Qualitative and Quantitative Analysis of the Major Bioactive Components of L. Using LC-QTOF-MS and LC-MSMS and Investigation of Antibacterial Activity against Pathogenic Bacteria.

Plants in the genus have been reported to produce a variety of chemical components, such as coumarins, flavonoids, lignans, sterols, and terpenoids. Here, ultra-high-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC-QTOF-MS) and ultra-high-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) were applied to qualitatively and quantitatively analyze the major bioactive components in an ethanolic crude extract from the leaves of L., which grows naturally in Korea.

Identification and Comparison of Bioactive Components of Two sp. Extract Using LC-QTOF-MS.

sp. is known for its various pharmacological effects and is used as a traditional medicine in Asia. The present study investigated the chemical composition and antimicrobial activity of sp.

TSA32-1 as a Promising Agent for Biocontrol of Plant Pathogenic Fungi.

The use of synthetic fungicides has caused major problems such as soil and water pollution and negatively affects non-target species. Microbial biocontrol agents are needed for crop disease management to reduce agrochemical use. and related genera produce secondary metabolites with agricultural applications, such as the pathogen-control agent We isolated TSA32-1 from soil and identified its characteristics by sequencing its 16S rRNA.

Middle East Respiratory Syndrome Coronavirus Superspreading Event Involving 81 Persons, Korea 2015.

Since the first imported case of Middle East respiratory syndrome coronavirus (MERS-CoV) infection was reported on May 20, 2015 in Korea, there have been 186 laboratory-confirmed cases of MERS-CoV infection with 36 fatalities. Ninety-seven percent (181/186) of the cases had exposure to the health care facilities. We are reporting a superspreading event that transmitted MERS-CoV to 81 persons at a hospital emergency room (ER) during the Korean outbreak in 2015.

Idiopathic pleuroparenchymal fibroelastosis presenting in recurrent pneumothorax: a case report.

Idiopathic pleuroparenchymal fibroelastosis (PPFE) is a rare, recently classified entity that consists of pleural and subjacent parenchymal fibrosis predominantly in the upper lungs. In an official American Thoracic Society/European Respiratory Society statement in 2013, this disease is introduced as a group of rare idiopathic interstitial pneumonias. We describe a case of a 76-year-old woman with cough and recurrent pneumothorax.

Association between occupational dust exposure and prognosis of idiopathic pulmonary fibrosis: a Korean national survey.

Background: Previous studies have investigated the relationship between occupational and environmental agents and idiopathic pulmonary fibrosis (IPF). However, there have been few studies regarding the prognosis of patients with IPF according to patient occupation.

Methods: We investigated whether occupational dust exposure was associated with clinically decreased lung function and poor prognosis.

Thrombin induces epithelial-mesenchymal transition via PAR-1, PKC, and ERK1/2 pathways in A549 cells.

Thrombin activates protease-activated receptor (PAR)-1 and induces a myofibroblast phenotype in normal lung fibroblasts. The origins of myofibroblasts are resident fibroblasts, fibrocytes, and epithelial-mesenchymal transition (EMT). We investigated the effects of thrombin, an important mediator of interstitial lung fibrosis, on EMT in A549 human alveolar epithelial cells.

A multicenter phase II study of belotecan, a new camptothecin analogue, in elderly patients with previously untreated, extensive-stage small cell lung cancer.

Purpose: Belotecan is a new camptothecin analogue and a potent topoisomerase I inhibitor. The aim of this phase II study was to investigate the efficacy and toxicity of belotecan in previously untreated elderly patients with small cell lung cancer (SCLC).

Methods: A total of 26 patients, aged ≥65 years, with previously untreated, extensive-stage SCLC were enrolled in the study.

Clinical Utility of Two Interferon-gamma Release Assays on Pleural Fluid for the Diagnosis of Tuberculous Pleurisy.

Background: The release of interferon-gamma (IFN-γ) by T lymphocytes increases after rechallenge with Mycobacterium tuberculosis antigen, especially, at a localized site of tuberculosis (TB) infection. We aimed to compare the clincial efficacy of two commercial IFN-γ release assays from pleural fluid for the diagnosis in tuberculous pleurisy.

Methods: We performed T-SPOT.

Inhibitory effect of receptor for advanced glycation end products (RAGE) on the TGF-β-induced alveolar epithelial to mesenchymal transition.

Idiopathic pulmonary fibrosis (IPF) is a lethal parenchymal lung disease characterized by myofibroblast proliferation. Alveolar epithelial cells (AECs) are thought to produce myofibroblasts through the epithelial to mesenchymal transition (EMT). Receptor for advanced glycation end products (RAGE) is a member of the immunoglobulin superfamily of cell surface receptors whose activation is associated with renal fibrosis during diabetes and liver fibrosis.

A multicenter phase II study of belotecan, a new camptothecin analogue, as a second-line therapy in patients with small cell lung cancer.

Belotecan (Camtobell, CKD602) is a new camptothecin derivative antitumor agent that belongs to the topoisomerase inhibitors. The aim of this phase II study was to evaluate the efficacy and safety of single agent belotecan as a second-line therapy in patients with small cell lung cancer (SCLC). Patients who were previously treated for SCLC were entered into the study.

Inhibitory effects of anti-immunoglobulin E antibodies on airway remodeling in a murine model of chronic asthma.

Background: Airway remodeling is one of the cardinal features of asthma and is thought to play a pivotal role in refractory or persistent asthma. Immunoglobulin E (IgE) has a major effect on the pathogenesis of asthma. The aim of this study was to investigate the effects of anti-IgE antibody not only on airway inflammation and bronchial hyperresponsiveness, but also on airway remodeling in a murine model of chronic asthma.

