Motores de propulsão em veículos elétricos: tipos, características e perspetivas de evolução

Os sistemas de propulsão baseados em motores síncronos de ímanes permanentes (MSIP) e motores de indução (MI) têm sido as principais opções para veículos híbridos (VH) e elétricos (VE). As limitações das reservas e os elevados custos das terras-raras (constituinte essencial dos ímanes permanentes (IP)) têm motivado o interesse por motores sem IP ou com menores quantidades de terras-raras. Várias configurações têm vindo a ser desenvolvidas e/ou aperfeiçoadas, com vista a ultrapassar as limitações dos MI, sendo que a otimização do seu projeto também tem sido alvo de atenção. De modo não exaustivo, o objetivo deste artigo é incidir sobre os tipos de motores atualmente aplicados na propulsão elétrica. No final, apresenta-se uma breve referência às principais tecnologias emergentes.info:eu-repo/semantics/publishedVersio

Neurovascular unit in chronic pain.

Chronic pain is a debilitating condition with major socioeconomic impact, whose neurobiological basis is still not clear. An involvement of the neurovascular unit (NVU) has been recently proposed. In particular, the blood-brain barrier (BBB) and blood-spinal cord barrier (BSCB), two NVU key players, may be affected during the development of chronic pain; in particular, transient permeabilization of the barrier is suggested by several inflammatory- and nerve-injury-based pain models, and we argue that the clarification of molecular BBB/BSCB permeabilization events will shed new light in understanding chronic pain mechanisms. Possible biases in experiments supporting this theory and its translational potentials are discussed. Moving beyond an exclusive focus on the role of the endothelium, we propose that our understanding of the mechanisms subserving chronic pain will benefit from the extension of research efforts to the NVU as a whole. In this view, the available evidence on the interaction between analgesic drugs and the NVU is here reviewed. Chronic pain comorbidities, such as neuroinflammatory and neurodegenerative diseases, are also discussed in view of NVU changes, together with innovative pharmacological solutions targeting NVU components in chronic pain treatment

Non-neuronal cells, inflammation and epilepsy (Commentary on Aronica et al.).

Comment on: * Eur J Neurosci. 2010 Mar;31(6):1100-7

Leukocyte trafficking mechanisms in epilepsy.

Epilepsy is a chronic disorder that affects 1% of the world population and is characterized by chronically reoccurring seizures. Seizures are initiated by abnormal excessive or synchronous neuronal activity in the brain. Epilepsy requires life long anti-convulsant therapy and current therapies for epilepsy selectively target neuronal activity. In the last decade, cytokines and vascular alterations have been discussed in relation to the pathogenesis of epilepsy, suggesting a potential role for inflammation mechanisms in seizure induction. More recently, it has been shown that leukocyte trafficking plays a key role in seizure generation, and that anti-leukocyte adhesion therapy has therapeutic and preventative effects in an experimental model of human epilepsy. These results were supported by evidence in humans showing that leukocytes accumulate in the brain parenchyma of patients with different types of epilepsy. Finally, recent clinical observations suggest that therapies able to interfere with leukocyte trafficking may have a therapeutic effect in epilepsy. The emerging role for leukocytes and leukocyte adhesion mechanisms in seizure generation provides insight into the mechanisms of brain damage and may contribute to the development of novel therapeutic strategies in epilepsy

Early onset of age-related changes on neural processing in rats

Item does not contain fulltextAltered perceptual and emotional processing might bind impaired cognitive mechanisms during aging; however the nature of these sensory perception modifications is still unknown. In the present experiment we analyzed in rats, from early to mature life (2 to 11 months old), the response to unattended auditory evoked stimulation (Auditory evoked potential, AEP) and the power spectrum of spontaneous electroencephalogram (EEG), with the aim of unraveling the onset and target functional effects of aging. Somatosensory and cingulate cortex, mediodorsal thalamus and CA3 hippocampus were chosen for examination based on their involvement in sensory processing and age-related deficits. The main finding of this study is the early onset of age-related changes in adult rats as can be established with both AEP's and frequency analyses, and its diversity between brain regions during normal aging

Drug resistance and hippocampal damage after delayed treatment of pilocarpine-induced epilepsy in the rat

