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Biomedical subjects

J De Keyser

Publications and source records attributed to J De Keyser.

At least 19 recordsLinked to original sources
PubMed1992

Serum concentrations of vitamins A and E and early outcome after ischaemic stroke.

Formation of free radicals and subsequent lipid peroxidation may have an important role in tissue injury and neuronal cell death after cerebral ischaemia. We conducted a prospective, controlled study to determine whether the endogenous antioxidant vitamins A and E had a protective function in acute ischaemic stroke. The study population consisted of 80 patients seen at the Free University Hospital in Brussels. Entry criteria were occurrence of sudden focal neurological deficit lasting more than 3 h; deficit due to acute ischaemia in the territory of the middle cerebral artery; and investigation within 24 h of onset of the episode. Outcome was assessed within the first 21 days. 80 controls matched for age and sex had various neurological disorders other than acute ischaemia. Serum concentrations of vitamins A and E were similar in the study and control groups. In the study population a serum vitamin A concentration higher than the mean of 2.27 mumol/l was associated with a higher frequency of complete recovery within the first 24 h (p less than 0.05), decreased mortality (p = 0.038), and a better outcome as assessed by the Mathew scale of neurological deficit (p less than 0.03) and the Barthel index. There was no significant difference in outcome between patients with vitamin E concentrations above or below the mean of 35.3 mumol/l. Our results suggest a beneficial effect of a high serum vitamin A concentration on early outcome in ischaemic stroke.

Aged↗
PubMed1992

Idiopathic hemiparetic parkinsonism, a syndrome distinct from idiopathic parkinsonism.

Two women had a syndrome of progressive parkinsonism with ipsilateral rigidity, mild resting tremor, paresis, hyperreflexia, and an extensor plantar response. Symptoms had started 24 and 3 months after a surgical procedure in the affected limb. Neuroimaging studies were unhelpful. Both the parkinsonian features and the pyramidal tract signs responded well to dopaminergic drug treatment. We propose that the syndrome be called "idiopathic hemiparetic parkinsonism".

Adult↗
PubMed1992

Regional distribution of alpha 2A- and alpha 2B-adrenoceptor subtypes in postmortem human brain.

The newly available and highly selective radiolabeled antagonist [3H]RX 821002 was used to examine the distribution of alpha 2 adrenoceptors in human brain. High densities of alpha 2 adrenoceptors were found in the hippocampus, frontal cortex, thalamus, amygdala, pons, and medulla oblongata. Intermediate densities were observed in the striatum (nucleus accumbens, nucleus caudatus, and putamen), globus pallidus, and substantia nigra. The KD values for [3H]RX 821002 were similar in all regions (ranging from 2.8 to 7.5 nM). On the basis of their different affinities for prazosin and oxymetazoline, the alpha 2 adrenoceptors have been divided into alpha 2A and alpha 2B subtypes. To examine the alpha 2A/alpha 2B-adrenoceptor ratio in the different brain regions, we performed oxymetazoline and prazosin/[3H]RX 821002 competition binding experiments. In frontal cortex membranes, the competition curves with prazosin were steep, indicating a single class of binding sites, whereas the competition curves with oxymetazoline were shallow and fitted by computer best to a two-site model. However, in the presence of GTP, the high-affinity sites for oxymetazoline were partially converted into low-affinity sites, indicating that this agonist interacts with high- and low-affinity states of the alpha 2 adrenoceptors. This implies that oxymetazoline is not very suitable for discriminating the alpha 2A- and alpha 2B-receptor subtypes in radioligand binding studies. Therefore, prazosin/[3H]RX 821002 competition binding experiments were used to investigate the distribution of the alpha 2-adrenoceptor subtypes in human brain. The alpha 2A-receptor subtype was detected in all brain regions examined. In contrast, alpha 2B receptors were only observed in striatum and globus pallidus.

Adrenergic alpha-Antagonists↗
PubMed1991

Autoradiographic distribution of alpha 2 adrenoceptors, NAIBS, and 5-HT1A receptors in human brain using [3H]idazoxan and [3H]rauwolscine.

The regional distribution of [3H]idazoxan and [3H]rauwolscine was studied autoradiographically in human brain. [3H]Idazoxan binds with high affinity to alpha 2 adrenoceptors as well as to non-adrenergic sites (NAIBS). [3H]Rauwolscine, besides binding to alpha 2 adrenoceptors, also binds to 5-HT1A receptors. Both radioligands labelled the same population of alpha 2 adrenoceptors, defined as the epinephrine-displaceable binding component. The highest densities of alpha 2 adrenoceptors occur in the leptomeninges, cerebral cortex and claustrum; lower densities were visualised in the basal ganglia, thalamus, pons, substantia nigra, cerebellum and medulla oblongata; no alpha 2 adrenoceptors were detected in amygdala and nucleus ruber. NAIBS were present in all the examined brain areas, with the highest densities found in the basal ganglia and substantia nigra. The finding that certain brain regions, such as the amygdala, contained NAIBS but no detectable alpha 2 adrenoceptors, suggests that the binding sites are independent from each other. The regional distribution of 5-HT1A receptors labelled by [3H]rauwolscine is in agreement with previous studies using [3H]8-OH-DPAT.

Adult↗
PubMed1991

Meningoencephalitis caused by Rickettsia conorii.

Case report of Mediterranean spotted fever in an 18 year old male heroin addict, caused by Rickettsia Conorii. The typical "tache noir" was absent. The patient developed meningoencephalitis within 5 days after onset of the systemic symptoms. Diagnosis was based on serological findings. Treatment with doxycycline led to rapid recovery without sequelae.

Adolescent↗
PubMed1991

Sudden hypotonic paraparesis caused by tophaceous gout of the lumbar spine.

