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Biomedical subjects

R E Peter

Publications and source records attributed to R E Peter.

At least 19 recordsLinked to original sources
PubMed1992

Distinct sequence of gonadotropin-releasing hormone (GnRH) in dogfish brain provides insight into GnRH evolution.

In vertebrates, gonadotropin-releasing hormone (GnRH) belongs to a family of decapeptides characterized by the conservation of residues 1, 2, 4, 9, and 10. In the jawed vertebrates only positions 5, 7, and 8 in the GnRH molecules vary. We have now purified two forms of GnRH from the brains of spiny dogfish (Squalus acanthias) by using reverse-phase high-performance liquid chromatography. The primary structures were established by automated Edman degradation and mass spectral analysis. The distinct structure of the first form (dogfish GnRH) is pGlu-His-Trp-Ser-His-Gly-Trp-Leu-Pro-Gly-NH2 (pGlu represents pyroglutamyl). The second peptide is identical to a form of GnRH originally isolated from chicken brains (chicken GnRH-II; pGlu-His-Trp-Ser-His-Gly-Trp-Tyr- Pro-Gly-NH2) and is widespread throughout the vertebrates. We are aware of no other species of cartilaginous fish in which the primary structures of two forms of GnRH have been determined. The presence of chicken GnRH-II in dogfish supports the idea that chicken GnRH-II is the oldest GnRH to evolve in jawed vertebrates. With the addition of the dogfish GnRH structure to the family, two main structural branches of GnRH can be delineated. The physiological effects of dogfish GnRH included the release of not only gonadotropin but also growth hormone from goldfish pituitary fragments.

Amino Acid Sequence↗
PubMed1992

Activity of vertebrate gonadotropin-releasing hormones and analogs with variant amino acid residues in positions 5, 7 and 8 in the goldfish pituitary.

All non-mammalian vertebrates as well as marsupial mammals have two or more forms of gonadotropin-releasing hormone (GnRH) in the brain. Goldfish brain and pituitary contains two molecular forms of GnRH, salmon GnRH ([Trp7, Leu8]m-GnRH; s-GnRH) and chicken GnRH-II ([His5, Trp7, Tyr8]m-GnRH; cII-GnRH). Both sGnRH and cII-GnRH stimulate gonadotropin (GtH) as well as growth hormone (GH) release from the goldfish pituitary. The purpose of the present study was to study the activity of the five known forms of GnRHs as well as analogs of mammalian GnRH (m-GnRH) with variant amino acid residues in positions 5, 7 and 8 in terms of binding to GnRH receptors, and release of GTH and GH from the perifused fragments of goldfish pituitary in vitro. All five vertebrate GnRH peptides stimulated both GtH and GH release in a dose-dependent manner, although their potencies were very different. cII-GnRH was somewhat more active than s-GnRH in releasing GtH, whereas s-GnRH tended to have a greater potency than cII-GnRH in terms of GH release. Both chicken GnRH-I (cI-GnRH) and lamprey GnRH (l-GnRH) were significantly less potent than mGnRH, s-GnRH and cII-GnRH in releasing GtH and GH. cII-GnRH binds with higher affinity for the high affinity binding sites compared to all other native peptides. The activity of [Trp7]-GnRH was similar to both s-GnRH and cII-GnRH in releasing GtH and GH. Substitution of His5 resulted in a significant decrease in GtH releasing potencies compared to mGnRH, sGnRH and cII-GnRH. [His5]-GnRH also had lower GH releasing potency than mGnRH and sGnRH. Tyr8, His8 and Leu8 substitutions caused significant decreases in GtH releasing potencies compared to mGnRH, s-GnRH and cII-GnRH, but did not cause a significant change in GH releasing potency. The combination of [His5, Trp7]-GnRH had GtH and GH releasing activities similar to m-GnRH, s-GnRH and cII-GnRH.(ABSTRACT TRUNCATED AT 400 WORDS)

Amino Acid Sequence↗
PubMed1992

Properties of common carp gonadotropin I and gonadotropin II.

