ࡱ> OQNq` &bjbjqPqP .:::N8,$P$)*(v)x)x)x)x)x)x)$!+h-)$$$))((($v)($v)(((t _q+ژ%p( )l)0)(.&>.((.(`jp(v!>))>(X)$$$$ PP  Reference 200542 Comparison of dendritic cell maturation and migration in patients undergoing cardiac surgery with and without cardiopulmonary bypass (CPB) Fundamental to the body's defence system are specialised lookout cells in tissues (dendritic cells), which quickly move to lymph nodes to alert immune defence cells (lymphocytes) that a danger signal has been received. Movement of these cells has been observed during uncomplicated cardiac surgery. At cardiac surgery using the heart-lung machine, inflammatory mediators, also activated by this defence system, can damage organs. Various strategies, described as perioperative inflammatory limitation strategies (PILS), are employed to reduce this. However, PILS such as steroid administration, whilst reducing the inflammation, may, as a side-effect, also reduce the ability of the dendritic cells to give the danger signal, thus reducing immune defences. Cardiac surgery without the use of the heart-lung machine (OPCAB) has reduced activation of these mediators and can therefore act as a PILS without the need for steroid intervention. This study aims to prove that, although this surgical technique will reduce inflammation, it will not reduce dendritic cell function, and consequently it will not affect immune defences. Research Team: Dr Marilyn Armstrong, Department of Microbiology and Immunology, Queens University Belfast, Grosvenor Road, Belfast, BT12 6BN Dr William McBride, Cardiac Anaesthesia, Royal Victoria Hospital, Grosvenor Rd., Belfast, BT12 6BN Dr Stephen McQuaid Department of Pathology, Royal Victoria Hospital, Grosvenor Rd., Belfast, BT12 6BN Location: Queens University, Belfast Grant Value: 21,030 Start Date: August 2005 End Date: August 2007 Reference 200544 Endothelial dysfunction: Interaction of hyperglycaemia and fatty acids to cause oxidative damage and monocyte binding to endothelial cells Cardiovascular disease is the leading cause of morbidity and premature death in people with diabetes. The incidence of diabetes is reaching epidemic proportions in the western world and this increase can be attributed directly to increased obesity and physical inactivity and represents a major health economics problem. Diabetes is thought to cause changes within the vascular wall however the underlying mechanisms by which diabetes increases cardiovascular disease are poorly understood. The monounsaturate-rich Mediterranean diet in contrast to the polyunsaturate-rich Northern European diet may protect against cardiovascular disease by improving the function of the endothelium, a component of the vascular wall. This project aims to investigate the effects of fatty acids, (monounsaturated versus polyunsaturated versus saturated) in combination with diabetes on markers of endothelial dysfunction. Moreover, this study will determine whether vascular cell function in diabetes can be modified following dietary intervention with specific fatty acids. It is anticipated that the results from this study will help in the prevention and treatment of diabetes-related cardiovascular disease. Research Team: Professor Elisabeth Trimble, Clinical Biochemistry & Metabolic Medicine, Queens University Belfast, Institute of Clinical Science, Grosvenor Road, Belfast, BT12 6BJ Dr Lesley Powell, Clinical Biochemistry & Metabolic Medicine, Queens