Fraud Detection Report: Early Hydrogen-Rich Water and Exercise Intervention Study on Cardiac β3-AR Expression Following Myocardial Infarction

Academic fraud report · Geng Detector

Summary

This report flags a confirmed serious integrity issue (verdict: 实锤 / substantiated) in Chen Ting et al. (2016), published in the Journal of Beijing Sport University (DOI: 10.19582/j.cnki.11-3785/g8.2016.09.010). The core problem is a fatal timeline conflict with established cardiac pathophysiology: the Methods state that all endpoints (hemodynamics, Masson trichrome staining, Western blot sampling) were collected 45 minutes after myocardial infarction (MI) surgery, yet the Results report a collagen volume fraction (CVF) of 59.64% ± 4.83% in the MI group versus 5.16% ± 1.09% in sham, with intervention groups at 19.92%, 19.58%, and 34.14%. Fibrotic scarring visualized by Masson trichrome is biologically impossible at 45 minutes post-MI; it requires days to weeks of remodeling. The paper also mixes acute-phase endpoints with chronic-phase molecular and histological claims (β3-AR, eNOS, anti-remodeling discussion), strongly suggesting data stitching across mismatched time points. Image-level analysis was not possible because original figures were unavailable. Confidence is high regarding the timeline/fibrosis inconsistency; overall scope of misconduct (fabrication vs. assembly error) cannot be determined without raw data.

Verdict

🔴 Substantiated (实锤) — The paper contains a decisive internal contradiction between its reported sampling timeline and its histopathological findings that violates established cardiac pathophysiology, and shows signs of data assembled across mismatched experimental time points.

Key findings

Biologically impossible fibrosis at 45 minutes post-MI: Methods specify that hearts were harvested 45 minutes after MI surgery for Masson trichrome staining. Results report an MI-group collagen volume fraction (CVF) of 59.64% ± 4.83% versus sham 5.16% ± 1.09%. Collagen-rich scar tissue detectable by Masson trichrome requires days to weeks of post-MI remodeling; a 45-minute time point cannot produce this signal.
Implausibly effective acute interventions: Intervention groups show CVF of 19.92% (EM), 19.58% (HM), and 34.14% (HEM) — reportedly reduced from a value that cannot exist at the stated sampling time.
Acute/chronic experimental mismatch: Hemodynamic measurement and tissue harvest are described as acute (45 min), while Western blot endpoints (β3-AR, eNOS) and the Discussion (Section 3.1) invoke chronic post-MI ventricular remodeling mechanisms. This indicates probable stitching of data from a chronic MI model (e.g., 4 or 8 weeks) into an acute-protocol manuscript frame.
Image analysis not performed: Figures 1–5 were not available in analyzable form; pixel-level and gel-level checks were deferred. The text-level contradictions alone are sufficient to question data authenticity.

Evidence highlights

Methods quote (Section 1.5–1.7): five groups of rats anesthetized 45 min post-MI, hemodynamic indices measured, hearts excised, portions fixed in neutral formalin for Masson staining.
Results quote (Section 2.2): MI-group CVF = 59.64% ± 4.83%; sham CVF = 5.16% ± 1.09%; EM = 19.92%; HM = 19.58%; HEM = 34.14%.
Cardiac collagen deposition sufficient to register as ~60% CVF on Masson staining is incompatible with a 45-minute post-ischemia sampling window.
DOI preserved as reported: 10.19582/j.cnki.11-3785/g8.2016.09.010.

Notes

Scope of misconduct (fabrication vs. assembly of data from different time points) cannot be conclusively determined without the authors' raw experimental records and original images.
The reported affiliations are Shaanxi Normal University and Xizang Minzu University; institutional investigation would be needed to confirm time-point provenance.
Confidence: high for the timeline–fibrosis inconsistency; moderate-to-low for any broader claim of deliberate falsification until raw data are examined.