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O Mäentausta

Publications and source records attributed to O Mäentausta.

At least 19 recordsLinked to original sources
PubMed1994

Immunohistochemical localization of estrogen-specific 17 beta-hydroxysteroid oxidoreductase in the human and mouse prostate.

The estrogen-specific 17 beta-hydroxysteroid oxidoreductase (17 beta-HSOR) enzyme protein was stained immunohistochemically in the newborn and adult human prostate as well as in the mouse prostate. In the newborn human prostate, ductal and urethral epithelia were faintly stained, whereas in the adult human prostate, intense staining for 17 beta-HSOR enzyme antigen could be detected in the epithelium of the collecting ducts and urethral epithelium as well as in the epithelium of the intraprostatic vas deferens and seminal vesicle epithelium. Immunostaining was weak in the prostatic tissues of both newborn and adult prostate. No positive cells were found in stroma. The activity of NADPH-dependent 3H-estrone reductase was detectable in cell-free homogenates prepared from human prostatic tissues. The activities showed a good correlation with immunocytochemical findings. In the mouse, neonatal estrogenization resulted in intensively stained epithelium of the collecting ducts at the age of 14 days. Moreover, when adult control and neonatally estrogenized mice were implanted with 17 beta-estradiol, the metaplastic epithelium of the periurethral collecting ducts of neonatally estrogenized mice was intensively stained with 17 beta-HSOR. These findings suggest that metaplastic epithelium rises from 17 beta-HSOR-positive cells. The similar distributions of 17 beta-HSOR-positive cells confirm the concept of homology in the posterior estrogen-responsive periurethral region (containing the periurethral ducts and periurethral glands) of the mouse and humans. Our findings further suggest that the 17 beta-HSOR-positive cells may have the same origin and hormonal control in both species.

Adult↗
PubMed1993

The effects of an antiprogestin, mifepristone, and an antiestrogen, tamoxifen, on endometrial 17 beta-hydroxysteroid dehydrogenase and progestin and estrogen receptors during the luteal phase of the menstrual cycle: an immunohistochemical study.

The effects of a progesterone antagonist, mifepristone (RU486), and an estrogen antagonist, tamoxifen, given during the early luteal phase on endometrial 17 beta-hydroxysteroid dehydrogenase (17HSD) and estrogen (ER) and progesterone (PR) receptors were studied. Eleven regularly menstruating women were studied during control and treatment cycles. In the treatment cycle on day LH + 2 (2 days after the peak serum LH concentration), 10 subjects received a single dose of 200 mg mifepristone, and 9 received 2 doses of 40 mg tamoxifen on days LH + 2 and LH + 3. In addition, 4 subjects received 400 mg mifepristone in a separate treatment cycle. 17HSD, ER, and PR were measured immunohistochemically in endometrial tissue specimens taken on days LH + 6 to LH + 8. Blood samples were conducted during control and treatment cycles, and serum estradiol, progesterone, and LH concentrations were quantified by RIA. Administration of mifepristone blocked the induction of 17HSD by progesterone and prevented the expression of 17HSD in gland and surface epithelial cells in 8 patients. In 2 patients, staining of 17HSD was seen during both the control and mifepristone treatment cycles. The higher dose of mifepristone additionally given to four subjects did not block the expression of 17HSD in 2 cases where blocking was observed with the lower dose of mifepristone, and in 1 of these patients, very strong staining of 17HSD was observed in basal cells beneath the epithelial cells. ER and PR showed intense staining in the nuclei of both gland and stromal cells in mifepristone treatment cycles, whereas receptor staining was faint or absent in the respective control cycles. Tamoxifen did not have any significant effect on staining of 17HSD or the abundance of receptors. Serum concentrations of estradiol, progesterone, and LH were not significantly affected by the administration of mifepristone or tamoxifen. This study reveals that mifepristone, administered in the early luteal phase, usually blocks the expression of 17HSD and the down-regulation of PR and ER. However, the expression of 17HSD in some patients may reflect the ineffectiveness of the mifepristone treatment used to prevent implantation in certain subjects.

17-Hydroxysteroid Dehydrogenases↗
PubMed1992

Immunohistochemical study of the human 17 beta-hydroxysteroid dehydrogenase and steroid receptors in endometrial adenocarcinoma.

