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Search Results: 1 - 10 of 4179 matches for " Irfan Rahman "
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Vitamin D and Susceptibility of Chronic Lung Diseases: Role of Epigenetics
Irfan Rahman
Frontiers in Pharmacology , 2011, DOI: 10.3389/fphar.2011.00050
Abstract: Vitamin D deficiency is linked to accelerated decline in lung function, increased inflammation, and reduced immunity in chronic lung diseases. Epidemiological studies have suggested that vitamin D insufficiency is associated with low lung function in susceptible subjects who are exposed to higher levels of environmental agents (airborne particulates). Recent studies have highlighted the role of vitamin D and vitamin D receptor (VDR) in regulation of several genes that are involved in inflammation, immunity, cellular proliferation, differentiation, and apoptosis. Vitamin D has also been implicated in reversal of steroid resistance and airway remodeling, which are the hallmarks of chronic obstructive pulmonary disease (COPD) and severe asthma. VDR protein level is decreased in lungs of patients with COPD. VDR deficient mice develop an abnormal lung phenotype with characteristics of COPD, such as airspace enlargement and decline in lung function associated with increased lung inflammatory cellular influx, and immune-lymphoid aggregates formation. Dietary vitamin D may regulate epigenetic events, in particular on genes which are responsible for COPD susceptibility. Active metabolite of vitamin D, 1,25-dihydroxyvitamin D3 plays an essential role in cellular metabolism and differentiation via its nuclear receptor (VDR) that cooperates with several other chromatin modification enzymes (histone acetyltransferases and histone deacetylases), thereby mediating complex epigenetic events in vitamin D signaling and metabolism. This review provides an update on the current knowledge and understanding on vitamin D, and susceptibility of chronic lung diseases in relation to the possible role of epigenetics in its molecular action. Understanding the molecular epigenetic mechanism of vitamin D/VDR would provide rationale for dietary vitamin D-mediated intervention in prevention and management of chronic lung diseases linked with vitamin D deficiency.
OILCROP-SUN Model for Nitrogen Management of Diverse Sunflower (Helianthus annus L.) Hybrids Production under Agro-Climatic Conditions of Sargodha, Pakistan  [PDF]
Muhammad Irfan Ahmad, Amjed Ali, Aaqil Khan, Sikandar Ali Jamro, Alam Sher, Shafeeq-ur Rahman, Arif Rashid
American Journal of Plant Sciences (AJPS) , 2017, DOI: 10.4236/ajps.2017.83028
Abstract: Decision support system for agro-technology transfer (DSSAT), OIL CROP-SUN Model was used to stimulate the phenology, growth, yield of different two sunflower hybrids. i.e. Hysun-33 and S-78 by applying different nitrogen levels. The effect of nitrogen (N) on growth and yield components of different sunflower (Helianthus annuus L.) hybrids were evaluated under agro-climatic conditions of Sargodha, Pakistan during spring 2013. The experiment was laid out in a randomized complete block design with split plot arrangement having three replications, keeping cultivars in the main plots and nitrogen levels (0, 45, 90,135 and 180 kg/ha) in sub plots. OIL CROP-SUN Model showed that the model was able to simulate the growth and yield of sunflower with an average of 10.44 error% between observed and simulate achene yield (AY). The result of simulation indicates that nitrogen rate of 180 kg/ha produced highest achene yield in S-78 hybrid as compared to other treatments and Hysun-33 cultivar.
