Search PubMed⌕ Search

Biomedical subjects

I Hrsak

Publications and source records attributed to I Hrsak.

At least 37 records · Page 2Linked to original sources
PubMed1982

Correlation of substance(s) immunologically cross-reactive with insulin, glucose and growth hormone in Hodgkin lymphoma patients.

The levels of substance(s) detectable by insulin specific radioimmunoassay (RIA), glucose and growth hormone (GH) were determined in the blood of patients suffering from Hodgkin lymphoma. In the relapse phase of the disease, the levels of substances immunologically cross-reactive with insulin (SICRI) were elevated and glucose concentrations were below normal. In these patients the basal and hypoglycemia-induced levels of GH in blood were strongly elevated. Contrary to this, both SICRI and glucose levels were normal in the blood of patients in remission, and GH levels were significantly reduced compared to those measured in patients in relapse.

Adolescent↗
PubMed1982

Immunosuppression related to ascitic fluid in patients with ovarian carcinoma.

The immune response to SRBC (PFC assay) was suppressed in mice injected with cell-free ascitic fluid from patients with ovarian carcinoma. The immunosuppressive effect of ascitic fluid obtained from stage IV patients was stronger than that of stage III patients. These data were correlated with the patient's immune status (number of E and EAC rosettes, PHA reactivity of lymphocytes, skin reactivity in recall antigens) and with changes in protein fractions in the serum and ascitic fluid. A good correlation was found between the immunosuppressive effect in the mouse PEC assay and the increased quantity of alpha-1-globulins in ascites. Skin nonreactivity to PPD also correlated with the immunosuppressive effect of ascitic fluid. However, the lymphocyte response to PHA and the numbers of E and EAC rosettes did not correlate either with skin reactivity or recall antigens or with the suppression of PFC response in mice.

Adult↗
PubMed1981

The metabolic fate of 14C-labeled immunoadjuvant peptidoglycan monomer. II. In vitro studies.

Peptidoglycan monomer (GlcNAc-MurNAc-L-Ala-D-isoglutamine-meso-diaminopimelic acid-D-Ala-D-Ala), labeled with 14C both in the disaccharide and pentapeptide portions, was incubated with slices of mouse liver, kidney or spleen as well as with mouse and human blood, blood cells plasma and serum. Peptidoglycan monomer was isolated unchanged after incubations with mouse organs and blood cells. However, upon incubation with mouse or human blood, 10-50% of the peptidoglycan monomer underwent hydrolysis to the corresponding disaccharide and pentapeptide. After incubations with plasma and serum more than 90% of the [14C]peptidoglycan monomer was metabolized: about 50% of the administered radioactive dose was recovered in the disaccharide unit and about 35% in the pentapeptide part. These results suggest that in blood, plasma and serum of mouse and man, an N-acetylmuramoyl-L-alanine amidase (mucopeptide amidohydrolase, EC 3.5.1.28) exists which splits the amide bond between the lactyl carboxyl group of the muramyl residue and the amino group of the peptide moiety in the peptidoglycan molecule.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1980

The metabolic fate of 14C-labeled peptidoglycan monomer in mice. I. Identification of the monomer and the corresponding pentapeptide in urine.

The distribution of radioactive products in mouse urine following intravenous administration of the 14C-labeled peptidoglycan monomer, GlcNAc-MurNaC-L-Ala-D-isoglutamine-meso-diaminopimelic acid-D-Ala-D-Ala, has been studied. 60--80% of radioactivity was recovered within first 3 h, 4--8% in the next 3 h and 2--7% in the following 18 h. The majority of the label was associated with the unchanged peptidoglycan monomer (42--56% of the dose). 14--21% of the label was incorporated into a compound which was isolated and tentatively identified as L-Ala-D-isoglutamine-meso-diaminopimelic acid-D-Ala-D-Ala. The kinetics of excretion and the distribution of radioactivity did not differ in immunized, when compared to non-immunized, mice.

Animals↗
PubMed1979

Stimulation of humoral immunity by peptidoglycan monomer from Brevibacterium divaricatum.

Peptidoglycan monomer (PGM), a water soluble and nontoxic disaccharide pentapeptide unit obtained from Brevibacterium divaricatum, was administered intravenously into mice, and the humoral immune response to sheep erythrocytes was assayed by means of Jerne's technique for plaque-forming cells (PFC) in the spleen. The PFC response was evidently stimulated. The counts were increased to practically the same extent over a great range of doses of PGM (from 25 to 1600 microgram per animal), and the effect was present in the mice immunised with optimal, as well as in those immunised with suboptimal, doses of antigen. The magnitude of the immunostimulation depend only on the timing of PGM administration: it was maximal if PGM was injected 1 or 2 days after the antigen. In vitro, in a 4-day culture of spleen cells, PGM did not stimulate PFC formation. We conclude that stimulation of the humoral immune response to sheep red blood cell antigens by PGM probably occurs without cell multiplication and probably involves more than simply a contact of immunocompetent cells with PGM.

Adjuvants, Immunologic↗
PubMed1979

[The influence of treatments with a quinine-lithium-salicylate combination or acetylsalicylic acid on hematopoiesis in mice (author's transl)].

The effects of an 8-week treatment with the quinine-lithium-salicylate combination Togal and sole acetylsalicylic acid (ASA) on the hemopoietic bone marrow cells of mice were studied. In general, both substances caused only minor changes. A slight leukopenia caused by higher doses as well as a transitory erythropenia observed a little bit more distinctly in ASA treated animals than in Togal treated animals need more detailed discussion, especially so because after a short two-week Togal treatment some animals showed an increase of hemopoietic cell colonies which a sole ASA dose did not cause. On the other hand, these results indicate a lower toxicity of Togal in comparison with acetylsalicylic acid as has been already shown in several other publications. It was proven that after a several weeks' treatment with therapeutic doses no pernicious influence on blood producing organs or pathological processes of the blood picture occurred. Only doses that border on the toxic region lead to insignificant bone marrow changes. As these over-doses are ten times the highest therapeutical dose the use of Togal does any damage to the blood forming tissue or pathological changes in the blood count are not likely. This has also been proved by other authors by means of long-term tests on humans.

Animals↗
PubMed1978

Effect of immunosuppression on the growth of six murine tumors.

Mice have been immunosuppressed with cyclophosphamide, cortisone-acetate, irradiation, or Ehrlich ascitic fluid (EAF) and then grafted with Ehrlich tumor or with one of the following strain-specific tumors: thymoma, methylcholanthrene-induced fibrosarcoma, B-16 melanoma, lymphatic leukaemia, and myeloid leukaemia. Immunosuppression of the host influenced very differently the growth of transplanted malignancies. The growth of thymoma and of Ehrlich tumor was regularly enhanced. The growth of fibrosarcoma and of melanoma, on the other hand, was retarded in mice pretreated with EAF and X-rays, or remained unchanged in mice pretreated with drugs. Leukaemia growth was not influenced by any immunosuppressive treatment; the only exception was enhanced growth of lymphoid leukaemia in animals pretreated with EAF. Thus different tumors grew differently in animals immunosuppressed by the same immunosuppressive agent, while different immunosuppressive treatment changed the growth of one particular tumor always in the same way. From this we concluded: (1) there is no rule as to how immunosuppression of the host will influence tumor growth; and (2) the way in which the malignant growth will be changed depends mainly upon the type of the tumor and probably not very much upon the type of immunosuppressive treatment.

Animals↗