17 beta-Hydroxysteroid dehydrogenase (17HSD) and estrogen (ER) and progestin (PR) receptors were analyzed immunohistochemically in tissue specimens of 66 patients with endometrial adenocarcinoma. Plasma steroid concentrations were correlated to immunohistochemical data. 17HSD was detected in 48% of the specimens and was stained in the cytoplasm of epithelial cells. The tissues were characterized by a heterogeneous staining pattern for 17HSD. In some patients, intensively stained epithelial cell clusters were seen, indicating that local factors were responsible for the expression of the protein. Poorly differentiated adenocarcinoma specimens tended to have no 17HSD more frequently than did well or moderately differentiated tissues. ER and PR were detectable in 24% and 28% of patients, respectively, and were localized in the nuclei of epithelial and stromal cells. There was a significant correlation between 17HSD and PR staining and an inverse correlation between plasma progesterone concentrations and 17HSD staining. This is contrary to the data obtained with normal endometrium. The main reason for this inverse relation between endometrial 17HSD staining and plasma progesterone concentrations was that, in some postmenopausal patients with low plasma progesterone concentrations, intense staining for 17HSD was detectable in the endometrial carcinoma specimens. This indicates a major difference in the regulation of 17HSD expression in endometrial adenocarcinomas, compared with normal tissues of premenopausal women.

17-Hydroxysteroid Dehydrogenases↗
PubMed1992

Distribution of estradiol-17 beta hydroxysteroid oxidoreductase in the urogenital tract of control and neonatally estrogenized male mice: immunohistochemical, enzymehistochemical, and biochemical study.

The present study was conducted to investigate the regional distribution of the enzymes catalyzing the interconversion of the hydroxyl and carbonyl groups at C-17 of the estrogen molecule within the male urogenital tract of adult mouse and to test the hypothesis, whether regional differences in the distribution are critical for estrogen responses. The highest ratios of NADPH-dependent 3H-estrogen reduction to oxidation at C-17 of cell-free homogenates were obtained from coagulating gland and seminal vesicle as well as from the prostatic and lower intrapelvic urethra, which are considered the most estrogen-sensitive parts of the male urogenital tract. Both NADP- and NAD-dependent oxidation of 3H-17 beta-estradiol were low or nondetectable at these sites. The epithelium of the lower and prostatic urethra as well as the periurethral collecting ducts were stained with the antibody prepared against human placental 17 beta-hydroxysteroid oxidoreductase. The NAD-dependent 3H-estradiol-17 beta oxidase activity was highest in the bladder epithelium, and the activity declined sharply in the urinary tract from the bladder downward. The lowest detectable activities were found in vas deferens and prostate (combined ventral and dorsolateral lobes). The uneven distribution of estradiol-17 beta oxidase activity may provide additional explanation for the regional differences of estrogen responses. The NADPH-dependent 17 beta-reduction of estrone and the immunohistochemical staining of the human placental estradiol-17 beta oxidoreductase antigenicity were not significantly altered after neonatal estrogenization. These findings do not lend any support to the idea that the increased estrogen sensitivity observed after neonatal estrogenization is associated with changes in 17 beta-oxidoreduction. However, the possibility remains that there are specific sites (e.g., epithelium of prostatic urethra and collecting ducts) in which the changes in 17 beta-oxidoreduction of estrogen does play a role in the regulation of estrogen action.

17-Hydroxysteroid Dehydrogenases↗
PubMed1992

Immunohistochemical detection of human estrogen receptor with region D-specific antipeptide antibodies.

To study the possibility of using antipeptide antibodies for the immunohistochemical determination of human estrogen receptors (ER), three peptides corresponding to the putative major antigenic regions of the human ER (Met12-Leu26, or ERP1; Thr227-Gln267, or ERP2; Leu256-Gly275, or ERP3) were used to produce site-specific rabbit polyclonal antipeptide antisera. High titer antibodies were obtained against all the peptides used, as judged by time-resolved fluoroimmunoassay. The antibodies against region D (ERP3) specifically immunoprecipitated the ER proteins in vitro, as did the antiERP2 antibodies to a much smaller extent. With one of the region D-specific antibodies (antiERP3 Ab2) ER could also be immunohistochemically detected. When benign and malignant human breast and normal endometrial tissues were used, the immunohistochemical staining observed with these antipeptide antibodies correlated well with the staining obtained with an established method. Thus, the results reported here show that this part of region D in ER is a potential antigenic epitope for the production of site-specific antibodies against ER. Antipeptide antibodies produced against this region can be used to immunolocalize the ER in various normal and pathological human tissues.

Breast Neoplasms↗
PubMed1991

Immunohistochemical localization of 17 beta-hydroxysteroid dehydrogenase in the human endometrium during the menstrual cycle.

