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Biomedical subjects

H G Bohnet

Publications and source records attributed to H G Bohnet.

81 records · Page 5Linked to original sources
PubMed1976

Lack of a direct effect of homocysteic acid on growth hormone and prolactin receptors.

The effects of homoystine derivatives upon GH and prolactin receptors which are reported to stimulate growth in the rat were investigated. Several concentrations of homocysteic acid, homocysteine, homocysteinethiolactone, homoystine as well as other amino-acids were used in GH and prolactin receptor assay systems to determine their growth promoting or the lactogenic activities. None of the aminoacids used displaced labelled hGH or ovine PRL. It os concluded that derivatives of homoystine stimulate growth by an indirect mechanism and exhibit a lack of a direct stimulation of GH and prolactin receptors.

Animals↗
PubMed1976

Human pituitary gonadotrophin index. II LHRH test and clomiphene response before and after LHRH stimulation.

To monitor the effect of LHRH treatment on hypothalamo-pituitary-gonadal function, women with functional amenorrhoea were investigated by standardized LHRH and repeated clomiphene tests before and after LHRH therapy. The actual pituitary gonadotrophin reserve was defined by a Human Pituitary Gonadotrophin Index (HPGI). Clomiphene response served as hypothalamic function test, plasma oestradiol and progesterone concentrations were measured for assessment of the gonadal function. LHRH treatment as performed in this study did not change basal gonadotrophin levels or the pituitary responsiveness in our standardized LHRH test. Plasma oestradiol concentrations remained unaltered at the lower limit of the early follicular phase values of a normal menstrual cycle. The inability to respond to clomiphene was changed to clomiphene responsiveness during therapy in eighteen out of twenty-nine women with anovulation. The majority of the responders had HPG-Indices of R2. Patients with hyperprolactinaemic anovulation did not convert. The possibility of an ultrashort feedback action of LHRH on its own production in the human is discussed.

Adult↗
PubMed1975

Human pituitary gonadotropin index. I. Standardized LRH test criteria for evaluation of functional amenorrhea.

LRH test were carried out by giving 339 amenorrheic women and 74 normally menstruating volunteers an intravenous injection of 25 mug LRH (Hoe 471). Plasma LH and FSH were measured by RIA in two laboratories (Tuebingen and Ulm) using two standard reference preparations: LER 907 and 2nd IRP-HMG. The average conversion factors between the two standard preparations were calculated at 5.0 for LH and 25.0 for FSH. Furthermore, the estradiol-17beta levels were measured in 139 out of the 339 patients immediately before and 60 minutes after LRH injection. Taking the episodic and cyclic plasma gonadotropin fluctuations into consideration a shorthand system classifying the gonadotropin baseline (BI-BIV) and LH responses to 25 mug LRH (R0-R2) has been established and is referred to as Human Pituitary Gonadotropin Index (HPGI). It is possible to achieve reproducible gonadotropin results in two different laboratories using two different standard reference preparations. Two separate, randomly selected groups of amenorrheic women were found to have the same percent distribution of the HPGI. A correlation coefficient of r equal 0.67 between basal and LRH stimulated plasma LH levels does not sufficiently characterize the individual LH response behavior. A significant increase of plasma LH and FSH within the test period (60') reveals that the iv administration of 25 mug LRH represents an adequate dose for the LRH test in women. The HPGI which characterizes the functional state of gonadostat, may become a useful diagnostic index for evaluating women with anovulatory disease before, during, and after therapy.

Adolescent↗
PubMed1975

[The pulsatile LH fluctuation (spiking) dependent on the circulating prolactin. Studies during physiological (puerperium), functional pathological and TRH induced hyperprolactinemia].

