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Biomedical subjects

M Lucas

Publications and source records attributed to M Lucas.

At least 199 records · Page 11Linked to original sources
PubMed1986

Autologous rosette-forming T cells and their relationship to OKT4+ and OKT8+ cells in chronic HBV infection.

A percentage of human T lymphocytes forms rosettes with autologous erythrocytes and this property has been considered as a marker for post-thymic precursor suppressor cells capable of providing suppression under the influence of inducer cells. We quantitated autologous rosette-forming T cells (ARFC) in the peripheral blood of 37 patients with chronic HBV infection: 8 healthy carriers, 9 chronic persistent hepatitis (CPH-B) and 20 chronic active hepatitis (CAH-B). Two control groups were studied, one consisting of 26 healthy individuals and the other of 8 individuals with non-HBV-associated CAH. Patients with non-HBV-associated CAH had a significant reduction in the proportion of ARFC, whereas CAH-B patients fell into 2 distinct patterns, one with increased and the other with decreased proportions of ARFC. This was unrelated to the degree of biochemical activity of the disease or to degree of viral replication as defined by HBeAg status and HBV-DNA in the serum. Healthy carriers and CPH-B had no changes in ARFC. Simultaneous quantitation of OKT4 and OKT8+ cells was done and a positive correlation was found between the proportions of ARFC and the proportions of OKT8+ cells. The possible significance of this correlation and the relevance of the bimodal distribution of autologous rosette-forming cells in CAH-B are discussed.

Antibodies, Monoclonal↗
PubMed1986

Calmodulin and ATP dependence of the high and low calcium affinity p-nitrophenylphosphatase from human erythrocyte membranes.

In calmodulin depleted membranes from human erythrocytes, the Ca2+-dependent phosphatase showed different sensitivity to calmodulin and ATP with variable affinity towards free calcium concentrations: a calmodulin-dependent activity with high calcium affinity, K1/2 = 1.2 X 10(-7) mol/l calcium, that was fully activated at submicromolar calcium concentrations, higher concentrations being rather inhibitory; an ATP-dependent activity with lower calcium affinity, K1/2 = 10(-6) mol/l calcium, that was fully activated at 10(-5) mol/l calcium in the presence of 50-200 mumol/l ATP and was insensitive to calmodulin, and a calcium dependent phosphatase that was active at a wider ranger of free calcium, 10(-8)-10(-5) mol/l, and required the presence of both calmodulin and ATP.

4-Nitrophenylphosphatase↗
PubMed1985

Stimulation by calcium and carbamoylcholine of the ouabain-sensitive uptake of 86Rb+ in isolated rat pancreatic acinar cells.

The uptake of 86Rb+ was assayed in isolated rat pancreatic acinar cells to determine the effect of calcium and carbamoylcholine on the ouabain-sensitive and ouabain-insensitive components. The presence of calcium in the medium bathing the cells during the preincubation and the main incubation periods was needed to preserve in optimum conditions the uptake of 86Rb+, the stimulation by carbamoylcholine and the sensitivity to ouabain. In the presence of calcium, the ouabain-sensitive component of 86Rb+ uptake was higher than the ouabain-insensitive. The ouabain-sensitive component was 3-times lower in cells incubated in a medium lacking calcium and containing 1 mM EGTA, as compared to cells incubated in the presence of calcium. Carbamoylcholine, at 5 X 10(-4) M, stimulated the uptake of 86Rb+ and this effect depended on the presence of calcium in the bathing medium. Maximal stimulation by carbamoylcholine was reached at 0.2 mM calcium. The nett stimulation by carbamoylcholine was inhibited up to 85% by 1 mM ouabain. As judged by digitonin-disruption of plasma membrane, the above-indicated effects were limited to a cytoplasmic pool of 86Rb+ and a leaky plasma membrane could be ruled out. The results suggest that in rat pancreatic acinar cells, carbamoylcholine stimulated the ouabain-sensitive uptake of 86Rb+ and required the presence of calcium in the bathing medium.

Amylases↗
PubMed1985

Irreversible blockade of beta-adrenergic receptors with a bromoacetyl derivative of pindolol.

