Application of bronchoscopic argon plasma coagulation in the treatment of tumorous endobronchial tuberculosis: Historical controlled trial

ObjectiveThe purpose of this study was to evaluate the efficacy and safety of bronchoscopic argon plasma coagulation for tumorous endobronchial tuberculosis.MethodsWe analyzed the records of 115 patients with tumorous endobronchial tuberculosis who did not show luminal narrowing of the bronchus at diagnosis. Of these 115 patients, 41 patients received bronchoscopic argon plasma coagulation plus routine antituberculosis chemotherapy (argon plasma coagulation group) and the other 74 patients received only routine antituberculosis chemotherapy (chemotherapy group). The treatment effects between these 2 groups were compared based on changes in lesions, rate of lesion disappearance, and complications associated with bronchoscopic argon plasma coagulation.ResultsThe complete removal rate was 100% in patients in argon plasma coagulation group. About 84.6% lesions disappeared completely in patients in the chemotherapy group. The rate of disappearance of lesions in the argon plasma coagulation group was faster than that of the chemotherapy group. There were no severe complications in the argon plasma coagulation group.ConclusionsBronchoscopic argon plasma coagulation can accelerate the healing of tumorous endobronchial tuberculosis and can help prevent progressive bronchial stenosis resulting from tumorous endobronchial tuberculosis, and it is a very safe method

Dipeptidyl Peptidase-4 (DPP-4) Inhibitor Saxagliptin Alleviates Lipopolysaccharide-Induced Acute Lung Injury via Regulating the Nrf-2/HO-1 and NF-κB Pathways

Purpose We aimed at investigating the effects of Dipeptidyl peptidase-4 (DPP-4) inhibitor saxagliptin (Saxa) on mouse acute lung injury (ALI)-induced by lipopolysaccharide (LPS) and the potential mechanisms. Materials/methods Animals were divided into four groups: control, Saxa, LPS, and LPS + Saxa. Histopathology changes of lung tissues were assessed by hematoxylin and eosin staining and periodic acid-Schiff staining. The degree of edema was determined by wet/dry ratio. The levels of oxidative stress markers and inflammatory cytokines in lung homogenate and bronchoalveolar lavage fluid were detected using kits. Terminal deoxynucleotidyl transferase dUTP nick end labeling assay was used to test apoptosis and Western blotting was applied to measure the expression of apoptosis-associated proteins. The expression of nuclear factor erythroid 2-related factor 2 (Nrf-2)/heme oxygenase-1 (HO-1) and nuclear factor-kappa B (NF-κB) pathways were detected by Western blotting. Results The results revealed that Saxa attenuated LPS-induced pathological injury and edema. Saxa decreased the levels of reactive oxygen species (ROS), malondialdehyde (MDA), myeloperoxidase (MPO) and increased the levels of superoxide dismutase (SOD) and catalase (CAT). The contents of inflammatory cytokines were reduced in the Saxa intervention group. Saxa attenuated apoptosis accompanied by alterations in the expression of apoptosis-associated proteins. Furthermore, the expression of Nrf-2 and HO-1 were upregulated whereas phospho (p)-NF-κB p65 and phospho-inhibitory subunit of NF-κB alpha (p-IκB-α) were downregulated after Saxa treatment. Conclusion These findings concluded that Saxa alleviates oxidative stress, inflammation and apoptosis in ALI induced by LPS via modulating the Nrf-2/HO-1 and NF-κB pathways, which provides evidence for employing Saxa in ALI treatment

Thymosin alpha1 based immunomodulatory therapy for sepsis: a systematic review and meta-analysis

Objectives: Thymosin alpha1 (Tα1) is considered a promising immunomodulatory drug. However, it is still unclear whether Tα1 should be recommended for the management of sepsis. Here we conducted a systematic review and meta-analysis to assess the efficacy of Tα1 based immunomodulatory therapy on the clinical outcomes of septic patients. Methods: We searched for relevant clinical trials published before Dec. 12, 2014 through electronic databases. All articles about Tα1 based immunomodulatory therapy for sepsis were included regardless of language. Two authors independently selected studies, extracted data and assessed the quality of each included study. We polled the data related to all-cause mortality with Review Manager 5.1. Results: Twelve controlled trials were evaluated in all. Tα1 based immunomodulatory therapy had a significant trend toward lower all-cause mortality among patients with sepsis (pooled risk ratio 0.68, 95%CI 0.59-0.78, p < 0.00001, 12 trials, n = 1480). Conclusions: Tα1 based immunomodulatory therapy was associated with a lower mortality in septic patients. Nevertheless, these findings should be interpreted cautiously because of the poor quality and small number of participants of the included trials. More well-designed worldwide multicenter clinical trials are needed to provide a conclusive guideline for clinical practice

Endothelial Semaphorin 7A Promotes Inflammation in Seawater Aspiration-Induced Acute Lung Injury

Inflammation is involved in the pathogenesis of seawater aspiration-induced acute lung injury (ALI). Although several studies have shown that Semaphorin 7A (SEMA7A) promotes inflammation, there are limited reports regarding immunological function of SEMA7A in seawater aspiration-induced ALI. Therefore, we investigated the role of SEMA7A during seawater aspiration-induced ALI. Male Sprague–Dawley rats were underwent seawater instillation. Then, lung samples were collected at an indicated time for analysis. In addition, rat pulmonary microvascular endothelial cells (RPMVECs) were cultured and then stimulated with 25% seawater for indicated time point. After these treatments, cells samples were collected for analysis. In vivo, seawater instillation induced lung histopathologic changes, pro-inflammation cytokines release and increased expression of SEMA7A. In vitro, seawater stimulation led to pro-inflammation cytokine release, cytoskeleton remodeling and increased monolayer permeability in pulmonary microvascular endothelial cells. In addition, knockdown of hypoxia-inducible factor (HIF)-1α inhibited the seawater induced increase expression of SEMA7A. Meanwhile, knockdown of SEMA7A by specific siRNA inhibited the seawater induced aberrant inflammation, endothelial cytoskeleton remodeling and endothelial permeability. These results suggest that SEMA7A is critical in the development of lung inflammation and pulmonary edema in seawater aspiration-induced ALI, and may be a therapeutic target for this disease