Two gonadotropins, GtH I and GtH II, were extracted with 35% ethanol-10% ammonium acetate, pH 6.1, from female common carp pituitary glands and purified by ion-exchange chromatography on a DE-52 column followed by gel filtration on a Sephadex G-75 column. Molecular weights of GtH I and GtH II as determined by SDS-PAGE were 45,000 and 35,000, respectively. Both GtHs dissociate into two subunits following reduction with beta-mercaptoethanol. These subunits contain different N-terminal amino acids (Tyr and Gly for GtH I; Tyr and Ser for GtH II). GtH I was acid stable and did not dissociate into subunits following treatment with 0.1% trifluoroacetic acid; GtH II readily dissociated into subunits by this treatment. GtH I and GtH II have distinct elution profiles on reverse-phase HPLC. The N-terminal amino acid sequence of the beta-subunit of GtH II was identical to that of common carp maturational GtH described by other workers suggesting that GtH I is a newly identified molecule. This was supported by radioimmunoassay analysis. GtH II and a common carp maturational GtH preparation (F11 cGtH; Peter et al., 1982, J. Interdiscipl. Cycle Res. 13, 229-239) had similar immunological activity in tests with antisera to the beta-subunit of maturational GtH whereas GtH I had low (less than 6%) cross-reactivity. GtH I, GtH II, and F11 cGtH were equipotent in tests with antisera to the alpha-subunit of maturational GtH suggesting these molecules contain a similar alpha-subunit. In vitro bioassays using goldfish revealed that GtH I and GtH II share the same spectrum of biological activities causing stimulation of ovarian and testicular steroidogenesis and induction of oocyte final maturation. The demonstration of two chemically distinct GtHs in common carp is similar to what has been described for chum and coho salmon.

Amino Acid Sequence↗
PubMed1992

A reduction in pituitary dopamine turnover is associated with sex pheromone-induced gonadotropin secretion in male goldfish.

In goldfish, the gonadal steroid, 17 alpha,20 beta-dihydroxy-4-pregnen-3-one (17,20 beta-P), functions as a potent preovulatory female sex pheromone which stimulates rapid elevations in serum gonadotropin (GtH) levels and subsequent increases in milt production in males. GtH secretion in goldfish is known to be regulated by the stimulatory actions of gonadotropin-releasing hormone (GnRH) and the inhibitory actions of dopamine (DA). This study specifically examined whether the 17,20 beta-P-induced elevation in male GtH is caused by pheromone-mediated changes in DA inhibition at the level of the pituitary. First, we have demonstrated that dihydroxyphenylacetic acid (DOPAC) is the primary metabolite of DA catabolism in the brain and pituitary gland of goldfish. Second, we measured changes in circulating levels of GtH and changes in pituitary content of DA and its metabolite, DOPAC, as well as possible alterations in DA turnover rate (DOPAC/DA ratio) following short-term exposure of male goldfish to water-borne 17,20 beta-P. Water-borne 17,20 beta-P consistently increased serum GtH levels in males within 20 min of exposure and maintained elevated levels for up to 120 min. Although changes in pituitary DA content were not observed during periods of high GtH release, coincident reductions in pituitary levels of DOPAC were measured within 45 min of exposure to the pheromone. More importantly, there was a significant decrease in the rate of DA turnover in the pituitary, as assessed by comparing the ratio of DOPAC to DA present, at 20, 45, and 120 min of exposure. Since the reduction of DA turnover in the pituitary is inversely correlated with periods of increased GtH release, the present results suggest that water-borne 17,20 beta-P causes an abatement of DA release to the pituitary. Based on the latency of the GtH response to water-borne 17,20 beta-P, a rapid reduction of DA turnover in the pituitary appears to be at least part of the neuroendocrine trigger for 17,20 beta-P-induced GtH release in male goldfish.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1992

Adrenergic and dopaminergic regulation of gonadotropin-releasing hormone release from goldfish preoptic-anterior hypothalamus and pituitary in vitro.

