Search PubMed⌕ Search

Biomedical subjects

M Boranić

Publications and source records attributed to M Boranić.

At least 19 recordsLinked to original sources
PubMed1990

Opposing influence of age on the growth and colony-forming ability of mouse melanoma B16 and mammary adenocarcinoma: correlation with natural killer activity.

C57B1 and CBA mice of different ages (6, 12, 26 or 35 weeks) received intramuscular inocula of melanoma B16 or mammary adenocarcinoma (MCa), respectively. Median survival time was shorter, the younger the recipients. Tumor enlargement was correspondingly retarded in older mice. This was associated with decrease of natural killer (NK) activity in the spleens. However, the cytotoxicity against fresh syngeneic tumor cells, increased with age in CBA mice. In contrast to the growth of intramuscular tumors, the ability of intravenously injected B16 or MCa cells to form nodules in the lungs was significantly superior in old animals (35 weeks or more), with low levels of NK activity, than in young ones (6 weeks) with high levels of NK activity. Stimulation of NK activity by poly(I).poly(C) reduced the number of MCa colonies by 50% in the lungs of old mice, but had no effect on colony-forming ability in young animals. The observed association of tumor growth with age and NK activity levels may reflect (a) an interplay of tumor-inhibiting and tumor-promoting effects of NK cells, changing with age, and (b) the accessibility of tumor cells, inoculated intramuscularly or captured in the lungs, to these influences.

Adenocarcinoma↗
PubMed1990

Immune response of stressed rats treated with drugs affecting serotoninergic and adrenergic transmission.

Stressful conditions interfere with immune response. One of the principal mechanisms is activation of hypothalamo-pituitary-suprarenal axis by central serotoninergic and adrenergic pathways. Alternative mechanisms bypassing the axis also take part in stress-induced immunomodulation. Immunosuppression caused by repeated restraints or over-crowding was usually accompanied by increased metabolism of serotonin in the brain (as indicated by increased level of its metabolite, 5-HIAA) and by increased levels of corticosterone in plasma. Changes in lymphatic tissues of stressed animals that result in suppression of immune response apparently "outlive" fluctuating changes in neurotransmitter and corticosterone levels. Drugs that alter serotoninergic or adrenergic transmission interfere with immunosuppressive effect of stress either synergistically (augmenting suppression) or antagonistically (preventing it). Since immunocompetent cells possess serotoninergic and adrenergic receptors, such drugs may exert their effect either via central neuroendocrine mechanisms, or by direct effects on immunocompetent cells.

Animals↗
PubMed1989

In vivo and in vitro modulation of NK and ADCC activities of mouse spleen cells by peptidoglycan monomer (PGM).

The ability of peptidoglycan monomer (PGM), an immunomodulator obtained from Brevibacterium divaricatum, to modulate NK and ADCC activities of spleen cells was tested in mice with constitutively weak (C57B1) or strong NK activity (CBA, C3H). In weak reactors, i.v. injection of PGM enhanced the NK and ADCC activity as effectively as a known stimulator, poly I.C, and the dynamics of the response was comparable. In strong reactors, PGM caused two peaks of the ADCC response, and one peak of NK stimulation (after an initial decline), whereas poly I.C caused more or less persistent stimulation of both activities. Incubation of spleen cells with PGM was generally less effective than the treatment in vivo. No alteration of NK activity was recorded at high effector-to-target ratio (E:T), and at low ones, PGM caused suppression. This was true both for weakly and strongly reactive cells. ADCC was either unchanged (CBA spleen cells), stimulated (C3H), or suppressed at high E:T and enhanced at low E:T (C57B1). PGM apparently activates an interlocked regulatory mechanism, and the final outcome probably depends on relative concentrations of regulatory and effector cells and on their per cell activities. Hence the effect varied with the time interval between treatment and assay, with strain-related constitutive reactivity, and with the E:T ratio.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1989

Expression of haematopoietic progenitor cell-associated antigen BI-3C5/CD34 in leukemia.

