Objective To investigate the expression of aquaporin-1（AQP-1） on pleura in rats with carrageenan-induced pleural effusion and explore the role of AQP-1 in effusion formation.Methods Fifty-six healthy Wistar rats were randomly divided into a normal control group and 6 pleuritis groups（6，12，24，36，48 and 72 h groups respectively）.The rat model of inflammatory pleurisy was induced by injecting l-Carrageenan into the pleural cavity.The expression of AQP-1 on pleura was detected with immunohistochemistry.The mRNA and protein expression of AQP-1 on visceral pleura and parietal pleura were measured by RT-PCR and Western blot assay respectively.The volume of pleural effusions were measured.Results The volume of pleural effusion was 2.10±0.22，4.10±0.15，4.40±0.36，3.20±0.27，2.60±0.18，0.12±0.02 mL in the 6，12，24，36，48 and 72 h pleuritis groups respectively.AQP-1 were mainly expressed on visceral and parietal pleural mesothelial cells and capillary endothelial cells，and significantly increased in all pleuritic rats The mRNA and protein expression of AQP-1 on parietal pleura increased after 6 h and reached peak level at 24 h in pleuritic groups.The mRNA and protein expression of AQP-1 on visceral pleura increased after 12 h and reached peak level at 24 h in pleuritic groups.The expression of AQP-1 on parietal pleura at 12 h and 24 h in pleuritic groups was correlated positively with the volume of pleural effusion（r=0.857，r=0.846，all Plt;0.01）.The expression of AQP-1 on visceral pleura at 24 h in pleuritic groups was positively correlated with the volume of pleural effusion（r=0.725，Plt;0.05）.Conclusion The expression of AQP-1 on pleura were increased in rats with e carrageenan-induced pleural effusion.AQP-1 may play a role in pleural fluid transportation in pleural effusion.
Objective To investigate the expression of aquaporin-1( AQP1 ) in visceral and parietal pleura in SD rats and to examine the effect of AQP1 on pleural fluid turnover. Methods Five groups( n = 24 ) of SD rats were randomly assigned to received intrapleural injection of dexamethasone,lipopolysaccharide, erythromycin, hypertonic saline and normal saline, respectively. The AQP1 protein in pleural was detected with immunohistochemistry. The mRNA expression of AQP1 under stimulations at different time points was measured by real time RT-PCR. Results AQP1 was immunolocalized predominantly to the microvessels and mesothelial cells of visceral and parietal pleura. The extent of AQP1expression in parietal pleura was less than that in visceral pleura[ ( 4. 14 ±1. 12) ×104 copy /μg vs ( 7. 43 ±2. 02) ×104 copy / μg, P lt;0. 05] . AQP1 expression increased at all phases in the dexamethasone group andthe hypertonic saline group, whereas decreased in the erythromycin group and the lipopolysaccharide group.Conclusion The stimulations of dexamethasone, lipopolysaccharide, erythromycin and hypertonic saline can significantly change the AQP1 expression in pleura, which indicate that AQP1 may contribute to the accumulation and clearance of pleuritic fluids.
