South Australian primary schools bicycle helmet usage survey

This was a school-based survey that was conducted to assess bicycle helmet compliance rates amongst South Australian primary school students riding to school. 32% of South Australian primary schools chose to participate in the survey. The total number of students surveyed in the participating schools accounted for approximately 42% of all primary school children. It was estimated that 4% of primary school children ride their bicycle to school. Of the students riding a bicycle to school, 92% wore a helmet. The highest rate of helmet-compliance was reported in Catholic and independent primary schools (100%). Geographically, the lowest rate was reported in the metropolitan Adelaide region (89%).H Thomas, R.L. Somers and R.W.G. Anderso

Survival of motor neurone protein is required for normal postnatal development of the spleen

Funding S.H.P. received an Anatomical Society PhD Studentship award for A.K.T. T.H.G. received an Anatomical Society PhD Studentship award for R.A.P. and funding from the SMA Trust (UK SMA Research Consortium), Euan MacDonald Centre for Motor Neurone Disease Research, and Muscular Dystrophy UK. K.J.S received funding for pathologic studies in human subjects from NICHD grant R01-HD054599.Peer reviewedPostprin

EORTC Group Phase II Study of Oral Etoposide for Pretreated Soft Tissue Sarcoma

Purpose. This study investigates the efficacy and toxicity of daily oral etoposide in chemotherapy for non-heavily pretreated advanced and metastatic soft tissue sarcoma (STS)

Dysregulation of ubiquitin homeostasis and β-catenin signaling promote spinal muscular atrophy

Acknowledgements The authors are grateful to Nils Lindstrom and members of the Gillingwater laboratory for advice and assistance with this study and helpful comments on the manuscript; Neil Cashman for the NSC-34 cell line; and Ji-Long Liu for the DrosophilasmnA and smnB lines. This work was supported by grants from the SMA Trust (to T.H. Gillingwater, P.J. Young, and R. Morse), BDF Newlife (to T.H. Gillingwater and S.H. Parson), the Anatomical Society (to T.H. Gillingwater and S.H. Parson), the Muscular Dystrophy Campaign (to T.H. Gillingwater), the Jennifer Trust for Spinal Muscular Atrophy (to H.R. Fuller), the Muscular Dystrophy Association (to G.E. Morris), the Vandervell Foundation (to P.J. Young), the Medical Research Council (GO82208 to I.M. Robinson), Roslin Institute Strategic Grant funding from the BBSRC (to T.M. Wishart), the BBSRC (to C.G. Becker), the Deutsche Forschungsgemeinschaft and EU FP7/2007-2013 (grant no. 2012-305121, NeurOmics, to B. Wirth), the Center for Molecular Medicine Cologne (to B. Wirth and M. Hammerschmidt), and SMA Europe (to M.M. Reissland). We would also like to acknowledge financial support to the Gillingwater lab generated through donations to the SMASHSMA campaign.Peer reviewedPublisher PD

Ethanolamine is a novel STAT-3 dependent cardioprotective agent

Ethanolamine is a biogenic amine found naturally in the body as part of membrane lipids and as a metabolite of the cardioprotective substances, sphingosine-1-phosphate (S1P) and anandamide. In the brain, ethanolamine, formed from the breakdown of anandamide protects against ischaemic apoptosis. However, the effects of ethanolamine in the heart are unknown. Signal transducer and activator of transcription 3 (STAT-3) is a critical prosurvival factor in ischaemia/reperfusion (I/R) injury. Therefore, we investigated whether ethanolamine protects the heart via activation of STAT-3. Isolated hearts from wildtype or cardiomyocyte specific STAT-3 knockout (K/O) mice were pre-treated with ethanolamine (Etn) (0.3 mmol/L) before I/R insult. In vivo rat hearts were subjected to 30 min ischaemia/2 h reperfusion in the presence or absence of 5 mg/kg S1P and/or the FAAH inhibitor, URB597. Infarct size was measured at the end of each protocol by triphenyltetrazolium chloride staining. Pre-treatment with ethanolamine decreased infarct size in isolated mouse or rat hearts subjected to I/R but this infarct sparing effect was lost in cardiomyocyte specific STAT-3 deficient mice. Pre-treatment with ethanolamine increased nuclear phosphorylated STAT-3 [control 0.75 ± 0.08 vs. Etn 1.50 ± 0.09 arbitrary units; P < 0.05]. Our findings suggest a novel cardioprotective role for ethanolamine against I/R injury via activation of STAT-3