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Biomedical subjects

D Ayalon

Publications and source records attributed to D Ayalon.

At least 55 records · Page 3Linked to original sources
PubMed1988

The role of increased prolactin levels under GnRH analogue treatment in advanced prostatic carcinoma.

The role of prolactin in the progress of prostatic carcinoma still is obscure. It is known to modulate testosterone metabolism and may have a prognostic value in determining disease progression. Prolonged treatment with a GnRH analogue has been introduced recently as a therapeutic alternative to surgical castration in advanced prostatic carcinoma. It has been reported that prolactin levels remain unchanged or even decrease in GnRH analogue treatment. By contrast, in this series of 15 prostatic carcinoma patients treated with GnRH analogue, a significant rise was demonstrated in clinical responders as well as nonresponders. In the latter group, prolactin rise was more pronounced. These results suggest that frequent prolactin determinations might be of prognostic value in determining early disease progression under GnRH analogue treatment.

Buserelin↗
PubMed1988

Correlation between PGE2 production and suppressor activity of alveolar macrophages from patients with interstitial lung diseases.

The suppressive activity of alveolar macrophages (AM) obtained from bronchoalveolar lavage (BAL), on PHA stimulation of autologous peripheral blood lymphocytes (APL) was evaluated. The effect on lymphocyte stimulation was evaluated by coculturing the AM and APL cells at a ratio of 1:1. PGE2 released by AM during the culture period was measured by a radioimmune assay. The patients included in the study were 11 cases with interstitial lung disease (ILD), 8 cases of lung cancer (CA), and 5 controls (CO). Addition of AM of patients from the CA group resulted in slight suppression of lymphocyte stimulation in 4 cases, slight enhancement in 3 cases and no effect in one case. AM from the CO group induced slight suppression in 4 out of 5 cases. AM from all 11 ILD cases exerted a significant high suppressive activity (65.6% +/- 18.2 - P less than 0.001 by comparison with the CO and CA groups). In ILD cases, a dichotomous pattern was found in regard to relation between high suppressive activity of AM and release of PGE2: in idiopathic pulmonary fibrosis (IPF) patients, high suppressive activity of AM (70.4% +/- 15.4) correlated well with elevated secretion of PGE2: 3.58 +/- 0.26 ng/ml/10(5) cells (P less than 0.02 compared to CO). AM from sarcoidosis patients suppressed PHA stimulation by 61.6% +/- 19.3 but secreted only 0.357 +/- 0.26 ng/ml/10(5) cells of PGE2 (P less than 0.02 compared with the idiopathic pulmonary fibrosis group). Therefore, it seems that other factors, in addition to PGE2, might be involved in the suppressive activity of AM from interstitial lung diseases.

Aged↗
PubMed1988

Receptors for gonadotropin releasing hormone are present in rat oocytes.

Specific receptors for gonadotropin releasing hormone (GnRH) in the rat oocyte have been identified by using two independent methods. Light microscopic autoradiography, utilizing an iodinated biologically active photoaffinity derivative of GnRH, revealed specific binding of the neurohormone to rat oocytes. Furthermore, the presence of GnRH-receptor is also evident from indirect fluorescent immunocytochemistry that shows binding of GnRH-receptor antibodies to rat oocytes which is neither detected with non immune serum nor with antiserum depleted of GnRH-receptor antibodies. These antibodies to the GnRH-receptor, also bind to both cumulus and granulosa cells but not to rat basophilic leukemia cells. The presence of specific GnRH receptors on rat oocytes provides an experimental basis for understanding the molecular events involved in GnRH-induced oocyte maturation.

Animals↗
PubMed1988

Gonadotropin-releasing hormone-induced rise in cytosolic free Ca2+ levels: mobilization of cellular and extracellular Ca2+ pools and relationship to gonadotropin secretion.

