[en] Much spider silk research to date has focused on its mechanical properties. However, the webs of many orb-web spiders have evolved for over 136 million years to evade visual detection by insect prey. It is therefore a photonic device in addition to being a mechanical device. Herein we use optical surface profiling of capture silks from the webs of adult female St Andrews cross spiders (Argiope keyserlingi) to successfully measure the geometry of adhesive silk droplets and to show a bowing in the aqueous layer on the spider capture silk between adhesive droplets. Optical surface profiling shows geometric features of the capture silk that have not been previously measured and contributes to understanding the links between the physical form and biological function. The research also demonstrates non-standard use of an optical surface profiler to measure the maximum width of a transparent micro-sized droplet (microlens).

[en] Dysphagia is a frequent and the most common symptom of malignant disease in the oesophagus. Adequate palliation with low morbidity in dysphagia due to inoperable oesophageal carcinoma is difficult to achieve. Surgery probably provides the most effective palliation of dysphagia, but it is associated with a high morbidity. Self-expanding metal stents seem to offer excellent palliation with minimal morbidity for patients with inoperable carcinoma of the oesophagus. Stent treatment has a good and prompt effect on dysphagia and can be recommended for palliation of patients with malignant oesophageal strictures. A combination of radiotherapy (40 Gy) and the self-expanding metal stents can result in a prolonged palliation. This combined treatment was generally well tolerated

[en] Short communication

No abstract available

[en] Highlights: • 1, miR-616-3p was up-regulated in GC cell lines and tissues, indicating a poor prognosis. • 2, miR-616-3p promoted angiogenesis and EMT in vitro. • 3, miR-616-3p exerted its biological function might through AKT/mTOR pathway by targeting PTEN. • 4, miR-616-3p might be a potential therapeutic target in GC. Dysregulation of microRNAs has been demonstrated to be involved in a variety of biological events related to cancer, including proliferation, metastasis, angiogenesis and immune escape. MiR-616-3p is located on the chromosome region 12q13.3, however, its potential role and clinical implications in gastric cancer remain poorly understood. The current study aimed to investigate the potential role of miR-616-3p in gastric cancer. The results showed that miR-616-3p was up-regulated in cancer tissues. Higher expression of miR-616-3p in tumor tissues also predicted poor prognosis. Furthermore, loss- and gain-of-function in vitro revealed that miR-616-3p promoted angiogenesis and EMT in gastric cancer cells. Mechanistically, further analysis demonstrated that the effects of miR-616-3p on metastasis and angiogenesis occurred through the down-regulation of PTEN, a direct target of miR-616-3p. We propose that the restoration of PTEN expression may block miR-616-3p-induced EMT and angiogenesis. Collectively, our findings suggest that the miR-616-3p-PTEN signaling axis might be a potential therapeutic target for gastric cancer.

[en] Highlights: • The crystal structure of BdcA in complex with NADPH is determined. • NADPH binding stabilizes a potential substrate binding pocket of BdcA. • The substrate binding pocket is conversely involved in BdcA recognizing NADPH. • Both NADPH and substrate binding are essential for BdcA inducing biofilm dispersal. Biofilm dispersal is characterized by the cell detachment from biofilms and expected to provide novel “anti-biofilm” approaches of prevention and treatment of biofilms in clinical and industrial settings. The E.coli protein BdcA has been identified as a biofilm dispersal factor and designed to be an important component in engineered applications to control biofilm formation. It belongs to short-chain dehydrogenase/reductase (SDR) family with the specific affinity to NADPH. Here, we show the structure of BdcA in complex with NADPH and confirm that NADPH binding is requisite for BdcA facilitating cell motility and increasing biofilm dispersal. Especially, we observe a potential substrate binding pocket surrounded by hydrophobic residues upon NADPH binding and present evidences that this pocket is essential for BdcA binding NADPH and exerting its biological functions. Our study provides the clues for illuminating the molecular mechanism of BdcA regulating biofilm dispersal and better utilizing BdcA to eliminate the biofilms.

No abstract available

[en] Studying the effects of NPs on proteins may help understanding potential biological injuries such as changes in protein fibrillation, exposure of new antigenic epitopes, and loss of function such as enzymatic activity impairment. In this mini-review we present recent data which help understand the basis of NP-protein interactions and their subsequent potential effects on key mediators of biological functions such as enzymes.

No abstract available

[en] Lung cancer is the most frequent cause of cancer-related deaths worldwide, but its molecular pathogenesis is poorly understood. The tumor suppressor candidate 3 (TUSC3) gene is located on chromosome 8p22 and is universally acknowledged as a cancer suppressor. However, our research has demonstrated that TUSC3 expression is significantly upregulated in non-small-cell lung cancer compared to benign controls. In this study, we analyzed the consequences of TUSC3 knockdown or overexpression on the biological functions of non-small-cell lung cancer cell lines. To identify the molecules and signaling pathways with which TUSC3 might interact, we completed immunoblotting, quantitative polymerase chain reaction, microarray, co-immunoprecipitation, and immunofluorescence assays. We demonstrated that TUSC3 knockdown leads to decreased proliferation, migration, and invasion, and reduced xenograft tumor growth of non-small-cell lung cancer cell lines, whereas opposite results were observed with overexpression of TUSC3. In addition, TUSC3 knockdown suppressed epithelial-mesenchymal transition by downregulating the expression of claudin-1, which plays an indispensable role in EMT progress. On the contrary, overexpression of TUSC3 significantly enhanced EMT progress by upregulating claudin-1 expression. Overall, our observations suggest that TUSC3 accelerates cancer growth and induces the epithelial-mesenchymal transition in non-small-cell lung cancer cells; we also identified claudin-1 as a target of TUSC3.