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O Bakke

Publications and source records attributed to O Bakke.

66 records · Page 4Linked to original sources
PubMed1984

T-lymphocytes and the subpopulations of T-helper and T-suppressor cells measured by monoclonal antibodies (T11, T4, and T8) in relation to surgery under epidural and general anaesthesia.

Monoclonal antibodies reacting with specific determinants on lymphocytes and their subpopulations were used to study the influence of surgery under general or epidural anaesthesia on the number of T-cell (T11), T-suppressor cells (T8), and T-helper cells (T4). The T-cell fraction decreased significantly during surgery, but was only moderately reduced on the first postoperative day. The change in the T-cell fraction was the same under both types of anaesthesia. The helper and suppressor cell fractions were not significantly altered at any time during the study, and again there was no difference between the two anaesthetic regimens. The ratio of helper cells to suppressor cells (the T4/T8 ratio), which is widely used as an indicator of immunosuppression, showed no significant variations during the study, even though there were individual variations. Changes in the T4/T8 ratio were not correlated to the amount of blood transfusions, nor was there any correlation between the T4/T8 ratio and the thymidine uptake in mitogen-(PHA)-stimulated lymphocytes. T-lymphocytes are depressed during and after surgery under general anaesthesia. From the present study, this does not seem to be due to changes in the balance between helper- and suppressor T-cells.

Aged↗
PubMed1983

Soluble cytostatic factor(s) released from human monocytes. II. Effects on target cell kinetics.

Human monocytes release a stable cytostatic factor during in vitro culture after stimulation with lymphokine and endotoxin. The cell cycle time of synchronized NHIK 3025 cells increased from 20.3 to 23.2 h in the first cell cycle when the target cells were exposed to the factor during the whole cell cycle. In exponentially growing NHIK 3025 cell cultures the cell doubling time increased from 18.9 h to 23.1 h under continuous factor exposure for 70 h. These cells regained normal cell division rate when fresh culture medium replaced the cytostatic factor. Continuous exposure to the cytostatic factor for 96 h increased the cell doubling time of asynchronous K-562 cells from 19.7 to 31.8 h. The target cell DNA synthesis, evaluated by thymidine incorporation, was markedly depressed after culture with the factor for 24 h, and this depression was detectable already within 4 h of culture. The factor showed no cytolytic effect on the two cell lines tested. The cytostatic factor influenced the cell cycle distribution of both target cells tested, since cell cycle analysis by DNA flow cytometry demonstrated a reversible inhibition of factor-exposed NHIK 3025 cells in G1- and early S-phase, whereas K-562 cells accumulated in G1-phase.

Cell Cycle↗
PubMed1982

The role of protein metabolism in glucocorticoid-induced prolongation of G1 phase in human NHIK 3025 cells.

It has previously been found that human NHIK 3025 cells have a glucocorticoid-sensitive restriction point in mid-G1 phase of the cell cycle. When these cells were synchronized by mitotic selection and exposed to dexamethasone before the restriction point, G1 phase was prolonged whereas the rest of the cell cycle was unperturbed by the hormone. These observations were confirmed by flowcytometric measurements of synchronized cells in the present study. Cells that received dexamethasone (10(-6) M) just after mitotic selection had a 4 hour prolongation of both G1 and the total cell cycle. However, the general rates of both protein synthesis and protein degradation were found not to be altered by the hormone, i.e., the rate of protein accumulation in dexamethasone exposed cells was equal to that of control cells. Dexamethasone exposed NHIK 3025 cells were found to be larger than control cells at the time of cell division. This is a direct consequence of a prolonged cell cycle duration with no change in general protein metabolism. It thus appears that the dexamethasone-induced prolongation of G1 phase is the result of a steroid-regulated G1 specific process(es) leading toward DNA replication, a process that does not alter general protein accumulation.

Cervix Uteri↗
PubMed1982

Structure requirements for glucocorticoid growth of a human cell line (NHIK 3025).

The human cell line NHIK 3025 has a cytoplasmic dexamethasone receptor. When these cells are exposed to glucocorticoids, the cell cycle time is prolonged. The structural requirements for this effect were investigated by measuring cell number after 4 days exposure to different glucocorticoid analogues at concentrations of 10(-6) M and 10(-7) M. Growth inhibition at 10(-7) M required the 4-5 double bond, the 3,20 ketone--and the 11 beta, 17 alpha and 21 hydroxygroups of the glucocorticoid structure, e.g. cortisol, dexamethasone and prednisolone. Other synthetic glucocorticoids like bimetrazol and triamcinolone acetonide were also active at this dose whereas corticosterone, lacking the 17 alpha hydroxygroup, was only active at 10(-6) M. The effect was steroid specific and could be inhibited by anti-cortisol antiserum or by glucocorticoid antagonists.

