A new and important relationship between miRNA-147a and PDPK1 in radiotherapy.

It was found that the expression level of miR-147a was significantly increased and the pathway of PI3K/AKT was dramatically inhibited after radiation. In view of the relationship between miRNA and target genes, we put forward the question, what is the relationship between PI3K/AKT and miR-147a? In order to find the answer to the question, we used bioinformatics techniques to analyze the relationship between miR-147 (a or b) and PI3K/AKT signaling pathway. miR-147a overexpression plasmid and PDPK1 3'UTR luciferase reporter gene plasmid were constructed. Dual luciferase reporter gene system validation experiments were carried out on miR-147a and PDPK1 relationship. The verification experiments were also carried out. Bioinformatics analysis showed that there is a miR-147a binding site in the non-coding region (3'UTR) of PDPK1. In the experimental groups transfected with wild type PDPK1 gene of 3'UTR plasmid, the luciferase activity decreased (or increased) significantly in miR-147a (or inhibitor) group compared with miR-NC (or anti-miR-NC); There was no significant difference between the miR-147a group (or inhibitor) and the miR-NC group (or anti-miR-NC) in the transfection of PDPK1-3'UTR-Mut gene vector. PDPK1 was a target gene for direct regulation of miR-147a downstream. Verifying test results showed that the expression of PDPK1 mRNA and protein was reduced after overexpression of miR-147a, which was up-regulated after silencing miR-147a in TC, and V79 cells. These results suggest that miR-147a could be involved in the regulation of PDPK1 transcription by binding to the target site in PDPK1 mRNA 3'UTR, and then regulated AKT.

Activating AKT to inhibit JNK by troxerutin antagonizes radiation-induced PTEN activation.

Radiotherapy is one of the most effective non-surgical treatments for many tumors. However, radiation damage remains a major negative consequence of radiotherapy. At present, radio-protective effect of troxerutin has been confirmed, but the mechanism of this radioprotection has not been elucidated. Here, this study showed that troxerutin protected thymus tissue of irradiated mice, and its radio-protective effect on thymocytes was significant in the range of 0.625-10µg/ml. Troxerutin significantly inhibited apoptosis of irradiated thymocytes at the concentration of 10µg/ml. Computer-aided drug design was used to investigate potential candidate targets for troxerutin, and an excellent correlation was identified between troxerutin and AKT (Pharm mapper and KEGG signal pathway). Troxerutin inhibited the activation of PTEN to stimulate AKT, which in turn prevented the activation of JNK to protect cells. Our results showed that troxerutin enhanced radioprotection at least partially by activating AKT to inhibit the activation of JNK.

Flavonoids of Rosa roxburghii Tratt act as radioprotectors.

BACKGROUND: To study the radioprotective effects of flavonoids from Rosa roxburghii Tratt (FRT). MATERIALS AND METHODS: The radioprotective effects of FRT were investigated by examining cell viability, 30-day survival of mice and the number of colony-forming units in spleen (CFU-S) after total-body 60Co irradiation. RESULTS: The survival rates of irradiated cells gradually increased with increasing concentrations of FRT. The survival rate was the highest at 87% with a concentration of 30 µg/mL. Pretreatment with FRT was needed to realize its radioprotective activity in mice at the dose of 60 mg/kg. With the increasing doses of 30 mg/kg, 60 mg/kg and 120 mg/kg, the numbers of CFU-S increased, and were significantly different compared with the control group. CONCLUSIONS: Pretreatment with FRT prior to irradiation resulted in significantly higher cell survival at 24 h after 5 Gy radiation, increased 30-day survival in mice after exposure to a potentially lethal dose of 8 Gy, and resulted in a higher number of CFU-S in mice after exposure to a dose of 6 Gy. These results collectively indicate that FRT is an effective radioprotective agent.

[X-ray hardening correction for ICT in testing workpiece].

