Publications
91 results found
Wilson MR, O'Dea KP, Dorr AD, et al., 2010, Efficacy and safety of inhaled carbon monoxide during pulmonary inflammation in mice, PLOS One, Vol: 5, ISSN: 1932-6203
Patel BV, Wilson MR, Takata M, 2010, A physiologcal characterisation of injury, inflammation and resolution in murine aspiration pneumonitis., British-Thoracic-Society-Winter-Meeting, Pages: A183-A183
Wakabayashi K, Wilson MR, O'Dea KP, et al., 2009, ROLE OF INTRAVASCULAR LEUCOCYTES IN VENTILATOR-INDUCED LUNG INJURY IN THE ISOLATED PERFUSED MOUSE LUNG, Winter Meeting of the British-Thoracic-Society, Publisher: B M J PUBLISHING GROUP, Pages: A48-A49, ISSN: 0040-6376
Dorr AD, Wilson MR, O'Dea KP, et al., 2009, SOURCES OF INCREASED PLASMA SOLUBLE TNF RECEPTORS DURING INJURIOUS MECHANICAL VENTILATION IN MICE, Winter Meeting of the British-Thoracic-Society, Publisher: B M J PUBLISHING GROUP, Pages: A46-A47, ISSN: 0040-6376
Wilson MR, O'Dea KP, Zhang D, et al., 2009, Role of Lung-marginated Monocytes in an <i>In Vivo</i> Mouse Model of Ventilator-induced Lung Injury, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 179, Pages: 914-922, ISSN: 1073-449X
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- Citations: 64
O'Dea KP, Wilson MR, Dokpesi JO, et al., 2009, Mobilization and Margination of Bone Marrow Gr-1<SUP>high</SUP> Monocytes during Subclinical Endotoxemia Predisposes the Lungs toward Acute Injury, JOURNAL OF IMMUNOLOGY, Vol: 182, Pages: 1155-1166, ISSN: 0022-1767
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- Citations: 58
Bertok S, Wilson MR, Dokpesi J, et al., 2009, Tumour Necrosis Factor-α (TNF) Receptor p75 Plays a Substantial Role in TNF-Mediated Upregulation of Leukocyte Adhesion Molecules in Mouse Lung Microvasculature, Publisher: AMER THORACIC SOC, ISSN: 1073-449X
Dorr AD, Wilson MR, Wakabayashi K, et al., 2009, Injurious Ventilation and Intratracheal Lipopolysaccharide Increase Soluble TNF Receptors in the Alveoli Via Distinct Mechanisms, Publisher: AMER THORACIC SOC, ISSN: 1073-449X
Bertok S, Wilson MR, Dokpesi J, et al., 2008, ROLE OF TUMOUR NECROSIS FACTOR a RECEPTOR SUBTYPES IN TUMOUR NECROSIS FACTOR-INDUCED MOUSE LUNG MICROVASCULAR ENDOTHELIAL CELL ACTIVATION, Winter Meeting of the British-Thoracic-Society, Publisher: B M J PUBLISHING GROUP, Pages: A141-A141, ISSN: 0040-6376
Waite AC, Wilson MR, Takata M, 2008, HIGH TIDAL VOLUME VENTILATION INDUCES RECRUITMENT OF ACTIVATED LEUCOCYTES TO EXTRAPULMONARY ORGANS IN AN IN-VIVO MOUSE MODEL, Winter Meeting of the British-Thoracic-Society, Publisher: B M J PUBLISHING GROUP, Pages: A149-A149, ISSN: 0040-6376
Dorr AD, Wilson MR, Wakabayashi K, et al., 2008, INJURIOUS VENTILATION AND INTRATRACHEAL LIPOPOLYSACCHARIDE INCREASE SOLUBLE TUMOUR NECROSIS FACTOR RECEPTORS IN THE ALVEOLI VIA TWO DISTINCT MECHANISMS, Winter Meeting of the British-Thoracic-Society, Publisher: B M J PUBLISHING GROUP, Pages: A71-A71, ISSN: 0040-6376
Rippon HJ, Lane S, Qin M, et al., 2008, Embryonic stem cells as a source of pulmonary epithelium in vitro and in vivo., Proc Am Thorac Soc, Vol: 5, Pages: 717-722, ISSN: 1546-3222
Embryonic stem cells (ESCs) derived from the preimplantation blastocyst are pluripotent and capable of indefinite expansion in vitro. As such, they present a cell source to derive a potentially inexhaustible supply of pulmonary cells and tissue. ESC-derived pulmonary epithelium could be used for in vitro cell or tissue models or, in the future, implanted into the damaged or diseased lung to effect repair. Efforts to date have largely focused on obtaining distal lung epithelial phenotypes from ESCs, notably alveolar epithelium. Several disparate methods have been developed to enhance differentiation of ESCs into pulmonary epithelial lineages; these are broadly based on recapitulating developmental signaling events, mimicking the physical environment, or forcibly reprogramming the ESC nucleus. Early findings of our preclinical experiments implanting differentiated ESCs into the injured lung are also described here. Future efforts will focus on maximizing ESC differentiation efficiency and yield of the target phenotype, as well as characterizing the function of derived cells in vivo and in vitro.
