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Biomedical subjects

E Petersen

Publications and source records attributed to E Petersen.

At least 19 recordsLinked to original sources
PubMed1992

Capture ELISA for IgM antibodies against Plasmodium falciparum glutamate rich protein.

This report describes a novel mu chain capture ELISA for the detection of IgM antibodies against a Plasmodium falciparum antigen. A fragment of the 220 kDa P. falciparum glutamate rich protein containing amino acid residues 489-1271 was expressed in E. coli as a recombinant chimeric beta-galactosidase fusion protein and used as antigen after purification and biotinylation. Specific IgM antibodies were found in 51% (39/77) of sera from adult Liberians immune to malaria. The binding of IgM antibodies was specific for the malaria portion of the fusion protein and no cross-reactivity was found in sera from patients with IgM antibodies due to other diseases. Inhibition studies with a fusion protein containing amino acid residues 816-1134 (GLURP816-1134) representing the carboxy-terminal repeat region suggested a different use of epitopes for IgM antibodies in different individuals.

Animals↗
PubMed1992

[Parasitic diseases in patients with impaired immune response. Clinical picture and diagnosis].

Patients with impaired immune system are frequently infected with various parasitic diseases. The clinical picture is characterized by unusual manifestations and frequently severe recurrences of infections which are not normally serious. Some almost parasitic microorganisms produce symptoms exclusively in patients with impaired immune system. Parasitic infections have become increasingly common with the increasing number of patients who live for prolonged periods with impaired immune systems, often as a result of infection with HIV. Among the numerous parasitic infections which are observed in man, there are a few which occur particularly frequently in patients with impaired immune systems. This is a brief review of the clinical pictures and diagnostic options in parasitic disease in individuals with impaired immune system with particular emphasis on infections caused by: Pneumocystis carinii, Toxoplasma gondii, Cryptosporidium ssp., Microspora, Entamoeba histolytica, Leishmania ssp., and Strongyloides stercoralis. In patients with impaired immunity, parasitic infections frequently cause nonspecific symptoms and, on account of the impaired immunity, antibodies to the parasite are not always produced. The diagnosis of these infections is, therefore, based on morphological demonstration of the microorganism concerned, culture, specific antigen or DNA defections.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Transient expression of recombinant glycoprotein Ib alpha polypeptides in COS cells that inhibit von Willebrand factor binding to the platelet glycoprotein Ib/IX complex.

The cDNA encoding the glycoprotein Ib alpha polypeptide has been expressed in COS cells. Transfection with full-length cDNA and a cDNA truncated at an internal XbaI site produced a recombinant polypeptide doublet with estimated molecular weights of 48 and 46 kDa (rGpIb alpha L318) which could be resolved into a single band of molecular weight 36 kDa following digestion with endoglycosidase F. A portion of the truncated polypeptide was retained in the endoplasmic reticulum of COS cells and slowly released. A second fraction was rapidly secreted into COS cell-conditioned medium and could be used for functional studies. Soluble rGpIb alpha L318 harvested from COS cell-conditioned medium inhibited ristocetin-dependent binding of [125I]-vWF to fixed washed human platelets (IC50 20 nM). Binding was inhibited by reduction and alkylation of "rGp1b alpha L318" suggesting the need for a critical disulfide bond to maintain biological activity of the recombinant polypeptide. We conclude that the recombinant polypeptides produced by transfection of GpIb alpha cDNA into heterologous cells are secreted, soluble, and can inhibit vWF binding to platelet GpIb/IX.

Binding Sites↗
PubMed1992

[Congential toxoplasmosis and ocular involvement. A review with 6 case reports].

A review is presented of the ocular affections in congenital toxoplasmosis. The epidemiological, pathogenetic and pathological conditions are reviewed together with the clinical manifestations and the diagnostic and therapeutic possibilities. On the basis of incidence investigations and knowledge from the literature, it must be assumed that approximately 190 infants with congenital toxoplasmosis are born annually in Denmark. Only approximately 15% of the infections will be symptom-producing and will be diagnosed neonatally, but more than 85% of the children with congenital toxoplasmosis will develop chorioretinitis on delivery or later in life and this will frequently cause reduction in vision or blindness. Congenital toxoplasmosis must be regarded as the commonest cause of chorioretinitis and it is probable that congenital toxoplasmosis and chorioretinitis due to toxoplasmosis are considerably underdiagnosed in Denmark. Treatment of congenital toxoplasmosis from birth improve the prognosis. Toxoplasmosis should be suspected in all cases of chorioretinitis. When antibodies to Toxoplasma gondii are demonstrated and the clinical picture is compatible with toxoplasmosis and when there is no other diagnosis, anti-Toxoplasma treatment should be considered. It is important to inform pregnant women about prophylactic measures. If investigations for toxoplasmosis were introduced in the prenatal or perinatal examinations, treatment could be initiated from birth and the diagnosis could be confirmed by possible activation of the chorioretinitis at a later date. Six case reports are presented.

Adult↗
PubMed1992

Functional analysis of a recombinant glycoprotein Ib alpha polypeptide which inhibits von Willebrand factor binding to the platelet glycoprotein Ib-IX complex and to collagen.

