Açaí (Euterpe oleracea Mart.) reduces the inflammatory response triggered in vitro by the antipsychotic drug olanzapine in RAW 264.7 macrophage cells.

BACKGROUND: Açaí (Euterpe oleracea Mart), a Brazilian fruit, is considered a "superfruit" due its energetic properties and bioactive compounds. The açai's anti-inflammatory effects could attenuate the undesirable metabolic and pro-inflammatory side effects triggered by some antipsychotic drugs, such as Olanzapine (OLZ). It is possible to infer that açai supplement could potentially minimize the adverse effects of OLZ. Aim. This study tested the potential in vitro effects of açai hydroalcoholic extract on the inflammatory activation of the RAW 264.7 macrophage line triggered by OLZ antipsychotic drugs. METHODS: An in vitro protocol was performed using commercial RAW 264.7 macrophages, cultured under sterile conditions at 37°C with 5% CO2 saturation. Initially, a pharmacological curve was defined to determine the concentration of Olanzapine to be used. After this, the cells were supplemented with different concentrations of hydroalcoholic extract of açaí, which had been previously chemically characterized. After 24 and 72 hours of treatment, oxidative and inflammatory tests were performed. Therefore, the aim of this study was to verify whether the hydroalcoholic extract of açaí can modulate the oxy-inflammatory response of olanzapine in vitro. RESULTS: From a preliminary analysis, the açai extract at 5 mg/mL presented higher activity against inflammation triggered by OLZ (0.03 µg/mL). At this concentration, açai was able to reduce several oxidative and inflammatory markers triggered by OLZ (0.03 µg/mL) exposure, such as nitric oxide (NO), reactive oxygen species (ROS), and pro-inflammatory cytokine levels (IL-1b, IL-6, TNF-a, IFN-g) caused by OLZ (0.03 µg/mL). Moreover, açaí reverted the levels of anti-inflammatory cytokine IL-10 that had been dropped by OLZ exposure to their pre-exposure treatments. CONCLUSIONS: The results suggest that açai extract could be useful in attenuating the peripheral inflammatory states triggered by OLZ. Additional pre-clinical and clinical investigations could be useful in testing therapeutic açai extract supplements.

Feeding cycle alters the biophysics and molecular expression of voltage-gated Na+ currents in rat hippocampal CA1 neurones.

The function of hippocampus as a hub for energy balance is a subject of broad and current interest. This study aims at providing more evidence on this regard by addressing the effects of feeding cycle on the voltage-gated sodium (Na+ ) currents of acutely isolated Wistar rat hippocampal CA1 neurones. Specifically, by applying patch clamp techniques (whole cell voltage clamp and single channel in inside-out patches) we assessed the influence of feeding and fasting conditions on the intrinsic biophysical properties of Na+ currents. Additionally, mass spectrometry and western blotting experiments were used to address the effect of feeding cycle over the Na+ channel population of the rat hippocampus. Na+ currents were recorded in neurones obtained from fed and fasted animals (here termed "fed neurones" and "fasted neurones", respectively). Whole cell Na+ currents of fed neurones, as compared to fasted neurones, showed increased mean maximum current density and a higher "window current" amplitude. We demonstrate that these results are supported by an increased single channel Na+ conductance in fed neurones and, also, by a greater Nav1.2 channel density in plasma membrane-enriched fractions of fed samples (but not in whole hippocampus preparations). These results imply fast variations on the biophysics and molecular expression of Na+ currents of rat hippocampal CA1 neurones, throughout the feeding cycle. Thus, one may expect a differentiated regulation of the intrinsic neuronal excitability, which may account for the role of the hippocampus as a processor of satiety information.

Ion Fluxes through KCa2 (SK) and Cav1 (L-type) Channels Contribute to Chronoselectivity of Adenosine A1 Receptor-Mediated Actions in Spontaneously Beating Rat Atria.

