MicroRNA 494 increases chemosensitivity to doxorubicin in gastric cancer cells by targeting phosphodiesterases 4D.

Acquired drug resistance is one of the main limitations in pharmacological therapy of malignancies including gastric cancer. MicroRNAs (miRNAs) are a class of small noncoding RNAs that suppress their targets by binding to the 3'UTR region of genes. In this study, we explored investigate the target gene of miR-494 and its roles in chemoresistance of gastric cancer. We found that miR-494 was significantly down-regulated in gastric cancer cells lines compared to the normal gastric epithelial cell line. Exogenous overexpression of miR-494 increased the chemosensitivity of gastric cancer cells to doxorubicin. Moreover, miR-494 expression was reduced in a doxorubicin-resistant gastric cancer cells (AGS/dox) compared with the parental cells. MTT assay showed that AGS/dox cells exhibited an elevated viability compared with the parental cells. Enforced expression of miR-494 inhibited AGS/dox cell viability and colony formation ability. In addition, we demonstrated that elevated expression of miR-494 inhibited the mRNA and protein expression of phosphodiesterases 4D (PDE4D) in gastric cancer cell. Luciferase assay showed that miR-494 directly targeted the 3'UTR region of PDE4D. Furthermore, restoration of PDE4D recovered the chemoresistance in miR-494-overexpressed gastric cancer cells. Taken together, this study demonstrated that miR-494 enhanced doxorubicin sensitivity via regulation of PDE4D expression, suggesting a novel therapeutic strategy for anti-chemoresistance in gastric cancer.

Fully integrated InGaAs/InP single-photon detector module with gigahertz sine wave gating.

InGaAs/InP single-photon avalanche diodes (SPADs) working in the regime of GHz clock rates are crucial components for the high-speed quantum key distribution (QKD). We have developed for the first time a compact, stable, and user-friendly tabletop InGaAs/InP single-photon detector system operating at a 1.25 GHz gate rate that fully integrates functions for controlling and optimizing SPAD performance. We characterize the key parameters of the detector system and test the long-term stability of the system for continuous operation of 75 h. The detector system can substantially enhance QKD performance and our present work paves the way for practical high-speed QKD applications.

[Inhibitory effects of Salvia miltiorrhiza injection coordinated with dexamethasone on interleukin-13 and eotaxin expression in lung of asthmatic rats].

OBJECTIVE: To investigate the molecular mechanism of inhibitory effect of Salvia miltiorrhiza Injection (SMI) coordinated with dexamethasone (DXM) on allergic airway inflammation in asthmatic rats. METHODS: Forty SD rats were randomly divided into 5 groups equally: the normal group, the asthma model group, the DXM group, the SMI group and the DXM + SMI group, they were treated with correspondant herbal medicines. Pathologic changes of lung tissue were obseved with HE stain, count of WBC and eosinophil (Eos) in bronchoalveolar lavage fluid (BALF) were estimated and the expressions of interleukin-13 (IL-13) and Eotaxin in lung tissue were measured by RT-PCR and SP method of immunohistochemistry assay. RESULTS: There was moderate inflammation in lung tissue in the SMI group, and mild inflammation in the DXM + SMI and the DXM group, which was similar to that in the normal group. Compared with the asthma model group, Eos and WBC count in BALF and the expression of IL-13 and Eotaxin in the lung tissue were significantly lower in the three treated groups (P < 0.05), particularly in the DXM + SMI group, showing a significant difference as compared with the other two groups (P < 0.05 or P < 0.01). Additionally, IL-13 expression was positively correlated with Eotaxin expression (r = 0.92, P < 0.01). CONCLUSION: SMI could inhibit the expression of IL-13 and Eotaxin in the lung of asthmatic rats, showing inhibitory effects synergistic with DXM on airway inflammation.