Since energy spectrum of X-ray is polychromatic source in X-ray industrial computerized tomography, the variation of attenuation coefficient with energy leads to the lower energy of X-ray radiation being absorbed preferentially when X-ray is transmitting the materials. And the higher the energy of X-ray, the lower the attenuation coefficient of X-ray. With the increase in the X-ray transmission thickness, it becomes easier for the X-ray to transmit the matter. Thus, the phenomenon of energy spectrum hardening of X-ray takes place, resulting from the interaction between X-ray and the materials. This results in false images in the reconstruction of X-ray industrial computerized tomography. Therefore, hardening correction of energy spectrum of X-ray has to be done. In the present paper, not only is the hardening phenomenon of X-ray transmitting the materials analyzed, but also the relation between the X-ray beam sum and the transmission thickness of X-ray is discussed. And according to the Beer law and the characteristics of interaction when X-ray is transmitting material, and by getting the data of X-ray beam sum, the relation equation is fitted between the X-ray beam sum and X-ray transmission thickness. Then, the relation and the method of equivalence are carried out for X-ray beam sum being corrected. Finally, the equivalent and monochromatic attenuation coefficient fitted value for X-ray transmitting the material is reasoned out. The attenuation coefficient fitted value is used for product back-projection image reconstruction in X-ray industrial computerized tomography. Thus, the effect caused by X-ray beam hardening is wiped off effectively in X-ray industrial computerized tomography.

[Beam hardening simulated correction research for X-ray TICT in testing composites workpiece].

In X-ray TICT, when X-ray is transmitted in the materal, the phenomenon of energy spectrum hardening takes place, resulting in artifacts. Thus, hardening correction has to be done. In the present paper, the phenomenon of X-ray beam hardening resulting in analyized, and the relation between the X-ray beam sum and the transmission thickness in testing composites workpiece is discussed. According to the Beer law and the characteristics of the interaction between X-ray and the material, and getting the data of X-ray beam sum, the relation equation between the beam sum and transmission thickness is simulated firstly, and testing composites workpiece. Then, the relation and the method of equivalence are carried out between the equivalent transmission thickness and the transmission thickness for X-ray beam sum being corrected for monochromatic ray beam. Finally, the attenuation coefficient beam hardening simulated value for X-ray equivalent monochromatic is reasoned out in testing composites workpiece. Then, the attenuation coefficient simulated value that has been corrected is used for product back-projection reconstruction. Thus, the effect caused by X-ray beam hardening is wipped off effectively in testing composites workpiece.

[Hardening correction model of energy spectrum for X-ray TICT in testing composites workpiece].

In the case of a polychromatic source in X-ray TICT, the variation of attenuation coefficient with energy leads to low energy radiation being absorbed preferentially. In other words, the higher the energy, the lower the attenuation coefficient. With the transmission thickness augmenting, it is easier for X-ray to transmit the matter. The phenomenon is energy spectrum hardening. Thus, hardening correction has to be done. In the present paper, not only is energy spectrum hardening analyzed by theory and the relation stated between attenuation coefficient and transmission thickness in testing composites workpiece, but also the precise accurate theory model for hardening correction of energy spectrum and theory method are reasoned out in testing composites workpiece, which results from Beer's law and the characteristics of X-ray interaction with composites. Then, the attenuation coefficient that has been corrected is used for product back-projection reconstruction. Thus, the effect caused by X-ray beam hardening is wipped out effectively in testing composites workpiece.

[An anti-tumor research of recombinant phage vaccine expressed xenogenic EGFR].

A recombinant phage vaccine expressing EGFR on it's capsid was constructed and used to study the anti-tumor effect. The T7 phage display system was applied to display seven xenogenic (human, chicken) epidermal growth factor receptor extracellular domain fragments. The EGFR fragment was expressed as fused protein with 10B capsid on the surface of T7 phage. The T7-EGFR phage vaccines were injected into C57BL/6J mice, and then Lewis lung cancer cells were inoculated after 4 weeks immunization. The tumor tissue was excised and weighed after 10 days to evaluate the anti-tumor effect of each experimental group. The EGFR expression of the phage vaccine was verified by western-blot analysis. The A431 cells with high expressed EGFR was used to detect the anti-EGFR antibody by flow cytometry analysis. The results showed that the A431 cell can react with the serum obtained from the mice after three-week immunization. The experimental results confirmed that special EGFR antibody could be induced by the T7-EGFR phage vaccine. The T7-EGFR phage vaccine can elicit endogenous special EGFR antibody in mice and is capable of suppressing the tumor proliferation and retarding the growth of Lewis lung cancer. This research can be used to develop an anti-tumor vaccine for the target-therapy of EGFR(+) tumor.