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Biomedical subjects

C Boyer

Publications and source records attributed to C Boyer.

At least 19 recordsLinked to original sources
PubMed1992

Role of CD3 delta in surface expression of the TCR/CD3 complex and in activation for killing analyzed with a CD3 delta-negative cytotoxic T lymphocyte variant.

The TCR is composed of two chains (alpha/beta) containing variable regions associated at the cell surface with invariant chains (CD3 gamma-, delta-, epsilon-, and zeta/eta chains). The latter control assembly and surface expression of the TCR/CD3 complex, as well as its cytoplasmic association with signal transduction relays. In differentiated CTL, stimulation through the TCR leads to the transcriptional activation of genes coding secreted cytokines such as gamma-IFN as well as transcription-independent activation of the lytic machinery. It is not known which of the CD3 components is necessary to transduce the required signals. CD3 gamma- and delta-chains have high sequence homology, in particular in their cytoplasmic domain, and it has been proposed that alpha beta gamma epsilon zeta and alpha beta delta, epsilon zeta may be expressed and function in signal transduction independently. Here, we characterize a CTL clone that has selectively lost expression of the CD3 delta mRNA. This results in expression of partial CD3 complexes devoid of TCR alpha beta chains at the surface of the clone, which are not functional for activation of cytolysis or for gamma-IFN production. Transfection of the clone with either the native or a cytoplasmic exon-deleted CD3 delta gene restores full TCR/CD3 surface expression as well as Ag- or CD3-mediated activation for killing and for gamma-IFN production, indicating that the CD3 delta chain is essential for surface expression of the TCR alpha beta, but that the CD3 delta cytoplasmic portion is not required either for complex assembly or for signal transduction involved in the functions studied.

Amino Acid Sequence↗
PubMed1992

Delineation of immunoreactive, conserved regions in the external glycoprotein of the human immunodeficiency virus type 1.

Immunization of mice and rats with purified external glycoprotein gp120 from two divergent human immunodeficiency virus type 1 (HIV-1) isolates resulted in the development of seven hybridomas secreting monoclonal antibodies able to recognize regions of gp120 which are common among divergent strains of HIV-1. These monoclonal antibodies cross-reacted with env glycoproteins from one African (Rutz), one Haitian (RF), and three North American viral isolates, namely IIIB, MN, and 451 by either immunoblot or radioimmunoprecipitation assays. All recognized denatured gp120 in immunoblots with the exception of one which required a conformationally intact glycoprotein for reactivity. The gp120 epitopes identified by these antibodies were mapped by screening of an env gene library in the lambda gt11 expression system. Three out of four epitopes were found to reside in the amino-terminal half of gp120 (Cys9 to Cys35, Thr44 to Glu72 and Val108 to Met130), the other was located in the middle region (Thr221 to Ser255). By virtue of their extent of cross-reactivity these reagents might provide a unique resource for the detection of new viral isolates related to HIV-1.

Amino Acid Sequence↗
PubMed1991

T cell receptor/CD3 complex internalization following activation of a cytolytic T cell clone: evidence for a protein kinase C-independent staurosporine-sensitive step.

The fate of the T cell receptor (TcR)/CD3 complex was examined on a cytotoxic T lymphocyte (CTL) clone (KB5.C20) activated either via binding of an anti-TcR monoclonal antibody (mAb) or by a Ca2+ ionophore and phorbol 12-myristate 13-acetate (PMA). After binding of the anti-TcR mAb, electron microscopy revealed internalization through coated vesicles followed by slow degradation of the antibody as shown by use of radiolabeled mAb. The influence of activation on TcR/CD3 internalization was analyzed. The Ca2+ ionophore alone had no effect on internalization, whereas PMA induced an accelerated internalization of anti-TcR mAb. PMA-induced internalization was dependent on protein kinase C (PKC) as shown by its absence in PKC-depleted cells or in the presence of the PKC inhibitor staurosporine. Anti-TcR mAb-induced internalization was maintained in PKC-depleted cells, but unexpectedly remained sensitive to inhibition by staurosporine. The monovalent anti-TcR mAb Fab fragment is non-stimulatory for the CTL. It was poorly internalized but its internalization was induced by PMA. Surprisingly, on PKC-depleted cells, the Fab was internalized more readily than in untreated cells and this internalization was sensitive to inhibition by staurosporine. Inhibition of PMA-induced phosphorylation of gamma and epsilon subunits of CD3 was demonstrated after depletion of PKC or in the presence of staurosporine, confirming that PKC function was inhibited in those conditions. Cross-linking of the TcR via plastic-coated anti-TcR mAb led to phosphorylation of CD3 gamma and epsilon and also of zeta, known to be phosphorylated on tyrosines. All of these phosphorylation events were inhibited by treatment with staurosporine. Our results indicate that staurosporine inhibits the receptor internalization induced by anti-TcR mAb by means other than inhibition of PKC, suggesting that other kinases may control a step of this internalization process.