Nitrogen Management of Diverse Sunflower (Helianthus annus L.) Hybrids Production under Agro-Climatic Conditions of Sargodha, Pakistan  [PDF]
Muhammad Irfan Ahmad, Amjed Ali, Aaqil Khan, Alam Sher, Arif Rashid, Sikandar Ali Jamro, Shafeeq ur-Rahman, Saboor Ahmad
American Journal of Plant Sciences (AJPS) , 2017, DOI: 10.4236/ajps.2017.86092
Abstract: A field study was carried out with the objective to determine the effect of various levels of nitrogen on growth, development, yield and yield components of different sunflower (Helianthus annuus L.) hybrids i.e. Hysun-33 and S-78 were evaluated under agro-climatic conditions of Sargodha, Pakistan during spring 2013. The experiment was laid out in a randomized complete block design with split plot arrangement having three replications, keeping cultivars in the main plots and N levels in the subplots. The net plot size was 4.2 m × 6 m. The growth parameters such are leaf area, leaf area duration and yield parameters were observed are Days to a thesis, Days to maturity, head diameter (cm), No. of achene’s per head, Achene yield (kg·ha-
Differential effects of cigarette smoke on oxidative stress and proinflammatory cytokine release in primary human airway epithelial cells and in a variety of transformed alveolar epithelial cells
Aruna Kode, Se-Ran Yang, Irfan Rahman
Respiratory Research , 2008, DOI: 10.1186/1465-9921-9-6
Abstract: In Figure 2 (Figure 1 in this paper) 'Cigarette smoke extract caused necrosis with no or little evidence of apoptosis in human lung cancer cells (H1299)' of our published article [1], panels d, e, and f show an identical red-staining pattern. The corrected figure, with the red staining pattern overlaying the green fluorescent staining of each group is given here as Figure 1.In addition in Figure 7 (Figure 2 in this paper) 'Cigarette smoke extract caused necrosis with no or little evidence of apoptosis in primary human small airway epithelial cells (SAEC)' of our published article [1], the cell morphology and histogram shown is identical to the cell morphology histogram given in Figure 3. The histogram for Figure 3 [1] is correct (and a corrected version of Figure 7 is given here as Figure 2) [1].These errors inadvertently occurred during the preparation of these figures from the images of the fluorescent microscope. We sincerely apologize for the error and any inconvenience or confusion it may have caused.
Differential effects of cigarette smoke on oxidative stress and proinflammatory cytokine release in primary human airway epithelial cells and in a variety of transformed alveolar epithelial cells
Aruna Kode, Se-Ran Yang, Irfan Rahman
Respiratory Research , 2006, DOI: 10.1186/1465-9921-7-132
Abstract: Primary human SAEC, transformed human (A549, H1299, H441), and rodent (murine MLE-15, rat L2) alveolar epithelial cells were treated with different concentrations of CSE (0.2–10%) ranging from 20 min to 24 hr. Cytotoxicity was assessed by lactate dehydrogenase release assay, trypan blue exclusion method and double staining with acridine orange and ethidium bromide. Glutathione concentration was measured by enzymatic recycling assay and 4-hydroxy-2-nonenal levels by using lipid peroxidation assay kit. The levels of proinflammatory cytokines (e.g. IL-8 and IL-6) were measured by ELISA. Nuclear translocation of the transcription factor, NF-κB was assessed by immunocytochemistry and immunoblotting.Cigarette smoke extract dose-dependently depleted glutathione concentration, increased 4-hydroxy-2-nonenal (4-HNE) levels, and caused necrosis in the transformed cell lines as well as in SAEC. None of the transformed cell lines showed any significant release of cytokines in response to CSE. CSE, however, induced IL-8 and IL-6 release in primary cell lines in a dose-dependent manner, which was associated with the nuclear translocation of NF-κB in SAEC.This study suggests that primary, but not transformed, lung epithelial cells are an appropriate model to study the inflammatory mechanisms in response to cigarette smoke.Cigarette smoke, a complex admixture of more than 4700 chemical compounds and oxidants [1], is an important etiological factor in the development of chronic obstructive pulmonary disease (COPD). It contains 1014–1016 free radicals/puff, which include reactive aldehydes, quinones and benzo(a)pyrene [2]. Many of these are relatively long lived, such as tar-semiquinone, which can also generate hydroxyl radicals (?OH) and hydrogen peroxide (H2O2) by Fenton reaction in presence of free iron. These agents induce an oxidative burden by disturbing the oxidant:antioxidant balance and could lead to cellular damage in the lungs. Oxidative stress caused by cigarette smoking c
