Second-hand smoke and chronic bronchitis in Taiwanese women: a health-care based study

<p>Abstract</p> <p>Background</p> <p>Cigarette smoking cannot fully explain the epidemiologic characteristics of chronic obstructive pulmonary disease (COPD) in women, particularly for those who rarely smoke, but COPD risk is not less than men. The aim of our study is to investigate the relationship between second-hand smoke (SHS) exposure and chronic bronchitis in Taiwanese women.</p> <p>Methods</p> <p>We used Taiwan's National Health Insurance Bureau claims data in 1999, and cross-checked using criteria set by the American Thoracic Society; there were 33 women with chronic bronchitis, 182 with probable chronic bronchitis, and 205 with no chronic bronchitis during our interview time between 2000 and 2005. We measured second-hand smoke (SHS) exposure by self-reported measures (household users and duration of exposure), and validated this by measuring urinary cotinine levels of a subset subjects. Classification of chronic bronchitis was also based on spirometry defined according to the GOLD guidelines to get the severity of COPD.</p> <p>Results</p> <p>Women who smoked and women who had been exposed to a lifetime of SHS were 24.81-fold (95% CI: 5.78-106.38) and 3.65-fold (95% CI: 1.19-11.26) more likely to have chronic bronchitis, respectively, than those who had not been exposed to SHS. In addition, there was a significant increasing trend between the severity of COPD and exposure years of SHS (<it>p </it>< 0.01). The population attributable risk percentages of chronic bronchitis for smokers and those exposed to SHS were 23.2 and 47.3% respectively.</p> <p>Conclusions</p> <p>These findings indicate that, besides cigarette smoking, exposure to SHS is a major risk factor for chronic bronchitis in Taiwanese women.</p

Epigallocatechin Gallate Attenuates Proliferation and Oxidative Stress in Human Vascular Smooth Muscle Cells Induced by Interleukin-1β via Heme Oxygenase-1

Proliferation of vascular smooth muscle cells (VSMCs) triggered by inflammatory stimuli and oxidative stress contributes importantly to atherogenesis. The association of green tea consumption with cardiovascular protection has been well documented in epidemiological observations, however, the underlying mechanisms remain unclear. This study aimed to elucidate the effects of the most active green tea catechin derivative, (−)-epigallocatechin-3-gallate (EGCG), in human aortic smooth muscle cells (HASMCs), focusing particularly on the role of a potent anti-inflammatory and antioxidative enzyme heme oxygenase-1 (HO-1). We found that pretreatment of EGCG dose- and time-dependently induced HO-1 protein levels in HASMCs. EGCG inhibited interleukin- (IL-)1β-induced HASMC proliferation and oxidative stress in a dose-dependent manner. The HO-1 inducer CoPPIX decreased IL-1β-induced cell proliferation, whereas the HO-1 enzyme inhibitor ZnPPIX significantly reversed EGCG-caused growth inhibition in IL-1β-treated HASMCs. At the molecular level, EGCG treatment significantly activated nuclear factor erythroid-2-related factor (Nrf2) transcription activities. These results suggest that EGCG might serve as a complementary and alternative medicine in the treatment of these pathologies by inducing HO-1 expression and subsequently decreasing VSMC proliferation

Curcumin Inhibits LIN-28A through the Activation of miRNA-98 in the Lung Cancer Cell Line A549

[[abstract]]Metastasis is common in lung cancer and is associated with poor clinical outcomes and increased mortality. Curcumin is a natural anti-cancer agent that inhibits the metastasis of various cancers by modulating the expression of micro (mi) RNAs such as miR-98, which acts as a tumor suppressor. This study investigated the effect of curcumin on miR-98 expression and in vitro cell line growth and invasiveness in lung cancer. Curcumin treatment enhanced the expression of miR-98 and reduced that of the miR-98 target gene LIN28A as well as matrix metalloproteinase (MMP) 2 and MMP9 in vitro and in vivo. MiR-98 overexpression suppressed lung cancer cell migration and invasion by inhibiting LIN28A-induced MMP2 and MMP9 expression. Meanwhile, LIN28A level was downregulated by overexpression of miR-98 mimic. Induction of miR-98 by curcumin treatment suppressed MMP2 and MMP9 by targeting LIN28A. These findings provide insight into the mechanisms by which curcumin suppresses lung cancer cell line growth in vitro and in vivo and invasiveness in vitro. Curcumin Inhibits LIN-28A through the Activation of miRNA-98 in the Lung Cancer Cell Line A549 (PDF Download Available). Available from: https://www.researchgate.net/publication/317377715_Curcumin_Inhibits_LIN-28A_through_the_Activation_of_miRNA-98_in_the_Lung_Cancer_Cell_Line_A549 [accessed Oct 30 2017]

