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S Kallio

Publications and source records attributed to S Kallio.

6 recordsLinked to original sources
PubMed1986

A new triphenylethylene compound, Fc-1157a. I. Hormonal effects.

The basic pharmacological and biochemical properties of a new antiestrogen, Fc-1157a, are described. Fc-1157a is bound specifically and with high affinity to estrogen receptors. The binding is competitive with estradiol. Fc-1157a treatment induces translocation of estrogen receptors from cytoplasm to nucleus. The turnover rate of nuclear estrogen receptors is markedly lower than with estradiol, but is more rapid than after tamoxifen. Fc-1157a is an almost pure antiestrogen in rat uterus, but has intrinsic estrogenic activity in mouse uterus. In animal experiments Fc-1157a has shown antitumor properties, which are described in the companion paper.

Animals↗
PubMed1986

A new triphenylethylene compound, Fc-1157a. II. Antitumor effects.

The antitumor effects of a new antiestrogen, Fc-1157a have been studied in vitro and in vivo. In vitro the effect of Fc-1157a was comparable to that of tamoxifen. The effect was dose-dependent, and at concentrations higher than 10(-6) mol/1 Fc-1157a induced real cell death of the MCF-7 cells. In DMBA-induced mammary cancer in rats Fc-1157a decreased the number of new tumors and inhibited the growth of existing tumors, these effects being statistically highly significant. The ratio of growing tumors to stable and regressing tumors was significantly decreased. Although these effects were slightly stronger with Fc-1157a than with tamoxifen, the difference between these two compounds was not statistically significant. Murine uterine sarcoma, an estrogen receptor-negative tumor, was resistant to tamoxifen, but was statistically significantly inhibited by high doses (100 and 200 mg/kg-1 day-1 for 5 days) of Fc-1157a. The antitumor effects of Fc-1157a are due mainly to the antiestrogenic activity. At high concentrations in vitro and at high doses in vivo Fc-1157a exerts antitumor effects some of which are different from those of tamoxifen and are directed even against estrogen receptor-negative tumors. The exact mechanism of the observed cytolytic effect at high doses is unknown.

Animals↗
PubMed1982

Steroid receptors in normal and neoplastic female reproductive tissues.

The presence of cytosol estrogen (ER) and progestin (PR) receptors in specimens of normal uterine cervix, endometrium, myometrium, Fallopian tubes and corpora lutei or in samples of neoplastic female reproductive tissues was investigated. The material consisted of PR and ER measurements of tissue samples obtained from fertile and postmenopausal women, receptor assays were performed by a dextran-coated charcoal technique. The radio PR/ER was highest in specimens from the Fallopian tubes (44) and endometrium (4-10),2-3 in specimens of uterine ecto- or endocervical epithelium and about 4 in the myometrium. No ER or PR were found in the four corpora lutei examined. PR or PR/ER ratio in specimens of myoma tissues did not differ from that found in the myometrium specimens. The highest ER and PR values in the endometrium were measured in specimens taken during the late proliferative or intermediate phase of the menstrual cycle. The PR values in specimens from postmenopausal myometrium were lower in comparison with the samples taken from the myometrium of fertile women in contrast to ER values. In the specimens of carcinoma of the vulva and the uterine cervix ER levels were very low, with no measureable values of PR. In the endometrial carcinoma samples the PR/ER ratio was lower than in the normal endometrium. 4 out of 7 specimens taken from ovarian adenocarcinoma had a measureable amount of ER and in 2 out of 7 cases PR.

Female↗
PubMed1981

HLA-B27 frequency and MLC reactions in acute anterior uveitis.

HLA-A and B antigens were determined in 37 unrelated patients with acute non-granulomatous anterior uveitis (AAU) and in 114 control subjects. HLA-B27 was identified in 31 patients with AAU (83.8%) and in 15 control subjects (13.2%). Fifteen patients (40.5%) had associated rheumatic diseases and all of them (100%) had HLA-B27. Of the 22 patients without any associated disease, 16 (72.7%) had HLA-B277. To study the HLA-D composition MLC tests were done as one-way microcultures between members of four groups consisting of 10, 10, 8, 8 patients with AAU and two or three healthy controls in each test group. No difference between patient-to-patient reactions as compared with the control reactions could be observed. The results show that AAU is very closely associated with HLA-B27 but not with any of the HLA-D antigens.

Adult↗
PubMed1980

Increased urinary protein excretion after intravenous injection of furosemide in man.

The furosemide-induced increase in protein excretion, and its relations to 1) the size of protein molecules as reflected by three enzymes, and 2) glomerular filtration rate (GFR), plasma renin activity (PRA) and prostaglandin (PG) E2 and F2 alpha excretions were studied in 14 outpatients with normal renal function and 13 healthy males. Furosemide (120 mg) was given intravenously, and thereafter the protein excretion and the above parameters were monitored for 1--2 hours. In both groups, furosemide caused a transient increase in protein excretion. The excretion of the largest molecule, beta-glucuronidase, rose to 6.3-fold, while those of N-acetyl-beta-D-glucosaminidase and of the smallest molecule, alpha-amylase, increased by 91 and 37%, respectively. GFR increased, too, but markedly less than the protein excretion. PGE2 and PGF2 alpha excretions increased more than GFR and changed simultaneously with the excretion of proteins. Furosemide also caused a marked increase in PRA. This lasted, however, much longer than the rise in PG and protein excretion or GFR. The results suggest that the furosemide-induced increase in protein excretion is 1) related to the molecular size of proteins, 2) partly due to the rise in GFR, 3) simultaneous with the change in PG excretion. Our findings also agree with the view that furosemide causes changes in glomerular permeability.

Acetylglucosaminidase↗