Objective To analyze the expression and predictive value of serum tumor markers spectrum and chemokine protein in lung cancer and predictive value.Methods One hundred and fifty patients with lung cancer were selected as the observation group and contemporaneous 150 individuals undergoing physical examination served the control group.The levels of ProGRP,CEA,SCC and Cyfra21-1 were measured by chemiluminescence microparticle immunoassay.The chemokine protein was determined by multiple immunofluorescent assay.Results The levels of CCL28,LIF,LIGHT and GRO in the observation group were significantly higher than those in the control group (P＜0.05).The levels of CCL28,LIF,LIGHT and GRO in the observation group were higher than those in the control group.The levels of CCL28,NAP-2 and MDC in the observation group were lower than those in the control group (P＜0.05).Conclusion The regular detection of serum tumor markers spectrum and chemokine protein can predict the treatment prognosis and evaluate the clinical curative effect.

Objective:To design a semi-spherical applicator for delivery of semi-spherical dose distributions and assess its dosemetric characteristics.Methods:The applicator was designed in the following way. First, the scattering angle and dose rate of the electron beam having passed through a series of scattering foils of different thicknesses were calculated to determine the thickness of the scattering foil. And then, a series of location model was designed, and the variances of the mean electron energy on the surface of these models were calculated to determine the foil location. Finally, the relationship between the geometric characteristics of the layer and the surface dose on the applicator was established to design the modulator. Monte Carlo (MC) codes EGSnrc/BEAMnrc and EGS4/DOSXYZ were employed to model the head of the Mobetron, the location model, the layer, the semi-spherical applicator, and to calculate the dose distributions.Results:A semi-spherical applicator was designed for electron beam of energy 12 MeV, which consisted of a 2.5 cm diametre cylindrical collimator with 0.5 cm thick wall made of 0.3 cm thick steel and 0.2 cm thick water equivalent material (WEM), a 0.14 cm-thick foil made of tansgen, and a 2.5 cm diametre hollow semi-sphere containing a crescent modulator made of WEM. The dose rate was about 160 cGy/min, and the depth of the 50% isodose curve was 0.85 cm.Conclutions:We designed and performed a MC simulation of a semi-spherical applicator to deliver a semi-spherical dose distribution from a high energy electron beam.

ObjectiveTo investigate the regulatory effect and potential mechanisms of isocitrate dehydrogenase 3A （IDH3A） on cardiomyocyte hypertrophy. MethodsThe expression of IDH3A in the myocardium of healthy volunteers （n=10） and patients with heart failure （HF） （n=10）， and in the myocardium of mice subjected to transverse aortic constriction （TAC） surgery and sham operation， as well as in phenylephrine （PE）-induced neonatal rat ventricular cardiomyocytes （NRVCs）， was assessed by real-time quantitative polymerase chain reaction （RT-qPCR） and Western blot assay. The effect of adenovirus-mediated overexpression of IDH3A on the expression of hypertrophy-related genes in PE-induced NRVCs was also evaluated. The effect of IDH3A on NRVCs area was examined by phalloidin staining assay. A mutant of IDH3A with abolished enzymatic activity， IDH3A_D208A， was generated through site-directed mutagenesis. The impact of this IDH3A mutant on the hypertrophic phenotype， ATP and ROS levels in NRVCs was evaluated to investigate whether the regulatory role of IDH3A in cardiomyocyte hypertrophy was dependent on its enzymatic activity. The effect of exogenous α-ketoglutaric acid （AKG） on cardiomyocyte hypertrophy was also detected by Western blot and phalloidin staining assay， respectively. ResultsIDH3A was significantly decreased in the myocardium of HF patients， in the myocardium of TAC-operated mice， and in PE-induced NRVCs （P = 0.005 2，P = 0.026 6，P = 0.041 3 and P = 0.006 6， respectively）. Overexpression of IDH3A markedly suppressed the expression of hypertrophy-related genes and the increase of cell size of PE-induced NRVCs （P < 0.000 1， P = 0.000 1 and P = 0.000 2， respectively）. The ATP and ROS analysis indicated that IDH3A inhibited the increases of ATP and ROS levels in PE-induced NRVCs （P = 0.001 2 and P<0.000 1， respectively）， whereas the enzymatically inactive IDH3A mutant lacked this effect. Exogenous AKG provision could， but overexpression of IDH3A mutant failed to suppress PE-induced NRVCs hypertrophy. ConclusionIDH3A inhibits cardiomyocyte hypertrophy via elevating AKG level， providing scientific evidence for study on IDH3A-based treatment of cardiac hypertrophy.