• Tuberculosis and Respiratory Diseases
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• v.39 no.4
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• pp.299-303
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• 1992

• BMB Reports
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• v.33 no.6
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• pp.427-439
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• 2000

The activity of the phagocyte respiratory burst oxidase is regulated by complex and dynamic alterations in protein-protein interactions that result in the rapid assembly of an active multicomponent NADPH oxidase enzyme on the plasma membrane. While the enzymatic activity has been studied for the past 20 years, the past decade has seen remarkable progress in our understanding of the enzyme and its activation at the molecular level. This article describes the current state of knowledge, and proposes a model for the mechanism by which protein-protein interactions regulate enzyme activity in this system.

• Journal of Oriental Neuropsychiatry
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• v.27 no.2
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• pp.89-101
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• 2016

Objectives In human, there is a diversity in the breathing pattern, for instance inspiratory and expiratory time, volume, breathing frequency, and breath-to-breath variation. Expecially, respiratory variability can provide important information about breathing regulation and physiological flexibility. it is significant to not only breathing index but also physiological index.Methods Thus this paper reviews the literature on respiratory variability with the aim of clinical application.Results We could find the interrelationships and respiratory variability between emotions, psychopathy, sighing, mental and physical activity.Conclusions As a result, respiratory variability can serve an important physiological index in the clinical area and reflects how our bodies act in diverse environments under various condition.

• The Journal of Korean Physical Therapy
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• v.25 no.5
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• pp.330-336
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• 2013

Purpose: Respiratory is an essential vital component for conservation of life in human, which is controlled by respiratory muscles and its related neuromuscular regulation. The purpose of this study is to assess lung capacity and respiratory pressure in healthy children, and to investigate relationship and predictability between respiratory pressure and other related respiratory functions. Methods: A total of 31 healthy children were recruited for this study. Demographic information and respiratory related factors were assessed in terms of body surface area (BSA), chest mobility, lung capacity, and respiratory pressure. Correlation between respiratory pressure and the rested variables was analyzed, and multiple regression using the stepwise method was performed for prediction of respiratory muscle strength, in terms of respiratory pressure as the dependent variable, and demographic and other respiratory variables as the independent variable. Results: According to the results of correlation analysis, respiratory pressure showed significant correlation with age (r=0.62, p<0.01), BSA (r=0.80, p<0.01), FVC (r=0.80, p<0.01), and FEV1 (r=0.70, p<0.01). In results of multiple regression analysis using the backward elimination method, BSA and FVC were included as significant factors of the predictable statistical model. The statistical model showed a significant explanation power of 71.8%. Conclusion: These findings suggest that respiratory pressure could be a valuable measurement tool for evaluation of respiratory function, because of significant relationship with physical characteristics and lung capacity, and that BSA and FVC could be possible predictable factors to explain the degree of respiratory pressure. These findings will provide useful information for clinical assessment and treatment in healthy children as well as those with pulmonary disease.

• Molecules and Cells
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• v.37 no.9
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• pp.664-671
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• 2014

MiR-217 can function as an oncogene or a tumour suppressor gene depending on cell type. However, the function of miR-217 in lung cancer remains unclear to date. This study aims to evaluate the function of miR-217 in lung cancer and investigate its effect on the sensitivity of lung cancer cells to cisplatin. The expression of miR-217 was detected in 100 patients by real-time PCR. The effects of miR-217 overexpression on the proliferation, apoptosis, migration and invasion of SPC-A-1 and A549 cells were investigated. The target gene of miR-217 was predicted by Targetscan online software, screened by dual luciferase reporter gene assay and demonstrated by Western blot. Finally, the effects of miR-217 up-regulation on the sensitivity of A549 cells to cisplatin were determined. The expression of miR-217 was significantly lower in lung cancer tissues than in noncancerous tissues (p < 0.001). The overexpression of miR-217 significantly inhibited the proliferation, migration and invasion as well as promoted the apoptosis of lung cancer cells by targeting KRAS. The up-regulation of miR-217 enhanced the sensitivity of SPC-A-1 and A549 cells to cisplatin. In conclusion, miR-217 suppresses tumour development in lung cancer by targeting KRAS and enhances cell sensitivity to cisplatin. Our results encourage researchers to use cisplatin in combination with miR-217 to treat lung cancer. This regime might lead to low-dose cisplatin application and cisplatin side-effect reduction.

• Applied Biological Chemistry
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• v.33 no.3
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• pp.264-267
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• 1990

Representative synthetic piericidin-like compounds, such as hydroxypyridine and hydroxyquinoline derivatives, which showed high inhibition activity against NADH-ubiquinone oxidoreductase on the respiratory chain revealed good fungicide activity. Especially, hydrolrypyridine ones showed high activity against rice blast (Pyricularia oryzae) and barley powdery mildew (Erysiphe graminis).

