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Biomedical subjects

G Pasvol

Publications and source records attributed to G Pasvol.

At least 91 records · Page 5Linked to original sources
PubMed1984

Pneumonia due to Legionella bozemanii: first report of a case in Europe.

Pneumonia caused by Legionella bozemanii and acquired by a 75-year-old man while on holiday in Majorca is described. This appears to be the first report of such a case from Europe. Despite artificial ventilation and intravenous erythromycin the patient died. The causative organism was isolated from part of the lung obtained post mortem. Examination of a single sample of serum by means of an indirect immunofluorescence test gave a titre of 32 in respect of L. bozemanii antigen.

Aged↗
PubMed1983

Lectin-like polypeptides of P. falciparum bind to red cell sialoglycoproteins.

Attempts to control human malaria by immunological means could be compromised by antigenic variability within and between different strains of malarial parasites1. A useful alternative approach might be to block parasite antigens which are important in the mechanisms of invasion of red cells. As the major human parasite Plasmodium falciparum is highly specific for human red cells, isolation of the proteins involved in the recognition of red cells by this parasite might be of particular value. Recent studies suggest that the major red cell sialoglycoproteins (SGPs), glycophorins A, B and possibly C, may carry the sites recognized by the parasite2-4. Furthermore, because certain carbohydrates present on SGPs such as N-acetylglucosamine are able to block invasion by the parasite5, they may be involved in the initial interaction between parasite and red cell. We have now identified parasite proteins which bind to SGP or N-acetylglucosamine on Sepharose 4B columns. Three proteins, of molecular weights (MWs) 140,000 (140K), 70K and 35K, seem to be specifically bound by N-acetylglucosamine.

Acetylglucosamine↗
PubMed1983

Glycophorins and red cell invasion by Plasmodium falciparum.

The major red cell sialoglycoproteins, the glycophorins, play a central role in the invasion of human red cells by Plasmodium falciparum. En(a-) cells deficient in glycophorin A (alpha) and S-s-U- cells deficient in glycophorin B (delta) are relatively resistant to invasion, while trypsin treatment of S-s-U- cells, which removes most of the remaining sialoglycoprotein, renders these cells almost totally resistant to invasion. Parasites inside these glycophorin-deficient cells develop normally. Invasion of erythroid precursors in vitro by merozoites of P. falciparum parallels the appearance of glycophorins on the surface of these nucleated cells, even though parasites fail to develop inside them. However, another type of cell from an erythroleukaemic line (K562) which expresses glycophorins on its surface is resistant to invasion. Furthermore, the observed increased invasion of young cells as opposed to an older cell population is not related quantitatively to the presence of glycophorins on the cell surface. Thus, although the role of glycophorins is both specific and important in the invasion of cells by P. falciparum, it is clearly only part of a complex process.

Animals↗
PubMed1983

High-dose intravenous acyclovir in the treatment of zoster: a double-blind, placebo-controlled trial.

In a randomised, double-blind, controlled trial, 40 patients with zoster of short duration (rash present for less than three days) were given either 10 mg/kg acyclovir (20) or placebo (20) intravenously three times daily for five days. Pain was reduced in the treatment group both in the acute phase and at follow-up, when compared with the placebo group, but this difference did not reach statistically significant levels. Healing of the lesions was also better, but not significantly so, in the acyclovir group. No complications of the disease were seen in the six cases of ophthalmic zoster given acyclovir whereas, of the four cases in the placebo group, two developed seventh cranial nerve palsies and one secondary glaucoma. No evidence of renal or other major toxicity was detected in the acyclovir group, although three patients developed mild thrombophlebitis. We conclude that acyclovir, given by the route and in the dose and frequency as used in this study, is free from major side effects, but is only of marginal benefit in the treatment of zoster.

Acyclovir↗
PubMed1983

A lectin-like receptor is involved in invasion of erythrocytes by Plasmodium falciparum.

Glycophorin both in solution and inserted into liposomes blocks invasion of erythrocytes by the malaria parasite Plasmodium falciparum. Furthermore, one sugar, N-acetyl-D-glucosamine (GlcNAc), completely blocks invasion of the erythrocyte by this parasite. GlcNAc coupled to bovine serum albumin to prevent the sugar entering infected erythrocytes was at least 100,000 times more effective than GlcNAc alone. Bovine serum albumin coupled to lactose or bovine serum albumin alone had no effect on invasion. These results suggest that the binding of P. falciparum to erythrocytes is lectin-like and is determined by carbohydrates on glycophorin.

Animals↗
PubMed1982

Glycophorin as a possible receptor for Plasmodium falciparum.

