ORCID Profile
0000-0003-2854-0116
Current Organisations
Faculdade de Ciencias e Tecnologia Universidade Nova de Lisboa
,
CSIRO Energy Centre Newcastle
,
CSIRO
Does something not look right? The information on this page has been harvested from data sources that may not be up to date. We continue to work with information providers to improve coverage and quality. To report an issue, use the Feedback Form.
Related Links
Publications
LIGAND-INDUCED DIFFERENTIATION OF GLUCOCORTICOID RECEPTOR (GR) TRANS-REPRESSION AND TRANSACTIVATION
Publisher: Portland Press Ltd.
Date: 05-1996
DOI: 10.1042/BST024267S
Steroid Resistance in Asthma: Molecular Mechanisms
Publisher: American Thoracic Society
Date: 08-1996
DOI: 10.1164/AJRCCM/154.2_PT_2.S58
Abstract: Biochar is widely used to remove hexavalent chromium [Cr(VI)] from wastewater through adsorption, which is recognized as a facile, cost-efficient, and high-selectivity approach. In this study, a versatile strategy that combines delignification with subsequent carbonization and KOH activation is proposed to prepare a novel woody biochar from waste poplar sawdust. By virtue of the unique multilayered and honeycomb porous structure induced by delignification and activation processes, the resultant activated carbonized delignified wood (ACDW) exhibits a high specific surface area of 970.52 m
Effects of inhaled beta agonist and corticosteroid treatment on nuclear transcription factors in bronchial mucosa in asthma
Publisher: BMJ
Date: 06-1999
DOI: 10.1136/THX.54.6.488
Abstract: Inhaled corticosteroids and beta agonists are the most commonly used treatments in asthma and are often used together. Recent evidence suggests that many of the anti-inflammatory actions of corticosteroids are mediated by cross-talk between the activated glucocorticoid receptor (GR) and other transcription factors such as the pro-inflammatory nuclear factor kappa B (NFkappaB). Beta agonists can activate the transcription factor cAMP response element binding protein (CREB). A mutual inhibition between GR and CREB occurs in vitro which raises the possibility of a negative interaction between corticosteroid and beta agonist drugs. A study was undertaken to determine whether these interactions occur during treatment with beta2 agonists and corticosteroids in asthma. Seven subjects who were participating in a randomised, placebo controlled, crossover study of six weeks treatment with inhaled budesonide (400 microg twice daily), terbutaline (1 mg four times daily), and combined treatment were recruited. Biopsy s les of the bronchial mucosa were obtained after each treatment and analysed for the DNA binding activity of GR, CREB, and NFkappaB. Budesonide increased GR activity (p<0.05) and decreased NFkappaB activity (p<0.05). No treatment combination altered CREB activity and terbutaline had no significant effects on any transcription factor. Inhaled corticosteroids have significant effects on GR and NFkappaB activity in bronchial mucosa. A negative interaction between inhaled corticosteroids and beta agonists was not found.
Renewable-powered hydrogen economy from Australia’s perspective
Publisher: Elsevier BV
Date: 09-2020
Solar-powered PCC: An upfront levy for sustainable carbon capture
Publisher: Elsevier BV
Date: 03-2022
NF-κB involvement in IL-1β-induction of GM-CSF and COX-2: inhibition by glucocorticoids does not require I-κB
Publisher: Portland Press Ltd.
Date: 05-1997
DOI: 10.1042/BST025154S
Abstract: The S100/calgranulin gene appears to modulate neuroinflammation following cerebral ischemia and could be a valuable biomarker for stroke prognosis, according to growing research. This study aimed at evaluating the correlation between calgranulin gene variants and susceptibility to ischemic stroke (IS) in the Southern Chinese population. Using an enhanced multi-temperature ligase detection reaction genotyping, 310 IS patients and 324 age-matched healthy controls were genotyped to identify five calgranulin gene variants. According to the obtained results, the S100A8 rs3795391, rs3806232, and S100A12 rs2916191 variants were linked to a higher risk of IS, while the S100A9 rs3014866 variant was associated with a lower risk of IS. Moreover, the T-T-C-A-T, T-T-C-G-T, or C-C-C-G-C haplotypes have been linked to a greater risk of developing IS, according to haplotype analysis. The occurrence of the variant C allele there in S100A8 rs3795391, rs3806232, and S100A12 rs2916191 variants may impart a greater risk of stroke in the LAA subtype, according to further stratification by IS subtypes, while the T allele of the S100A9 rs3014866 variant may be linked to a reduced risk of stroke of all subtypes. Furthermore, patients with the variant C allele of the S100A8 rs3795391, rs3806232, and S100A12 rs2916191 variants presented with increased circulating S100A8 and S100A12 levels and larger infarct volumes relative to those with the major TT genotype. Our findings suggest that calgranulin gene variants are linked to IS susceptibility, implying that the calgranulin gene may be a potential biomarker for IS prevention and personalized treatment.
Transcription factors and asthma
Publisher: European Respiratory Society (ERS)
Date: 07-1998
DOI: 10.1183/09031936.98.12010221
Abstract: Asthma is characterized by the expression of multiple genes for inflammatory proteins, such as cytokines, enzymes, receptors and adhesion molecules. This is orchestrated by transcription factors, which are proteins that bind to the promoter regions of these genes and may be activated by inflammatory stimuli, such as cytokines. Several transcription factors are involved in asthmatic inflammation, including nuclear factor-kappaB (NF-kappaB), activator protein-1 (AP-1), nuclear factor of activated T-cells (NF-AT), cyclic AMP response element binding protein (CREB) and signal transduction-activated transcription factors (STAT). These transcription factors lead to coordinated expression of multiple inflammatory genes. There is increasing evidence that synergistic interaction of these transcription factors (e.g. NF-kappaB and AP-1) results in the optimal expression of particular genes, resulting in the specific inflammatory pattern seen in asthmatic airways. Transcription factors are a target for antiasthma therapy. Corticosteroids activate glucocorticoid receptors, which themselves are transcription factors, and interact with other transcription factors to inhibit their actions. The interaction between transcription factors may be important in lifying and inhibiting the inflammatory process. Many transcription factors interact with a large co-activator molecule CREB-binding protein (CBP) that coordinates the activation of several transcription factors and controls transcription through the regulation of deoxyribonucleic acid coiling around histone residues in the chromatin structure. Understanding transcription factors in asthma has given new insights into the complex chronic inflammatory process, the mechanism of action of corticosteroids, and may lead to new approaches to therapy in the future.
