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Objective To explore the diagnostic value of SPECT/CT on fracture healing.Methods A total of 28 patients (13 males,15 females; average age 45.3 years) with fracture were enrolled.All underwent metal fixation.SPECT/CT scans were performed at least 6 months after the metal fixation.X-ray examination before SPECT/CT showed equivocal fracture healing.The fracture delayed union or nonunion were judged by degree of uptake as well as uptake pattern around fracture site.Final diagnosis was confirmed by surgery or follow-up X-ray film.Results Among 28 patients,15 showed delayed union (confirmed by follow-up),and 13 showed nonunion (confirmed by surgery).There were 13 screws in 6 patients showed abnormal uptake,suggesting screw loose (confirmed by surgery).Conclusions SPECT/CT imaging could be of clinical significance in assessing fracture healing.
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Objective To detect the chromosomal aberration in the cells of renal carcinoma and to evaluate the rela-tionship between the chromosomal aberration and development of renal carcinoma.Methods CGH technology was used to analyze the global genomic aberration in cancer cells from 12 patients with renal carcinoma.Results All of 12 cases deeeted by CGH showed chromosomal aberrations.The common extension regions of renal carcinoma were 1p,4p,5q,7p,9p and 16p.The common deletion regions of renal carcinoma were 3q,4q,6q,9q,14q and 18q.Conclusion The hereditary material of renal carcinoma is unbalanced.The extension and/or deletion of chro-mosome may facilitate the occurrence of renal carcinoma.
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In order to investigate the expression of leukemia inhibitory factor (LIF) in airway epithelial tissues of normal and asthmatic rats, the influence of dexamethasone and the role of LIF in pathogenesis of asthma, 30 Sprague-Dawley (SD) rats were randomly divided into 3 groups (10 for each group): normal group, asthma model group, and dexamethasone-interfered group. In asthmamodel group and dexamethasone-interfered group, asthma rat models were established by intraperitoneal (i.p.) injection of 10% ovalbumin (OVA) and challenge with 1% OVA via inhalation. Rats in dexamethasone-interfered group were pretreated with dexamethasone (2 mg/kg, i.p) 30 min before each challenge. The expression of LIF protein in lung was detected by immunohistochemistry. The results showed that LIF protein was mainly expressed in cytoplasm of bronchial epithelial cells. The expression of LIF protein in the airway epithelial tissue of asthma model group was significantly higher than that in normal group and dexamethasone-interfered group (P＜0.01), but there was no significant difference between normal group and dexamethasone-interfered group (P＞0.05). It was concluded that the expression of LIF was increased significantly in the airway epithelial tissue of the asthma rats, and dexamethasone could down-regulate the expression of LIF. It was suggested that LIF might play an important role in the pathogenesis of asthma as an inflammation regulator.
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The expression of interleukin-17 (IL-17) in lung and peripheral blood of asthmatic rats and the influence of dexamethasone, and the role of IL-17 in the pathogenesis of asthma were inves-tigated. Thirty Sprague-Dawley (SD) adult rats were randomly divided into three groups (n=10 in each group): normal group, asthmatic group, and dexamethasone-interfered group. Rat asthmatic model was established by intraperitoneal (I.p.) injection of 10% ovalbumin (OVA) and challenge with 1% OVA via inhalation. Rats in dexamethasone-interfered group were pretreated with dexa-methasone (2 mg/kg, I.p.) 30 rain before each challenge. The expression of IL-17 protein in serum and bronchoalveolar lavage fluid (BALF) was detected by ELISA. The expression of IL-17 mRNA in peripheral blood mononuclear cells (PBMC) and BALF cells was semi-quantitatively detected by RT-PCR. The expression of IL-17 protein in serum and BALF of asthmatic rats was significantly elevated as compared with normal rats and dexamethsone-interfered rats (P<0.01), and there was sig- nificant difference between normal rats and dexamethsone-interfered rats (P<0.05). The expression of IL-17 mRNA in PBMC and BALF cells of asthmatic rats was markedly increased as compared with normal rats and dexamethsone-interfered rats (P<0.01), and significant difference was found between normal rats and dexamethsone-interfered rats (P<0.05). It was concluded that the expression of IL-17 was increased significantly in asthmatic rats and could be inhibited partly by dexamethasone, sug-gesting that IL-17 might play an important role in the pathogenesis of asthma as an inflammation regulation factor.
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The transcription activity of ectogenic human carcinoembryonic antigen (CEA) promoter in lung adenocarcinoma cells A549 was investigated for the further gene-targeting therapy. The reporter gene green fluorescent protein (GFP) driven by CEA promoter and human cytomegalovirus (CMV) promoter were relatively constructed and named plasmid pCEA-EGFP and pCMV-GFP respectively. The intensity of fluorescence was detected by fluorescence microscope and flow cytometry analysis after the pCEA-GFP and pSNAV-GFP plasmids were transfected into A549 cells through liposome respectively. The results showed (4.08+/-0.63) % of the A549 cells transfected with pCEA-AFP plasmid expressed, significantly lower than that of the A549 cells transfected with pCMV-GFP [(43.27+/-3.54) %]. It was suggested that ectogenic human CEA promoter in lung adenocarcinoma cells A549 was weakly expressed. The distinct specificity of CEA promoter in CEA high expression cells was regarded as a tool in selective gene therapy, but the transcription activity of ectogenic human CEA promoter was needed to increase in the future.
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The transcription activity of ectogenic human carcinoembryonic antigen (CEA) promoter in lung adenocarcinoma cells A549 was investigated for the further gene-targeting therapy. The reporter gene green fluorescent protein (GFP) driven by CEA promoter and human cytomegalovirus (CMV) promoter were relatively constructed and named plasmid pCEA-EGFP and pCMV-GFP respectively. The intensity of fluorescence was detected by fluorescence microscope and flow cytometry analysis after the pCEA-GFP and pSNAV-GFP plasmids were transfected into A549 cells through liposome respectively. The results showed (4.08±0.63) % of the A549 cells transfected with pCEA-AFP plasmid expressed, significantly lower than that of the A549 cells transfected with pCMV-GFP [(43.27±3.54) %]. It was suggested that ectogenic human CEA promoter in lung adenocarcinoma cells A549 was weakly expressed. The distinct specificity of CEA promoter in CEA high expression cells was regarded as a tool in selective gene therapy, but the transcription activity of ectogenic human CEA promoter was needed to increase in the future.