Pinhu L, Wilson M, Takata M, et al., 2007, Cyclo-oxygenase-2 induction by cyclic mechanical strain in human primary alveolar type 2 cells and in murine whole lung is dependent on activation of erk1/2, Winter Meeting of the British-Thoracic-Society, Publisher: B M J PUBLISHING GROUP, Pages: A60-A61, ISSN: 0040-6376
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- Citations: 1
Wilson MR, O'Dea KP, Zhang D, et al., 2007, Marginated monocytes exacerbate pulmonary oedema in a murine model of ventilator-induced lung injury, Winter Meeting of the British-Thoracic-Society, Publisher: B M J PUBLISHING GROUP, Pages: A61-A62, ISSN: 0040-6376
O'Dea KP, Wilson MR, Dokpesi JO, et al., 2007, Lung-marginated monocytes play a central role in a two-hit LPS-zymosan model of acute lung injury in mice, Winter Meeting of the British-Thoracic-Society, Publisher: B M J PUBLISHING GROUP, Pages: A36-A37, ISSN: 0040-6376
Wilson MR, Goddard ME, O'Dea KP, et al., 2007, Differential roles of p55 and p75 tumor necrosis factor receptors on stretch-induced pulmonary edema in mice, AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, Vol: 293, Pages: L60-L68, ISSN: 1040-0605
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- Citations: 58
Shearman AD, Wilson MR, O'Dea KP, et al., 2007, High stretch mechanical ventilation promotes the recruitment of activated inflammatory subset monocytes to the lung in mice, Meeting of the Anaesthetic-Research-Society, Publisher: OXFORD UNIV PRESS, Pages: 289P-290P, ISSN: 0007-0912
Wilson MR, Choudhury S, Takata M, 2005, Stretch induced pulmonary oedema is mediated by tumour necrosis factor receptor I signalling in mice, Winter Meeting of the British-Thoracic-Society, Publisher: B M J PUBLISHING GROUP, Pages: II15-II15, ISSN: 0040-6376
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- Citations: 1
Pinhu L, Wilson MR, Takata M, et al., 2005, Chemokine production by mouse lungs subjected to injurious mechanical ventilation requires extracellular regulated kinase 1/2 pathway activity, Winter Meeting of the British-Thoracic-Society, Publisher: BMJ PUBLISHING GROUP, Pages: II15-II15, ISSN: 0040-6376
Ghosh S, Wilson MR, Choudhury S, et al., 2005, Effects of inhaled carbon monoxide on acute lung injury in mice, AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, Vol: 288, Pages: L1003-L1009, ISSN: 1040-0605
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- Citations: 34
Wilson MR, Choudhury S, Takata M, 2005, Pulmonary inflammation induced by high-stretch ventilation is mediated by tumor necrosis factor signaling in mice, AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, Vol: 288, Pages: L599-L607, ISSN: 1040-0605
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- Citations: 80
Preston JE, Wilson MR, Chen RL, 2005, Aging of the choroid plexus and CSF system: Implications for neurodegeneration, The Blood-Cerebrospinal Fluid Barrier, Editors: Zheng, Chodobski, Boca Raton, Florida USA, Publisher: Taylor & Francis Books, Pages: 361-376
Choudhury S, Wilson MR, Goddard ME, et al., 2004, Mechanisms of early pulmonary neutrophil sequestration in ventilator-induced lung injury in mice, AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, Vol: 287, Pages: L902-L910, ISSN: 1040-0605
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- Citations: 79
Wilson MR, Choudhury S, Goddard ME, et al., 2003, High tidal volume upregulates intrapulmonary cytokines in an in vivo mouse model of ventilator-induced lung injury, JOURNAL OF APPLIED PHYSIOLOGY, Vol: 95, Pages: 1385-1393, ISSN: 8750-7587
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- Citations: 166
Thomas SA, Preston JE, Wilson MR, et al., 2001, Leptin transport at the blood--cerebrospinal fluid barrier using the perfused sheep choroid plexus model., Brain Res, Vol: 895, Pages: 283-290, ISSN: 0006-8993
