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1.  Retracted manuscript 
Small GTPases  2013;4(2):61.
The following article from Small GTPases, “Scientific Yellow Journalism” by Anica Klockars and Michael J. Williams, published online on 20 September 2012  (doi: 10.4161/sgtp.22289; by Landes Bioscience and subsequently published in print in Small GTPases 2012 3(4):201 has been retracted by agreement between the authors and the journal’s Editor in Chief, Michael J. Williams (also an author of the paper). 
PMCID: PMC3747257  PMID: 23485921
2.  Effects of Community-Based Cardiac Rehabilitation on Body Composition and Physical Function in Individuals with Stable Coronary Artery Disease: 1.6-Year Followup 
BioMed Research International  2013;2013:903604.
Objective. To examine long-term changes in physical function and body composition in coronary artery disease (CAD) patients participating in ongoing community-based cardiac rehabilitation (CR). Design. Thirty-four individuals (69.7 ± 8.2 years; 79% men) participated in this longitudinal observational study. Baseline and follow-up assessments included incremental shuttle walk, short physical performance battery, handgrip strength, chair stands, body composition, last year physical activity, and CR attendance. Results. Participants attended 38.5 ± 30.3% sessions during 1.6 ± 0.2 year followup. A significant increase in 30-second chair stands (17.0 ± 4.7 to 19.6 ± 6.4, P < 0.001), body weight (75.8 ± 11.1 to 77.2 ± 12.1 kg, P = 0.001), and body fat (27.0 ± 9.5 to 29.1 ± 9.6%, P < 0.001) and a decline in handgrip strength (36.4 ± 9.4 to 33.0 ± 10.6 kg·f, P < 0.001) and muscle mass (40.8 ± 5.6 to 39.3 ± 5.8%, P < 0.001) were observed during followup. There was no significant change in shuttle walk duration. CR attendance was not correlated to observed changes. Conclusions. Elderly CAD patients participating in a maintenance CR program improve lower-body muscle strength but experience a decline in handgrip strength and unfavourable changes in body composition, irrespective of CR attendance.
PMCID: PMC3707214  PMID: 23865071
3.  Rho GTPases 
Small GTPases  2012;3(1):1.
PMCID: PMC3398910  PMID: 22710727
4.  Small GTPases 
Small GTPases  2011;2(4):189.
PMCID: PMC3225907  PMID: 22145090
5.  Scientific yellow journalism 
Small GTPases  2012;3(4):201.
PMCID: PMC3520881  PMID: 22995950
6.  Scientific dialogue in the electronic age 
Small GTPases  2011;2(1):1.
PMCID: PMC3116613  PMID: 21686275
7.  The peer review process from an editor's point of view 
Small GTPases  2010;1(2):77.
PMCID: PMC3116592  PMID: 21686258
8.  Introduction to Small GTPases 
Small GTPases  2010;1(1):1.
PMCID: PMC3109482  PMID: 21686116
9.  Real-Time Analysis of Drosophila Post-Embryonic Haemocyte Behaviour 
PLoS ONE  2012;7(1):e28783.
The larval stage of the model organism Drosophila is frequently used to study host-pathogen interactions. During embryogenesis the cellular arm of the immune response, consisting of macrophage-like cells known as plasmatocytes, is extremely motile and functions to phagocytise pathogens and apoptotic bodies, as well as produce extracellular matrix. The cellular branch of the larval (post-embryonic) innate immune system consists of three cell types—plasmatocytes, crystal cells and lamellocytes—which are involved in the phagocytosis, encapsulation and melanisation of invading pathogens. Post-embryonic haemocyte motility is poorly understood thus further characterisation is required, for the purpose of standardisation.
In order to examine post-embryonic haemocyte cytoskeletal dynamics or migration, the most commonly used system is in vitro cell lines. The current study employs an ex vivo system (an adaptation of in vitro cell incubation using primary cells), in which primary larval or pre-pupal haemocytes are isolated for short term analysis, in order to discover various aspects of their behaviour during events requiring cytoskeleton dynamics.
The ex vivo method allows for real-time analysis and manipulation of primary post-embryonic haemocytes. This technique was used to characterise, and potentially standardised, larval and pre-pupal haemocyte cytoskeleton dynamics, assayed on different extracellular matrices. Using this method it was determined that, while larval haemocytes are unable to migrate, haemocytes recovered from pre-pupae are capable of migration.
PMCID: PMC3252279  PMID: 22242151
10.  The Rho-Family GTPase Rac1 Regulates Integrin Localization in Drosophila Immunosurveillance Cells 
PLoS ONE  2011;6(5):e19504.