Impulse generation in supraventricular tissue is inhibited by adenosine and acetylcholine via the activation of A1 and M2 receptors coupled to inwardly rectifying GIRK/KIR3.1/3.4 channels, respectively. Unlike M2 receptors, bradycardia produced by A1 receptors activation predominates over negative inotropy. Such difference suggests that other ion currents may contribute to adenosine chronoselectivity. In isolated spontaneously beating rat atria, blockade of KCa2/SK channels with apamin and Cav1 (L-type) channels with nifedipine or verapamil, sensitized atria to the negative inotropic action of the A1 agonist, R-PIA, without affecting the nucleoside negative chronotropy. Patch-clamp experiments in the whole-cell configuration mode demonstrate that adenosine, via A1 receptors, activates the inwardly-rectifying GIRK/KIR3.1/KIR3.4 current resulting in hyperpolarization of atrial cardiomyocytes, which may slow down heart rate. Conversely, the nucleoside inactivates a small conductance Ca(2+)-activated KCa2/SK outward current, which eventually reduces the repolarizing force and thereby prolong action potentials duration and Ca(2+) influx into cardiomyocytes. Immunolocalization studies showed that differences in A1 receptors distribution between the sinoatrial node and surrounding cardiomyocytes do not afford a rationale for adenosine chronoselectivity. Immunolabelling of KIR3.1, KCa2.2, KCa2.3, and Cav1 was also observed throughout the right atrium. Functional data indicate that while both A1 and M2 receptors favor the opening of GIRK/KIR3.1/3.4 channels modulating atrial chronotropy, A1 receptors may additionally restrain KCa2/SK activation thereby compensating atrial inotropic depression by increasing the time available for Ca(2+) influx through Cav1 (L-type) channels.

Effective Hypothermic Storage of Human Pluripotent Stem Cell-Derived Cardiomyocytes Compatible With Global Distribution of Cells for Clinical Applications and Toxicology Testing.

UNLABELLED: To fully explore the potential of human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs), efficient methods for storage and shipment of these cells are required. Here, we evaluated the feasibility to cold store monolayers and aggregates of functional CMs obtained from different PSC lines using a fully defined clinical-compatible preservation formulation and investigated the time frame that hPSC-CMs could be subjected to hypothermic storage. We showed that two-dimensional (2D) monolayers of hPSC-CMs can be efficiently stored at 4°C for 3 days without compromising cell viability. However, cell viability decreased when the cold storage interval was extended to 7 days. We demonstrated that hPSC-CMs are more resistant to prolonged hypothermic storage-induced cell injury in three-dimensional aggregates than in 2D monolayers, showing high cell recoveries (>70%) after 7 days of storage. Importantly, hPSC-CMs maintained their typical (ultra)structure, gene and protein expression profile, electrophysiological profiles, and drug responsiveness. SIGNIFICANCE: The applicability of human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs) in the clinic/industry is highly dependent on the development of efficient methods for worldwide shipment of these cells. This study established effective clinically compatible strategies for cold (4°C) storage of hPSC-CMs cultured as two-dimensional (2D) monolayers and three-dimensional (3D) aggregates. Cell recovery of 2D monolayers of hPSC-CMs was found to be dependent on the time of storage, and 3D cell aggregates were more resistant to prolonged cold storage than 2D monolayers. Of note, it was demonstrated that 7 days of cold storage did not affect hPSC-CM ultrastructure, phenotype, or function. This study provides important insights into the cold preservation of PSC-CMs that could be valuable in improving global commercial distribution of hPSC-CMs.

Modeling human neural functionality in vitro: three-dimensional culture for dopaminergic differentiation.

