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A Espino

Publications and source records attributed to A Espino.

At least 19 recordsLinked to original sources
PubMed2005

Quantification of the drawing of an Archimedes spiral through the analysis of its digitized picture.

We have developed a new quantitative analysis of spiral drawing that is able to evaluate any spiral execution and it has not temporal or spatial limitations in the obtaining of specimens. Thirty-one patients with action tremor and 24 control subjects were asked to draw an Archimedes spiral over a print template. Specimens were scanned and then treated through a semiautomatic computer program that reconstructs the temporal sequence of the spiral drawing by the subject. The spirals were first analysed by means of the cross-correlation coefficient with the spiral template. Secondly, the mean and the standard deviation of the distance between each point of the spiral drawing and the corresponding point of the spiral model were determined. Finally, the reconstructed spiral was analysed using the Fourier Transform. Its results were interpreted with the aid of a computer model of a tremulous spiral. The experimental variables were greater in the patients group respect to age-matched controls. There was also a high linear correlation between them and the clinical score given by three neurologists. Finally, Receiver Operating Characteristic (ROC) curves analysis shown that the method classified the spirals better than human ratters.

Adult↗
PubMed1996

MPP+ toxicity in rat striatal slices: relationship between non-selective effects and free radical production.

Incubations of rat striatal slices have been used to assay MPP+ neurotoxicity. MPP+, at concentrations of 1 mM or higher, caused a marked increase in hydroxyl radicals, measured as malondialdehyde (MDA) accumulation, but not in nitric oxide production. At these doses, MPP+ showed an effect on dopamine terminals, causing a massive dopamine decrease, and on non-neuronal glial cells, where a marked reduction in glutamine synthetase activity was detected. At lower concentrations (25 mu M), the toxic effect on dopaminergic endings was maintained without increasing malondialdehyde concentrations or inhibiting glutamine synthetase activity. The effect on glutamine synthetase was prevented by the addition to the medium of 0.5% dimethyl sulfoxide, a hydroxyl-radical scavenger, but this did not protect the effect of dopamine depletion. We propose that non-selective effects of MPP+, at doses of 1 mM or higher, are mediated by extracellular overproduction of hydroxyl radicals. The main factor responsible for this overproduction would not be the released dopamine but rather the MPP+ itself through non selective inhibition of the mitochondrial respiratory chain or through a redox cycling that can trigger oxygen radical production.

1-Methyl-4-phenylpyridinium↗
PubMed1996

Apolipoprotein E epsilon4 association with dementia in a population-based study: The Framingham study.

Apolipoprotein E type 4 allele (apoE epsilon4) is associated with Alzheimer's disease (AD) in the late-onset familial form and in sporadic cases, but the age-associated risk in a randomly sampled elderly population is not established. We examined the association of apoE epsilon4 with AD and other dementias (mainly multi-infarct or dementia following stroke) in 1,030 persons aged 71 to 100 years in the population-based Framingham Study cohort. Kaplan-Meier survival analysis revealed that 55% of the apoE epsilon4/epsilon4 homozygotes developed AD by age 80, whereas 27% of apoE epsilon3/epsilon4 heterozygotes developed AD by age 85, and 9% of those without a 4 allele developed AD by age 85 years. In comparison with persons without a 4 allele, the risk ration for AD was 3.7 (95% CI = 1.9 to 7.5) for apoE epsilon3/epsilon4 heterozygotes and 30.1 (95% CI = 10.7 to 84.4) for apoE epsilon4 homozygotes. ApoE epsilon2 (2/2, 2/3, or 2/4 genotypes) was associated with an absence of AD. One-half (n=21) of the 43 AD patients were either homozygous or heterozygous for apoE epsilon4. We found evidence for an association of apoE epsilon4 with other dementia, primarily multi-infarct dementia and stroke. The risk ratio was 2.3 (95% CI = 0.9 to 6.1) for non-AD dementias among persons with apoE epsilon3/epsilon4. Although the apoE epsilon4 allele is a potent risk factor for AD and may be associated with other forms of dementia, most apoE epsilon4 carriers do not develop dementia, and about one-half of AD is not apoE epsilon4 associated. The low positive predictive value of this marker (0.10) suggest that use of apoE genotyping as a screening test for AD is not supported.

