Rationale: Asthma is a disabling inflammatory disease of the airway, and bronchial epithelial cells (BECs) play a key role in its pathogenesis. Although many drugs are available, some asthmatic patients remained poorly controlled with the currently available treatment. MicroRNAs (miRNAs) are one of major cellular regulators and have become potential targets for developing new therapeutic strategies. Methods: Total RNA was extracted from asthmatic primary BECs and normal primary BECs. The small RNA library construction and deep sequencing was carried out with next-generation sequencing (NGS), and the mRNA microarray were carried out with microarray. The data generated were further analyzed with Ingenuity Pathway Analysis (IPA) software (Ingenuity, Systems, Redwood City, CA, USA): gene expression change known for asthma were selected, and possible miRNA-mRNA pairs with highly predicted confidence were identified with microRNA Target Filter in IPA. Results: The levels of miR-3176, miR-212-3p, and miR-424-5p were markedly lower in asthmatic BECs than in normal BECs, which might be correlated to the markedly higher expression levels of ALOX5, MMP9, SPON2, respectively. Conclusions: Medications with up-regulating effect on the identified microRNAs might be worthy to develop as a novel anti-asthmatic treatment.
We reviewed 400 cases whose P-A and lateral chest radiographs were used. These were divided into three groups. Group A was composed of 235 cases of normal radiographs. This group was used to evaluate the incidence of visibility of some anatomic structures on a lateral radiograph. Group B consisted of 143 cases with various diseases including pleural effusion (20 cases), peri-diaphragmatic lesions (15 cases), abscess (12 cases), emphysema (20 cases), lung tumor (15 cases), mediastinal tumor (10 cases), obstructive atelectasis (16 cases), infiltrative pattern (15 cases), and pneumonia (20 cases). This group was used to evaluate what information the lateral view could add to an abnormal chest P-A radiograph. Group C had 22 cases with additional findings on the lateral view which were not seen on the chest P-A radiographs. This group was used to evaluate the applicability of sings of thickening of the posterior tracheal band, thickening of the posterior wall of the bronchus intermedius and posterior displacement of the left main bronchus in the diagnosis of specific diseases. The results showed A) there was no difference in the incidence of visibility of anatomic structures evaluated in this study on the right and the left lateral view. The visible incidence of these structures in 235 cases was 97% for the posterior tracheal band, 45% for the right upper lobe bronchus orifice, 83% for the left upper lobe bronchus orifice, 70% for the inferior vena cava, 92% for the posterior wall of the bronchus intermedius, 87% for the aorta, 97% for the right pulmonary artery, 71% for the left pulmonary artery, 69% for stomach air and 99% for the tracheal air column. B) unless the diagnosis could not be reached on the chest P-A radiograph or localization of the lesion was expected, the lateral view should be ordered only for patients with lesions of the peridiaphragm, mediastinum, hilum, midline, middle or lingual lobe, sternum, retrosternum or spine. C) the high incidence of visibility of the posterior tracheal band, posterior wall of the application of these signs available for diagnosis of specific diseases.
Unilateral absence of pulmonary artery (UAPA) is a rare congenital malformation. Some cases cause deadly complications during childhood, others are usually diagnosed incidentally in asymptomatic patients in adulthood by chest plain film. The image feature on plain film is often a hypoplastic lung on the affected side. Confirmatory CT angiography or magnetic resonance angiography may be needed. The common symptoms of UAPA are hemoptysis, dyspnea, and recurrent pulmonary infections. However, high-altitude pulmonary edema has been thought to be a possible complication recently. Herein, we present an asymptomatic 15-year-old adolescent with absence of a right pulmonary artery. Magnetic resonance angiography confirmed this diagnosis and revealed associated left inferior pulmonary vein stenosis, which has not been reported previously.
Short-term oral steroid use may improve lung function and respiratory symptoms in patients with stable chronic obstructive pulmonary disease (COPD). However, long-term oral steroid (LTOS) use is not recommended owing to its potential adverse effects. Our study aimed to investigate whether chronic use of oral steroids for more than 4 months would increase mortality and vertebral fracture risk in patients with stable COPD. A systemic search of the PubMed database was conducted, and meta-analysis was performed using Review Manager 5.3. Five studies with a total of 1795 patients showed there was an increased risk of mortality in patients using LTOS (relative risk, 1.63; 95% confidence interval (CI), 1.19–2.23; p < 0.0001; I 2 = 86%). In addition, four studies with a total of 17,764 patients showed there was an increased risk of vertebral fracture in patients using LTOS (odds ratio, 2.31; 95% CI, 1.52–3.50; p = 0.03; I 2 = 65%). Our meta-analysis showed LTOS was associated with increased mortality and vertebral fracture risk in patients with COPD, and this risk may be due to the adverse effects of LTOS and progression COPD.
