Impact of end-expiratory pressure fluctuation on tidal volume in the trilevel positive airway pressure mode.

INTRODUCTION: In noninvasive positive-pressure ventilation (NPPV), the changes in the expiratory positive airway pressure (EPAP) directly affect the magnitude of the tidal volume. OBJECTIVES: This experimental study aims to verify the precise effects of end-expiratory fluctuation on the body tidal volume to better assist NPPV in clinical practice. METHODS: We selected the TestChest-simulated lung simulation of different populations, including healthy subjects (normal group), patients with chronic obstructive pulmonary disease (COPD) with emphysema as their primary phenotype (COPD1 group), and patients with COPD with bronchitis as their primary phenotype (COPD2 group). RESULTS: Regarding the tidal volume curves of the three groups under various conditions, sixfold charts revealed that the tidal volume changed with the end-expiratory pressure fluctuations. In addition, regression coefficients for end-expiratory pressure fluctuations, (IPAP-EPAP) and (IPAP-EEPAP) exhibited a significant contribution to the tidal volume. The two coefficients in the normal, COPD1 and COPD2 groups were 52.294 and 10.414, 46.192 and -8.816, and 11.922 and 17.947, respectively. The circuit simulation results showed that the simulation curve fitted the experimental curve better by changing the coefficient of the descending edge of the expiratory phase. CONCLUSIONS: The study results suggest that the end-expiratory pressure fluctuation affects the body tidal volume. Compared with the bilevel positive airway pressure (PAP), the trilevel PAP provides additional respiratory support to the body during a respiratory difference in initial respiration and descent.

Bronchobiliary fistula following radiofrequency ablation for liver metastases from breast cancer: A case report and literature review.

RATIONALE: Bronchobiliary fistula (BBF) is a rare clinical condition which is characterized by a channel between biliary tract and bronchial tree. BBF can present with fever, dyspnea, and cough. However, it can be easily misdiagnosed as biliary vomiting, dyspnea, or even severe pneumonia. PATIENT CONCERNS: A 53-year-old woman was diagnosed with breast cancer in April 2011 and underwent radical mastectomy and lymph node dissection, chemotherapy, and radiotherapy. Unfortunately, the patient suffered from bone metastasis during the 1st year and liver metastasis during the 2nd year after radical mastectomy. In 2013, the patient underwent transcatheter arterial chemoembolization therapy twice for liver metastasis. The patient was then treated with radiofrequency ablation (RFA) in 2016. Unfortunately, the patient developed a cough with bitter-tasting yellow sputum and chest tightness 2 weeks after the RFA treatment. Approximately 6 months later, the patient still complained of a cough with yellow sputum and persistent chest tightness. The patient was then admitted to our department. DIAGNOSES: The presence of bile in the sputum supported a diagnosis of BBF. Bronchoscopy was performed, and the presence of bile in the lavage fluid confirmed the diagnosis of BBF. INTERVENTIONS: The patient was treated with antibiotics including sulbactam, cefoperazone, levofloxacin and meropenem, was well as hepatoprotectants, nutritional support and other supportive treatments in our department. OUTCOMES: The patient died because of liver failure. LESSONS: This case demonstrates that we should consider the possibility of BBF when patients experience a recurrent cough with discolored sputum after RFA. In particular, a diagnosis of BBF should be considered in patients who do not respond to antibiotic treatment.

Tracing type 1 diabetic Tibet miniature pig's bone marrow mesenchymal stem cells in vitro by magnetic resonance imaging (1).

BACKGROUND: Traditional cell-tracking methods fail to meet the needs of preclinical or clinical research. Thus, the aim of the present study was to establish a new method of double labeling bone marrow mesenchymal stem cells (BMSCs) from type 1 diabetic (T1D) minipigs with super-paramagnetic iron oxide (SPIO) and enhanced green fluorescent protein (eGFP) and tracing them using MRI in vitro. METHODS: Isolated BMSCs from T1D minipigs were labeled with eGFP and different concentrations of SPIO. The effects of lentivirus (LV)-eGFP transfection and SPIO on the viability and growth curves of BMSCs were determined by Trypan blue exclusion, the 3-(4,5-dimethyl-2 thiazoyl)-2,5-diphenyl-2H-tetrazolium bromide assay and flow cytometry. Cellular ultrastructure was evaluated by transmission electron microscopy. Magnetic resonance imaging was used to evaluate BMSCs labeled with SPIO-eGFP complexes 6 weeks after labeling. RESULTS: Expression of eGFP in BMSCs peaked 96 h after transfection with LV-eGFP. Prussian blue staining revealed scattered blue granules in the cytoplasm of SPIO-labeled cells. Transmission electron microscopy revealed that the dense granules aggregated mainly in secondary lysosomes. On MRI, T2* -weighted imaging was far more sensitive for SPIO-labeled BMSCs than other image sequences 3 and 6 weeks after the cells had been labeled with SPIO-eGFP. CONCLUSIONS: We have developed a relatively simple and safe method for double labeling of BMSCs from T1D minipigs using SPIO and LV-eGFP and tracing them in vitro by MRI for 6 weeks.