The involvement of adrenergic and dopaminergic receptor subtypes on in vitro release of radioimmunoassayable gonadotropin-releasing hormone (GnRH) from incubated preoptic-anterior hypothalamic (P-AH) slices and pituitary fragments of sexually mature male goldfish was studied. Norepinephrine (NE) produced a dose-related stimulation of GnRH from P-AH slices, but not from pituitary fragments. The effects of some adrenergic receptor agonists (1 microM) on GnRH release from P-AH slices were tested: phenylephrine (alpha 1-agonist) significantly stimulated GnRH release; clonidine (alpha 2-agonist) and isoproterenol (beta-agonist) were ineffective. Incubation of P-AH slices with phentolamine (alpha 1/alpha 2-antagonist) and prazosin (alpha 1-antagonist), at a concentration of 1 microM, inhibited the release of GnRH induced by NE (60 microM); the alpha 2-antagonist yombibin and the beta-antagonist propanolol were ineffective. None of the adrenergic antagonists (1 microM) tested produced significant effects on spontaneous release of GnRH from both tissue preparations. Spontaneous release of GnRH from both P-AH slices and pituitary fragments was reduced by dopamine (DA) in a dose-related manner. The effects of some DA agonists (1 microM) were tested: apomorphine (D1/D2-agonist) and SKF 38398 (D1-agonist), but not bromocriptine and LY-171555 (D2-agonists) significantly reduced spontaneous GnRH release from P-AH slices in vitro. On the other hand, D2-agonists, but not D1-agonists, significantly reduced GnRH release from pituitary fragments. The effects of DA antagonists (1 microM) were also tested: in P-AH slices, addition of SKF-83566 (D1-antagonist) significantly reduced spontaneous GnRH release; pimozide and domperidone (D2-antagonist) were ineffective when tested alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗
PubMed1992

Amino acid neurotransmitters and dopamine in brain and pituitary of the goldfish: involvement in the regulation of gonadotropin secretion.

An isocratic high-performance liquid chromatographic technique was developed to measure levels of gamma-aminobutyric acid (GABA), glutamate, and taurine in the brain and pituitary of goldfish. Accuracy of this procedure for quantification of these compounds was established by evaluating anesthetic and postmortem effects and by selectively manipulating GABA concentrations by intraperitoneal administration of the glutamic acid decarboxylase (GAD) inhibitor 3-mercaptopropionic acid or the GABA transaminase inhibitor gamma-vinyl GABA. The technique provided a simple, rapid, and reliable method for evaluating the concentrations of these amino acids without the use of complex gradient chromatographic systems. To investigate the relationship between neurotransmitter amino acids and the control of pituitary secretion of gonadotropin, the effects of injection of taurine, GABA, or monosodium glutamate on GABA, glutamate, taurine, and, in some instances, monoamine concentrations in the brain and pituitary were evaluated and related to serum gonadotropin levels. Injection of taurine caused an elevation in serum gonadotropin concentrations. In addition, injection of the taurine precursor hypotaurine but not the taurine catabolite isethionic acid elevated serum gonadotropin levels. Intracerebroventricular injection of either GABA or taurine also elevated serum gonadotropin concentrations. Pretreatment of recrudescent fish with alpha-methyl-p-tyrosine reduced pituitary dopamine concentrations and also potentiated the serum gonadotropin response to taurine. Injection of monosodium glutamate caused an increase of glutamate content in the pituitary at 24 h; this was followed by a decrease at 72 h after administration. Pituitary GABA, taurine, and dopamine concentrations underwent a transient depletion after monosodium glutamate administration, and this was associated with an elevation of serum gonadotropin content.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Mercaptopropionic Acid↗
PubMed1992

Influence of GABA on gonadotrophin release in the goldfish.

