.01％)and FWCI(0.67＜global baseline 1.0).Its international collaboration rate(2.8％)lagged significantly behind global peers(e.g.,NUH Singapore:53.5％).Entropy weighting identified Q1 publications(31.8％)and FWCI(28.5％)as core drivers.WCSH ranked 9th among 12 global institutions(4th domestically).Conclusion WCSH exhibits"scale advantage with quality gaps and collaboration deficit".Strategic recommendations include quality-fo-cused incentive reform,enhanced international networks,and dynamic monitoring.The study provides a data-driven transnational evaluation paradigm for the disciplinary development of obstetrics and gynecology.

Aim To explore whether the polypeptide vaccines CKL9 and YL20 can induce immune response and anti-tumor effect on HER-2 (+) tumors in vitro and in vivo, and to provide suggestions for clinical use.Methods The proliferation of specific lymphocytes and cytotoxic T lymphocyte activity(CTL) stimulated by CKL9 and YL20 were studied with CCK-8 assay and LDH assay, and the antitumor activity of CKL9 and YL20 was evaluated in vivo.Results The lymphocyte proliferation was promoted by incubation with CKL9 and YL20, and the relative increase of cells was 11.1% and 16.7% respectively at the concentration of 50 mg·L-1 of CKL9 and YL20.The LDH assay confirmed the CTL effect induced by CKL9 and YL20 on HER2-positive tumor cells, not on HER2-negtive tumor cells.With an effector-target ratio of 80 ∶1, the inhibition of tumor cell by cytotoxic T lymphocyte stimulated by CKL9 and YL20 could reach 89.8% and 84.3%, respectively.The HER2(+) tumor cell N87 transplanted in Babes mice was inhibited by pre-immune polypeptide CKL9 and YL20.Conclusion The HER2-specific polypeptide vaccines CKL9 and YL20 could induce persistent specific CD4 and CD8 T cell immune and inhibit the growth of HER2 positive tumor cells.