Search PubMed⌕ Search

Biomedical subjects

J Spona

Publications and source records attributed to J Spona.

At least 253 records · Page 14Linked to original sources
PubMed1976

Optimization of determination of ovulation after clomiphene therapy.

A total of 131 cycles of 71 sterility patients, who suffered from anovulatory cycles at least previous 6 months, were monitored daily by a rapid radioimmunoassay for LH and by gynecological examinations before we attempted to induce ovulations with Clomiphene. The width of the cervix, spinnbarkeit, transparency of the cervical mucus and karyopycnotic and acidophilic index of the vagina were recorded daily. 18 subjects exhibited hypoplasia of the uterus and 32 husbands of the 71 patients suffered from severe to medium oligospermia. Homologous inseminations were performed in 15 patients. Different patterns of LH serum levels were observed during and after Clomiphene treatment. The response of LH to Clomiphene and preovulatory LH rise was recorded in 73 cycles. No Clomiphene response with preovulatory LH peak was observed in 31 cycles. 11 patients out of 71 subjects failed to ovulate. 12 patients (30.7%) out of 39 subjects with normospermatic husbands became pregnant. 6 patients (18.7%) of 32 subjects whose husbands suffered from oligospermia became pregnant. A total pregnancy rate of 30% calculated, when the 11 patients with negative responses are excluded. The conclusion is reached that sterility patients benefit most, when both gynecological as well as rapid LH estimations by radioimmunoassay are used to time imminent ovulations in Clomiphene treated subjects.

Anovulation↗
PubMed1976

[Serum levels of LH and FSH in patients with adreno-genital syndrome (AGS) (author's transl)].

Serum levels of LH, FSH, testosterone and 17beta-estradiol were estimated by radioimmunoassay in 13 children suffering from AGS. Hormone levels were determined during and after substitution therapy and were compared with values registered in normal subjects. After therapy was stopped a statistically significant rise of testosterone and 17beta-estradiol was observed, but no changes in the serum levels of LH and FSH was noted. The discrepancies between the two observations are discussed.

Adrenal Hyperplasia, Congenital↗
PubMed1976

Action of steroids on LH-RH provoked gonadotropin release.

The action of mesterolone (1 alpha-methyl-17-beta-hydroxy-5 alpha-androsten-3-one) mesterolone cipionate, testosterone, 17 alpha-methyl-testosterone, 17 beta-hydroxy-5 alpha-androstane-3-one, cyproterone actetate and D-norgestrel on basal and LH-RH stimulated, gonadotropin release was studied in vitro. Hemi-gland preparation of the anterior pituitary were incubated in the presence or absence of steroids and/or LH-RH. Steroid hormones were added at a concentration of 25, 5 and 1 mug per ml medium. Basal levels of LH and FSH discharge were not influenced by mesterolone, whereas inhibition of LH-RH stimulated gonadotropin release was noted at 25 mug mesterolone/ml medium. The addition of mesterolone cipionate to the incubation medium did not significantly change basal FSH levels, whereas an inhibition of LH-RH provoked FSH discharge was noted. Basal LH release was stimulated by the presence of 1 mug mesterolone cipionate per 1 ml medium. LH-RH stimulated LH release in the presence of 25, 5 and 1 mug mesterolone cipionate per 1 ml medium was indistinguishable from control levels. Basal levels of LH and FSH were not affected by testosterone, whereas an impaired gonadotropin response to LH-RH was observed in the presence of testosterone. At 1 mug testosterone per 1 ml medium only LH response to LH-RH was found. Basal gonadotropin levels in the presence of 17 alpha-methyl-testosterone were indistinguishable from control values. The only inhibition of LH-RH action was found for stimulation of LH release at 25 mug 17 alpha-methyl-testosterone/ml medium. On the other hand, 17 beta-hydroxy-5 alpha-androstane-3-one stimulated basal LH and FSH discharge, and LH-RH actions were not impaired. Results of our studies with cyproterone acetate indicate that this steroid stimulates basal pituitary gonadotropin discharge at high concentration, without blunting responses to LH-RH. No action of D-norgestrel on basal and LH-RH stimulated gonadotropin release was observed. These experiments add further evidence that steroids modulate LH-RH actions at the pituitary level. It is concluded that the fine control of gonadotropin release resides at the adenohypophysis whereas the coarse control of LH and FSH discharge is at the hypothalamus and/or other centers of the central nervous system.

Androstenes↗
PubMed1976

[Influence of allylestrenol on hpl serum levels in high-risk pregnancies (author's transl)].