Immunoaffinity-purified polyclonal anti-rabbit antibody against human placental 17 beta-hydroxysteroid dehydrogenase (17HSD) was used to localize 17HSD in frozen sections of 21 human endometrial tissue specimens, taken at different stages of the menstrual cycle, and in the human placenta. The presence and distribution of estrogen and progesterone receptors were also analyzed in endometrial specimens using commercial immunohistochemical techniques. In addition, 17HSD was localized by immunoelectron microscopy in the endometrium and the placenta. In the endometrium, immunostaining of 17HSD appeared in the cytoplasm of surface epithelial and gland cells during the early and midluteal phase. During the late luteal phase, it gradually disappeared. No immunostaining was observed in the endometrium during the follicular phase of the menstrual cycle. The changes in staining intensity of 17HSD were associated with changes in the concentration of serum progesterone as judged by radioimmunoassay. An apparent inverse correlation between 17HSD expression and the concentrations of estrogen and progesterone receptors was observed. These results strongly support the concept that progesterone induces an increase in the amount of 17HSD, in the glandular and surface epithelial cells of the human endometrium. In the human term placenta, 17HSD immunostaining was detected exclusively in the cytoplasm of syncytiotrophoblasts. In immunoelectron microscopic studies of the endometrium and placenta, 17HSD staining was observed in the cytoplasm and it was associated with cytoplasmic membranes unrelated to the endoplasmic reticulum.

17-Hydroxysteroid Dehydrogenases↗
PubMed1991

Time-resolved immunofluorometric assay of 17 beta-hydroxysteroid dehydrogenase in plasma.

We describe a time-resolved immunofluorometric assay (TR-IFMA) for human 17 beta-hydroxysteroid dehydrogenase (17HSD) in which antibody-coated microtiter strip wells and europium chelate-labeled polyclonal antibodies are used. In preparing the label, a polyclonal antibody is affinity-purified and derivatized with diethylenetriamine-pentaacetic acid. With this derivative, five to eight europium ions can be combined with one antibody molecule without decreasing the antibody's immunoreactivity. The minimum detectable concentration of 17HSD is 0.13 microgram/L; the intra- and interassay CVs are less than 8% and less than 15%, respectively, for concentrations between 0.3 and 100 micrograms/L. There is no difference between the concentrations of 17HSD in plasma specimens taken during the proliferative and luteal phases of the menstrual cycle, the measured mean concentration being 0.22 microgram/L. We found no correlation between plasma 17HSD and progesterone concentrations. The plasma concentrations of 17HSD increase during pregnancy, the mean concentrations being 1.5, 4.4, and 12.5 micrograms/L, during the first, second, and third trimesters of pregnancy, respectively. In the specimens from 18 men, the mean concentration was 0.18 microgram/L. In six plasma specimens from patients with endometrial adenocarcinoma, the mean concentration was 0.20 micrograms/L. Pre-analytical aspects are important in the assay of 17HSD because of the lability of the enzyme protein. Preferably, blood should be sampled into EDTA-containing tubes, plasma should be separated within 15 min, and glycerol must be added without delay to a final volume of 200 mL/L.

17-Hydroxysteroid Dehydrogenases↗
PubMed1990

Immunological measurement of human 17 beta-hydroxysteroid dehydrogenase.

Human placental 17 beta-hydroxysteroid dehydrogenase (17-HSD) was purified to apparent homogeneity using ammonium sulfate precipitation and chromatography on Red-Agarose and DEAE-Sepharose columns. Electrophoresis on polyacrylamide gels under denaturing conditions and using silver staining showed a single protein with an apparent molecular weight of 37,800. Antibodies to the purified protein were raised in rabbits and were found by immunoblotting to be specific to 17-HSD. A sensitive radioimmunoassay was established using 125I-labeled 17-HSD as a tracer, an appropriate dilution of the antibody, and a kaolin-coupled double antibody for separating the antibody-bound and free fractions. The detection limit of the assay was approximately 150 pg/tube (1.5 micrograms/l). The cytosol fraction (105,000 g) of term placental tissue contained approximately 0.7 mg of 17-HSD per gram of protein, and the concentrations of 17-HSD measured by immunoassay and enzymatic activity proved to be strictly parallel in different partly purified placental preparations. The supernatants from centrifugations of human endometrial homogenates at 800 g and 105,000 g (after detergent treatment) displayed cross-reactivity with the antibody. The mean concentration of the cross-reacting substance in the radioimmunoassay was 14.1 micrograms/g protein (range 2-62.3) in specimens taken on different days in the cycle. These concentrations showed a significant correlation with the 17-HSD activities measured in the endometrial specimens (r = 0.722, P less than 0.001, n = 21). Mean concentrations of substance were 8.3 micrograms/g protein in endometrial specimens taken during the follicular phase (days 4-12, n = 8) and 22.9 micrograms/g protein during the luteal phase (days 16-22, n = 6) were obtained using the radioimmunoassay. There was excellent parallelism between the competition curves for [125I]iodo-17-HSD with purified 17-HSD standards and placental and endometrial homogenate dilutions. These data strongly suggest that the substance measured in the endometrial specimens was 17-HSD.

