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6 recordsLinked to original sources
PubMed1978

beta-thromboglobulin and deep vein thrombosis.

The measurement of plasma beta-thromboglobulin as a potential diagnostic test for venous thrombosis has been investigated in 16 normal volunteers, 24 patients presenting with deep vein thrombosis (DVT) or pulmonary embolism and 46 patients screened by 125I fibrinogen test (IFT) for post-operative DVT. The normal mean was 33 ng/ml (range 15-117 ng/ml). Of the 24 patients with clinical thrombotic disease 22 presented with DVT confirmed by phlebogram or IFT and 2 presented with embolism confirmed by lung scan. At the time of first presentation 12 out of 24 had betaTG values greater than 70 ng/ml. All except 3 of this group of 24 patients had values of greater than 70 ng/ml at some stage during a subsequent week of daily sampling. DVT was detected in 13 out of 46 screened post-operative patients. There was a rise om betaTG observed within 24 hr of the IFT becoming positive but the mean rise did not reach significance at the 5% level. An association between DVT and high betaTG values has been confirmed. However, its clinical value cannot yet be fully elucidated until factors, probably related to blood sampling and clearance, are further investigated.

Beta-Globulins↗
PubMed1979

Studies on antibodies against feline leukaemia virus (FeLV) in cat sera and rabbit anti-FeLV sera: cross reaction and differences.

The indirect immunoferritin technique (IFT) that enables us to distinguish clearly whether an antibody reacts with a virus particle or only with the cell membrane, was used to study 25 cat sera and one rabbit anti-feline leukaemia virus (FeLV) serum using FL-74 cells as target. (1) All sera contained antibodies against FeLV even though 11 of the cats were viraemic at the same time; (2) from the effect of glutaraldehyde fixation of the FL-74 cells on the reaction with cat sera and the results of blocking experiments, it could be concluded that cat sera and rabbit anti-FeLV sera react partly with different antigenic specificities of FeLV, partly with the same antigens; and (3) the indirect membrane immunofluorescence test using FL-74 cells as target is not a good test to detect the presence of antibodies against feline oncornavirus-associated cell membrane antigen (FOCMA) because FL-74 cells produce a large quantity of FeLV and the fluorescence measured could be from antibodies against FeLV.

Animals↗
PubMed1975

Identification of T. brucei-subgroup strains isolated from game.

Several T. brucei-subgroup strains isolated from game were investigated with the blood incubation infectivity test (BIIT) and in human volunteers. Original isolates and their clones derivatives were tested. In order to check the validity of the BIIT, volunteer tested clones were used under modified BIIT conditions. Inoculation of different trypanosome strains into volunteers yielded positive parasitaemia for original isolates from lion, hyaena, and Coke's hartebeest. Changing antibody titers during the course of infection in the volunteers were checked with the indirect fluorescent antibody test (IFT). The BIIT WAs reliable (consistently positive) for cloned T. b. rhodesiense. When testing T. b. brucei, the BIIT results depended on the number of incubated parasites and on the parasitaemia peak number the tested trypanosomes derived from. It was further shown that the in vivo part of the BIIT is actually essential for the complete neutralization of T. b. brucei induced by the action of human plasma. Tests with trypanosomes originating from experimentally mixed T. b. rhodesiense and brucei infections gave inconsistent results. On the other hand, pure populations mixed in vitro-prior to incubation for BIIT-revealed results depending on the proportion of the 2 species: up to 20% T. b. rhodesiense gave negative, higher concentrations consistently positive results.

Animals↗
PubMed1975

Sperm antibodies in men from infertile couples. Analysis of sperm agglutinins and immunofluorescent antibodies in 657 men.

Sera from 657 men from infertile couples were tested for sperm agglutinins and spermatozoal antibodies detectable by the indirect immunofluorescense technique (IFT), and the results were correlated to the clinical examinations of the couples. Sperm agglutinins were found in 6.7%. Spontaneous agglutination of the ejaculated spermatozoa was observed only among these men, most commonly among those with high serum titres. IF-antibodies against the four spermatozoal antigens located beneath the cell membrane occurred in 15.2% of the patients. Antibodies against the front part of the acrosome and the postnuclear cap were mainly IgM. Antibodies against the equatorial segment of the acrosome were predominantly IgG and in a few cases IgA, whereas straining of the main tail piece was caused by IgG antibodies. Considering the clinical fertility status of the couples, sperm agglutinins in high titres (greater than or equal to 10) against the equatorial segment and the main tail piece of the spermatozoa were found significantly more often among men from couples with unexplained infertility than among clinically normal men from couples where the findings in the women could be assumed to cause infertility. These results support the view that sperm agglutinins can cause infertility, whereas the significance of the IF-antibodies is still unclarified as, in some cases, these can be found even in high titres in men with proven fertility. The possible mechanism of autosensitization were evaluated by means of an anamnestic study.

Adult↗
PubMed1975

[Vital fluorochromasia of mikroorganisms using fluorescein-3',6'-diacetate (FDA). II; Communication: The influences of humoral and cellular defence-mechanisms on vitality of Toxoplasma gondii (author's transl)].

Fluorochromization by using the non-fluorescent, but fluorogenic substrate fluorescein-3',6'-diacetate indicates vitality and metabolic activity of extra- and intracellular Toxoplasma gondii. Specific humoral antibody diminishes the metabolism and, therefore, also the fluorochromization of these parasites; Because toxoplasms invade host cells mainly by active penetration, they are found not only in phagocytes but also in lymphocytes and in hepatocytes. In these cells, a further multiplication of parasites occurs. Only well functioning phagocytes are able to destroy the parasites; This process is supported by humoral antibody. Using IFT, the binding of humoral antibody to vital and killed toxoplasms in phagocytes of peritoneal exudate and spleen can be demonstrated in vivo and in vitro. The destroying effect of humoral antibody is limited by the rapid penetration of toxoplasms into the host cells. After infection, only an early administration of a high dose of antiserum will achieve a sufficient binding of antibodies to be able to influence the metabolism of toxoplasms. Due to this fact and according to the risk of a repression of humoral defence mechanisms in the host by IgG-antibodies the value of passive immunisation is limited.

Animals↗
PubMed2025

The RNA splicing factor PRPF8 is required for left-right organiser cilia differentiation and determination of cardiac left-right asymmetry via regulation of Arl13b splicing.

Cilia function in the left-right organizer (LRO) is critical for determining internal organ asymmetry in vertebrates. To further understand the genetics of left-right asymmetry, we isolated a mouse mutant with laterality defects, l11Jus27, from a random mutagenesis screen. l11Jus27 mutants carry a missense mutation in the pre-mRNA processing factor, Prpf8. cephalophŏnus (cph) mutant zebrafish, carrying a protein truncating mutation in prpf8, phenocopy the laterality defects of l11Jus27 mutants. Prpf8 mutant mouse and fish embryos have increased expression of an alternative transcript encoding the cilium-associated protein, ARL13B, that lacks exon 9. In zebrafish, over-expression of the arl13b transcript lacking exon 9 perturbed cilium formation and caused laterality defects. The shorter ARL13B protein isoform lacked interactions with intraflagellar transport proteins. Our data suggest that PRPF8 plays a prominent role in LRO cilia by through the regulation of alternative splicing of ARL13B, thus uncovering a new mechanism for cilia-linked developmental defects.

ARL13B↗