The photoluminescence (PL) properties of Si-doped cubic GaN with different carrier concentrations were investigated at room temperature. The epilayers were grown on GaAs (001) by radio-frequency molecular-beam epitaxy. It was found that when the carrier concentration is increased from 5×1015 to 2×1018 cm−3, the PL peak shifted towards low energy, from 3.246 to 3.227 eV, and the PL linewidth increased from 77.1 to 121 meV. The PL peak shift is explained by the band gap narrowing effect due to the high doping concentration. The PL linewidth includes two parts: one is doping concentration independent, which is caused by the imperfection of samples and phonon scattering; the other is doping concentration dependent. We assign the second part to the broadening by the microscopic fluctuation of the doping concentration. The experimental measurements are in good agreement with the model.
ABSTRACT. The objective of this paper was to identify hub genes and pathways associated with retinoblastoma using centrality analysis of the co-expression network and pathway-enrichment analysis. The coexpression network of retinoblastoma was constructed by weighted gene co-expression network analysis (WGCNA) based on differentially expressed (DE) genes, and clusters were obtained through the molecular complex detection (MCODE) algorithm. Degree centrality analysis of the co-expression network was performed to explore hub genes present in retinoblastoma. Pathway-enrichment analysis was performed using the Kyoto Encyclopedia of Genes and Genomes (KEGG) database. Validation of hub gene expression in retinoblastoma was performed by reverse transcription-polymerase chain reaction (RT-PCR) analysis. The coexpression network based on 221 DE genes between retinoblastoma and normal controls consisted of 210 nodes and 3965 edges, and 5 clusters of the network were evaluated. By assessing the centrality analysis of the co- (2015) expression network, 21 hub genes were identified, such as SNORD115-41, RASSF2, and SNORD115-44. According to RT-PCR analysis, 16 of the 21 hub genes were differently expressed, including RASSF2 and CDCA7, and 5 were not differently expressed in retinoblastoma compared to normal controls. Pathway analysis showed that genes in 2 clusters were enriched in 3 pathways: purine metabolism, p53 signaling pathway, and melanogenesis. In this study, we successfully identified 16 hub genes and 3 pathways associated with retinoblastoma, which may be potential biomarkers for early detection and therapy for retinoblastoma.
ABSTRACT. The aim of this study was to investigate the expression of AIB1 in human esophageal squamous cell carcinoma and its correlation with Ki67 expression. The immunohistochemical method streptavidinperosidase was used to analyze the expression of AIB1 and Ki67 in specimens from 60 patients with esophageal squamous cell carcinoma and in 20 control individuals with normal esophageal tissue. Expression correlation, clinical significance, and relationships between the two groups were determined. In the 20 individuals with normal esophageal mucosa cells, AIB expression was primarily detected at low levels in the nucleus or not at all, whereas 41.6% of specimens from individuals with esophageal squamous cell carcinoma exhibited high levels of AIB1 expression (P < 0.05). Furthermore, overexpression of AIB1 was observed more frequently in carcinoma specimens with late T stages (T3/ T4) and lymph node metastases (P < 0.05). No significant differences were observed in AIB1 expression by gender, age, or pathological type (P < 0.05). Comparatively, the rate of positive expression of Ki67 In esophageal squamous cell carcinoma specimens was 65.0% (39/60) (P < 0.05). Of these, 29 specimens exhibited simultaneous expression of AIB1, 25 of which demonstrated AIB1 overexpression; expression of AIB1 and Ki67 was positively correlated (P < 0.01). In summary, the results from this study suggested that AIB1 protein expression was associated with the T stage and lymph node metastasis in esophageal squamous cell carcinoma, and that Ki67 might play a role in the AIB1 non-steroid receptor pathway.
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