Predictors for Identifying the Most Infectious Pulmonary Tuberculosis Patient

Background/PurposeClinicians need to decide whether to begin isolation and empiric therapy for patients suspected of having infectious tuberculosis (TB). This study aimed to identify the demographic, clinical and radiographic characteristics of acid-fast bacilli (AFB) smear-positive patients and to create a smear-positive TB prediction rule, which clinicians may use to predict risk.MethodsThis was a retrospective study involving 105 patients with AFB smear-positive TB and 52 patients with AFB smear-negative TB at Kaohsiung Municipal Hsiao-Kang Hospital in southern Taiwan from August 1, 2003 to July 31, 2006. All of the patients had at least one sputum culture that was positive for Mycobacterium tuberculosis. Demographic, clinical and radiographic data of patients with AFB smear-positive TB were compared to those of patients with AFB smear-negative TB.ResultsOn univariate analysis, young age (p = 0.033), alcoholism (p = 0.036), weight loss (p = 0.003), fever (p = 0.018), consolidation (p = 0.001), infiltration (p = 0.012), cavitary pattern (p = 0.005), right upper lung field (p < 0.001) and left upper lung field (p = 0.001) lesions on chest radiographs were found to be predictive of smear-positive TB patients. In contrast, end-stage renal disease (p = 0.035) and normal chest radiograph (p = 0.006) were predictive of smear-negative TB patients. On multivariate analysis, age less than 65 years (p = 0.004), fever (p = 0.004), right upper lung field (p = 0.044), left upper lung field (p = 0.041), consolidation (p = 0.018) and cavitary (p = 0.049) lesions on chest radiograph were independently associated with an increased risk of an AFB positive smear finding. The smear-positive TB prediction model was created based on the results of the multivariate analysis that had an area of 0.788 under the receiver operating characteristic curve.ConclusionThe smear-positive TB prediction model may help clinicians decide if a patient with pending sputum smear results should first be placed in isolation and empiric anti-tuberculous therapy started

Curcumin Inhibits LIN-28A through the Activation of miRNA-98 in the Lung Cancer Cell Line A549

Metastasis is common in lung cancer and is associated with poor clinical outcomes and increased mortality. Curcumin is a natural anti-cancer agent that inhibits the metastasis of various cancers by modulating the expression of micro (mi) RNAs such as miR-98, which acts as a tumor suppressor. This study investigated the effect of curcumin on miR-98 expression and in vitro cell line growth and invasiveness in lung cancer. Curcumin treatment enhanced the expression of miR-98 and reduced that of the miR-98 target gene LIN28A as well as matrix metalloproteinase (MMP) 2 and MMP9 in vitro and in vivo. MiR-98 overexpression suppressed lung cancer cell migration and invasion by inhibiting LIN28A-induced MMP2 and MMP9 expression. Meanwhile, LIN28A level was downregulated by overexpression of miR-98 mimic. Induction of miR-98 by curcumin treatment suppressed MMP2 and MMP9 by targeting LIN28A. These findings provide insight into the mechanisms by which curcumin suppresses lung cancer cell line growth in vitro and in vivo and invasiveness in vitro

Gene Expression Changes Associated with Nintedanib Treatment in Idiopathic Pulmonary Fibrosis Fibroblasts: A Next-Generation Sequencing and Bioinformatics Study

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, and fatal interstitial lung disease. Therapeutic options for IPF remain limited. Nintedanib, a tyrosine kinase inhibitor approved for IPF treatment, is known to inhibit fibroblasts proliferation, migration and transformation to myofibroblasts. However, how nintedanib changes gene regulations in IPF has never been systematically investigated. We conducted a next-generation sequencing and bioinformatics study to evaluate the changes of mRNA and miRNA profiles in IPF fibroblasts treated with 2 &micro;M and 4 &micro;M nintedanib, compared to those without treatment. We identified 157 upregulated and 151 downregulated genes and used STRING and DAVID databases for analysis of protein&ndash;protein interactions, biological pathways, and molecular functions. We found strong protein&ndash;protein interactions within these dysregulated genes, mostly involved in the pathways of cell cycle and mitotic cell cycle. We also discovered 13 potential miRNA&ndash;mRNA interactions associated with nintedanib treatment. After validation using miRDB, TargetScan, and RT-qPCR, we identified 4 downregulated genes (DDX11, E2F1, NPTX1, and PLXNA4) which might be repressed by the upregulated hsa-miR-486-3p. According to the proposed functions of DDX11, E2F1, and PLXNA4 reported in previous studies, these gene expression changes together might contribute to decreased proliferation of fibroblasts and decreased angiogenesis in the microenvironment of IPF. Our findings need further studies to confirm

