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F Daffos

Publications and source records attributed to F Daffos.

133 records · Page 8Linked to original sources
PubMedDate not supplied

A unique T-cell receptor complex expressed on human fetal lymphocytes displaying natural-killer-like activity.

We have recently derived a series of cloned cell lines displaying natural killer (NK) cell-like activity from normal human fetal blood (25 weeks). The lines were obtained after repeated stimulation of mononuclear cells with allogeneic Epstein-Barr virus (EBV)-transformed B lymphocytes and are interleukin-2 (IL-2) dependent. Initial characterization of the clones has been reported previously. Certain of these clones have been found to have unusual surface characteristics, namely, they are recognized by several well-defined anti-T3 antibodies, but do not react with WT31, which is thought to recognise an invariant epitope of the human (Ti-alpha beta) structure. Transcription of the genes encoding the alpha- and beta-chains of the T-cell receptor was assessed in two of these clones (F6A4 and F6C7). Ti-beta genes were found to be expressed, whereas alpha messenger RNA was not detected in Northern blot analysis. These data strongly suggest that these cells do not produce a stoichiometric T3/Ti-alpha beta receptor complex. However, experiments performed with a monoclonal antibody (anti-NKFi) developed against F6C7 cells demonstrated the existence of a unique clonotypic structure [relative molecular mass (Mr) 85,000 (85K)] which is surface-associated with T3 proteins. Furthermore, both anti-T3 and anti-NKFi were found to block cytotoxic effector function. Together, the results support the view that T3 proteins are involved in non-major histocompatibility complex (MHC)-restricted cytotoxic reactions mediated by certain circulating fetal lymphocytes which are likely to use a clonotypic structure distinct from both the 'first' (alpha beta) and the putative 'second' (gamma delta) T-cell receptor to recognize their target. The present studies were designed to characterize this structure.

Antibodies, Monoclonal↗
PubMedDate not supplied

In utero treatment of toxoplasmic fetopathy with the combination pyrimethamine-sulfadiazine.

The mothers of 52 fetuses with toxoplasma fetopathy diagnosed in utero were treated with a combination pyrimethamine-sulfa drug and spiramycine. Their infants were compared to a group of 51 infants whose mothers had received spiramycine alone. Postnatal treatment was identical in both groups. Parasitological investigation of the placenta was positive in 42 and 76.6%; the newborns had a specific IgM of 17.4 and 69% in groups 1 and 2, respectively. These differences were significant. The mean specific IgG titer was significantly reduced at birth and at 4-6 months of age in group 1. According to the results obtained in the present material the pyrimethamine-sufa drug combination, given to the mothers of fetuses infected with toxoplasma, has a significant effect on the parasitological and serological signs of evolutive fetopathy. It did not significantly alter the clinical pattern, probably because the onset of treatment was too long after maternal infection.

Antibodies, Protozoan↗
PubMedDate not supplied

Direct fetal blood examination for prenatal diagnosis of homozygous familial hypercholesterolemia.

Prenatal diagnosis of homozygous hypercholesterolemia was achieved at the 24th week of gestation by analysis of lipid values in a fetal blood sample obtained by a needle guided by ultrasound. These abnormal values were compared to values in blood obtained from normal fetuses at the same stage of gestation. After abortion, the diagnosis was confirmed by measuring LDL receptor activity on fibroblast cultures from a skin biopsy. The main advantages of this procedure over measuring LDL receptor activity on cultured amniotic cells are its simplicity and speed.

Adult↗
PubMedDate not supplied

[Fetal toxoplasmosis. In utero treatment with pyrimethamine sulfamides].

The mothers of 52 cases of toxoplasmic fetopathy diagnosed in utero by fetal blood and/or amniotic fluid sampling were treated with the combination pyrimethamine-sulfadiazine (or sulfisoxazole) and by spiramycine. The infants were compared with 51 other infants with congenital toxoplasmosis whose mothers had received spiramycine alone. Patients of both groups received the same pyrimethamine-sulfadiazine and spiramycine treatment after birth. Parasitologic examination of the placenta was positive in 42 and 76.6% of patients, in group I and group II respectively. The newborns had specific IgM in 17.4 and 69.2% of cases respectively in both groups. These differences were significant. The mean specific IgG titer was significantly reduced at birth and 4 to 6 months of age in the first group. Patients in group I had more often subclinical infection than patients of the comparison group: 57% vs 33.3%. They had less often a high cerebro-spinal protein content during the first week. Prenatal treatment with pyrimethamine-sulfadrugs resulted in a less progressing infection at birth. However in cases with clinically patent toxoplasmosis, the frequency of overt localizations and their sequellae was not significantly altered. This might be related to a relatively late onset of the treatment. The pyrimethamine-sulfadrug combination given to mothers of proved infected fetuses can be rewarding. The indication might be extended to well-documented seroconverted mothers if, in the future, the acquired experience and necessary pharmacological studies bring the proof of its innocuousness.

Drug Therapy, Combination↗
PubMedDate not supplied

[Fetomaternal therapeutic follow-up of spiramycin during pregnancy].

In the preventive treatment of congenital toxoplasmosis it is admitted that spiramycin is concentrated in the placenta and crosses the placental barrier at the end of pregnancy. However, little is known about its entry in the fetal circulation. We studied fetal spiramycin blood levels during the 2nd and 3rd trimesters of pregnancy in women who, having presented with toxoplasmosis during the 1st trimester, had been given spiramycin until delivery. Microbiological titrations of spiramycin were performed--in the maternal blood at the onset of treatment, at the time of fetal blood sampling and during delivery), in the fetal blood at the time of prenatal diagnosis of toxoplasmosis, in cord blood and placenta at birth. We were able to confirm transplacental crossing of spiramycin. Fetal blood levels during the 2nd trimester were about 47% of the maternal ones and there was no correlation between maternal and fetal levels. Levels at birth showed that (1) there was no accumulation in the course of treatment, (2) spiramycin was concentrated in placenta and (3) there was a correlation between fetal and maternal levels during the 3rd trimester.

Female↗