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Radiation medicine, one of the clinical medicine majors, is mainly engaged with the cultivation of special talents for radiotherapy, nuclear medicine, diagnosis and management of radiation occupational diseases, radiation protection, and medical emergency for nuclear accident. By 2022, there have been a total of 9 universities in China where undergraduate talents in radiation medicine are cultivated. Based on the demand for radiation medicine talents and the developmental trend in disciplines in China, this paper analyzes the deficiencies in the discipline status, discipline construction and teaching staff of radiation medicine. It also suggests the construction of a nation-wide organization for the radiation medicine talent training to improve the major status, the establishment of the new medicine development concept in consistency with the developmental trend of interdisciplinary integration, the building of high-quality educational resources of radiation medicine based on internet technology, and the improvement of grassroots teaching institutions, so as to adapt to the development of radiation medicine in the future.
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Objective:To construct a random forest classification model of DNA double strand breaks (DSB) induced by ionizing radiation and investigate the genome-wide distribution of DSB.Methods:The GRCh38 reference genome was divided into 50 kilobase fragments. Then these genomic fragments were separated into low-level or high-level regions of ionizing radiation-induced DSB according to the sequencing data of MCF-7 cells. The data of eight epigenetic features were used as input. Two thirds of the data were randomly assigned to the training set, and the rest of the data was assigned to the test set. A random forest classification model with 100 decision trees was constructed. The importance of epigenetic features in the classification model was analyzed and displayed.Results:The accuracy score of the random forest classification model on the test set was 99.4%, the precision score was 98.9% and the recall score was 99.9%. The area under the receiver operating characteristic curve was 0.994. Among the eight epigenetic features, H3K36me3 and DNase markers were the most important variables. The enrichments of the two markers in DSB high-level regions were much higher than those in DSB low-level regions.Conclusions:The random forest classification model could precisely predict the genome-wide levels of DSB induced by ionizing radiation in the 50 kilobase window based on epigenetic features. Analysis revealed that these DSB might primarily distribute in the actively transcribed sites in the genome.
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Objective To investigate the effects of titanium dioxide ( TiO2 ) nanoparticles coupled with nuclear localization sequence ( NLS ) on the radiosensitivity of U251 glioma cells. Methods Synthesis and characterization of the TiO2-NLS nanoparticles with nuclear targeting property. U251 cells were treated with nanoparticles and/or ionizing radiation. Flow cytometry analysis was performed to measure the ROS content and the cell apoptotic percentage. The DNA damage was detected by using γ-H2AX foci staining. Clonogenic survival assay was used to evaluate the radiosensitivity of U251 cells. Results NLS modification promoted nuclear translocation of TiO2 nanoparticles. Compared with the control nanoparticles, TiO2-NLS treatment increased radiation-induced cell apoptosis (t=8. 96, P<0. 05). Clonogenic survival assay showed the radiosensitization ratios of TiO2 nanoparticle-treated group and TiO2-NLSnanoparticle-treated group were 1. 18 and was 1. 29, respectively. These two ratios had statistically difference ( t =14. 72, P< 0. 05). Conclusions Nuclear targeting TiO2 nanoparticles enhances the radiosensitivity of U251 glioma cells.
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Objective To evaluate the clinical efficacy of thoracoscopic surgery combined with chemorad-iotherapy in patients with N2 stage ⅢA non-small cell lung cancer (NSCLC). Methods 40 patients (study group) received thoracoscopic surgery and another 40 patients (control group) received traditional thoracotomy. Combination therapy with navelbine and cisplatin were postoperatively administered for four cycles and one cycle lasted for 3 weeks. 7 to 14 days after chemotherapy , sequential conformal radiotherapy were delivered. The one-year survival and two-year survival rates , duration of tatal treatment , and adverse reactions were compared between the two groups. Results In the study group, duration of total treatment time and time to postoperative chemotherapy were significantly shorter (χ2=9.45,P=0.002 andχ2=41.324, P=0.000), and the KPS score was significantly higher (χ2 = 15.118,P = 0.002). No significant differences were found between the two groups in bone marrow suppression,gastrointestinal reactions,and one- or two-year survival rate. Conclusions As compared with conventional surgery,post-thoracoscopic surgery sequential chemoradiotherapy for patients with N2 stage ⅢA NSCLC could achieve a better efficacy with less surgical trauma , shorter hospital stay , faster recovery , and shorter time to postoperative chemotherapy and total treatment duration;it is worth further researching and popularizing.
