Acute pyelonephritis in children. Preliminary results obtained with NMR imaging.
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Biomedical subjects
Publications and source records attributed to J Bamberger.
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An acute, transient aplastic crisis in a 15-month old boy revealed the presence of homozygous beta-thalassaemia. The crisis was very likely due to a parvovirus infection, in view of the presence of specific IgM at the onset and of seroconversion to total antibodies. Later, requirements for transfusions were in favour of an intermediate type thalassaemia. The responsibility of the parvovirus is discussed in the light of recent data concerning the inhibitory action of this virus on bone marrow erythropoiesis.
Maternal toxoplasma infection was responsible for congenital toxoplasmosis with ocular and cerebral manifestations in the infant. The acquired character of the toxoplasmosis in the 5th month of pregnancy was confirmed by serologic data and isolation of the parasite from the placenta. Five years later, an evolutive chorioretinitis was found in the mother. The toxoplasma origin of the ocular injury was proven by the study of aqueous humor. This case report is compared with the rare similar cases in the literature. The late discovery of ocular impairment is discussed.
Glycopeptide and oligosaccharide fractions obtained from fucosidosis urine contains more Lea activity (4-8 fold) than control urine. Both fucosidosis fractions also contained Leb and H activities, no A activity in contrast to the salivary and erythrocyte phenotypes (A, Le a+ b-). The amount of Leb activity is lower in both fractions (1) and (2) than that of Leb control children (4-16 fold decrease). Blood group A activity was not detected at any concentration used (less than or equal to 50 fold-concentrated urine) whereas A activity was found in (A, Le a- b+) control urine. On the contrary, both fucosidosis fractions contained H activity, whereas A (Le a- b+) control children fractions had none (less than or equal to 50-fold concentrated urine). H and Leb activity might originate from Lea precursor apart from the "non-secretory" type of the patient.
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A pregnancy from a family at risk for fucosidosis was monitored. Determinations of fucosidase and mannosidase were performed on the serum and white blood cells of several members of the family, om amniotic fluid and amniotic fluid cells of the fetus at several passages, and on fibroblast cell lines from index cases. The fetus was diagnosed as being free from the disease. This conclusion was confirmed after birth by fucosidase determination in plasma and white cells from cord blood, and in the placenta. Fluctuations in fucosidase activity were observed in extracts from cultured amniotic cells at various passages. The possible causes of this variability are discussed.
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