Comparative study of radiomics, tumor morphology, and clinicopathological factors in predicting overall survival of patients with rectal cancer before surgery.

We compared the ability of a radiomics model, morphological imaging model, and clinicopathological risk model to predict 3-year overall survival (OS) in 206 patients with rectal cancer who underwent radical surgery and had magnetic resonance imaging, clinicopathological, and OS data available. The patients were randomized to a training cohort (n = 146) and a verification cohort (n = 60). Radiomics features were extracted from preoperative T2-weighted images, and a radiomics score model was constructed. Factors that were significant in the Cox multivariate analysis were used to construct the final morphological tumor model and clinicopathological model. A comprehensive model in the form of a line chart was established by combining the three models. Ten radiomics features significantly related to OS were selected to construct the radiomics feature model and calculate the radiomics score. In the morphological model, mesorectal extension depth and distance between the lower tumor margin and the anal margin were significant prognostic factors. N stage was the only significant clinicopathological factor. The comprehensive model combined with the above factors had the best prediction performance for OS. The C-index had a predictive performance of 0.872 (95% confidence interval [CI]: 0.832-0.912) in the training cohort and 0.944 (95% CI: 0.890-0.990) in the verification cohort, which was better than for any single model. The comprehensive model was divided into high-risk and low-risk groups. Kaplan-Meier curve analysis showed that all factors were significantly correlated with poor OS in the high-risk group. A comprehensive nomogram based on multi-model radiomics features can predict 3-year OS after rectal cancer surgery.

Fibroblast growth factor 21, assisted by elevated glucose, activates paraventricular nucleus NUCB2/Nesfatin-1 neurons to produce satiety under fed states.

Fibroblast growth factor 21 (FGF21), liver-derived hormone, exerts diverse metabolic effects, being considered for clinical application to treat obesity and diabetes. However, its anorexigenic effect is debatable and whether it involves the central mechanism remains unclarified. Moreover, the neuron mediating FGF21's anorexigenic effect and the systemic energy state supporting it are unclear. We explored the target neuron and fed/fasted state dependence of FGF21's anorexigenic action. Intracerebroventricular (ICV) injection of FGF21 markedly suppressed food intake in fed mice with elevated blood glucose. FGF21 induced c-Fos expression preferentially in hypothalamic paraventricular nucleus (PVN), and increased mRNA expression selectively for nucleobindin 2/nesfatin-1 (NUCB2/Nesf-1). FGF21 at elevated glucose increased [Ca2+]i in PVN NUCB2/Nesf-1 neurons. FGF21 failed to suppress food intake in PVN-preferential Sim1-Nucb2-KO mice. These findings reveal that FGF21, assisted by elevated glucose, activates PVN NUCB2/Nesf-1 neurons to suppress feeding under fed states, serving as the glycemia-monitoring messenger of liver-hypothalamic network for integrative regulation of energy and glucose metabolism.