Neutrophils are Essential in Short Hairpin RNA of Indoleamine 2,3- Dioxygenase Mediated-antitumor Efficiency

Indoleamine 2,3-dioxygenase (IDO) is a rate limiting enzyme in tryptophan-degrading pathways and IDO activity results in immune suppression. Targeting IDO is a strategy of cancer immunotherapies. Our previous studies demonstrate that delivery of short hairpin against IDO (IDO shRNA) suppresses tumor growth and increases neutrophils infiltration into tumor. Neutrophils reveal antitumorigenic “N1” or protumorigenic “N2” phenotype in tumor microenvironment. However, the function of IDO shRNA-induced neutrophils is not clear. The LLC1 lung cancer model was used to investigate the role of these neutrophils. Intramuscular injection of IDO shRNA or IDO inhibitor treatment delayed tumor growth and both treatments increased neutrophil infiltration in tumor. Enriched tumor-infiltrating neutrophils expressed both high level of tumor necrosis factor-α and tumor necrosis factor-β (N1 and N2 associated molecules, respectively). In addition, IDO shRNA treatment induced interferon-γ and tryptophan transfer RNA expression in splenocytes. Systematic depletion of neutrophils abolished the IDO shRNA-induced therapeutic effect but did not affect the effect of IDO inhibitor. The levels of interferon-γ and tumor necrosis factor-α were suppressed in IDO shRNA treatment splenocytes after neutrophils depletion. In conclusion, these tumor-infiltrating neutrophils show antitumorigenic phenotype in spleen after IDO shRNA treatment in a murine lung cancer model

Combination of Whole-Brain Radiotherapy with Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors Improves Overall Survival in EGFR-Mutated Non-Small Cell Lung Cancer Patients with Brain Metastases

Brain metastases (BM) cause morbidity and mortality in patients with non-small cell lung cancer (NSCLC). The use of upfront epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) and withholding of whole-brain radiation therapy (WBRT) is controversial. We aim to investigate the impact of WBRT on overall survival (OS). After screening 1384 patients, a total of 141 EGFR-mutated patients with NSCLC and BM were enrolled. All patients received EGFR-TKIs between 2011 and 2015. Ninety-four patients (66.7%) were treated with WBRT (TKI + WBRT group). With a median follow-up of 20.3 months (95% confidence interval (CI), 16.9&ndash;23.7), the median OS after the diagnosis of BM was 14.3 months (95% CI, 9.5 to 18.3) in the TKI + WBRT group and 2.3 months (95% CI, 2 to 2.6) in the TKI alone group. On multivariate analysis, WBRT (p &lt; 0.001), female, surgery to primary lung tumor, and surgery to BM were associated with improved OS. The 1-year OS rate was longer in the TKI+WBRT group than that in the TKI alone group (81.9% vs. 59.6%, p = 0.002). In conclusion, this is the first study to demonstrate the negative survival impact from the omission of WBRT in patients with EGFR-mutant NSCLC

Safety of Performing Percutaneous Dilational Tracheostomy in Patients with Preexisting Barotrauma

Since its introduction in 1985 by Ciaglia et al, percutaneous dilational tracheostomy (PDT) has gradually become the procedure of choice in establishing a long-term airway in many intensive care units (ICU). However, the safety of performing PDT in patients with barotrauma is still unknown and has never been reported. We present the case of a 35-year-old man with AIDS, who was admitted to our medical ICU for pneumonia and acute respiratory distress syndrome. He developed subcutaneous emphysema and pneumomediastinum as complications of mechanical ventilation. After stabilization of the barotrauma, he underwent PDT with the standard Ciaglia Blue Rhino technique. However, rapid and extensive progression of preexisting barotrauma occurred shortly after PDT. This severe complication was nearly fatal. The prolonged procedure during which the susceptible lung was exposed to longer duration of high airway pressure was thought to be the mechanism of rapid deterioration of the preexisting barotrauma. With aggressive supportive care, the patient survived. To prevent further deterioration of preexisting barotrauma during and after PDT in future cases, we propose some principles that should be strictly followed. Under administration of these principles, we safely performed PDT in another case with preexisting barotrauma 1 month later