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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 (doi: 10.4161/sgtp.22289; by Landes Bioscience and subsequently published in print in Small GTPases 2012 3(4):201 has been retracted by agreement between the authors and the journal’s Editor in Chief, Michael J. Williams (also an author of the paper).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.  Drosophila Insulin-Producing Cells Are Differentially Modulated by Serotonin and Octopamine Receptors and Affect Social Behavior 
PLoS ONE  2014;9(6):e99732.
A set of 14 insulin-producing cells (IPCs) in the Drosophila brain produces three insulin-like peptides (DILP2, 3 and 5). Activity in IPCs and release of DILPs is nutrient dependent and controlled by multiple factors such as fat body-derived proteins, neurotransmitters, and neuropeptides. Two monoamine receptors, the octopamine receptor OAMB and the serotonin receptor 5-HT1A, are expressed by the IPCs. These receptors may act antagonistically on adenylate cyclase. Here we investigate the action of the two receptors on activity in and output from the IPCs. Knockdown of OAMB by targeted RNAi led to elevated Dilp3 transcript levels in the brain, whereas 5-HT1A knockdown resulted in increases of Dilp2 and 5. OAMB-RNAi in IPCs leads to extended survival of starved flies and increased food intake, whereas 5-HT1A-RNAi produces the opposite phenotypes. However, knockdown of either OAMB or 5-HT1A in IPCs both lead to increased resistance to oxidative stress. In assays of carbohydrate levels we found that 5-HT1A knockdown in IPCs resulted in elevated hemolymph glucose, body glycogen and body trehalose levels, while no effects were seen after OAMB knockdown. We also found that manipulations of the two receptors in IPCs affected male aggressive behavior in different ways and 5-HT1A-RNAi reduced courtship latency. Our observations suggest that activation of 5-HT1A and OAMB signaling in IPCs generates differential effects on Dilp transcription, fly physiology, metabolism and social interactions. However the findings do not support an antagonistic action of the two monoamines and their receptors in this particular system.
PMCID: PMC4055686  PMID: 24923784
3.  Cerebral blood flow and cerebrovascular reactivity at rest and during sub-maximal exercise: Effect of age and 12-week exercise training 
Age  2012;35(3):905-920.
Chronic reductions in cerebral blood flow (CBF) and cerebrovascular reactivity to CO2 are risk factors for cerebrovascular disease. Higher aerobic fitness is associated with higher CBF at any age; however, whether CBF or reactivity can be elevated following an exercise training intervention in healthy individuals is unknown. The aim of this study was to assess the effect of exercise training on CBF and cerebrovascular reactivity at rest and during exercise in young and older individuals. Ten young (23 ± 5 years; body mass index (BMI), 26 ± 3 kg m−2; \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$ {\mathop{V}\limits^{ \cdot }{_{\text{O2}}}}\max $$\end{document}, 35 ± 5 ml kg−1 min−1) and 10 older (63 ± 5 years; BMI, 25 ± 3.0 kg m−2; \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$ {\mathop{V}\limits^{ \cdot }{_{\text{O2}}}}\max $$\end{document}, 26 ± 4 ml kg-1 min−1) previously sedentary individuals breathed 5 % CO2 for 3 min at rest and during steady-state cycling exercise (30 and 70 % heart rate range (HRR)) prior to and following a 12-week aerobic exercise intervention. Effects of training on middle cerebral artery blood velocity (MCAv) at rest were unclear in both age groups. The absolute MCAv response to exercise was greater in the young (9 and 9 cm s−1 (30 and 70 % HRR, respectively) vs. 5 and 4 cm s−1 (older), P < 0.05) and was similar following training. Cerebrovascular reactivity was elevated following the 12-week training at rest (2.87 ± 0.76 vs. 2.54 ± 1.12 cm s−1 mm Hg−1, P = 0.01) and during exercise, irrespective of age. The finding of a training-induced elevation in cerebrovascular reactivity provides further support for exercise as a preventative tool in cerebrovascular and neurological disease with ageing.
PMCID: PMC3636405  PMID: 22669592
Ageing; Exercise training; Fitness; Cerebral blood flow; CO2 reactivity
4.  Biogeography and body size shuffling of aquatic salamander communities on a shifting refuge 
Freshwater habitats of coastal plains are refugia for many divergent vertebrate lineages, yet these environments are highly vulnerable to sea-level fluctuations, which suggest that resident communities have endured dynamic histories. Using the fossil record and a multi-locus nuclear phylogeny, we examine divergence times, biogeography, body size evolution and patterns of community assembly of aquatic salamanders from North American coastal plains since the Late Cretaceous. At least five salamander families occurred on the extensive Western Interior Coastal Plain (WICP), which existed from the Late Cretaceous through the Eocene. Four of these families subsequently colonized the emergent Southeastern Coastal Plain (SECP) by the Early Oligocene to Late Miocene. Three families ultimately survived and underwent extensive body size evolution in situ on the SECP. This included at least two major size reversals in recent taxa that are convergent with confamilial WICP ancestors. Dynamics of the coastal plain, major lineage extinctions and frequent extreme changes in body size have resulted in significant shuffling of the size structure of aquatic salamander communities on this shifting refuge since the Cretaceous.
PMCID: PMC3619470  PMID: 23466988
Amphibia; Caudata; coastal plain; body size evolution; community evolution; incumbency
5.  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
6.  Rho GTPases 
Small GTPases  2012;3(1):1.
PMCID: PMC3398910  PMID: 22710727
7.  Scientific yellow journalism 
Small GTPases  2012;3(4):201.
PMCID: PMC3520881  PMID: 22995950
8.  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
10.  Sarcoidosis presenting with Polyarthritis 
Annals of the Rheumatic Diseases  1961;20(2):138-143.
PMCID: PMC1007197  PMID: 13785473

Results 1-10 (10)