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Biomedical subjects

U Bicker

Publications and source records attributed to U Bicker.

51 records · Page 3Linked to original sources

Experimental investigations on increased resistance to infections with Candida albicans and Staphylococcus aureus Smith by 4-imino-1,4-diazobicyclo-(3.1.0)-hexane-2-on BM 06.002 (prop. INN imexon) in mice.

BM 06.002 increases the resistance of mice to experimentally induced chronic infection with Candida albicans. Furthermore, BM 06.002 leads to increased resistance in the case of experimentally induced infection with Staphylococcus aureus Smith, when a subtherapeutic dose of sulfadiazine is applied. In mice immunosuppressively pretreated with hydrocortisone, BM 06.002 effectuates immunorestauration.

Animals↗

Immunestimulation by 4-imino-1,3-diazabicyclo(3.1.0.)-hexan-2-on (BM 06.002).

The new cancerostatic substance 4-imino-1,3-diazabicycle- (3.1.0.)-hexan-2-on was investigated in DBF1 mice in respect to its effects on antibody producing B-lymphocytes and T-lymphocytes. It was shown that BM 06.002 has no definitive influence on immunocompetence when used at a low concentration (1 mg/kg). At higher concentrations of 5 up to 20 mg/kg a stimulation of T-lymphocytes was found which was constant at a concentration of 20 mg/kg for more than three weeks after the single injection of 20 mg/kg. Using the haemolytic plaque test, a stimulation of the antibody producing B-cells was observed on day 3 and 12 after treatment. On day 5 a transitory suppression of the lymphocyte functions was observed in both test systems.

Animals↗

Immunestimulation in cancer patients by a new synthetic compound: BM 06 002.

A new synthetic compound 4-imino-1,3-diazobicyclo (3,1,0)-hexan-2-on (BM 06 002) has been shown in animal models to stimulate humoral and cell-mediated immune reactions. In a Phase I study in man a total absence of toxic side effects after intravenous injection of BM 06 002 has been demonstrated. In the present investigation in patients with advanced incurable cancer one single injection of this substance induced a significant stimulation of lymphocyte blastogenesis response to PHA and PWM. Delayed cutaneous hypersensitivity reactions, tested before and after drug application, were also found increased. According to thses findings BM 06 002 might be considered as an immune-stimulating compound.

Antibody Formation↗

Effect of the immune modulators BM 12.531 (azimexone) and BM 41.332 on the subsets of T-lymphocytes in mice.

The immunomodulating 2-cyanaziridine derivatives BM 12.531 (azimexone) and BM 41.332 have no effects on the total amount of T-lymphocytes in the spleen of mice but increase dose-dependently the percentage of Ly1-, 2+, 3+ T-lymphocytes (killer/suppressor) and decrease the percentage of Ly1+, 2-, (helper) cells. These investigations were carried out by means of specific monoclonal antibodies and fluorescence-activated cell sorting. The increase in Ly2+-cells is mainly due to increased suppressor activity.

Adjuvants, Immunologic↗

Lack of correlation between cytotoxicity of agonists and antagonists of platelet activating factor [paf-acether] in neoplastic cells and modulation of [3H]-paf-acether binding to platelets from humans in vitro.

The 3 ether-lipids ET-18-OCH3, SRI 63-154 and paf-acether, the TLP BM 41.440, the ester-linked 2-LPC and CV-3988, were tested for cytostatic/antiproliferative [3H]-thymidine uptake) and cytotoxic (trypan blue dye exclusion, HTCA) activity in 11 neoplastic human cell lines (U 698-M, Nall-1, Su-DHL-4, RPMI 8226, K 562-4, Li-A, HTB-47, HTB-38, CCL218, 85 HG-59, 85 HG-63) and 1 ALL in vitro. 2-LPC and paf-acether showed either no, or only minor, CV-3988 varying activity. There were no significant differences in the activity of ET-18-OCH3, SRI63-154 and BM 41.440, which showed IC50- and LC50-values of less than or equal to 10 micrograms/ml after incubation periods greater than or equal to 48 hours with or during continuous exposure to the cells. The latter three compounds were then tested for interaction with [3H]-paf-acether binding to intact human platelets: ET-18-OCH3 and SRI63-154 reduced [3H]-paf-acether binding in a time-dependent manner. BM 41.440 did not show this interaction. Thus, since the in vitro cytotoxicity of these lipids did not correlate with their modulation of [3H]-paf-acether binding to human platelets, it was concluded that cytotoxicity of ether-lipids is not mediated by specific paf-acether binding sites similar to those present on human platelets. This finding is important for the future design of antineoplastic lipids.

Antineoplastic Agents↗

[Effects of therapy, serology, stage and activity of rheumatoid arthritis on lymphocyte stimulation in whole blood].

We utilized a new, whole blood method to study the stimulation of lymphocytes by phytohemagglutinin in patients with rheumatoid arthritis and healthy volunteers. We observed that lymphocytes of patients with rheumatoid arthritis were significantly less stimulated by phytohemagglutinin than lymphocytes of controls (p less than 0.05). The underlying T-cell defect appeared to be present at all stages and activity levels of disease, and in both seropositive and seronegative patients.

Adrenal Cortex Hormones↗