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Theranostic nanoparticles with combined imaging and therapy functions show great promise in cancer precision medicine. In this study, we constructed near-infrared (NIR) "OFF-ON" fluorescent nanohybrids (F-PNDs) for synchronous tumor imaging and microRNA (miRNA) modulation therapy against esophageal cancer. Nanodiamond clusters (NDs) were first functionalized for protamine sulfate immobilization (PNDs) on their surfaces via a noncovalent self-assembling approach and simultaneous encapsulation of NIR emitting fluorescence dye cyanine 5 (Cy-5) (F-PNDs). Tumor suppressor miRNA-203 (miR-203) was then adsorbed onto the surface of F-PNDs to form miR-203/F-PNDs via electrostatic interactions. The size, morphology, photophysical and stability properties of miR-203/F-PNDs were analyzed. We found that the NIR fluorescence of miR-203/F-PNDs could be activated to the "ON" state in intracellular environment while remaining in the "OFF" state in extracellular or blood environment. Furthermore, in vivo live imaging experiments showed that miR-203/F-PNDs could be predominantly accumulated in tumor tissues and image the tumor sites 24 h postintravenous injection. In addition, intravenous and intratumoral injection of miR-203/F-PNDs could efficiently inhibit tumor growth through down-regulation of the expressions of oncogenes Ran and Δp63. Our study indicated that miRNA/F-PNDs could serve as a promising theranostic platform for synchronous tumor imaging and miRNA-based modulation therapy against cancer.

MicroRNAs are highly conserved non-coding RNAs that regulate gene expression at the post-transcriptional level, and play pivotal roles in cancer development and progression. miR-100 has been reported to be significantly downregulated in a variety of cancers, including esophageal cancer. However, the role of miR-100 in human esophageal cancer has not been fully elucidated. We demonstrated that overexpression of miR-100 in esophageal cancer cells markedly inhibited cell proliferation, migration and invasion as well as tumor growth. We subsequently showed that CXCR7 is a direct target gene of miR-100. Our results indicated that miR-100 plays a tumor-suppressor role in esophageal cancer and suggest its potential application for esophageal cancer treatment.

The expression of miR-203 has been reported to be significantly down-regulated in esophageal cancer. We showed here that overexpression of miR-203 in esophageal cancer cells dramatically increased cell apoptosis and inhibited cell proliferation, migration and invasion as well as tumor growth and down-regulated miR-21 expression. We subsequently identified that small GTPase Ran was a target gene of miR-203. Furthermore, Ran restoration partially counteracted the tumor suppressive effects of miR-203 and increased miR-21 expression. Taken together, our findings suggest that miR-203 may act as novel tumor suppressor in esophageal cancer through down-regulating the expression of Ran and miR-21.

Introduction A potent mesenchymal stem cell (MSC) population was recently isolated from the Wharton's jelly of human umbilical cord (UC). The aim of the current experiments was to determine the potential of human UC-derived MSC (UC-MSC) in cartilage healing. Materials and methods Chondrogenic differentiation of collagen hydrogel-embedded cells was induced in standard chondrocyte conditioning medium and further detected by real-time PCR, histochemistry and immunohistochemistry analyses. Cell viability and apoptosis of the MSCs in the collagen I hydrogels were monitored using apoptosis detection kit. Results Cells isolated from UC were positive for MSC biomarkers and negative for haematopoietic lineage and endothelial biomarkers and possess the capacity to differentiate along osteogenic lineage. UC-MSCs embedded in collagen hydrogel can undergo chondrogenesis characterised by significantly increased expressions of collagen II, aggrecan, COMP (cartilage oligomeric matrix protein) and sox9 after exposed cells-embedded hydrogels to chondrogenic factors. The most of cells remained viable throughout the hydrogels after 3 weeks of cultivation in chondrogenic differentiation medium. Conclusions Collagen hydrogel can provide an appropriate 3-D environment for the chondrogenesis of UC-MSCs. UC-MSCs embedded in biocompatible scaffold may have great potential for cartilage engineering.

Vehicle Routing Problem (VRP) is one of critical problems in modern logistics service. Due to small batch and dynamic changes of VRP, an effective and fast algorithm solution of VRP is greatly needed. But in traditional Ant Colony Algorithm, the searching speed is slow, and it is easy to fall into the local optimization when solve this problem. In order to overcome these disadvantages, basing on the new hybrid algorithm of Ant Colony Algorithm and Artificial Fish School Algorithm, this paper further improves the Aswarm Degree in the Artificial Fish School Algorithm and proposes the Insertion Point Algorithm to solve the problem rapidly. The simulation results show that the improved algorithm has a better searching ability of global optimization. The improved algorithm is an effective algorithm of solving the VRP optimization problem.

Esophageal cancer, including Squamous Cell Carcinoma and Adenocarcinoma, is one of the most common causes of cancer and cancer death globally, with China alone accounting for about half of the new cases worldwide in 2012. In this study we analyzed the presence of human papilloma virus (HPV) DNA and Tp53 mutations in 52 cancer patients, including 26 Squamous Cell Carcinoma cases, 21 Adenocarcinomas and 5 of non-described histology from Tangshan China. Overall 44 patients were positive for HPV L1 consensus, 28 were positive for HPV16 and 34 for HPV18 (84.62%, 53.82% and 65.38% respectively); 23 samples (44.23%) were positive for both HPV16 and HPV 18. We detected however a very low rate of Tp53 mutations in exons 5 through 8, which may possible be related to the elevated percentage of high risk HPV. Our findings corroborate our previous study on Esophageal Squamous Cell carcinoma in the same area but a further analysis on other Tp53 exons polymorphisms are necessary to understand the reason behind the low level of Tp53 mutations we reported.