By deletion mutagenesis and transient expression in COS cells, a 96-amino acid hydrophilic sequence in the glycoprotein Ib alpha polypeptide located between L220 and L318 was identified which appeared to contain its von Willebrand factor- (vWF) binding site. The cDNA encoding this fragment was then expressed in Escherichia coli and purified from the bacterial cell lysate. The recombinant polypeptide, rGpIb alpha Q221-L318, was monomeric and had an apparent molecular weight of 14,000 by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. It inhibited both ristocetin-induced binding of 125I-vWF to fixed washed platelets and ristocetin-induced platelet agglutination. The recombinant polypeptide also inhibited the binding of 125I-vWF to immobilized type I and III collagen. Inhibition of 125I-vWF binding to platelets and collagen was dose-dependent, with IC50 values of 500 and 200 nM rGpIb alpha Q221-L318, respectively. Fifty % inhibition of ristocetin-induced platelet agglutination required 500 nM rGpIb alpha Q221-L318. Although rGpIb alpha Q221-L318 inhibited vWF binding to collagen it did not, itself, bind to collagen-coated surfaces. Reduction of the disulfide bond between C248 and C264 abolished activity. 125I-rGpIb alpha Q221-L318 bound directly to GpIb/IX sites on multimeric vWF. These studies document that a portion of the sequence between Q221 and L318 is needed for recognition and binding to vWF and that binding requires an intact disulfide bond between C248 and C264. The binding of this recombinant polypeptide to vWF multimers inhibits vWF interaction with two important substrates, platelet GpIb/IX and collagen.

Adenosine Diphosphate↗
PubMed1992

The antibody response to well-defined malaria antigens after acute malaria in individuals living under continuous malaria transmission.

The IgG and IgM antibody responses to the C-terminal 783 amino acids of the P. falciparum glutamate-rich protein, GLURP489-1271, expressed as an E. coli fusion protein, the IgG response to a 18-mer synthetic peptide EDKNEKGQHEIVEVEEIL (GLURP899-916) representing the C-terminal repeats of GLURP, and a synthetic peptide (EENV)6 representing the C-terminal repeats from Pf155/RESA, were investigated longitudinally in 13 children and 7 adults living under conditions of continuous, intense malaria transmission. Some subjects did not recognize the antigens after malaria infection, and in subjects recognizing the antigens, the responses were often short-lived. In adults, the antibody responses to the GLURP489-1271 fusion protein and the (EENV)6 peptide peaked after 2 weeks, and not all individuals responded to all antigens. The antibody response, even against large fragments of conserved antigens, is not uniformly elicited by natural malaria infection in previously primed donors.

Adolescent↗
PubMed1992

Antibodies to a recombinant glutamate-rich Plasmodium falciparum protein: evidence for protection of individuals living in a holoendemic area of Liberia.

A Plasmodium falciparum antigen gene coding for a 220-kD glutamate-rich protein (GLURP) has been cloned, and the 783 C-terminal amino acids of this protein (GLURP489-1271) have been expressed as a beta-galactosidase fusion protein in Escherichia coli. The encoded 783 amino acid residues contain two areas of repeated amino acid sequences. Antibodies against recombinant GLURP489-1271, as well as against a synthetic peptide corresponding to GLURP899-916, and against a synthetic peptide representing the major glutamate rich repeat sequence from the P. falciparum ring erythrocyte surface antigen (Pf155/RESA) (EENV)6 were examined in 423 individuals (age range 30 days-78 years) living in a malaria holoendemic area of Liberia. In the 5-9-year-old age group, subjects with anti-GLURP489-1271 antibody concentrations greater than the mean value of the group had lower parasite densities than those with low antibody concentrations (P = 0.0151). High levels of anti-GLURP899-916 antibodies did not correlate with low parasite densities. However, high levels of anti-(EENV)6 antibodies were associated with significantly lower parasite densities in the 2-4-year-old age group (P = 0.0189). There was no correlation between the anti-GLURP489-1271 and anti-(EENV)6 antibody responses. The data provide indirect evidence for a protective role of antibodies reacting with recombinant GLURP489-1271 as well as with the synthetic peptide (EENV)6 from the Pf155/RESA.

Adolescent↗
PubMed1992

Neonatal screening for congenital toxoplasmosis in Denmark: presentation of the design of a prospective study.

The design of a two year prospective study of 45,000 mothers and their newborn children aiming at determining the incidence of congenital toxoplasmosis in Denmark is presented. Toxoplasma IgG antibodies in a bloodspot from the newborn, routinely collected on filterpaper (the Guthrie card), and IgG antibodies in a stored serum sample from the mother collected in the first trimester are compared. Seroconversion identify mothers infected with T. gondii during pregnancy and identify newborn children at risk of congenital toxoplasmosis. All children at risk will be treated and followed until congenital toxoplasmosis is verified or excluded. Children with verified congenital toxoplasmosis will be followed clinically and the effectiveness of the treatment will be evaluated. The study design allows determination of the materno-fetal transmission rate in untreated pregnancies, and will furthermore allow a good estimate of the incidence of congenital toxoplasmosis in Denmark. In addition we hope that the diagnosis and treatment of cases of subclinical toxoplasmosis will prevent chorioretinitis and minor cerebral disorders later in life. Of 6355 pregnancies tested during the first 3 month of the study, 14 cases of maternal seroconversions have been diagnosed. Only one child had detectable toxoplasma specific IgM antibodies at birth.

Antibodies, Protozoan↗
PubMed1992

The effect of splenectomy on immunity to Plasmodium malariae and P. falciparum in a malaria immune donor.

A 55 year old Liberian male was splenectomized after an abdominal trauma. A few days after splenectomy he experienced a pure Plasmodium malariae infection with high fever. He was later followed for 12 months with monthly blood films and temperature measurements, and did never show any signs of clinical malaria. The parasite densities observed during the longitudinal follow after splenectomy did not differ from parasite densities in villagers with intact spleens.

Animals↗