Objective To compare the effects of heparin versus urokinase injection intrapleurally in the management of pleural thickening and adhesion due to tuberculous exudative pleurisy. Methods Sixty patients with tuberculous pleurisy were allocated into three groups randomly. Sodium heparin ( heparin group) , urokinase ( urokinase group) , and 0. 9% saline ( control group) were intrapleurally injected respectively. The concentrations of fibrinogen and D-dimer in pleural effusion were measured before and after the injection. The duration of absorption and the total drainage volume of pleural effusion were recorded. The pleural thickness and adhesion were observed two months after the injection. Results In 72 hours after the intrapleural injection, the concentration of fibrinogen( g/L) in the pleural effusion was significantly increased in the heparin group( 1. 13 ±0. 44 vs 0. 34 ±0. 19, P lt; 0. 001) , and significantly decreased in the urokinase group( 0. 25 ±0. 16 vs 0. 38 ±0. 15, P lt; 0. 05) when compared with baseline. Concentrations of D-dimer in the pleural effusions were significantly higher than those at baseline in both the heparin group and the urokinase group( 57. 0 ±17. 6 vs 40. 0 ±15. 4, P lt; 0. 05; 74. 5 ±16. 4 vs 43. 8 ±14. 9, P lt; 0. 001) . There were no significant differences in the absorption duration of pleural effusion among the three groups( P gt;0. 05) . The total drainage volume of pleural effusion was higher in the heparin group and the urokinase group compared to the control group( P lt;0. 01) . And the total volume of pleural effusion was significantly higher in the heparin group and the urokinase group than that in the control group( 2863 mL and 2465 mL vs 1828 mL,P lt;0. 01) . Two months after the intervention, the pleura were thinner[ ( 1. 37 ±0. 82) mm and ( 1. 33 ±0. 85) mmvs ( 3. 06 ±1. 20) mm, P lt; 0. 01] and the incidence of pleural adhesion was significantly lower[ 15% and 20% vs 50% , P lt; 0. 05] in the heparin and the urokinase groups than those in the control group.Conclusion Intrapleural heparin has similar effects with urokinase for prevention pleural thickness andadhesion in tuberculous pleurisy with good availability and safety.
Objective To evaluate the clinical, radiological and pathological manifestations of lipoid pneumonia, to improve the diagnosis of this rare disease. Methods Retrospective analysis of clinical data of 19 cases with confirmed lipoid pneumonia was conducted. Results There was 13 male and 6 female patients with an average age of 54. 4 years ranging from 24 to 71 years. Lipoid pneumonia presented a chronic clinical course with few physical signs. The main complaints included cough, expectation, bloody phlegmand chest pain. Finding of chest mass in routine physical examination was also a common reason for doctor visiting. Radiological features of lipoid pneumonia could be non-specific, usually presenting mass shadow in the chest, with lymph nodes enlargement in some cases. Eighteen cases were diagnosed by the histopathology of pulmonary tissue and one case was diagnosed through a combination of bronchoscopy, thoracoscopy and CT-guided percutaneous lung puncture biopsy. Histopathological finding showed accumulation of foamy macrophages in the alveolar spaces. Conclusions The clinical and radiological manifestations of lipoid pneumonia are non-specific. Histopathological examination for diagnosis is essential. If the medical therapy is not responsive, pulmonary lobectomy might be necessary.
Objective To measure the level of circulating endothelial progenitor cells ( EPCs) in peripheral blood of patients with acute exacerbation of chronic obstructive pulmonary disease ( AECOPD) , and to explore the relationship between EPCs and severity markers of the disease and cardiovascular adverse outcome predictors.Methods Forty patients with COPD were recruited, including 27 at acute exacerbation phase and 13 with stable COPD from December 2010 to December 2011. Sixteen healthy nonsmokers were included as controls. Circulating EPCs were isolated by Ficoll density-gradient centrifugation and purified by Magnetic Activated Cell Sorting system. High-sensitivity C-reactive protein ( hsCRP) was estimated by using a latex immunoturbidimetric assay kit, and matrix metalloproteinase-9 ( MMP-9) was measured by enzymelinked immunosorbent assay ( ELISA) . Arterial blood gas analysis and echocardiograph were performed in the AECOPD patients. The correlations between circulating EPCs, lung function, and cardiovascular markers were investigated. Results Circulating EPCs were significantly lower in AECOPD and stable COPD patients compared with the healthy controls [ ( 5.1 ±2.6) ×103 /mL and ( 6.0 ±3.2) ×103 /mL vs. ( 9.0 ±4.3) × 103 /mL, Plt;0. 05] . EPCs had a weak correlation with hsCRP ( P = 0. 033) , but not with MMP-9. In the AECOPD patients, EPC counts were significantly inversely correlated with PASP ( pulmonary artery systolic pressure) and NT-proBNP ( amino-terminal pro-brain natriuretic peptide) levels, and positively with left ventricular ejection fraction. No correlations were found between EPCs and lung function, blood gas, hospital stays or smoking index. Conclusions Circulating EPCs were significantly lower in AECOPD patients compared with healthy controls, in which systemic inflammation might be involved. Decreased EPCs were correlated with cardiac dysfunction in patients with AECOPD, which may account for the increased cardiovascular risk in this population.