The expression of progenitor cell-associated antigen CD34, defined with monoclonal antibody BI-3C5, was investigated in cells from 109 patients with leukaemia. No reactivity was found in chronic leukaemias, whereas 31% of acute myelogenous leukaemia (AML) and most non-T, non-B acute lymphoblastic leukaemia (ALL) expressed CD34. Examples of BI-3C5+ AML included M1 and M2 FAB types only; all but one were myeloperoxidase positive. In combination with pan-myeloid markers, BI-3C5 is useful for identification of immature myeloid cells.

Adult↗
PubMed1989

Defect of NK activity in children with untreated acute lymphocytic leukemia (ALL). I. Dependence on the blast count and phenotype, and response to exogenous and endogenous alpha-interferon.

Endogenous NK-activity (eNK) against K-562 cells was determined in peripheral blood of 68 children with acute lymphocytic leukemia (ALL) before treatment. In 53% of them it was depressed, and in 47% it was within the range of control children (27) and adults (104). There was a significant negative correlation between blast contamination of peripheral blood and the level of eNK-activity. In spite of this general trend, 8 patients with high blast count have had normal eNK-activity, and 10 patients with relatively low blast count (below 50%) have had depressed eNK-activity. Examples of T ALL showed significantly lower eNK-activity than CALLA ALL. The ability of exogenous alpha-interferon (IFN) to stimulate eNK-activity was impaired in 18 of 40 examples of ALL and preserved in 22. The IFN-induced NK-response was also negatively correlated to the blast burden, but again with exceptions: Six nonresponders in spite of low blast count, and six responders in spite of high blast count in peripheral blood. IFN-inducer, poly-IC, stimulated eNK-activity only in 6 of 26 ALL samples. Surprisingly, positive correlation was found between poly-IC-induced NK-stimulation and blast count in peripheral blood. Poly-IC induced significant IFN production only in one of six cultures of ALL. Impaired eNK-activity has been attributed, in part, to "dilution" of NK cells by the blasts. Defects in production of IFN, and in response to it, may be additional reasons for depressed NK-activity in about 50% of children with untreated ALL.

Adolescent↗
PubMed1988

Defects of natural killer cell activity in children with untreated acute lymphocytic leukemia.

Natural killer (NK) activity against cells of the K-562 line was significantly depressed in 12 of 18 children (66%) with untreated acute lymphocytic leukemia (ALL). No suppression of allogeneic NK activity was observed with sera of the patients, regardless of the level of NK depression. The ability of peripheral blood lymphocytes (PBLs) to suppress allogeneic NK activity was tested in two ALL patients - one with no detectable NK activity, and one with high NK activity. No NK-suppressive activity was found with PBLs of the areactive patient; PBLs of the reactive patients exhibited some suppressive activity, but only at a particular suppressor-to-effector cell ratio. Leukemic blasts were resistant to killing by autologous NK cells stimulated by IFN, as well as to killing by allogeneic, IFN-stimulated PBLs. Leukemic blasts of an ALL patient inhibited lysis of K-562 cells in an 18-h, but not in a 4-h NK assay. The inhibition could partly be reversed by pretreatment of ALL cells with alpha interferon, suggesting that the blasts might inhibit the lysis of K-562 targets in a competitive manner. Disturbed function and/or regulation of NK cells may influence attempts at NK cell activation by lymphokines.

Acute Disease↗
PubMed1988

NK cell activity and estrogen hormone levels during normal human pregnancy.

NK cell activity was determined in peripheral blood of 24 women during pregnancy, and compared to NK activity of 40 healthy nonpregnant women in generative age. An increase in the first trimester was followed by a significant decline of NK activity in the second trimester, and a further fall in the third trimester of pregnancy. The initial rise of NK activity was predominantly due to primigravidas, whereas the fall in the second trimester was mainly due to multigravidas. There was a significant negative correlation between NK activity and the increasing levels of estrogen hormones (beta-estradiol, estriol and estrone) in the sera of pregnant women. However, when analyzed for each trimester of pregnancy separately, a significant (p less than 0.02) negative correlation was only found with beta-estradiol, suggesting that high doses of this hormone could contribute to pregnancy-associated NK suppression.

Adolescent↗
PubMed1988

Subsets of childhood acute lymphoblastic leukaemia in Croatia.

