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Pathogen research abs 1 || Pathogen research abs 2 || Pathogen research abs 3 || Pathogen research abs 4 || Pathogen research abs 5 || Hormone and endocrine research abs 1 || Hormone and endocrine research abs 2 || Hormone and endocrine research abs 3 || Hormone and endocrine research abs 4 || Hormone and endocrine research abs 5

Am J Obstet Gynecol. 1979 Nov 15;135(6):737-42.
Plasma thyrotropin-releasing hormone, prolactin, thyrotropin, and thyroxine concentrations following the intravenous or oral administration of thyrotropin-releasing hormone.

Andreassen B, Huth J, Tyson JE.

In a further evaluation of the use of oral thyrotropin-releasing hormone (TRH) in puerperally lactating women, a radioimmunoassay for its measurement has been developed. Its concentration in plasma as well as that of prolactin (PRL), thyrotropin (TSH) and thyroxine (T4) were measured following either intravenous or oral administration of TRH. Basal concentrations of TRH in 14 normally cycling women ranged from less than 5 to 17 pg/ml. Two luteal phase studies produced peaks in plasma TRH 5 to 10 minutes after 100 micrograms of TRH administered intravenously with a return to basal concentrations within 2 to 3 hours. In 10 normally menstruating women, ingestion of 10 mg of TRH orally resulted in plasma TRH which peaked at 423 +/- 123 pg/ml (standard error of the mean) at 30-minutes. Plasma PRL, TSH, and T4 also increased and remained slightly elevated at 4 hours. These 8-hour studies were performed in a puerperal lactating woman who had ingested 10 mg of TRH orally twice a day for 7 days prior to blood sampling. TRH concentrations declined throughout each day while TSH rose slightly in the first 1 to 2 hours but remained within normal limits. The prolonged administration of 10 mg of TRH orally twice daily to three puerperally lactating women resulted in elevations in plasma TRH 2 to 3 hours following hormone administration, yet no significant increases in plasma TSH were observed. Both endogenous TRH and TSH were measured before and after 22 nursing events in nine puerperally lactating women. There was no change in the concentration of either substance and all values were similar to those obtained in normally menstruating women.

PIP: A radioimmunassay was developed and is described for use in evaluating the effect of oral thyrotropin-releasing hormone (TRH) in puerperally lactating women. After either intravenous or oral administration, TRH plasma levels, prolactin, thyrotropin (TSH), and thyroxine (T4) levels were measured by this radioimmunoassay. Basal concentrations of TRH in 14 normally cycling women ranged from 5-17 pg/ml. Peaks in plasma TRH were produced in 2 luteal-phase studies 5-10 minutes after 100 mcg of TRH was administered intravenously, returning to basal concentrations within 2-3 hours. 10 normally menstruating women ingested 10 mg of TRH orally; plasma TRH peaked at 423 pg/ml at 30 minutes. Plasma prolactin, TSH, and T4 levels also increased and remained slightly elevated at 4 hours. 8-hour studies were performed in a puerperal lactating woman who had ingested 10 mg of TRH orally 2 times/day for 7 days before blood sampling. TRH levels declined throughout each day, whereas TSH rose slightly in the 1st 1-2 hours but remained within normal limits. Prolonged ingestion of 10 mg of TRH 2 times/day was studied in 3 puerperally lactating women and resulted in elevations in plasma TRH 2-3 hours after hormone administration, but no significant increases in plasma TSH were observed. Both endogenous TRH and TSH were measured before and after 22 nursing events in 9 puerperally lactating women, and there was no change in the level of either substance; all values were similar to those obtained from normally menstruating women.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=115316&dopt=Abstract

Br J Pharmacol. 1979 Nov;67(3):323-5.
Thyrotrophin releasing hormone stimulates release of [3H]-dopamine from slices of rat nucleus accumbens in vitro.

Kerwin RW, Pycock CJ.