The influence of GABA on pituitary gonadotrophin (GTH) release in the goldfish was studied by means of in vivo and in vitro techniques. It was found that GABA injected intraperitoneally caused an increase of serum GTH levels in regressed or early maturing fish, but not in late maturing animals. Moreover, injection of a GABA transaminase inhibitor caused a significant increase of GABA within the hypothalamus and pituitary, and a dose-dependent increase in serum GTH levels. To determine if this effect could be exerted directly at the level of the pituitary, dispersed pituitary cells in static incubation or in perifusion were exposed to increasing concentrations of GABA or its agonists muscimol and baclofen. None of these drugs was able to modify the spontaneous or GnRH-induced secretion of GTH, indicating that the in vivo effect of GABA was most likely mediated via another hypothalamic factor. Using in vitro incubation of pituitary slices, it was found that GABA caused a dose-related stimulation of GnRH release at the level of the pituitary, providing a possible explanation for the observed in vivo stimulatory effect of GABA on GTH release. Since the seasonal effect of GABA in vivo indicated a possible interaction of GABA with sexual steroids, GABA was given intraperitoneally to female goldfish implanted with either testosterone or estradiol. We found that the stimulatory effect of GABA on GTH release was abolished in estradiol-treated females but was still observed in testosterone-implanted fish. Moreover, estradiol but not testosterone caused a decrease of the GABA concentration within the telencephalon.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Aminobutyrate Transaminase↗
PubMed1992

Interactions of estradiol with gonadotropin-releasing hormone and thyrotropin-releasing hormone in the control of growth hormone secretion in the goldfish.

The effects of testosterone (T) and estradiol (E2) on serum growth hormone (GH) concentrations were investigated throughout the seasonal reproductive cycle of the female goldfish. Gonad-intact female goldfish were implanted intraperitoneally for 5 days with silastic pellets containing no steroid (blank), T(100 micrograms/g) or E2 (25-100 micrograms/g). In blank-implanted females, seasonal variations in serum GH were evident; maximal serum GH levels were found in spring while minimal GH levels were found in summer and early autumn. Implantation of E2-containing silastic capsules stimulated increases (2-4 times control) in serum GH levels throughout the reproductive cycle. Implantation of T did not affect serum GH at any time of the year. One possible mechanism by which E2 could exert its effects may be through alteration of pituitary sensitivity to GH-releasing factors. The decapeptide salmon gonadotropin-releasing hormone (sGnRH) is found in the brain and pituitary of goldfish and stimulates gonadotropin (GTH) and GH secretion. In contrast, thyrotropin-releasing hormone (TRH) stimulates GH, but not GTH, release from pars distalis fragments obtained from sexually regressed (ED50 = 5.7 +/- 3.8 nM; August) or sexually mature (ED50 = 0.53 +/- 0.28 nM; March) fish; in vivo E2 treatment resulted in a 3-fold increase in the in vitro GH response to TRH. Furthermore, E2 treatment increased sGnRH-stimulated GH release by approximately 4-fold. These results demonstrate that E2 but not T stimulates GH secretion throughout the reproductive cycle of female goldfish. Furthermore, sGnRH and TRH stimulate GH release in a teleost, and these stimulatory responses are enhanced by physiological levels of E2.

Animals↗
PubMed1992

Isolation and characterization of hypothalamic growth-hormone releasing factor from common carp, Cyprinus carpio.

A growth hormone-releasing factor (GRF)-like peptide was isolated from the hypothalamus of common carp, Cyprinus carpio, by acid extraction, gel filtration chromatography, immunoaffinity chromatography using antiserum directed against rat GRF, and multiple steps of HPLC using octadecyl columns. Based on Edman degradation and peptide mapping, this teleost GRF was established to be a 45-residue peptide with the following primary structure: His-Ala-Asp-Gly-Met-Phe-Asn-Lys-Ala-Tyr-Arg-Lys-Ala-Leu-Gly-Gln-Leu-Ser- Ala-Arg - Lys-Tyr-Leu-His-Thr-Leu-Met-Ala-Lys-Arg-Val-Gly-Gly-Gly-Ser-Met-Ile-Glu- Asp-Asp-Asn-Glu-Pro-Leu-Ser. Carp GRF is closely related structurally to peptides of the glucagon-secretin superfamily, and more particularly to mammalian vasoactive intestinal peptide (VIP) precursors and the N-terminal portion of mammalian GRFs. A synthetic replicate of this peptide is highly potent [50% effective dose (ED50) approximately 0.08 nM] in stimulating GH release from cultured goldfish pituitary glands and in elevating serum GH levels 30 min after injection (0.1 micrograms/g) in goldfish.