Gouty arthritis of the axial skeleton is rare, and neurological complications due to spinal cord or nerve root compression secondary to tophaceous deposits have been seldom reported. We describe a patient with chronic gouty arthritis who developed an acute paraparesis caused by tophaceous cauda equina compression. Surgical removal of the mass resulted in complete recovery.

Arthritis, Gouty↗
PubMed1991

Increase in serum myoglobin, creatine kinase, and free fatty acids, during recovery from a paralytic attack in hypokalemic periodic paralysis.

In a patient with hypokalemic periodic paralysis (HPP), recovery from a paralytic attack, coinciding with the restoration of plasma potassium, was associated with a rise in serum myoglobin (Mb) and creatine kinase (CK). The increase of muscle proteins in serum was preceded by an increase in serum free fatty acids (FFA). An increased permeability of the sarcolemma, caused by an accumulation of FFA within the muscle cell, might underly the reflux of potassium into the circulation. This might represent a mechanism by which the paralytic attacks in HPP terminate.

Adolescent↗
PubMed1991

D1 and D2 dopamine receptors in human substantia nigra: localization and the effect of aging.

D1 and D2 receptor densities in human substantia nigra were examined by use of the specific binding of, respectively, [3H]SCH 23390 [R(+)-7-chloro-8-hydroxy-3-[3H]methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3- benzazepine] and [3H]spiperone. A unilateral loss of striato- and pallidonigral pathways by an infarction (n = 4) had no effect on the ipsilateral nigral D2 receptors, but reduced the ipsilateral nigral D1 receptors by 48-60% compared with the intact side. These data suggest that a substantial fraction of D1 receptors in human substantia nigra is located on terminals of striato- and/or pallidonigral neurons, whereas D2 receptors are confined to intrinsic nigral cells. We also examined the effect of aging on the D1 and D2 receptors in substantia nigra obtained from 25 postmortem human brains (age range 19-88 years). The densities of both receptor types were not affected by the aging process. Since nigrostriatal dopaminergic neurons degenerate with aging, these results suggest either that the nigral D2 receptors are up-regulated in response to a progressive depletion of dopamine in the substantia nigra or that, in contrast to the rat, they are not located on dopaminergic neurons.

Aged↗
PubMed1990

D1-dopamine receptor abnormality in frontal cortex points to a functional alteration of cortical cell membranes in Alzheimer's disease.

D1-dopamine receptors and their high-agonist affinity (RH) sites were determined in postmortem-obtained frontal cortex from seven patients with histopathologically confirmed Alzheimer's disease and from seven controls matched for sex, age, and postmortem delay. Total D1-dopamine receptor concentration was unchanged in patients with Alzheimer's disease compared with controls, but the RH sites were significantly reduced in number. Since the RH sites are thought to represent a conformational change of the receptors, induced by the interaction of agonist-bound receptor with a signal transduction protein located in the cell membrane, the reduced ratio of RH sites to total receptors suggests a functional alteration of cortical cell membranes in Alzheimer's disease. Such a cell membrane abnormality might explain why substitution therapy in Alzheimer's disease has been largely disappointing.

Aged↗
PubMed1990

Age-related changes in the human nigrostriatal dopaminergic system.

A deficiency of dopamine in the striatum may contribute to the decline in motor function associated with aging. We examined the effect of aging on the densities of the D1 and D2 dopamine receptors, their high-agonist affinity sites, and the dopamine uptake sites in postmortem human putamen (n = 32; age range, 19-88 years). With aging a steady decrease was seen in dopamine uptake sites (p less than 0.001), confirming previous morphometric and biochemical data of an age-related loss of nigrostriatal axons. In contrast, the concentrations of the D1 and D2 dopamine receptors and their high-agonist affinity sites, which are believed to represent the functionally active receptors, were not affected by the aging process. These results may have implications for the pharmacological treatment of the age-related decline in motor function.

Adult↗
PubMed1990

Human M1-, M2- and M3-muscarinic cholinergic receptors: binding characteristics of agonists and antagonists.

The muscarinic acetylcholine receptors were identified in membrane preparations from human tissues by the specific binding of 1-[benzilic-4,4'-3H] quinuclidinyl benzilate. Saturation binding isotherms of this radioligand yielded a total amount of receptors of 435 +/- 208, 159 +/- 65 and 913 +/- 89 fmol/mg protein, respectively, in the hippocampus, pons and submandibular gland. Non linear least squares analysis of competition binding studies with the antagonists pirenzepine and AF-DX 116 indicates that the majority of receptors are of the M1-type in the hippocampus (83%, high affinity for pirenzepine, intermediate affinity for AF-DX 116), the M2-type in the pons (low affinity for pirenzepine and high affinity for AF-DX 116), and the M3-type in the submandibular gland (low affinity for pirenzepine and AF-DX 116). Competition binding parameters of the agonists carbachol, arecoline, oxotremorine, pilocarpine and MCN-A-343 were compared for M1, M2 and M3 receptors in the human hippocampus, pons and submandibular gland. GTP caused a shift to the right and a steepening of the shallow agonist competition curves in the 3 tissues but did not affect the initially steep ones. This effect is explained by a GTP-mediated conversion of high- to low-agonist affinity sites. The extent of the nucleotide shift was much greater for M2 receptors as compared with M1 and M3 receptors. The GTP effect was impaired by the sulphydryl reagent N-ethylmaleimide, probably due to alkylation of GTP-binding proteins. Moreover, the reagent provoked also an increase of the agonist affinity for the uncoupled muscarinic receptors. For all agonists, this increase was more pronounced for the M2 receptors than for the M1 and M3 receptors. These findings suggest structural differences between the agonist binding sites of M1 and M3 receptors versus the M2 receptors.

Binding, Competitive↗