Feasibility of annual dry anaerobic digestion temperature-controlled by solar energy in cold and arid areas.

In cold and arid areas, variations of ambient temperature not only lead to a large amount of heat loss from anaerobic digestion reactors but also greater challenges in the stable production of biogas. Common temperature-controlled methods of biogas production, such as coal combustion, electric heating, biogas combustion and so on, are expensive and high energy-consuming. Openly, solar energy is economical and suitable for stable biogas production. However, no pilot studies have yet shown the feasibility of controlling the temperature of annual biogas production with solar energy in cold and arid areas. This paper first theoretically analyzed the energy balance between evacuated tube solar collectors and anaerobic reactors. Then a biogas production system was developed in Lanzhou City, China, consisting mainly of a 3 m3 insulated anaerobic reactor and a solar collector with 30 sticks Φ58 × L1800mm evacuated tubes. Annual batch experiments have been carried out to test the feasibility of stable biogas production at a temperature-controlled by solar energy in cold and arid areas. The results show that dry anaerobic digestion with 20% total solid (TS) can start and operate smoothly even under the condition of low solar irradiation for 3-4 consecutive days. The system can run stability by anaerobic digestion at 26 ± 1 °C in winter and spring, by mesophilic (37 ± 1 °C) and thermophilic (52 ± 1 °C) anaerobic digestion in summer and autumn, which implies a highly efficient operation strategy for agricultural and animal husbandry wastes treatment. These theoretical and experimental results provide a scientific basis and engineering reference for the application of biogas production temperature-controlled by solar energy and have important value for the efficient and low-cost anaerobic digestion treatment of agricultural and animal husbandry wastes in cold and arid areas.

Dual-Aptamer-Targeted Immunomagnetic Nanoparticles to Accurately Explore the Correlations between Circulating Tumor Cells and Gastric Cancer.

It has been acknowledged that circulating tumor cells (CTCs) are promising biomarkers in liquid biopsy for cancer diagnosis and prognosis. However, the relationship between the CTC number and gastric cancer has scarcely been quantitatively investigated. Moreover, the single criterion of epithelial cell adhesion molecule (EpCAM) antibody/aptamer to specifically recognize epithelial CTCs cannot be universally applied for clinical applications, as it fails to recognize EpCAM-negative CTCs. Herein, we propose simple, low-cost, dual-aptamer (EpCAM and PTK7)-modified immunomagnetic Fe3O4 particles (IMNs) for efficient capture of heterogeneous CTCs and downstream analysis in gastric cancer patients. High PTK7 expression and a significant negative correlation between PTK7 and EpCAM expression were observed in primary gastric cancer tissues. Taking MGC-803 and BGC-823 cells as CTC models, the obtained dual-targeting IMNs could distinguishably recognize these cells with both high or low EpCAM and PTK7 expressions, which enhanced the accuracy of CTC recognition in gastric cancer. More than 95% of these two kinds of cells could be captured within 20 min of incubation, which was significantly more efficient than that of single EpCAM- or PTK7-modified IMNs. With this strategy, as low as five CTCs could be captured from phosphate-buffered saline (PBS), a cell mixture containing THP-1 cells, and lysed blood mediums. Moreover, the obtained CTCs can be used for subsequent gene analysis. Finally, the fabricated IMNs were successfully applied for CTC capture in 1.0 mL of peripheral blood samples from patients with gastric cancer. The detected CTC numbers in 72 participants were found to have close relationships with chemotherapy sensitivity, diagnosis, stage, and distant metastasis of patients. This work provides important references for further investigations on CTC-related diagnosis and individualized treatment.

Targeting the ILK/YAP axis by LFG-500 blocks epithelial-mesenchymal transition and metastasis.

Metastasis is the main cause of mortality in patients with cancer. Epithelial-mesenchymal transition (EMT), a crucial process in cancer metastasis, is an established target for antimetastatic drug development. LFG-500, a novel synthetic flavonoid, has been revealed as a potential antitumor agent owing to its various activities, including modulation of EMT in the inflammatory microenvironment. Here, using a transforming growth factor beta (TGF-ß)-induced EMT models, we found that LFG-500 inhibited EMT-associated migration and invasion in human breast cancer, MCF-7, and lung adenocarcinoma, A549, cell lines, consistent with the observed downregulation of YAP activity. Further studies demonstrated that LGF-500-induced suppression of YAP activation was mediated by integrin-linked kinase (ILK), suggesting that the ILK/YAP axis might be feasible target for anti-EMT and antimetastatic treatments, which was verified by a correlation analysis with clinical data and tumor specimens. Hence, our data support the use of LGF-500 as an antimetastatic drug in cancer therapy and provide evidence that the ILK/YAP axis is a feasible biomarker of cancer progression and a promising target for repression of EMT and metastasis in cancer therapy.

6H2L, a novel synthetic derivative of bifendate, induces apoptosis in hepatoma cells via mitochondrial and MAPK pathway.

Hepatocellular carcinoma (HCC) is a major cause of cancer-related death worldwide. Our previous study indicated that 6H2L, a novel synthetic bifendate derivative, shows multidrug resistance reversal activity, while its antitumor effect has not been revealed. Here, the potent antitumor effects of 6H2L on hepatoma cells both in vitro and in vivo were investigated. 6H2L inhibited cell viability of HepG2 and SMMC-7721 cells with less sensitivity to normal human liver L-02 cells. 6H2L induced apoptosis in hepatoma cells. It upregulated Bax expression, while simultaneously decreasing Bcl-2 expression. Further elucidation of the mechanism revealed that 6H2L induced mitochondrial dysfunction, with transmitochondrial membrane potential collapse and cytochrome c release, which activated caspase-9 and caspase-3 and subsequently cleaved PARP, suggesting that 6H2L induced apoptosis via triggering mitochondrial pathway. Moreover, 6H2L decreased the phosphorylation of ERK1/2, whereas it increased the expression of p-JNK and p-p38. Then, specific inhibitors of the mitogen-activated protein kinase (MAPK) pathway were employed to confirm the roles of the MAPK pathway in the apoptosis-inducing effects of 6H2L. Additionally, 6H2L obviously inhibited the tumor growth in H22-bearing ICR mice. Meanwhile, 6H2L remarkably up-regulated Bax while suppressing Bcl-2 in tumors. Importantly, neither significant weight loss, white blood cell (WBC) count, nor histopathological abnormalities of major organs were observed in the mice receiving 6H2L treatment, indicating that 6H2L exerted strong anticancer activities with low toxicity in vivo. In contrast, fluorouracil inhibited tumor growth with significant decreased body weight and WBC count. Taken together, these results suggested 6H2L is a potential therapeutic candidate for HCC.