Addition of GnRH to pituitary gonadotrophs preloaded with Quin 2 resulted in a rapid (approximately 8 s) mobilization of an ionomycin-sensitive intracellular Ca2+ pool. A second component of Ca2+ entry via voltage dependent channels contributed about 45% of the peak cytosolic free Ca2+ concentration ([Ca2+]i). Thereafter, influx of Ca2+ via voltage-sensitive and -insensitive channels is responsible for maintenance of elevated [Ca2+]i during the second phase of GnRH action. Addition of inositol 1,4,5-trisphosphate (IP3) to permeabilized pituitary cells resulted in a Ca2+ transient, released from a nonmitochondrial pool, which maintained ambient free Ca2+ concentration around 170 nM in an ATP-dependent mechanism. Successive stimulations of the cells with IP3 produced an attenuated response. Elevation of the gonadotroph [Ca2+]i by ionomycin, to levels equivalent to that induced by GnRH, resulted in LH release amounting to only 45% of the response to the neurohormone. Activation of the voltage-dependent Ca2+ channels by the dihydropyridine Ca2+-agonist [methyl 1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoromethylphenyl)-pyridine- 5-carboxylate (BAYK8644)] stimulated LH release, 36% of the GnRH (100 nM) response being reached by 10(-8) M of the drug, both [Ca2+]i elevation and GnRH-induced LH release were inhibited similarly (40-50%) by the dihydropyridine Ca2+-antagonist nifedipine. The results indicate that peak [Ca2+]i induced by GnRH in pituitary gonadotrophs is derived mainly from ionomycin-sensitive cellular stores most likely via IP3 formation.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1988

Induction of ovulation with D-Trp6-LHRH combined with purified FSH in patients with polycystic ovarian disease.

Seventeen patients with polycystic ovarian disease (PCOD) and evidence of mild or severe ovarian hyperstimulation syndrome (OHSS) during therapy with CC/hCG, FSH/hCG or hMG/hCG were treated with D-Trp6-LHRH until medical gonadectomy was attained. Under the suppressive therapy with the GnRH agonist (GnRHa) ovulation was induced with FSH/hCG. In 15 out of 17 patients, ovulatory cycles were obtained with this new modality of treatment. Seven patients conceived (3 viable pregnancies and 4 early abortions) after the 1st treatment cycle. Fourteen of the 17 patients demonstrated symptoms of mild OHSS which did not require hospitalization. Only 1 patient developed severe OHSS after the combined treatment. Our results suggest that therapy with GnRHa, especially in its delayed release formulation, is effective for the prevention of severe ovarian hyperstimulation in PCOD patients undergoing treatment with menotropins for the induction of ovulation.

Adult↗
PubMed1988

Sonographic monitoring of ovarian volume during LHRH analogue therapy in women with polycystic ovarian syndrome.

Polycystic ovarian disease is characterized by menstrual disorders, infertility, obesity, and large ovaries. Large ovaries with multiple cysts are the direct cause of the high incidence of ovarian hyperstimulation during ovulation induction. Lately, gonadotropin-releasing hormone (GnRH) analogues have been employed to decrease ovarian steroidogenesis and thus reduce the incidence of ovarian hyperstimulation. In this study the ovarian size was ultrasonographically assessed during chronic GnRH analogue treatment, revealing a significant reduction in ovarian volume. This decrease in volume results in a reduced incidence of hyperstimulation, and we think the ultrasonic scanning can be effectively used to assess the success of GnRH treatment.

Female↗
PubMed1987

Serum myoglobin in detection of myocardial necrosis in patients with "coronary insufficiency".

Myoglobin, an oxygen-binding protein, is synthesized exclusively in striated and cardiac muscle, and is normally found in blood. Serum myoglobin determination has been used in the diagnosis of acute myocardial infarction. Experimental work has shown that myoglobin is released only after muscular necrosis. This prospective study included 101 patients: 62 with acute coronary insufficiency, 16 with acute myocardial infarction, and 23 controls. In all the patients with infarction the serum myoglobin levels were elevated. None of the controls showed serum myoglobin above normal. In patients with coronary insufficiency the peak serum myoglobin ranged from normal to 280 ng/ml. Half of all the patients with coronary insufficiency had a significant elevation of serum myoglobin (p less than 0.001). The obvious explanation of this finding is that myocardial necrosis to some extent develops in cases of so-called coronary insufficiency. Furthermore, this study confirms previous findings that serum myoglobin assessment constitutes a very early marker of myocardial damage.

Acute Disease↗
PubMed1987

Cytosolic free calcium levels in cultured pituitary cells separated by centrifugal elutriation: effect of gonadotropin-releasing hormone.

