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Background To investigate the clinical features of septic pulmonary embolism (SPE) cases and prognostic factors for in-hospital mortality in China. Methods A retrospective analysis was conducted of SPE patients hospitalized between January 2007 and June 2018 in the Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Guangxi Medical University. Results A total of 98 patients with SPE were identified. All patients had bilateral multiple peripheral nodules on chest computed tomography. The most common pathogen found in blood culture was Staphylococcus aureus (10/33, 30.3%). Transthoracic echocardiography was performed in 39 patients and 20 showed vegetations. Bronchoscopy was performed in 24 patients. Bronchoalveolar lavage fluid (BALF) was obtained from 15 patients (62.5%) and showed predominantly polymorphonuclear cell infiltration (52%, range of 48%~ 63%). Four patients received transbronchial lung biopsy, and histopathological examinations revealed suppurative pneumonia and organizing pneumonia. The in-hospital mortality rate was 19.4%. Age (odds ratio [OR] 1.100; 95% confidence interval [CI] 1.035–1.169), hypotension (OR 7.260; 95% CI 1.126–46.804) and ineffective or delay of empirical antimicrobial therapy (OR 7.341; 95% CI 1.145–47.045) were found to be independent risk factors for in-hospital mortality, whereas drainage treatment was found to be a protective factor (OR 0.33; 95% CI 0.002–0.677). Conclusions SPE cases presented with nonspecific clinical manifestations and radiologic features. Blood cultures and bronchoscopy are important measures for early diagnosis and differential diagnosis. There is relationship between primary infection sites and the type of pathogen. Maintaining normal blood pressure and providing timely and appropriate initial antimicrobial therapy for effective control of the infection could improve prognosis.

The polyphenol ellagic acid is found in many natural food sources and has been proposed as a candidate compound for clinical applications due to its anti-oxidative capacity and as a potential anti-tumorigenic compound. The objective of the present study was to evaluate the sensitivity to and possible apoptosis mechanism induced by ellagic acid in neuronal tumor cells. As a model the human neuroblastoma SH-SY5Y cell line was used. The methods applied were bright field and phase contrast microscopy, XTT- and LDH-assays, western blot, and flow cytometric analysis of DNA degradation and mitochondrial membrane potential. Ellagic acid treatment was found to induce a reduction in cell number preceded by alterations of the mitochondrial membrane potential and activation of caspase-9 and -3, DNA-fragmentation and cell death by apoptosis. The apoptotic cell death studied was not due to anoikis since it was significant in the adherent fraction of the cells. We conclude that ellagic acid induces dose- and time-dependent apoptosis, at least partly by the mitochondrial pathway, in an embryonal neuronal tumor cell system. This finding is in agreement with previously reported data on adult carcinoma cells thus suggesting a more general effect of ellagic acid on tumor cells.

This study was designed to investigate the p38 mitogen-activated protein kinase (MAPK) signaling pathway involved in Aquaporin1 (AQP1) expression caused by staphylococcal peptidoglycan (PGN) in cultured rat pleural mesothelial cells (rPMCs) in vitro.RT-PCR and immunoblot analysis were used to determine the relative mRNA and protein levels of AQP1 by PGN in rPMCs. P38 kinase inhibitor SB203580, JNK inhibitor SP600125, and ERK1/2 inhibitor PD98059 were used to determine the effects of PGN-induced AQP1 expression by immunoblot. Activation of p38 by PGN was reflected by detecting the phosphorylation constituent of p38, using immunoblot. The shift of localization after activation of p38 by PGN was investigated by immunofluorescence assay.AQP1 transcription and protein expression were decreased by PGN in dose-dependent and time-dependent manners in rPMCs. Down-regulation of AQP1 by PGN was blocked only by SB203580, neither by SP600125 nor by PD98059. Furthermore, rPMCs exposed to PGN showed activation of p38 MAPK. Phospho-p38 protein production was increased by PGN stimulation in rPMCs. The localization of phospho-p38 was both in the cytosol and nuclei after PGN treatment, while its normal distribution is mainly in the cytosol in rPMCs.AQP1 expression was decreased by PGN in both dose-dependent and time-dependent manners in rPMCs. This down-regulation by PGN-induced AQP1 in rPMCs may be mediated by the activation of p38 MARK pathway.