Alkaloids↗
PubMed1991

Biochemical and functional association between CD8 and H-2 at the surface of a T cell clone.

In an attempt to define structures interacting with CD8 molecules during activation of CD8+ cells, immunoprecipitates of CD8 and Tcr-CD3 molecules from lysates of a surface-labeled CTL clone were analyzed. No proteins other than the known Tcr alpha/beta and associated CD3 components were detected in either anti-Tcr or anti-CD3 immunoprecipitates, whether or not the CTL clone had been activated. However, anti-CD8 antibodies co-precipitated class I MHC heavy chain and associated beta 2-microglobulin in all conditions. The latter co-precipitation was shown to result from "cis-type" interactions between CD8 and class I MHC proteins on the same cell and to involve a degree of selectivity, as class I MHC molecules were absent from immunoprecipitates of highly expressed cell surface molecules such as LFA-1. A further analysis of cell surface molecular distribution during antigen-dependent CTL-target cell interaction by double fluorescence-microscopy in non-activating conditions indicated that an increased density of CTL class I molecules was found in the CTL-target cell contact zone of most conjugates with redistributed CD8 molecules. A possible role for "cis-type" class I MHC-CD8 interactions in the dynamics of CTL-target cell contacts is proposed.

Animals↗
PubMed1991

Wild type and tailless CD8 display similar interaction with microfilaments during capping.

We examined the influence of the intracytoplasmic region of CD8 alpha on capping and interaction with microfilaments. We used cell clones obtained by transfecting a CD4+ T-cell hybridoma with (a) T-cell receptor (TCR) alpha and beta chains from a cytolytic clone and (b) CD8 alpha genes that were either native or modified by extensive deletion of the intracytoplasmic region or replacement of the transmembrane and intracytoplasmic domains with those of a class I major histocompatibility complex gene (Letourneur et al. (1990). Proc. natn. Acad. Sci. U.S.A. 87, 2339-2343). Different cell surface structures were cross-linked with anti-T-cell receptor, anti-CD8 or anti-class I monoclonal antibodies and anti-immunoglobulin (Fab')2. Double labeling and quantitative image analysis were combined to monitor fluorescence anisotropy and correlation between different markers. Microfilaments displayed maximal polarization within two minutes. The correlation between these structures and surface markers was then maximal and started decreasing, whereas the redistribution of surface markers remained stable or continued. Furthermore, wild type and altered CD8 alpha exhibited similar ability to be capped and to induce co-capping of TCR and MHC (major histocompatibility complex) class I: the fraction of cell surface label redistributed into a localized cap ranged between 40% and 80%. Finally, cytochalasin D dramatically decreased CD8 capping in all tested clones. It is concluded that the transmembrane and/or intracellular domains of CD8 molecules are able to drive the extensive redistributions of membrane structures and cytoskeletal elements that are triggered by CD8 cross-linking.

Actin Cytoskeleton↗
PubMed1979

Long-term results of permanent atrioventricular sequential demand pacing.