The cytosolic concentration of free Ca2+ ([Ca2+]i) in normal rat pituitary cells separated by centrifugal elutriation was monitored with the fluorescent Ca2+ indicator Quin 2. GnRH (10(-7) M) induced a rapid rise (6-8 sec) in the gonadotroph's [Ca2+]i, followed by a plateau phase of prolonged elevated [Ca2+]i which lasted about 15 min. The stimulatory effect of GnRH was dose dependent, with an ED50 of 10(-9) M, and was blocked by the potent antagonist [Dp-Glu1,pclPhe2,DTrp3.6]GnRH. GnRH elevated [Ca2+]i only in gonadotroph-enriched cell fractions, whereas TRH and GH-releasing factor (GRF) elevated [Ca2+]i in mammotroph- and somatotroph-enriched cells fractions, respectively. A rapid increase (first phase) in [Ca2+]i induced by GnRH was observed in Ca2+-free medium containing EGTA, but this rapid phase was terminated within 2 min. Readdition of Ca2+ to the medium induced a second slower rise in [Ca2+]i (plateau phase). Addition of K+ caused a rapid rise in [Ca2+]i, which was dependent on extracellular Ca2+, but was not affected by prior stimulation with GnRH. On the other hand, stimulation of gonadotroph's [Ca2+]i response by GnRH desensitized the cells to a subsequent GnRH challenge within the time frame studied. These findings indicate an elevation of [Ca2+]i induced by GnRH, TRH, and GRF in their respective separated target cells in the rat pituitary. The rise in [Ca2+]i in GnRH-stimulated gonadotrophs originates partly from intracellular Ca2+ pools and partly from influx of Ca2+ across the cell membrane.

Aminoquinolines↗
PubMed1986

Calcium-dependent actions of gonadotropin-releasing hormone agonist and luteinizing hormone upon cyclic AMP and progesterone production in rat ovarian granulosa cells.

The Ca2+ dependency of the direct stimulatory effect of the gonadotropin-releasing hormone (GnRH) agonist analog [D-Ser(t-Bu)6]des-Gly10-GnRH-N-ethylamide (GnRHa) on progesterone production was investigated and compared to that of luteinizing hormone (LH) in rat granulosa cells from preovulatory follicles. Removal of extracellular Ca2+ by EGTA, or the use of the Ca2+ channel blockers verapamil and La3+, resulted in complete inhibition of GnRHa-induced progesterone production and a partial inhibition of LH-stimulated progesterone production (80, 80 and 50% inhibition respectively for EGTA, verapamil and La3+). Removal of extracellular Ca2+ increased the ED50 for LH-induced cAMP production by four-fold (from 80 to 330 ng/ml) and decreased maximal nucleotide formation by 44%. LH-induced cAMP production was also inhibited partially by verapamil (35%) at 10(-4) M drug concentration. GnRHa had no effect on cAMP production in the presence or absence of Ca2+. GnRHa and LH were found to have maximal effects on progesterone production at about 0.5 mM of Ca2+ in the incubation medium. On the other hand the stimulatory effect of dibutyryl cAMP [Bu)2cAMP) on progesterone production showed little dependency on extracellular Ca2+. The calmodulin antagonist trifluoperazine (TFP) caused concentration-dependent inhibition of the stimulatory action of GnRHa and LH on progesterone production with IC50 values of 3 and 8 microM, respectively. The stimulatory effect of (Bu)2cAMP on progesterone synthesis was attenuated by verapamil and TFP. These results indicate that the direct stimulatory effect of GnRH on ovarian progesterone production is absolutely dependent on Ca2+.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

The effect of delta 1tetrahydrocannabinol on luteinizing hormone release in castrated and hypothalamic deafferented male rats.

delta 1Tetrahydrocannabinol (THC) acutely suppresses tonic serum luteinizing hormone (LH) and prolactin levels in adult male rats. The exact site of its action has not been identified. We have performed complete hypothalamic deafferentation (CHD), which disrupts the medial basal hypothalamus (MBH) from the rest of the CNS, but did not abolish the ability of THC to suppress hypothalamic-pituitary responses in gonadectomized male rats. This was shown by the equal reduction in serum levels of LH and prolactin in non-deafferented (ND) and CHD animals. These results indicate that THC is able to act inside the MBH and that the MBH-pituitary axis remains responsive to its inhibitory effect despite interruption of the neural connections between the MBH and extrahypothalamic areas. However, the corticotropin releasing factor neurons in the MBH appear functionally impaired as a result of the transection and become unresponsive to the normally produced THC stimulation. Different patterns of action seem to govern the various hypophyseal hormones controlled by the hypothalamus, suggesting that the release of LH releasing hormone and prolactin inhibiting factor might be maintained by the activity of neurons surviving inside the island.

Afferent Pathways↗
PubMed1985

Induction of ovulation in amenorrheic patients with gonadotropin-releasing hormone and human menopausal gonadotropin.