Stomach cancer has a high mortality, which is partially caused by an absence of suitable biomarkers to allow detection of the initiation stages of cancer progression. Thus, identification of critical biomarkers associated with gastric cancer (GC) is required to advance its clinical diagnoses and treatment. Recent studies using tracing models for lineage analysis of GC stem cells indicate that the cell fate decision of the gastric stem cells might be an important issue for stem cell plasticity. They include leucine-rich repeat-containing G-protein-coupled receptor 5 (Lgr5+), Cholecystokinin receptor 2 (Cckr2+), and axis inhibition protein 2 (Axin2+) as the stem cell markers in the antrum, Trefoil Factor 2 (TFF2+), Mist1+ stem cells, and Troy+ chief cells in the corpus. By contrast, Estrogen receptor 1 (eR1), Leucine-rich repeats and immunoglobulin-like domains 1 (Lrig1), SRY (sex determining region Y)-box 2 (Sox2), and B lymphoma Mo-MLV insertion region 1 homolog (Bmi1) are rich in both the antrum and corpus regions. These markers might help to identify the cell-lineage identity and analyze the plasticity of each stem cell population. Thus, identification of marker genes for the development of GC and its environment is critical for the clinical application of cancer stem cells in the prevention of stomach cancers.
Infective endocarditis has been the major cause of morbidity and mortality among intravenous drug users (IDUs) with infections, mostly involving the tricuspid valve and presenting multiple septic pulmonary embolisms. Numerous pulmonary complications of septic pulmonary embolism have been described, but only a few have reported spontaneous pneumothorax. Our patient, a 23‐year‐old heroin addict, was hospitalized for tricuspid endocarditis and septic pulmonary embolism. Acute onset of respiratory distress occurred on his seventh hospital day and rapidly resulted in hypoxemia. Immediate bedside chest radiograph demonstrated left pneumothorax. It was thought to be a spontaneous pneumothorax, because he had not undergone any invasive procedure before the occurrence of pneumothorax. His clinical condition improved after the insertion of an intercostal chest tube. He later underwent surgery to replace the tricuspid valve as a result of the large size of the vegetation and poor control of infection. He ultimately survived. Pneumothorax is a possible lethal complication of septic pulmonary embolism in IDUs with right‐sided endocarditis and should be considered in such patients when respiratory distress occurs acutely during their hospitalization.
// Ya-Ling Hsu 1, * , Jen-Yu Hung 2, 3, * , Yen-Lung Lee 4 , Feng-Wei Chen 5 , Kuo-Feng Chang 6 , Wei-An Chang 3, 5 , Ying-Ming Tsai 1, 3 , Inn-Wen Chong 3, 7 and Po-Lin Kuo 5, 8, 9 1 Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan 2 School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan 3 Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan 4 Division of Thoracic surgery, Department of Surgery, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan 5 Graduate Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan 6 Welgene Biotech. Inc, Taipei, Taiwan 7 Department of Respiratory Therapy, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan 8 Center for Biomarkers and Biotech Drugs, Kaohsiung Medical University, Kaohsiung, Taiwan 9 Institute of Medical Science and Technology, National Sun Yat-Sen University, Kaohsiung, Taiwan * These authors have contributed equally to this work Correspondence to: Inn-Wen Chong, email: chong@kmu.edu.tw Po-Lin Kuo, email: kuopolin@seed.net.tw Keywords: next-generation sequencing, bioinformatics, microRNA, messenger RNA, lung adenocarcinoma Received: July 31, 2017 Accepted: August 28, 2017 Published: September 18, 2017 ABSTRACT Lung adenocarcinoma is one of the leading causes of cancer-related death worldwide. We showed transcriptomic profiles in three pairs of tumors and adjacent non-tumor lung tissues using next-generation sequencing (NGS) to screen protein-coding RNAs and microRNAs. Combined with meta-analysis from the Oncomine and Gene Expression Omnibus (GEO) databases, we identified a representative genetic expression signature in lung adenocarcinoma. There were 9 upregulated genes, and 8 downregulated genes in lung adenocarcinoma. The analysis of the effects from each gene expression on survival outcome indicated that 6 genes (AGR2, SPDEF, CDKN2A, CLDN3, SFN, and PHLDA2) play oncogenic roles, and 7 genes (PDK4, FMO2, CPED1, GNG11, IL33, BTNL9, and FABP4) act as tumor suppressors in lung adenocarcinoma. In addition, we also identified putative genetic interactions, in which there were 5 upregulated microRNAs with specific targets - hsa-miR-183-5p-BTNL9, hsa-miR-33b-5p-CPED1, hsa-miR-429-CPED1, hsa-miR-182-5p-FMO2, and hsa-miR-130b-5p-IL33. These 5 microRNAs have been shown to be associated with tumorigenesis in lung cancer. Our findings suggest that these genetic interactions play important roles in the progression of lung adenocarcinoma. We propose that this molecular change of genetic expression may represent a novel signature in lung adenocarcinoma, which may be developed for diagnostic and therapeutic strategies in the future.
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