17-Hydroxysteroid Dehydrogenases↗
PubMed1990

Direct solid-phase time-resolved fluoroimmunoassay of 17 alpha-hydroxyprogesterone in serum and dried blood spots on filter paper.

We describe a direct, solid-phase time-resolved fluoroimmunoassay (TRFIA) for measuring 17 alpha-hydroxyprogesterone (17OHP) in serum and blood spots on filter paper. We used 17OHP-3-carboxymethyloxime (17OHP3CMO) coupled to polylysine as the label, which enabled incorporation of up to 34 atoms of europium per molecule of 17OHP, for a very high specific activity. The assay is based on competition between labeled 17OHP3CMO and 17OHP in blood specimens for polyclonal rabbit anti-17OHP antibodies. The antibody-label complex is separated by binding to anti-rabbit antibodies coated onto microtiter strips. The assay buffer contains danazol to displace 17OHP from steroid-binding proteins in serum. For serum samples, the assay is accomplished in 1 h of incubation at room temperature. The blood spot assay with filter paper discs involves incubation overnight at 4 degrees C. Results for both types of specimens from the same subjects correlated well. The lowest measurable concentrations of 17OHP (nmol/L) were 0.10 (3 SD) and 0.75 (3 SD) for serum and dried blood on filter paper, respectively. Intra- and interassay CVs were about 5-15% for both types of samples.

17-alpha-Hydroxyprogesterone↗
PubMed1989

Relationship of Campylobacter pylori and duodenogastric reflux.

We have examined the relationship of Campylobacter-like organism (CLO) and duodenogastric reflux (DGR) in 107 patients with unoperated stomachs. Neither the extent of externally measured bile reflux nor the concentrations of bile acids or lysolecithin in the gastric fluid differed significantly in the groups with different numbers of CLO in the gastric mucosa. Our results suggest that DGR, in the quantities commonly present in unoperated stomachs, does not effect the presence of C. pylori in the gastric mucosa.

Adult↗
PubMed1988

Complete amino acid sequence of human placental 17 beta-hydroxysteroid dehydrogenase deduced from cDNA.

cDNA clones for 17 beta-hydroxysteroid dehydrogenase (17-HSD; EC 1.1.1.62) were isolated from a placental lambda gt11 expression library using polyclonal antibodies against placental 17-HSD. The largest cDNA contained 1325 nucleotides, consisting of a short 5'-noncoding segment, a coding segment of 987 nucleotides terminated by a TAA codon, and a 329 nucleotide long 3'-noncoding segment. The open reading frame encoded a polypeptide of 327 amino acid residues with a predicted Mr of 34853. The amino acid sequence of 23 N-terminal amino acids determined from purified 17-HSD agreed with the sequence deduced from cDNA. The deduced amino acid sequence also contained two peptides previously characterized from the proposed catalytic area of placental 17-HSD.

17-Hydroxysteroid Dehydrogenases↗
PubMed1988

Time-resolved immunofluorometric assay of sex-hormone binding globulin.

A time-resolved immunofluorometric assay (trlFMA) for human sex-hormone binding globulin (SHBG) is described in which antibody-coated tubes or microliter strip-wells and a europium (Eu) chelate-labeled monoclonal antibody are used. The trlFMA sensitivity is similar to that of other SHBG immunoassays, and other analytical variables compare favorably with an SHBG immunoradiometric assay (IRMA) kit and a steroid binding capacity assay: the interassay coefficient of variation (CV) is less than 8% and the intra-assay CV is less than 6% for concentrations between 6 and 200 nmol/L. The reference intervals (means +/- SD) for SHBG concentrations (nmol/L) in serum from 10 men, 10 women, and 10 pregnant women were 23 +/- 12, 65 +/- 39, and 439 +/- 122, respectively. In 14 hirsute women the mean +/- SD serum SHBG concentration (37 +/- 21 nmol/L) was significantly lower (P less than 0.01) than the mean for an age-matched, nonhirsute female comparison group. The trlFMA is technically simple, requires no centrifugation or separation reagent, and takes a counting time of only 1 s. In addition, the Eu-label is nontoxic, presents no waste-disposal problems, and has a long shelf life.