The magnitude and frequency of episodic LH-fluctuations have been observed to change during the different phases of the menstrual cycle. A hypothalamic control center appears to be responsible for these variations. Disturbances of the hypothalamus often make themselves known through a lack of LH-episodes. Ahypothalamic derangement in women with functional amenorrhoea can result in a disregulation of gonadotropins as well as prolactin, thereby leading to hyperprolactinemia. One finds an inverse relationship between high prolactin secretion and cessation of or decreased pulsatile LH-secretion (spiking). LH-spiking was tested in physiological post partum, functional pathological and TRH-induced hyperprolactinemias. No LH-episodes were observed post partum after the end of HCG clearance although prolactin had returned to normal levels at 12 days p.p. The mode of LH-secretion in a group of functionally amenorrhoic patients was changed by a TRH-induced prolactin increase: the previously observed LH-spikes in these women could no longer be seen. Normal cycling women, however, were not affected. In patients with hyperprolactinemic anovulatory syndromes, prolactin suppressed LH-fluctuations reappeared after administration of 2-Bromo-alpha-ergocryptin. The inhibitory influence of hyperprolactinemia on the function of the gonadostat will be discussed. High plasma prolactin levels influence the cyclic and tonic hypothalamic function. Furthermore, prolactin appears to have a peripheral inhibitory influence on ovarian gonadotropin stimulation. Post partum anovulation and amenorrhoea can be caused by an antigonadotropic and antigonadic effect of prolactin.

Amenorrhea↗
PubMed1975

[TRH stimulation as an attempt at demonstration of the induction and involution of prolactin-secreting pituitary cells in pregnancy and puerperium and in pathological hyperprolactinemia].

The present paper discusses the relationship between functional hypertrophia or hyperplasia of the prolactin secreting cells in the pituitary and actual pituitary prolactin reserves in pregnant and post partum women. 35 randomly selected post partum patients from the 3rd to 12th day p.p. and 14 women in their 11th to 14th weeks of pregnancy volunteered to undergo a standard TRH-test. The control group consisted of 60 normoprolactinemic patients. Eleven pathologically hyperprolactinemic patients were compared to the normoprolactinemic and physiologically hyperprolactinemic groups. In all cases, plasma prolactin showed a linear decrease from the 3rd to 12th days post partum. The TRH induced increase became correspondingly greater as the basal prolactin levels decreased, i.e. an inverse relationship between these two parameters was seen. The TRH-induced increase was also always greater than the increase caused by suckling. A connection between prolactin and parity was not found. The inverse relationship between basal prolactin levels and the actual reserves which could be released by TRH stimulation can be explained in that there are two regulatory systems for prolactin. The estrogens stimulate basal prolactin and inhibit prolactin reserves. The actual prolactin reserve is, on the one hand, directly dependent on the degree of endogenous neurohormonal stimulation and, on the other hand, indirectly dependent on the endogenous estrogens through a feedback mechanism. The TRH-stimulation test is not suitable for determining a functional hypertrophia or hyperplasia of lactotropic pituitary cells.

Estrogens↗
PubMedDate not supplied

[Personality markers, physical complaints and microsomal thyroid antibody titer in postpartum women].

OBJECTIVE: To define the relation between mood, anxiety, puerperal-depression and autoimmune-thyroid-disfunction. PATIENTS AND METHODS: We screened 292 mothers 2 to 3 days after delivery for anxiety, depression and mood disturbances as well as thyroid-function and microsomal antithyroid-antibody status. Ten autoantibody positive woman were compared with an equal number of age-matched controls. The state-trait-anxiety inventory which consists of 20 questions concerning state-anxiety (anxiety in a given situation) and 20 questions concerning trait-anxiety (anxiety as a quality of personality) was used to describe anxiety. The Beck-depression-inventory was applied to measure depressive illness. To assess the mood we used the "Giessener Beschwerdebogen". RESULTS: We found subclinical hypothyroidism in 40% of the antibody positive women and their matched pairs. Another 10% of these 20 women showed clinical hypothyroidism. There was no significant association of thyroid-function or disfunction with neither anxiety nor depressive illness or mood disturbance. The incidence of state-anxiety was significantly higher in the antibody positive group than in the antibody negative group (Chi2 = 3,3; P < 0.04). Trait-anxiety showed a tendency to be higher in the antibody positive group, but the difference was not significant (Chi2 = 2; P < 0,08). The frequency of depressive illness or mood disturbance at the time of assessment was not significantly different in thyroid-antibody positive group compared with antibody negative group. CONCLUSION: Autoantibody induced thyroiditis may contribute to anxiety in the postpartum period.

Adolescent↗