PubMed Health⌕ Search

Biomedical subjects

F Du

Publications and source records attributed to F Du.

At least 91 records · Page 5Linked to original sources
PubMed1993

Plasma Na-K ATPase inhibitor activity and intracellular ions during hemodialysis.

We have investigated the relationship between plasma Na-K ATPase inhibitor activity (EDLS) and intracellular ions in 37 uremic hemodialysed hypertensive patients, and in 20 normotensive non uremic controls (NC). As compared with the NC population, significantly enhanced values for erythrocyte (RBC) Na, Ca, platelet cytosolic Ca and EDLS were observed in all the uremic patients tested just before a dialysis session, as well as a decrease in RBC Ca ATPase and in the platelet pH. In uremia, significant correlations have been noted between RBC Na and platelet Ca (r = 0.6) or systolic BP (r = 0.45); between platelet Ca and systolic blood pressure (r = 0.8) or diastolic BP (r = 0.5) and between EDLS and RBC Na, Ca or platelet Ca (r = 0.5). Anti-hypertensive treatment has no influence on these parameters. During dialysis, a significant decrease has been noted in RBC Na, Ca, platelet Ca, SBP (only in untreated patients) and EDLS and an increase in RBC Ca ATPase and platelet pH. These modifications are significantly correlated with the weight change.

Adult↗
PubMed1992

Aminooxyacetic acid causes selective neuronal loss in layer III of the rat medial entorhinal cortex.

Aminooxyacetic acid (AOAA) was used to produce a selective lesion in the rat entorhinal cortex (EC). As assessed 7 days following the injection of AOAA (75 micrograms/0.75 microliter) into the EC, neuronal loss in layer III of the medial EC, particularly in its ventral portion, was consistently observed in Nissl-stained horizontal sections. This selective neurodegeneration was seen even when AOAA was injected laterally or in deeper layers. Behavioral seizures occurred between 2 and 4 h after the AOAA injection. AOAA-induced EC lesions may provide experimental models for the study of human diseases in which the EC, particularly layer III neurons, is involved.

Aminooxyacetic Acid↗
PubMed1992

Immunocytochemical localization of kynurenine aminotransferase in the rat striatum: a light and electron microscopic study.

Kynurenine aminotransferase is the biosynthetic enzyme for kynurenic acid, an antagonist of excitatory amino acid receptors. Because of the possible role of kynurenic acid in basal ganglia diseases, the distribution of kynurenine aminotransferase immunoreactivity was examined in the adult rat striatum at the light and electron microscopic levels. Kynurenine aminotransferase immunoreactivity was detected in glial cells and in neurons. The preadsorption control vastly reduced or eliminated specific staining at both the light and electron microscopic levels. Kynurenine aminotransferase positive glial cells were abundant and contained a robust and homogeneous distribution of reaction product in both the nucleus and cytoplasm. The majority of neurons, both medium and large, were immunostained and exhibited granular kynurenine aminotransferase immunoreactivity in the cytoplasm of somata and proximal dendrites. At the ultrastructural level, kynurenine aminotransferase immunoreactive astrocytic processes were apparent throughout the neuropil where they often encircled capillaries and surrounded axospinous synapses. Reaction product was associated with the cytoplasmic matrix, filaments, rough endoplasmic reticulum, and the nucleus. In neurons, the majority of label occurred in round membrane-bound cytoplasmic organelles located adjacent to the Golgi apparatus, rough endoplasmic reticulum, and the cell or nuclear membranes. Cisternae and vesicles were identifiable in some of the labeled profiles. Polyribosomes and rough endoplasmic reticulum were also labeled. These data provide an anatomical basis for biochemical studies that have suggested the presence of striatal kynurenine aminotransferase in both astrocytes and neurons.

Animals↗
PubMed1992

Localization of kynurenine aminotransferase immunoreactivity in the rat hippocampus.

