RESUMO
Objective Study the endobronchial ultrasound features of mediastinal tubercular lymphadenopathy and sarcoidosis to probe a new method for the differential diagnosis. Methods The endobronchial ultrasound features of 74 lymph nodes in 16 mediastinal tubercular lymphadenopathy and 30 sarcoidosis patients diagnosed in our department were studied retrospectively, and the sizes, borders, fusion and echo features of mediastinal tubercular lymphadenopathy were compared to sarcoidosis. Results Both of the long size and the short size of mediastinal tubercular lymphadenopathy were smaller than sarcoidosis [(15.77 ± 4.10) vs (19.76 ± 5.83), t = 3.28, P = 0.021;(12.67 ± 4.09) vs (16.81 ± 5.54), t = 3.56, P = 0.001]. And the following features were statistically significant of tubercular lymphadenopathy as compared to sarcodosis: indistinct borders, fusion of lymph nodes, hyperechoic echotexture and patchy anechoic/hypoechoic areas [50.0% (11/22) vs 17.3% (9/52), χ2 = 8.38, P = 0.004; 18.2%(4/22) vs 0.0% (0/52), P = 0.008; 50.0% (11/22) vs 0.0% (0/52), P = 0.000; 63.6% (14/22) vs 0.0% (0/52), P = 0.000, respectively). However, there was no significant difference in the existence of central hilar structure [9.1% (2/22) vs 19.2% (10/52), P = 0.491] between mediastinal tubercular lymphadenopathy and sarcoidosis. Conclusions The endobronchial ultrasound features of mediastinal lymph nodes, including sizes, borders, fusion, hyperechoic echotexture and patchy anechoic/hypoechoic areas are helpful in the differential diagnosis of mediastinal tubercular lymphadenopathy and sarcoidosis.
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The purpose of this study was to investigate the changes of protein kinase Calpha (PKCalpha) and cyclin D1 expressions in pulmonary arteries from smokers with normal lung function and smokers with mild to moderate chronic obstructive pulmonary disease (COPD). The peripheral lung tissues were obtained from 10 non-smokers with normal lung function (non-smoker group), 14 smokers with normal lung function (smoker group), 11 smokers with mild to moderate COPD (COPD group). The morphological changes of pulmonary arteries were observed by HE-staining. The expressions of alpha-smooth muscle actin (alpha-SMA), proliferating cell nuclear antigen (PCNA), PKCalpha and cyclin D1 proteins in pulmonary artery smooth muscle cells (PASMCs) were immunohistochemically determined. The percentages of PCNA-positive cells were taken as the smooth muscle cells proliferation index (PI). The mRNA expressions of PKCalpha and cyclin D1 in PASMCs were evaluated by real-time fluorescence PCR. Morphometrical analysis showed that the ratio of pulmonary artery wall area to total area (WA%) in smoker group and COPD group was significantly greater than that in non-smoker group (P<0.01). The PASMCs proliferation index in smoker group and COPD group was significantly higher than that in nonsmoker group (P<0.01). The protein levels of PKCalpha and cyclin D1 in PASMCs were significantly increased in smoker group and COPD group as compared with non-smoker group (P<0.01). The mRNA expressions of PKCalpha and cyclin D1 in PASMCs were significantly elevated in smoker group and COPD group as compared with non-smoker group (P<0.01). Significant correlations were found between PKCalpha protein and WA% or PI (P<0.01). Correlations between cyclin D1 protein and WA% or PI also existed (P<0.01). The expression of PKCalpha was positively correlated with the expression of cyclin D1 at both protein and mRNA levels (P<0.01). In conclusion, increased expressions of PKCalpha and cyclin D1 might be involved in the pathogenesis of abnormal proliferation of PASMCs in smokers with normal lung function and smokers with mild to moderate COPD.
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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.
RESUMO
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.
RESUMO
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.