University Belfast, Institute of Clinical Science, Grosvenor Road, Belfast, BT12 6BJ Location: Queens University, Belfast Grant Value: 20,050 Start Date: September 2005 End Date: September 2007 Reference 200545 Viral infection in presymptomatic smokers with COPD COPD is a severe disabling disease, which progresses throughout the life of susceptible smokers. It is the commonest respiratory disease causing hospitalization. Seasonal increases in COPD admissions contribute to the recurrent winter pressures. It is the sixth commonest cause of death, and is set to rise to the third commonest cause of death by 2015. Not all smokers get this disease. In fact only 20% are affected. We have studied people with severe disease and found that they frequently have viruses in their sputum which are not present in unaffected (healthy) smokers. This is associated with a rise in an inflammatory chemical, called granulocyte-macrophage colony stimulating factor, which causes pus cells to accumulate in the airways. It is these pus cells which cause the damage to the airways. Unfortunately all our patients studied have had severe disease which warranted hospitalization and treatment. This treatment, particularly steroids, may have altered their immunity and allowed these viruses to proliferate. We now wish to study patients who are younger, have only a mild disease, and have not had steroids. We want to see do they have these viruses and the inflammatory chemical for the pus cells in their airway. If this study is successful it will indicate that anti-viral treatment, which is already available, could be beneficial. This would be the first disease modifying treatment ever in COPD Research Team: Dr Joe Kidney, Respiratory Medicine, Mater Infirmorum Hospital, Crumlin Rd, Belfast, BT14 6AB Dr Peter Coyle, Department of Virology, Royal Victoria Hospital, Grosvenor Rd., Belfast, BT12 6BA Location: Mater Infirmorum Hospital Grant Value: 45,944 Start Date: August 2005 End Date: August 2006 Reference 200546 Effects of chronic exposure to IL-13 on mucociliary differentiation of bronchial epithelial cells obtained from normal and asthmatic children Asthma is a chronic disease caused by inflamed airways that restrict airflow, which is increasing in prevalence. Epithelial cells that line the airways are highly specialised, performing critical functions against outside invaders. One population of these epithelial cells have cilia, small hair-like structures that move mucus, dust and other debris out of the lungs into the windpipe where they can be coughed up. The other population (goblet cells) maintain normal mucus secretion, an essential component of airway defences. Asthma is characterised by abnormalities in epithelial cells, which impair their function. Most of the research in this area to date has been conducted on animals or adult human cells; however for the majority asthma begins in childhood. Childhood is therefore the ideal time to address the pathology of the disease onset before irreversible changes have become established and when therapeutic interventions are more likely to change the natural history of the disease. We have established a unique method of obtaining bronchial epithelial cells from children when they are undergoing elective surgery using a small brush and a model of differentiating bronchial epithelial cells in the laboratory. In this system, lung cells from asthmatic and normal children will