OBJECTIVE: To investigate the gene expression profile by using gene chip technology and probe into the role of corresponding gene in the pathogenesis of nasal polyps by analysing the difference of the gene depression. METHOD: The total RNAs were respectively extracted from 6 pairs of inferior turbinates and nasal polyps, and then were reversely transcribed to cDNAs with incorporation of fluorescent dUTP as the hybridization probes. The mixed probes were then hybridized with the BiostarH-40 s gene chips, it was scanned by laser scanner and the acquired image was analyzed by software. RESULT: 1887 genes were differently expressed in gene profile of nasal polyps, among which 1099 were upregulated and 788 were down-regulated. Six genes were found in all gene chips, among which 4 genes were upregulated and 2 were down-regulated. The 6 genes encoded the protein of the transmembrane 4 superfamily, highly similar to GAMMA-interferon-inducible protein IP-30 precursor, highly similar to complement factor I precursor and insulin-like growth factor binding protein 3 (IGFBP3). CONCLUSION Detecting the differently expressed genes will provide clues and theoretical foundation for the pathogenesis of nasal polyps. The nasal polyps is a polygenic disease and the genes of GAMMA-interferon-inducible protein, insulin-like growth factor binding protein may play an important role in its pathogenesis.
Adult ; Gene Expression Profiling ; methods ; Humans ; Male ; Middle Aged ; Nasal Polyps ; genetics ; Oligonucleotide Array Sequence Analysis ; methods ; Young Adult

Objective:To investigate the differences in dosimetric impacts of the systematic errors induced by the leaf positions of a multi-leaf collimator (MLC) on the volumetric modulated arc therapy (VMAT) for patients with different T stages of nasopharyngeal carcinoma (NPC).Methods:A total of 44 patients with T 1-4N 1M 0 NPC were selected to design the VMAT plans using the Pinnacle planning system as the initial plans. The prescribed doses to the primary gross tumor volume (PGTV) were 68-70 Gy in 33 fractions for patients with T 1 and T 2 stage NPC and 71 Gy in 33 fractions for patients with T 3 and T 4 stage NPC. The prescribed doses to other target volumes were identical. In the initial plan files, a systematic error ranging from ±0.2 to ±1 mm was introduced to the position of each MLC leaf, leading to an increase or decrease in the subfield area. Then, potential error plans at the positions of MLC leaves during VMAT treatment were simulated. Dose evaluation indices involved target volumes and organs at risk (OARs). The indices related to target volumes consisted of the D98% of PGTV and PGTVnd, while those concerning OARs included the D0.1 cm 3 of the brainstem, spinal cord, and optic chiasm. Results:After the systematic errors induced by the positions of MLC leaves were introduced, the sensitivity range of each dose index range was (3.87%-9.87%)/mm ( R2 = 0.932-0.998, P < 0.01). Specifically, patients with stage T 4 NPC displayed higher sensitivity to the D98% of PGTV than those with stage T 1, T 2 and T 3 NPC ( Z = -3.12, -2.86, -2.59, P < 0.05), patients with stage T 3 NPC exhibited lower sensitivity to the D0.1 cm 3 of optic chiasm than those with stage T 1 and T 2 NPC ( Z = -2.92, -2.72, P < 0.05), and patients with stage T 4 NPC manifested lower sensitivity to the D0.1 cm 3 of chiasma than those with stage T 1 and T 2 NPC ( Z = -3.51, -3.25, P < 0.05). The relationship between the sensitivity of MU/Gy and PGTV D98% was y=-3.020+ 0.025 x ( r = 0.80, P < 0.05). Conclusion:The MU/Gy in the plans increased with the T stage of NPC, and the D98% of PGTV was more significantly affected by the systematic errors induced by the positions of MLC leaves. After the systematic errors induced by the positions of MLC leaves were introduced into the VMAT plans, doses to patients with T 4 stage NPC changed more significantly than those to patients with other T stages of NPC. Therefore, stricter quality control of leaf positions is required for patients with T 4 stage NPC, and it is recommended that the systematic errors should be less than 0.42 mm.

Objective: To investigate the inhibitory effect of AKR1B10 inhibitor combined with sorafenib on hepatocellular carcinoma (HCC) xenograft growth. Methods: HepG2 xenograft model was established in nude mice. The mice were then randomly divided into four groups: control group, epalrestat monotherapy group, sorafenib monotherapy group and combination treatment group. Tumor volume, tumor weight, T/C ratio and the change in body weight of nude mice in each group were compared to evaluate the curative effect. Immunohistochemistry staining was used to detect the expression of Ki-67 in tumor tissues to evaluate the proliferation status of tumor cells. One-way analysis of variance was used to compare the differences between the groups. Student’s t-test was used to test means of two groups and chi-square test was used for multiple samples. Results: The differences of the grafted tumor volume before and after treatment between the control group, epalrestat group, sorafenib group and combined therapy group was 238.940 ± 39.813, 124.991 ± 84.670, -26.111 ± 11.518, and -54.072 ± 17.673(mm³), respectively, (F = 37.048, P < 0.001). The tumor mass were 0.273 ± 0.140, 0.158 ± 0.078, 0.079 ± 0.054, 0.045 ± 0.024 (g), (F = 16.594, P < 0.001); T/C ratio were 100%, 57.9%, 28.9%, 16.5%, and Ki-67 positive rate were 23.295 ± 6.218, 13.503 ± 3.392, 7.325 ± 2.257, 4.664 ± 1.189 (%), (χ² = 822.203, P < 0.001) . The tumor volume (t = -3.579, P = 0.002) and Ki-67 positive rate (t = -10.003, P < 0.001) in epalrestat monotherapy group were significantly lower than control group. The tumor volume (t = 2.056, P = 0.025), tumor mass (t = 2.101, P = 0.043), and Ki-67 positive rate (t = -2.850, P = 0.005) in combination treatment group were significantly lower than sorafenib monotherapy group. Compared with the control group, the body weight of nude mice in the treatment group decreased to a certain extent, but there was no statistically significant difference between epalrestat monotherapy group and control group (t = -1.599, P = 0.262), and combined therapy and sorafenib monotherapy group (t = -0.051, P = 0.96). Conclusion AKR1B10 inhibitor enhanced the inhibitory effect of sorafenib on hepatocellular carcinoma xenograft.