Entomotoxicology in burnt bodies: a case of maternal filicide-suicide by fire.

One of the most common methods of maternal filicide is by fire. In this case study, a 40-year-old female and her children were found completely burned in a burnt out car. All bodies showed a degree of destruction by fire consisting to a level 3 of the Crow-Glassman Scale (CGS) and early stage of insect activity. Toxicological analyses were performed on soft tissues and body fluids still available. The results were positive for diazepam and its metabolites only for children with blood concentrations consistent with therapeutic doses of benzodiazepines. Home video surveillance cameras confirmed sedation prior to death recording the mother while administering some drops of sedative drugs in a soft drink to the children just a couple of hours before setting fire to the car. Based on autopsy findings, all victims were still alive at the time of fire. The cause of death was determined as carbon monoxide poisoning and fatal thermal injuries by fire. This case study has a special focus on the entomotoxicology and the potential role of insects in death investigations of burnt bodies, supposed to be an inadequate substratum for insect colonization. It demonstrates that in burnt bodies, arthropod colonization can be quite immediate after fire is extinguished. Toxicological analyses performed on larvae actively feeding on the children's bodies were positive for diazepam and its metabolites in small amount compared with blood concentrations, whereas the larvae collected from the mother's body were totally negative. These data, according to the autopsy findings and the toxicological results from the victim's blood and tissues, supported the suspect of a non-lethal sedation prior to death, which is a common behaviour in maternal filicide.

The appropriateness of opt-out consent for monitoring childhood obesity in Australia.

Childhood obesity monitoring is a fundamental component of obesity prevention but is poorly done in Australia. Monitoring obesity prevalence in children provides important population health data that can be used to track trends over time, identify areas at greatest risk of obesity, determine the effectiveness of interventions and policies, raise awareness and stimulate action. High participation rates are essential for effective monitoring because these provide more representative data. Passive ('opt-out') consent has been shown to provide high participation rates in international childhood obesity monitoring programs and in a recent Australian federal initiative monitoring early child development. A federal initiative structured like existing child development monitoring programs, but with the authority to collect height and weight measurements using opt-out consent, is recommended to monitor rates of childhood obesity in Australia.

Full characterization of Gaussian bipartite entangled states by a single homodyne detector.

We present the full experimental reconstruction of Gaussian entangled states generated by a type-II optical parametric oscillator below threshold. Our scheme provides the entire covariance matrix using a single homodyne detector and allows for the complete characterization of bipartite Gaussian states, including the evaluation of purity, entanglement, and nonclassical photon correlations, without a priori assumptions on the state under investigation. Our results show that single homodyne schemes are convenient and robust setups for the full characterization of optical parametric oscillator signals and represent a tool for quantum technology based on continuous variable entanglement.

From neuroscience to application in neuropharmacology: A generation of progress in electrophysiology.

A continuum from neuronal cellular/subcellular properties to system processes appears to exist in many instances and to allow privileged approaches in neuroscience and neuropharmacology research. Brain signals and the cholinergic and GABAergic systems, in vivo and in vitro evidence from studies on the retina, or the "gamma band" oscillations in neuron membrane potential/spiking rate and neuronal assemblies are examples in this respect. However, spontaneous and stimulus-event-related signals at any location and time point reflect brain state conditions that depend on neuromodulation, neurotransmitter interaction, hormones (e.g., glucocorticois, ACTH, estrogens) and neuroendocrine interaction at different levels of complexity, as well as on the spontaneous or experimentally-induced changes in metabolism (e.g., glucose, ammonia), blood flow, pO2, pCO2, acid/base balance, K activity, etc., that occur locally or systemically. Any of these factors can account for individual differences and/or changes over time that often are (or need to be) neglected in pharmaco-EEG studies or are dealt with statistically and by controlling the experimental conditions. As a result, the electrophysiological effects of neuroactive drugs are to an extent non-specific and require adequate modeling and precise correlation with independent parameters (e.g., drug kinetics, vigilance, hormonal profile or metabolic status, etc.) to avoid biased results in otherwise controlled studies.

Fibroblast growth factor-2 over-rides insulin-like growth factor-I induced proliferation and cell survival in human neuroblastoma cells.

The insulin-like growth factor (IGF) system is a key regulator of cell growth, survival and differentiation, and these functions are co-modulated by other growth factors including fibroblast growth factor-2 (FGF-2). To investigate IGF/FGF interactions in neuronal cells, we employed neuroblastoma cells (SK-N-MC). In serum free conditions proliferation of the SK-N-MC cells was promoted by IGF-I (25 ng/ml), but blunted by FGF-2 (50 ng/ml). IGF-I-induced proliferation was abolished in the presence of FGF-2 even when IGF-I was used at 100 ng/ml. In addition to our previously described FGF-2 induced proteolytic cleavage of IGFBP-2, we found that FGF-2 increased IGFBP-6 levels in conditioned medium (CM) without affecting IGFBP-6 mRNA abundance. Modulation of IGFBP-2 and -6 levels were not significant mechanisms involved in the blockade of IGF-I action since the potent IGF-I analogues [QAYL]IGF-I and des(1-3)IGF-I (minimal IGFBP affinity) were unable to overcome FGF-2 inhibition of cell proliferation. FGF-2 treated cells showed morphological differentiation expressing the TUJ1 neuronal marker while cells treated with IGF-I alone showed no morphological change. When IGF-I was combined with FGF-2, however, cell morphology was indistinguishable from that seen with FGF-2 alone. FGF-2 inhibited proliferation and enhanced differentiation was also associated with a 70% increase in cell death. Although IGF-I alone was potently anti-apoptotic (60% decreased), IGF-I was unable to prevent apoptosis when administrated in combination with FGF-2. Gene-array analysis confirmed FGF-2 activation of the intrinsic and extrinsic apoptotic pathways and blockade of IGF anti-apoptotic signaling. FGF-2, directly and indirectly, overcomes the proliferative and anti-apoptotic activity of IGF-I by complex mechanisms, including enhancement of differentiation and apoptotic pathways, and inhibition of IGF-I induced anti-apoptotic signalling. Modulation of IGF binding protein abundance by FGF-2 does not play a significant role in inhibition of IGF-I induced mitogenesis.