Amino Acid Sequence↗
PubMed1992

Dopamine stimulates growth hormone release from the pituitary of goldfish, Carassius auratus, through the dopamine D1 receptors.

Previously, we have demonstrated that ip injection of apomorphine, a nonselective dopamine (DA) agonist, increases serum GH levels in the goldfish, suggesting a possible role of DA in GH regulation. In the present study, the effects of DA on GH release in the goldfish were further characterized using an in vitro perifusion system for pituitary fragments. DA increased GH release in a dose-dependent manner with an ED50 of 0.26 +/- 0.06 microM. SKF38393, a DA D1 agonist, mimicked the GH-releasing effect of DA with an ED50 of 0.41 +/- 0.12 microM. Stereoselectivity consistent with mammalian DA D1 systems was demonstrated for the GH response to SKF38393; only the (+)- but not (-)-enantiomer of SKF38393 induced a dose-dependent GH release. Two other D1 agonists, SKF77434 and SKF82958, were also found to have GH-releasing activity. In contrast, high doses (up to 1 microM) of the DA D2 agonists, bromocriptine and LY171555, did not affect basal GH levels. The receptor specificity for DA-stimulated GH release was further investigated by using D1 and D2 antagonists; the D1 antagonists SCH23390 and SKF83566 completely abolished the GH response to DA or the D1 agonist SKF38393, whereas the D2-specific antagonists domperidone and (-)-sulpiride were not effective in this respect. Taken together, the present study demonstrates that DA is stimulatory to GH release from the pituitary of goldfish, and its action is mediated through receptors resembling the mammalian DA D1 receptors. The apparent similarities of the DA D1 receptor pharmacology between the goldfish and the mammals also indicate that D1 receptor is highly conserved during vertebrate evolution.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1992

Effects of porcine follicular fluid, inhibin-A, and activin-A on goldfish gonadotropin release in vitro.

Inhibin and activin are important reproductive regulators in mammalian species and have been demonstrated to be highly conserved in structure. The present study examines the effects of porcine follicular fluid (pFF; a crude inhibin and activin preparation) and purified porcine inhibin-A and activin-A on goldfish gonadotropin-II (GTH-II) release. In studies using primary cultures of dispersed goldfish pituitary cells in static incubation, treatments with pFF, inhibin-A, and activin-A for 10 h caused dose-dependent increase in GTH-II release. In perifusion studies using goldfish pituitary fragments, basal GTH-II release was significantly elevated after 12-h exposure to 500 micrograms/ml pFF. Furthermore, GnRH-induced GTH-II secretion was potentiated by pretreatment with pFF. When pFF was applied in the form of 5-min pulses, a rapid dose-related stimulation of GTH-II was observed. Similarly, challenges with 2-min pulses of 15, 150, and 1500 pM inhibin-A and activin-A stimulated GTH-II release by goldfish pituitary fragments in a rapid and dose-dependent manner. This acute stimulatory action of inhibin on goldfish GTH-II release was completely abolished after pretreatment with specific inhibin antibodies. The acute actions of inhibin and activin on GTH-II release are probably not due to the release of endogenous GnRH from nerve terminals in the pituitary fragments or binding to the GnRH receptors. First, a specific GnRH antagonist did not block the actions of inhibin and activin. Second, dopamine, a potent inhibitor of GnRH-stimulated GTH-II secretion in goldfish, was only partially effective in decreasing inhibin- and activin-induced GTH-II release. Third, the stimulatory effects of inhibin and GnRH on GTH-II release were additive. These lines of evidence also indicate that the mechanisms mediating inhibin and activin stimulation of goldfish GTH-II release may be somewhat different from those of GnRH. These results demonstrate that in contrast with the usual inhibitory effects of inhibin on GTH release in mammals, both inhibin and activin exert long term and acute stimulatory actions on GTH-II release in the goldfish.

