Search

To investigate the heat transfer coefficient (HTC) of a newly developed rare-earth wrought magnesium alloy under different cooling rates, the experiment of solution treatment followed by water quenching or air cooling process was carried out for calculation by lumped capacitance method (LCM) and optimized by inverse heat transfer method (IHTM), and cooling temperature curves were simulated afterward. In water quenching, the larger the temperature difference between the sample and water, the larger the maximum HTC, and the earlier it reached the maximum value, and in air cooling the HTC became larger with the airflow speeds increased. In LCM, the peak values of the HTC were 2840 W/(m2·°C) in water quenching and 54 W/(m2·°C) in air cooling. The corresponding HTC was 2388 W/(m2·°C) in IHTM. The maximum absolute average relative error (AARE) of temperature simulation in water quenching decreased from 8.46% in LCM to 2.45% in IHTM. The residual stress(RS) of a large conical component was simulated using both non-optimized and optimized HTC, the RS in the IHTM was ~30 MPa smaller than that in the ILCM, because the corresponding HTC was smaller, and the comparison of the simulation results with the measurements revealed that the RS using HTC in the IHTM is more accurate. [ABSTRACT FROM AUTHOR]

Resistance to radiotherapy and to EGFR tyrosine kinase inhibitors (EGFR‐TKIs), as well as therapy‐related lung toxicity, are serious problems in the treatment of lung cancer. NF‐κB has been reported to be associated with radioresistance. Therefore, we evaluated its effects on sensitivity to irradiation and to EGFR‐TKIs; irradiation‐induced lung toxicity; and the effects of irradiation on sensitivity to EGFR‐TKIs. We used IKKβ inhibitor IMD 0354 or p65 depletion to explore their effects on sensitivity to irradiation and to EGFR‐TKIs in vitro and in vivo. We evaluated the efficacy of IMD 0354 in a radiation‐induced pulmonary‐fibrosis mouse model. Irradiation enhanced activation and expression of MET and therefore suppressed the sensitivity of lung cancer cells to irradiation or EGFR‐TKIs. Inhibition of NF‐κB by IMD 0354 or by p65 depletion reversed irradiation‐induced MET activation and increased the sensitivity of lung cancer cells to irradiation, to EGFR‐TKIs and to the combination thereof in vitro and in vivo. In addition, IMD 0354 significantly reduced lung toxicity in a murine model of irradiation‐induced pneumonia and lung fibrosis. These findings indicated that NF‐κB inhibition can improve sensitivity to irradiation and to EGFR‐TKIs and can decrease irradiation‐inducedlung toxicity in lung cancer. What's new? The efficacy of lung cancer treatment is limited by various factors, including resistance to radiotherapy and epidermal growth factor receptor‐tyrosine kinase inhibitors (EGFR‐TKIs). The mechanisms underlying therapeutic resistance, however, remain unclear. In this study, investigation of the effects on treatment sensitivity of NF‐κB, a factor previously associated with radioresistance in cancer cells, shows that irradiation reduces lung cancer cell susceptibility to EGFR‐TKIs. This effect was overcome by NF‐κB inhibition, which increased radiosensitivity via effects on MET signaling. The findings indicate that irradiation‐induced NF‐κB activation and subsequent MET upregulation serve a critical role in therapeutic resistance in lung cancer. [ABSTRACT FROM AUTHOR]

Breast cancer is a highly heterogeneous disease at the molecular level and >90% of mortalities are due to metastasis and its associated complications. The present study determined the impact of molecular subtypes on metastatic behavior and overall survival (OS) of patients with metastatic breast cancer. The influence of molecular subtypes on the sites and number of metastases in 166 patients with metastatic breast cancer from a single center were assessed; and the influence of molecular subtypes on the sites and number of metastases and OS in 15,322 metastatic cases among 329,770 patients with primary breast cancer from the Surveillance, Epidemiology and End Results database were assessed. Analysis of both datasets revealed that different molecular subtypes exhibited differences in the prevalence of different metastatic sites and number of metastases. A larger proportion of bone metastasis was observed in the hormone receptor (HR)+/human epidermal growth factor receptor 2 (HER2)+ subtype than in other subtypes, more lung metastasis was observed in the HR-/HER2+ subtype and more liver metastasis occurred in the HR+/HER2+ and HR-/HER2+ subtypes. Single-site metastasis was more common for the HR+/HER2− subtype than in other subtypes, while 2–3 sites of metastases were more common for the HR+/HER2+ subtype and ≥4 sites of metastases were more frequent in the HR-/HER2+ and HR-/HER2- subtypes. The mean OS of patients with primary breast cancer in the HR+/HER2− subtype group was the longest (78.5 months), while the HR-/HER2- group had the shortest mean OS (69.1 months). The mean OS of the metastatic HR+/HER2+ group was the longest (46.0 months), while the mean OS of the metastatic HR-/HER2- group was the shortest (18.5 months). In conclusion, the results of the present study suggested that different molecular subtypes of breast cancer have different metastatic behavior, as well as mean OS. [ABSTRACT FROM AUTHOR]