Local Government's effective community responses

Speech given at the conference 'Reducing criminality: partnerships and best practice', Perth, 31 July to 1 August 2000, by Adam Graycar, Director, Australian Institute of Criminology. This speech is made available under the CC-BY-NC-ND 4.0 license: http://creativecommons.org/licenses/by-nc-nd/4.0/The challenge before us is to find the right set of interventions to prevent criminal behaviour among young people, and prevent that behaviour becoming a lifelong activity. The two main strategies are on the one hand to reduce the supply of motivated offenders, and on the other to make crime more difficult to commit. Crime is the result of complex changes in economic, social and cultural factors such as unemployment, dysfunctional families, child abuse, poor education, community breakdown, economic inequality and substance abuse. If crime prevention is to succeed it should focus on broad social outcomes, for example reducing social exclusion. Compelling evidence suggests that those who feel excluded from participation in community life are more likely to offend against that community. Addressing this sense of exclusion can reduce the risk of offending. In simple terms the criminal justice domain plays only a small part in crime prevention and preventing the supply of motivated offenders

Different levels of neuroprotection by two insulin-like growth factor-I splice variants

We compared the neuroprotective effects of a liver-type isoform of insulin-like growth factor-I (IGF-IEa) and its splice variant, mechano-growth factor (MGF), isolated from active skeletal muscle. cDNAs of these peptides were injected into the facial muscle of adult rats prior to facial nerve avulsion. This resulted in significant neuroprotection of 88% and 37%, respectively, of motoneurons compared to control plasmid and avulsion-only groups. MGF is markedly more effective than the liver-type, systemic IGF-I for motoneuron survival, suggesting a major role for the peripheral target in adult neuronal maintenance and survival.Michael Aperghis, Ian P. Johnson, John Cannon, Shi-Yu Yang and Geoffrey Goldspin

Age, diet and injury affect the survival of facial motoneurons

Using the model of facial nerve avulsion, we have compared the effects of injury, age and diet on motoneuronal survival. One to four weeks after nerve avulsion, 50–75% motoneuron loss was quantified in ad libitum-fed rats aged 7 days (neonate), 6 months (adult) and 24 months (aging) at the time of injury. Evidence of apoptosis was found for neonatal rats at 3 days post-injury, but not for neonates examined 7 days or adult or aging rats examined 1 month after injury. Non-operated, ad libitum-fed rats showed no significant loss of facial motoneurons by 24 months. Surprisingly, non-operated rats whose food intake was restricted to 15 g standard rat chow per day from the age of 6 months lost 50% of their motoneurons by 24 months. Facial nerve avulsion of 24-month-old rats raised on this restricted diet did not result in any additional loss of motoneurons one month after injury. These results challenge the common view that aging results in neuronal loss and that dietary restriction is universally beneficial.M. Aperghis, I. P. Johnson, N. Patel, A. Khadir, J. Cannon and G. Goldspin