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<p><b>OBJECTIVE</b>To identify specific serum glycoprotein profiles that correspond to the carcinogenic process of primary liver cancer (PLC) by analyzing a population with high-incidence of PLC using lectin affinity microarray.</p><p><b>METHODS</b>Serum samples were collected from individuals classified as high risk for PLC (including patients with liver cirrhosis and hepatitis B) and development of PLC was recorded. Healthy individuals served as normal controls. The serum samples were subjected to glycoprotein profling by using lectin microarrays and the results were confirmed by lectin blot. Between-group differences were statistically analyzed.</p><p><b>RESULTS</b>PLC carcinogenesis was found to be correlated with enhanced affinity for AAL, ACL, ConA, LCA, MPL, NML, PHA-E, PHA-L, PSA, RCA-I, STL, VAL,WGA, and SNA (P less than 0.05). These data implied that changes in specific glycan structures, such as aFuc, GlcNAc, GalNAc, mannose, bisecting GlcNAc and terminal beta1-4 Gal, may be involved in PLC carcinogenesis . The PLC group showed significantly different results for all detected lectins, except SNA (P less than 0.05). However, among the PLC group, the SNA affinity was not significantly different for the hepatitis B group (P =0.443, P more than 0.05).</p><p><b>CONCLUSION</b>Glycans may be associated with the carcinogenic process of PLC and may be developed as diagnostic and prognostic biomarkers of PLC in the future.</p>
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Humans , Carcinogenesis , Chromatography, Affinity , Cohort Studies , Glycoproteins , Blood , Lectins , Blood , Liver Neoplasms , Blood , PathologyABSTRACT
OBJECTIVE: Angiopoietin-1 (Ang1) is a potent angiogenic factor that can increase synovial angiogenesis and also enhance osteoblast maturation and bone formation. However, its role in rheumatoid arthritis (RA) has not been well documented. Thus, we investigated roles of Ang1 in collagen-induced arthritis (CIA). METHODS: A recombinant adenovirus carrying the gene that encodes either cartilage oligomeric matrix protein (AdCOMP)-Ang1 (a modified form of Ang1) or LacZ (AdLacZ) was injected intravenously into CIA mice. Clinical, radiological, histopathological, and immunofluorescent analyses were performed. Serum levels of receptor activators of nuclear factor kappaB ligand (RANKL) and osteoprotegerin (OPG) and expression of osteoblast maturation genes were analyzed. RESULTS: AdCOMP-Ang1-injected mice developed more severe inflammation than the AdLacZ-injected mice. However, there were no significant differences in cartilage damage and bone erosion. More PECAM-1-positive blood vessels were seen in the synovium of the AdCOMP-Ang1-injected mice than in those injected with AdLacZ. Interestingly, a lower number of TRAP-positive osteoclasts were observed in AdCOMP-Ang1-injected CIA mice than in the AdLacZ group when comparing sections obtained from joints showing similar synovial proliferation. The serum OPG/RANKL ratio and expression of osteoblast maturation genes, such as runt-related transcription factor 2, bone sialoprotein, type 1 collagen, osteopontin, and osterix, were significantly upregulated in the AdCOMP-Ang1 group. CONCLUSION: COMP-Ang1 facilitates arthritis onset and increases synovial inflammation, but enhances osteoblast maturation, which in turn inhibits osteoclastogenesis by increasing the OPG/RANKL ratio in CIA. Our results suggest that careful investigation is necessary to delineate the possible therapeutic use of COMP-Ang1 as an adjunctive agent, in combination with anti-inflammatory therapies, for the prevention of bone destruction in RA.