Objective To investigate the value of tumor type M2 pyruvate kinase ( M2-PK) in the differential diagnosis of pleural effusion. Methods A total of 146 patients with pleural effusion during January 2006 to December 2008 were recruited at the department of respiratory medicine of the Shantou Affiliated Hospital and the First Affiliated Hospital of Sun Yat-sen Medical College. Pleural effusion was malignant in 72 cases ( 52 cases with lung cancer and 20 cases with metastatic lung cancer) and benign in 74 cases ( 54 cases with infective pleural effusion and 20 with transudation effusion) . The patients were divided into a malignant pleural effusion group, an infective pleural effusion group, and a transudation group.Then the infective group was further divided into subgroups of tuberculosis pleural effusion group andparapneumonic effusion group. The concentration of tumor M2-PK in pleural fluid obtained during the first thoracocentesis was measured by enzyme-linked immunosorbent assay( ELISA) . Results The concentration of tumor M2-PK was significantly higher in the malignant pleural effusion group compared with the benignpleural effusion groups ( P lt; 0. 01) . Significant differences were also found in the concentration of tumor M2-PK between malignant pleural effusion caused by lung cancer and metastatic lung cancer( P lt; 0. 05) .When the cutoff value of tumor M2-PK was set at 18. 68 U/mL, the sensitivity, specificity, and accuracy for the diagnosis of malignant pleural effusion was 87. 6% , 86. 0% , and 87. 4%, respectively. Furthermore,the detection of tumor M2-PK in combination with CEA showed better diagnostic sensitivity( 96. 0% ) ,specificity ( 85. 0% ) , and accuracy ( 91. 1% ) . Conclusions The detection of tumor M2-PK in pleural effusion is of some clinical significance in the differential diagnosis of benign and malignant pleural effusion.The detection of tumor M2-PK in combination with CEA is a good diagnostic tool with high sensitivity andspecificity.
Objective To investigate the depression status，score of asthma control test (ACT) and quality of life in asthma patients before and after health care education according to Global Initiative for Asthma guidelines.Methods 59 enrolled outpatients with asthma were asked to self-administer the CES-D (center for epidemiologic studies-depression) scale，ACT scale and the quality of life (QOL) questionnaire respectively.All the patients were educated and treated by health care professionals under the guidance of GINA 2004.After average of 2.5 months ± 15 days，they were asked to self-administer all the scales and questionnaire mentioned above once again on return visit.The data was collected and analyzed statistically based on whether or not the patient had depression according to the CES-D score and the data before and after the education was compared statistically.Results （A）40.7% (24/59) of the patients had depression emotion before guided treatment，and after that the percentage significantly decreased to 13.6% (8/59) (Plt;0.05).（B）Comparing the depressive and non-depressive groups，there was significant difference in 3 of 5 domains in QOL excluding limitation of activity and self concern about health (Plt;0.05) before guided treatment.While on return visit 3 domains in QOL excluding limitation of activity and psychologic status had shown a significant difference (Plt;0.05).There was no significant difference in ACT score before guided treatment，while wise versa after that (Plt;0.05).（C）Before guided treatment the depression status was inversely correlated with 3 in 5 domains of QOL (symptoms of asthma，psychologic status and response to irritant)，as well as QOL as a whole (Plt;0.05)，but not with the other two domains of QOL scale and ACT score.After guided treatment，the depression status had inverse correlation with QOL and 3 in 5 domains of QOL scale (excluding limitation of activity and psychologic status) (Plt;0.05)，as well as ACT score (Plt;0.05).Conclusions The symptoms of asthma and response to irritants are common factors that influence the depressive emotion in asthma population.While psychologic status and self concern about health are both important factors that can not be overlooked.Health care education is important for asthma patients in view of appropriate treatment，symptom control and relief of depression emotion.