Adult↗
PubMed1995

Chronic effects of single intrastriatal injections of 6-hydroxydopamine or 1-methyl-4-phenylpyridinium studied by microdialysis in freely moving rats.

Extracellular dopamine (DA) and its main cerebral metabolites, dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), were measured by bilateral striatal microdialysis in rats at different times (2, 7, 15 and 60 days) after unilateral administration into the right striatum of 1-methyl-4-phenylpyridinium ion (MPP+) or 6-hydroxydopamine (6-OHDA). In both cases the decrease in extracellular dopamine did not exceed 40% of control values. The response of DOPAC and HVA depended on the treatment: MPP+ caused a marked acute decrease in the dopamine metabolites but allowed a progressive recovery that was very evident after 60 days; 6-OHDA caused a progressive decrease in the dopamine metabolites throughout the two months of the study. Tyrosine hydroxylase immunostaining revealed severe neuronal loss in substantia nigra two months after striatal administration of 6-OHDA, whereas no significant neuronal loss was found at the same time after MPP+ administration. A bilateral challenge infusion of MPP+ through the microdialysis probe was used to assess the dopaminergic capacity of both striata: at all the times studied there was a sharp depletion of DA on the non-lesioned side; both MPP(+)- and 6-OHDA-treated striata were unresponsive after a short time (2 days); after 2 months the response in MPP(+)-lesioned rats was similar on both sides, whereas 6-OHDA-lesioned striata were still unresponsive to MPP+. In rats, then, the effects of MPP+ could be partly reversed whereas the effects of 6-OHDA were not. These results suggest that neurotoxins causing striatal dopamine loss may act through different mechanisms, which could be significant for the etiopathogenic development of Parkinson's disease.

1-Methyl-4-phenylpyridinium↗
PubMed1995

[Possible relationship between overweightness and prevalence of hyperlipemia in the children of patients with heterozygote familial hypercholesterolemia and combined familial hyperlipemia].

BACKGROUND: Heterozygote familial hypercholesterolemia and combined familial hyperlipemia are associated to a greater risk of coronary disease. Combined familial hyperlipemia has classically been indicated to manifest after the second decade in life. The aim of this study was to establish whether a systematic search would demonstrate the existence of combined familial hyperlipemia earlier and analyze whether the antropometric parameters related with the overweightedness accompany the appearance of the lipid disorders of this disease found at an early age. PATIENTS AND METHODS: Different lipid parameters were studied in 89 subjects under the age of 18 who were children of patients with heterozygote familial hypercholesterolemia and combined familial hyperlipemia. Likewise the weight, height and waist/hip quotient were evaluated. Hyperlipemia was considered as the presence of cholesterol/LDL and/or triglicerides greater than the 95 percentile for age and sex. RESULTS: Hyperlipemia was observed in 51% and 40% of the children of patients with heterozygote familial hypercholesterolemia and combined familial hyperlipemia, respectively. The body mass index and the waist/hip quotient of the latter children significantly correlated with the cholesterol-HDL values and the LDL/HDL quotient. CONCLUSIONS: The patients with known combined familial hyperlipemia have a high percentage of children with hyperlipemia during infancy. These data suggest a possible association between obesity in the appearance of hyperlipemia in the children of patients with combined familial hyperlipemia at this age.

Adolescent↗
PubMed1995

Cerebrospinal dopamine metabolites in rats after intrastriatal administration of 6-hydroxydopamine or 1-methyl-4-phenylpyridinium ion.

