The gastrointestinal (GI) tract is not a common site of metastasis in primary lung cancer. The aim of the present study was to reveal the clinical and prognostic characteristics of gastrointestinal metastases of lung cancer (GMLC). Information on 366 cases of GMLC was collected and factors that affect severe GI complications were analyzed. Univariate and multivariate survival analyses were performed using the Cox proportional hazards model. Of the cases analyzed, the small intestine (59.6%) and colorectum (25.6%) were the two organs where lung cancer was most likely to metastasize in the GI tract. Squamous cell carcinoma (28.5%), adenocarcinoma (27.6%) and large cell carcinoma (20.9%) were the three most common histological types. However, compared with the histological distributions of primary lung cancer, patients with large cell carcinoma exhibited the highest elevated risk of GMLC [relative risk (RR), 4.07; P<0.001] and those with adenocarcinoma exhibited the lowest risk (RR, 0.58; P<0.001). Differences in organ involvement and in histological type led to varying GI complications. It was also indicated that chemotherapy was associated with a decreased risk of hemorrhage (P=0.006), but there was no reduction in the risk of hemorrhage associated with perforation and obstruction (P>0.05). The median overall survival time of GMLC patients was 2.8 months (range, 0–108 months). The survival analyses revealed that perforation and extra-GI metastasis were negative prognostic factors but abdominal surgery was identified a positive prognostic factor. In conclusion, the histological distribution of GMLC differed from that of primary lung cancer. Sufficient and careful patient evaluation, targeted surgeries and systemic therapies for specific patients are able to increase patient survival rate and improve the quality of life.

Deoxynivalenol (DON) is a toxic secondary metabolite produced by several Fusarium species that infest wheat and corn. Food and feed contaminated with DON pose a health risk to both humans and livestock and form a major barrier for international trade. Microbial detoxification represents an alternative approach to the physical and chemical detoxification methods of DON-contaminated grains. The present study details the characterization of a novel bacterium, Devosia mutans 17-2-E-8, that is capable of transforming DON to a non-toxic stereoisomer, 3-epi-deoxynivalenol under aerobic conditions, mild temperature (25–30°C), and neutral pH. The biotransformation takes place in the presence of rich sources of organic nitrogen and carbon without the need of DON to be the sole carbon source. The process is enzymatic in nature and endures a high detoxification capacity (3 μg DON/h/108 cells). The above conditions collectively suggest the possibility of utilizing the isolated bacterium as a feed treatment to address DON contamination under empirical field conditions.

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Curcumin, which is the effective component of turmeric (Curcuma longa), has previously been shown to exert potent antioxidant, antitumor and anti‑inflammatory activities in vitro and in vivo. However, the mechanism underlying the protective effects of curcumin against oxidative damage in endothelial cells remains unclear. The present study aimed to examine the effects of curcumin on hydrogen peroxide (H2O2)‑induced apoptosis and autophagy in EA.hy926 cells, and to determine the underlying molecular mechanism. Cultured EA.hy926 cells were treated with curcumin (5‑20 µmol/l) 4 h prior to and for 4 h during exposure to H2O2 (200 µmol/l). Oxidative stress resulted in a significant increase in the rate of cell apoptosis, which was accompanied by an increase in the expression levels of caspase‑3 and B‑cell lymphoma 2 (Bcl‑2)‑associated X protein (Bax), and a decrease in the expression levels of Bcl‑2. Treatment with curcumin (5 or 20 µmol/l) significantly inhibited apoptosis, and reversed the alterations in caspase‑3, Bcl‑2 and Bax expression. Furthermore, curcumin induced autophagy and microtubule‑associated protein 1A/1B‑light chain 3‑Ⅱ expression, and suppressed the phosphorylation of Akt and mammalian target of rapamycin (mTOR). These results indicated that curcumin may protect cells against oxidative stress‑induced damage through inhibiting apoptosis and inducing autophagy via the Akt/mTOR pathway.