Advances in mechanistic knowledge of human neurological disorders have been hindered by the lack of adequate human in vitro models. Three-dimensional (3D) cellular models displaying higher biological relevance are gaining momentum; however, their lack of robustness and scarcity of analytical tools adapted to three dimensions hampers their widespread implementation. Herein we show that human midbrain-derived neural progenitor cells, cultured as 3D neurospheres in stirred culture systems, reproducibly differentiate into complex tissue-like structures containing functional dopaminergic neurons, as well as astrocytes and oligodendrocytes. Moreover, an extensive toolbox of analytical methodologies has been adapted to 3D neural cell models, allowing molecular and phenotypic profiling and interrogation. The generated neurons underwent synaptogenesis and elicit spontaneous Ca(2+) transients. Synaptic vesicle trafficking and release of dopamine in response to depolarizing stimuli was also observed. Under whole-cell current-and-voltage clamp, recordings showed polarized neurons (Vm=-70 mV) and voltage-dependent potassium currents, which included A-type-like currents. Glutamate-induced currents sensitive to α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid and N-methyl-D-aspartate antagonists revealed the existence of functional glutamate receptors. Molecular and phenotypic profiling showed recapitulation of midbrain patterning events, and remodeling toward increased similarity to human brain features, such as extracellular matrix composition and metabolic signature. We have developed a robust and reproducible human 3D neural cell model, which may be extended to patient-derived induced pluripotent stem cells, broadening the applicability of this model.

Galantamine inhibits slowly inactivating K+ currents with a dual dose-response relationship in differentiated N1E-115 cells and in CA1 neurones.

Galantamine, one of the major drugs used in Alzheimer's disease therapy, is a relatively weak acetylcholinesterase inhibitor and an allosteric potentiating ligand of nicotinic acetylcholine receptors. However, a role in the control of excitability has also been attributed to galantamine via modulation of K+ currents in central neurones. To further investigate the effect of galantamine on voltage-activated K+ currents, we performed whole-cell voltage-clamp recordings in differentiated neuroblastoma N1E-115 cells and in dissociated rat CA1 neurones. In both cell models, one can identify two main voltage-activated K+ current components: a relatively fast inactivating component (Ifast; time constant approximately hundred milliseconds) and a slowly inactivating one (Islow; time constant approximately 1 s). We show that galantamine (1 pM-300 microM) inhibits selectively Islow, exhibiting a dual dose-response relationship, in both differentiated N1E-115 cells and CA1 neurones. We also demonstrate that, in contrast with what was previously reported, galantamine-induced inhibition is not due to a shift on the steady-state inactivation and activation curves. Additionally, we characterized a methodological artefact that affects voltage-dependence as a function of time in whole-cell configuration, observed in both cell models. By resolving an inhibitory role on K+ currents in a non-central neuronal system and in hippocampal neurones, we are attributing a widespread role of galantamine on the modulation of cell excitability. The present results are relevant in the clinical context, since the effects at low dosages suggest that galantamine-induced K+ current inhibition may contribute to the efficiency of galantamine in the treatment of Alzheimer's disease.

Insulin increases excitability via a dose-dependent dual inhibition of voltage-activated K+ currents in differentiated N1E-115 neuroblastoma cells.

A role in the control of excitability has been attributed to insulin via modulation of potassium (K(+)) currents. To investigate insulin modulatory effects on voltage-activated potassium currents in a neuronal cell line with origin in the sympathetic system, we performed whole-cell voltage-clamp recordings in differentiated N1E-115 neuroblastoma cells. Two main voltage-activated K(+) currents were identified: (a) a relatively fast inactivating current (I(fast) - time constant 50-300 ms); (b) a slow delayed rectifying K(+) current (I(slow) - time constant 1-4 s). The kinetics of inactivation of I(fast), rather than I(slow), showed clear voltage dependence. I(fast) and I(slow) exhibited different activation and inactivation dependence for voltage, and have different but nevertheless high sensitivities to tetraethylammonium, 4-aminopyridine and quinidine. In differentiated cells - rather than in non-differentiated cells - application of up to 300 nm insulin reduced I(slow) only (IC(50) = 6.7 nm), whereas at higher concentrations I(fast) was also affected (IC(50) = 7.7 microm). The insulin inhibitory effect is not due to a change in the activation or inactivation current-voltage profiles, and the time-dependent inactivation is also not altered; this is not likely to be a result of activation of the insulin-growth-factor-1 (IGF1) receptors, as application of IGF1 did not result in significant current alteration. Results suggest that the current sensitive to low concentrations of insulin is mediated by erg-like channels. Similar observations concerning the insulin inhibitory effect on slow voltage-activated K(+) currents were also made in isolated rat hippocampal pyramidal neurons, suggesting a widespread neuromodulator role of insulin on K(+) channels.

