Reclaiming human machine nature

Extending and modifying his domain of life by artifact production is one of the main characteristics of humankind. From the first hominid, who used a wood stick or a stone for extending his upper limbs and augmenting his gesture strength, to current systems engineers who used technologies for augmenting human cognition, perception and action, extending human body capabilities remains a big issue. From more than fifty years cybernetics, computer and cognitive sciences have imposed only one reductionist model of human machine systems: cognitive systems. Inspired by philosophy, behaviorist psychology and the information treatment metaphor, the cognitive system paradigm requires a function view and a functional analysis in human systems design process. According that design approach, human have been reduced to his metaphysical and functional properties in a new dualism. Human body requirements have been left to physical ergonomics or "physiology". With multidisciplinary convergence, the issues of "human-machine" systems and "human artifacts" evolve. The loss of biological and social boundaries between human organisms and interactive and informational physical artifact questions the current engineering methods and ergonomic design of cognitive systems. New developpment of human machine systems for intensive care, human space activities or bio-engineering sytems requires grounding human systems design on a renewed epistemological framework for future human systems model and evidence based "bio-engineering". In that context, reclaiming human factors, augmented human and human machine nature is a necessityComment: Published in HCI International 2014, Heraklion : Greece (2014

GABAB receptor-mediated activation of astrocytes by gamma-hydroxybutyric acid

The gamma-aminobutyric acid (GABA) metabolite gamma-hydroxybutyric acid (GHB) shows a variety of behavioural effects when administered to animals and humans, including reward/addiction properties and absence seizures. At the cellular level, these actions of GHB are mediated by activation of neuronal GABAB receptors (GABABRs) where it acts as a weak agonist. Because astrocytes respond to endogenous and exogenously applied GABA by activation of both GABAA and GABABRs, here we investigated the action of GHB on astrocytes on the ventral tegmental area (VTA) and the ventrobasal (VB) thalamic nucleus, two brain areas involved in the reward and proepileptic action of GHB, respectively, and compared it with that of the potent GABABR agonist baclofen. We found that GHB and baclofen elicited dose-dependent (ED50: 1.6 mM and 1.3 µM, respectively) transient increases in intracellular Ca2+ in VTA and VB astrocytes of young mice and rats, which were accounted for by activation of their GABABRs and mediated by Ca2+ release from intracellular store release. In contrast, prolonged GHB and baclofen exposure caused a reduction in spontaneous astrocyte activity and glutamate release from VTA astrocytes. These findings have key (patho)physiological implications for our understanding of the addictive and proepileptic actions of GHB

Gamma-hydroxybutyrate does not maintain self-administration but induces conditioned place preference when injected in the ventral tegmental area

Gamma-hydroxybutyric acid (GHB) is an endogenous brain substance that has diverse neuropharmacological actions, including rewarding properties in different animal species and in humans. As other drugs of abuse, GHB affects the firing of ventral tegmental neurons (VTA) in anaesthetized animals and hyperpolarizes dopaminergic neurons in VTA slices. However, no direct behavioural data on the effects of GHB applied in the VTA or in the target regions of its dopaminergic neurons, e.g. the nucleus accumbens (NAc), are available. Here, we investigated the effects of various doses of intravenous GHB in maintaining self-administration (from 0.001 to 10 mg/kg per infusion), and its ability to induce conditioned place preference (CPP) in rats when given orally (175-350 mg/kg) or injected directly either in the VTA or NAc (from 10 to 300 microg/0.5 microl per side). Our results indicate that while only 0.01 mg/kg per infusion GHB maintained self-administration, although not on every test day, 350 mg/kg GHB given orally induced CPP. CPP was also observed when GHB was injected in the VTA (30-100 microg/0.5 microl per side) but not in the NAc. Together with recent in-vitro findings, these results suggest that the rewarding properties of GHB mainly occur via disinhibition of VTA dopaminergic neurons

Toxic effects of phenothiazines on the eye

Publications about the retinotoxic action of phenothiazine derivatives led the author to undertake an ophthalmological investigation in two psychiatric hospitals in The Netherlands. The pharmacological actions of phenothiazine preparations are listed and a survey of the phenothiazine derivatives which are at present in use is given. Some retinotoxic substances are discussed and a survey is given of the literature on the ocular complications of phenothiazine therapy. The eyes of 561 patients were examined. of whom 541 are included in this study. 343 of these patients(63.4 %) were found to have retinopathy. The correlation between the retinopathy and the total dose of phenothiazine preparations taken. and between the retinopathy and the duration of treatment. was highly significant. The correlation between the retinopathy and the average daily dose taken was significant. The retinopathy was associated with a reduced standing potential of the eye. as determined by electro-oculography. It was possibly responsible for diminished visual acuity in some cases, and for an abnormally large proportion of protans in the group of patients with colour defects. It was not possible to ascribe a more severe retinotoxic action to one or more specific phenothiazine derivatives than to others. In the author's opinion regular examination of the eyes of patients who are being treated with phenothiazine preparations in high dosage and for for a long period of time is indicated

Bases biologiques du comportement social

Pour bien comprendre le comportement humain dans un environnement social,il est necessaire de comprendre comment fonctionne le systÂ?me nerveux central. L'une des principales fonctions du cerveau est de crÂ?er des relations entre leshumains.. .................A talk on the biological implications on a behavior in social environmen