Questions éthiques et cliniques posées par l'adoption de l'initiative sur l'internement à vie des délinquants particulièrement dangereux par le peuple suisse

Une initiative populaire se concluant par un vote national a conduit le peuple suisse à demander une modification de sa constitution pour permettre d'interner définitivement certains délinquants particulièrement dangereux. Une fois la décision prise, aucune véritable réévaluation de la situation ne pourra être effectuée. Cette décision se basera principalement sur l'expertise psychiatrique qui devra se prononcer sur le caractère inamendable ou inaccessible à tout traitement de tels sujets. Cet article présente l'historique de la démarche populaire qui a conduit à ce vote et la manière dont l'Etat suisse a rendu compte de cette votation en tentant de l'inscrire dans son code pénal. Pourtant le texte voté se présentait d'une manière telle qu'il rendait impossible son inscription autant dans un discours juridique que dans un discours psychiatrique. Il confronte maintenant les praticiens à des questions éthiques majeures. Doit-on accepter de s'inscrire dans un tel processus pénal? Peut-on valider par une expertise un pronostic qui engage la vie entière d'une personne lorsque l'on connaît le caractère incertain et donc discutable des approches prédictives? Comment tout un Etat de droit a-t-il pu laisser se développer un tel leurre quant à la place de la psychiatrie dans la cité? [Auteurs]]]> Sex Offenses; Commitment of Mentally Ill; Forensic Psychiatry fre oai:serval.unil.ch:BIB_43D14F96D4A2 2022-05-07T01:16:46Z openaire documents urnserval <oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"> https://serval.unil.ch/notice/serval:BIB_43D14F96D4A2 ECIL-6 guidelines for the treatment of invasive candidiasis, aspergillosis and mucormycosis in leukemia and hematopoietic stem cell transplant patients. info:doi:10.3324/haematol.2016.152900 info:eu-repo/semantics/altIdentifier/doi/10.3324/haematol.2016.152900 info:eu-repo/semantics/altIdentifier/pmid/28011902 Tissot, F. Agrawal, S. Pagano, L. Petrikkos, G. Groll, A.H. Skiada, A. Lass-Flörl, C. Calandra, T. Viscoli, C. Herbrecht, R. info:eu-repo/semantics/review article 2017-03 Haematologica, vol. 102, no. 3, pp. 433-444 info:eu-repo/semantics/altIdentifier/eissn/1592-8721 urn:issn:0390-6078 <![CDATA[The European Conference on Infections in Leukemia (ECIL) provides recommendations for diagnostic strategies and prophylactic, pre-emptive or targeted therapy strategies for various types of infection in patients with hematologic malignancies or hematopoietic stem cell transplantation recipients. Meetings are held every two years since 2005 and evidence-based recommendations are elaborated after evaluation of the literature and discussion among specialists of nearly all European countries. In this manuscript, the ECIL group presents the 2015-update of the recommendations for the targeted treatment of invasive candidiasis, aspergillosis and mucormycosis. Current data now allow a very strong recommendation in favor of echinocandins for first-line therapy of candidemia irrespective of the underlying predisposing factors. Anidulafungin has been given the same grading as the other echinocandins for hemato-oncological patients. The beneficial role of catheter removal in candidemia is strengthened. Aspergillus guidelines now recommend the use of either voriconazole or isavuconazole for first-line treatment of invasive aspergillosis, while first-line combination antifungal therapy is not routinely recommended. As only few new data were published since the last ECIL guidelines, no major changes were made to mucormycosis recommendations

Vasopressin modulates social recognition-related activity in the left temporoparietal junction in humans

The neuropeptide vasopressin is a key molecular mediator of social behavior in animals and humans, implicated in anxiety and autism. Social recognition, the ability to assess the familiarity of others, is essential for appropriate social interactions and enhanced by vasopressin; however, the neural mechanisms mediating this effect in humans are unknown. Using functional magnetic resonance imaging (fMRI) and an implicit social recognition matching task, we employed a double-blinded procedure in which 20 healthy male volunteers self-administered 40 UI of vasopressin or placebo intranasally, 45 min before performing the matching task in the scanner. In a random-effects fMRI analysis, we show that vasopressin induces a regionally specific alteration in a key node of the theory of mind network, the left temporoparietal junction, identifying a neurobiological mechanism for prosocial neuropeptide effects in humans that suggests novel treatment strategies

Effects of extracellular calcium and of light adaptation on the response to dim light in honey bee drone photoreceptors.