Model-based analysis of CO2 revalorization for di-methyl ether synthesis driven by solar catalytic reforming
Publisher: Elsevier BV
Date: 09-2016
Ligand‐induced differentiation of glucocorticoid receptor (GR) trans‐repression and transactivation: preferential targetting of NF‐κB and lack of I‐κB involvement
Publisher: Wiley
Date: 06-1999
A model-based analysis of CO2 utilization in methanol synthesis plant
Publisher: Elsevier BV
Date: 06-2015
Computer-aided design for high efficiency latent heat storage – a case study of a novel domestic solar hot water process
Publisher: Elsevier
Date: 2017
Enhancing the performance of a solar-assisted adsorption chiller using advanced composite materials
Publisher: Elsevier BV
Date: 11-2018
T CELL RECEPTOR REPERTOIRE IN PERIPHERAL BLOOD AND BRONCHIAL BIOPSIES FROM NORMAL AND ASTHMATIC SUBJECTS
Publisher: Portland Press Ltd.
Date: 05-1996
DOI: 10.1042/BST024316S
Identification of the protein kinase C isoenzymes in human lung and airways smooth muscle at the protein and mRNA level
Publisher: Elsevier BV
Date: 07-1997
DOI: 10.1016/S0006-2952(97)00165-2
Abstract: The protein kinase C (PKC) isoenzymes expressed by human peripheral lung and tracheal smooth muscle resected from in iduals undergoing heart-lung transplantation were identified at the protein and mRNA level. Western immunoblot analyses of human lung identified multiple PKC isoenzymes that were differentially distributed between the soluble and particulate fraction. Thus, PKC alpha, PKC betaII, PKC epsilon, and PKC zeta were recovered predominantly in the soluble fraction whereas the eta isoform was membrane-associated together with trace amounts of PKC alpha and PKC epsilon. PKC beta1-like immunoreactivity was occasionally seen although the intensity of the band was uniformly weak. Immunoreactive bands corresponding to PKCs gamma, delta, or theta were never detected. Reverse transcription-polymerase chain reaction (RT-PCR) of RNA extracted from human lung using oligonucleotide primer pairs that recognise unique sequences in each of the PKC genes lified cDNA fragments that corresponded to the predicted sizes of PKC alpha, PKC betaI, PKC betaII, PKC epsilon, PKC zeta, and PKC eta (consistent with the expression of PKC isoenzyme protein) and, in addition, mRNA for PKC delta PCR fragments of the expected size for the supposedly muscle-specific isoform, PKC theta, or the atypical isoenzyme, PKC lambda, were never obtained. The complement and distribution of PKC isoforms in human trachealis were similar, but not identical, to human lung. Thus, immunoreactive bands corresponding to the alpha, betaI, betaII, epsilon, and zeta isoenzymes of PKC were routinely labelled in the cytosolic fraction. In the particulate material PKC alpha, PKC epsilon, PKC alpha, PKC eta, and PKC mu were detected by immunoblotting. With the exception of PKC zeta, RT-PCR analyses confirmed the expression of the PKC isoforms detected at the protein level and, in addition, identified mRNA for PKC delta. Collectively, these data clearly demonstrate the expression of multiple PKC isoenzymes in human lung and tracheal smooth muscle, suggesting that they subserve erse multifunctional roles in these tissues.
Inducible nitric oxide synthase after sensitization and allergen challenge of Brown Norway rat lung
Publisher: Wiley
Date: 07-1997
Agile solar roof tile HVAC
Publisher: IOP Publishing
Date: 04-2020
DOI: 10.1088/1757-899X/778/1/012103
Abstract: This paper studies the technical feasibility of a novel solar roof tile (SRT) to be used for HVAC (heating, ventilation and air conditioning) in buildings. The SRT utilizes a phase change material (PCM) for thermal storage. The SRT works like a conventional thermal storage tank while featuring compact size and lower cost. Two heat exchangers are connected one each on the top and bottom of the PCM matrix. The top heat exchanger functions as an absorber of solar heat. Aqueous sodium hydroxide passes to the top heat exchanger from a storage sump. The bottom heat exchanger is the condenser and evaporator with water passing through the heat exchanger. The cooling system is integrated inside the customised roof tile interlocking system. This system uses roof tiles that have higher performance during extreme weather conditions and lower maintenance costs. In this paper, we have investigated the thermal performance and technical feasibility of the proposed solar SRT-HVAC system. This proposition eliminates conventional thermal storage tanks used in solar thermal collectors. The dynamic performance of the SRT under transient conditions is evaluated using the TRNSYS modelling package, which shows the influence of design variables like insulation points and charging/discharging durations on thermal storage performance.
Cytokine induction of cytosolic phospholipase A2 and cyclooxygenase-2 mRNA is suppressed by glucocorticoids in human epithelial cells
Publisher: Elsevier BV
Date: 11-1996
DOI: 10.1016/S0024-3205(96)00590-5
Abstract: Prostaglandin (PG) release, which is increased in vivo by inflammatory conditions and in vitro by pro-inflammatory cytokines, is decreased by glucocorticoids. Two phospholipase A2 isoforms, secretory (sPLA2) and cytosolic (cPLA2,), have been implicated in inflammation. These enzymes catalyse the release of arachidonic acid which is then converted to prostaglandins by the cyclooxygenases (COX-1 and COX-2). Regulation of these events at the mRNA level is poorly characterised in epithelial cells. We have used a human epithelial-like cell line (A549) as a model system to study mRNA expression of sPLA2, cPLA2, COX-1 and COX-2. Following treatment of cells and extraction of RNA, semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) was used to examine expression of these genes. We show a coordinate induction of both cPLA2 and COX-2 mRNA by pro-inflammatory cytokines which correlated with increased PGE2 release. By contrast, sPLA2 mRNA was undetectable and COX-1 was found to be expressed at a constant low level. In addition dexamethasone pretreatment significantly reduced both cPLA2 and COX-2 mRNA levels as well as PGE2 release following cytokine stimulation. These data indicate a major role for control of prostaglandin synthesis at the mRNA level of key synthetic genes in epithelial cells. Furthermore we show that a major mechanism of glucocorticoid action in preventing prostaglandin release occurs by suppression of cPLA2 and COX-2 mRNA levels.
