Objectives: This study aims to identify prognostic factors associated with metastatic recurrence-free survival of cervical carcinoma (CC) patients treated with radical radiotherapy and assess the cure probability of radical radiotherapy from metastatic recurrence. Methods: Data were from 446 cervical carcinoma patients with radical radiotherapy for an average follow up of 3.96 years. We applied a mixture cure model to investigate the association between metastatic recurrence and prognostic factors and the association between noncure probability and factors, respectively. A nonparametric test of cure probability under the framework of a mixture cure model was used to examine the significance of cure probability of the definitive radiotherapy treatment. Propensity-score-matched (PSM) pairs were generated to reduce bias in subgroup analysis. Results: Patients in advanced stages (p = 0.005) and those with worse treatment responses in the 3rd month (p = 0.004) had higher metastatic recurrence rates. Nonparametric tests of the cure probability showed that 3-year cure probability from metastatic recurrence was significantly larger than 0, and 5-year cure probability was significantly larger than 0.7 but no larger than 0.8. The empirical cure probability by mixture cure model was 79.2% (95% CI: 78.6–79.9%) for the entire study population, and the overall median metastatic recurrence time for uncured patients (patients susceptible to metastatic recurrence) was 1.60 (95% CI: 1.51–1.69) years. Locally advanced/advanced stage was a risk factor but non-significant against the cure probability (OR = 1.078, p = 0.088). The interaction of age and activity of radioactive source were statistically significant in the incidence model (OR = 0.839, p = 0.025). In subgroup analysis, compared with high activity of radioactive source (HARS), low activity of radioactive source (LARS) significantly contributed to a 16.1% higher cure probability for patients greater than 53 years old, while cure probability was 12.2% lower for the younger patients. Conclusions: There was statistically significant evidence in the data showing the existence of a large amount of patients cured by the definitive radiotherapy treatment. HARS is a protective factor against metastatic recurrence for uncured patients, and young patients tend to benefit more than the elderly from the HARS treatment.
BackgroundTitanium dioxide (TiO2) with nanofractions is increasingly applied in food products as a food additive, which makes consumers under the health risks of titanium dioxide nanoparticles (TiO2-NPs) oral exposure. The recent ban of food additive TiO2 (E171) use in France aggravated public controversy on safety of orally ingesting TiO2-NPs. This work aimed to determine biological effects of TiO2-NPs (38.3 ± 9.3) oral consumption (100 mg/kg bw, 10 days) on TNBS-induced colitis mice and healthy mice, and the additional vitamin E administration was also conducted to explore the possible mechanism of TiO2-NPs on colitis development.ResultsOral consumption of TiO2-NPs exacerbated oxidative stress status in colitis mice by decreasing the colonic glutathione (GSH) and total glutathione (T-GSH) levels, however, TiO2-NPs administration repaired the dysbacteriosis of colitis mice, and downregulated the Toll-like receptors (TLRs), nuclear factor kappa-B (NF-κB) signal pathway and inflammatory factor (IL-1β and TNF-α) transcription levels in colon tissue, which finally decreased the TNF-α expression level and participated in the mitigation of colitis symptoms. Moreover, further vitamin E intervention after TiO2-NPs consumption could relieve the oxidative stress status (mainly by scavenging reactive oxygen species, ROS) and the inflammatory factor over-transcription in colonic epithelium of colitis mice, but the effect of TiO2-NPs on dysbacteriosis repair would not be further changed by Vitamin E. At last, TiO2-NPs induced oxidative stress status and increased NF-κB signal transcription level in colonic epithelium, which increased daily disease activity index (DAI) score and caused mild mucosal inflammatory cell infiltrate in healthy mice. ConclusionOur present work showed that oral TiO2-NPs administration indeed induced oxidative stress and made an adverse effect on the development of colitis, but TiO2-NPs could also downregulate the NF-κB signal transduction level by repairing gut dysbacteriosis, which made a predominant role in alleviating colitis. On the other hand, it should also be noticed that TiO2-NPs oral ingestion caused potential colonic inflammation risks in healthy mice.
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