Pervenous atrioventricular sequential demand pacemakers (AVSDPs) were implanted in 18 patients using an atrial electrode positioned in the right atrial appendage and a ventricular electrode positioned at the apex of the right ventricle. The indications included 13 patients with the sick sinus syndrome (72%), five of whom had the tachycardia-bradycardia syndrome, three with paroxysmal supraventricular tachycardia, one with cardiomyopathy and one with carotid sinus syncope. The follow-up ranged from 6 to 38 months, with a mean of 19.4 months (a total of 350 pacing months). Seventeen patients (94%) are asymptomatic. One patient had persistent episodes of paroxysmal supraventricular tachycardia. In the remaining patients with tachyarrhythmia, pacing alone (three patients) or in combination with antiarrhythmic drugs (four patients) controlled the tachyarrhythmia. There was one displacement of the atrial electrode (5.5%). Extrusion of the pacer occurred in three patients. It is concluded from this experience that AV sequential pacing is an effective technique and may be useful in patients with sick sinus syndrome, in patients with tachyarrhythmia and/or patients with poor myocardial function. However, continued research is needed to prolong battery life and to reduce the size of the pacemaker.

Aged↗
PubMed1977

Haemostatic disorders and respiratory distress in the newborn.

Coagulation and fibrinolysis studies were performed on 64 newborns; 16 premature infants with hyaline membrane disease (HMD), 17 newborns with other forms of respiratory distress syndrome (RDS) (8 of them were premature), 31 healthy newborns (11 of them were premature). All the babies were studied once in the first 48 hours of life. There was no significant difference between sick and healthy babies for 5 parameters; platelet count, factor VIII, fibrinogen, fibrin(ogen) degradation products, euglobulin lysis time. Factor II, VII and X were low in all infants, and premature infants had significantly lower levels compared to full term newborns. Factor V, plasminogen, alpha 2 macroglobulin (alpha 2M) and antithrombin III (AT III) levels were significantly lower in sick infants. Except for AT III, these deficiencies were not related to prematurity. No significant difference was found between HMD and other RDS. Of the 33 sick infants, 5 developed laboratory findings consistent with disseminated intravascular coagulation (DIC). The results indicate that the coagulation and fibrinolytic abnormalities reported are not specific to HMD.

Antithrombins↗
PubMed1977

Immunologic study of the age-related loss of activity of six enzymes in the red cells from newborn infants and adults--evidence for a fetal type of erythrocyte phosphofructokinase.

Blood from 10 normal healthy adults and cord blood from 8 healthy full term infants were infiltrated through a mixture sulfoethylethycellulose-Sephadex G 25 in order to eliminate the platelets and the leukocytes. Then the erythrocytes were fractionated into young and old cells by centrifugation in microhematocrit tubes. The enzyme activity and the immunologic reactivity of glucose phosphate isomerase (EC.5.3.1.9), phosphoglycerate kinase (EC.2.7.2.3), pyruvate kinase (ec.2.7.1.40), glucose 6-phosphate dehydrogenase (EC. 1.1.1.49), and 6-phosphogluconate dehydrogenase (EC.1.1.1.44) were measured in every fraction. As previously reported, the enzyme activities were far higher in cord blood than in adult blood red cells; nevertheless, the age-related loss of enzyme activity was similar in both cord and adult blood. The decrease of the enzyme activity of glucose phosphate isomerase and phosphoglycerate kinase in old cells was singly associated with a lowered concentration of the enzyme-related antigen; by contrast, the age-related decrease of the enzyme activity of pyruvate kinase, glucose-6-phosphate dehydrogenase, and 6-phosphogluconate dehydrogenase was associated with both a lowered concentration of the enzyme-related antigen and a lowered "molecular specific activity" (i.e., a lowered ratio of enzyme activity to enzyme-related antigen concentration). This phenomenon was especially marked for pyruvate kinase, which had a molecular specific activity in old cells that was 68% of that in young cells. Phosphofructokinase had a lower enzyme activity in cord blood erythrocytes than in adult blood erythrocytes; the difference was especially important in old cells from infants in which phosphofructokinase activity was 53% of that in old cells from adults. Phosphofructokinase from old cells of full term infants and from unfractionated cells from two premature infants (21 and 32 weeks of gestation) was less neutralized by anti-muscle phosphofructokinase serum and more inhibited by ATP than the enzyme from adult blood erythrocytes.

Adenosine Triphosphate↗
PubMed1976

Causal mechanisms of multiple acquired red cell enzyme defects in a patient with acquired dyserythropoiesis.