P21-PARP-1 Pathway Is Involved in Cigarette Smoke-Induced Lung DNA Damage and Cellular Senescence
Hongwei Yao, Isaac K. Sundar, Vera Gorbunova, Irfan Rahman
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0080007
Abstract: Persistent DNA damage triggers cellular senescence, which may play an important role in the pathogenesis of cigarette smoke (CS)-induced lung diseases. Both p21CDKN1A (p21) and poly(ADP-ribose) polymerase-1 (PARP-1) are involved in DNA damage and repair. However, the role of p21-PARP-1 axis in regulating CS-induced lung DNA damage and cellular senescence remains unknown. We hypothesized that CS causes DNA damage and cellular senescence through a p21-PARP-1 axis. To test this hypothesis, we determined the levels of γH2AX (a marker for DNA double-strand breaks) as well as non-homologous end joining proteins (Ku70 and Ku80) in lungs of mice exposed to CS. We found that the level of γH2AX was increased, whereas the level of Ku70 was reduced in lungs of CS-exposed mice. Furthermore, p21 deletion reduced the level of γH2AX, but augmented the levels of Ku70, Ku80, and PAR in lungs by CS. Administration of PARP-1 inhibitor 3-aminobenzamide increased CS-induced DNA damage, but lowered the levels of Ku70 and Ku80, in lungs of p21 knockout mice. Moreover, 3-aminobenzamide increased senescence-associated β-galactosidase activity, but decreased the expression of proliferating cell nuclear antigen in mouse lungs in response to CS. Interestingly, 3-aminobenzamide treatment had no effect on neutrophil influx into bronchoalveolar lavage fluid by CS. These results demonstrate that the p21-PARP-1 pathway is involved in CS-induced DNA damage and cellular senescence.
Multiple Levels of Abstraction in the Simulation of Microthreaded Many-Core Architectures  [PDF]
Irfan Uddin
Open Journal of Modelling and Simulation (OJMSi) , 2015, DOI: 10.4236/ojmsi.2015.34017
Abstract: Simulators are generally used during the design of computer architectures. Typically, different simulators with different levels of complexity, speed and accuracy are used. However, for early design space exploration, simulators with less complexity, high simulation speed and reasonable accuracy are desired. It is also required that these simulators have a short development time and that changes in the design require less effort in the implementation in order to perform experiments and see the effects of changes in the design. These simulators are termed high-level simulators in the context of computer architecture. In this paper, we present multiple levels of abstractions in a high-level simulation of a general-purpose many-core system, where the objective of every level is to improve the accuracy in simulation without significantly affecting the complexity and simulation speed.
Hemoglobin α and β are ubiquitous in the human lung, decline in idiopathic pulmonary fibrosis but not in COPD
Nobuhisa Ishikawa, Steffen Ohlmeier, Kaisa Salmenkivi, Marjukka Myll?rniemi, Irfan Rahman, Witold Mazur, Vuokko L Kinnula
Respiratory Research , 2010, DOI: 10.1186/1465-9921-11-123
Abstract: Proteomics of fibrotic vs. control lung tissue suggested decreased levels of several spots in the lung specimens of IPF patients, which were identified as Hemoglobin (Hb) α and β monomers and Hbα complexes. The Hbα and β monomers and complexes were investigated in more detail in normal lung and lung specimens of patients with IPF and COPD by immunohistochemistry, morphometry and mass spectrometry (MS).Both Hb monomers, in normal lung, were expressed especially in the alveolar epithelium. Levels of Hbα and β monomers and complexes were reduced/lost in IPF but not in the COPD lungs when compared to control lung. MS-analyses revealed Hbα modification at cysteine105 (Cysα105), preventing formation of the Hbα complexes in the IPF lungs. Hbα and Hbβ were expressed as complexes and monomers in the lung tissues, but were secreted into the bronchoalveolar lavage fluid and/or induced sputum supernatants as complexes corresponding to the molecular weight of the Hb tetramer.The abundant expression of the oxygen carrier molecule Hb in the normal lung epithelium and its decline in IPF lung are new findings. The loss of Hb complex formation in IPF warrants further studies and may be considered as a disease-specific modification.Idiopathic pulmonary fibrosis (IPF) (histopathology of usual interstitial pneumonia, UIP) is classified as one of the idiopathic interstitial pneumonias, representing an entity with unknown etiology, aggressive fibrogenesis and a very poor prognosis [1,2]. IPF is considered primarily as a disease associated with epithelial/fibroblastic pathology [3,4]. Chronic obstructive pulmonary disease (COPD) is a slowly progressive but very common lung disease, with most of the cases being related to smoking. COPD involves not only airway inflammation/obstruction but also varying degrees of parenchymal lung damage i.e. emphysema combined with small airway fibrosis and the occurrence of patchy fibrotic lesions in the lung parenchyma. Despite recent advances in our under