Activins↗
PubMed1992

Treatment of humeral diaphyseal fractures with Hackethal stacked nailing: a report of 33 cases.

Hackethal's technique of stacked intramedullary (IM) nailing was used to treat 43 consecutive acute fractures of the humeral diaphysis. Of these, 6 were lost to follow-up and 4 additional patients were excluded for pathologic fractures. All of the remaining 33 traumatic fractures were followed until union. The average age was 34 years. Mean operative time was 90 min. Usually four or five 2- or 3-mm IM Kirschner wires were introduced in a retrograde manner, through a posterior unicortical window under radioscopic control. Closed reductions were performed in 28 patients, and open reductions were performed in the other five. Time to follow-up averaged 3 years 5 months (range 8 months to 13 years). There were no infections. There were three nonunions (9%), and two nails in 1 patient penetrated the greater tuberosity and one nail migrated distally in another patient. This method of internal fixation is not complicated and causes minimal trauma. It provides good stability at the fracture site and permits early mobilization of patients with excellent functional results.

Adolescent↗
PubMed1991

Demonstration of gonadotropin releasing-hormone receptors on gonadotrophs and somatotrophs of the goldfish: an electron microscope study.

Dispersed pituitary cells of the goldfish were incubated with biotinylated [D-Lys6, Pro9-N-ethylamide] salmon gonadotropin-releasing hormone (sGnRH-A) then avidingold (10 nm), and were fixed, embedded and sectioned. Cells were identified as gonadotrophs, somatotrophs, or prolactin cells using specific hormone antisera and protein-A gold (20 nm) as a marker. Attachment of the biotinylated sGnRH-A to the pituitary cell sections was determined by scanning cell surfaces for the smaller gold particles using the transmission electron microscope. Attachment was observed on gonadotrophs and somatotrophs, but was negligible on prolactin cells. Preincubation with unlabelled salmon gonadotropin-releasing hormone or chicken II gonadotropin-releasing hormone, or omission of the salmon gonadotropin-releasing hormone analog, prevented the reaction. The direct visualization of specific gonadotropin-releasing hormone receptors on gonadotrophs and somatotrophs supports the existence of direct stimulatory actions of gonadotropin-releasing hormone on gonadotropin and somatotropin release in gold-fish.

Animals↗
PubMed1991

Isolation and characterization of a gonadotropin-releasing hormone binding protein in goldfish serum.

A binding protein (BP) specific for gonadotropin-releasing hormone (GnRH) was previously demonstrated in goldfish serum. In the present study the binding protein was isolated and further characterized. The GnRH-BP, partially purified from goldfish serum using polyacrylamide gel electrophoresis (PAGE) under nondenaturing conditions, was concentrated in a single band, separate from all major components of serum proteins. The binding ability of the partially purified GnRH-BP was conserved; the isolated GnRH-BP specifically bound salmon GnRH and chicken GnRH-II, the native forms of GnRH present in goldfish, but not other forms of GnRH. The relative binding affinity of the partially purified GnRH-BP was [D-Arg6,Pro9-NEt]-salmon GnRH greater than chicken GnRH-II greater than or equal to salmon GnRH. The GnRH-BP, in raw serum or partially purified by PAGE, was specifically covalently labeled using 125I-[D-Lys6,Pro9-NEt]-salmon GnRH and the bifunctional cross-linking reagent, disuccinimidyl suberate, and then subjected to sodium dodecyl sulfate-PAGE under reducing conditions. The location of the radiolabeled GnRH-BP on PAGE gels was determined by cutting gels into sections and counting the radioactivity, or by autoradiography; the molecular weight of the GnRH-BP was estimated to be 40 KD. The covalently labeled GnRH-BP extracted from SDS-PAGE was subjected to high pressure liquid chromatography, and it coeluted with a single protein peak of the GnRH-BP partially purified by PAGE under nonreducing conditions. These studies demonstrate that the GnRH-BP is a minor component of serum proteins in goldfish; it is a single nonglycoprotein of about 40 kDa.