A potent irreversible beta-adrenergic derivative of pindolol possessing a chemically reactive group (Br-AAM-pindolol) was synthesized. This compound devoid of agonist properties, competed for all (3H)-dihydroalprenolol (3H-DHA) binding sites in C6 glioma cell and rat cerebellum membranes. Pretreatment of C6 glioma cell membranes with Br-AAM-pindolol and subsequent washing resulted in a time- and dose-dependent blockade of beta-adrenergic receptors. A 50% blockade was achieved in the presence of 1.6 nM Br-AAM-pindolol. This blockade occurs specifically at the beta-adrenergic receptor level, as: 1) it induced a decrease of maximal isoproterenol stimulated adenylate cyclase activity with no modification of basal and sodium fluoride stimulated activity and 2) decreases of (3H)-DHA binding and stimulation of adenylate cyclase activity by the agonist were suppressed in the presence of isoproterenol, a beta-adrenergic agonist. Furthermore, Br-AAM-pindolol treatment did not affect (3H)-diazepam binding in C6 glioma cell membranes. Pretreatment of C6 glioma cells with Br-AAM-pindolol also reduced the response of adenylate cyclase to isoproterenol and the number of beta-adrenergic receptors. The blockade of beta-adrenergic receptors of C6 glioma cells by Br-AAM-pindolol was non-competitive, whereas the blockade obtained with AM-pindolol, a derivative of pindolol devoid of alkylating properties, was competitive. The irreversible blockade of beta-adrenergic receptors by Br-AAM-pindolol in rat erythrocyte membranes was substantiated by the demonstration that no recovery of beta-adrenergic receptors occurred during long term incubation of the membranes (48 h) following Br-AAM-pindolol treatment and subsequent washing.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗
PubMed1985

[Sutton's periadenitis mucosa necrotica recurrens. An optical-ultrastructural case study].

An optic-ultrastructural study is realized, emphazising the presence of: a) Intermediate lymphocytes, that we interpret as T-activated; b) Activated endothelial cells (prominent, rich in Weibel-Palade's bodies, well developed nuclei- and cytoskeletons); c) Classic and native myofibroblasts, partially responsible for the cicatricial contraction. We postulate that the changes in the connective-vascular tissue of the chorion represent an anarchic and reactive fibroangioblastic hyperplasia and favors the typical recurrences of this process.

Adolescent↗
PubMed1984

Beta adrenergic receptor repopulation of C6 glioma cells after irreversible blockade and down regulation.

C6 glioma cells possess beta adrenergic receptors coupled with adenylate cyclase which can be irreversibly blocked by bromoacetylaminomethylpindolol (Br-AAM-pindolol), a beta adrenergic antagonist. With 1 microM Br-AAM-pindolol, more than 80% of beta adrenergic receptors, labeled by (3H)-dihydroalprenolol [3H)-DHA), were blocked. After this blockade, new beta adrenergic receptors were synthesized only during cell division. However, at cell confluency when the cell number was constant, turnover of beta adrenergic receptors was barely detectable. Cycloheximide (1 microgram/ml) inhibited cell growth as well as reappearance of beta adrenergic receptors. A 90% loss of beta adrenergic receptors in C6 glioma cells was obtained after down-regulation for 15 h with 10 microM isoproterenol, a beta adrenergic agonist. After removal of the agonist, recovery of beta-adrenergic-sensitive adenylate cyclase was complete within 2 to 3 days, whereas beta adrenergic receptors reached 90% of control value within 6 days. The half-life of the receptor recovery was 2 to 3 days. Pretreatment of C6 glioma cells by Br-AAM-pindolol and subsequent cell exposure to isoproterenol indicated that down regulation and recovery of unblocked beta adrenergic receptors did occur; however isoproterenol did not accelerate the biosynthesis of beta adrenergic receptors. The recovery of both biological response and beta adrenergic receptor occupancy was restored both in the presence or absence of cycloheximide (1 microgram/ml), a concentration which blocked 90% of protein synthesis. Our results suggest that reappearance of beta adrenergic receptors in C6 glioma cells, following isoproterenol-induced down regulation, was not due to synthesis of new receptors but to recycling of the beta adrenergic receptors.

Cells, Cultured↗
PubMed1984

Turnover of adrenergic receptors under normal and desensitized conditions.