Temporal lobe epilepsy (TLE) is the most common and pharmacoresistant form of epilepsy. Problems that cause pharmacoresistance may include delayed therapy due to late consultation, especially in developing countries. Our study aimed at unraveling consequences of delayed drug treatment using a rat model of TLE. Following pilocarpine-induced status epilepticus interrupted after 4h, rats were continuously videorecorded for onset and recurrence of spontaneous convulsive seizures. The animals were then treated for 50 days with carbamazepine (CBZ; first-line drug in TLE and effective also in rats), starting at seizure onset (27.22+/-3.38 days after status epilepticus) or 50 days later, and compared with epileptic untreated rats and non-epileptic CBZ-treated ones. Convulsive seizure frequency and duration, and hippocampal cell changes were evaluated. In particular, parvalbumin-containing hippocampal interneurons, astrocytes and microglia were characterized with immunohistochemistry and quantitative analyses. Prompt administration of CBZ suppressed seizures; delayed treatment only decreased frequency of convulsive seizures, which were also relatively prolonged. In hippocampal regions, histopathological damage, parvalbumin immunoreactivity loss, and glial activation were very marked after delayed treatment, and were reduced only slightly compared to untreated epilepsy, but enhanced compared to early treatment. The data on high frequency and duration of convulsive seizures in late-therapy rats indicate that delayed CBZ administration caused a high degree of drug resistance. This condition was subserved by severe damage in the hippocampus, presumably consequent to long-term seizure recurrence. Overall the data indicate that the paradigm of delayed treatment of limbic epilepsy could provide a model of drug-refractory TLE with hippocampal sclerosis

Different patterns of neuronal activation and neurodegeneration in the thalamus and cortex of epilepsy-resistant Proechimys rats versus Wistar rats after pilocarpine-induced protracted seizures

PURPOSE: To analyze cellular mechanisms of limbic-seizure suppression, the response to pilocarpine-induced seizures was investigated in cortex and thalamus, comparing epilepsy-resistant rats Proechimys guyannensis with Wistar rats. METHODS: Fos immunoreactivity revealing neuronal activation, and degenerating neurons labeled by Fluoro-Jade B (FJB) histochemistry were analyzed on the first day after onset of seizures lasting 3 h. Subpopulations of gamma-aminobutyric acid (GABA)ergic cells were characterized with double Fos-parvalbumin immunohistochemistry. RESULTS: In both cortex and thalamus, degenerating neurons were much fewer in Proechimys than Wistar rats. Fos persisted at high levels at 24 h only in the Proechimys thalamus and cortex, especially in layer VI where corticothalamic neurons reside. In the parietal cortex, about 50% of parvalbumin-containing interneurons at 8 h, and 10-20% at 24 h, were Fos-positive in Wistar rats, but in Proechimys, Fos was expressed in almost all parvalbumin-containing interneurons at 8 h and dropped at 24 h. Fos positivity in cingulate cortex interneurons was similar in both species. In the Wistar rat thalamus, Fos was induced in medial and midline nuclei up to 8 h, when <30% of reticular nucleus cells were Fos-positive, and then decreased, with no relationship with cell loss, evaluated in Nissl-stained sections. In Proechimys, almost all reticular nucleus neurons were Fos-positive at 24 h. DISCUSSION: At variance with laboratory rats, pilocarpine-induced protracted seizures elicit in Proechimys limited neuronal death, and marked and long-lasting Fos induction in excitatory and inhibitory cortical and thalamic cell subsets. The findings implicate intrathalamic and intracortical regulation, and circuits linking thalamus and cortex in limbic seizure suppression leading to epilepsy resistance

The thalamus of the Amazon spiny rat Proechimys guyannensis, an animal model of resistance to epilepsy, and pilocarpine-induced long-term changes of protein expression

The thalamus of the spiny rat Proechimys guyannensis (casiragua), a common rodent of the Amazon basin, was investigated with immunohistochemistry, using as markers GABA and glutamic acid decarboxylase, and calcium binding proteins. As in all mammals, GABAergic neurons containing also parvalbumin filled the reticular nucleus, and GABAergic cells were seen in the dorsal lateral geniculate nucleus. At variance with the laboratory rat, GABAergic and parvalbumin-containing neurons were also seen in the laterodorsal and anterodorsal nuclei, in which the two markers were co-distributed. Calbindin-immunopositive cells were widely distributed in dorsal thalamic domains, except for the intralaminar nuclei, and prevailed in the laterodorsal nucleus. The distribution of calretinin-immunopositive neurons was more restricted, and they were especially concentrated in the laterodorsal and midline nuclei. At variance with the laboratory rat, in which systemic pilocarpine administration induces status epilepticus and results in chronic limbic epilepsy, pilocarpine elicited in casiragua an acute seizure that was not followed by spontaneous seizures up to 1 month, when changes were evaluated in the thalamus using also image analysis. Parvalbumin immunostaining in reticular nucleus neurons and in the dorsal thalamus neuropil, and the number of parvalbumin-positive and GABAergic cells in the laterodorsal and anterodorsal nuclei, exhibited an increase with respect to controls. Calbindin immunostaining was also enhanced, whereas calretinin immunostaining was mostly reduced, but was preserved in midline neurons. The findings show, after an acute seizure induced in an animal model of anti-convulsant mechanisms, regional long-term neurochemical alterations that could reflect functional changes in inhibitory and excitatory thalamic neurons