Evolution of transbronchial needle aspiration technique.

Transbronchial needle aspiration (TBNA) is an established technique to collect cell and tissue specimens from lesions outside the airway wall, generally guided by flexible bronchoscope under the direct visualization of the puncture site. TBNA has been utilized for 30 years, and now there is renewed interest in utilizing it in conjunction with endobronchial ultrasound. Although the basic operational principles have remained the same, conventional TBNA (cTBNA) and endobronchial ultrasound-guided TBNA (EBUS-TBNA) have been greatly improved over the years with the increased application in clinic and the advance of new technology. In this article we briefly discussed the evolution of TBNA technique and its future.

Insight into the differences in classification of mediastinal and hilar lymph nodes between Wang's lymph node map and the International Association for the Study of Lung Cancer lymph node map.

Lung cancer is the leading cause of malignant-tumor-related morbidity and mortality worldwide. Transbronchial needle aspiration (TBNA) has for the past 30 years been an effective technique for the diagnosis and staging of lung cancer. Understanding the anatomy of mediastinal and hilar lymph nodes is essential to improve the yield of TBNA. Wang's lymph node map is based on the lymph node map of the American Thoracic Society (ATS), and on the TBNA technique; it was published in 1994, and has promoted the development of both conventional TBNA (cTBNA) and endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA). In 2009, the International Association for the Study of Lung Cancer (IASLC) developed a new chest lymph node map to reconcile the differences between the Naruke and The Mountain-Dresler (MD)-ATS lymph node maps. The IASLC lymph node map was incorporated into the seventh edition of the tumor, node, metastasis (TNM) staging system for lung cancer, which directly affected the treatment and prognosis of lung cancer. There are significant differences between Wang's lymph node map and the IASLC lymph node map in TNM staging, and it is imperative to understand these differences and correlate these maps for the prognosis and staging of lung cancer using cTBNA or EBUS-TBNA.

A comparison of APACHE II and CPIS scores for the prediction of 30-day mortality in patients with ventilator-associated pneumonia.

OBJECTIVE: The aim of this study was to compare the Acute Physiology and Chronic Health Evaluation II (APACHE II) score and the Clinical Pulmonary Infection Score (CPIS) for the prediction of 30-day mortality in patients with ventilator-associated pneumonia (VAP). METHODS: A single-center, prospective cohort study design was employed between January 1, 2010 and January 1, 2014. APACHE II and CPIS scores were determined on the day of VAP diagnosis. Discrimination was tested using receiver-operating characteristic (ROC) curves and the areas under the curve (AUC). Calibration was tested using the Hosmer-Lemeshow statistic. RESULTS: Of 135 patients with VAP, 39 died; the 30-day mortality was 28.9%. APACHE II and CPIS scores were significantly higher in non-survivors compared to survivors (23.1±4.8 vs. 16.7±4.6, p<0.001; 6.8±1.3 vs. 6.2±1.3, p=0.016). APACHE II had excellent discrimination for predicting 30-day mortality in patients with VAP, with AUC 0.808 (95% confidence interval (CI) 0.704-0.912, p<0.001). However, the CPIS score did not have discrimination power for predicting mortality, with AUC 0.612 (95% CI 0.485-0.739, p=0.083). The Hosmer-Lemeshow statistic showed good goodness-of-fit for observed 30-day mortality and APACHE II expected mortality (Chi-square=1.099, p=0.785). However, CPIS expected 30-day mortality did not fit the observed mortality (Chi-square=6.72, p=0.004). CONCLUSIONS: These data suggest that APACHE II is useful for predicting 30-day mortality in patients with VAP, but that the CPIS does not have good discrimination and calibration for predicting mortality.

Ovalbumin enhances YKL-40, IL-5, GM-CSF, and eotaxin expression simultaneously in primarily cultured mouse tracheal epithelial cells.

Epithelial inflammation and eosinophil infiltration are crucial for the pathogenesis of asthma. Many inflammatory mediators, such as YKL-40, interleukin -5 (IL-5), granulocyte-macrophage colony-stimulating factor (GM-CSF), and eotaxin, are important for the development of allergic airway inflammation. This study is aimed at investigating the impact of treatment with ovalbumin (OVA) on the levels of those inflammatory mediators in primarily cultured mouse tracheal epithelial cells. Mouse tracheal epithelial cells were isolated and identified by immunofluorescent staining; the isolated mouse tracheal epithelial cells expressed cytokeratins. Treatment with OVA for 24 or 48 h significantly increased the relative levels of YKL-40, IL-5, GM-CSF, and eotaxin mRNA transcripts and YKL-40, IL-5, GM-CSF, and eotaxin proteins secreted in the supernatants of cultured cells, as compared with that in the untreated control cells (P < 0.01, P < 0.05, respectively). The levels of YKL-40 expression were correlated positively with the levels of IL-5, GM-CSF, and eotaxin expression in the OVA-treated cells. These data indicated that treatment with OVA simultaneously enhanced YKL-40, IL-5, GM-CSF, and eotaxin expression in the cultured mouse tracheal epithelial cells in vitro. These inflammatory mediators may synergistically contribute to the pathogenesis of allergic inflammation, and this study may help to understand the role of YKL-40 in the pathogenesis of asthma.

