Background Lymphovascular invasion (LVI) status facilitates the selection of optimal therapeutic strategy for breast cancer patients, but in clinical practice LVI status is determined in pathological specimens after resection. Purpose To explore the use of dynamic contrast‐enhanced (DCE)‐magnetic resonance imaging (MRI)‐based radiomics for preoperative prediction of LVI in invasive breast cancer. Study Type Prospective. Population Ninety training cohort patients (22 LVI‐positive and 68 LVI‐negative) and 59 validation cohort patients (22 LVI‐positive and 37 LVI‐negative) were enrolled. Field Strength/Sequence 1.5 T and 3.0 T, T1‐weighted DCE‐MRI. Assessment Axillary lymph node (ALN) status for each patient was evaluated based on MR images (defined as MRI ALN status), and DCE semiquantitative parameters of lesions were calculated. Radiomic features were extracted from the first postcontrast DCE‐MRI. A radiomics signature was constructed in the training cohort with 10‐fold cross‐validation. The independent risk factors for LVI were identified and prediction models for LVI were developed. Their prediction performances and clinical usefulness were evaluated in the validation cohort. Statistical Tests Mann–Whitney U‐test, chi‐square test, kappa statistics, least absolute shrinkage and selection operator (LASSO) regression, logistic regression, receiver operating characteristic (ROC) analysis, DeLong test, and decision curve analysis (DCA). Results Two radiomic features were selected to construct the radiomics signature. MRI ALN status (odds ratio, 10.452; P < 0.001) and the radiomics signature (odds ratio, 2.895; P = 0.031) were identified as independent risk factors for LVI. The value of the area under the curve (AUC) for a model combining both (0.763) was higher than that for MRI ALN status alone (0.665; P = 0.029) and similar to that for the radiomics signature (0.752; P = 0.857). DCA showed that the combined model added more net benefit than either feature alone. Data Conclusion The DCE‐MRI‐based radiomics signature in combination with MRI ALN status was effective in predicting the LVI status of patients with invasive breast cancer before surgery. Level of Evidence: 1 Technical Efficacy Stage: 2 J. Magn. Reson. Imaging 2019;50:847–857.

The research tries to establish Wistar rat's model of atherosclerosis for evaluating the antiatherosclerotic effect of hederagenin and exploring its antiatherosclerosis-related mechanisms. The statistical data have shown that hederagenin exhibits multiple pharmacological activities in the treatment of hyperlipidemia, antiplatelet aggregation, liver protection, and anti-inflammation, indicating that hederagenin may exert a protective effect on vascular walls by improving lipid metabolism disorders and lipid deposition. The results show that hederagenin can correct the imbalance of endothelial function by inhibiting the release of large amounts of iNOS and increasing eNOS contents and inhibits the IKKβ/NF-κB signaling pathway to reduce the release of IL-6, IFN-γ, TNF-α, and other inflammatory factors. The experimental results indicated that hederagenin can inhibit or ameliorate the pathological changes associated with AS, displaying an excellent preventive function against AS.

ObjectiveThe objective was to further investigate apoptosis induction by Babao Dan (BBD), which supports its anti-tumor mechanisms, using two human gastric cancer cell lines (AGS and MGC80-3).MethodsAfter treatment with various BBD concentrations, cell viability and cytotoxic effects were investigated using methyl thiazolyl tetrazolium (MTT) and lactate dehydrogenase (LDH) assays, respectively. The following indicators of cell apoptosis were evaluated: Annexin V-APC staining, caspase-3/-8/-9 activation, and mitochondrial membrane potential loss. Apoptosis-related protein levels (including Bcl-2-associated X protein [Bax], B-cell CLL/lymphoma 2 [Bcl-2], factor associated suicide [Fas], and Fas ligand [FasL]) were determined by western blot. The following multi-pathway factors were also assessed: p-ERK1/2, p-JNK, p-p38, and p-NF-κB.ResultsThe MTT and LDH assays both demonstrated increased BBD cytotoxicity. BBD induced cell apoptosis by stimulating caspase-3/-8/-9 activity and destroying the mitochondrial membrane potential. BBD also regulated key factor expression levels including Bcl-2, Bax, Fas, and FasL and down-regulated protein phosphorylation via the MAPK and NF-κB pathway.ConclusionsThe possible anti-tumor mechanism is that BBD induces apoptosis via the MAPK and NF-κB signaling pathways.

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These results indicate that TBD and SBO are safe and effective procedures for treating patients with intractable pneumothorax.