ABSTRACT
Closure of bronchopleural fistula remains a difficult challenge for clinicians. Although several therapeutic approaches have been proposed, the clinical results are commonly unsatisfactory. Previous reports have indicated that autologous mesenchymal stem cells (MSCs) are useful for aiding treatment of bronchopleural fistula. We report here the use of umbilical cord MSCs to effect the successful closure of a bronchopleural fistula (5 mm) in a 33-year-old woman 6 months after a lobectomy. A review of the relevant literature is included. The use of MSCs may be a promising therapeutic method for the closure of bronchopleural fistula. Randomized controlled trials with larger samples are required.
Subject(s)
Bronchial Fistula/therapy , Mesenchymal Stem Cell Transplantation/methods , Mesenchymal Stem Cells/cytology , Pleural Diseases/therapy , Pneumonectomy/adverse effects , Adult , Bronchial Fistula/diagnosis , Bronchoscopy , Female , Fistula/diagnosis , Fistula/therapy , Humans , Injections , Pleural Diseases/diagnosis , Postoperative Complications/therapy , Tomography, X-Ray ComputedABSTRACT
BACKGROUND: Location of the affected bronchus of pleural air leaks is the most important step of trans-bronchoscopic bronchial occlusion for the treatment of intractable pneumothorax. The balloon occlusion test is the most commonly used technique, but has failed in some cases. The aim of the present study was: (1) to determine if endo-bronchial end-tidal CO2 (EtCO2) measurement can identify the affected bronchus that is the source of a persistent pleural air leak; and (2) to establish a methodology for endo-bronchial EtCO2 testing in locating affected bronchus in intractable pneumothorax. METHODS: A total of 28 patients with intractable pneumothorax underwent bronchoscopy with (1) the balloon occlusion test for the identification of the affected bronchus; and (2) endo-bronchial EtCO2 measurement (EtCO2 test) at the orifices of the bronchus of the affected lung. The effectiveness of these two methods of affected bronchus identification were compared. The threshold EtCO2 (T-EtCO2) was determined. RESULTS: The positive rates of locating the affected bronchus by the endo-bronchial EtCO2 test, balloon occlusion test, and combination of the two techniques were 60.7% (17/28), 64.3% (18/28) and 96.4% (27/28), respectively. The average differences in EtCO2 between the affected bronchus and the main carina, main bronchus, and non-affected bronchus were (in mmHg) 4.41 ± 1.99 (95% confidence interval: 3.5, 5.3), 4.73 ± 2.10 (3.80, 5.66 ) and 5.57 ± 2.53 (4.45, 6.69), respectively. CONCLUSIONS: (1) The endo-bronchial EtCO2 test is complementary to the balloon occlusion test of the leading bronchus. (2) A threshold (T-EtCO2) value of >5 mmHg is optimal for this technique.
Subject(s)
Breath Tests/methods , Bronchi/metabolism , Bronchoscopy/methods , Carbon Dioxide/metabolism , Pneumothorax/diagnosis , Aged , Biomarkers/metabolism , Breath Tests/instrumentation , Bronchi/physiopathology , Bronchoscopes , Bronchoscopy/instrumentation , Catheters , Humans , Male , Middle Aged , Pneumothorax/metabolism , Pneumothorax/physiopathology , Pneumothorax/therapy , Predictive Value of Tests , Prognosis , Prospective Studies , Reproducibility of ResultsABSTRACT
The aim of the present study was to explore the expression of POLD4 in human lung adenocarcinoma A549 cells under 4-nitroquinoline-1-oxide (4NQO) stimulation to investigate the role of POLD4 in smoking-induced lung cancer. The lung cancer A549 cell line was treated with 4NQO, with or without MG132 (an inhibitor of proteasome activity), and subsequently the POLD4 level was determined by western blot analysis. Secondly, the cell sensitivity to 4NQO and Taxol was determined when the POLD4 expression level was downregulated by siRNA. The POLD4 protein levels in the A549 cells decreased following treatment with 4NQO; however, MG132 could reverse this phenotype. Downregulation of the POLD4 expression by siRNA enhanced A549 cell sensitivity to 4NQO, but not to Taxol. In conclusion, 4NQO affects human lung adenocarcinoma A549 cells by regulating the expression of POLD4.