目的 研究无创通气(NIPPV)治疗对肾移植术后巨细胞病毒(CMV)肺炎患者的疗效。方法 1998年1月~2005年12月间入住中山大学附属第一医院内科重症监护病房(MICU)的78例肾移植术后CMV肺炎患者，根据是否接受无创通气治疗而分为非NIPPV组和NIPPV组，比较两组患者在接受有创机械通气比例、病死率、住院时间及并发症等方面的差异。对52例NIPPV组患者，比较无创通气治疗前后生命体征及血气分析指标的变化。结果 NIPPV组与非NIPPV组相比，接受有创机械通气比例(30.8％ 比80.8％)、医院获得性肺炎发生率（32.7％ 比61.5％)及病死率(30.8％ 比57.7％)较低，两组比较均有显著性差异(P均lt;0.05)；而住院时间、气压伤发生率无显著差异。NIPPV组患者无创通气治疗后患者呼吸频率有所减慢，动脉血pH值逐渐降低，PaCO2水平缓慢上升，PaO2、PaO2 ／FiO2及SaO2明显升高，两组比较均有显著差异(P均lt;0.05)。而无创通气治疗前后心率、血压的变化则无明显规律。结论 NIPPV治疗能够改善肾移植术后CMV肺炎患者的低氧血症，缓解呼吸窘迫症状，降低有创机械通气治疗比例及医院获得性肺炎的发生率，从而降低病死率。用无创通气治疗巨细胞病毒肺炎值得在临床上推广使用。
ObjectiveTo investigate the clinical features of primary tracheal or pulmonary malignant glomus tumor (MGT).MethodsA patient with primary tracheal MGT was reported. Wanfang, CNKI, Embase, Ovid, Cochrance and PubMed databases were searched with key words "tracheal malignant glomus tumor" and " pulmonary malignant glomus tumor” both in English and in Chinese for literature of primary tracheal or pulmonary MGT. Their clinical manifestations, imaging findings, bronchoscopic findings, pathological findings, especially immunohistochemical characteristics, diagnosis and differential diagnosis, treatment, and prognosis of primary tracheal or pulmonary MGT were summarized.ResultsThis male patient who manifested as cough, chest tightness, shortness of breath and dyspnea was diagnosed as tracheal MGT and received a treatment of radiofrequency ablation and cryotherapy under bronchoscopy. He refused to receive the chemotherapy and died after two months with a lung metastases. A total of 17 cases of primary tracheal or pulmonary MGT were retrieved in 16 articles, of which 5 were primary in the trachea and 12 were primary in the lung. Their clinical manifestations, imaging findings, and bronchoscopic findings were non-specific. The diagnosis relied on pathology, especially immunohistochemical staining. The preferred treatment of tracheal MGT may be surgical resection, the prognosis was acceptable. Treatment of lung MGT included lobectomy or airway interventional treatment and its prognosis was poor. The treatment of primary tracheal or pulmonary MGT needed early treatment. Because the curative effect of airway interventional treatment and chemotherapy was dubious, surgical plan should be first considered.ConclusionsBoth of primary tracheal and primary pulmonary MGT are rare. They usually lack specific clinical manifestations, laboratory tests, and imaging, and are easy to be misdiagnosis or miss diagnosis. The diagnosis can be confirmed by the results of biopsy for pathological analysis, especially by the immunohistochemical staining analysis. The treatment of tracheal and pulmonary MGT need further study.