Publications
415 results found
Usmani OS, Watson EM, Meah SN, et al., 2009, DECLINING RESPIRATORY CLINICAL ACADEMICS: A MODEL FOR REVERSING THE TREND?, Winter Meeting of the British-Thoracic-Society, Publisher: B M J PUBLISHING GROUP, Pages: A165-A166, ISSN: 0040-6376
Armstrong PCJ, Dhanji AA, Tucker AT, et al., 2009, URINARY 11-DEHYDRO-THROMBOXANE B2 AS A MARKER OF THE ANTI-PLATELET EFFECTS OF CLOPIDOGREL OR ASPIRIN THERAPY IN HEALTHY MALE VOLUNTEERS, Spring Meeting of the British-Society-for-Cardiovascular-Research, Publisher: B M J PUBLISHING GROUP, ISSN: 1355-6037
Ali FY, Hall MG, Desvergne B, et al., 2009, PPARβ/δ Agonists Modulate Platelet Function via a Mechanism Involving PPAR Receptors and Specific Association/Repression of PKCα-Brief Report, ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, Vol: 29, Pages: 1871-1873, ISSN: 1079-5642
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- Citations: 38
Armstrong PCJ, Dhanji A-R, Truss NJ, et al., 2009, Utility of 96-well plate aggregometry and measurement of thrombi adhesion to determine aspirin and clopidogrel effectiveness, THROMBOSIS AND HAEMOSTASIS, Vol: 102, Pages: 772-778, ISSN: 0340-6245
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- Citations: 34
Belvisi MG, Mitchell JA, 2009, Targeting PPAR receptors in the airway for the treatment of inflammatory lung disease, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 158, Pages: 994-1003, ISSN: 0007-1188
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- Citations: 90
Mitchell JA, 2009, Oxidative stress by environmental and host derived sources leading to lung inflammation, 46th Congress of the European-Societies-of-Toxicology, Publisher: ELSEVIER IRELAND LTD, Pages: S44-S44, ISSN: 0378-4274
Wort SJ, Ito M, Chou P-C, et al., 2009, Synergistic Induction of Endothelin-1 by Tumor Necrosis Factor α and Interferon γ Is due to Enhanced NF-κB Binding and Histone Acetylation at Specific κB Sites, JOURNAL OF BIOLOGICAL CHEMISTRY, Vol: 284, Pages: 24297-24305
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- Citations: 58
Piqueras L, Jesus Sanz M, Perretti M, et al., 2009, Activation of PPARβ/δ inhibits leukocyte recruitment, cell adhesion molecule expression, and chemokine release, JOURNAL OF LEUKOCYTE BIOLOGY, Vol: 86, Pages: 115-122, ISSN: 0741-5400
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- Citations: 55
Secher T, Vasseur V, Poisson DM, et al., 2009, Crucial Role of TNF Receptors 1 and 2 in the Control of Polymicrobial Sepsis, JOURNAL OF IMMUNOLOGY, Vol: 182, Pages: 7855-7864, ISSN: 0022-1767
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- Citations: 40
Ali FY, Armstrong PCJ, Dhanji A-RA, et al., 2009, Antiplatelet Actions of Statins and Fibrates Are Mediated by PPARs, ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, Vol: 29, Pages: 706-711, ISSN: 1079-5642
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- Citations: 104
Paul-Clark MJ, McMaster SK, Sorrentino R, et al., 2009, Toll-like Receptor 2 Is Essential for the Sensing of Oxidants during Inflammation, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 179, Pages: 299-306, ISSN: 1073-449X
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- Citations: 47
Armstrong PCJ, Truss NJ, Ali FY, et al., 2008, Aspirin and the <i>in vitro</i> linear relationship between thromboxane A<sub>2</sub>-mediated platelet aggregation and platelet production of thromboxane A<sub>2</sub>, JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Vol: 6, Pages: 1933-1943, ISSN: 1538-7933
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- Citations: 55