Human red cells deficient in glycophorin B are partly resistant to invasion by Plasmodium falciparum and become completely resistant when glycophorin A is removed from their surface by trypsin treatment. Similar treatment of cells which have a hybrid glycophorin molecule renders them glycophorin-deficient and resistant to invasion. Tn and Wrb -ve cells with defined alterations in glycophorin A or B are also resistant to invasion. These findings suggest that both glycophorins A and B are involved in parasite invasion, indicate which parts of these molecules may be involved in this process, and provide the basis for a tentative model of parasite/red-cell interactions.

Blood Group Antigens↗
PubMed1980

The interaction between sickle haemoglobin and the malarial parasite Plasmodium falciparum.

The mechanism whereby heterozygous carriers of the sickle cell gene are protected against fatal malarial infections due to Plasmodium falciparum has been examined in a short term in vitro cultivation system. The results have shown that both parasite invasion of red cells and parasite growth within red cells containing sickle haemoglobin (Hb-S) is restricted, but only under conditions of low (5%) oxygen tensions. To bring this about, the cells containing Hb-S need not sickle. Furthermore the growth retardation observed in the presence of Hb-S was also found to apply to the mature forms of the parasite. These findings offer a plausible mechanism for the protection of sickle heterozygotes against falciparum malaria.

Adult↗
PubMed1980

The increased susceptibility of young red cells to invasion by the malarial parasite Plasmodium falciparum.

The relationship between red cell age and susceptibility to invasion by the malarial parasite Plasmodium falciparum has been examined by several different methods including short-term cultures of parasitized human blood. The results indicate that reticulocytes and young red cells are more susceptible to invasion by this parasite as compared with metabolically older cell populations. This is contrary to the current belief that red cells of all ages are invaded indiscriminately by P. falciparum. This observation has important theoretical, clinical and practical implications; its mechanism remains as yet unclear.

Age Factors↗
PubMed1978

Differentiation of gametocytes in microcultures of human blood infected with Plasmodium falciparum.

Gametocytes differentiated from ring-stage parasites in microcultures of human blood infected with Plasmodium falciparum. Immature gametocytes could be distinguished morphologically from late asexual trophozoites after approximately 40 h of culture. Differentiation into crescentic forms took several days and the incorporation of [3H]-isoleucine by developing gametocytes was demonstrated. About 1% of red cells contained gametocytes at the maxiumum densities attained. Differentiation of gametocytes occurred either directly from rings placed in culture or from the progeny of subsequent cycles of schizogony and invasiton in vitro. The latter occurrence was confirmed by the development of gametocytes in marker fetal red cells added to cultures, although fetal red cells provide a less favorable environment than those with HbA for growth of the parasites.

Erythrocytes↗
PubMed1977

Invasion and growth of Plasmodium falciparum in different types of human erythrocyte.

The susceptibility of human red blood cells to invasion by Plasmodium falciparum was investigated in microtissue cultures with different populations of erythrocytes containing fetal haemoglobin (HbF). Preferential invasion of HbF-containing erythrocytes was observed with umbilical cord blood. The parasites showed no preference for HbF cells in blood from a subject with hereditary persistence of fetal haemoglobin (HPFH). By contrast, a significant preference for HbA-containing erythrocytes was found with blood from young infants. Further experiments demonstrated that falciparum parasites preferentially invade "young" erythrocytes. This could explain the distribution of parasites found in blood containing HbF, because HbF-containing erythrocytes are "younger" on average in cord blood, "older" in the blood of infants, and of the same average age as HbA-containing cells in HPFH. We concluded that the susceptibility of human erythrocytes to invasion by P. falciparum is not correlated with the presence of HbF, but that aging of red cells in vivo decreases their susceptibility to invasion. Semi-quantitative measurements were made of parasite growth in cells containing HbA or HbF. The growth of individual parasites in cells containing HbF was significantly retarded. This might confer a selective advantage on individuals with thalassaemia and sickle cell trait, in which HbF levels are raised in early life.

Animals↗
PubMed1976

Fetal haemoglobin and malaria.

The distribution and growth of Plasmodium falciparum was compared in red blood-cells containing either adult or fetal haemoglobins. In in-vitro cultures, cord blood-cells were invaded more readily, but there was a paucity of parasites in cells containing haemoglobin F in the blood of infected infants aged 3-6 months. These findings suggest that P. falciparum may preferentially invade young, metabolically active erythrocytes. There was a significant retardation of parasite growth in vitro in cells containing haemoglobin F. This latter finding suggests a further mechanism for the resistance to malaria in the first months of life and for high gene frequencies (in areas in which malaria was endemic) of the thalassaemias and related haemoglobinopathies in which the rate of decline of fetal-haemoglobin production is retarded.

Adult↗