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Biomedical subjects

Y Koch

Publications and source records attributed to Y Koch.

At least 73 records · Page 4Linked to original sources

Gonadotropin-releasing hormone in milk.

The hypothalamic hormone gonadotropin-releasing hormone (GnRH) has been found in milk of man, cow, and rat. Radioimmunoassays of acidified milk indicate concentrations of GnRH ranging between 0.1 and 3 nanograms per milliliter. Multistep extractions, followed by electrophoresis, reveal gonadotropin-releasing activity in the fraction that comigrates with the GnRH-marker. A second hypothalamic hormone, thyrotropin-releasing hormone, is present in milk at a much lower concentration. "Milk -GnRH" may influence the secretion of the gonadotropic hormones in neonates.

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On the role of tryptophan in luteinizing-hormone-releasing hormone (luliberin).

The tryptophan residue of luteinizing-hormone-releasing hormone (luliberin) was chemically modified to produce the following analogs: [Trp(o)3]luliberin, Trp-(2,4-dinitrophenylsulfenyl)-luliberin, Trp-(2-hydroxy-5-nitrobenzyl)luliberin, (Trp-S-luliberin)2, Trp-CH3S-luliberin and Trp-formyl-luliberin. The luteinizing-hormone-releasing activity of those analogs was determined by bioassay in vitro and found to be 0.2%, 0.2%, 0.6%, 1.5%, 1.7% and 7% of that of the natural hormone, respectively. These results demonstrate that alterations in the indole moiety of tryptophan-3, which lead to a reduction in its electron density or sterically restrict its electron avaliability, are associated with a dramatic loss of biological activity.

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Evidence for the dependence of serum luteinizing hormone surge on a transient, enhanced secretion of gonadotropin-releasing hormone from the hypothalamus.

Data that a substantial, transient release of gonadotropin-releasing hormone (GnRH) from the hypothalamus is a prerequisite for the serum luteinizing hormone (LH) surge are presented. Ovariectomized rats, in which daily afternoon LH peaks can be induced by estradiol benzoate (EB), were used as the experimental model. These rats present a homogenous, synchronized population having low hypothalamic stores of GnRH, thus facilitating detection of small physiological fluctuations in the levels of hypothalamic GnRH. Blockade, by Nembutal administration, of the serum LH surge on 2 consecutive afternoons results in elevated GnRH levels in the hypothalamus (1.79 ng in blocked rats vs 0.94 ng in controls). Abolition of LH secretion by administration of antiserum to GnRH, unlike the Nembutal blockade, does not affect GnRH levels. These results indicate that the afternoon LH surge is dependent on a transitory, enhanced release of GnRH from the hypothalamus, reflected by a depletion of GnRH stores.

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Suppression of prolactin and thyrotropin secretion in the rat by antiserum to thyrotropin-releasing hormone.

Administration of antiserum to synthetic thyrotropin-releasing hormone (TRH) to male and female rats cause a 50% and a 70% suppression in serum levels of prolactin and thyrotropin, respectively, as compared with controls injected with normal rabbit serum. The degree of suppression was similar in diestrous and proestrous female rats and in male rats. These findings support the view that, in addition to its original designation, TRH also has a physiological role in regulating release of pituitary prolactin.

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Endocrine and reproductive repercussions of immunization against progesterone and oestradiol in female rats.

Mature female rats were immunized with BSA-conjugates of oestradiol-17beta-6-carboxymethyloxime or progesterone-11-hymisuccinate. Sera tested two months later at 1/2000 dilution bound 63.3% +/- 3.1 SEM and 21.2% +/- 2.3 of the homologous tritiated hormone (10 pg),--oestradiol-17beta(Oe2) and progesterone (P), respectively. Rats immunized against Oe2 had a significantly longer oestrous cycle (8.2 days vs. 4.5 days in BSA-immunized rats), with a prolonged leukocytic phase. The cycle of rats immunized against P was also prolonged (10.5 days), but in this group the cornified smear phase was abnormally extended. The luteinizing hormone (LH) normally observed on the afternoon of pro-oestrus failed to occur in the rats immunized against Oe2 and in 70% of rats immunized against P. The latter animals, however, showed sporadic LH discharges during periods of persistent cornification. Immunization against P resulted in elevated total (free plus bound) plasma P levels; immunization against Oe2 prevented the pro-oestrous rise in plasma P. Mating of rats immunized against Oe2 resulated in normal pregnanices, while none of the rats immunized against P delivered.

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Purification of the gonadotropin-releasing hormone-degrading enzyme by affinity chromatography.

A crude preparation of Kallikrein inactivator, which inhibits the gonadotropin-releasing hormone (GnRH)-degrading enzyme(s) from rat hypothalamus and anterior pituitary, was fractionated by passage through an ion-exchange column. The enzyme-inhibiting fraction was coupled to Sepharose and the resin obtained was used for, affinity-chromatography purification of the GnRH-degrading enzyme. The enzyme from crude tissue preparations was retained on this column and eluted by 0.05 M phosphate buffer. A 9-12 fold increase in the specific activity of the enzyme was achieved. Bacitracin, an effective peptide inhibitor of the degradation of GnRH, was also coupled to Sepharose. Three different such Sepharose-bacitracin conjugates were synthesized, two of which inhibited the degradation of GnRH by hypothalamic and pituitary extracts. They all failed, however, to separate the active enzymic fraction from the bulk of accompanying proteins, using affinity chromatographic techniques.

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