Harrington LS, Lucas R, McMaster SK, et al., 2008, COX-1, and not COX-2 activity, regulates airway function: relevance to aspirin-sensitive asthma, FASEB JOURNAL, Vol: 22, Pages: 4005-4010, ISSN: 0892-6638
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- Citations: 41
Ali FY, Warner TD, Mitchell JA, 2008, Comparison of responses in IP and PPARβ deleted murine platelets, HEART, Vol: 94, ISSN: 1355-6037
Zain ZNM, Armstrong PCJ, Pearson NJ, et al., 2008, Evaluation of aspirin inhibition of platelet aggregation induced by combination of collagen and adrenaline in a 96-well plate format, HEART, Vol: 94, ISSN: 1355-6037
Armstrong PCJ, Zain ZNM, Truss NJ, et al., 2008, Linear relationship between platelet aggregation and thromboxane A<sub>2</sub> production, HEART, Vol: 94, ISSN: 1355-6037
Dhanji AA, Truss NJ, Bishop-Bailey D, et al., 2008, Generation of clonal populations of prostaglandin I<sub>2</sub>-producing rat vascular smooth muscle cells:: Potential utility for production of bypass vessels, HEART, Vol: 94, ISSN: 1355-6037
Moreno L, McMaster SK, Paul-Clark M, et al., 2008, The PPAR target gene CD36 is a rate limiting factor for the sensing of gram positive <i>S-aureus</i> in vascular smooth muscle cells but not in macrophages, FUNDAMENTAL & CLINICAL PHARMACOLOGY, Vol: 22, Pages: 48-48, ISSN: 0767-3981
Moreno L, Bailey LK, Cartwright N, et al., 2008, Rip2 mediates NOSII-induction by NOD1 activation in vascular smooth muscle cells but not by TLR4 activation in macrophages, FUNDAMENTAL & CLINICAL PHARMACOLOGY, Vol: 22, Pages: 86-87, ISSN: 0767-3981
Sorrentino R, de Souza PM, Sriskandan S, et al., 2008, Pattern recognition receptors and interleukin-8 mediate effects of Gram-positive and Gram-negative bacteria on lung epithelial cell function, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 154, Pages: 864-871, ISSN: 0007-1188
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- Citations: 12
Issa R, Sorrentino R, Sukkar MB, et al., 2008, Differential regulation of CCL-II/eotaxin-I and CXCL-8/IL-8 by Gram-positive and Gram-negative bacteria in human airway smooth muscle cells, Respiratory Research, Vol: 9, ISSN: 1465-993X
Background: Bacterial infections are a cause of exacerbation of airway disease. Airway smoothmuscle cells (ASMC) are a source of inflammatory cytokines/chemokines that may propagate localairway inflammatory responses. We hypothesize that bacteria and bacterial products could inducecytokine/chemokine release from ASMC.Methods: Human ASMC were grown in culture and treated with whole bacteria or pathogenassociated molecular patterns (PAMPs) for 24 or 48 h. The release of eotaxin-1, CXCL-8 orGMCSF was measured by ELISA.Results: Gram-negative E. coli or Gram-positive S. aureus increased the release of CXCL-8, as didIL-1β, LPS, FSL-1 and Pam3CSK4, whereas FK565, MODLys18 or Poly I:C did not. E. coli inhibitedeotaxin-1 release under control conditions and after stimulation with IL-1β. S. aureus tended toinhibit eotaxin-1 release stimulated with IL-1β. E. coli or LPS, but not S. aureus, induced the releaseof GMCSF.Conclusion: Gram-positive or Gram-negative bacteria activate human ASMC to release CXCL-8.By contrast Gram-negative bacteria inhibited the release of eotaxin-1 from human ASMCs. E. coli,but not S. aureus induced GMCSF release from cells.Our findings that ASMC can respond directly to Gram-negative and Gram-positive bacteria byreleasing the neutrophil selective chemokine, CXCL-8, is consistent with what we know about therole of neutrophil recruitment in bacterial infections in the lung. Our findings that bacteria inhibitthe release of the eosinophil selective chemokine, eotaxin-1 may help to explain the mechanismsby which bacterial immunotherapy reduces allergic inflammation in the lung.