Mechanisms underlying activation of the slow AHP in rat hippocampal neurons.

The firing of a train of action potentials in hippocampal pyramidal neurons is terminated by an afterhyperpolarization (AHP) that displays two main components; the medium AHP (I(mAHP)), lasting a few hundred milliseconds and the slow AHP (I(sAHP)), that has a duration of several seconds. It is unclear how much of I(mAHP) is dependent on the entry of calcium ions (Ca(2+)), whereas it is accepted that I(sAHP) is caused by activation of Ca(2+)-activated potassium channels. There has been controversy regarding the subcellular localization and mechanism of activation of these channels. Whole-cell recordings from CA1 neurons in the hippocampal slice preparation showed that inhibition of L-type, but not N-, P/Q-, T- and R-type Ca(2+) channels, reduced both I(mAHP) and I(sAHP). Inhibition of both AHP components by L-type Ca(2+) channel antagonists was not complete, with I(sAHP) being significantly more sensitive than I(mAHP). Somatic extracellular ionophoresis of BAPTA during I(sAHP) caused a transient inhibition, but had no effect on I(mAHP). Cell-attached patch recordings from the soma of CA1 neurons within a slice displayed channels that produced an ensemble waveform reminiscent of I(sAHP) when the patch was subjected to a train of action potential waveforms. The channels were Ca(2+)-activated, exhibited a limiting slope conductance of 19 pS and were not observed in dendritic membrane patches. These data demonstrate that the I(sAHP) is somatic in origin and arises from continued Ca(2+) entry through functionally co-localized L-type channels.

Co-assembly of N-type Ca2+ and BK channels underlies functional coupling in rat brain.

Activation of large conductance Ca(2+)-activated potassium (BK) channels hastens action potential repolarisation and generates the fast afterhyperpolarisation in hippocampal pyramidal neurons. A rapid coupling of Ca(2+) entry with BK channel activation is necessary for this to occur, which might result from an identified coupling of Ca(2+) entry through N-type Ca(2+) channels to BK channel activation. This selective coupling was extremely rapid and resistant to intracellular BAPTA, suggesting that the two channel types are close. Using reciprocal co-immunoprecipitation, we found that N-type channels were more abundantly associated with BK channels than L-type channels (Ca(V)1.2) in rat brain. Expression of only the pore-forming alpha-subunits of the N-type (Ca(V)2.2) and BK (Slo(27)) channels in a non-neuronal cell-line gave robust macroscopic currents and reproduced the interaction. Co-expression of Ca(V)2.2/Ca(V)beta(3) subunits with Slo(27) channels revealed rapid functional coupling. By contrast, extremely rare examples of rapid functional coupling were observed with co-expression of Ca(V)1.2/Ca(V)beta(3) and Slo(27) channels. Action potential repolarisation in hippocampal pyramidal neurons was slowed by the N-type channel blocker omega-conotoxin GVIA, but not by the L-type channel blocker isradipine. These data showed that selective functional coupling between N-type Ca(2+) and BK channels provided rapid activation of BK channels in central neurons.

The role of muscarinic receptors and intracellular Ca2+ in the spectral reflectivity changes of squid iridophores.

