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Mary Ann Liebert 2013 Antioxidants & redox signaling Vol.18 No.12
<P>The corresponding author has sought retraction of this work from ARS. The author statement is copied below: We, the authors, wish to retract 'Cigarette Smoke-Induced Oxidative/Nitrosative Stress Impairs VEGF- and Fluid Shear Stress-Mediated Signaling in Endothelial Cells' by Edirisinghe et al. (Antioxid Redox Signal 12: 1355-1369; DOI:10.1089/ars.2009.2874) because we are not satisfied with the quality of some of the data presented in the article. Overall, however, the data are reproducible and the conclusions drawn were not affected. We apologize for any inconvenience this may have caused to the readers.</P>
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Rahman, Irfan Korean Society for Biochemistry and Molecular Biol 2003 Journal of biochemistry and molecular biology Vol.36 No.1
Inflammatory lung diseases are characterized by chronic inflammation and oxidant/antioxidant imbalance. The sources of the increased oxidative stress in patients with chronic inflammatory lung diseases such as asthma and chronic obstructive pulmonary disease (COPD) derive from the increased burden of inhaled oxidants, and from the increased amounts of reactive oxygen species (ROS) generated by several inflammatory, immune and various structural cells of the airways. Increased levels of ROS produced in the airways is reflected by increased markers of oxidative stress in the airspaces, sputum, breath, lungs and blood in patients with lung diseases. ROS, either directly or via the formation of lipid peroxidation products such as 4-hydroxy-2-nonenal may play a role in enhancing the inflammation through the activation of stress kinases (JNK, MAPK, p38) and redox sensitive transcription factors such as NF-${\kappa}B$ and AP-1. Recent evidences have indicated that oxidative stress and pro-inflammatory mediators can alter nuclear histone acetylation/deacetylation allowing access for transcription factor DNA binding leading to enhanced pro-inflammatory gene expression in various lung cells. Understanding of the mechanisms of redox signaling, NF-${\kappa}B$/AP-1 regulation, the balance between histone acetylation and deacetylation and the release and expression of pro- and anti-inflammatory mediators may lead to the development of novel therapies based on the pharmacological manipulation of antioxidants in lung inflammation and injury. Antioxidants that have effective wide spectrum activity and good bioavailability, thiols or molecules which have dual antioxidant and anti-inflammatory activity, may be potential therapeutic agents which not only protect against the direct injurious effects of oxidants, but may fundamentally alter the underlying inflammatory processes which play an important role in the pathogenesis of chronic inflammatory lung diseases.
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( Irfan Rahman ) 생화학분자생물학회 2003 BMB Reports Vol.36 No.1
Inflammatory lung disease are characterized by chronic inflammation and oxidant/antioxidant imbalance. The sources of the increased oxidative stress in patients with chronic inflammatory lung disease such as asthma and chronic obstructive pulmonary disease (COPD) derive from the increased burden of inhaled oxidants, and from the increased amounts of reactive oxygen species (ROS) generated by several inflammatory, immune and various structural cells of the airways. Increased levels of ROS produced in the airways is reflected by increased markers of produced in the airways is reflected by increased markers of oxidative stress in the airspaces, sputum, breath, lungs and blood in patients with lung disease. ROS, either directly or via the formation of lipid peroxidation products such as 4-hydroxy-2-noneunal may play a role in enhancing the inflammation through the activation of stress kinases (JNK, MAPK, p38) and redox sensitive transcription factors such as NF-кB and AP-1. Recent evidences have indicated that oxidative stress and pro-inflammatory mediators can alter nuclear histone aceylation/deacetylation allowing access for transcription factor DNA binding leading to enhanced pro-inflammatory gene expression in various lung cells. Understanding of the mechanisms of redox signaling, NF-кB/AP-a regulation, the balance between histone acetylation and deacetylation and the release and expression of pro- and anti- inflammatory mediators may lead to the development of novel therapies based on the pharmacological manipuolation of antioxidants in lung inflammation and injury. Antioxidant that have effective wide spectrum activity and good bioavailablity, thoils or molecules which have dual antioxidants and anti-inflammatory activity, may be potential therapeutic agents which not only protect against the direct injurious effects of oxidants, but may fundamentally alter the underlying inflammatory processes which play an important role in the pathogenesis of chronic inflammatory lung diseases.