Inhibitory effect of CXC chemokine receptor 4 antagonist AMD3100 on bleomycin induced murine pulmonary fibrosis.

CXC chemokine receptor 4 (CXCR4), which binds the stromal cell-derived factor-1 (SDF-1), has been shown to play a critical role in mobilizing the bone marrow (BM)-derived stem cells and inflammatory cells. We studied the effects of AMD3100, CXCR4 antagonist, on a murine bleomycin-induced pulmonary fibrosis model. Treatment of mice with AMD3100 in bleomycin-treated mice resulted in the decrease of SDF-1 in bronchoalveolar lavage (BAL) fluids at an early stage and was followed by the decrease of fibrocytes in the lung.

Effects of elastase inhibitor on the epithelial cell apoptosis in bleomycin-induced pulmonary fibrosis.

Alveolar epithelial cell injury and apoptosis is consistent findings in human idiopathic pulmonary fibrosis (IPF). Epithelial cell apoptosis is known to be induced by leukocyte elastase in vitro. The authors hypothesized that synthetic neutrophil elastase inhibitor, sivelestat (ONO-5046), can inhibit the bleomycin-induced pulmonary fibrosis in rats by blocking the apoptotic pathways in epithelial cells.

Risk factors for acute respiratory distress syndrome during neutropenia recovery in patients with hematologic malignancies.

Introduction: Neutropenia recovery may be associated with deterioration in oxygenation and exacerbation of pre-existing pulmonary disease. However, risk factors for acute respiratory distress syndrome (ARDS) during neutropenia recovery in patients with hematologic malignancies have not been studied.

Methods: We studied critically ill patients with hematologic malignancies with the dual objectives of describing patients with ARDS during neutropenia recovery and identifying risk factors for ARDS during neutropenia recovery.

The soluble tumor necrosis factor-alpha receptor suppresses airway inflammation in a murine model of acute asthma.

Purpose: Tumor necrosis factor-alpha (TNF-alpha) is a proinflammatory cytokine that has been implicated in many aspects of the airway pathology in asthma. TNF-alpha blocking strategies are now being tried in asthma patients. This study investigated whether TNF-alpha blocking therapy inhibits airway inflammation and airway hyperresponsiveness (AHR) in a mouse model of asthma.

Inflammatory and remodeling events in asthma with chronic exposure to house dust mites: a murine model.

Although animal models with ovalbumin have been used to study chronic asthma, there are difficulties in inducing recurrence as well as in maintaining chronic inflammation in this system. Using a murine model of house dust mite (HDM)-induced bronchial asthma, we examined the airway remodeling process in response to the chronic exposure to HDM. During the seventh and twelfth weeks of study, HDM were inhaled through the nose for three consecutive days and airway responsiveness was measured.

Time sequence of airway remodeling in a mouse model of chronic asthma: the relation with airway hyperresponsiveness.

During the course of establishing an animal model of chronic asthma, we tried to elucidate the time sequence of airway hyperresponsiveness (AHR), airway inflammation, airway remodeling, and associated cytokines. Seven-week-old female BALB/c mice were studied as a chronic asthma model using ovalbumin (OVA). After sensitization, mice were exposed twice weekly to aerosolized OVA, and were divided into three groups depending on the duration of 4 weeks, 8 weeks, and 12 weeks.

Nitric oxide induces MUC5AC mucin in respiratory epithelial cells through PKC and ERK dependent pathways.

Background: Nitric oxide (NO) is generally increased during inflammatory airway diseases. This increased NO stimulates the secretion of mucin from the goblet cell and submucosal glands but the mechanism is still unknown precisely. In this study, we investigated potential signaling pathways involving protein kinase C (PKC) and mitogen-activated protein kinase (MAPK) in the NO-induced MUC5AC mucin gene and protein expression in A549 cells.

Co-administration of vaccination with DNA encoding T cell epitope on the Der p and BCG inhibited airway remodeling in a murine model of chronic asthma.

Therapeutic modalities of airway remodeling in asthma have proved to be unsuccessful regarding reversing the previously established chronic airway changes. Recently, the potential of plasmid DNA to inhibit the Th2 immune response has been demonstrated in animal models of asthma. Bacillus Calmette-Guerin (BCG) immunization also induced immunomodulation, which appeared to be reliant on the properties of the interferon-gamma that was produced.

Neutrophil elastase causes MUC5AC mucin synthesis via EGF receptor, ERK and NF-kB pathways in A549 cells.

Background: Neutrophil elastase (NE) was found to increase the respiratory mucin gene, MUC5AC, although the molecular mechanisms of this process remain unknown. We attempted to determine the signal transduction pathway through which NE induces MUC5AC gene expression in bronchial epithelial cells.

Methods: A fragment of 1.

A case of chronic myelomonocytic leukemia with severe eosinophilia having t(5;12)(q31;p13) with t(1;7)(q10;p10).

We describe an unusual case of chronic myelomonocytic leukemia with severe eosinophilia having t(5;12)(q31;p13) with t(1;7)(q10;p10). The eosinophilic proliferation was severe in peripheral blood and bone marrow, and they revealed marked dysplastic features. We performed fluorescence in situ hybridization (FISH) and immunohistochemistry to evaluate the clonality of eosinophils.

The role of nitric oxide in the particulate matter (PM2.5)-induced NFkappaB activation in lung epithelial cells.

NFkappaB is one of key transcription factors that are involved in the inflammatory responses to the particulate matter (PM) in the lungs. In order to further understand the molecular mechanism, the effects of antioxidants and an inducible nitric oxide synthase (iNOS) inhibitor on PM-induced NFkappaB activation were examined in A549 lung epithelial cells. NFkappaB activation by 2.