The extracellular Ca++ -independent component of luteinzing hormone (LH) secretion is manifest under the steroidal conditions known to induce gonadotrophine-releasing hormone (GnRH) self-potentiation

Quartered pituitaries obtained from intact males or gonadectomized males and females (72h) ± estradiol (24h) and/or testosterone (72h) implants were perifused at 0.25 ml/minute with Ca++ -free medium at 37°C, and sequential effluent fractions collected every 10 minutes, in an attempt to determine if the steroidal conditions known to induce or prevent GnRH self-potentiation would activate or inhibit the extracellular Ca++ -independent component of luteinizing hormone (LH) secretion. Continuous infusions (4h) of 1nmol GnRH or 1µmol of phorbol 12-myristate 13-acetate (PMA) did not stimulate LH secretion from the pituitaries of castrated males, intact males, estradiol-treated intact males or ovariectomized females. In contrast, estradiol induced delayed (20-30 minutes), protein synthesis-dependent components of LH secretion in response to both GnRH and PMA from pituitaries of gonadectomized males and females. Implantation of testosterone capsules immediately following gonadectomy resulted in an inhibition of the estradiol- induced GnRH- and PMA-stimulated responses from pituitaries of castrated or ovariectomized animals. These results suggest that estradiol can induce extracellular Ca++ -independent components of LH secretion from pituitaries of gonadectomized animals; responses which depend on de novo protein synthesis and which could involve protein kinase C. Additionally, the effects of estradiol are prevented by testosterone, indicating that this component of LH secretion is only apparent under the steroidal conditions known to facilitate GnRH self-potentiation.

The extracellular Ca++ -independent component of luteinzing hormone (LH) secretion is manifest under the steroidal conditions known to induce gonadotrophine-releasing hormone (GnRH) self-potentiation

Quartered pituitaries obtained from intact males or gonadectomized males and females (72h) ± estradiol (24h) and/or testosterone (72h) implants were perifused at 0.25 ml/minute with Ca++ -free medium at 37°C, and sequential effluent fractions collected every 10 minutes, in an attempt to determine if the steroidal conditions known to induce or prevent GnRH self-potentiation would activate or inhibit the extracellular Ca++ -independent component of luteinizing hormone (LH) secretion. Continuous infusions (4h) of 1nmol GnRH or 1µmol of phorbol 12-myristate 13-acetate (PMA) did not stimulate LH secretion from the pituitaries of castrated males, intact males, estradiol-treated intact males or ovariectomized females. In contrast, estradiol induced delayed (20-30 minutes), protein synthesis-dependent components of LH secretion in response to both GnRH and PMA from pituitaries of gonadectomized males and females. Implantation of testosterone capsules immediately following gonadectomy resulted in an inhibition of the estradiol- induced GnRH- and PMA-stimulated responses from pituitaries of castrated or ovariectomized animals. These results suggest that estradiol can induce extracellular Ca++ -independent components of LH secretion from pituitaries of gonadectomized animals; responses which depend on de novo protein synthesis and which could involve protein kinase C. Additionally, the effects of estradiol are prevented by testosterone, indicating that this component of LH secretion is only apparent under the steroidal conditions known to facilitate GnRH self-potentiation.

The effect of DPT inoculation on the hormonal control of glucose homeostasis in children recovered from malnutrition

The effect of a controlled stress (DPT inoculation) on the hormonal control of glucose homeostasis was investigated in children nutritionally rehabilitated from severe malnutrition. The age range of the 15 children studied was 6-26 months. Plasma insulin (INS), growth hormone (GH) and interleukin-1 (IL-1) were measured by radioimmunoassay; plasma glucose (GLU) by a glucoseoxidase method; and red cell insulin binding ( percentSB) was determined, using A-14 monoiodinated insulin. Measurements were made on two occasions: (T-O) at 10 a.m.,12 hr before DPT inoculation, and (T-36) 36 hr. after inoculation. On both occasions, 4 hr post-prandial blood samples were used, and the mean body temperature(T) on the day of the test was determined. Red cell insulin binding ( percentSB) was significantly higher at T-36 than at T-O (16.8 ñ 1.7 vs 12.1 ñ 1.2 (14), p=0.005). (Results were expressed as mean ñ SEM, numbers of paired observations in parentheses). The higher percentSB after DPT was accompanied by an increase in the number of receptor sites (S) (29.05 ñ 6.5 vs 15.6 ñ 2.5 (14),p=0.025). However, insulin receptor affinity (K x 10(9)M(-1)) was decreased 0.7 ñ 0.1 vs 1.5 ñ 0.3(14), p=0.008). There were no significant differences in the plasma levels of insulin, glucose and interleukin-1, but plasma growth hormone (æU/ml) was increased after DPT, (18.0 ñ 3.0 vs 11.5 ñ 1.2 (13), p=0.04). Body temperature (§C) was also significantly increased after DPT,(99.9 ñ 0.4 vs 98.3 ñ 0.2(14), p=0.006). The change in plasma glucose from T-O to T-36 tended to be associated with both a change in plasma insulin (p=0.06) and plasma growth hormone (p=0.07). Increased insulin binding, as one index of increased insulin sensitivity during fever, can contribute to a reduction in blood glucose. However, the elevation in plasma growth hormone cold buffer the hypoglycaemic effect of insulin, and help to maintain glucose homeostasis (AU)

Insulin and growth hormone inter-relationships in vitro and in vivo - abstract

The effect of growth hormone on insulin release was observed in rabbit pancreas in vitro. Isolated islets and pancreas slices were incubated with varying concentrations of human growth hormone. Insulin released in the medium was measured by double antibody immunoassay. Human growth harmone stimulated insulin release in both pancreas preparations (p=.01). However the response was concentration dependent in that insulin release was inhibited at high concentrations of growth hormone. These observations support the concept that growth hormone plays a physiological role in the control of insulin release. Correlation between insulin and growth hormone levels in vivo was investigated in infants recovering from malnutrition. Plasma immunoreactive insulin was measured by a specially modified assay which descriminated between 0, 3, 6 and 12 uu/ml (P=.01). Growth hormone assay was equally sensitive, detecting 0.16 uu/ml. Fasting hormone levels were observed during acute malnutrition, rapid catch-up growth and recovery. In 19 acutely malnourished children insulin levels were low (2.3ñ0.3 uu/ml) (mean ñ SEM) while growth hormone levels were high (32.5 ñ 7.1). During the phase of rapid growth, insulin levels were significantly increased (4.5 ñ 0.6) (p = 0.025) while growth hormone level was 21.7 ñ 4.1. When growth curves plateaued with recovery, mean insulin level was 2.8 ñ 0.3 while growth hormone was 17.6 ñ 3.4. It is concluded that rapid catch-up after protein-calorie malnutrition is associated with a significant elevation of plasma insulin (AU)

Observations on carcinoma of the breast in Jamaica

Data on 127 cases of carcinoma of the breast treated in the University College Hospital of the West Indies are presented. Additional information from the registrar general is given. Carcinoma of the breast occurs commonly in Jamaica. Patients attend for treatment at a late stage of the disease which makes the prognosis bad. X-ray therapy is hopelessly inadequate. This makes the prognosis worse and necessitates modification in treatment. The histological types are the same as for other countries. (AU)

Oral contraceptives: beyond pregnancy prevention, Part 1

Combined oral contraceptives (COC) have become an integral part of birth control. A growing body of knowledge is pointing to several non contraceptive benefits of COCs while illuminating the potential risks of the "pills". Pharmacists have a critical role to play in promoting the safe and effective use of these medications