Preoperative Prediction of Perineural Invasion and Prognosis in Gastric Cancer Based on Machine Learning through a Radiomics-Clinicopathological Nomogram.

PURPOSE: The aim of this study was to construct and validate a nomogram for preoperatively predicting perineural invasion (PNI) in gastric cancer based on machine learning, and to investigate the impact of PNI on the overall survival (OS) of gastric cancer patients. METHODS: Data were collected from 162 gastric patients and analyzed retrospectively, and radiomics features were extracted from contrast-enhanced computed tomography (CECT) scans. A group of 42 patients from the Cancer Imaging Archive (TCIA) were selected as the validation set. Univariable and multivariable analyses were used to analyze the risk factors for PNI. The t-test, Max-Relevance and Min-Redundancy (mRMR) and the least absolute shrinkage and selection operator (LASSO) were used to select radiomics features. Radscores were calculated and logistic regression was applied to construct predictive models. A nomogram was developed by combining clinicopathological risk factors and the radscore. The area under the curve (AUC) values of receiver operating characteristic (ROC) curves, calibration curves and clinical decision curves were employed to evaluate the performance of the models. Kaplan-Meier analysis was used to study the impact of PNI on OS. RESULTS: The univariable and multivariable analyses showed that the T stage, N stage and radscore were independent risk factors for PNI (p < 0.05). A nomogram based on the T stage, N stage and radscore was developed. The AUC of the combined model yielded 0.851 in the training set, 0.842 in the testing set and 0.813 in the validation set. The Kaplan-Meier analysis showed a statistically significant difference in OS between the PNI group and the non-PNI group (p < 0.05). CONCLUSIONS: A machine learning-based radiomics-clinicopathological model could effectively predict PNI in gastric cancer preoperatively through a non-invasive approach, and gastric cancer patients with PNI had relatively poor prognoses.

Mechanisms and targeted reversion/prevention of hepatic fibrosis caused by the non-hereditary toxicity of benzo(a)pyrene.

The effect of long term exposure to low concentrations of environmental pollutants on hepatic disorders is a major public health concern worldwide. Polycyclic aromatic hydrocarbons (PAHs) are a class of persistent organic pollutants. In recent years, an increasing number of studies have focused on the deleterious effects of low concentrations of PAHs in the initiation or exacerbation of the progression of chronic liver disease. However, the underlying molecular mechanisms and effective intervention methods remain unclear. Here, we found that in hepatocytes, a low concentration of benzo(a)pyrene (B[a]P, an indicator of PAHs) chronic exposure continuously activated 14-3-3η via an epigenetic accumulation of DNA demethylation. As a "switch like" factor, 14-3-3η activated its downstream PI3K/Akt signal, which in turn promoted vascular endothelial growth factor (VEGF) production and secretion. As the characteristic fibrogenic paracrine factor regulated by B[a]P/14-3-3η, VEGF significantly induced the neovascularization and activation of hepatic stellate cells, leading to the development of hepatic fibrosis. Importantly, targeted 14-3-3η by using its specific inhibitor invented by our lab could prevent B[a]P-induced hepatic fibrosis, and could even reverse existent hepatic fibrosis caused by B[a]P. The present study not only revealed novel mechanisms, but also proposed an innovative approach for the targeted reversion/prevention of the harmful effects of exposure to PAHs on chronic liver disease.

[Comparison of efficacy and safety between two kinds of injection therapy in the treatment of I-II degree rectal prolapse].

OBJECTIVE: To explore the safety and efficacy of Shaobei injection in the management of I(-II( degree rectal prolapse. METHODS: A total of 80 patients eligible for the inclusion criteria were divided into 2 groups: 40 patients in the treatment group (treated with Shaobei injection) and 40 cases in the control group (treated with Xiaozhiling) respectively. The short-term efficacy was identified by the length of rectal prolapse and the depth of rectocele demonstrated by the defecography while the long-term efficacy was evaluated by the length of rectal prolapse. In addition, the safety was assessed by the occurrence of postoperative complications. RESULTS: The variation of the lengths of rectal prolapse and the depth of rectocele demonstrated by the defecography at the sixth month follow up in the two groups did not reach significant difference (P>0.05). After 2 year follow up, 37 patients (92.5%) in the treatment group and 35 cases(87.5%) in the control group was cured. Therefore, there was no significant difference in the long term efficacy between the two groups (P>0.05). The adverse events in the therapy group(10%) was less than that in the control group (45%)(P<0.01). CONCLUSIONS: Shaobei injection in the management of I(-II( degree rectal prolapse has a similar efficacy of short-term and long-term higher safety compared to Xiaozhiling injection.

The influence of insulin on secretion of IGF-I and IGFBP-I in cultures of human endometrial stromal cells.

OBJECTIVES: To study the influence of insulin on IGF-I and IGFBP-I secretion of the human endometrial stromal cells. METHODS: Late proliferative phase endometrial stromal cells were isolated from endometrium tissues and then cultured for 24 h in Hams F-12 only as a control and in Hams F-12 with different concentrations of estradiol (E2) and insulin (INS) as treated groups. Simultaneously, the endometrial stromal cells from late secretory phase endometrium were cultured for 24 h in Hams F-12 only as a control and in Hams F-12 supplemented with different concentrations of progesterone (P) and insulin as treated groups. After 24 h of culturing, the mediums were collected for either IGF-I or IGFBP-I assays. RESULT: The concentrations of IGF-I in medium from cultured endometrial stromal cells in the proliferative phase were 0.78 +/- 0.47 ng/ml in the hormone-free control group; 1.44 +/- 0.59 ng/ml and 1.39 +/- 0.33 ng/ml in 100 pg/ml E2 group and 20 microU/ml INS group, which was higher than that of the control group (P < 0.05 and P < 0.01, respectively). The IGF-I concentration in the 100 microU/ml INS group was 2.03 +/- 0.53 ng/ml, which was higher than that of the 20 micro U/ml INS group (P < 0.01). Levels of IGF-I in the 100 pg/ml E2 plus 20 microU/ml INS group was 2.18 +/- 0.36 ng/ml, which was significantly higher than that of the 20 microU/ml INS and 100 pg/ml E2 group (P < 0.01), but lower than that of the 100 pg/ml E2 plus 100 microU/ml INS group (3.42 +/- 0.75 ng/ml), P < 0.01. The concentration of IGFBP-I in medium from cultured endometrial stromal cells in the secretory phase was 2.50 +/- 1.39 ng/ml in the hormone-free control group and 5.44 +/- 2.09 ng/ml in the 10 pg/ml P group, which was significantly higher than that of the control (P < 0.01). IGFBP-I concentration in 20 microU/ml INS group was 0.16 +/- 0.58 ng/ml, which was lower compared with control, but higher compared with the 100 microU/ml INS group (P < 0.01). The level of IGFBP-I in the 10 ng/ml P plus 20 microU/ml INS group was 2.10 +/- 1.17 ng/ml, lower compared with the 10 ng/ml P group, but higher compared with the 10 pg/ml P plus 100 microU/ml INS group, P < 0.01. CONCLUSIONS: Insulin can stimulate basal (without hormone) and E2-stimulated IGF-I secretion in cultured stromal cells from human late proliferative endometrium in a dose-dependent manner. Insulin can suppress basal (without hormone) and P-stimulated IGFBP-I secretions in cultured stromal cells from human secretory endometrium in a dose-dependent manner.