Biomedical subjects

J C Furtado

Publications and source records attributed to J C Furtado.

5 recordsLinked to original sources

PubMed2001

Constructive genetic algorithm for clustering problems.

Genetic algorithms (GAs) have recently been accepted as powerful approaches to solving optimization problems. It is also well-accepted that building block construction (schemata formation and conservation) has a positive influence on GA behavior. Schemata are usually indirectly evaluated through a derived structure. We introduce a new approach called the Constructive Genetic Algorithm (CGA), which allows for schemata evaluation and the provision of other new features to the GA. Problems are modeled as bi-objective optimization problems that consider the evaluation of two fitness functions. This double fitness process, called fg-fitness, evaluates schemata and structures in a common basis. Evolution is conducted considering an adaptive rejection threshold that contemplates both objectives and attributes a rank to each individual in population. The population is dynamic in size and composed of schemata and structures. Recombination preserves good schemata, and mutation is applied to structures to get population diversification. The CGA is applied to two clustering problems in graphs. Representation of schemata and structures use a binary digit alphabet and are based on assignment (greedy) heuristics that provide a clearly distinguished representation for the problems. The clustering problems studied are the classical p-median and the capacitated p-median. Good results are shown for problem instances taken from the literature.

Algorithms↗

PubMed1996

Behavioral characterization of quinolinate-induced lesions of the medial striatum: relevance for Huntington's disease.

Huntington's disease (HD) in an inherited neurodegenerative disorder in which the striatum undergoes marked atrophic changes. Patients with HD typically have impaired cognitive function, including deficient visuospatial skills, lack of cognitive flexibility and poor recall of memories. The relationship between these cognitive abnormalities and the striatal degeneration of HD is incompletely understood. In order to explore this issue, we studied the behavior of rats with histologically confirmed bilateral quinolinate (QUIN)-induced lesions of the medial striatum. In a series of Morris Water Maze (MWM) experiments and Delayed Alternation (DA) tests, QUIN-lesioned animals exhibited: (i) impaired acquisition of visuospatial skills; (ii) impaired "transfer of learning"; (iii) preseverative behavior; (iv) deficient retrieval or retention of stored memories. The lesioned rats were unimpaired with swimming to a visible platform, while moving spontaneously in behavior boxes, and when performing various specialized tests of motor function. These results indicate that QUIN-induced lesions of the medial striatum can produce impairments of visuospatial skills, cognitive flexibility, and recall. These are the categories of cognitive function that are disturbed in HD. This suggests that the striatal degeneration of HD could be a sufficient explanation for the cognitive abnormalities associated with the illness.

Animals↗

PubMed1996

Dopamine-glutamate interactions in the striatum: behaviourally relevant modification of excitotoxicity by dopamine receptor-mediated mechanisms.

The two most important afferent projections to the striatum contain glutamate and dopamine, respectively. Excitotoxic damage resulting from excessive stimulation of the N-methyl-D-aspartate subtype of glutamate receptor has been implicated in pathophysiology of ischaemic stroke, hypoglycaemic brain damage and Huntington's disease. We studied the ability of the dopamine system to modify the anatomical, neurochemical and behavioural consequences of glutamatergic toxicity in the striatum. In a first set of experiments, the specific N-methyl-D-aspartate receptor agonist quinolinate was injected unilaterally into the striatum of rats pretreated with one of (i) intraperitoneal (i.p.) saline (controls); (ii) i.p. haloperidol, a D2 dopamine receptor agonist; or (iii) 6-hydroxydopamine lesion of the ipsilateral nigrostriatal tract. Quinolinate-induced striatal damage, as assessed by morphometric and neurochemical criteria, was significantly attenuated in the animals with 6-hydroxydopamine lesions and in those pretreated with haloperidol, compared with saline-pretreated controls. There were no significant differences between the 6-OHDA and haloperidol groups. In a second set of experiments, animals received (i) bilateral intrastriatal quinolinate plus perioperative i.p. saline; (ii) bilateral intrastriatal quinolinate plus i.p. haloperidol; or (iii) bilateral intrastriatal saline. Again, the quinolinate-lesioned animals treated with perioperative haloperidol had significantly less striatal damage than the bilateral quinolinate rats. Behavioural assessment in the Morris Water Maze showed the bilateral quinolinate+haloperidol group to be significantly less impaired on a spatial acquisition task than the bilateral quinolinate animals. Measures of spontaneous daytime motor activity showed significant differences in average speed and rest time between the bilateral quinolinate+haloperidol rats and the bilateral quinolinate group. The performance of the bilateral quinolinate+haloperidol group was not significantly different from that of controls on any of the behavioural tasks. These results indicate an important role for D2 dopamine receptor-mediated mechanisms in striatal excitotoxicity. Since the excitotoxic process involves the same fundamental signalling mechanism that is involved in normal glutamatergic transmission, these findings imply an ability of D2 receptor blockade to modify glutamate signalling in the striatum. These results may have implications for treatment strategies in ischaemic stroke, hypoglycaemic brain damage and schizophrenia.

Analysis of Variance↗

PubMed1991

MPTP-induced neurotoxicity and the quest for a preventative therapy for Parkinson's disease.

Less than 10 years have passed since the discovery that 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is capable of producing parkinsonism in both humans and non-human primates. In that time, there has been considerable interest in the possibility that the pathogenesis of idiopathic Parkinson's disease (PD) might involve a process analogous to that of MPTP toxicity. One hypothesis holds that PD might arise, at least in part, from exposure to an MPTP-like environmental toxin. Rapid progress has been made towards elucidating the precise mechanism by which MPTP exerts toxicity, and clarifying the relationship of MPTP toxicity to idiopathic PD. The goal of these efforts is to develop a therapy that inhibits the underlying disease process in PD.

Environmental Pollutants↗

PubMed1991

Concurrent language and motor performance in bilinguals: a test of the age of acquisition hypothesis.

The objective of the present study was to test the hypothesis that the age at which a second language is acquired influences the pattern of cerebral lateralization associated with that language. Subjects who differed in terms of the age at which they had acquired their second language (English or French) were tested on a concurrent task paradigm involving motor and language performance. Hemispheric processing was inferred from the pattern of lateralized and generalized interference between the tasks. No support was found for the age-of-acquisition hypothesis. Instead, the data indicated a language-specific effect. Regardless of age of acquisition and of whether the first language was English or French, bilingual subjects showed lateralized interference effects consistent with left-hemisphere processing when reading in English and translating from French into English, but no lateralized interference when reading in French and translating from English into French. Whether this effect reflects characteristics of the two languages or the influence of social factors in subject-experimenter interaction is considered.

Adult↗