Alpha 1 and beta adrenergic receptor metabolism was investigated by studying receptor reappearance after an irreversible blockade. Phenoxybenzamine was used to irreversibly block alpha 1 adrenergic receptors both in vitro in the BC3H1 cell line and in vivo in rat submaxillary glands. In these two systems, the alpha 1 adrenergic receptor reappearance followed a monoexponential kinetic allowing to determine the half-life of the receptor (23h in vitro, 33h in vivo) as well as the rate of receptor synthesis and degradation. the receptor reappearance was due to receptor synthesis since it was blocked by cycloheximide. The irreversible blockade of beta adrenergic receptors was done with an alkylating beta adrenergic antagonist that we recently developed: Br-pindolol (1). This ligand has high efficiency and blocked at 10(-7)M 80-90% of the beta adrenergic receptors present in C6 glioma cells in culture. After this irreversible blockade, receptors reappeared only during cell division. At confluency, when cells did not significantly divide, receptor synthesis could hardly be detectable. Therefore, at confluency, the metabolic stability of the beta adrenergic receptor is considerable, compared to that of the alpha 1 adrenergic receptor. This stability was confirmed by the observation that after an almost complete "down-regulation" of the beta adrenergic receptor, receptor repopulation of the C6 glioma cells was total and occurred in the presence of cycloheximide.

Animals↗
PubMed1984

[Paget's disease involving the face. Apropos of 4 cases].

This study describes four cases of Paget's deforming dystrophy involving the jaw. In three of them the course of the disease affected only the bone involved whilst in the fourth the bones of the vault of the skull and some cranial nerves were affected in time. The prevalence of the female sex and of involvement of the maxilla was evident. The mandible was involved in only one case. Biochemical abnormalities were the same in all cases as well as being identical to those in cases of Paget's disease with multiple bone involvement. The authors suggest medical treatment (calcitonin, Na etidronate, mitramycin ) and surgery only when required for bone remodelling when there is interference with function.

Aged↗
PubMed1983

Compartmentation of calcium in digitonin-disrupted guinea pig pancreatic acinar cells.

The treatment of guinea pig pancreatic acinar cells with digitonin leads to disruption of the plasma membrane, as judged by the liberation of cytosolic enzymes, without significant alteration of the mitochondrial membrane. The transport of calcium by the particulate residue was studied, and two different pools could be distinguished. One was supported by ATP or ADP, succinate providing the respiratory substrate, and was sensitive to the inhibitors, Ruthenium red and azide. The other pool needed the presence of ATP, ADP being ineffective, and also was unaffected by Ruthenium red or by azide, but was stimulated several-fold by oxalate. The Ruthenium red-sensitive calcium pool has characteristics resembling those of the transport of calcium by a mitochondrial fraction prepared from digitonin-treated acinar cells. In contrast, the Ruthenium red-insensitive calcium transport has characteristics resembling those of a microsomal fraction obtained from guinea pig pancreas. When the transport of calcium in digitonized cells was assayed at a calcium concentration range of 10(-8)-10(-4) M, preferential Ruthenium red-insensitive calcium transport could be observed at submicromolar calcium concentrations.

Animals↗
PubMed1983

Determination of acid surface pH in vivo in rat proximal jejunum.

Surface pH of rat intestine was measured in vivo in exteriorised loops using pH-electrodes. Surface pH was approximately 6.1 in Krebs-phosphate buffer in proximal jejunum and was significantly more acid (p less than 0.01) than the bulk medium pH of 7.2. Values for the midgut were approximately 6.5, yet the distal ileum gave values of 7.3, which was marginally more alkaline than the buffer. These results agree with the known acidification phenomenon in the jejunum and the alkalinisation process in the ileum. No difference in surface pH was detected when bicarbonate buffer was used, nor when glucose was included in the buffer. The acid surface pH was almost completely inhibited when jejunal loops were made anoxic by completely occluding the blood supply, showing that the low surface pH is not itself a consequence of preparative anoxia. If glucose was included in the buffer, allowing glucose access from the luminal surface, surface pH was not significantly altered after occlusion. This indicates that previously reported in vitro results in the presence of glucose are similar to the present in vivo findings. The present experiments confirm the existence in vivo of the 'acid-microclimate' proposed to alter the absorption profiles of some dissociable drugs.

Animals↗
PubMed1983

[Salivary lithiasis as a complication of surgically treated Robin syndrome].

A 15-year-old girl, operated upon (surgical ankyloglossia) at birth for glossoptosis due to Pierre Robin's syndrome provoking respiratory distress, presented with lithiasis of Wharton's duct. The pathogenesis of the lithiasis is considered to be related to the wounds and scars following the sublingual surgery, findings in this case also strongly suggesting the role of mechanical and inflammatory factors in the etiology of salivary gland lithiasis in general.

Adolescent↗