Endocrinology: The effect of growth hormone on granulosa cell function during in-vitro fertilization

The effect of growth hormone addition to human menopausal gonadotrophin(HMG), after pituitary down-regulation, on granulosa cell function,in in-vitro fertilization (IVF) was evaluated. Growth hormoneor placebo were added in a prospective, randomized and double-blindmanner to an existing IVF stimulation protocol. Forty-two normalovulatory women (38 years old) with mechanical factor infertilityand normal male factor were included in the study. Gonadotrophin-releasinghormone agonist (GnRHa) was given from day 21 of the previouscycle until human chorionic gonadotrophin (HCG) administration.Follicular stimulation with HMG was started after pituitarydown-regulation. Growth hormone 12 IU/day or placebo were administeredon alternate days, beginning day 1 until day 7 of HMG treatment.Granulosa cell function was evaluated, in all patients, by follicularfluid levels of ovarian steroids and insulin-like growth factor-I(IGF-I). In 14 patients, chosen arbitrarily granulosa luteincells were cultured in the presence and absence of additionalHCG. Follicular fluid levels of oestradiol, progesterone, testosteroneand IGF-I were similar in both growth hormone and placebo groups.Basal and post-HCG levels of oestradiol and progesterone didnot differ significantly between the two groups of granulosalutein cell cultures. We conclude that after pituitary down-regulation,in-vivo administration of growth hormone with HMG in young ovulatorywomen does not seem to affect granulosa cell function when comparedto the administration of HMG alone.     

Concordant and discordant effects on cardiovascular risks exerted by oestrogen and progestogen in women using oral contraception and hormone replacement therapy. ESHRE Capri Workshop Group

The major indications for the clinical use of oestrogen and progestogen are oral contraception (OC) in young women, and hormonal replacement therapy (HRT) in menopause. Over the past few years, epidemiological data have associated the use of these hormones to different cardiovascular conditions such as myocardial infarction, cerebrovascular disease and venous thromboembolism. This review summarizes the data discussed and the conclusions achieved by the ESHRE Capri Workshop Group, recently published in Human Reproduction.     

Growth hormone as an early embryonic growth and differentiation factor

In this review we consider the evidence that growth hormone (GH) acts in the embryo as a local growth, differentiation, and cell survival factor. Because both GH and its receptors are present in the early embryo before the functional differentiation of pituitary somatotrophs and before the establishment of a functioning circulatory system, the conditions are such that GH may be a member of the large battery of autocrine/paracrine growth factors that control embryonic development. It has been clearly established that GH is able to exert direct effects, independent of insulin-like growth factor-I (IGF-I), on the differentiation, proliferation, and survival of cells in a wide variety of tissues in the embryo, fetus, and adult. The signaling pathways behind these effects of GH are now beginning to be determined, establishing early extrapituitary GH as a bona fide developmental growth factor.     

Fetal development in experimental uremia

Summary Uremic women on hemodialysis with metabolic bone disease (hyperparathyroidism, osteomalacia resulting from defective vitamin D metabolism) and anemia (erythropoietin deficiency) are known to give birth to infants without bone disease or anemia. Therefore, skeletal development (enchondral and desmal bone formation) and hepatic erythropoiesis were evaluated in fetuses of uremic rats. These fetuses failed to show defective mineralisation or evidence of bone disease. Bolus injection of high doses of exogenous PTH into the maternal or fetal organism did not affect fetal bone histology. In addition, no apparent defect of bone mineralisation or bone formation was found in fetuses of ricketic rats. Normal mineralisation in the offspring of uremic rats may be explained by fetal hyperphosphatemia and/or insensitivity of fetal (woven) bone mineralisation to vitamin D.Absence of fetal anemia (normal hematocrits, normal density of hematopoietic cells in the liver) in the presence of maternal anemia is presumably due to the insensitivity of fetal erythropoiesis to erythropoietin.With the support of Deutsche Forschungsgemeinschaft     

Freeze-fracture studies of muscle plasma membranes in myopathic patients with hypo-and hyperthyroidism

To examine the influence of thyroid hormone on the skeletal muscle plasma membrane, we analyzed the changes in ultrastructural architecture and membrane area complexed with digitonin of muscle plasma membrane in myopathic patients with hypo-and hyperthyroidism by the conventional freeze-fracture (F-F) technique and F-F cytochemistry using the sterol-specific ligand digitonin. The densities of flask-shaped invaginations, which are mainly thought to correspond to caveolae, intramembranous particles, and orthogonal arrays, and the changes of digitoninreacted membrane areas in the muscle plasma membranes in three patients with hypothyroid myopathy and one patient with both myasthenia gravis and hyperthyroidism were compared with those in age-matched controls. In the conventional F-F study, the muscle plasma membrane of hypothyroid patients showed increased invagination density, whereas that of the hyperthyroid patient was normal ultrastructurally. In the F-F cytochemistry study, however, the ratio of digitonin-reacted membrane areas versus fractured membrane areas was not different between hypothyroid patients and controls, whereas that of the hyperthyroid patient was lowered in comparison with that of control. These results suggest that thyroid hormone may alter the biochemical properties and ultrastructural architecture of muscle plasma membrane.This study was presented at the 29th annual meeting of the Clinical Electron Microscopy Society of Japan, Sapporo, October 2–3, 1997     