Cell Cycle↗
PubMed1982

Effects of potassium dichromate on the cell cycle of an established human cell line (NHIK 3025).

The effect of K2Cr2O7 exposure on the cell cycle phases of the human cell line NHIK 3025 has been studied. Inhibition of cell proliferation was found to depend on the concentration and length of exposure. An effect on cell proliferation was observed 6-9 h after addition of K2Cr2O7, whereas cell death was not observed until 3-4 days later. The cells were most sensitive in G2 phase. After exposure to 8 mumol/l K2Cr2O7 the greatest prolongation of the cell cycle was in G2 + M phase, but an increase of S phase was also observed. No prolongation of G1 phase could be measured. Our results thus indicate that K2Cr2O7 delays progression through the cell cycle.

Cell Cycle↗
PubMed1981

Cell cycle-specific glucocorticoid growth regulation of a human cell line (NHIK 3025).

It has been reported that the human cell line NHIK 3025 has a specific cytoplasmic glucocorticoid receptor. When these cells were exposed to glucocorticoids, the cell cycle time was prolonged. Cells, synchronized by mitotic selection, were subjected to the synthetic glucocorticoid dexamethasone throughout the cell cycle. Only cells exposed in the first half of G1 phase had a lengthened cell cycle time. Most of the prolongation was also located within the G1 phase. The dexamethasone growth inhibition was reversible and could be detected only in the cell cycle where the cells were exposed to the steroid. DNA-histograms of asynchronous cells were recorded by flow cytometry at various times after steroid exposure. These histograms also showed G1 phase sensitivity and G1 phase prolongation after exposure to dexamethasone. Our results thus indicate that these cells have a dexamethasone-sensitive restriction point in mid-G1 phase of the cell cycle.

Carcinoma in Situ↗
PubMed1977

A change in the oxygen effect throughout the cell-cycle of human cells of the line NHIK 3025 cultivated in vitro.

NHIK 3025 cells were synchronized by repeated mitotic selection. The S-phase was determined by 3H-thymidine incorporation and scintillation counting. By comparing the age-response surves of aerobic cells irradiated with 500 rad with those of extremely hypoxic (less than4 p.p.m. O2) cells irradiatedwith 1500 rad, it was found that the sensitizing effect of oxygen was not constant throuhgout the cycle. It was significantly higher in S, G2 and mitosis than in G1. No significant sensitizing effect of 120 p.p.m. O2 (compared with less than4 p.p.m.O2) was found on cells in G1 when the cells were irradiated with 1500 rad. In S, G2 and mitosis, however, the sensitizing effect of oxygen at 120 p.p.m. is considered to be significant. Experiments performed with cells irradiated with 2000 rad incontact with either less than4 p.p.m. O2 or 80 p.p.m. O2 showed the same trend, little sensitizing effect in G1 and higher in S, G2 andmitosis. Dose-response curves for cells in mid-G1 and mid-S under aerobic and extremely hypoxic conditions were well fitted by the formula S=exp (-alphaD-betaD2). From the dose-response curves it was conculded that the change in the sensitizing effect of oxygen throughout the cell-cycle only appeared for low doses (in the dose region where alpha dominates). The sensitizing effect of oxygen on cells in mid-G1 was found to be increasing with increasing dose.

Cell Division↗
PubMed1977

Cell cycle characteristics of synchronized and asynchronous populations of human cells and effect of cooling of selected mitotic cells.

The method of synchronizing cells by means of mitotic selection has been adapted to the human line NHIK 3025. Increase in cell number as a function of time in asynchronous and synchronous populations was studied as well as mitotic index as a function of time after selection of synchronized populations. Phase durations of the cell cycle of synchronous populations were determined by 3H-thymidine incorporation and scintillation counting. The relative phase durations of exponentially growing asynchronous populations were determined by mathematical analysis of DNA-histograms recorded by flow cytofluorimetry. Both the generation time and the various phase durations of the cell cycle were found to be the same in asynchronous and synchronous populations. It was found that NHIK 3025 cells are damaged by cooling to 4 and 0 degrees C so that cooling of selected cells in order to increase the yield would reduce the quality of the synchronized populations.

Cell Count↗
PubMed1976

A fast and accurate method for calculating Engelberg's synchronization index.

A method is described which makes a fast and accurate calculation of Engelberg's synchronization index possible. The calculation is only based on the growth curve for the synchronous and the corresponding asynchronous population, and makes it unnecessary to calculate the curve for the normalized rate of cell division.

Cell Division↗