Apple pomace is a wasted resource produced in China in large quantities, disposal of which has caused serious environmental problems. In order to make the best of this residue, apple pomace together with cottonseed powder was used as a raw material to produce β-mannanase in solid-state fermentation (SSF) by Aspergillus niger SN-09. Optimization of fermentation conditions for maximizing β-mannanase production was carried out using Plackett-Burman and Central Composite designs. A mixture of apple pomace and cottonseed powder (3:2, w/w) with 59.2 % (w/w) initial moisture, together with certain ionic compounds and salts, proved to be the optimal medium. The test fungi were inoculated in the optimized medium and incubated at 30°C for 48 h. The activity of β-mannanase reached 561.3 U/g, an increase of 45.7 % compared with that in basal medium, and reached the same level of production as that achieved using wheat bran and soybean meal as raw materials as in most factories in China. This is the first report of the use of apple pomace as a raw material to produce β-mannanase in SSF. This will not only reduce the production cost of β-mannanase, but also represents a new and effective way to make the best use of apple pomace, which can consequently help to reduce the environmental pollution caused by this waste.

Summary Background Serum concentrations of soluble mesothelin-related peptides (SMRP) have been reported to be higher in patients with malignant mesothelioma than in healthy subjects and in patients with non-malignant mesothelioma diseases. The aim of the present meta-analysis was to establish the overall diagnostic accuracy of the measurement of SMRPs for diagnosing malignant mesothelioma. Methods After a systematic review of English language studies, sensitivity, specificity, and other measures of accuracy of serum SMRPs in the diagnosis of malignant mesothelioma were pooled using random-effects models. Summary receiver operating characteristic curves were used to summarize overall test performance. Results Eleven publications from 12 studies met our inclusion criteria. The summary estimates for SMRPs in the diagnosis of malignant mesothelioma in the studies included were sensitivity 0.64 (95% confidence interval 0.61–0.68), specificity 0.89 (0.88–0.90), positive likelihood ratio 7.10 (4.44–11.35), negative likelihood ratio 0.39 (0.31–0.48), and diagnostic odds ratio 19.35 (10.95–34.17). Conclusions Serum SMRP determination plays a role in the diagnosis of malignant mesothelioma. The results of SMRP assays should be interpreted in parallel with clinical findings and the results of conventional tests.

BACKGROUND Triggering receptors expressed on myeloid cells (TREM) proteins are a family of cell surface receptors expressed broadly by cells of the myeloid lineage. The aim of this study was to investigate the clinical significance of soluble TREM-1 (sTREM-1) in pleural effusions, and to determine the effects of pneumonia on pleural sTREM-1 concentrations. METHODS Pleural fluid was collected from 109 patients who presented to the respiratory institute (35 with malignant pleural effusion, 31 with tuberculous pleural effusion, 21 with bacterial pleural effusion, and 22 with transudate). The concentrations of sTREM-1, tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) were determined in effusion and serum samples by enzyme linked immunosorbent assay (ELISA). RESULTS The concentrations of sTREM-1 in bacterial pleural effusion were significantly higher than those in malignant, tuberculous, and transudative groups (all P < 0.001). An sTREM-1 cutoff value of 768.1 ng/L had a sensitivity of 86% and a specificity of 93%. Pleural sTREM-1 levels were positively correlated with levels of TNF-alpha and IL-1beta. Patients with complicating bacterial pneumonia did not have elevated concentration of sTREM-1 in pleural effusion when compared with patients without pneumonia. CONCLUSIONS Determination of pleural sTREM-1 may improve the ability of clinicians to differentiate pleural effusion patients of bacterial origin from those with other etiologies. The occurrence of bacterial pneumonia did not affect pleural sTREM-1 concentrations.