Light responses in honey bee drone photoreceptors were recorded with intracellular micro-electrodes in superfused slices of retina. The effects of changes in extracellular calcium on the size and the shape of the response to dim light were studied and compared with the effects of light adaptation. Dim light stimuli were used so that the amplitude of the response was linearly related to the number of the photons absorbed, the effects of voltage-dependent mechanisms were negligible and no detectable light adaptation was produced by the stimulus. Lowering the extracellular calcium concentration increased the amplitude and the duration of the response. Raising the extracellular calcium concentration produced the opposite effects. Changing the extracellular calcium concentration modified the response without altering either the linearity of the intensity--response relation or the resting membrane potential in the dark. Light adaptation decreased the amplitude and the duration of the response in a manner that could be quantitatively simulated, in the same photoreceptors, by an increase in the extracellular calcium concentration. Changing the extracellular calcium concentration, or light-adapting the preparation, modified the response without altering its early depolarizing phase. Lowering external calcium either did not affect, or slightly increased, the maximum rate of the light-induced depolarization; raising external calcium, or light-adapting the preparation, either did not affect, or slightly decreased, the maximum rate of the light-induced depolarization. The experimental data can be quantitatively described by a mathematical model with the basic assumption that calcium acts in the process of light adaptation by decreasing the mean open time of the light-activated channels

Vasopressin- and oxytocin-induced activity in the central nervous system: electrophysiological studies using in-vitro systems

During the last two decades, it has become apparent that vasopressin and oxytocin, in addition to playing a role as peptide hormones, also act as neurotransmitters/neuromodulators. A number of arguments support this notion: (i) vasopressin and oxytocin are synthesized not only in hypothalamo-neurohypophysial cells, but also in other hypothalamic and extrahypothalamic cell bodies, whose axon projects to the limbic system, the brainstem and the spinal cord. (ii) Vasopressin and oxytocin can be shed from central axons as are classical neurotransmitters. (iii) Specific binding sites, i.e. membrane receptors having high affinity for vasopressin and oxytocin are present in the central nervous system. (iv) Vasopressin and oxytocin can alter the firing rate of selected neuronal populations. (v) In-situ injection of vasopressin and oxytocin receptor agonists and antagonists can interfere with behavior or physiological regulations. Morphological studies and electrophysiological recordings have evidenced a close anatomical correlation between the presence of vasopressin and oxytocin receptors in the brain and the neuronal responsiveness to vasopressin or oxytocin. These compounds have been found to affect membrane excitability in neurons located in the limbic system, hypothalamus, circumventricular organs, brainstem, and spinal cord. Sharp electrode intracellular recordings and whole-cell recordings, done in brainstem motoneurons or in spinal cord neurons, have revealed that vasopressin and oxytocin can directly affect neuronal excitability by opening non-specific cationic channels or by closing K(+) channels. These neuropeptides can also influence synaptic transmission, by acting either postsynaptically or upon presynaptic target neurons or axon terminals. Whereas, in cultured neurons, vasopressin and oxytocin appear to mobilize intracellular Ca(++), in brainstem slices, the action of oxytocin is mediated by a second messenger that is distinct from the second messenger activated in peripheral target cells. In this review, we will summarize studies carried out at the cellular level, i.e. we will concentrate on in-vitro approaches. Vasopressin and oxytocin will be treated together. Though acting via distinct receptors in distinct brain areas, these two neuropeptides appear to exert similar effects upon neuronal excitability

