Andrographolide radiosensitizes human esophageal cancer cell line ECA109 to radiation in vitro.

To explore the radiosensitivity of andrographolide on esophageal cancer cell line ECA109. The inhibition effects of andrographolide were measured using 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium (MTT) assay. Clonogenic survival assay was used to evaluate the effects of andrographolide on the radiosensitivity of esophageal cancer cells. Immunofluorescence was employed to examine Bax expression. The changes in cell cycle distribution and apoptosis were assayed using flow cytometry. The expression of NF-κb/Cleaved-Caspase3/Bax/Bcl-2 was measured using Western blot analysis. DNA damage was detected via γ-H2AX foci counting. With a clear dose and time effects, andrographolide was found to inhibit the proliferation of esophageal cell line ECA109. The results of the clonogenic survival assay show that andrographolide could markedly enhance radiosensitivity (P < 0.05) with a sensitizing enhancement ratio of 1.28. Andrographolide caused a dose-dependent increase in Cleaved-Caspase3/Bax protein expression and a decrease in Bcl-2/NF-κb expression. Apoptosis in andrographolide-treated ECA-109 increased significantly compared with the apoptosis in the simple drug and radiation combined with drug groups (P < 0.001; P < 0.05). Moreover, compared with the independent radiation group, the andrographolide combined with radiation group increased the number of DNA double chain breaks. Andrographolide can increase the radiosensitivity of esophageal cell line ECA109. This result may be associated with the decrease in the NF-κb level and the induced apoptosis of esophageal cancer cells.

Association between C-myc and K-ras gene polymorphisms and non-Hodgkin lymphoma.

OBJECTIVE: To explore the association between c-myc and K-ras gene polymorphisms and non-Hodgkin lymphoma (NHL). PATIENTS AND METHODS: A total of 200 NHL patients in our hospital in the past 3 years were collected as disease group, while 200 healthy people were taken as control group. The genomic deoxyribonucleic acid (DNA) in the peripheral blood was extracted in both groups, amplified via Polymerase Chain Reaction (PCR) and sent to the company for the detection of c-myc and K-ras gene polymorphisms. The expressions of c-myc and K-ras were detected via Reverse Transcription-quantitative PCR (RT-qPCR), and the levels of clinical indexes hemoglobin (Hb), platelet (PLT) and lactate dehydrogenase (LDH) were determined in the Laboratory Department. RESULTS: The allele distribution at c-myc gene locus rs121918684 was different between control group and disease group (p=0.000), and the G allele frequency was 202 (0.505) in the control group and 263 (0.657) in the disease group. In the disease group, the GG genotype frequency at c-myc gene locus rs121918684 [97 (0.485)], the CC genotype frequency at rs775522201 [98 (0.490)], and the GA genotype frequency at K-ras gene locus rs1137188 [127 (0.635)] were all significantly higher than those in the control group (p=0.000, p=0.002, p=0.011). In the disease group, the frequency of recessive model GC+CC (p=0.003), heterozygous model GC (p=0.035), and homozygous model CC (p=0.037) at c-myc gene locus rs121918684 was significantly lower than that in the control group, and the frequency of recessive model CT+TT (p=0.046) at c-myc gene locus rs775522201 was also markedly lower than that in the control group. The haplotype frequency of c-myc CC (p=0.000), GC (p=0.000), and GT (p=0.018) in the disease group was different from that in the control group. Moreover, the CT genotype at c-myc gene locus rs775522201 was remarkably correlated with the c-myc gene expression, and the gene expression was markedly increased in the disease group. The TT genotype at K-ras gene locus rs12245 was correlated with the K-ras gene expression, and the gene expression was notably increased in the disease group. There was an association between GG genotype at c-myc gene locus rs121918684 and LDH level (p=0.000), between CT genotype at c-myc gene locus rs775522201 and PLT level (p=0.002), and between AA genotype at K-ras gene locus rs1137188 and Hb level (p=0.003). CONCLUSIONS: The c-myc and K-ras gene polymorphisms are associated with susceptibility to NHL, gene expression and levels of Hb, PLT, and LDH.

First Observation of z-Dependent Electron-Beam Microbunching Using Coherent Transition Radiation.

We report the first measurements of the electron-beam microbunching z dependence in a self-amplified spontaneous-emission (SASE) free-electron laser (FEL) experiment by the observation of visible wavelength coherent transition radiation (CTR). In this case the fundamental SASE wavelength was at 537 nm, and the CTR exhibited an exponential intensity growth similar to the SASE radiation. In addition, we observed for the first time structure in the CTR angular distribution patterns that may be useful for optimizing SASE FEL performance.

The cyclic hexapeptide AcF attenuates sepsis-induced acute lung injury and mortality in rats.

OBJECTIVE: The purpose of this study was to elucidate the possible beneficial effects of AcF on acute lung injury (ALI) in a rat model of sepsis. MATERIALS AND METHODS: Male Sprague-Dawley rats were randomly divided into the following four experimental groups (n = 10 per group): animals undergoing a sham cecal ligature puncture (CLP) (Sham group); animals undergoing CLP (control group); or animals undergoing CLP and treated with saline (Saline group) and animals undergoing CLP and treated with AcF (AcF group). At 24 h after CLP, blood, bronchoalveolar lavage fluid (BALF) and lung tissue were collected. The lung wet/dry weight ratio, Protein concentration and the count of inflammatory cells or neutrophils in the BALF were determined. The pathologic changes in lungs were examined with the optical microscopy. Myeloperoxidase (MPO) activity, the expression of inflammatory cytokines were measured in lung tissue and BALF respectively. Survival rates were recorded at 120h in the four groups in another experiment. RESULTS: Histology findings revealed acute lung injury in rats in the CLP group, whereas those in the AcF-treated group had mild lung injury. Treatment with AcF significantly attenuated the CLP-induced pulmonary edema and inflammation, as it significantly decreased lung wet/dry ration, protein concentration and the infiltration of inflammatory cells and neutrophils in the lung tissues. In addition, the secretion of inflammatory cytokines, such as TNF-α, IL-6, IL-1b and macrophage inflammatory protein-2 (MIP-2) was decreased in AcF treated group compared with the control saline treated group. CONCLUSIONS: AcF administration ameliorates acute lung injury in a rat model of sepsis induced by CLP. AcF can be developed as a novel treatment for severe sepsis-induced ALI.