The localization and distribution of kynurenine aminotransferase (KAT), the biosynthetic enzyme of the excitatory amino acid receptor antagonist, kynurenic acid, was studied in the rat hippocampal formation with immunohistochemical methods. The enzyme was found mainly in glial cells that could be distinguished as 3 types on the basis of their shapes and locations. Typically, these cells shared the morphological features of astrocytes and exhibited glial fibrillary acidic protein immunoreactivity as demonstrated by a double-labeling technique. The distribution of KAT-containing glial cells was heterogeneous throughout the hippocampal formation. In the hippocampus, the stratum lacunosum-moleculare of Ammon's horn and the hilus contained a higher density of KAT-positive glial cells than other regions, whereas the lowest density of KAT glial cells was observed in the granule cell layer of the dentate gyrus and in the stratum radiatum of CA subfields. In the subicular complex, the density of KAT-containing glial cells was generally higher in the superficial than in the deep layer. Hippocampal neurons exhibiting KAT immunoreactivity, distinguished as nonpyramidal cells, were very few in number and mainly distributed in strata oriens and pyramidale of Ammon's horn. Substantially more KAT-positive neurons were observed in layers II and III of the subicular complex. The organization of cellular elements containing KAT may be of relevance for the function and possible dysfunction of kynurenic acid in the rat hippocampal formation.

Animals↗
PubMed1992

Low sodium diet in essential hypertension. Effect on blood cell ions and hemodynamic parameters.

The influence of salt restriction for 3 months on blood pressure, peripheral vascular resistance (observed by occlusive plethysmography), erythrocyte sodium, platelet calcium, and pH, was studied in eight untreated essential hypertensive patients. A low salt diet decreases blood pressure, vascular resistances, erythrocyte sodium, and platelet calcium, but not platelet pH. A strong positive correlation was noted between baseline platelet calcium and vascular resistances (r = 0.95, P less than .01). But during the salt restriction period, a negative correlation has been observed between the changes in these parameters, which casts doubt on the use of the platelet as a model of the smooth muscle cell.

Adult↗
PubMed1992

[Effect of dietary sodium in hypertension not treated with drugs].

The usefulness of salt restriction in essential hypertension is still now disputed. This study was designed to test the influence of a diet with and without salt restriction in 19 untreated essential hypertensives (12 with and 7 without family history of hypertension) and free of cardiovascular and renal complications. Each patient was examined after a placebo period, after 1 month of salt restriction, and after 1 month of salt supplementation. Weight, blood pressure, 24 hours urinary sodium excretion and red blood cell ionic fluxes were measured. In patients with hypertensive heredity, the blood pressure did not change. The intracellular sodium concentration, the cotransport and the countertransport remained stable. The ouabain sensitive sodium pump slightly increased during salt restriction and remained stable after salt supplementation. In patients without such hypertensive heredity (who were older and heavier), sodium restriction period was characterized by significant decrease in blood pressure, weight, intracellular sodium concentration and increase in sodium pump activity. When salt was increased, all the parameters remained stable. A more balanced diet with sodium restriction decreases the blood pressure in relation to age, weight and the blood pressure level. Hypertensive heredity does not seem to be a parameter of salt sensitivity. The blood pressure decrease is also related to the quantitative importance of sodium restriction. The ouabain sensitive pump activity changes during diet especially in relation to weight loss and decreasing salt intake.

Adult↗
PubMed1991

Quinolinic acid catabolism is increased in cerebellum of patients with dominantly inherited olivopontocerebellar atrophy.

We measured the activities of the enzymes responsible for the metabolism of the excitotoxin quinolinic acid, 3-hydroxyanthranilate oxygenase and quinolinic acid phosphoribosyltransferase, in autopsied brain of 11 patients with olivopontocerebellar atrophy. In cerebellar cortex, severe Purkinje cell loss was evident but with relative preservation of granule cells. As compared with the control subjects (n = 14), mean activity of 3-hydroxyanthranilate oxygenase was normal in cerebellar cortex from the patients with olivopontocerebellar atrophy, whereas quinolinic acid phosphoribosyltransferase activity was markedly increased (+92%, p less than 0.02). No significant changes in enzyme activities were found in samples from occipital cortex. Increased quinolinic acid phosphoribosyltransferase activity may represent a mechanism, in the degenerating cerebellum, to protect quinolinic acid-sensitive granule cells in patients with olivopontocerebellar atrophy.

Adult↗
PubMed1991

Focal injection of aminooxyacetic acid produces seizures and lesions in rat hippocampus: evidence for mediation by NMDA receptors.