Background Conventional tests are not always helpful in making a diagnosis of tuberculous pleurisy. Many studies have investigated the usefulness of interferon (IFN)-γ measurements in pleural fluid for the early diagnosis of tuberculous pleurisy. We conducted a metaanalysis to determine the accuracy of IFN-γ measurements in the diagnosis of tuberculous pleurisy. Methods After a systematic review of English-language studies, sensitivity, specificity, and other measures of accuracy of IFN-γ concentrations in the diagnosis of pleural effusion were pooled using random-effects models. Summary receiver operating characteristic curves were used to summarize overall test performance. Results Twenty-two studies met our inclusion criteria. The summary estimates for IFN-γ in the diagnosis of tuberculous pleurisy in the studies included were as follows: sensitivity, 0.89 (95% confidence interval [CI], 0.87 to 0.91); specificity, 0.97 (95% CI, 0.96 to 0.98); positive likelihood ratio, 23.45 (95% CI, 17.31 to 31.78); negative likelihood ratio, 0.11 (95% CI, 0.07 to 0.16); and diagnostic odds ratio, 272.7 (95% CI, 147.5 to 504.2). Conclusions IFN-γ determination is a sensitive and specific test for the diagnosis of tuberculous pleurisy. The measurement of IFN-γ levels in pleural effusions is thus likely to be a useful tool for diagnosing tuberculous pleurisy. The results of IFN-γ assays should be interpreted in parallel with clinical findings and the results of conventional tests.

The objective of the present study was to investigate the presence of interleukin (IL)-27 in pleural effusions and to evaluate the diagnostic significance of pleural IL-27. The concentrations of IL-27 were determined in pleural fluids and sera from 68 patients with tuberculous pleural effusion, 63 malignant pleural effusion, 22 infectious pleural effusion, and 21 transudative pleural effusion. Flow cytometry was used to identify which pleural cell types expressed IL-27. It was found that the concentrations of pleural IL-27 in tuberculous group were significantly higher than those in malignant, infectious, and transudative groups, respectively. Pleural CD4(+) T cells, CD8(+) T cells, NK cells, NKT cells, B cells, monocytes, macrophages, and mesothelial cells might be the cell sources for IL-27. IL-27 levels could be used for diagnostic purpose for tuberculous pleural effusion, with the cut off value of 1,007 ng/L, IL-27 had a sensitivity of 92.7% and specificity of 99.1% for differential diagnosing tuberculous pleural effusion from non-tuberculous pleural effusions. Therefore, compared to non-tuberculous pleural effusions, IL-27 appeared to be increased in tuberculous pleural effusion. IL-27 in pleural fluid is a sensitive and specific biomarker for the differential diagnosing tuberculous pleural effusion from pleural effusions with the other causes.

Purpose: The aim of this study was to explore the presence of the chemokines CCL22 and CCL17 in malignant pleural effusion, and the chemoattractant activity of these chemokines on CD4-positive CD25-positive Foxp3-positive regulatory T cells infiltrating into the pleural space.Experimental Design: The concentrations of CCL22 and CCL17 in both pleural effusions and sera from 33 patients with lung cancer were determined. Flow cytometry was done to determine T lymphocyte subsets in cell pellets of pleural effusion. Pleural cells were analyzed for the expression of CCL22 and CCL17. The chemoattractant activity of CCL22 for regulatory T cells in vitro and in vivo was also observed.Results: The concentration of CCL22 in malignant pleural effusion was significantly higher than that in the corresponding serum. Pleural fluid from lung cancer patients was chemotactic for regulatory T cells, and this activity was partly blocked by an anti-CCL22, but not by an anti-CCL17 antibody. Intrapleural administration of CCL22 of patients produced a marked progressive influx of regulatory T cells into pleural space.Conclusions: Compared with serum, CCL22 seemed to be increased in malignant pleural effusion, and could directly induce regulatory T cell infiltration into the pleural space in patients with malignant effusion.