A patient with an unclassified form of acquired dyserythropoiesis was found to have multiple defects in erythrocyte enzyme activity, involving especially pyruvate kinase (PK), glucose phosphate isomerase (GPI), and phosphofructokinase (PFK). The PK activity defect was associated with a normal concentration of PK-related antigen, and the enzyme could be reactivated during the procedure of partial purification of the enzyme. The concentration of GPI-related antigen was as reduced as the GPI enzymatic activity, and the defect was not improved by any treatment (cross-incubation of red cells or treatment of the hemolysate by SH reagents); the residual enzyme had a normal stability to heat, and a normal electrophoretic and electrofocusing pattern. The PFK activity defect was not improved either by cross-incubation of red cells or by treatment with SH reagents. Immunologic data with antimuscle and antileukocyte antisera seemed to indicate that the defect involved especially the muscle-type subunit of erythrocyte PFK. In agreement with this assumption was the fact that deficient PFK was markedly more inhibited by ATP than normal enzyme. Changes similar to those of deficient PFK herein studied were noted for PFK of unfractionated erythrocytes from premature newborns or of "old" erythrocytes from full-term infants. It appeared that each of the three enzyme defects detected in the patient could be due to a different mechanism, involving post-translational changes, decreased synthesis, and possible reversion of the genetic regulation mechanisms of the abnormal erythroid precursors toward a fetal type. The possible relationships between these various phenomena and the nature of a hypothetical common underlying cause are discussed.

Anemia, Hemolytic, Congenital Nonspherocytic↗
PubMed1976

[Atrioventricular "sequential" stimulation by implantable "bifocal" stimulator].

The "bifocal pacemaker achieves a sequential" stimulation which reproduces the physiological atrio-ventricular sequence. This type of stimulation has the advantages of atrial stimulation without the disadvantages of being inefficient when an atrio-ventricular block exists or supervenes. The pacemaker was used by the endocavity route in 12 patients. The indications included a disease of the sinus node (8 cases), supra-ventricular arrhythmias associated to conduction disorders (3 cases) and a cardiomyopathy with conduction disorders (1 case). The preliminary results were appraised after two to twenty four months. One displacement of the ventricular electrode was noted. On the other hand no displacement of the atrial electrode was reported. One battery was worn out after 19 months. The "bifocal" pacemaker was efficient in the treatment of symptoms which justified its implantation. Or particular interest were the results obtained in patients with no supraventricular arrhythmias. This pacemaker may be of use: 1) in the disease of the sinus node, in particular in the tachycardia-bradycardia syndrome; 2) in supraventricular arrhythmias associated to paroxystic conduction disorders; 3)in patients with an alteration of the myocardial function and for whom the atrial contribution to cardiac output is essential.

Aged↗
PubMedDate not supplied

[Favorable course of a bilateral postoperative diaphragmatic paralysis].

Writing about a case of post-operative diaphragmatic bilateral palsy (bilateral thoracotomies for oesocoloplasty and oesophagectomy necessited by a caustic oesophagitis) on a 8 years old boy, palsy which was cured 6 months after, the authors tell about causes, prognostic and treatment of diaphragmatic palsies. In that observation, treatment consisted essentially in artificial ventilation for months and a half, and on intensive kinesitherapy.

Abdomen↗
PubMedDate not supplied

[When the leg is the victim of the foot].

Man (homo-erectus, plantigrade) is in constant contact with the ground via his feet which are platforms on which the legs and, above all, the entire body rest. When the body moves, the only segment which remains stable and fixed is the foot, which forms the point of departure of all the muscular actions of this moving body. The slightest deformity of this platform, this foot, will lead to skeletal, musculotendinous and neurovascular problems in the legs, and to pain. Pain due to skeletal problems may be related to fatigue fractures (tibia, fibula) and to posterior tibial periostitis. Pain may also be due to musculotendinous problems which are characterised by a muscle bed syndrome (anterolateral, posterior) or tensosynovitis. Neurovascular problems are typified by a tarsal sinus syndrome, a musculocutaneous nerve syndrome and dysfunction of Lejears' sole during filling in flat feet and during emptying in hollow feet.

Foot Diseases↗