The prognostic value of pulmonary embolism severity index in acute pulmonary embolism: a meta-analysis.

BACKGROUND: Prognostic assessment is important for the management of patients with acute pulmonary embolism (APE). Pulmonary Embolism Severity Index (PESI) and simple PESI (sPESI) are new emerged prognostic assessment tools for APE. The aim of this meta-analysis is to assess the accuracy of the PESI and the sPESI to predict prognostic outcomes (all-cause and PE-related mortality, serious adverse events) in APE patients, and compare between these two PESIs. METHODS: MEDLINE and EMBASE database were searched up to June 2012 using the terms "Pulmonary Embolism Severity Index" and "pulmonary embolism". Summary odds ratio (OR) with 95% confidence intervals (CIs) for prognostic outcomes in low risk PESI versus high risk PESI were calculated. Summary receiver operating characteristic curve (SROC) used to estimate overall predicting accuracies of prognostic outcomes. RESULTS: Twenty-one studies were included in this meta-analysis. The results showed low-risk PESI was significantly associated with lower all-cause mortality (OR 0.13; 95% CI 0.12 to 0.15), PE-related mortality (OR 0.09; 95% CI 0.05 to 0.17) and serious adverse events (OR 0.34; 95% CI 0.29 to 0.41), with no homogeneity across studies. In sPESI subgroup, the OR of all-cause mortality, PE-related mortality, and serious adverse events was 0.10 (95% CI 0.08 to 0.14), 0.09 (95% CI 0.03 to 0.26) and 0.40 (95% CI 0.31 to 0.51), respectively; while in PESI subgroup, the OR was 0.14 (95% CI 0.13 to 0.16), 0.09 (95% CI 0.04 to 0.21), and 0.30 (95% CI 0.23 to 0.38), respectively. For accuracy analysis, the pooled sensitivity, the pooled specificity, and the overall weighted AUC for PESI predicting all-cause mortality was 0.909 (95% CI: 0.900 to 0.916), 0.411 (95% CI: 0.407 to 0.415), and 0.7853±0.0058, respectively; for PE-related mortality, it was 0.953 (95% CI: 0.913 to 0.978), 0.374 (95% CI: 0.360 to 0.388), and 0.8218±0.0349, respectively; for serious adverse events, it was 0.821 (95% CI: 0.795 to 0.845), 0.389 (95% CI: 0.384 to 0.394), and 0.6809±0.0208, respectively. In sPESI subgroup, the AUC for predicting all-cause mortality, PE-related mortality, and serious adverse events was 0.7920±0.0117, 0.8317±0.0547, and 0.6454±0.0197, respectively. In PESI subgroup, the AUC was 0.7856±0.0075, 0.8158±0.0451, and 0.6609±0.0252, respectively. CONCLUSIONS: PESI has discriminative power to predict the short-term death and adverse outcome events in patients with acute pulmonary embolism, the PESI and the sPESI have similar accuracy, while sPESI is easier to use. However, the calibration for predicting prognosis can't be calculated from this meta-analysis, some prospective studies for accessing PESI predicting calibration can be recommended.

The dynamic changes of LDH isoenzyme 3 and D-dimer following pulmonary thromboembolism in canine.

INTRODUCTION: To investigate the time course of changes of lactic acid dehydrogenase (LDH), LDH isoenzymes and D-dimer levels following acute pulmonary thromboembolism (PTE). MATERIALS AND METHODS: Eighteen dogs were randomly divided into three groups. Acute PTE was induced by injection of preformed blood clots into pulmonary artery through femoral vein. Thrombin and human fibrinogen were delivered into blood clots in embolism group I. Only thrombin was delivered into blood clots in embolism group II. The control group received normal saline and human fibrinogen in the same manner. Series of blood samples were collected pre-embolism and post-embolism. LDH isoenzymes proportion and D-dimer levels were measured. RESULTS: At 30 min, 1 h, 2 h, 4 h, 24 h post-embolism, the plasma D-dimer levels from embolism group I were significantly higher than pre-embolism and those from control group at the same intervals (p<0.05). The peak appeared at 2 h post-embolism (2.336+/-0.326 vs. 0.016+/-0.013, p<0.05). At 4 h, 24 h and 48 h post-embolism, total serum LDH activity and LDH-3 proportion from two embolism groups were significantly higher than pre-embolism (p<0.05). The peak of LDH-3 proportion in two embolism groups both appeared at 24 h post-embolism (0.225+/-0.021 vs. 0.108+/-0.030, 0.214+/-0.011 vs. 0.096+/-0.031, respectively. p<0.05). CONCLUSIONS: The LDH-3 and D-dimer levels were changed dynamically with a relative specificity manner during the course of acute massive PTE. Combination the D-dimer assay with LDH-3 may have a potential value in diagnosing acute massive PTE.