Affinity Labels↗
PubMed1991

Metabolism of gonadotropin-releasing hormone in goldfish: serum clearance and tissue uptake studies.

The metabolic clearance rate (MCR) and initial half-disappearance time (T(1/2)i) of salmon gonadotropin-releasing hormone (sGnRH) and its agonist analog [D-Arg6,Pro9-NEt]-sGnRH (sGnRH-A) were investigated in goldfish, following a single intraarterial injection of radioiodinated sGnRH and sGnRH-A. The tissue uptake of radioiodinated sGnRH-A was also investigated. 125I-sGnRH had a MCR of 0.01173 ml min-1 35 g-1 and a (T(1/2)i) of 32.38 min; 125I-sGnRH-A had a MCR of 0.0192 ml min-1 35 g-1 and a (T(1/2)i) of 72.95 min. In the tissue uptake experiments, high levels of accumulated labeled sGnRH-A were generally found in the gills, kidney, liver, and pituitary compared to air bladder, brain, gonad, eyes, and muscle. Coinjection of excess amount of cold sGnRH-A caused decreased uptake of labeled sGnRH-A only in pituitary, but increased accumulation of labeled sGnRH-A in some other tissues. Our results show a correlation between the T(1/2)i and the affinity of the peptides for a serum GnRH binding protein present in the goldfish, suggesting that the formation of a hormone-binding protein complex may decrease the MCR of GnRH in the circulation in goldfish. Our data also indicate specific uptake of 125I-sGnRH-A by the pituitaries of both male and female goldfish, confirming the pituitary as a major target organ of GnRH in goldfish.

Air Sacs↗
PubMed1991

Evaluation of a specific gonadotropin-releasing hormone binding protein in the serum of goldfish: a study on the influence of sex, season, GnRH injection and estradiol treatment in vivo.

A gonadotropin releasing hormone (GnRH) binding protein (GnRH-BP) from goldfish serum was isolated and characterized. In the present studies, the differences in serum titer of GnRH-BP between male and female goldfish, and between goldfish at different stages of gonadal development, were investigated. The effects of estradiol (E2) treatment or multiple injections of [D-Arg6-Pro9-NEt]-salmon GnRH (sGnRH-A) treatment on the serum titer of GnRH-BP were also studied. GnRH-BP in individual serum samples was quantified with a ligand binding assay using 125I-sGnRH-A as tracer; GnRH-BP-tracer complex was separated from free tracer by gel filtration using Sephadex G-50 mini-columns. GnRH-BP was detected in every individual sample; however, no differences between males and females, nor seasonal changes in either sex, were detected. Serum total protein content doubled with E2 treatment, but no effects of E2 on GnRH-BP titer were detected. Long-term treatment with sGnRH-A stimulated an increase in serum gonadotropin levels; the long-term treatment with sGnRH-A did not alter the serum titer of GnRH-BP. Although the GnRH-BP is present in excess relative to the low concentration of GnRH in goldfish serum, it is not a major component of serum proteins. It is concluded that the serum titer of GnRH-BP was not fine tuned by GnRH, gonadotropin, or estradiol. Therefore physiological regulators have yet to be discovered.

Animals↗
PubMed1991

External fixation of the sternum for thoracic trauma.

A flail chest with a manubriosternal separation in a man with multiple injuries was treated with an external fixator applied to the sternum and the manubrium. Pain and ventilatory function were improved, permitting immediate postoperative extubation and prompt patient mobilization. The external fixator was removed after fracture union at 2 months. One year after injury, the patient's pulmonary function was normal. External fixation is an alternative to other methods of sternal fracture stabilization.

Abdominal Injuries↗