Leptin is secreted by adipose tissue and thought to regulate appetite at the central level. Several studies have explored the central nervous system (CNS) entry of this peptide across the blood-brain and blood-cerebrospinal fluid (CSF) barriers in parallel, but this is the first to explore the transport kinetics of leptin across the choroid plexus (blood-CSF barrier) in isolation from the blood-brain barrier (BBB). This is important as the presence of both barriers can lead to ambiguous results from transport studies. The model used was the isolated Ringer perfused sheep choroid plexus. The steady-state extraction of [(125)I]leptin (7.5 pmol l(-1)) at the blood face of the choroid plexus was 21.1+/-5.7%, which was greater than extraction of the extracellular marker, giving a net cellular uptake for [(125)I]leptin (14.0+/-3.7%). In addition, trichloroacetic acid precipitable [(125)I] was detected in newly formed CSF, indicating intact protein transfer across the blood-CSF barrier. Human plasma concentrations of leptin are reported to be 0.5 nM. Experiments using 0.5 nM leptin in the Ringer produced a concentration of leptin in the CSF of 12 pM (similar to that measured in humans). [(125)I]Leptin uptake at the blood-plexus interface using the single-circulation paired tracer dilution technique (uptake in <60 s) indicated the presence of a saturable transport system, which followed Michaelis-Menten-type kinetics (K(m)=16.3+/-1.8 nM, V(max)=41.2+/-1.4 pmol min(-1) g(-1)), and a non-saturable component (K(d)=0.065+/-0.002 ml min(-1) g(-1)). In addition, secretion of new CSF by the choroid plexuses was significantly decreased with leptin present. This study indicates that leptin transport at the blood-CSF barrier is via saturable and non-saturable mechanisms and that the choroid plexus is involved in the regulation of leptin availability to the brain.
Wilson MR, Hughes SJ, 1998, Impaired glucose-stimulated insulin release in islets from adult rats malnourished during foetal-neonatal life., Mol Cell Endocrinol, Vol: 142, Pages: 41-48, ISSN: 0303-7207
Poor foetal and neonatal nutrition may impair normal pancreatic beta-cell development and predispose to diabetes in later life. We investigate here the nature of the pancreatic beta-cell dysfunction in sucrose-fed adult offspring malnourished during the foetal-neonatal period and examine glucose metabolism and the generation of signals involved in the secretory mechanism. In islets from sucrose-fed previously malnourished rats, rates of glucose utilisation (production of 3H2O) and oxidation (production of 14CO2), at 2, 6 and 10 mM glucose, were not lower than those of controls. ATP concentrations in islets from previously malnourished rats fed sucrose at 2 and 10 mM glucose were similar to those of controls. Glucose-stimulated insulin release was impaired (by 49-55%) in islets from these animals as was the response to keto-isocaproate (by 70%) and tolbutamide (by 70%). Under conditions in which ATP-sensitive K+ channels were clamped open (40 mM K+ and diazoxide), glucose-stimulated insulin release in islets from previously malnourished rats fed sucrose was reduced. These findings show that defects in insulin secretion in islets isolated from previously malnourished animals are located in both ATP-sensitive K+ channel dependent and independent pathways. They do not involve alterations in the early steps of glucose handling in the beta-cell, including glucose metabolism and ATP generation.
Wilson MR, Hughes SJ, 1997, The effect of maternal protein deficiency during pregnancy and lactation on glucose tolerance and pancreatic islet function in adult rat offspring, JOURNAL OF ENDOCRINOLOGY, Vol: 154, Pages: 177-185, ISSN: 0022-0795
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- Citations: 62
Wilson MR, Hughes SJ, 1997, The effect of poor foetal and neonatal nutrition on islet function in neonatal rats, European Association for the Study of Diabetes, Pages: 522-522, ISSN: 0012-186X
Wilson M, Hughes SJ, 1996, Impaired glucose tolerance and mild hyperglycemia in sucrose-fed rats does not impair insulin secretion, ACTA DIABETOLOGICA, Vol: 33, Pages: 211-215, ISSN: 0940-5429
Wilson MR, Hughes SJ, 1996, The effect of poor foetal and neonatal nutrition on islet function and glucose tolerance in high fat fed-rats, European Association for the Study of Diabetes, Pages: 412-412, ISSN: 0012-186X
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