Adult↗
PubMed1988

Rapid equilibrium radioimmunoassay for the amino-terminal propeptide of human type III procollagen.

This is an equilibrium-type radioimmunoassay for the amino-terminal propeptide of type III procollagen (PIIINP), which overcomes the problem of nonparallelism between the standard and human serum samples encountered with earlier assays. Proper selection of antiserum and reaction conditions diminishes interference from degradation products of the propeptide in serum. Because a rapid solid-phase-bound second-antibody step is included, the assay takes only 3 h. The intra-assay and the interassay CVs are both about 5%. In infants and children the concentration of PIIINP in serum closely parallels the growth-velocity curve. For 88 presumably healthy adults, the PIIINP concentration was 1.7-4.2 micrograms/L, about a third that measured with the previously available commercial assay. This is because of lack of inhibition by small Col 1 domain-related degradation products.

Adolescent↗
PubMed1987

Campylobacter-like organisms and gastritis: histopathology, bile reflux, and gastric fluid composition.

We studied a prospective series of 107 randomly chosen dyspepsia patients without gastric ulcer for the association of spiral Campylobacter-like organisms (CLO) with features of antral and fundal gastritis and duodenogastric reflux. CLO were observed in 38% of the patients. The scores for all classes of inflammatory cells in both antral and body mucosa were significantly higher in the CLO-positive patients than in the CLO-negative ones (p less than 0.001), and foveolar hyperplasia was also associated with CLO (p less than 0.05). Metaplasia and glandular atrophy in the antral mucosa were significantly commoner in the CLO-positive group (p less than 0.05 and p less than 0.01, respectively). The body gastritis score correlated significantly with age in the CLO-negative patients (R = 0.33, p less than 0.01) but not in the CLO-positive ones. There were no significant differences between the groups with regard to duodenogastric reflux or intragastric pH. The results confirm that CLO are associated with gastritis, most notably superficial gastritis in the body and atrophic gastritis in the antrum, but their aetiological significance remains to be proved.

Adult↗
PubMed1984

Gallbladder function and maternal bile acids in intrahepatic cholestasis of pregnancy.

Ultrasonic measurement of the gallbladder volume was taken in 8 nonpregnant, healthy women, in 7 women with normal pregnancies and in 7 women whose pregnancies were complicated by intrahepatic cholestasis of pregnancy, in the fasting state and 30, 60, 120 and 180 min after a test meal. At the same time the serum concentrations of cholic acid and chenodeoxycholic acid were measured. The fasting and ejection volumes of the gallbladder in cholestasis of pregnancy were greater than in normal pregnancy. The fasting volume of the gallbladder was greater, but the ejection volume smaller in normal pregnancy than in nonpregnant women. No difference in the ultrasonic appearance of the intra- and extrahepatic bile ducts was found between the groups. Serum bile acids were increased in cholestasis of pregnancy and did not display any decreasing tendency after the postprandial rise during the following 3 h. The results indicate that in cholestasis of pregnancy the gallbladder function and the enterohepatic circulation of bile acids are different from normal pregnancy. This may be associated with the great tendency to gallstones in these women. The large size of the gallbladder in cholestasis of pregnancy has differential diagnostic importance in the ultrasonic evaluation of a pregnant woman with liver disease.

Bile Acids and Salts↗
PubMed1982

Serum bile acids during biphasic contraceptive treatment with ethinyl estradiol and norgestrel.

Twenty-nine women were treated with biphasic combined oral contraceptive pills containing ethinyl estradiol 0.05 mg and levonorgestrel 0.050-0.125 mg. Serum primary bile acids (cholic acid and chenodeoxycholic acid) and one secondary bile acid (deoxycholic acid) were measured by radioimmunoassay. The serum samples were collected before the treatment and at one, three and twelve months during the treatment. No significant changes were found in these bile acid levels during the treatment. The ratio of cholic/chenodeoxycholic acid did not change either. No pathological values were found in the conventional liver function tests although serum alanine aminotransferase activity was significantly increased after twelve months' treatment. It can therefore be concluded that the present contraceptive pill does not cause any liver dysfunction detectable by bile acid measurements of other "classical" liver function tests.

Adolescent↗