Predicted lower limit of normal reduces misclassification risk of airflow limitation in asymptomatic elderly never-smokers.

BACKGROUND: It remains controversial what better defines abnormal lung function at the extremes of age. This study aimed to establish new spirometric reference equations for residents in Jinan and compare the most accepted two spirometric definitions of chronic obstructive pulmonary disease (COPD)-a fixed post-bronchodilator ratio of forced expiratory volume in one second to forced vital capacity (FEV1/FVC) below 70% vs. FEV1/FVC < lower limit of normal (LLN)-in an elderly population (age ≥60 years). METHODS: Among 10 002 cases, only never-smokers who had no respiratory symptoms or diagnoses of cardiopulmonary diseases and whose lung function measurements strictly followed the American Thoracic Society guidelines, were included in the statistical analysis. For each gender, prediction equations of FEV1, FVC, FEV1/FVC and corresponding LLN values were developed using multiple regression models. RESULTS: In this cross-sectional study, spirometric reference values were statistically derived from a sample of 1328 healthy never-smokers (672 males, 656 females), age 56-84 years. As expected, age and height were the main predictors for all lung function parameters. Using the two spirometric definitions, the number of pulmonary function test results interpreted as obstructed varied markedly in the elderly population for both genders (males: χ(2) = 19.59, P < 0.01; females: χ(2) = 5.67, P = 0.017). CONCLUSIONS: The Global Initiative for Chronic Obstructive Lung Disease (GOLD) criterion probably leads to overdiagnosis in asymptomatic elderly never-smokers. Our study suggests that the predicted LLN values will reduce the misclassification risk instead. However, cohort studies are urgently needed for clinical validation.

[Higher levels of urokinase plasminogen activator system components in the airways of chronic obstructive pulmonary disease patients].

OBJECTIVE: To investigate the state and the pathophysiologic significances of urinary plasminogen activator system components in airways of patients with chronic obstructive pulmonary disease (COPD). METHODS: (1) Assay of induced sputum: 56 patients with COPD in stable clinical conditions (COPD group), aged (51 +/- 11) years with forced expiratory volume in one second of predicted % (FEV1% predicted) (53.5 +/- 14.4)% predicted, and 26 healthy control subjects (control group), aged (46 +/- 9) years; FEV1% predicted (85.1 +/- 1.0)% were studied. Levels of urokinase plasminogen activator system components in induced sputum, urokinase plasminogen activator (u-PA), urokinase plasminogen activator receptor (u-PAR), plasminogen activator inhibitor-1 (PAI-1) and interleukin-8 (IL-8), interferon-gamma (IFN-gamma), tumor necrosis factor (TNF-alpha), and interleukin-10 (IL-10) were determined by enzyme linked immunosorbent assay. (2) Pathological section of resected lung tissue: The study subjects included 11 patients receiving lung lobectomy for COPD with emphysematous bullae, aged (53 +/- 7) years, FEV1% predicted (58.3 +/- 6.6)%; as well as 10 non-COPD patients receiving lung lobectomy for local lesions with normal lung function, aged (47 +/- 12) years, FEV1% predicted (84.3 +/- 1.6)%, of which 3 were inflammatory pseudotumor, 5 were hamartoma, and 2 tuberculoma as the control. Cell expression of u-PA, u-PAR, PAI-1 in the pulmonary pathologic sections was investigated by immunohistochemistry. RESULTS: Induced sputum of COPD patients showed significant increase in u-PAR, PAI-1, and IL-8 compared to the control subjects, (570 +/- 614) ng/L vs (97 +/- 74) ng/L (t = 5.629, P < 0.01), (6162 +/- 9247) ng/L vs (574 +/- 731) ng/L (t = 4.346, P < 0.01) and (12,370 +/- 17,292) ng/L vs (1868 +/- 1905) ng/L (t = 4.486, all P < 0.01); and there were no differences in u-PA, IFN-gamma, TNF-alpha, and IL-10. Correlation analysis showed that u-PAR and PAI were positively correlated with IL-8 in COPD patients (r = 0.483, 0.770, all P < 0.01), while PAI negatively correlated with FEV1% (r = -0.272, P < 0.05). No correlation was found in healthy control subjects. u-PAR was localized in alveolar epithelial cells, macrophages, neutrophils and lymphocytes in COPD subjects, while u-PAR was mainly localized in alveolar epithelial cells in the control subjects. The ratio of positive expression in alveolar epithelial cells of control subjects was significantly lower than in that of COPD subjects (33 +/- 18)% vs (49 +/- 16)% (t = 2.213, P < 0.05), while the detectable intensity of expression in these cells of control subjects was also weaker than that of COPD subjects. PAI-1 was localized in fibroblasts, macrophages and neutrophils in COPD subjects, while mainly localized in fibroblasts in control subjects; the ratio of positive expression in fibroblasts in control subjects was also significantly lower than that in COPD subjects (37 +/- 16)% vs (61 +/- 16)% (t = 3.419, P < 0.05), meanwhile the detectable intensity of expression in these cells of control subjects was weaker than that of COPD one. CONCLUSION: u-PA system components are important inflammatory mediators in airways of COPD. PAI-1 is most likely to play a significant role in airway remodelling of COPD.