[50] Induction of nuclear factor-κB by exposure to ozone and inhibition by glucocorticoids
Publisher: Elsevier
Date: 2000
Superinduction of COX‐2 mRNA by cycloheximide and interleukin‐1β involves increased transcription and correlates with increased NF‐κB and JNK activation
Publisher: Wiley
Date: 24-11-1997
DOI: 10.1016/S0014-5793(97)01362-8
Abstract: Many primary response genes, including cyclooxygenase-2 (COX-2), exhibit mRNA superinduction following agonist stimulation in the presence of translational blockers such as cycloheximide. This is widely assumed to result from mRNA stabilisation. However, superinduction of IL-1beta-induced COX-2 mRNA levels by cycloheximide in pulmonary type II A549 cells occurred by increased transcription and not by mRNA stabilisation. Furthermore, equivalent effects were observed on NF-kappaB binding to COX-2 promoter kappaB sites and activation of the Jun N-terminal kinases (JNK), p54 and p46. These signalling pathways play important roles in COX-2 induction and may therefore account for the observed increases in COX-2 transcription. These data are consistent with negative feed-back involving down-regulation of NF-kappaB by de novo IkappaB alpha synthesis and suggest that JNK activation may also be down-regulated by a cycloheximide sensitive process.
Assessing the current state of biomass gasification technology in advancing circular economies: A holistic analysis from techno-economic-policy perspective in Malaysia and beyond
Publisher: Elsevier BV
Date: 11-2023
Asthma: Application of Cell and Molecular Biology Techniques to Unravel Causes and Pathophysiological Mechanisms
Publisher: Humana Press
Date: 2000
Abstract: The condition termed "asthma" has been difficult to define satisfactorily. Much of this problem arises from poor understanding of its causes, natural history, and pathophysiology, and also from a lack of a specific marker(s) of the disease. To the clinician, the diagnosis of asthma is not difficult in most cases, particularly if patients present early with symptoms of intermittent wheeze and chest tightness, and if their symptoms respond to particular treatments, such as β-adrenergic agonists. Early definitions of asthma included the presence of airway obstruction that could spontaneously reverse with treatment, and also the increased narrowing of the airways to non-specific bronchoconstrictor stimuli, i.e., bronchial hyperresponsiveness (BHR). The essential elements of this definition were useful in separating asthma from other conditions, such as chronic bronchitis, chronic obstructive pulmonary disease, and emphysema, which could sometimes be diagnostically confused with asthma. More recently, the definition of asthma has been enhanced by the recognition that the airway submucosa of patients with asthma are chronically inflamed with a typical inflammatory infiltrate, and that inflammatory processes are important causes of the chief characteristics of asthma: airway obstruction and BHR. In addition, the loss of reversibility of airway obstruction as a long-term effect of the chronic inflammatory process is recognized:
Corticosteroid-resistant bronchial asthma is associated with increased c-fos expression in monocytes and T lymphocytes.
Publisher: American Society for Clinical Investigation
Date: 15-12-1998
DOI: 10.1172/JCI2680
Mechanistic qualities of steroids in chronic–severe asthma
Publisher: Wiley
Date: 06-2001
Albuterol Does Not Antagonize the Inhibitory Effect of Dexamethasone on Monocyte Cytokine Release
Publisher: American Thoracic Society
Date: 03-1998
DOI: 10.1164/AJRCCM.157.3.9707116
Abstract: Beta2-adrenoceptor agonists given by the inhaled route are the most effective bronchodilators known, yet high doses of these drugs may be associated with an increase in asthma mortality and morbidity. One theory for this paradox is that chronic use of beta2-adrenoceptor agonists compromises the anti-inflammatory action of glucocorticosteroids. This hypothesis derives from the ability of albuterol and fenoterol to inhibit the interaction of the glucocorticosteroid receptor (GR) with proinflammatory transcriptional activators acting on the promoter region of certain target genes that encode cytokines such as tumor necrosis factor-alpha (TNF alpha) and granulocyte/macrophage colony-stimulating factor (GM-CSF). However, the functional relevance of these results has not been formally investigated. We have tested the hypothesis that albuterol reduces the ability of dexamethasone to inhibit the generation of TNF alpha and GM-CSF from lipopolysaccharide (LPS)-stimulated human monocytes. Pretreatment of human monocytes with albuterol (1 and 100 microM) for 5 and for 180 min inhibited maximally TNF alpha generation by approximately 25%. However, regardless of the concentration of albuterol, or the time of preincubation, the inhibitory effect of dexamethasone was not significantly affected with respect to the EC50 or the maximal effect produced. Qualitatively identical data were obtained when GM-CSF release was used as an index of monocyte activation. We conclude that high concentrations of albuterol do not compromise the ability of dexamethasone to suppress the generation of TNF alpha and GM-CSF from LPS-stimulated human monocytes.
Induction of Phosphodiesterases 3B, 4A4, 4D1, 4D2, and 4D3 in Jurkat T-cells and in Human Peripheral Blood T-lymphocytes by 8-Bromo-cAMP and Gs-coupled Receptor Agonists
Publisher: Elsevier BV
Date: 08-1998
Glucocorticoid Receptor Recruitment of Histone Deacetylase 2 Inhibits Interleukin-1β-Induced Histone H4 Acetylation on Lysines 8 and 12
Publisher: Informa UK Limited
Date: 09-2000
Optimizing an advanced hybrid of solar-assisted supercritical CO2 Brayton cycle: A vital transition for low-carbon power generation industry
Publisher: Elsevier BV
Date: 09-2017
Dynamic modelling and analysis of a novel latent heat battery in tankless domestic solar water heating
Publisher: Elsevier BV
Date: 10-2017
Techno-Economic Analysis of ‘Solar-Powered’ Post-Combustion Carbon Capture
Publisher: Elsevier BV
Date: 2021
DOI: 10.2139/SSRN.3812039
Glucocorticoid-mediated transrepression is regulated by histone acetylation and DNA methylation
Publisher: Elsevier BV
Date: 10-2001
DOI: 10.1016/S0014-2999(01)01332-2
Abstract: Glucocorticoids are highly effective in controlling chronic inflammatory diseases by inhibiting the expression of cytokines and chemokines. Glucocorticoids act through binding of their receptor resulting to inhibition of transcription factors such as nuclear factor kappa B (NF-kappa B). This may occur via the transcription integrator protein, CREB binding protein (CBP), which has intrinsic histone acetylase (HAT) activity. Interleukin (IL)-1 beta caused a significant increase in NF-kappa B-mediated granulocyte/macrophage colony stimulating factor (GM-CSF) release, which was inhibited by the glucocorticoid mometasone furoate (MF) (EC(50)=2 x 10(-11) M). This effect was inhibited by CBP over-expression. The role of histone acetylation and DNA methylation in the transcription of GM-CSF was indicated by trichostatin A (TSA), an inhibitor of histone deacetylases, and 5-azacytidine (5-aza), a DNA methylase inhibitor, to increase GM-CSF expression partially blocking glucocorticoid inhibition of IL-1 beta-stimulated GM-CSF release. These data suggest that the mechanism of glucocorticoid action in suppressing interleukin-1 beta-stimulated GM-CSF release in A549 cells may involve modulation of CBP-mediated histone-acetylase activity and DNA methylation.
