PGE2 involvement in experimental infection with Trypanosoma cruzi subpopulations

PGE₂ involvement in experimental Trypanosoma cruzi infection depends on the lethal capacity of the parasite subpopulation used. Mice acutely infected with non-lethal K98 displayed an enhancement in PGE₂ serum levels during the acute period, while those infected with lethal T. cruzi subpopulations (RA or K98-2) showed levels not different from normal mice. The enhancement detected in K98 group could be related both to an increased number of CD8+ T cell number and to enhanced PGE₂ release per cell by CD8+; values of PGE₂ release by adherent cells were not altered in this group. Treatment with cyclooxygenase inhibitors enhanced mortality rates of mice infected with K98, and administration of 16,16-dimethyl PGE₂ (dPGE) reversed this effect. However, mice infected with RA did not reduce their mortality rates by administration of diverse doses of dPGE. These findings suggest that PGE₂ could play a role in resistance in mice infected with K98.     

Exclusion of the APC gene as the cause of a variant form of familial adenomatous polyposis (FAP)

Familial adenomatous polyposis (FAP) is a premalignant disease inherited as an autosomal dominant trait, characterized by hundreds to thousands of polyps in the colorectal tract. Recently, the syndrome has been shown to be caused by mutations in the APC (adenomatous polyposis coli) gene located on chromosome 5q21. We studied two families that both presented a phenotype different than that of the classical form of FAP. The most important findings observed in these two kindreds are (a) low and variable number of colonic polyps (from 5 to 100) and (b) a slower evolution of the disease, with colon cancer occurring at a more advanced age than in FAP in spite of the early onset of intestinal manifestations. To determine whether mutations of the APC gene are also responsible for this variant syndrome, linkage studies were performed by using a series of markers both intragenic and tightly linked to the APC gene. The results provide evidence for exclusion of the APC gene as the cause of the variant form of polyposis present in the two families described.     

Primate terminal complement inhibitor homologues of human CD59

The nucleotide sequence data reported in this paper have been submitted to the GenBank nucleotide sequence database and have been assigned the accession numbers L22862 (African green monkey CD59) and L22863 (baboon CD59)     

Haemaphysalis concinna Koch, 1844 in Italy

The authors provide here the data concerning the first italian finding of tick Hemaphysalis concinna (Ixodidae). Two males of this species--which has a large geographic diffusion--were actually caught for the first time in Italy, in July 1977. They were found on the ground of the Castel Porziano estate (Rome) at sealevel, in two different grassy places. The authors describe their morphological characters and provide some essential data on the environment of Castel Porziano.     

A high throughput assay for inhibitors of HIV-1 protease. Screening of microbial metabolites

A novel method for discovery of HIV-1 protease inhibitors in complex biological samples has been developed. The assay is based on two specific reagents: a recombinant protein constituted by a portion of the HIV-1 Gag polyprotein comprising the p17-p24 cleavage site, fused to E. coli beta-galactosidase, and a monoclonal antibody which binds the fusion protein in the Gag region. Binding occurs only if the fusion protein has not been cleaved by the HIV-1 protease. The assay has been adapted for the screening of large numbers of samples in standard 96-well microtiter plates. Using this method about 12000 microbial fermentation broths have been tested and several HIV-1 protease inhibitory activities have been detected. One of these has been studied in detail.     

Dictyocaulus viviparus: The role of pepsin in the exsheathment of infective larvae

Following the report of Silverman and Podger (1964) that pepsin formed an association with larval receptor sites on D. viviparus and that exsheathment had an absolute requirement for pepsin, the role of pepsin was studied in greater detail. A range of enzyme incubation, pepsin labeling, histochemical and electron microscopical techniques were used. Pepsin did cause exsheathment of D. viviparus but, it was not an absolute requirement. Exsheathment occurred in a range of proteolytic enzymes each at its optimum pH. Findings suggest that the area of weakness around the anterior end of the larvae is digested by external protease and that, in vivo, exsheathment is caused by the gut enzymes of the host.