Effect of dexamethasone on the expression of binding sites for high-density lipoproteins in cultured rat hepatocytes (Independence of the hormone effect on the intracellular cholesterol pool)

It is shown that glucocorticoids play a key regulatory role directed toward the maintenance of an optimal level of binding and internalization of HDL₃ in hepatocytes. Their stimulatory effect on the expression of HDL receptors proves to be independent of changes in the CH content in parenchymal cells. Translated fromByulleten' Eksperimentalnoi Biologii i Meditsiny, Vol. 117, N ^o 1, pp. 50–53, January, 1994     

Hormonelle Grundlagen der normalen und pathologischen somatischen Sexualentwicklung

Summary Normal sexual development is the consequence of three sequential interrelated processes: establishment of genetic, gonadal and somatic sex. It is the terminal phase of sexual differentiation-the translation of gonadal into somatic sex, which is governed by the presence or absence of both testosterone and Müllerian-inhibiting hormone and of dihydrotestosterone, which is formed in its respective target tissues. Thus, despite a testis, somatic male sexual differentiation will proceed to a normal male phenotype only if all three hormones are synthesized and act during a critical period of uterine development. Many clinically distinct syndromes are the results of abnormalities in the synthesis or action of the above-mentioned hormones; these syndromes are described in detail. In contrast to male somatic differentiation, female somatic development is independent of these hormones.

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Abkürzungen DHT 5-Dihydrotestosteron - HY-Antigen Histocompatibilitätsantigen-Y - MIH Müllerian-Inhibiting-Hormon - SSW Schwangerschaftswoche Die eigenen Untersuchungen wurden durch die Deutsche Forschungsgemeinschaft Schw 168/5–7 unterstützt     

Effects of veratridine, tetrodotoxin and other drugs that alter electrical behaviour on secretion of melanocyte-stimulating hormone from melanotrophs of the pituitary pars intermedia

Since melanotrophs are electrically active and exhibit spontaneous Na spikes, a study was made of the effects, on melanotroph secretion, of drugs known to influence electrical properties. The output of melanocyte-stimulating hormone was measured from perifused neurointermediate lobes of mice or melanotrophs dispersed from such lobes of mice or rats. Veratridine (200 microM), which is known to increase Na permeability in a variety of cells, caused a large, although transient, increase in secretion from the melanotrophs that required extracellular Ca2+ and was blocked by the Na-channel blocker tetrodotoxin (1 microM). Tetraethylammonium (10 mM), which blocks K channels and thus prolongs the duration of the action potential in many cells, also stimulated secretion in the melanotrophs in a Ca-dependent manner. This response was not, however, blocked by tetrodotoxin, and is thus not attributable to prolongation of Na spikes in these cells. Moreover, tetrodotoxin did not inhibit basal secretion. The stimulant effect of veratridine on secretion in melanotrophs and its suppression by tetrodotoxin suggests that voltage-dependent Na channels can participate in the regulation of hormone output in these cells of the pituitary pars intermedia. However, the apparent lack of effect of tetrodotoxin on basal secretion suggests that the spontaneous Na spikes previously observed in these cells are not required for promoting the Ca influx which other evidence shows is important for basal secretion.     

Growth hormone deficiency,aortic dilation,and neurocognitive issues in Feingold syndrome 2

We report three patients with Feingold 2 syndrome with the novel features of growth hormone deficiency associated with adenohypophyseal compression, aortic dilation, phalangeal joint contractures, memory, and sleep problems in addition to the typical features of microcephaly, brachymesophalangy, toe syndactyly, short stature, and cardiac anomalies. Microdeletions of chromosome 13q that include the MIR17HG gene were found in all three. One of the patients was treated successfully with growth hormone. In addition to expanding the phenotype of Feingold 2 syndrome, we suggest management of patients with Feingold 2 syndrome include echocardiography at the time of diagnosis in all patients and consideration of evaluation for growth hormone deficiency in patients with short stature.     

181例柯兴氏综合征的临床病理

本文收集自1957至1984年181例柯兴氏综合征的肾上腺标本,对30例作了电镜观察。对88例用电子计算机作逐步回归分析,结果表明治疗方式、病理类型、紫纹和性征异常对预后影响较大。并对肾上腺皮腺癌诊断标准的掌握、皮质增生中腺瘤样结节和皮质腺瘤间可能存在的转化关系、肾上腺皮质增生的诊断标准以及柯兴氏综合征病例肾上腺病损的超微结构进行了讨论。