Sustainable transformation of fly ash industrial waste into a construction cement blend via CO2 carbonation
Publisher: Elsevier BV
Date: 07-2017
Waste tire pyrolysis using thermal solar energy: An integrated approach
Publisher: Elsevier BV
Date: 08-2018
Low‐dose theophylline does not exert its anti‐inflammatory effects in mild asthma through upregulation of interleukin‐10 in alveolar macrophages
Publisher: Wiley
Date: 11-2001
DOI: 10.1034/J.1398-9995.2001.00097.X
Abstract: There is accumulating evidence that theophylline has anti-inflammatory or immunomodulatory effects. This may be, in part, mediated via an upregulation in the production of the anti-inflammatory cytokine interleukin (IL)-10. We determined whether low-dose theophylline (LDT) would increase the production of IL-10, and attenuate the production of proinflammatory cytokines by alveolar macrophages. In a double-blind, placebo-controlled, crossover study involving 15 steroid-free patients with mild asthma, fiberoptic bronchoscopy and bronchoalveolar lavage (BAL) were performed at the end of the treatment and placebo periods. Alveolar macrophages were cultured in vitro, and we measured their release of IL-10, GM-CSF, and TNF-alpha. We also measured IL-10 production in whole blood together with the number of monocytes and T cells expressing intracellular IL-10 by flow cytometry. LDT did not increase the production of IL-10, or attenuate the production of GM-CSF or TNF-alpha by alveolar macrophages. However, after theophylline treatment, there was a significant reduction in mean (SD) (95% CI) BAL eosinophil number from 3.4 (1.7)% (95% CI 2.4-4.4) to 1.7 (1.0)% (95% CI 1.1-2.3) compared with placebo (P<0.05). Similarly, there was no increase in whole-blood IL-10 release or in the number of monocytes and T cells expressing intracellular IL-10 after treatment. LDT has an anti-inflammatory effect in asthma however, this effect is not mediated via the production of IL-10 or the attenuation of GM-CSF or TNF-alpha. The mechanisms of theophylline activity remain to be determined.
A Modelling Framework for the Conceptual Design of Low-Emission Eco-Industrial Parks in the Circular Economy: A Case for Algae-Centered Business Consortia
Publisher: MDPI AG
Date: 31-12-2020
DOI: 10.3390/W13010069
Abstract: This article describes a unique industrial symbiosis employing an algae cultivation unit (ACU) at the core of a novel eco-industrial park (EIP) integrating fossil-fuel fired power generation, carbon capture, biofuel production, aquaculture, and wastewater treatment. A new modelling framework capable of designing and evaluating materials and energy exchanges within an industrial eco-system is introduced. In this scalable model, an algorithm was developed to balance the material and energy exchanges and determine the optimal inputs and outputs based on the industrial symbiosis objectives and participating industries. Optimizing the functionality of the ACU not only achieved a substantial emission reduction, but also boosted aquaculture, biofuel, and other chemical productions. In a power-boosting scenario (PBS), by matching a 660 MW fossil fuel-fired power plant with an equivalent solar field in the presence of ACU, fish-producing aquaculture and biofuel industries, the net CO2 emissions were cut by 60% with the added benefit of producing 39 m3 biodiesel, 6.7 m3 bioethanol, 0.14 m3 methanol, and 19.55 tons of fish products annually. Significantly, this article shows the potential of this new flexible modelling framework for integrated materials and energy flow analysis. This integration is an important pathway for evaluating energy technology transitions towards future low-emission production systems, as required for a circular economy.
Glucocorticoid receptor localization in normal and asthmatic lung.
Publisher: American Thoracic Society
Date: 09-1996
DOI: 10.1164/AJRCCM.154.3.8810618
Abstract: The localization and distribution of the human glucocorticoid receptor (GR) mRNA and protein was investigated in human lung obtained from transplant donors and recipients by in situ hybridization, RNA blot analysis, immunolocalization, and Western analysis. Subjects were either nonasthmatic or had mild asthma requiring only beta(2)-agonists. No difference in amount of GR mRNA was found in total RNA isolated from nonasthmatic or asthmatic donor lung. In situ hybridization showed the highest concentration of GR mRNA in the alveolar walls and vascular endothelium and smooth muscle, with lesser amounts in the airway epithelium and smooth muscle. There was no change in the level or sites of expression of GR mRNA between normal and asthmatic subjects. Immunolocalization of GR confirmed the in situ hybridization data. There was no change in the level or sites of expression of GR, in either the lung or airway, between normal and asthmatic subjects. Immunolocalization of GR in bronchial biopsies from two normal and asthmatic subjects confirmed the localization and distribution of GR. Western analysis and mobility shift assays confirmed no differences in GR levels between the two subject groups. The localization of GR mRNA and protein to specific cell types within lung and airway will make it possible to study the cellular targets of glucocorticoid therapy in inflammatory lung diseases such as asthma.
Process enhancement in aqueous ammonia PCC using a direct contact condenser
Publisher: Wiley
Date: 11-01-2019
DOI: 10.1002/GHG.1842
Pilot-plant and laboratory demonstration of advanced aqueous ammonia-based CO2 capture technologies Final report
Publisher: CSIRO
Date: 2020
Expression of GATA family of transcription factors in T-cells, monocytes and bronchial biopsies
Publisher: European Respiratory Society (ERS)
Date: 09-2001
DOI: 10.1183/09031936.01.00040701
Abstract: GATA-binding proteins are a subfamily of zinc finger transcription factors with six members (GATA-1-6) that interact with the GATA deoxyribonucleic acid (DNA) sequence. This sequence is found in the regulatory regions of many genes including those encoding T-helper 2 (Th2)-like cytokines, receptors, adhesion molecules and enzymes, which may be important in the pathogenesis of bronchial asthma. The expression of GATA-3, -4 and -6 was investigated in peripheral blood T-lymphocytes and monocytes and bronchial biopsies from 11 normal subjects and 10 steroid-naïve asthmatic patients. Using Western blot analysis, T-cells from asthmatic subjects expressed 5 times the level of GATA-3 compared to that in normals. Confocal microscopy indicated that GATA-3 expression was both nuclear and cytoplasmic. GATA DNA binding complex containing GATA-3 was elevated in Th2 cells as determined by electrophorectic mobility shift assay. In contrast, monocytes from normal and asthmatic subjects expressed GATA-4 and -6 in equal amounts, but no GATA-3 was found. Using immunohistochemistry in bronchial biopsies, epithelial cells expressed high levels of GATA-3, GATA-4 and GATA-6 proteins. Comparison of Western blots of bronchial biopsies showed no significant differences between normal and asthmatic subjects. In conclusion, the increased expression of GATA-3 in asthmatic T-cells may underlie augmented T-helper 2-like cytokines in this disease. However, the unaltered GATA-3 expression in epithelial cells suggests a distinct role for GATA-3 in these cells unrelated to T-helper 2-like cytokine release. Finally, no evidence was found for an increased expression of GATA-4 and GATA-6 in asthma.