Emphysema is associated with increased inflammation in lungs of atherosclerosis-prone mice by cigarette smoke: implications in comorbidities of COPD
Gnanapragasam Arunachalam, Isaac K Sundar, Jae-woong Hwang, Hongwei Yao, Irfan Rahman
Journal of Inflammation , 2010, DOI: 10.1186/1476-9255-7-34
Abstract: Adult male and female wild-type (WT) mice of genetic background C57BL/6J and ApoE-/- mice were exposed to CS, and lung inflammatory responses, oxidative stress (lipid peroxidation products), mechanical properties as well as airspace enlargement were assessed.The lungs of ApoE-/- mice showed augmented inflammatory response and increased oxidative stress with development of distal airspace enlargement which was accompanied with decline in lung function. Interestingly, the levels and activities of matrix metalloproteinases (MMP-9 and MMP-12) were increased, whereas the level of eNOS was decreased in lungs of CS-exposed ApoE-/- mice as compared to air-exposed ApoE-/- mice or CS-exposed WT mice.These findings suggest that CS causes premature emphysema and a decline of lung function in mice susceptible to cardiovascular abnormalities via abnormal lung inflammation, increased oxidative stress and alterations in levels of MMPs and eNOS.Chronic obstructive pulmonary disease (COPD) is characterized by chronic airflow limitation resulting from excessive airway inflammatory response mediated by cigarette smoke (CS). Comorbidities such as cardiovascular disease, diabetes, lung cancer, and osteoporosis are more prevalent in smokers and patients with COPD [1-3]. Recent studies have shown that smokers with altered forced expiratory volume in one second (FEV1) and airflow limitation are associated with arterial stiffness, exaggerated atherosclerosis and vice-versa [2,4,5]. Growing evidence also indicates that inflammation, endothelial dysfunction and oxidative modification of lipids play an important role in the pathogenesis of atherosclerosis and COPD [3,6,7]. In addition to CS, alcohol consumption is also one among the important contributing factors involved in the pathogenesis of COPD and atherosclerosis and their co-morbidities [8,9].Apolipoprotein E-deficient (ApoE-/-) mice develop atherosclerosis due to an accumulation of cholesterol ester-enriched particles in the blood resul
Airway biomarkers of the oxidant burden in asthma and chronic obstructive pulmonary disease: Current and future perspectives
Noora Louhelainen,Marjukka Myllärniemi,Irfan Rahman,Vuokko L Kinnula
International Journal of COPD , 2008,
Abstract: Noora Louhelainen1, Marjukka Myll rniemi1, Irfan Rahman2, Vuokko L Kinnula11Department of Medicine, Division of Pulmonary Medicine, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland; 2Department of Environmental Medicine and the Lung Biology and Disease Program, University of Rochester Medical Center, Rochester, New York, USAAbstract: The pathogenesis of asthma and chronic obstructive pulmonary disease (COPD) has been claimed to be attributable to increased systemic and local oxidative stress. Detection of the oxidant burden and evaluation of their progression and phenotypes by oxidant biomarkers have proved challenging and difficult. A large number of asthmatics are cigarette smokers and smoke itself contains oxidants complicating further the use of oxidant biomarkers. One of the most widely used oxidant markers in asthma is exhaled nitric oxide (NO), which plays an important role in the pathogenesis of asthma and disease monitoring. Another oxidant marker that has been widely investigated in COPD is 8-isoprostane, but it is probably not capable of differentiating asthma from COPD, or even sensitive in the early assessment of these diseases. None of the current biomarkers have been shown to be better than exhaled NO in asthma. There is a need to identify new biomarkers for obstructive airway diseases, especially their differential diagnosis. A comprehensive evaluation of oxidant markers and their combinations will be presented in this review. In brief, it seems that additional analyses utilizing powerful tools such as genomics, metabolomics, lipidomics, and proteomics will be required to improve the specificity and sensitivity of the next generation of biomarkers.Keywords: sputum, condensate, smoking, nitric oxide, 8-isoprostane, biomarker
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