Aminooxyacetic acid (AOAA), a potent yet nonspecific transaminase inhibitor, is known to cause convulsions when administered at high doses to experimental animals. The present study was designed to explore the mechanism(s) underlying the epileptogenic properties of AOAA. To this end, the drug was injected into the hippocampus of unanesthetized rats. Injection of 1.8 to 450 nmol AOAA produced dose-dependent EEG abnormalities including, at the higher doses, limbic seizures. Coadministration of the selective NMDA receptor antagonist D-2-amino-7-phosphonoheptanoic acid (APH) at doses of 45 and 225 nmol caused an almost complete inhibition of seizures produced by 225 nmol AOAA. At 225 and 450 nmol, AOAA also caused selective neuronal damage, which was restricted to the CA1 region at the lower dose and also affected the CA3/CA4 area in two of six rats injected with the higher dose. Co-injection of 225 nmol APH completely protected the hippocampus from AOAA-induced damage. In separate experiments, microiontophoretic application of AOAA to CA1 pyramidal neurons failed to increase the firing rate of each of the 10 cells tested, thus indicating that the drug does not directly activate NMDA receptors. These experiments suggest that seizures and neurotoxicity produced by AOAA are mediated indirectly via NMDA receptor activation.

Aminooxyacetic Acid↗
PubMed1991

Immunohistochemical localization of quinolinic acid phosphoribosyltransferase in the human neostriatum.

The localization and distribution of quinolinic acid phosphoribosyltransferase, the degradative enzyme of the endogenous excitotoxin quinolinic acid, were studied in the post mortem human neostriatum by immunohistochemistry. In eight neurologically normal human brains, quinolinic acid phosphoribosyltransferase immunoreactivity was detected in both glial cells and neurons. Typically, glial cells containing quinolinic acid phosphoribosyltransferase immunoreactivity had numerous processes radiating from the cell bodies. In Nissl-counterstained sections, most quinolinic acid phosphoribosyltransferase-immunoreactive glial cells showed round, large and pale nuclei. These morphological features indicate that they are probably astrocytes. Neurons containing quinolinic acid phosphoribosyltransferase immunoreactivity had different sizes and shapes and were tentatively classified into three subpopulations. Most were medium-sized cells with ovoid or elongated perikarya. Small quinolinic acid phosphoribosyltransferase-immunoreactive neurons, often spheroid in shape, were particularly noted in a zone of the caudate nucleus adjacent to the lateral ventricle. A few large quinolinic acid phosphoribosyltransferase-positive neurons were also present in both the caudate and putamen. The somatic and dendritic morphology of quinolinic acid phosphoribosyltransferase-immunoreactive neurons closely resembles that of aspiny neurons seen in Golgi preparations. The localization of the specific quinolinic acid-catabolizing enzyme in distinct populations of neostriatal cells suggests specific functional correlates. It remains to be examined how the anatomical organization of quinolinic acid phosphoribosyltransferase immunoreactivity relates to the degradation of quinolinic acid in the striatum, and if the morphological characteristics and distribution of quinolinic acid phosphoribosyltransferase-immunoreactive cells are of relevance for the pathogenesis of neurodegenerative basal ganglia disorders.

Adult↗
PubMed1991

[Comparative analysis of the trends of atherosclerotic cardiovascular diseases in rural and urban monitored population of Jiangsu province].

This study was done on acute myocardial infarction (AMI), coronary sudden death(CSD) and stroke in 424,318 population in Hai Men county and Nanjing city by registration according to WHO "Monica Project" from 1983 to 1987. The results showed that the age-adjusted average annual incidence of coronary events and stroke were 18.6/100,000 and 103.1/100,000, respectively, in a resident population aged 25-74 for 135,429 year-persons in Nanjing. They were significantly higher than 8.4/100,000 and 61.6/100,000 in a group of peasants for 1,040,127 year-persons in Hai Men county of Jiangsu province (u = 2.1, 4.38, P less than 0.05). The age-adjusted average annual mortality of AMI was also higher in Nanjing (4.7 vs. 0.3/100,000; u = 4.6, P less than 0.01) than in Hai Men. Following the effectiveness of hypertensive community control in the monitored population in Nanjing from 1985 to 1987, the mortality of AMI, CSD and stroke decreased significantly and the annual incidence of stroke was also tended to lower. Both the annual incidence of coronary and stroke events and the fatality of stroke at acute stage were still unchanged from 1983 to 1987 owing to the hypertensive community control being delayed in rural population in Hai Men.

Adult↗
PubMed1990

Purification and characterization of kynurenine-pyruvate aminotransferase from rat kidney and brain.