A novel process for direct solvent regeneration via solar thermal energy for carbon capture
Publisher: Elsevier BV
Date: 04-2017
Effects of Inhaled Corticosteroid Therapy on Expression and DNA-Binding Activity of Nuclear Factor κ B in Asthma
Publisher: American Thoracic Society
Date: 2000
DOI: 10.1164/AJRCCM.161.1.9809019
Abstract: We determined whether inhaled corticosteroid therapy modulates the expression of the transcription factor, nuclear factor kappa B (NF-kappaB), in patients with asthma. Fifteen stable patients with mild asthma underwent bronchoalveolar lavage (BAL) with bronchial biopsies in a double-blind, placebo-controlled and crossover study after placebo or after inhaled fluticasone propionate (500 microg twice daily). Fluticasone reduced the number of eosinophils in BAL fluid (BALF) and in airway biopsies, together with an improvement of bronchial responsiveness to methacholine. However, NF-kappaB DNA-binding in alveolar macrophages and in bronchial biopsies was not affected by fluticasone treatment. NF-kappaB expression was also measured by immunohistochemical staining with an antibody to the p65 component of NF-kappaB. Fluticasone caused an increase in the number of positive nuclear staining cells in the airway epithelium from 34. 1 +/- 5.0 to 64.1 +/- 8.0 per mm(2) (p = 0.002). In vitro studies of A549 epithelial cells stimulated by interleukin-1beta (IL-1beta) showed that dexamethasone increased p65 protein expression analyzed by Western blot. Despite an anti-inflammatory effect of fluticasone, there was no decrease in NF-kappaB-DNA binding and activation, indicating that this may not be a mechanism by which corticosteroids act in asthma. The significance of corticosteroid-induced increase in p65 protein expression is not known.
Integration of solar energy in coal-fired power plants retrofitted with carbon capture: A review
Publisher: Elsevier BV
Date: 10-2014
Green pathways for urea synthesis: A review from Australia’s perspective
Publisher: Elsevier BV
Date: 2022
Evidence for Involvement of NF-κB in the Transcriptional Control of COX-2 Gene Expression by IL-1β
Publisher: Elsevier BV
Date: 08-1997
Abstract: The cyclooxygenase (COX) isoforms COX-1 and COX-2 convert arachidonic acid to prostaglandin (PG) precursors and are a limiting step in PG production. Interleukin-1beta (IL-1beta) treatment of type II A549 cells increases PGE2 synthesis via transcription- and translation-dependent induction of COX-2. IL-1beta produces a 10-fold induction of COX-2 mRNA and an 8-fold increase in COX-2 transcription that was temporally preceded by activation of the transcription factor nuclear factor-kappaB (NF-kappaB). The protein-tyrosine phosphatase inhibitor phenylarsine oxide (PAO) prevented both NF-kappaB activation and induction of COX-2 mRNA. We show that two putative NF-kappaB motifs, kappaBu (-447/-438) and kappaBd (-224/-214), from the COX-2 promoter bind p50 65 NF-kappaB heterodimers in an IL-1beta-dependent manner and that the upstream element has the greater affinity. Finally, we demonstrate that the two NF-kappaB subunits, p50 and p65, synergistically activate a -917/+49 COX-2 promoter construct. We conclude that IL-1beta stimulates PG production via transcriptional activation of COX-2 and provide evidence that this may involve NF-kappaB.
Glucocorticoid-regulated Transcription Factors
Publisher: Elsevier BV
Date: 06-2001
Analysis of Transcription Factor Activation: NFκ B as Regulator of Inflammatory Genes in Epithelial Cells
Publisher: Humana Press
Date: 2000
DOI: 10.1385/1-59259-072-1:143
Abstract: In addition to being essential for differentiation and maturation, regulated gene expression governs many cellular responses to their local environment. For ex le, cytokines, viral infection, and numerous other inflammatory stimuli elicit the expression of specific response genes. Such signals are generally.
Renewable Energy Integration in Combined Cooling, Heating, and Power (CCHP) Processes
Publisher: Elsevier
Date: 2019
Analysis of di-methyl ether production routes: Process performance evaluations at various syngas compositions
Publisher: Elsevier BV
Date: 07-2016
A novel design protocol for solar-powered carbon capture
Publisher: Elsevier BV
Date: 12-2021
Albuterol-induced downregulation of Gsα accounts for pulmonary β2-adrenoceptor desensitization in vivo
Publisher: American Society for Clinical Investigation
Date: 07-2000
DOI: 10.1172/JCI8374
Pathophysiological Mechanisms of Asthma: Application of Cell and Molecular Biology Techniques
Publisher: Springer Science and Business Media LLC
Date: 2001
DOI: 10.1385/MB:18:3:213
Projecting Movement, Union, Synergy, Interplay & Cultural-collaboration across the Silk Road (& beyond)
Publisher: Center for Open Science
Date: 04-06-2019
Abstract: Interplay between culture and globalisation, and in particular the musical connection between the two has been forwarded as an illustrative, hopeful, and harmonious ex le of how humanity as a global race may enhance mutual understanding and cross-cultural appreciation of its many erse groups. In particular, this study aims to investigate the global community-building behind the relatively recent Silkroad initiative, and to what degree has its aims been achieved, and how.
Analysis for flexible operation of supercritical CO2 Brayton cycle integrated with solar thermal systems
Publisher: Elsevier BV
Date: 04-2017
NF-kB: a pivotal role in asthma and a new target for therapy
Publisher: Elsevier BV
Date: 02-1997
DOI: 10.1016/S0165-6147(97)89796-9
Abstract: Preoperative optimization programs have demonstrated positive effects on perioperative physical function and surgical outcomes. In nonsurgical populations, physical activity and healthy diet may reduce pain and pain medication requirement, but this has not been studied in surgical patients. Our aim was to determine whether a preoperative diet and exercise intervention affects postoperative pain and pain medication use. Patients undergoing abdominal colorectal surgery were invited to participate in a web-based patient engagement program. Those enrolling in the first and third time periods received information on the standard perioperative pathway (enhanced recovery after surgery [ERAS]). Those enrolling in the second time period also received reminders on nutrition and exercise (PREHAB + ERAS). The primary outcome was postoperative inpatient opioid use. The secondary outcomes were inpatient postoperative pain scores and nonopioid pain medication use. The ERAS and PREHAB + ERAS groups were similar in demographic and operative characteristics. Subgroup analysis of patients who activated their accounts demonstrated that the two groups had similar average maximum daily pain scores, but the PREHAB + ERAS group (n = 158) used 15.9 fewer oral morphine equivalents per postoperative inpatient day than the ERAS group (n = 92), representing a 30% decrease (53 mg versus 37.1 mg, P = 0.04). The two groups used comparable amounts of acetaminophen, gabapentin, and ketorolac. Generalized linear models demonstrated that PREHAB + ERAS, minimally invasive surgery, and older age were associated with lower inpatient opioid use. Access to a web-based preoperative diet and exercise program may reduce inpatient opioid use after major elective colorectal surgery. Further studies are necessary to determine whether the degree of adherence to nutrition and physical activity recommendations has a dose-dependent effect on opioid use.