In five hypothalamic amenorrhea patients who underwent chronic intermittent gonadotropin-releasing hormone (GnRH) therapy for induction of ovulation, small doses (2 to 4 ampules/day) of human menopausal gonadotropin (hMG) were administered 9 to 32 days after the start of GnRH treatment. In seven treatment cycles, the addition of hMG initiated a sudden rise of 17 beta-estradiol concentrations, followed by a luteinizing hormone and follicle-stimulating hormone surge and ultrasonographic evidences of ovulation. Four of five patients conceived (singleton pregnancies) after the first or second treatment course. There were no clinical signs of ovarian hyperstimulation. Combined therapy of GnRH and hMG may be useful, therefore, for the treatment of hypothalamic amenorrhea patients who demonstrate prolonged follicular phases or luteinized unruptured follicle syndrome under chronic treatment with pulsatile GnRH alone.

Adult↗
PubMed1985

Pseudohypoaldosteronism in a female infant and her family: diversity of clinical expression and mode of inheritance.

Pseudohypoaldosteronism was diagnosed in an infant that clinically presented severe failure to thrive and vomiting. Evaluation of her extended family revealed many other affected family members with a vast range of clinical expression. The mode of inheritance is most likely autosomal dominant. Salt supplementation during infancy was effective in restoring normal growth, weight gain and serum electrolytes.

Adult↗
PubMed1984

The suppressive effect of delta-1-tetrahydrocannabinol on the steroidogenic activity of rat granulosa cells in culture.

In previous study the major psychoactive ingredient of marihuana (delta 1-THC) has been shown to inhibit ovarian prostaglandin synthesis when administered to normally cycling rats in the early afternoon of proestrus. These results suggested a direct suppressive effect of the drug on the ovary. The purpose of this study was to evaluate the effect of delta 1-THC on steroidogenesis in granulosa cells (GC) in vitro. Incubation of GC with delta 1-THC (10-50 microM) effectively inhibited LH-stimulatable progestin production. This suppressive effect was not abolished by washing the cells after 24 h of culture in the presence of delta 1-THC, indicating the irreversible nature of the blocking effect of delta 1-THC. By contrast, estradiol production following incubation of GC with testosterone (1 microgram/ml) was not inhibited by similar concentrations of delta 1-THC, thus suggesting that delta 1-THC does not inhibit aromatase activity in GC. In addition, delta 1-THC was shown to inhibit cAMP production as well as 125I-hCG binding capacity to GC. Administration of 8-Br-cAMP did not abolish the delta 1-THC-induced block, suggesting that the drug probably acts distal to the cAMP site of action.

20-alpha-Dihydroprogesterone↗
PubMed1984

Chronic treatment with 2-alpha-bromocriptine in women with the hyperprolactinemic syndrome.

Seventeen hyperprolactinemic patients with or without radiological evidences of a pituitary adenoma, were submitted to a long term (7-36 months) suppressive treatment with bromocriptine. Nine patients conceived during the treatment. All of them had a normal pregnancy and delivered normal babies. In all patients (with the exception of one-patient Z.S.) the post treatment prolactin levels were significantly lower than the pre-treatment values suggesting a long lasting suppressive effect of this dopamine agonist on the pituitary lactotrophs. Three of the patients followed throughout a whole menstrual cycle (3-10 months after discontinuation of therapy) showed presumptive signs of ovulation in spite of relatively elevated circulating immuno-reactive prolactin concentrations. These observations might suggest a modification of the biological activity of the hormone, possibly related to the chronic treatment with bromocriptine.

Bromocriptine↗
PubMed1983

Dopaminergic regulation of prolactin secretion in the hyperprolactinemic syndrome.

The prolactin responses to an oral challenge of L-dopa (0.5 g) and bromocriptine (2.5 mg) were studied in 31 hyperprolactinemic females without radiological abnormalities of pituitary fossa, in 12 hyperprolactinemic patients with minor radiological evidence suggesting the presence of a pituitary adenoma and in 16 normal volunteers in the early puerperium with physiological hyperprolactinemia. Administration of bromocriptine was followed by a similar suppression of prolactin secretion in the functional as well as the adenomatous hyperprolactinemic patients. By contrast, a significantly blunted response to L-dopa was noted in the patients with pathological hyperprolactinemia (with and without radiological abnormalities of the pituitary fossa). These results suggest that the L-dopa suppression test might serve as a reliable indicator to detect prolactin-secreting microadenomas in patients with persistent hyperprolactinemia and radiologically normal pituitary fossae.

Adenoma↗