32 patients with high-risk pregnancies were treated with 3 X 5 mg of 17alpha-ally1-17beta-hydroxy-estr-4-ene (allylestrenol, Gestanon) daily. Only those patients entered this study, who had pathological HPL serum levels during two successive control investigations. In addition, cytological analyses of vaginal smears were performed before treatment was started. The patients were treated with allylestrenol until normal HPL levels were recorded, but at least during 14 days. HPL serum levels were estimated every second day through 14 days. Thereafter HPL assays were performed in weekly intervals. Determinations of HPL were done by radioimmunoassay. Analyses of vaginal smears were done weekly. Statistical analysis of HPL serum levels were performed by Student's-t-test. A statistical significant increase of HPL serum levels were registered during allylestrenol therapy. These results suggest that the pregnancy maintaining effect of allylestrenol is at least partly due to a stimulation of placental function. Analyses of vaginal smears indicate a progestational effect of the norsteroid.

Allylestrenol↗
PubMed1975

[About the estimation of fetal risk by evalution of the serum -- amniotic liqour -- ratio of HPL during the pregnancy (author's transl)].

Radioimmunoassay of human placental lactogen (HPL) is a valuable diagnostic tool for the early recognition of placental dysfunction. But, the rather wide normal range hampers HPL estimations to be used as a good prognostic tool. However, the simultaneous determination of HPL in maternal serum and in amniotic fluid allows a better diagnosis of the fetal well-being. Results of amniotic fluid HPL levels are expressed as percent of maternal serum levels. In this pilot study it was shown that this ratio of maternal serum HPL level to amniotic fluid level is below 10% in normal pregnancies. The ratio is between 10 to 20% in subjects where fetal distress was recorded, and dystrophic babies were observed. The value is above 20% in cases where intrauterine fetal deaths were found. This good correlation of the HPL ratio in maternal serum and amniotic fluid with the outcome of pregnancy offers a new means of using HPL estimation as prognostic tool.

Amniotic Fluid↗
PubMed1975

[Optimal monitoring in EPH gestosis and idiopathic placentar insufficiency (author's transl)].

EPH gestosis and placental insufficiency sui generis are cause of fetal hazards. Clinical symptomatology and anamnesis indicate different tests to detect pathological conditions for the fetus. HPL, HCG, urinary estriol, measuring the placental flow-rate, ultrasonic diagnosis as all other usual examinations during pregnancy were carried out. In EPH gestosis a reduction of all placental functions was found like as for thrombocytes and fibrinogen. Placental insufficiency showed an even greater reduction of placental function, only thrombocytes and fibrinogen remained constant. Weight and length of the newborn were according the pathological placental function reduced. Morphology of the placenta could proof the results of the previous done tests.

Adult↗
PubMed1975

Some structural requirements for LH-RH actions.

LH-RH and analogues of LH-RH, [2-4] LH-RH, [Lys8] LH-RH, [Ala4] LH-RH and [3-10] LH-RH were tested in vitro for their ability to stimulate LH and FSH release, respectively. Furthermore, the influence of these peptides on binding of LH-RH to the anterior pituitary plasma membrane fractions of female rats was studied to obtain some information on the structural requirements for LH-RH actions. Significant increase of LH release above the control level was recorded for LH-RH, [Lys8] LH-RH and [Ala4] LH-RH. LH release in the presence of the tripeptide [2-4] LH-RH and the octapeptide [3-10] LH-RH was statistically indistinguishable from that of basal levels. Significant stimulation of FSH release was noted only in the presence of LH-RH and [Lys8] LH-RH. Changes in the binding characteristics of LH-RH to the pituitary plasma membrane in the presence of the LH-RH analogues suggest a proportionality between releasing ability and receptor affinity. Glu and His residues of the LH molecule were found to be critical for binding to the receptor. Residual binding ability of TRH to LH-RH receptor is consistent with current molecular models of LH-RH and TRH, respectively. Furthermore, the data presented suggest that the amino acid in position 8 of the LH-RH molecule is of importance for the three dimensional structure of LH-RH.

Animals↗
PubMed1975

Sex steroids influence LH-RH-receptor interaction.