Overview of cellular electrophysiological actions of vasopressin

The nonapeptide vasopressin acts both as a hormone and as a neurotransmitter/neuromodulator. As a hormone, its target organs include kidney, blood vessels, liver, platelets and anterior pituitary. As a neurotransmitter/neuromodulator, vasopressin plays a role in autonomic functions, such as cardiovascular regulation and temperature regulation and is involved in complex behavioral and cognitive functions, such as sexual behavior, pair-bond formation and social recognition. At the neuronal level, vasopressin acts by enhancing membrane excitability and by modulating synaptic transmission. The present review will focus on the electrophysiological effects of vasopressin at the cellular level. A large proportion of the experiments summarized here have been performed in in vitro systems, especially in brain and spinal cord slices of the rat. Vasopressin exerts a powerful excitatory action on motoneurons of young rats and mice. It acts by generating a cationic inward current and/or by reducing a potassium conductance. In addition, vasopressin enhances the inhibitory synaptic input to motoneurons. By virtue of these actions, vasopressin may regulate the functioning of neuronal networks involved in motor control. In the amygdala, vasopressin can directly excite a subpopulation of neurons, whereas oxytocin, a related neuropeptide, can indirectly inhibit these same neurons. In the lateral septum, vasopressin exerts a similar dual action: it excites directly a neuronal subpopulation, but causes indirect inhibition of virtually all lateral septal neurons. The actions of vasopressin in the amygdala and lateral septum may represent at least part of the neuronal substrate by which vasopressin influences fear and anxiety-related behavior and social recognition, respectively. Central vasopressin can modulate cardiovascular parameters by causing excitation of spinal sympathetic preganglionic neurons, by increasing the inhibitory input to cardiac parasympathetic neurons in the nucleus ambiguus, by depressing the excitatory input to parabrachial neurons, or by inhibiting glutamate release at solitary tract axon terminals. By acting in or near the hypothalamic supraoptic nucleus, vasopressin can influence magnocellular neuron activity, suggesting that the peptide may exert some control on its own release at neurohypophyseal axon terminals. The central actions of vasopressin are mainly mediated by receptors of the V(1A) type, although recent studies have also reported the presence of vasopressin V(1B) receptors in the brain. Major unsolved problems are: (i) what is the transduction pathway activated following stimulation of central vasopressin V(1A) receptors? (ii) What is the precise nature of the cation channels and/or potassium channels operated by vasopressin? (iii) Does vasopressin, by virtue of its second messenger(s), interfere with other neurotransmitter/neuromodulator systems? In recent years, information concerning the mechanism of action of vasopressin at the neuronal level and its possible role and function at the whole-animal level has been accumulating. Translation of peptide actions at the cellular level into autonomic, behavioral and cognitive effects requires an intermediate level of integration, i.e. the level of neuronal circuitry. Here, detailed information is lacking. Further progress will probably require the introduction of new techniques, such as targeted in vivo whole-cell recording, large-scale recordings from neuronal ensembles or in vivo imaging in small animals

Nicotinic receptors in circuit excitability and epilepsy

Neuronal nicotinic acetylcholine receptors belong to the family of excitatory ligand-gated channels and result from the assembly of five subunits. Functional heteromeric nictonic receptors are present in the hippocampus and neocortex, thalamus, mesolimbic dopamine system and brainstem motor nuclei, where they may play a role, respectively, in memory, sensory processing, addiction and motor control. Some forms of autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) have been found to be associated with mutations in the genes coding for the alpha 4 or beta2 subunits of the nicotinic receptor. Mutant receptors display an increased acetylcholine sensitivity with respect to normal receptors. Since the thalamus and the cortex are strongly innervated by cholinergic neurons projecting from the brainstem and basal forebrain, an unbalance between excitation and inhibition, brought about by the presence of mutant receptors, could generate seizures by facilitating and synchronizing spontaneous oscillations in thalamo-cortical circuits

Mechanism of action of oxytocin in rat vagal neurones: induction of a sustained sodium-dependent current.

1. The mechanism of action of oxytocin on vagal neurones of the rat was studied using single-electrode voltage-clamp recordings from brainstem slices. The ionic basis of the oxytocin-induced current was examined by changing the composition of the perfusion solution and by making use of channel blockers. 2. In neurones clamped at or near their resting potential, oxytocin generated a sustained, TTX-insensitive inward current whose peak amplitude was concentration related. This current was detectable at 10 nM, was half-maximal at about 100 nM and was maximal at micromolar concentrations of peptide. 3. The oxytocin current was inward over membrane potentials ranging from -110 to -20 mV and was voltage dependent, since it increased in magnitude as the membrane was depolarized from the resting potential toward less negative potentials. 4. Partial replacement of extracellular sodium by equimolar N-methyl-D-glucamine reversibly attenuated or suppressed the oxytocin current. By contrast, substituting part of extracellular chloride or blocking calcium currents did not modify it. Increasing the transmembrane potassium gradient was also without effect and none of the potassium channel blockers TEA, 4-amino pyridine (4-AP), apamin, caesium or barium affected the oxytocin current. This current is thus at least in part carried by sodium. 5. The activation of the oxytocin current as a function of the membrane potential could be quantitatively simulated using a Boltzmann equation, suggesting that oxytocin acts by inducing the opening of a voltage-dependent channel which can exist in either of two states, open or closed. 6. Lowering the extracellular calcium concentration from 2 to 0.1 mM, while keeping the magnesium concentration constant at 1 mM, enhanced the response to oxytocin. This low calcium-induced potentiation of the oxytocin current was 1.4-3-fold and was reversible. 7. We conclude that oxytocin increases the excitability of vagal neurones by generating a persistent, voltage-gated current which is sodium dependent, is insensitive to TTX and is modulated by divalent cations