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AutoFe-Sel: A Meta-learning based methodology for Recommending Feature Subset Selection Algorithms
Irfan Khan,Xianchao Zhang,Ramesh Kumar Ayyasamy,Rahman Ali 한국인터넷정보학회 2023 KSII Transactions on Internet and Information Syst Vol.17 No.7
Automated machine learning, often referred to as "AutoML," is the process of automating the time-consuming and iterative procedures that are associated with the building of machine learning models. There have been significant contributions in this area across a number of different stages of accomplishing a data-mining task, including model selection, hyper-parameter optimization, and preprocessing method selection. Among them, preprocessing method selection is a relatively new and fast growing research area. The current work is focused on the recommendation of preprocessing methods, i.e., feature subset selection (FSS) algorithms. One limitation in the existing studies regarding FSS algorithm recommendation is the use of a single learner for meta-modeling, which restricts its capabilities in the meta-modeling. Moreover, the meta-modeling in the existing studies is typically based on a single group of data characterization measures (DCMs). Nonetheless, there are a number of complementary DCM groups, and their combination will allow them to leverage their diversity, resulting in improved meta-modeling. This study aims to address these limitations by proposing an architecture for preprocess method selection that uses ensemble learning for meta-modeling, namely AutoFE-Sel. To evaluate the proposed method, we performed an extensive experimental evaluation involving 8 FSS algorithms, 3 groups of DCMs, and 125 datasets. Results show that the proposed method achieves better performance compared to three baseline methods. The proposed architecture can also be easily extended to other preprocessing method selections, e.g., noise-filter selection and imbalance handling method selection.
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Mohib Ur Rahman,Irfan Ullah,Aurang Zeb 대외경제정책연구원 2023 East Asian Economic Review Vol.27 No.1
This paper analyzes the entire distribution of stock market returns/volatility in five emerging markets (ASEAN5) and figures out the conditional distribution of the CHI_EPU index. The aim is to examine the impact of CHI_EPU on the stock returns/volatility density of ASEAN5 markets. It also examined whether changes in CHI_EPU explain returns at higher or lower points (abnormal returns). This paper models the behaviour of stock returns from March 2011 to June 2018 using a non-parametric conditional density estimation approach. The results indicate that CHI_EPU diminishes stock returns and augments volatility in ASEAN5 markets, except for Malaysia, where it affects stock returns positively. The possible reason for this positive impact is that EPU is not the leading factor reducing Malaysian stock returns; but, other forces, such as dependency on other countries’ stock markets and global factors, may have a positive impact on stock returns (Bachmann and Bayer, 2013). Thus, the risk of simultaneous investment in Chinese and ASEAN5 stock markets, except Malaysia, is high. Further, the degree of this influence intensifies at extreme high/low intervals (positive/negative tails). The findings of this study have significant implications for investors, policymakers, market agents, and analysts of ASEAN5.
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Lee, Hanbyeol,Park, Jeong-Ran,Kim, Woo Jin,Sundar, Isaac K.,Rahman, Irfan,Park, Sung-Min,Yang, Se-Ran The Federation of American Societies for Experimen 2017 The FASEB Journal Vol.31 No.5
<P>The receptor for advanced glycan end products (RAGE) has been identified as a susceptibility gene for chronic obstructive pulmonary disease (COPD) in genome-wide association studies (GWASs). However, less is known about how RAGE is involved in the pathogenesis of COPD. To determine the molecular mechanism by which RAGE influences COPD in experimental COPD models, we investigated the efficacy of the RAGE-specific antagonist FPS-ZM1 administration in in vivo and in vitro COPD models. We injected elastase intratracheally and the RAGE antagonist FPS-ZM1 in mice, and the infiltrated inflammatory cells and cytokines were assessed by ELISA. Cellular expression of RAGE was determined in protein, serum, and bronchoalveolar lavage fluid of mice and lungs and serum of human donors and patients with COPD. Downstream damage-associated molecular pattern (DAMP) pathway activation in vivo and in vitro and in patients with COPD was assessed by immunofluorescence staining, Western blot analysis, and ELISA. The expression of membrane RAGE in initiating the inflammatory response and of soluble RAGE acting as a decoy were associated with up-regulation of the DAMP-related signaling pathway via Nrf2. FPS-ZM1 administration significantly reversed emphysema in the lung of mice. Moreover, FPS-ZM1 treatment significantly reduced lung inflammation in Nrf2(+/+) , but not in Nrf2(-/-) mice. Thus, our data indicate for the first time that RAGE inhibition has an essential protective role in COPD. Our observation of RAGE inhibition provided novel insight into its potential as a therapeutic target in emphysema/COPD.-Lee, H., Park, J.-R., Kim, W. J., Sundar, I. K., Rahman, I., Park, S.-M., Yang. S.-R. Blockade of RAGE ameliorates elastase-induced emphysema development and progression via RAGE-DAMP signaling.</P>
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