Role of CBP in glucocorticoid-induced gene repression
Publisher: Portland Press Ltd.
Date: 08-1998
DOI: 10.1042/BST026S255
Advanced control strategies for dynamic operation of a solar-assisted recompression supercritical CO2 Brayton power cycle
Publisher: Elsevier BV
Date: 05-2018
Histone Acetylation and Histone Deacetylation
Publisher: Humana Press
Date: 2000
DOI: 10.1385/1-59259-072-1:309
Abstract: In the resting cell, DNA is tightly compacted to prevent transcription factor accessibility. During activation of the cell, this compact inaccessible DNA is made available to DNA-binding proteins, thus allowing the induction of gene transcription (1 ,2). DNA is packaged into chromatin, a highly organized and dynamic protein-DNA complex. The fundamental subunit of chromatin, the nucleosome, is composed of an octomer of four core histones, an H3/H4 tetramer and two H2A/H2B dimers, surrounded by 146 bp DNA (2,3). The packaging of DNA into nucleosomes acts as a barrier to the initiation of transcription by preventing the access of transcriptional factors, and RNA polymerase II, to their cognate recognition sequences (4). Specific lysine residues in the N-terminal tails of the core histone can be post-translationally modified by acetylation of the ε-amino group. The dynamic equilibrium of core histone acetylation is established and maintained by histone acetyltransferase (HAT) and histone deacetylase (HDAC). Several transcriptional regulators possess intrinsic HAT and HDAC activities, strongly suggesting that histone acetylation and deacetylation play a causal role in regulating transcription (5-8). There is compelling evidence that increased gene transcription is associated with an increase in histone acetylation hypoacetylation of histone is correlated with reduced transcription or gene silencing (2 ,7,8 Fig 1).
Analysis of CO2 utilization for methanol synthesis integrated with enhanced gas recovery
Publisher: Elsevier BV
Date: 2016
TGFβ1 allele association with asthma severity
Publisher: Springer Science and Business Media LLC
Date: 27-10-2001
DOI: 10.1007/S00439-001-0617-Y
Abstract: Transforming growth factor beta1 (TGFbeta1) is a multifunctional cytokine involved in pro- and anti-inflammatory pathways and is expressed in several cell types. Subepithelial fibrosis is one of the principle features of airway remodelling in asthma and is increased in severe patients. TGFbeta1 is implicated in fibrosis, including the deposition of extracellular matrix proteins. TGFbeta1 mRNA levels in eosinophils are increased in severe asthmatics relative to mild asthmatics. Therefore, TGFbeta1 is a promising candidate gene for contributing to asthma severity. Four polymorphisms located in the promoter region and signal peptide (C-509T, 72insC, T869C and G915C) were genotyped in groups of severe asthmatic, mild asthmatic or control in iduals defined by steroid usage and pulmonary function. Significant differences ( P=0.016) were found between the groups for the genotype frequencies at C-509T, attributable mainly to a greater relative frequency of homozygosity for the -509T allele in the severe group compared to the mild and control groups. In iduals homozygous for -509T were also homozygous at the other variant sites for the 72C, 869C and 915G alleles (haplotype 1). The T allele creates a putative YY1 transcription factor binding site, but binding between YY1 and the DNA sequence of the T allele was not detected in vitro. In this study, we show that the -509T variant on haplotype 1 is the most informative marker of the TGFbeta1 contribution to asthma severity.
Activation and Localization of Transcription Factor, Nuclear Factor- κ B, in Asthma
Publisher: American Thoracic Society
Date: 11-1998
DOI: 10.1164/AJRCCM.158.5.9706116
Abstract: Asthma is associated with increased expression of inflammatory proteins including cytokines, enzymes, and adhesion molecules. Induction of many of the genes for these proteins is regulated by the transcription factor, nuclear factor-kappaB (NF-kappaB). We therefore examined whether airway cells from patients with asthma show increased activation of NF-kappaB. Nuclear proteins were extracted from cells of induced sputum and from bronchial biopsies of normal subjects and patients with asthma. NF-kappaB-binding to its consensus DNA binding site, as investigated with 32P-labeled oligonucleotides and electrophoretic-mobility-shift assay, showed a 2.5-fold increase (p < 0.003) in NF-kappaB-DNA binding in induced sputum of asthma patients. Nuclear staining, representing activated NF-kappaB, was observed in macrophages of induced sputum. Immunohistochemical examination of bronchial biopsy specimens with an antibody to p65, a constituent of NF-kappaB, showed more airway epithelial cells with nuclear staining in asthma patients (45.1 +/- 7.2% versus 20.7 +/- 3.9% n = 9 p < 0.01), and a 2.5-fold greater number of cells with cytoplasmic staining in the mucosal region (p < 0.05). Pooled nuclear extracts of bronchial biopsy specimens from asthma patients showed a 44% greater level of NF-kappaB-DNA binding. Activation of NF-kappaB may be the basis for increased expression of many inflammatory genes and for the perpetuation of chronic airway inflammation in asthma.