Objective It remains controversial whether intensified chemotherapy with hematopoietic progenitors (ICHP) is effective for small-cell lung cancer. This meta-analysis was performed to evaluate the efficacy and safety of ICHP in patients with small-cell lung cancer. Methods MEDLINE and EMBASE databases were searched for English-language studies published through October 12, 2008. Randomized phase II and III clinical trials comparing ICHP with control therapy. Response rates, overall survival, and toxicity were analyzed. Results Five assessable trials were identified including 641 patients. No significant increase in the odds ratio for response was attributable to ICHP (odds ratio, 1.29; 95% confidence interval, 0.87–1.93; p = 0.206). No statistically significant increase in overall survival was found when ICHP were compared to control regimens (hazard ratio, 0.94; 95% confidence interval, 0.80–1.10; p = 0.432). The toxicity of ICHP was significantly higher for hematologic toxicity, including hemoglobin nadir and platelet nadir. Conclusions ICHP was not superior to control chemotherapy in terms of both objective response and overall survival, and was related to more significant hemoglobin nadir and platelet nadir.

Background Active suppression by CD4 + CD25 + regulatory T lymphocytes plays an important role in the down-regulation of T cell responses to foreign and self-antigens. This study was conducted to analyze whether the CD4 + CD25 + regulatory T cells exist and function normally in tuberculous pleural effusion. Methods The percentages of CD4 + CD25 + T cells in pleural effusion and peripheral blood from patients with tuberculous pleurisy and peripheral blood from healthy control subjects were determined by flow cytometry. The expression of forkhead transcription factor Foxp3 was also examined. CD4 + CD25 + and CD4 + CD25 - T cells from pleural effusion and blood were isolated, and were cultured to observe the effects of CD4 + CD25 + T cells on proliferation response of CD4 + CD25 - T cells in vitro. Results There were increased numbers of CD4 + CD25 + T cells in tuberculous pleural effusion compared with peripheral blood from both patients with tuberculous pleurisy and normal subjects, and these cells demonstrated a constitutive high-level expression of Foxp3. Moreover, CD4 + CD25 + T cells mediated potent inhibition of proliferation response of CD4 + CD25 - T cells. Conclusion The increased CD4 + CD25 + T cells in tuberculous pleural effusion express a high level of Foxp3 transcription factor, while potently suppressing the proliferation of CD4 + CD25 - T cells.

Background and objective: Conventional tests are not always helpful in making a diagnosis of malignant pleural effusion (MPE). Many studies have investigated the utility of pleural carcinoembryonic antigen (CEA) in the early diagnosis of MPE. The present meta-analysis determined the accuracy of CEA measurement in the diagnosis of MPE. Methods: A systematic review of English language studies was conducted and data on the accuracy of pleural CEA concentrations in the diagnosis of MPE were pooled using random effects models. Receiver operating characteristic curves were used to summarize the overall test performance. Results: Forty-five studies met the inclusion criteria for the meta-analysis. The summary estimates for CEA in the diagnosis of MPE were: sensitivity 0.54 (95% CI: 0.52–0.55), specificity 0.94 (95% CI: 0.93–0.95), positive likelihood ratio 9.52 (95% CI: 6.97–13.01), negative likelihood ratio 0.49 (95% CI: 0.44–0.54) and diagnostic odds ratio 22.5 (95% CI: 15.6–32.5). Analysis of a subset of 11 studies which examined the value of pleural CEA in ruling out a diagnosis of malignant mesothelioma found that the sensitivity and specificity of a CEA level exceeding cut-off values were 0.97 (95% CI: 0.93–0.99) and 0.60 (95% CI: 0.55–0.65), respectively. Conclusions: Measurement of pleural CEA is likely to be a useful diagnostic tool for confirming MPE, and is also helpful in the differential diagnosis between malignant pleural mesothelioma and metastatic lung cancer. The results of CEA assays should be interpreted in parallel with clinical findings and the results of conventional tests.

