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Biomedical subjects

T Christensen

Publications and source records attributed to T Christensen.

At least 217 records · Page 12Linked to original sources
PubMed1980

Photodynamic effects on human cells exposed to light in the presence of hematoporphyrin. pH effects.

Human cells derived from a carcinoma in situ (NHIK 3025) were exposed in vitro to visible light and hematoporphyrin at different pH levels. The cells were inactivated more efficiently at pH 6.7 and 7.2 than at pH 7.8 The treatment with light and hematoporphyrin also induced DNA damage more efficiently at the former pH values than at the latter one. The variation in the efficiency of the photodynamic effect with the pH is mainly due to the fact that the cellular uptake of hematoporphyrin increases with decreasing pH.

Chromosome Aberrations↗
PubMed1980

Binding of hematoporphyrin to synchronized cells from the line NHIK 3025.

The binding of hematoporphyrin (HP) to human cells of the line NHIK 3025 has been studied with the aid of microfluorometry. HP is concentrated within cells when present in Hank's balanced salt solution in the concentration range 10(-5)--3 x 10(-3) M. The time course of binding is biphasic with a rapid initial binding and a slower accumulation at times longer than 30 min. The amount bound to HP increases linearly as the cells proceed through the cell cycle and is doubled from early G1 to late G2.

Carcinoma in Situ↗
PubMed1980

DNA single-strand breaks and sister chromatid exchanges induced by treatment with hematoporphyrin and light or by x-rays in human NHIK 3025 cells.

Alkali-labile sites resulting in single-stranded breaks in DNA and sister chromatid exchanges are produced when human cells (NHIK 3025) in vitro are exposed to sublethal doses of light in the presence of hematoporphyrin. The irradiation doses required to reduce the survival from 1 to 0.1 for 220-kV X-rays and treatment with 10(-4) M hematoporphyrin in phosphate-buffered saline and 380 nm light were 6.2 grays and 230 J/sqm, respectively. X-rays induce about 5 times more sister chromatid exchanges and about 80% more DNA single-strand breaks than exposure to hematoporphyrin plus light when the two modalities of treatment are compared on the same level of survival. In both cases, the single-strand breaks are practically completely repaired within 15 min.

Cell Line↗
PubMed1979

Photodynamic inactivation of cancer cells in vitro. Effect of irradiation temperature and dose fractionation.

Human cancer cells in vitro (NHIK 3025), derived from a carcinoma in situ are inactivated when exposed to visible light in the presence of hematoporphyrin. Irradiation at 4 degrees C results in much more efficient inactivation than irradiation at 37 degrees C. Furthermore, a given total light dose is more efficient when it is fractionated than when it is given in a single exposire. These findings may be taken advantage of in future photochemotherapy of cancer.

Cell Division↗
PubMed1979

The mechanism of photodynamic inactivation of human cells in vitro in the presence of haematoporphyrin.

The photosensitizing effect of haematoporphyrin (HP) on human cells of the established line NHIK 3025 has been studied. Fluorescence measurements show that HP is bound to these cells. Serum proteins also bind HP, and the presence of 10% human serum during incubation with HP (3 X 10(-4)M) reduces the cellular uptake of HP by 75% or more. The photosensitized inactivation is enhanced when the cells are suspended in D2O-buffer during irradiation. This indicates that singlet oxygen is involved in the inactivation. Two findings indicate that the photoinduced damage is repairable: firstly, the fraction of cells surviving a given light dose decreases with decreasing irradiation temperature, and secondly, the survival curves have a shoulder at low exposures of light.

Cell Line↗
PubMed1979

Photodynamic effect of haematoporphyrin throughout the cell cycle of the human cell line NHIK 3025 cultivated in vitro.

Cells from the established cell line NHIK 3025 were synchronized by repeated mitotic selections. Survival of the synchronized cells after treatment with haematoporphyrin and near-UV light was measured by testing the capacity of the cells to form macroscopic colonies. The sensitivity to photodynamic inactivation was small in early G1, late S and G2. The sensitivity increased throughout late G1 and early S to a maximum in mid S. More than a 100-fold variation is found in the survival after 20 min irradiation in the presence of 4 X 10(-4)M haematoporphyrin.

Cell Cycle↗
PubMed1979

Iron absorption and iron status in patients with chronic uremia on regular peritoneal dialysis.

Gastrointestinal iron absorption was measured by whole body counting in 18 patients on regular peritoneal dialysis. Ten patients received regular oral iron treatment prior to the study (iron treated group), 8 patients did not receive iron treatment (non-iron treated group). Whole body retention 14 days after oral administration of 10 microCi 59Fe together with a carrier dose of 10 mg Fe2+ was used as an estimate of absorption. The erythrocyte iron incorporation, i.e. the percentage of administered 59Fe incorporated into the total erythrocyte mass, was measured. Geometric mean iron absorption in the non-iron treated groups was 7.4+/-3.3 (S.D.) % and in the iron treated group 2.8+/-2.5% (p less than 0.01). Absorption in the non-iron treated group did not differ significantly from the value in a normal control group (p greater than 0.3). Absorption in the iron treated group was distinctly lower than in the controls (p less than 0.01), due to the high iron supplementation. Several patients in the non-iron treated group had latent or overt iron deficiency, while patients in the iron treated group had satisfactory iron status. The correlation between iron absorption and erythrocyte iron incorporation was highly significant (r=0.95, p less than 0.001). Peritoneal dialysis patients on the whole have a normally functioning iron absorption. However, due to increased iron losses and insufficient dietary iron intake, the maintenance of a satisfactory iron balance implies an adequate oral iron supplementation.