be grown exposed to the air as they grow in human body. It will allow us to study the role of key regulatory proteins, on development of mucus secreting cells and mucus production. Our goal is to add to the knowledge of the mechanisms involved in abnormal epithelial function in asthma, specifically in children, and provide information, which will be critical for the development of the new means of treatment. Research Team: Dr Grzegorz Skibinski, Department of Clinical Biochemistry, Queens University of Belfast, Grosvenor Road, Belfast, BT12 6BJ Dr Liam Heaney, Department of Medicine, Queens University of Belfast, Level 8, Belfast City Hospital, BT9 7AB Dr Michael D Shields, Department of Child Health, Queens University of Belfast, Clinical Institute, Grosvenor Road, Belfast, BT12 6BJ Location: Queens University of Belfast Grant Value: 46,642 Start Date: October 2005 End Date: October 2006     NICHSA Grants awarded in 2005  FILENAME \p G:\RESEARCH ASSISTANT\RESEARCH 2005\NICHSA Grants awarded in 2005 Laymans terms.doc  PAGE 1 P Q z R T    hqrqrsDF&wrkgkh7u heh7u h5heh5 heh heh{wh=Zh{w5h]6h{wheh=Zhe5h=Zh]65 h=Z5h=Zheh=Z5h7uCJOJQJaJheh7uCJOJQJaJheh7u5 h]65heh]65 hehn`$ heh]6(S T   ghrsEgd7ugdgd]6$a$gd7uN&&EF&'6xy01_`?@ ^`gd7u$a$gdgd=Zgdgd7u&'/6y01^_2>?@{̹̹h7u h=Zh7uh7u5CJOJQJaJh=Zh7u5CJOJQJaJh{wh5 heh{wh=Zh{w5hh{wheh=Zhe5h=Zh5 h=Z5heh5heh=Z5 heh48 !!X$Y$h$$T%%gd7u$a$gdvzgdvzgd=Zgd IJ !!X$Y$a$h$k$$$%%%%&&&&&%&&&3&4&=&J&K&M&N&O&Q&R&T&U&W&X&Z&x&깱깥ꏇuhzhf 5>*CJ aJ hR #jhR #U heh( heh{whvzh{wh=Zh{w5heh=Zhe5h=Zhvz5 h=Z5h=Zheh=Z5h7u heh7uheh7u5 hvz5 hehvzhehvz5 h=Zh.%%&&&&4&K&L&M&N&P&Q&S&T&V&W&Y&Z&x&y&z&&&&&$a$gdzgdgdvzx&z&{&&&&&&&&&&&&&& heh(hR #h7u0JmHnHu hf 0Jjhf 0JUhf mHnHujhf Uhf ,1h/ =!"#$% @@@ NormalCJ_HaJmH sH tH Z@Z ]6 Heading 1dd@&[$\$5CJ0KH$\aJ0mH sH DA@D Default Paragraph FontRi@R  Table Normal4 l4a (k@(No List O ]6greyZZ@Z]6 Plain Text$a$#CJOJQJaJmHnHsH tH u@@@ Header  9r  aJmH sH rR@"r Body Text Indent 2$0^`0a$5CJOJQJaJmH sH 4 @24 zFooter  !.)@A. z Page Number :ST ghrsE F & ' 6 x y 01_`?@8 XYhT4KLMNPQSTVWYZxyz0000000000000000000000000000000000000000000000000000000000000000000000@0@0000000000000000@0I00@0I00@0I00@0I00@0@0@0@0@0I00g& ' x y 0`@8 XYhTKLMNxK00K00K00 @0K00C00 C00C00C00HC00K0 0 ԙFK0 0 K00@0K00C00C00C00|FC00C00C00C00K00K00C0#0C0#0@0K00C00C00C00C00C00C00C0#0$,K0'0(8ZK0'0K00K00@0K0+0 ,ZC0,0 C00C00C00C00C00@0C070C070 0<K00 0 ,,&x&&E%&&,:!>#)##,4####k#T!#o#j#T#4n#+#̥## #<###d#|#)#7#7#,8#5#\5#5#5#<#<#$=#d=#̋# #L##"#T"#"#"#d###$#d#l8#,m8 #lm8 #m8 #m8 #,n8 #ln8#Q#7*urn:schemas-microsoft-com:office:smarttags PostalCode=>*urn:schemas-microsoft-com:office:smarttags PlaceName8;*urn:schemas-microsoft-com:office:smarttagsCity:9*urn:schemas-microsoft-com:office:smarttagsStreet==*urn:schemas-microsoft-com:office:smarttags PlaceType;:*urn:schemas-microsoft-com:office:smarttagsaddress9<*urn:schemas-microsoft-com:office:smarttagsplace P>=<;:9;7><>>:9;7<>>>:9;7>=<;>=<;<>>=:9;7<>>>:9;7<>>=<=>:9;7<=> LTe s !BMkst}NNPPQQSTVWYZNNPPQQSTVWYZ33PQRTqrqrssD F & & ' / 1XYahk%JMMNNPPQQSTVWYZzNNPPQQSTVWYZz6/7uf j=R #n`$L{=O=Zevz{wKO] (a]6z 8NPSVYxo033? o0o0o0o0o0o0@[z@UnknownGz Times New Roman5Symbol3& z Arials"Gill Alt One MT LightTimes New Roman"1h""wꗦ77 4??2QHP ?]62NICHSA Grants awarded in 2005 Sara Morrow Paul J HoldenOh+'0 ,8 X d p | NICHSA Grants awarded in 2005 Sara Morrow Normal.dotPaul J Holden2Microsoft Office Word@ @3@(ژ@(ژ՜.+,0 hp  NICHSA7? 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