Dopamine (DA) and its main cerebral metabolites, dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) were measured in striatum and cerebrospinal fluid (CSF) from cisterna magna in rats bilaterally lesioned by intrastriatal administration of 6-hydroxydopamine (6-OHDA) or 1-methyl-4-phenylpyridinium ion (MPP+). 6-OHDA caused a progressive lesion in striatum that is only moderately reflected in the decrease in dopamine metabolite concentration in CSF. MPP+ caused an acute but less selective lesion in the dopamine striatal system, as indicated by a significant reduction in striatal GABA content, followed by a slow recovery in dopamine striatal metabolism and content. The locomotor activity was dramatically reduced in both groups 48 hours after the treatment but remained significantly decreased after two months only in 6-OHDA lesioned animals. A positive correlation was found between HVA CSF concentration and striatal DA content in MPP+ lesioned rats, but not in 6-OHDA lesioned rats. It is concluded that the concentration of dopamine metabolites in CSF can be altered only after a severe striatal lesion: reduction of striatal dopamine content below 50% of normal values and involvement of neuronal or non-neuronal elements other than the dopaminergic system, similarly to the lesions caused by MPP+. These results may partly explain why CSF dopamine metabolites concentrations were significantly decreased both in advanced stages of parkinsonism and in other neurodegenerative disorders.

1-Methyl-4-phenylpyridinium↗
PubMed1995

CSF somatostatin increase in patients with early parkinsonian syndrome.

Somatostatin-like immunoreactivity levels (SLI) in cerebrospinal fluid (CSF) were determined in twenty-three patients with untreated parkinsonian syndrome (15 with Idiopathic Parkinson's disease (IPD) and 8 with other forms of parkinsonism) at the moment of clinical diagnosis (mean duration of disease 1.1 +/- 0.2 years), and in 26 subjects without neurological symptoms. None of the IPD patients had a diagnosis of dementia at the moment of inclusion in the study. CSF-SLI content was found to be significantly higher in patients with parkinsonian syndrome (107.9 +/- 9.8 pg/ml) than in control subjects (73.5 +/- 8.4 pg/ml). The increase was also significant when controls were compared with IPD patients. In addition, a positive correlation between SLI and homovanillic acid was found in CSF of all patients. A test of learning memory was used to evaluate the mental state of patients and a significant increase in CSF-somatostatin levels was observed in patients with Idiopathic Parkinson's disease and severe affectation of memory. These results indicate that in the early steps of untreated parkinsonian syndrome, somatostatin concentration in cerebrospinal fluid may increase, probably due to the neurodegenerative depletion of somatostatin from striatal or cortical neurons.

Aged↗
PubMed1995

Lipoprotein concentrations in normolipidemic males consuming oleic acid-rich diets from two different sources: olive oil and oleic acid-rich sunflower oil.

The effects on plasma lipid concentrations of two oleic acid-rich diets, prepared with two different plant oils--olive oil and sunflower oil high in monounsaturated fatty acids (MUFAs)-- were compared with a National Cholesterol Education Program (NCEP) I diet. Twenty-one healthy, normolipidemic, young males consumed an NCEP-I diet (30% of energy as fat) during a 25-d period. Subjects were then assigned to two 4-wk study periods, according to a randomized, crossover design. Group one was placed on an olive oil-enriched diet (40% fat, 22% MUFAs), followed by a 4-wk period of a sunflower oil-enriched diet (40% fat, 22% MUFAs). In group two, the order of the diets was reversed. Both MUFA dietary periods resulted in an increase in high-density-lipoprotein (HDL) cholesterol (7% for the olive oil diet and 4% for the sunflower oil diet) and in apolipoprotein (apo) A-I (9% for both) compared with the NCEP-I diet. Low-density-lipoprotein (LDL) cholesterol and apo B concentrations (x +/- SEM) were lower (P < 0.05) during the sunflower oil diet (2.40 +/- 0.11 mmol/L, 0.85 +/- 0.04 mg/L) than during the olive oil diet (2.64 +/- 0.15 mmol/L, 0.93 +/- 0.05 mg/L). No significant differences were observed in these variables between the sunflower oil and NCEP-I (2.48 +/- 0.13 mmol/L, 0.89 +/- 0.04 mg/L) diets.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

The effect of cyclosporine and methylprednisolone on plasma lipoprotein levels in rats.