When the parasitoid wasp Leptopilina boulardi lays an egg in a Drosophila larva, phagocytic cells called plasmatocytes and specialized cells known as lamellocytes encapsulate the egg. The Drosophila β-integrin Myospheroid (Mys) is necessary for lamellocytes to adhere to the cellular capsule surrounding L. boulardi eggs. Integrins are heterodimeric adhesion receptors consisting of α and β subunits, and similar to other plasma membrane receptors undergo ligand-dependent endocytosis. In mammalian cells it is known that integrin binding to the extracellular matrix induces the activation of Rac GTPases, and we have previously shown that Rac1 and Rac2 are necessary for a proper encapsulation response in Drosophila larvae. We wanted to test the possibility that Myospheroid and Rac GTPases interact during the Drosophila anti-parasitoid immune response.
In the current study we demonstrate that Rac1 is required for the proper localization of Myospheroid to the cell periphery of haemocytes after parasitization. Interestingly, the mislocalization of Myospheroid in Rac1 mutants is rescued by hyperthermia, involving the heat shock protein Hsp83. From these results we conclude that Rac1 and Hsp83 are required for the proper localization of Mys after parasitization.
We show for the first time that the small GTPase Rac1 is required for Mysopheroid localization. Interestingly, the necessity of Rac1 in Mys localization was negated by hyperthermia. This presents a problem, in Drosophila we quite often raise larvae at 29°C when using the GAL4/UAS misexpression system. If hyperthermia rescues receptor endosomal recycling defects, raising larvae in hyperthermic conditions may mask potentially interesting phenotypes.
PMCID: PMC3095607  PMID: 21603603
11.  Systemic inflammation and lung function in young adults 
Thorax  2007;62(12):1064-1068.
Impaired lung function is associated with systemic inflammation and is a risk factor for cardiovascular disease in older adults. It is unknown when these associations emerge and to what extent they are mediated by smoking, chronic airways disease, and/or established atherosclerosis. We explored the association between the forced expiratory volume in one second (FEV1) and the systemic inflammatory marker C‐reactive protein (CRP) in young adults.
Associations between spirometric lung function and blood CRP were assessed in a population based birth cohort of approximately 1000 New Zealanders at ages 26 and 32 years. Analyses adjusted for height and sex to account for differences in predicted lung function and excluded pregnant women.
There were significant inverse associations between FEV1 and CRP at both ages. Similar results were found for the forced vital capacity. These associations were similar in men and women and were independent of smoking, asthma, and body mass index.
Reduced lung function is associated with systemic inflammation in young adults. This association is not related to smoking, asthma, or obesity. The reasons for the association are unexplained, but the findings indicate that the association between lower lung function and increased inflammation predates the development of either chronic lung disease or clinically significant atherosclerosis. The association between poor lung function and cardiovascular disease may be mediated by an inflammatory mechanism.
PMCID: PMC2094275  PMID: 17604302
inflammation; C‐reactive protein; spirometry; cohort studies
12.  The Drosophila cell adhesion molecule Neuroglian regulates Lissencephaly-1 localisation in circulating immunosurveillance cells 
BMC Immunology  2009;10:17.
When the parasitoid wasp Leptopilina boulardi lays its eggs in Drosophila larvae phagocytic cells called plasmatocytes and specialized cells known as lamellocytes encapsulate the egg. This requires these circulating immunosurveillance cells (haemocytes) to change from a non-adhesive to an adhesive state enabling them to bind to the invader. Interestingly, attachment of leukocytes, platelets, and insect haemocytes requires the same adhesion complexes as epithelial and neuronal cells.
Here evidence is presented showing that the Drosophila L1-type cell adhesion molecule Neuroglian (Nrg) is required for haemocytes to encapsulate L. boulardi wasp eggs. The amino acid sequence FIGQY containing a conserved phosphorylated tyrosine is found in the intracellular domain of all L1-type cell adhesion molecules. This conserved tyrosine is phosphorylated at the cell periphery of plasmatocytes and lamellocytes prior to parasitisation, but dephosphorylated after immune activation. Intriguingly, another pool of Nrg located near the nucleus of plasmatocytes remains phosphorylated after parasitisation. In mammalian neuronal cells phosphorylated neurofascin, another L1-type cell adhesion molecule interacts with a nucleokinesis complex containing the microtubule binding protein lissencephaly-1 (Lis1) [1]. Interestingly in plasmatocytes from Nrg mutants the nucleokinesis regulating protein Lissencephaly-1 (Lis1) fails to localise properly around the nucleus and is instead found diffuse throughout the cytoplasm and at unidentified perinuclear structures. After attaching to the wasp egg control plasmatocytes extend filopodia laterally from their cell periphery; as well as extending lateral filopodia plasmatocytes from Nrg mutants also extend many filopodia from their apical surface.
The Drosophila cellular adhesion molecule Neuroglian is expressed in haemocytes and its activity is required for the encapsulation of L. boularli eggs. At the cell periphery of haemocytes Neuroglian may be involved in cell-cell interactions, while at the cell centre Neuroglian regulates the localisation of the nucleokinesis complex protein lissencephaly-1.
PMCID: PMC2667480  PMID: 19320973
13.  Sarcoidosis presenting with Polyarthritis 
Annals of the Rheumatic Diseases  1961;20(2):138-143.
PMCID: PMC1007197  PMID: 13785473

Results 1-14 (14)