In this paper we describe changes in spectral reflectivity of the light reflectors (iridophores) of the squid Alloteuthis subulata. The spectral changes that can be seen in living squid, can also be brought about by superfusing whole skin preparations with acetylcholine (ACh) (20 micro mol l(-1)) and muscarine (30 micro mol l(-1)) but not nicotine (up to 50 mmol l(-1)), suggesting that cholinergic muscarinic receptors are involved. Changing the osmolarity of the external solution had no effect on spectral reflectivity. To study the iridophores at the cellular level, iridophores were isolated enzymatically. Lucifer Yellow filled the iridophores uniformly, showing cellular individuality. Isolated iridophore cells were loaded with Fura-2 AM and cytoplasmic Ca(2+) was recorded ratiometrically. Intracellular Ca(2+) (resting concentration at 66.16 nmol l(-1)) increased transiently after addition of ACh (50 micro mol l(-1)), muscarine (25 micro mol l(-1)), but not nicotine (up to 5 mmol l(-1)). Ca(2+) also increased when superfused with potassium chloride (10 mmol l(-1)) and caffeine (2.5 mmol l(-1)). Hypo- and hyperosmotic solutions had no effects on the cytoplasmic Ca(2+). By presenting direct evidence that iridophores are polarised cellular structures containing Ca(2+) stores and that they are activated via cholinergic muscarinic receptors, we demonstrate that Ca(2+) is involved in the reflectivity changes of the iridophores of A. subulata. Specimens were prepared for transmission electron microscopy. It was found that the orientations of the plates with respect to the skin surface are in good agreement with the expected orientations based on the prediction that the iridophores act as multilayer reflectors.

Mechanisms underlying modulation of neuronal KCNQ2/KCNQ3 potassium channels by extracellular protons.

Changes in extracellular pH occur during both physiological neuronal activity and pathological conditions such as epilepsy and stroke. Such pH changes are known to exert profound effects on neuronal activity and survival. Heteromeric KCNQ2/3 potassium channels constitute a potential target for modulation by H+ ions as they are expressed widely within the CNS and have been proposed to underlie the M-current, an important determinant of excitability in neuronal cells. Whole-cell and single-channel recordings demonstrated a modulation of heterologously expressed KCNQ2/3 channels by extracellular H+ ions. KCNQ2/3 current was inhibited by H+ ions with an IC50 of 52 nM (pH 7.3) at -60 mV, rising to 2 microM (pH 5.7) at -10 mV. Neuronal M-current exhibited a similar sensitivity. Extracellular H+ ions affected two distinct properties of KCNQ2/3 current: the maximum current attainable upon depolarization (Imax) and the voltage dependence of steady-state activation. Reduction of Imax was antagonized by extracellular K+ ions and affected by mutations within the outer-pore turret, indicating an outer-pore based process. This reduction of Imax was shown to be due primarily to a decrease in the maximum open-probability of single KCNQ2/3 channels. Single-channel open times were shortened by acidosis (pH 5.9), while closed times were increased. Acidosis also recruited a longer-lasting closed state, and caused a switch of single-channel activity from the full-conductance state ( approximately 8 pS) to a subconductance state ( approximately 5 pS). A depolarizing shift in the activation curve of macroscopic KCNQ2/3 currents and single KCNQ2/3 channels was caused by acidosis, while alkalosis caused a hyperpolarizing shift. Activation and deactivation kinetics were slowed by acidosis, indicating specific effects of H+ ions on elements involved in gating. Contrasting modulation of homomeric KCNQ2 and KCNQ3 currents revealed that high sensitivity to H+ ions was conferred by the KCNQ3 subunit.

AMPA/kainate and NMDA-like glutamate receptors at the chromatophore neuromuscular junction of the squid: role in synaptic transmission and skin patterning.