The aim of this study was to evaluate in rats the effects of cyclosporine, methylprednisolone, and the combination of both (CyP) on plasma lipids and lipoproteins levels. Three groups received a low doses of cyclosporine, methylprednisolone, and CyP (cyclosporine, 15 mg/kg/day; methylprednisolone, 1 mg/kg/day; and CyP, 15 plus 1 mg/kg/day of cyclosporine and methylprednisolone, respectively). Three additional groups received high doses (cyclosporine, 30 mg/kg/day; methylprednisolone, 2 mg/kg/day; and CyP, 30 plus 2 mg/kg/day of cyclosporine and methyprednisolone, respectively). The administration of cyclosporine produced an increase in plasma levels of triglycerides, very low density lipoprotein (VLDL) triglycerides, low-density lipoprotein (LDL) cholesterol and in total cholesterol/HDL cholesterol and LDL cholesterol/high-density lipoprotein (HDL) cholesterol ratios. In addition, cyclosporine decreased plasma HDL cholesterol and HDL2 cholesterol levels. The administration of methylprednisolone produced an increase in triglycerides and VLDL triglycerides and a decrease in HDL cholesterol and HDL2 cholesterol levels. Total cholesterol/HDL cholesterol and LDL cholesterol/HDL cholesterol ratios did not change after administration of methylprednisolone. The association of both drugs resulted in a greater increase in triglycerides and VLDL triglycerides than the separated administration of either cyclosporine or methylprednisolone alone. In rats receiving cyclosporine the increase in triglycerides and VLDL triglycerides may be due to a significant decrease in plasma lipoprotein lipase activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Influence of mutation in human apolipoprotein A-1 gene promoter on plasma LDL cholesterol response to dietary fat.

The plasma lipid response to changes in dietary fat and cholesterol can vary between individuals. At present, responders cannot be identified in advance. An adenine to guanine (A-->G) mutation in the promoter of the apolipoprotein A1 gene (apoA-1) has been suggested as affecting plasma high-density lipoprotein cholesterol. In 50 young men we examined the effect of the same mutation on the responses of both high and low density lipoprotein cholesterol to low-fat diet. The frequency for the A allele was 0.14. Subjects were fed a low-fat diet for 25 days, followed by a diet rich in monounsaturated fatty acid (MUFA, 22% out of 40% fat) for 28 days and lipoproteins were measured at the end of each diet. There were no differences in initial total cholesterol between subjects with the G/G mutation (170 mg/dL: 100 mg/dL = 2.59 mmol/L) and the G/A mutation (169 mg/dL) genotypes. After consumption of the high monounsaturated fat diet, significant increases were noted in plasma LDL cholesterol (10 mg/dL, p = 0.035) in the G/A subjects but not in the G/G subjects (1 mg/dL, p = 0.996). These differences showed that a significant diet-gene interaction (p = 0.015) existed. No differences were observed on HDL cholesterol between groups. Plasma low-density lipoprotein cholesterol responsiveness to diet may be explained by variation at the apoA-I gene locus.

Adult↗
PubMed1994

Cerebrospinal monoamine metabolites and amino acid content in patients with parkinsonian syndrome and rats lesioned with MPP+.

Monoamine metabolites and amino acid concentration in cerebrospinal fluid (CSF) of 33 untreated patients with parkinsonian syndrome, and 20 control patients without specific neurological symptoms have been compared with those obtained in cerebrospinal fluid of rats intrastriatally lesioned with 1-methyl-4-phenylpyridinium ion (MPP+) and sham operated animals. Homovanillic acid content was found to be significantly lower in patients with severe parkinsonism (motor score of UPDRS > 24), but not in patients with mild symptoms (motor score < or = 24). A correlation between the loss of striatal dopamine and the decrease in cerebrospinal homovanillic acid has been established in rats treated with MPP+. The extrapolation of these results to those obtained from human patients could be important in assessing the degree of striatal dopamine loss shown by humans with parkinsonian syndrome at the moment of clinical diagnosis. No significant differences were found between the other monoamine metabolites analyzed and free amino acid content in human and rat CSF.

