P84 is a neuronal membrane glycoprotein that promotes the attachment and neurite outgrowth of cultured murine cerebellar cells. The heterophilic adhesive properties of P84 and its localization at sites of synaptogenesis suggest that it may be involved in regulation of synapse formation or maintenance. P84 is expressed in subsets of neurons throughout the CNS. By cloning the cDNA encoding murine P84, we have discovered that this molecule is a member of a family of phosphatasebinding proteins and is identical to the murine SHPS-1 cDNA. Here we report the cloning of two alternatively spliced forms of P84 and describe its localization within the CNS by in situ hybridization.

No abstract

This study directly tested the inhibin hypothesis by examining the ability of replacement with recombinant human (rh-) inhibin, either alone or in combination with testosterone (T), to maintain FSH secretion and FSH beta messenger RNA (mRNA) at intact levels after orchidectomy in the hypophysiotropically clamped juvenile rhesus monkey. Thirteen male monkeys (11-21 months of age) received an intermittent i.v. infusion of GnRH (0.1 microgram/min for 3 min every 3 h). After 4-6 weeks of GnRH stimulation, 10 animals were orchidectomized, and 3 monkeys were sham castrated. Hormone replacement was initiated at castration and maintained for 4 days. Three monkeys received a combination of inhibin and T replacement, 4 monkeys received replacement with inhibin alone, and 3 monkeys received T replacement alone. A continuous i.v. infusion of rh-inhibin (832 ng/h.kg) was used to replace the testicular protein, whereas SILASTIC capsules were implanted sc for T replacement. The FSH response to castration and hormone replacement was determined by measuring circulating concentrations of this gonadotropin before a GnRH pulse and for 3 h thereafter on the day before surgery and on days 2 and 4 postcastration. Circulating immunoactive inhibin was measured by a RIA that recognizes the free alpha-subunit of inhibin as well as inhibin dimers. At the end of the study, anterior pituitaries were collected for analysis of steady state levels of FSH beta, LH beta, and alpha-subunit mRNAs. Steroid replacement alone, which produced circulating T concentrations in the upper physiological range, failed to prevent the postcastration increases in circulating FSH concentrations and pituitary FSH beta mRNA levels. In contrast, when circulating immunoactive inhibin in T-replaced monkeys was maintained at precastration levels (approximately 2 ng/ml) by infusion of rh-inhibin, FSH secretion and synthesis were held at control values. When T was omitted from combined replacement, the FSH-suppressing action of the recombinant hormone was not compromised. These results demonstrate that rh-inhibin is biologically active in the monkey, and the action of inhibin to suppress FSH synthesis and secretion does not require a concomitant action of T. Moreover, because the hypophysiotropic drive to the pituitary-testicular axis was clamped, the FSH-suppressing action of rh-inhibin must be at the pituitary.

Estimations of urinary estrone glucuronide, pregnanediol glucuronide and human chorionic gonadotrophin were carried out by ELISA to see their potential in predicting an abnormal outcome in cases with vaginal bleeding in early pregnancy. Reference values were set up with samples from women without bleeding in present or past pregnancies and with normal ultrasonic findings. None of the parameters were found to be sensitive enough to predict an abnormal outcome. However, predictability of an abnormal value was found to be 95% for estrone-3-glucuronide (E1G), 93% for pregnanediol glucuronide (PdG) and 87% for human chorionic gonadotrophin (hCG).

No abstract