Trends in CO2 conversion and utilization: A review from process systems perspective
Publisher: Elsevier BV
Date: 10-2018
Multiscale modeling and performance analysis of evacuated tube collectors for solar water heaters using diffuse flat reflector
Publisher: Elsevier BV
Date: 02-2016
A design protocol for enhanced discharge exergy in phase change material heat battery
Publisher: Elsevier BV
Date: 05-2020
Solar repowering of PCC-retrofitted power plants; solar thermal plant dynamic modelling and control strategies
Publisher: Elsevier BV
Date: 09-2015
Process control strategies for solar-powered carbon capture under transient solar conditions
Publisher: Elsevier BV
Date: 2022
New drugs for asthma
Publisher: Elsevier BV
Date: 09-1998
Expression of Heme Oxygenase Isoenzymes 1 and 2 in Normal and Asthmatic Airways
Publisher: American Thoracic Society
Date: 11-2000
DOI: 10.1164/AJRCCM.162.5.9909081
Abstract: Heme oxygenase (HO) is considered to be an antioxidant enzyme that catabolizes heme to produce carbon monoxide (CO) and biliverdin. We determined the expression and distribution of HO-1 and HO-2, two isoenzymes of HO, in the airways of patients with asthma, and determined the effect of inhaled corticosteroid therapy. Immunostaining for both enzymes was widely distributed in the airways' submucosa, particularly in airway epithelium and submucosal macrophages (CD68(+)) as determined by double immunostaining. There was no difference in intensity and extent of staining in biopsies from normal subjects (n = 10) and subjects with asthma (n = 10). Following 1 mo of treatment with inhaled corticosteroids (budesonide 1,600 microg/d), there was no significant change in the expression and distribution of either HO-1 or HO-2 in the airways' submucosa in eight subjects with mild asthma, despite a significant reduction in airway eosinophils and a reduction in bronchial responsiveness to methacholine. Levels of exhaled nitric oxide were significantly reduced, but exhaled CO levels remained unchanged by the treatment. Treatment with a placebo inhaler (n = 8) had no effects on these parameters. Thus, both HO-1 and HO-2 are extensively distributed equally in normal subjects and subjects with asthma, and are not modulated by inhaled corticosteroid therapy in subjects with asthma. HO may be an important endogenous antioxidant enzyme.
Molecular mechanisms of corticosteroid actions
Publisher: Elsevier BV
Date: 06-2001
Abstract: Glucocorticoids are the most effective therapeutic agents used for the treatment of chronic inflammatory diseases of the lung. They act by interacting with, and thereby activating, a specific cytoplasmic receptor (GR) which then migrates to the cell nucleus and inhibits inflammatory gene transcription. Inflammatory gene transcription is enhanced by activation of several intracellular signalling pathways which activate transcription factor such as NF-kappaB and AP-1. These transcription factors bind to DNA and induce local unwinding of the DNA structure allowing increased gene transcription. Glucocorticoids interfere with the ability of NF-kappaB and AP-1 to induce transcription by increasing the compaction of unwound chromosomal DNA in a process that involves deacetylation of histone proteins. A small number of asthmatic patients are resistant to the beneficial effects of glucocorticoids. This defect does not appear to be due to a reduced expression of GR but may be associated with a failure of GR to translocate into the nucleus and/or a reduced ability to inhibit AP-1 actions.
Differential IκB Kinase Activation and IκBα Degradation by Interleukin-1β and Tumor Necrosis Factor-α in Human U937 Monocytic Cells
Publisher: Elsevier BV
Date: 07-1999
CO2 Conversion and Utilization Pathways
Publisher: Elsevier
Date: 2018
Tailored solar field and solvent storage for direct solvent regeneration: A novel approach to solarise carbon capture technology
Publisher: Elsevier BV
Date: 05-2020
Modeling and Simulation Environments for Sustainable Low-Carbon Energy Production – A Review
Publisher: Walter de Gruyter GmbH
Date: 06-2016
Abstract: This paper reviews research trends in modeling for low-carbon energy production. The focus is on two currently significant low-carbon energy processes namely, bioenergy and post-combustion carbon capture (PCC) processes. The fundamentals of these two processes are discussed and the role of modeling and simulation tools (MSTs) is highlighted. The most popular modeling software packages are identified and their use in the literature is analyzed. Among commercially available packages, it is found that no single software package can handle all process development needs such as, configuration studies, techno-economic analysis, exergy optimization, and process integration. This review also suggests that optimal modeling results reported in literature can be viewed as optimal at the in idual plant level, but sub-optimal for plant superstructure level. This review has identified key gaps pertinent to developing hybrid models that describe integrated energy production processes. ASPEN Plus is found to be dominant for modeling both bioenergy and PCC processes for both steady-state and dynamic modes respectively.
Analysis for a solar stripper design for carbon capture under transient conditions
Publisher: Elsevier BV
Date: 02-2021
Mineral sequestration of CO 2 using saprolite mine tailings in the presence of alkaline industrial wastes
Publisher: Elsevier BV
Date: 07-2018
Evaluation of using thermoelectric coolers in a dehumidification system to generate freshwater from ambient air
Publisher: Elsevier BV
Date: 06-2011
An intelligent platform for evaluating investment in low-emissions technology for clean power production under ETS policy
Publisher: Elsevier BV
Date: 10-2021
A review of potential routes to zero and negative emission technologies via the integration of renewable energies with CO2 capture processes
Publisher: Elsevier BV
Date: 03-2023
A CFD study of a direct solar-driven desorption process for carbon capture under transient conditions
Publisher: Elsevier BV
Date: 10-2021
Inhibition of ozone-induced lung neutrophilia and nuclear factor-κB binding activity by vitamin A in rat
Publisher: Elsevier BV
Date: 07-1999
DOI: 10.1016/S0014-2999(99)00405-7
Abstract: Vitamin A binds to retinoic acid receptors, which in turn may interact with other transcription factors. We determined its effect (2500 and 5000 IU/kg) on nuclear factor-kappaB binding activity in the lung, airway inflammation and bronchial hyperresponsiveness in rats exposed to ozone. Ozone (3 ppm, 3 h) caused neutrophil influx into bronchoalveolar lavage fluid (16.2+/-0.8 x 10(5) cells/ml, p < 0.01) and bronchial hyperresponsiveness (-logPC200ACh = 2.54+/-0.19, p < 0.05, compared to control animals, respectively). Vitamin A inhibited this neutrophilia dose-dependently together with the increased DNA-binding activity of nuclear factor-KB in lung extracts. Vitamin A did not affect bronchial hyperresponsiveness at both doses. Vitamin A inhibits ozone-induced neutrophilic inflammation through a reduction in nuclear factor-kappaB DNA binding activity.
