Biomedical subjects

J Lecomte

Publications and source records attributed to J Lecomte.

At least 127 records · Page 7Linked to original sources

PubMed1984

Blocking of influenza virus-induced cell-mediated cytotoxicity by hemagglutinin-specific monoclonal antibody.

The relative importance of three major proteins of influenza virus in the mechanism of induction of cell-mediated cytotoxicity (natural killer cell activity) was assessed by an overnight chromium-51-release assay using radiolabeled K-562 cells as target cells and Ficoll-Hypaque-purified peripheral-blood lymphocytes as effector cells. Incubation of peripheral-blood lymphocytes with influenza virus (whether type-A or type-B) showed that intact and formalin-inactivated influenza virus enhanced cell-mediated cytotoxicity equally. The stimulation by intact or inactivated virions was comparable to that induced by the two major internal mediators of positive natural killer cell regulation, namely interferon and interleukin-2. This virus-induced cell-mediated cytotoxicity, which was mediated by human natural-killer 1+ cells, could be blocked only with monoclonal antibodies to the hemagglutinin and not with antinucleoprotein or antimatrix protein monoclonal antibodies, results indicating that the hemagglutinin of influenza virus is a potent mediator of natural killer cell stimulation in vitro.

Antibodies, Monoclonal↗

PubMed1984

[Dopamine and the chemoregulation of ventilation in the rat].

In pentobarbitalized rats, exogenous dopamine inhibits ventilation by acting on peripheral chemoreceptors. This inhibition is suppressed by haloperidol and by domperidone. Almitrine bismesilate, a potent glomic stimulant, potentiates dopaminergic inhibitory responses by depletion of dopamine endogenous stores. After blockade by dopamine antagonists, as well as after dopamine depletion, ventilatory responses to NaCN i.v. is increased. This potentiation can be explained by the suppression of a negative feed-back control dependent on endogenous dopamine release during the glomic stimulation itself.

Almitrine↗

PubMed1984

Studies of the antigenic variation in poliovirus type 1. Selection and analysis of variant strains with monoclonal antibodies by neutralization.

Nine neutralizing monoclonal antibodies were used in a preliminary study of the antigenic variation of poliovirus type 1. Six antigenic variants were selected and five distinct epitopes involved in neutralization were identified. Four of these epitopes are thought to be clustered within a single antigenic site. In kinetic studies, the neutralization of poliovirus by monoclonal antibodies was shown to be a single hit process.

Animals↗

PubMed1984

Typing of herpes simplex virus isolates with selected monoclonal antibodies.

On the basis of their reactivity with a large panel of clinical isolates of herpes simplex viruses, three monoclonal antibodies were selected as serotyping reagents. By indirect immunofluorescence, the type 1 specific (6D4) and the group specific (1B5) reacted with a cytoplasmic antigen while the type 2 specific (G3) reacted with a nuclear antigen. These three monoclonal antibodies have not failed so far in identifying and typing 257 culture isolates. For rapid serotyping by immunofluorescence, all antibodies gave unambiguous results on 95 additional isolates tested as soon as cytopathic effect appeared after inoculation on primary monkey kidney cells.

Animals↗

PubMed1984

[The concept of mediators in acute inflammatory reactions].

The evolution of ideas about inflammation oscillates between two poles: sometimes the cell aspects of inflammation are described, with leucocyte adhesion to the vessel wall followed by migration into the tissues and phagocytosis - at other times it is the turn of the chemical intermediaries accounting for the damage to blood vessels, in which case vasodilatation, permeability and chemotaxis are given particular emphasis. The present tendency is to concentrate on the origin of these intermediaries and their relationship to the different cell populations found in situ. Before defining the relationship between cells and acute inflammatory mediators, an inventory needs to be drawn up of the latter. They can be divided into three main categories, according to the manner of their involvement at the site of inflammation: preformed agents, which are then released; mediators formed as a result of enzyme influences, cell-derived or not, from inactive precursors; the enzymes themselves which attack the structures involved in the lesion. These various mediators are thus traceable to specific mechanisms of formation or release, from cell populations that are now clearly identified. From an understanding of how the inflammatory focus has been colonised by the different leucocyte populations and a knowledge of their enzymatic potential, conclusions can be drawn not only about the mediators concerned but more especially about the pharmacological agents that must be mobilised in order to neutralise their clinically apparent effects.

Acute Disease↗

PubMed1984

[Circulating vasopressin (ADH) during immersion of short duration].

During immersion in sitting position to the neck of 9 normal adult males, no change has been observed in the concentration of circulating ADH (1.91 +/- 0.58 versus 2.08 +/- 0.76 pg.ml-1) after 45 minutes. In the same period, diuresis is significantly increased (1.26 +/- 0.14 versus 3.9 +/- 1.19 ml.min-1).

Adult↗

PubMed1984

[Natriuria during immersion of brief duration].

During immersion in sitting position to the neck of 10 normal adult males, natriuria is significantly increased even after pretreatment with captopril (2 mg X kg-1, p.o.). Inhibition of the renin-angiotensin-aldosterone cascade does not completely block the mechanisms causing natriuria during immersion.

Adult↗

PubMed1983

Mast-cell heterogeneity in the rat.

In the rat, O-hydroxy ethyl rutoside derivatives release histamine and serotonin from skin mast-cells, but not from peritoneal mast-cells. These cellular populations do not exhibit identical pharmacological properties.

Animals↗

PubMed1983