1-Methyl-4-phenylpyridinium↗
PubMed1994

Stereotaxic administration of 1-methyl-4-phenylpyridinium ion (MPP+) decreases striatal fructose 2,6-bisphosphate in rats.

The stereotaxic administration of 1-methyl-4-phenylpyridinium ion (MPP+) into the neostriatum of male rats caused a lesion that resulted in a large dose-dependent loss of striatal fructose 2,6-bisphosphate; initial values were restored 5 days after the treatment. This effect was not protected by systemic administration of MK-801 or by nitroarginine. The content of hexose 6-phosphates and ATP was also reduced by MPP+ treatment, whereas lactate was increased. Biochemical and histological results suggested that MPP+ caused a nonselective cell death, followed by a pronounced astroglial response, parallel to fructose 2,6-bisphosphate recovery. The stereotaxic administration of rotenone showed a different time effect on fructose 2,6-bisphosphate cerebral content, with a significantly faster recovery. These results indicate that cerebral fructose 2,6-bisphosphate may be a sensitive metabolite related to brain damage caused by potent neurotoxins such as MPP+. On the other hand, they show that MPP+ acts in the brain through a quick, strong cytotoxic mechanism, which probably involves mechanisms other than mitochondrial chain blockage.

1-Methyl-4-phenylpyridinium↗
PubMed1993

Low-density lipoprotein metabolism in rats treated with cyclosporine.

Metabolic mechanisms underlying the observations of elevated cholesterol concentration of low-density lipoprotein (LDL) in organ-transplanted patients on long-term immunosuppressant cyclosporine therapy were explored using cyclosporine-treated rats as an experimental model. As in patients, treatment with cyclosporine induced a significant elevation of plasma cholesterol level, mainly in LDL cholesterol, with a decrease in high-density lipoprotein (HDL) cholesterol level. In an in vivo cross-over study design, differentially radioiodinated homologous LDL from donor cyclosporine-treated rats (Cyc-LDL) and excipient-only-treated control rats (Exc-LDL) were injected into recipient cyclosporine-treated rats (Cyc-rats), excipient-only--treated control rats (Exc-rats), and untreated rats (Unt-rats). From the isotope disappearance curves, the fractional catabolic rate (FCR) and production rate were calculated. The results showed that FCR and production rate were significantly reduced in Cyc-rats compared with control Exc-rats and Unt-rats. The decrease was independent of the donor LDL source. In vitro LDL ligand-receptor assays indicated a twofold higher degradation of Cyc-LDL by cultured rat fibroblasts, and hence could not account for the decreased clearance observed in vivo. These results suggest that the elevated concentrations of LDL cholesterol associated with cyclosporine treatment result not from a cyclosporine-induced modification of the LDL molecule, which could diminish its receptor-mediated clearance/catabolism, but possibly from an in vivo pharmacological property of cyclosporine such as an induced hepatic dysfunction.

Analysis of Variance↗
PubMed1992

[Vertebral hemangioblastoma: an atypical localization].

The case of a 53 year old patient with spastic paraparesis, sphincter function impairment and a deficit of sensation at the T 10 level of 2 months of evolution is presented complementary explorations (simple x-ray of the vertebrae, CT, MR and arteriography) demonstrated the presence of a vascular lesion affecting the 7th thoracic vertebra and which invaded the rachidian channel, compressing the spinal cord. Biopsy study of the intraspinal lesion was diagnosed as hemangioblastoma. A spinal hemangioblastoma with involvement of the vertebra at the same level is reported. The authors present three diagnostic hypothesis: the lesion is a vertebral hemangioblastoma with invasion of the rachidian channel with a evolution similar to vertebral angioma; the lesion is a vertebral angioma which invaded the channel differentiated into hemangioblastoma in its intraspinal position; or it is a spinal hemangioblastoma which has infiltrated the vertebra.

Epidural Neoplasms↗