McMaster SK, Paul-Clark MJ, Walters M, et al., 2008, Cigarette smoke inhibits macrophage sensing of Gram-negative bacteria and lipopolysaccharide: relative roles of nicotine and oxidant stress, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 153, Pages: 536-543, ISSN: 0007-1188
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- Citations: 33
Paul-Clark MJ, Sorrentino R, Bailey LK, et al., 2008, Gram-positive and gram-negative bacteria synergize with oxidants to release CXCL8 from innate immune cells, MOLECULAR MEDICINE, Vol: 14, Pages: 238-246, ISSN: 1076-1551
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- Citations: 15
Warner TD, Mitchell JA, 2008, COX-2 selectivity alone does not define the cardiovascular risks associated with non-steroidal anti-inflammatory drugs, LANCET, Vol: 371, Pages: 270-273, ISSN: 0140-6736
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- Citations: 111
Mitchell JA, Ali F, Bailey L, et al., 2008, Role of nitric oxide and prostacyclin as vasoactive hormones released by the endothelium, EXPERIMENTAL PHYSIOLOGY, Vol: 93, Pages: 141-147, ISSN: 0958-0670
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- Citations: 189
Mitchell JA, Ali F, Bailey L, et al., 2008, Role of nitric oxide and prostacyclin as vasoactive hormones released by the endothelium, Life Science Conference 2007, Pages: 141-147
The endothelium lines the luminal surface of every blood vessel, allowing it contact with circulating blood elements, as well as the underlying vascular smooth muscle layer. In healthy vessels, the endothelium expresses constitutive forms of nitric oxide synthase (NOSIII) and cyclo-oxygenase (COX-1), which produce the vasoactive hormones NO and prostacyclin, respectively. Both NO and prostacyclin relax blood vessels and inhibit platelet activation. The actions of prostacyclin are mediated by cell surface prostacyclin (IP) receptors and/or intracellular peroxisome proliferator-activated receptors (PPAR)beta. The actions of NO are mediated predominately by activation of intracellular guanylyl cyclase, leading to the formation of cGMP. In platelets, the actions of NO and prostacyclin are synergistic, but in vessels their actions are additive. In diseased vessels, inducible forms of NOS (NOSII) and cyclo-oxygeanse (COX-2) are expressed in vascular smooth muscle, resulting in the release of large amounts of NO, prostacyclin and prostaglandin E-2. The relative contribution of NOSII and COX-2 to vascular inflammation is still debated, but is likely to result in both protective and damaging responses. The relative contribution of constitutive forms of NOS and COX, as well as interactions between IP, PPAR beta and guanylyl cyclase pathways in vessels and platelets, is discussed.
Oltmanns U, Walters M, Sukkar M, et al., 2008, Fluticasone, but not salmeterol, reduces cigarette smoke-induced production of interleukin-8 in human airway smooth muscle, PULMONARY PHARMACOLOGY & THERAPEUTICS, Vol: 21, Pages: 292-297, ISSN: 1094-5539
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- Citations: 14
Harrington LS, Belcher E, Moreno L, et al., 2007, Homeostatic role of toll-like receptor 4 in the endothelioum and heart, JOURNAL OF CARDIOVASCULAR PHARMACOLOGY AND THERAPEUTICS, Vol: 12, Pages: 322-326, ISSN: 1074-2484
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- Citations: 16
Mitchell JA, Ryffel B, Quesniaux VFJ, et al., 2007, Role of pattern-recognition receptors in cardiovascular health and disease, BIOCHEMICAL SOCIETY TRANSACTIONS, Vol: 35, Pages: 1449-1452, ISSN: 0300-5127
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- Citations: 40
Harrington LS, Evans RJ, Wray J, et al., 2007, Purinergic 2X<sub>1</sub> receptors mediate endothelial dependent vasodilation to ATP, MOLECULAR PHARMACOLOGY, Vol: 72, Pages: 1132-1136, ISSN: 0026-895X
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- Citations: 37
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