Glutamate receptor types were examined at the chromatophore synapses of the squids Alloteuthis subulata and Loligo vulgaris, where nerve-induced muscle contraction causes chromatophore expansion. Immunoblotting with antibody raised against a squid AMPA receptor (sGluR) demonstrated that AMPA/kainate receptors are present in squid skin. Application of l-glutamate evoked chromatophore muscle contractions in both ventral and dorsal skins, while NMDA was only active on a subpopulation of dorsal chromatophores. In dorsal skin, neurotransmission was partly blocked by either AMPA/kainate receptor antagonists (CNQX and DNQX) or NMDA receptor antagonists (AP-5 and MK-801) or completely blocked by simultaneous application of both classes of antagonists. In isolated muscle fibres, ionophoretic application of l-glutamate evoked fast inward CNQX- and DNQX-sensitive currents with reversal potentials around +14 mV and a high conductance to Na+. In fibres from dorsal skin only, a slower outward glutamate-sensitive current appeared at positive holding potentials. At negative potentials, currents were potentiated by glycine or by removing external Mg2+ and were blocked by AP-5 and MK-801. Glutamate caused a fast, followed by a slow, transient increase in cytoplasmic Ca2+. The slow component was increased in amplitude and duration by glycine or by lowering external Mg2+ and decreased by AP-5 and MK-801. In cells from ventral skin, no 'NMDA-like responses' were detected. Thus, while AMPA/kainate receptors mediated fast excitatory synaptic transmission and rapid colour change over the whole skin, activation of both AMPA/kainate and NMDA-like receptors in a subpopulation of dorsal chromatophores prolonged the postsynaptically evoked Ca2+ elevation causing temporally extended colour displays with behavioural significance.

Tratamento a longo prazo de pacientes psicóticos com a risperidona: um estudo brasileiro multicêntrico aberto / Long-term treatment of psychotic patients with risperidone: an open Brazilian multicentre study

Em um estudo aberto multicêntrico, 154 esquizofrênicos (DSM-III - R) com um escore total > 60 na PANSS foram tratados durante 7 meses com a risperidona depois de um período de "wash-out". As doses foram aumentadas até 3 mg duas vezes por dia na primeira semana e de forma flexível, de acordo com a ICG, a dose podia ser aumentada até 16 mg/dia no final do primeiro mês. A partir daí, foi recomendado manter-se dose estável nos próximos 6 meses do tratamento. Os parâmetros de eficácia foram: ICG aplicada mensalmente e PANSS aplicada nos meses 1, 4 e 7. A segurança da risperidona foi avaliada por meio de exame físico, testes laboratoriais, ECG e sinais vitais (PS,PD e FC). As reaçoes adversas foram registradas em todas as visitas do estudo, os sintomas extrapiramidais (SEP) foram avaliados segundo a Extrapyramidal Symptom Rating Scale (ESRS) e também ICG para gravidade de parkinsonismo e discinesia. Cerca de 77 porcento dos pacientes completaram o estudo e em apenas 9 porcento o térmico precoce foi atribuído a falta de eficácia. De uma maneira geral, a risperidona foi eficaz (diminuiçao da sintomatologia > 20 porcento) em cerca de 70 porcento dos pacientes. As reaçoes adversas mais freqüentes foram insônia (14,1 porcento ) e ganho de peso (10,9 porcento). A risperidona nao causou nenhuma alteraçao importante nos testes laboratoriais realizados antes do início e no final do tratamento. Durante o período de tratamento houve uma diminuiçao dos SEP apesar de ter havido um aumento da dose média diária. Isto foi atribuído à tolerância. A dose ótima foi de 6 a 8 mg/dia, contudo, para alguns pacientes mais pode ser necessário se aumentar a dose. Em conclusao, nossos dados sugerem que a risperidona é um medicamento seguro, tem um rápido início de açao e na dose média de 6 a 8 mg/dia foi eficaz tanto em sintomas positivos como negativos; a resposta terapêutica tende a aumentar ao longo do tratamento enquanto que os SEP, além de poucos, mant6em-se estáveis ou tendem a diminuir.