Kynurenine-pyruvate aminotransferase (KPT), the enzyme responsible for the biosynthesis of the endogenous excitatory amino acid receptor antagonist kynurenic acid, was purified to homogeneity from rat kidney, as judged by polyacrylamide and sodium dodecyl sulfate electrophoresis. The protein appeared to consist of 2 identical subunits of approximately 48 kDa. Kinetic analysis showed Km values of 2.8 mM (kynurenine) and 3.8 mM (pyruvate), respectively. KPT was also partially purified from rat brain. Kidney and brain KPT were found to be identical when analyzed by a spectrum of biochemical, physico-chemical and, after production of anti-kidney KPT antibodies, immunological methods. Partially purified anti-KPT antiserum was used for first immunohistochemical studies, which revealed the presence of the enzyme in astrocyte-like cells throughout the brain. Less frequently, KPT was also found in discretely arranged neurons. The availability of pure KPT and specific anti-KPT antibodies can be expected to be of value for the further examination of the neurobiology of kynurenic acid.

Animals↗
PubMed1990

Distribution of quinolinic acid phosphoribosyltransferase in the human hippocampal formation and parahippocampal gyrus.

The morphological distribution of quinolinic acid phosphoribosyltransferase (QPRT), the degradative enzyme of the endogenous excitotoxin quinolinic acid, was studied in the human hippocampal formation and parahippocampal gyrus by immunohistochemical techniques. In seven neurologically normal human brains obtained at autopsy, QPRT-immunoreactivity (QPRT-i) was found in both glial cells and neurons. Glial cells exhibiting QPRT-immunoreactivity morphological features of astrocytes, were observed in all hippocampal subfields. The polymorphic layer of the dentate gyrus contained the highest density of QPRT-i glial cells. Numerous QPRT-i glial cells were also found along both sides of the fused hippocampal fissure and in the white matter including the alveus of Ammon's horn, whereas only a few were observed in the granule cell layer and the stratum pyramidale. Neurons containing QPRT-i were found mainly in the subiculum and in the strata oriens and pyramidale of CA1. They were mostly small and polymorphic or fusiform, thus indicating that they may belong to a subpopulation of interneurons. Moderate numbers of QPRT-i glial cells and neurons were also observed throughout layers II-VI of parahippocampal cortex. The localization of QPRT-i in selected glial cells and neurons suggests that in the regions examined these cellular elements might play specific roles in the regulation of quinolinic acid function.

Adult↗
PubMed1988

Distribution of substance P and vasoactive intestinal polypeptide neurons in the chicken spinal cord, with notes on their postnatal development.

The distribution of substance P (SP) and vasoactive intestinal polypeptide (VIP) was investigated by immunohistochemistry in the adult chicken spinal cord. By using colchicine treatment, populations of neurons containing either SP or VIP was observed in several regions of the spinal cord. SP neurons were found dorsal to the central canal (CC) and in lamina IV throughout the cord. However, at the thoracic level, numerous relatively larger SP perikarya were located ventral to the CC and aligned on either side of the midline. The distribution of SP fibers is very similar to that reported previously in mammals: they were mostly observed in laminae I and II, in Lissauer's tract, in the dorsolateral funiculus, and dorsal to the CC. In addition, two dense plexuses of SP fibers were noticed in lamina IV. VIP neurons were located mainly in lamina I, in the nucleus of the dorsolateral funiculus, and in the lateral portion of the neck of the dorsal horn throughout the spinal cord. At the thoracic level, many also were located lateral to the CC. Occasionally, single VIP neurons also were encountered dorsal to the CC, in laminae II-IV, and in the intermediate zone. VIP fibers were observed in similar numbers at all spinal levels, occurring mainly in laminae II (probably I) and III, dorsal to the CC, and in the intermediate zone. In addition, examination of the developing chick spinal cords showed similar results as in adult chickens.

Animals↗
PubMed1988

Distribution and development of VIP immunoreactive neurons in the spinal cord of the embryonic and newly hatched chick.