Effect of dexamethasone on interleukin-1beta-(IL-1beta)-induced nuclear factor-kappaB (NF-kappaB) and kappaB-dependent transcription in epithelial cells
Publisher: Wiley
Date: 15-05-1998
DOI: 10.1046/J.1432-1327.1998.2540081.X
Abstract: The production of inflammatory mediators by epithelial cells in inflammatory lung diseases may represent an important target for the anti-inflammatory effects of glucocorticoids. Nuclear factor-kappaB (NF-kappaB) is a major activator of inflammatory genes and has been proposed as a target for inhibition by glucocorticoids. We have used human pulmonary type-II A549 and airway epithelial BEAS-2B cells to investigate the effect of glucocorticoids on NF-kappaB regulation and kappaB-dependent transcription. In A549 cells following interleukin-1beta (IL-1beta) treatment, there was no effect of dexamethasone on the disappearance of I kappaB alpha protein, its subsequent reappearance 90-min later or the rapid induction of I kappaB alpha mRNA and transcription rate. Expression of p65 and p50 105 proteins were also unaffected by dexamethasone. In addition, the rapid IL-1beta-induction of NF-kappaB DNA binding and p65 nuclear localisation was unaffected by short (1-6 hours) dexamethasone pre-treatments. Similarly, BEAS-2B cells showed no effect of dexamethasone on IL-1beta-induced NF-kappaB (p50 65). Stable transfection of a kappaB-dependent reporter in A549 cells resulted in an 8-9-fold activation by IL-1beta or phorbol ester, that was repressed 30-40% by dexamethasone. However, in these cells, IL-1beta induction of inducible nitric oxide synthase, granulocyte-macrophage colony stimulating factor and cyclooxygenase-2 mRNA showed 70-90% repression by dexamethsone. We, therefore, conclude that in these epithelial cells, the repressive effects of glucocorticoids are not mediated by up-regulation of I kappaB alpha, decreased p50 65 gene expression or inhibition of NF-kappaB DNA binding. Furthermore, since the maximal repression of IL-1beta or phorbol-ester-induced kappaB-dependent transcription by dexamethasone was less than 40%, simple inhibition of kappaB-dependent transcription cannot by itself account for the full repressive effects of glucocorticoids observed in these cells.
Potential for solar-assisted post-combustion carbon capture in Australia
Publisher: Elsevier BV
Date: 11-2013
Molecular Mechanisms of Glucocorticosteroid Actions
Publisher: Elsevier BV
Date: 06-2000
Phosphodiesterase expression in human epithelial cells
Publisher: American Physiological Society
Date: 10-1998
DOI: 10.1152/AJPLUNG.1998.275.4.L694
Abstract: Epithelial cells play a critical role in airway inflammation and have the capacity to produce many inflammatory mediators, including bioactive lipids and proinflammatory cytokines. Intracellular levels of cAMP and cGMP are important in the control of inflammatory cell function. These cyclic nucleotides are inactivated via a family of phosphodiesterase (PDE) enzymes, providing a possible site for drug intervention in chronic inflammatory conditions. We studied the expression of PDE activity in an epithelial cell line (A549) and in primary human airway epithelial cells (HAECs). We measured PDE function using specific inhibitors to identify the PDE families present and used RT-PCR to elucidate the expression of PDE isogenes. Both A549 cells and HAECs predominantly expressed PDE4 activity, with lesser PDE1, PDE3, and PDE5 activity. RT-PCR identified HSPDE4A5 and HSPDE4D3 together with HSPDE7. Inhibition of PDE4 and PDE3 reduced secretion by these cells. Epithelial PDE may be an important target for PDE4 inhibitors in the development of the control of asthmatic inflammation, particularly when delivered via the inhaled route.
Transcription Factors in Asthma
Publisher: Elsevier
Date: 1998
A comparative life cycle impact assessment for solar heat integration in post-combustion carbon capture
Publisher: Elsevier BV
Date: 12-2023
Dynamic modelling and start-up operation of a solar-assisted recompression supercritical CO2 Brayton power cycle
Publisher: Elsevier BV
Date: 08-2017
Experimentally validated model for atmospheric water generation using a solar assisted desiccant dehumidification system
Publisher: Elsevier BV
Date: 07-2014
p65-activated Histone Acetyltransferase Activity Is Repressed by Glucocorticoids
Publisher: Elsevier BV
Date: 08-2001
Water Storage Instead of Energy Storage for Desalination Powered by Renewable Energy—King Island Case Study
Publisher: MDPI AG
Date: 19-10-2016
DOI: 10.3390/EN9100839
A comparative study of solar heliostat assisted supercritical CO2 recompression Brayton cycles: Dynamic modelling and control strategies
Publisher: Elsevier BV
Date: 02-2017
CYTOKINE mRNA PROFILES OF NORMAL AND ASTHMATIC PERIPHERAL BLOOD CELLS AND ENDOBRONCHIAL BIOPSIES
Publisher: Portland Press Ltd.
Date: 05-1996
DOI: 10.1042/BST024315S
Interleukin-4 and Lipopolysaccharide Synergize to Induce Vascular Cell Adhesion Molecule-1 Expression in Human Lung Microvascular Endothelial Cells
Publisher: American Thoracic Society
Date: 05-1998
Abstract: Recent studies suggest that increased vascular cell adhesion molecule-1 (VCAM-1) expression on vascular endothelium in bronchial mucosa biopsies correlates with interleukin-4 (IL-4) levels in bronchiolar lavage fluid of allergic asthmatics. The severity of asthma in patients allergic to house dust mite has also been shown to correlate with lipopolysaccharide (LPS), rather than allergen, concentration in dust. We hypothesized that to induce effective VCAM-1 expression in human lung microvascular endothelial cells (HLMVEC), IL-4 may require the presence of a co-stimulus such as LPS. To test this hypothesis we measured, by enzyme-linked immunosorbent assay, induction of cell adhesion molecule expression on, and human eosinophil adhesion to, cultured HLMVEC monolayers pretreated with IL-4 alone or combined with LPS. IL-4 synergized with LPS to induce VCAM-1 expression at 24, 48, or 72 h, whereas IL-4 alone induced expression at 72 h only. IL-4 did not induce expression of intercellular adhesion molecule-1 or E-selectin or alter LPS-induced expression of either. Pre-exposure of HLMVEC to LPS or IL-4 (1 h), followed by IL-4 or LPS, respectively (23 h), also induced VCAM-1 expression. Eosinophil adhesion to HLMVEC monolayers treated with IL-4 and LPS together, but not alone, significantly (P < 0.001) increased from 9.6 +/- 1.5% (control) to 26.9 +/- 3.3% and was inhibited by a monoclonal antibody against the VCAM-1 ligand, very late antigen-4. Analysis of VCAM-1 mRNA revealed synergism between IL-4 and LPS which may, in part, contribute to enhanced VCAM-1 expression. These results suggest that the presence of a co-stimulus such as LPS may be necessary for IL-4 to effectively induce VCAM-1 expression in lung microvasculature.
Related Organisations
Faculdade De Ciencias E Tecnologia Universidade Nova De Lisboa
Location: Portugal
Commonwealth Scientific And Industrial Research Organisation
Location: Australia
Related Funding Activities
Teacher-made- Testa And WISC-V Scores In Class Six In Embu West Sub County, Kenya
Start Date: 2016
End Date: 2017
Funder:
View Funded Activity