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.7
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• pp.4033-4039
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• 2013

Links between cancer and metabolism have been suggested for a long time but compelling evidence for this hypothesis came from the recent molecular characterization of the LKB1/AMPK signaling pathway as a tumor suppressor axis. Besides the discovery of somatic mutations in the LKB1 gene in certain type of cancers, a critical emerging point was that the LKB1/AMPK axis remains generally functional and could be stimulated by pharmacological molecules such as metformin in cancer cells. In addition, AMPK plays a central role in the control of cell growth, proliferation and autophagy through the regulation of mTOR activity, which is consistently deregulated in cancer cells. Targeting of AMPK/mTOR is thus an attractive strategy in the development of therapeutic agents against non-small-cell lung cancer (NSCLC). In this review, the LKB1/AMPK/mTOR signaling pathway is described, highlighting its protective role, and opportunities for therapeutic intervention, and clinical trials in NSCLC.

• Sleep Medicine and Psychophysiology
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• v.16 no.1
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• pp.22-27
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• 2009

Regulation of respiration differs significantly between wakefulness and sleep. Respiration during wakefulness is influenced by not only automatic control but also voluntary and behavioral control. Sleep is associated with definite changes in respiratory function. With the onset of sleep, voluntary control of ventilation that overrides automatic control during wakefulness becomes terminated. Also ventilatory response to various stimuli including hypoxemia and hypercapnia is decreased. With these reasons respiration during sleep becomes fragile and unstable so that marked hypoxemia can be happened in patients with lung disease especially during REM sleep. Obstructive sleep apnea may also be developed if upper airway resistance is increased in addition to these blunted ventilatory responses.

• Clinical and Experimental Pediatrics
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• v.57 no.4
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• pp.157-163
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• 2014

Respiratory distress syndrome (RDS) among preterm infants is typically due to a quantitative deficiency of pulmonary surfactant. Aside from the degree of prematurity, diverse environmental and genetic factors can affect the development of RDS. The variance of the risk of RDS in various races/ethnicities or monozygotic/dizygotic twins has suggested genetic influences on this disorder. So far, several specific mutations in genes encoding surfactant-associated molecules have confirmed this. Specific genetic variants contributing to the regulation of pulmonary development, its structure and function, or the inflammatory response could be candidate risk factors for the development of RDS. This review summarizes the background that suggests the genetic predisposition of RDS, the identified mutations, and candidate genetic polymorphisms of pulmonary surfactant proteins associated with RDS.

• Tuberculosis and Respiratory Diseases
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• v.79 no.4
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• pp.257-266
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• 2016

Background: Idiopathic pulmonary fibrosis is a common interstitial lung disease; it is a chronic, progressive, and fatal lung disease of unknown etiology. Over the last two decades, knowledge about the underlying mechanisms of pulmonary fibrosis has improved markedly and facilitated the identification of potential targets for novel therapies. However, despite the large number of antifibrotic drugs being described in experimental pre-clinical studies, the translation of these findings into clinical practices has not been accomplished yet. NADH:quinone oxidoreductase 1 (NQO1) is a homodimeric enzyme that catalyzes the oxidation of NADH to $NAD^+$ by various quinones and thereby elevates the intracellular $NAD^+$ levels. In this study, we examined the effect of increase in cellular $NAD^+$ levels on bleomycin-induced lung fibrosis in mice. Methods: C57BL/6 mice were treated with intratracheal instillation of bleomycin. The mice were orally administered with ${\beta}$-lapachone from 3 days before exposure to bleomycin to 1-3 weeks after exposure to bleomycin. Bronchoalveolar lavage fluid (BALF) was collected for analyzing the infiltration of immune cells. In vitro, A549 cells were treated with transforming growth factor ${\beta}1$ (TGF-${\beta}1$) and ${\beta}$-lapachone to analyze the extracellular matrix (ECM) and epithelial-mesenchymal transition (EMT). Results: ${\beta}$-Lapachone strongly attenuated bleomycin-induced lung inflammation and fibrosis, characterized by histological staining, infiltrated immune cells in BALF, inflammatory cytokines, fibrotic score, and TGF-${\beta}1$, ${\alpha}$-smooth muscle actin accumulation. In addition, ${\beta}$-lapachone showed a protective role in TGF-${\beta}1$-induced ECM expression and EMT in A549 cells. Conclusion: Our results suggest that ${\beta}$-lapachone can protect against bleomycin-induced lung inflammation and fibrosis in mice and TGF-${\beta}1$-induced EMT in vitro, by elevating the $NAD^+$/NADH ratio through NQO1 activation.