Thyrotrophin releasing hormone (TRH) (25 to 100 microM) was found to stimulate the efflux of [3Hu-dopamine from small slices of rat nucleus accumbens, but not from similar slices of rat caudate nucleus. Uptake inhibition was not responsible for this action, since at 10 and 50 microM TRH had no effect on the ability of small slices of nucleus accumbens to accumulate radioactivity when incubated with 10(-7) M [3H]-dopamine. In addition the hormone had no effect on basal or dopamine-stimulated adenylate cyclase, nor did it displace [3H]-spiperone binding, in membrane preparations from nucleus accumbens.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=115532&dopt=Abstract

Calcif Tissue Int. 1979 Aug 24;28(1):17-22.
Disordered mineral metabolism produced by ketogenic diet therapy.

Hahn TJ, Halstead LR, DeVivo DC.

Vitamin D and mineral metabolism status was examined in five children maintained chronically on combined ketogenic diet-anticonvulsant drug therapy (KG), and the results compared to those obtained in 18 patients treated with anticonvulsant drugs alone (AD) and 15 normal controls. KG patients exhibited biochemical findings of vitamin D deficiency osteomalacia: decreased serum 25-hydroxyvitamin D (25OHD) and calcium concentrations, elevated serum alkaline phosphatase and parathyroid hormone concentrations, decreased urinary calcium and increased urinary hydroxyproline excretion, and decreased bone mass. Although the KG and AD groups demonstrated similar reductions in serum 25OHD concentration, the KG patients exhibited a significantly greater reduction in bone mass. In response to vitamin D supplementation (5000 IU/day), mean bone mass in the KG group increased by 8.1 +/- 0.9% (P less than 0.001) over a 12-month period. These results suggest that ketogenic diet and anticonvulsant drug therapy have additive deleterious effects on bone mass and that these effects are partially reversible by vitamin D treatment.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=115548&dopt=Abstract

J Biol Chem. 2003 Jun 27;278(26):24118-24. Epub 2003 Apr 21.
Solution structure of human proguanylin: the role of a hormone prosequence.

Lauber T, Neudecker P, Rosch P, Marx UC.

Lehrstuhl fur Biopolymere, Universitat Bayreuth, Universitatstrasse 30, 95447 Bayreuth, Germany.

The endogenous ligand of guanylyl cyclase C, guanylin, is produced as the 94-amino-acid prohormone proguanylin, with the hormone guanylin located at the COOH terminus of the prohormone. The solution structure of proguanylin adopts a new protein fold and consists of a three-helix bundle, a small three-stranded beta-sheet of two NH2-terminal strands and one COOH-terminal strand, and an unstructured linker region. The sequence corresponding to guanylin is fixed in its bioactive topology and is involved in interactions with the NH2-terminal beta-hairpin: the hormone region (residues 80-94) partly wraps around the first 4 NH2-terminal residues that thereby shield parts of the hormone surface. These interactions provide an explanation for the negligible bioactivity of the prohormone as well as the important role of the NH2-terminal residues in the disulfide-coupled folding of proguanylin. Since the ligand binding region of guanylyl cyclase C is predicted to be located around an exposed beta-strand, the intramolecular interactions observed between guanylin and its prosequence may be comparable with the guanylin/receptor interaction.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12707255&dopt=Abstract

Calcif Tissue Int. 1979 Aug 24;28(1):79-81.
Formation and serum disappearance of fragments of parathyroid hormone in the infused dog.

Neuman MW, Neuman WF, Lane K.

Radioiodinated parathyroid hormone [125I-PTH(1-84)] was infused into intact dogs. At various times venous samples were chromatographed to determine the levels of intact hormone (1-84) and large fragments in the circulation. Both bioactive (electrolytically iodinated) and inactive (chloramine-T-labeled) preparations were used. In both instances, plateau concentrations of intact hormone and of large metabolite(s) were quickly reached. After cessation of infusion the levels of intact hormone and metabolite(s) quickly declined. Clearly, in the dog, the peripheral formation and disappearance of large fragments of exogenous PTH occur at rates comparable to the clearance of the intact hormone itself.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=115556&dopt=Abstract

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