Tratamento a longo prazo de pacientes psicoticos com a risperidona: um estudo brasileiro multicentrico aberto

Em um estudo aberto multicentrico, 154 esquizofrenicos (DSM-III-R) com um escore total maior igual 60 na PANSS foram tratados durante 7 meses com a risperidona depois de um periodo de 'wash-out'. As doses foram aumentadas ate 3 mg duas vezes por dia na primeira semana e de forma flexivel, de acordo com a ICG, a dose podia ser aumentada ate 16 mg/dia no final do primeiro mes. A partir dai, foi recomendado manter-se a dose estavel nos proximos 6 meses do tratamento. Os parametros de eficacia foram: ICG aplicada mensalmente e PANSS aplicada nos meses 1, 4 e 7. A seguranca da risperidona foi avaliada por meio de exame fisico, testes laboratoriais, ECG e sinais vitais (PS, PD e FC). As reacoes adversas foram registradas em todas as visitas do estudo, os sintomas extrapiramidais (SEP) foram avaliados segundo a Extrapyramidal Symptom Rating Scale (ESRS) e tambem ICG para gravidade de parkinsonismo e discinesia. Cerca de 77 por cento dos pacientes completam o estudo e em apenas 9 por cento o termino precoce foi atribuido a falta de eficacia. De uma maneira geral, a risperidona foi eficaz (diminuicao da sintomatologia maior igual 20 por cento) em cerca de 70 por cento dos pacientes. As reacoes adversas mais frequencias foram insonia (14,1 por cento) e ganho de peso (10,9 por cento). A risperidona nao causou nenhuma alteracao importante nos testes laboratoriais realizados antes do inicio e no final do tratamento. Durante o periodo de tratamento houve uma diminuicao dos SEP apesar de ter havido um aumento da dose media diaria. Isto foi atribuido a tolerancia. A dose otima foi de 6 a 8 mg/dia, contudo, para alguns pacientes mais resistentes pode ser necessario se aumentar a dose. Em conclusao, nossos dados sugerem que a risperidona e um medicamento seguro, tem um rapido inicio de acao e na dose media de 6 a 8 mg/dia foi eficaz tanto em sintomas positivos como negativos; a resposta terapeutica tende a aumentar ao longo do tratamento enquanto que os SEP, alem de poucos, mantem-se estaveis ou tendem a diminuir.

SETA: um programa computacional de apoio ao tratamento farmacológico dos transtornos afetivos / SETA: a computer program aiding pharmacological treatment of affective disorders

Os autores situam o uso de Sistemas Especialistas em Psiquiatria e descrevem um desses sistemas desenvolvido para apoio ao tratamento farmacológico dos transtornos afetivos (SETA). O programa contém um módulo de consulta em que se encontram informaçöes sobre f rmacos utilizados nesses distúrbios: farmacocinética, farmacodinâmica, indicaçöes, contra-indicaçöes, efeitos colaterais e seu manejo, uso em crianças, gestantes, idosos e na presença de doenças físicas. Contém ainda um módulo especialista, que auxilia o usu rio a escolher a droga mais adequada às condiçöes do paciente (idade, perfil sintom tico, doenças físicas...). Submetido a uma avaliaçäo inicial, mostrou-se útil tanto na consulta ao banco de dados, como no auxílio à escolha dos psicof rmacos mais apropriados

SETA: um programa computacional de apoio ao tratamento farmacologico dos transtornos afetivos

Os autores situam o uso de Sistemas Especialistas em Psiquiatria e descrevem um desses sistemas desenvolvido para apoio ao tratamento farmacologico dos transtornos afetivos (SETA). O programa contem um modulo de consulta em que se encontram informacoes sobre os farmacos utilizados nesses disturbios: farmacocinetica, farmacodinamica, indicacoes, contra-indicacoes, efeitos colaterais e seu manejo, uso em criancas, gestantes, idosos e na presenca de doencas fisicas. Contem ainda um modulo especialista, que auxilia o usuario a escolher a droga mais adequada as condicoes do paciente (idade, perfil sintomatico, doencas fisicas...). Submetido a uma avaliacao inicial, mostrou-se util tanto na consulta ao banco de dados, como no auxilio a escolha dos psicofarmacos mais apropriados.