Summary Objective Cytologic approaches such as pleural lavage cytology (PLC) are considered as possible aids to assessing prognosis of lung cancer patients. We aimed to comprehensively review the evidence for use of PLC to predict prognosis of lung cancer. Methods Fifteen studies, including 6391 patients, were found to be eligible for the present meta-analysis. A meta-analysis was done on the log hazard ratios and their variances in these studies. Results Four studies dealt with pleural lavage before lung resection, six studies dealt with pleural lavage after lung resection, and five studies had PLC data from both before and after lung resection examination. For before lung resection studies, combined hazard ratios showed that positive PLC results had an unfavorable impact on survival: 3.96 (95% confidence interval 2.48–6.33), 4.55 (2.95–7.04), 5.00 (3.39–7.36), 5.67 (3.81–8.43), and 7.06 (5.04–9.90), for 1-, 2-, 3-, 4- and 5-year, respectively. For after lung resection studies, combined hazard ratios showed that positive PLC results had an unfavorable impact on survival: 6.02 (3.74–9.71), 6.64 (4.53–9.72), 7.06 (4.93–10.12), 7.29 (5.18–10.25), and 8.47 (6.12–11.73), for 1-, 2-, 3-, 4- and 5-year, respectively. Totally, the combined hazard ratio was 5.61 (3.98–7.90), showing a worse survival when PLC was positive. These findings could be overestimated because of publication and reporting bias. Conclusions PLC is a strong prognostic factor for survival in patients with lung cancer.

Conventional tests are not always helpful in making a diagnosis of tuberculous pleurisy. Many studies have investigated the usefulness of interferon (IFN)-gamma measurements in pleural fluid for the early diagnosis of tuberculous pleurisy. We conducted a metaanalysis to determine the accuracy of IFN-gamma measurements in the diagnosis of tuberculous pleurisy.After a systematic review of English-language studies, sensitivity, specificity, and other measures of accuracy of IFN-gamma concentrations in the diagnosis of pleural effusion were pooled using random-effects models. Summary receiver operating characteristic curves were used to summarize overall test performance.Twenty-two studies met our inclusion criteria. The summary estimates for IFN-gamma in the diagnosis of tuberculous pleurisy in the studies included were as follows: sensitivity, 0.89 (95% confidence interval [CI], 0.87 to 0.91); specificity, 0.97 (95% CI, 0.96 to 0.98); positive likelihood ratio, 23.45 (95% CI, 17.31 to 31.78); negative likelihood ratio, 0.11 (95% CI, 0.07 to 0.16); and diagnostic odds ratio, 272.7 (95% CI, 147.5 to 504.2).IFN-gamma determination is a sensitive and specific test for the diagnosis of tuberculous pleurisy. The measurement of IFN-gamma levels in pleural effusions is thus likely to be a useful tool for diagnosing tuberculous pleurisy. The results of IFN-gamma assays should be interpreted in parallel with clinical findings and the results of conventional tests.

Summary Background Conventional tests are not always helpful in making a diagnosis of tuberculous pleurisy. Many studies have investigated the usefulness of adenosine deaminase (ADA) in pleural fluid for the early diagnosis of tuberculous pleurisy. We conducted a meta-analysis to determine the accuracy of ADA measurements in the diagnosis of tuberculous pleurisy. Methods After a systematic review of English language studies, sensitivity, specificity, and other measures of accuracy of ADA concentration in the diagnosis of pleural effusion were pooled using random effects models. Summary receiver operating characteristic curves were used to summarize overall test performance. Results Sixty-three studies met our inclusion criteria. The summary estimates for ADA in the diagnosis of tuberculous pleurisy in the studies included were sensitivity 0.92 (95% confidence interval 0.90–0.93), specificity 0.90 (95% confidence interval 0.89–0.91), positive likelihood ratio 9.03 (95% confidence interval 7.19–11.35), negative likelihood ratio 0.10 (95% confidence interval 0.07–0.14), and diagnostic odds ratio 110.08 (95% confidence interval 69.96–173.20). Conclusions ADA determination is a relative sensitive and specific test for the diagnosis of tuberculous pleurisy. Measurement of ADA in pleural effusion is thus likely to be a useful diagnostic tool for tuberculous pleurisy. The results of ADA assays should be interpreted in parallel with clinical findings and the results of conventional tests.