Absorption↗
PubMed1979

17-Hydroxyprogesterone in normal children and congenital adrenal hyperplasia. Measurement in serum by radioimmunoassay after thin-layer chromatography.

Serum 17alpha-hydroxyprogesterone (17 OH-P) was measured by a specific radioimmunoassay technique combined with thin-layer chromatography. Normal values for children are less than 1.1 microgram/1 (less than 3.3 nmol/l)--corresponding to values found in the literature. In congenital adrenal hyperplasia (CAH) values up to several hundred microgram/l are found. The values rise after ACTH stimulation and are suppressed by decadrone or cortisone treatment. The rise in 17 ketosteroids and pregnanetriol in untreated CAH is relatively smaller (15--25 fold). This clinical sensitivity of 17 OH-P is thus valuable for the diagnosis of CAH (21 hydroxylase deficiency). Furthermore it is easier to take a blood sample than to collect urine for 24 hours. The usefulness in therapeutic monitoring is being studied.

17-Ketosteroids↗
PubMed1979

Photodynamic inactivation of synchronized human cells in vitro in the presence of hematoporphyrin.

Dose-response curves for inactivation of synchronized cells from the human cell line NHK 3025 in the presence of hematoporphyrin and light are shown. Sensitivity toward photodynamic inactivation is increasing as the cells move in the cell cycle from G1 to mid-S. The increase is mostly due to a change in the extent of the shoulder of the dose-response curve at low doses. The quasithreshold dose (Dq) is high in early G1 and much lower in mid-S. No great variations were found in the slope (1/Do) of the dose-response curves at high doses. The shape of the dose-response curves indicates a higher capacity for repair of sublethal damage in the early part of the cell cycle than in the later stages.

Cell Cycle↗
PubMed1979

A syndrome with lack of udder developments in a high-yielding Jersey herd.

A syndrome with lack of udder development in a high-yielding jersey herd is described. The syndrome first appeared in the herd about 10 years ago. To try to elucidate this syndrome the endocrine pattern visualized by serum estrogen (Fig. 1) and progesterone (Fig. 2) levels was followed in 12 parturient cows. One case of typical lack of udder development appeared and was followed up by slaughter and pathological and histological examinations (Fig. 3 and 4). Pedigree investigations indicated that genetics could be involved in the syndrome. The endocrine pattern observed combined with the lack of udder development seems to indicate a complex disorder in the hormonal regulation which trigger the maternal preparation and initiation of parturition.

Animals↗
PubMed1978

The effects of blood loss on the performance of physical exercise.

Seven male subjects were studied before and up to 53 days after the loss of 11 of blood. The resting hematocrit fell from 44.0 to 38.7% and returned to control level after 3 weeks. Maximal oxygen uptake decreased from 4.00 1/min to 3.54 1/min and returned to the initial level within 2 weeks. Submaximal oxygen uptake, pulmonary ventilation, maximal heart rate and blood lactate were not found to change significantly. Submaximal heart rate was increased from 125 beats . min-1 to about 135 beats . min-1 and remained elevated for 3 weeks, whereas blood lactate was increased only in the first week. Maximal work time decreased from 5.1 min to 3.8 min and remained low for the first 2 weeks, but rose thereafter above the starting level. Comparison with a control study suggested that there is some training effect, which, when allowed for, indicates that maximal work time returns to starting values at the same time as does the maximal oxygen uptake. It is concluded that the drop in Hct, maximal oxygen uptake and work capacity, found after the loss of 11 of blood, are related to each other both in magnitude and duration.

Adult↗
PubMed1978

Sex steroids and sex-hormone binding globulin in males with chronic alcoholism.

Thirty men with chronic alcoholism were studied. Biopsies of the liver and testis were performed in all. Serum concentrations of total and non-protein bound (free) testosterone and oestradiol, dihydrotestosterone and sex-hormone binding globulin (SHBG) were determined. Testosterone and dihydrotestosterone concentrations were normal in most patients, whereas oestradiol and free oestradiol were above normal in approximately 50% of the patients. None of the hormones measured differed significantly between patients with and without cirrhosis. SGBG was significantly higher in men with severely reduced spermatogenesis compared to those with intact germinal epithelium, but there was no difference between men with and without cirrhosis. No relation could be demonstrated between clinical signs of hypogonadism and any of the hormones measured. The results support the view that hormonal and sexual disturbances may occur in chronic alcoholism independent of the presence of liver disease.

Adult↗
PubMed1978

Relationship between haemoglobin and serum testosterone in normal children and adolescents and in boys with delayed puberty.

The concentrations of haemoglobin and of serum testosterone were measured in 215 normal children and adolescents aged 7--20 years, and in 8 boys with constitutional delayed puberty. From the age of 14 years onward haemoglobin and testosterone rose in normal boys and differed significantly from the stable levels observed in prepubertal children and pubertal girls. In the entire series of normal boys (n = 118, age 7--20 years) concentrations of haemoglobin and testosterone were found to be closely correlated (r = 0.73, p less than 0.001). These results provide further evidence for a major role of testosterone in the control of erythropoiesis. Therefore, this correlation suggests the use of serum testosterone determination for the proper selection of haemoglobin reference ranges in boys. The respective reference ranges of haemoglobin corresponding to testosterone levels at 0 and 30 nmol/l were 120.5--148.5 and 143.5--171.5 g/l (95% confidence limits). Boys with delayed puberty were found to have significantly reduced median values of haemoglobin and testosterone for their chronological age, and 6 of the 8 boys investigated were truly anaemic on this background. Nevertheless, their haemoglobin concentration did appear appropriate as judged from their testosterone levels. This observation supports the idea that the selection of the relevant reference range for haemoglobin in boys should depend on the state of physical development as expressed by serum testosterone.

Adolescent↗
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↗