As a contribution to epidemiological studies on distribution of acute lymphoblastic leukaemia (ALL) subsets in different countries, we investigated blast cell immunophenotype in 54 children with ALL from the western part of Yugoslavia. The subtype incidences were: common, 75.9%; null, 7.4%; T, 11.1%; B, 1.9%; and unclassifiable, 3.7%. This resembles the ALL pattern registered in developed countries. Hence, differences in socioeconomic status between our population and developed European countries do not result in an appreciably altered incidence of childhood leukaemia subtypes.

Burkitt Lymphoma↗
PubMed1987

Effect of diazepam on brain neurotransmitters, plasma corticosterone, and the immune system of stressed rats.

Rats were treated with injections of diazepam (1 or 10 mg/kg) and stressed by restraint lasting 3 hours. This was performed once or, in animals immunized with sheep erythrocytes, repeatedly for 4 consecutive days. After repeated stress and/or diazepam treatment, the levels of brain noradrenalin decreased in all treated groups. Although both treatments (stress and diazepam) diminished the 5-hydroxytryptamine (5-HT)/5-hydroxyindoleacetic acid (5-HIAA) ratio, treatment with either dose of diazepam prevented the stress-induced fall of this ratio. The activity of hypothalamic glutamate decarboxylase, the enzyme taking part in GABA synthesis, was affected neither by the acute nor by repeated stress and/or diazepam treatment. The levels of plasma corticosterone were enhanced in all stressed rats, with and without drug. This finding was in accordance with the enhanced weights of adrenal glands in repeatedly stressed rats. The tendency to a corticosterone rise after repeated treatment with diazepam, 10 mg/kg, coincided with the enhanced weights of adrenal glands in these animals. The plaque-forming cell (PFC) response was reduced in all stressed animals and in animals treated with diazepam, 10 mg/kg. Accordingly, high doses of diazepam given repeatedly to rats are immunosuppressive, achieving this effect presumably by an enhancement of glucocorticoid secretion. Neither the low nor the high doses of diazepam affect the stress-induced enhancement of hypothalamohypophysial-adrenal axis activity and consecutive immunosuppression.

Animals↗
PubMed1987

Suppression of immune response in rats by stress and drugs interfering with metabolism of serotonin.

Rats immunized with sheep erythrocytes were stressed by repeated restraint and/or treated with a precursor of serotonin (5-hydroxytryptophan, 5-HTP) or with an inhibitor of serotonin synthesis (parachlorophenylalanine, PCPA). As expected, repeated stress reduced the plaque-forming cell (PFC) response. Treatment with 5-HTP also reduced the PFC response, and potentiated the immunosuppressive effect of stress. This was accompanied by increased metabolism of serotonin in the brain, as indicated by increased concentration of its metabolite, 5-hydroxyindoleacetic acid (5-HIAA) in cerebral tissue. Treatment with PCPA also suppressed the PFC response, but this suppression was accompanied by decreased levels of brain serotonin and of 5-HIAA. Plasma corticosterone levels were elevated, reaching statistical significance, in rats treated with PCPA. Both drugs suppressed the in vitro PFC response of peripheral blood lymphocytes. Thus, although 5-HTP and PCPA altered serotonin metabolism in the brain in a diametrically opposite manner, their effects on the immune response were the same. Putative central effects of the drugs on serotoninergic regulation of the immune response were apparently obscured by their effects on corticosterone secretion as well as by their direct effects on immunocompetent cells.

Animals↗
PubMed1987

Reduction of cis-dichlorodiammineplatinum(II) caused nephrotoxicity by indazolone carboxylic acid.

To reduce the nephrotoxicity of cis-dichlorodiammineplatinum (cis-DDP) we have used tetrahydroindazolonedicarboxylic acid (HIDA) in doses of 200, 100 or 50 mg/kg 4, 2 and 1 h before or 1, 2 and 4 h after cis-DDP treatment (10 mg/kg). At any dose, given 2 or 1 h before or 1 h after cis-DDP, HIDA reduced the kidney damage as judged by the blood urea nitrogen (BUN) levels in blood. No protective effect was seen when HIDA was given 4 h before cis-DDP injection. Studies in vitro on L1210 cells have revealed that HIDA does not directly interact with cis-DDP.

Animals↗