Intact male rats (I) and rats 30 days after orchidectomy (OR) were treated in vivo with a single dose of 1.5 or 0.5 mg testosterone propionate (TP), 22.5 or 7.5 mug estradiol benzoate (EB) and a mixture of TP plus EB, respectively. The release of LH and FSH from anterior pituitaries of steroid hormone pretreated animals induced by the administration of LH-RH was studied in vitro. LH-RH stimulated FSH release from pituitaries of I and OR was inhibited by higher doses of EB or a mixture of EB plus TP. On the other hand, EB and combination of EB plus TP stimulated LH release in I, whereas EB and TP inhibited LH-RH induced release of LH in OR. At the lower dose levels no inhibition of LH-RH stimulated FSH release from pituitaries of steroid pretreated I or OR animals occured. LH-RH induced LH release was only observed at thise dose level in I pretreated with TP and OR pretreated with EB. On the other hand, pretreatment of ovariectomized rats (OV) with sex steroids (5 mug 17 beta-estradiol, 3 mg progesterone, and mixture of 5 mug 17 beta-estradiol and 3 mg progesterone, resp., each injected through 6 days) resulted in restoration of LH-RH induced FSH release lost 30 days after ovariectomy. Furthermore, LH-RH induced release of LH and FSH from male rat pituitaries at different times after orc dectomy exhibited a pattern from that recorded for ovariectomized animals. [125I] LH-RH binding assays with anterior pituitary plasma membrane fractions isolated from I revealed two binding sites with apparent affinity constants of 4.3 x 10(-9) M and 2.2 x 10(-8) M, respectively. The low affinity binding site is lost upon orchidectomy. Scatchard plot analyses of binding data obtained for LH-RH reaction with plasma membrane fractions isolated from anterior pituitaries of OR pretreated with sex steroids showed that the second binding site could be regenerated by treatment with the low dose of TP. From the present experiments it is concluded that: 1. LH-RH induced gonadotropin release is affected by sex steroids at the pituitary plasma membrane level. 2. One hypothalamic hormone may well specifically control LH and FSH release. 3. Mechanisms controlling LH-RH induced gonadotropin release are different in the male and female.

Animals↗
PubMed1975

Radioligand- receptor assay of LH-RH.

Characteristics of LH-RH interactions with the plasma membrane of the anterior pituitary were utilized to develop a radioligand- receptor assay for the hypothalamic decapeptide. Plasma membranes were prepared from rat adenohypophyses and association of 125I-LH-RH with the cell membrane was found to reach a plateau after 30 min incubation time. Sensitivity of the present competitive protein binding assay was 10 ng. The system was shown to be sensitive to structural changes in the LH-RH molecule. No cross-reactivity of (3--10) LH-RH, pyro-His-Trp-SerOMe and TRH was recorded with LH-RH, whereas slight cross-reaction was observed for (Lys8) LH-RH and (Ala4) LH-RH showed marked cross-reaction. Although the present system is not sensitive enough to estimate physiological levels of LH-RH it seems to be a valuable approach for setting up an LH-RH assay system.

Animals↗
PubMed1975

LH-RH-sensitive adenylate cyclase in isolated plasma membranes of rat adenohypophyses.

The adenylate cyclase system in isolated plasma membranes of rat adenohypophyses was studied. Formation of cAMP was found to be dependent on plasma membrane protein. Production of cAMP could be stimulated by the addition of LH-RH. This process was shown to be a function of LH-RH concentration. Basal and stimulated cAMP could be stimulated by NaF. The results of the present experiments suggest that cAMP formation is time dependent. The synthesis of cAMP is a possible effector of LH-RH actions.

Adenylyl Cyclases↗
PubMed1975

LH-RH interactions with pituitary receptors: Properties and characterization.

The plasma membrane initiator system for actions of LH-RH was characterized. Binding of 125-I-LH-RH to the anterior pituitary plasma membrane was studied at 4 degrees C and at 37 degrees C. Two binding sites were indentified which possessed apparent affinity constants of 2 times 10- minus 8M and 2 times 10- minus 7M, respectively. The high affinity binding site was competible and saturable by TRH. These data suggest that the low affinity binding site is the physiological receptor for mediation of LH-RH stimulated LHrelease. LH-RH-receptor interaction has been shown to be a temperature and pH-dependent process. Less binding was observed at 37 degrees C than at 4 degrees C. Below pH 6 and above pH 8 a sharp drop in LH-RH binding to the cell membrane was recorded. Ca++, Mg++ and Mn++ were shown to inhibit the binding. Mn++ (16 mM) showed 50 percent inhibition of binding of LH-RH to the anterior pituitary plasma membrane fractions. On the other hand, increasing ionic strength enhanced LH-RH binding. The results of our study on the LH-RH-receptor systems offer a new approach to the study of LH-RH actions and facilitate the interpretation of earlier observations.

Animals↗