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This study aimed to identify key transitional pathways in the criminal justice system from adolescence to adulthood and the risk factors associated with the escalation of criminal justice involvement over time. We retrospectively linked offending records from 1994 to 2022 and mental health records from 2001 to 2022 for a cohort of 1556 adolescents identified through four health surveys in New South Wales, Australia. Transition probabilities were calculated using the Aalen-Johansen method, and the hazards of transition-specific covariates were estimated. The median age of adolescent entry was 15 years. The cohort was predominantly male (87.5%) and non-Indigenous (65.6%). Among incarcerated adolescents, 76.8% transitioned to adult incarceration. Transition probabilities were the highest among those aged 10–13 years. Among those with mental disorders, psychosis was associated with transitions to adolescent and adult incarceration. Other risk factors for future incarceration include being male, Indigenous, socio-economically disadvantaged, having a history of adolescent incarceration, and being diagnosed with substance use and behavioural disorders. Younger adolescents have higher transition probabilities to more intense criminal justice involvement. Legislative and policy reforms are needed to delay the onset of adolescent criminal justice involvement and ensure age-appropriate rehabilitative strategies to reduce recidivism. • Multi-state modelling can be used to assess criminal justice transitions from adolescence to adulthood. • Younger adolescents have higher probabilities of further incarceration after entry into the criminal justice system. • Adolescent incarceration is associated with adult incarceration and has a leveling effect regardless of age at entry. • Mental disorders increase the risk of incarceration during adolescence and adulthood. [ABSTRACT FROM AUTHOR]

Reducing the over-representation of Aboriginal children in the child protection system is a key target for the Australian government. We aimed to provide more recent evidence on the population-level cumulative incidence of contacts for Aboriginal children with child protective services (CPS) in Western Australia (WA). Linked administrative data was provided for WA CPS between 2000 and 2015 for 33,709 Aboriginal children born in WA between 2000 and 2013. Descriptive summaries and cumulative incidence estimates were used to examine changes in CPS contact trends over time and within sibling groups. There was an increase in early-childhood contacts for children born more recently, with 7.6 % and 2.3 % of children born in 2000–2001 having a notification and placement in out-of-home care by age one, respectively, compared to 15.1 % and 4.3 % of children born in 2012–2013. Among sibling groups where at least one sibling had a CPS contact, approximately half of children had their first contacts on the same date as another sibling. For children born after one of their siblings had been placed in out-of-home care, 31.9 % had themselves been placed in out-of-home care by age one. Multiple children tend to be placed into out-of-home care when at least one sibling is, which is likely to have a significant impact on families affected. The additional risk of placement also carries over to children born after the first removal in a sibling group, highlighting the need for further support to prevent future removals. [ABSTRACT FROM AUTHOR]

Abstract: The loss of dopaminergic neurons induced by the parkinsonian toxins paraquat, rotenone, and 1-methyl-4-phenylpyridinium (MPP+) is associated with oxidative stress. However, controversial reports exist regarding the source/compartmentalization of reactive oxygen species (ROS) generation and its exact role in cell death. We aimed to determine in detail the role of superoxide anion (O2 •-), oxidative stress, and their subcellular compartmentalization in dopaminergic cell death induced by parkinsonian toxins. Oxidative stress and ROS formation were determined in the cytosol, intermembrane (IMS), and mitochondrial matrix compartments, using dihydroethidine derivatives and the redox sensor roGFP, as well as electron paramagnetic resonance spectroscopy. Paraquat induced an increase in ROS and oxidative stress in both the cytosol and the mitochondrial matrix prior to cell death. MPP+ and rotenone primarily induced an increase in ROS and oxidative stress in the mitochondrial matrix. No oxidative stress was detected at the level of the IMS. In contrast to previous studies, overexpression of manganese superoxide dismutase (MnSOD) or copper/zinc SOD (CuZnSOD) had no effect on alterations in ROS steady-state levels, lipid peroxidation, loss of mitochondrial membrane potential (ΔΨm), and dopaminergic cell death induced by MPP+ or rotenone. In contrast, paraquat-induced oxidative stress and cell death were selectively reduced by MnSOD overexpression, but not by CuZnSOD or manganese-porphyrins. However, MnSOD also failed to prevent ΔΨm loss. Finally, paraquat, but not MPP+ or rotenone, induced the transcriptional activation of the redox-sensitive antioxidant response elements (ARE) and nuclear factor kappa-B (NF-κB). These results demonstrate a selective role of mitochondrial O2 •- in dopaminergic cell death induced by paraquat, and show that toxicity induced by the complex I inhibitors rotenone and MPP+ does not depend directly on mitochondrial O2 •- formation. [Copyright &y& Elsevier]

Abstract: The studies presented here demonstrate the protective effect of acetyl-l-carnitine (ALC) against alcohol-induced oxidative neuroinflammation, neuronal degeneration, and impaired neurotransmission. Our findings reveal the cellular and biochemical mechanisms of alcohol-induced oxidative damage in various types of brain cells. Chronic ethanol administration to mice caused an increase in inducible nitric oxide synthase (iNOS) and 3-nitrotyrosine adduct formation in frontal cortical neurons but not in astrocytes from brains of these animals. Interestingly, alcohol administration caused a rather selective activation of NADPH oxidase (NOX), which, in turn, enhanced levels of reactive oxygen species (ROS) and 4-hydroxynonenal, but these were predominantly localized in astrocytes and microglia. Oxidative damage in glial cells was accompanied by their pronounced activation (astrogliosis) and coincident neuronal loss, suggesting that inflammation in glial cells caused neuronal degeneration. Immunohistochemistry studies indicated that alcohol consumption induced different oxidative mediators in different brain cell types. Thus, nitric oxide was mostly detected in iNOS-expressing neurons, whereas ROS were predominantly generated in NOX-expressing glial cells after alcohol ingestion. Assessment of neuronal activity in ex vivo frontal cortical brain tissue slices from ethanol-fed mice showed a reduction in long-term potentiation synaptic transmission compared with slices from controls. Coadministration of ALC with alcohol showed a significant reduction in oxidative damage and neuronal loss and a restoration of synaptic neurotransmission in this brain region, suggesting that ALC protects brain cells from ethanol-induced oxidative injury. These findings suggest the potential clinical utility of ALC as a neuroprotective agent that prevents alcohol-induced brain damage and development of neurological disorders. [ABSTRACT FROM AUTHOR]