The distribution and development of vasoactive intestinal polypeptide (VIP) immunoreactive elements were studied in the spinal cord of embryonic and newly hatched chicks with the indirect immunofluorescence method. VIP neurons were first detectable in the presumed dorsal horn at stages 27-28 (incubation day 5). Subsequently they increased in number, and by stage 39 (day 12) many occurred in lamina I, in the nucleus of the dorsolateral funiculus, and in the lateral portion of the neck of the dorsal horn throughout the cord. However, at the thoracic level many were also situated lateral to the central canal, with their processes running to the ipsilateral lateral and contralateral ventral funiculi. The pattern described above remained visible in both embryonic and colchicine-pretreated newly hatched chicks. During development, VIP fibers appeared later than cell bodies. In the gray matter, they were mainly scattered in the intermediate zone, especially around the central canal at all levels examined. In the white matter, however, longitudinal fibers were observed in the lateral funiculus throughout the cord, but mostly at the cervical level, though some also occurred in the ventral funiculus. This finding supports the idea that spinal VIP neurons might project rostrally via the lateral funiculus. In addition, no VIP immunoreactivity was found in the spinal ganglia, but examination of the sympathetic paravertebral ganglia showed immunoreactivity as described by others.

Age Factors↗
PubMed1988

Development and distribution of enkephalin-immunoreactive elements in the chicken spinal cord.

The development and distribution of methionine-enkephalin-immunoreactive elements were studied in the chicken spinal cord with the indirect immunofluorescence method. Methionine-enkephalin-like immunoreactivity was first detected in the chick spinal cord at embryonic stages 29-30 (incubation day 6). Before stage 35 (day 9), it was mainly observed in fibres almost throughout the white matter. Subsequently, fibres containing the peptide appeared in the ventral half of the gray matter, but mostly in the lateral portion of the neck of the dorsal horn. From stage 40 (day 13 or 14), fibres were especially noticed in laminae 1 and 2, and in the area dorsal to the central canal. In particular, many enkephalin-immunoreactive perikarya were observed in several spinal areas during this period. Such a distribution of both enkephalin-immunoreactive fibres and perikarya remained visible at later embryonic stages, but labelled cells gradually decreased in number and disappeared after hatching. With colchicine treatment, however, a similar distribution of the peptide was found in the spinal cord of adult chickens. As in the embryo, enkephalin-immunoreactive perikarya were mainly observed in the lateral portion of the neck of the dorsal horn, in lamina 1, and in the nucleus of the dorsolateral funiculus throughout the spinal cord. At the thoracic level, many were also located ventral to the central canal. Enkephalin-immunoreactive fibres increased notably in the gray matter of adult chickens. They mainly occurred in laminae 1 and 2, in the lateral portion of the neck of the dorsal horn, and in the area around, especially dorsal to, the central canal. In contrast, enkephalin-immunoreactive fibres decreased in the white matter and they were mainly observed in the dorsolateral funiculus, in Lissauer's tract, and in the lateral funiculus adjacent to the gray. The distribution of enkephalin-immunoreactive fibres was generally comparable at all spinal levels examined. In addition, examination of post-hatched chickens showed virtually the same results as in the adult.

Aging↗
PubMed1987

Development and distribution of substance P in the spinal cord and ganglia of embryonic and newly hatched chick: an immunofluorescence study.

The development and distribution of substance P (SP) immunoreactivity were studied in the spinal cord and ganglia of embryonic and newly hatched chick by using the indirect immunofluorescence method. Substance P immunoreactivity was first detected in the spinal cord at embryonic stages 18-20 (incubation day 3). Before stage 32 (day 7), it was mainly found in regions corresponding to the dorsolateral funiculus and Lissauer's tract. Subsequently, SP fibers appeared in the dorsal horn. By stage 38 (day 11), they were demonstrated almost throughout the gray matter, but mostly in laminae I and II. During this period, however, many SP-positive cells were found just ventral to the central canal at the thoracic level, although a few were also detected in other areas throughout the cord. In the white matter, very dense longitudinal SP fibers were observed in Lissauer's tract and the dorsolateral funiculus, where extremely dense plexuses of SP immunoreactivity were also detected around a group of nonimmunoreactive cell bodies. At later stages, no remarkable differences were noticed in the distribution of SP fibers, but the SP-positive cells decreased gradually in number and disappeared after hatching. However, they reappeared following colchicine treatment. In the spinal ganglia, SP immunoreactivity appeared initially at stage 25 (day 4). It was mostly located in small neurons of the mediodorsal region. These cells also decreased in number from later stages but increased by colchicine treatment after hatching. The development and distribution of SP immunoreactivity in the spinal cord and ganglia were generally comparable at all levels examined, except where indicated.

Animals↗