Amino-acid sequence of human placental lactogen.
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Amino Acid Sequence↗
Biomedical subjects
S Handwerger
Publications and source records attributed to S Handwerger.
Glucose intolerance in cystic fibrosis.
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Adolescent↗
Characterization of placental lactogen release from perifused human trophoblast cells.
The dynamics of the release of human placental lactogen (hPL) under basal conditions and response to various secretogogues has been studied in perifused enriched hPL-producing cells from term placentae prepared by the isopycnic centrifugation of collagenase/hyaluronidase-dispersed placental cells on Percoll gradients. Under basal conditions, the perifused cells released hPL at a relatively constant rate for up to 24 h in culture. The mean rates of hPL release from cells (5 x 10(6) cells) from 18 normal full-term placentae varied from 1.8 to 20.2 ng/5 min (mean 7.7 ng/5 min). The cells from term placentae, however, did not release detectable amounts of chorionic gonadotrophin or the cytosolic enzymes lactic dehydrogenase and alkaline phosphatase. The amounts of hPL released by the perifused cells were inversely related to cell density with mean rates of hPL release by 2, 5, and 10 x 10(6) cells of 15.8, 8.6, and 5.7 ng/10(6) cells/0.5 h. The perifused cells responded to provocative stimuli (high-density lipoproteins (HDL), apolipoproteins AI, AII, and CI, partially purified hPL-releasing factor, phorbol esters, sn-1,2-diacylglycerol, and cAMP) in a manner qualitatively similar to enriched trophoblast cells and placental explants in static culture. Release of hPL in response to HDL, apoproteins AI, AII, and CI, and partially purified hPL-releasing factor was dose-dependent and occurred within 5 min of exposure. Basal and stimulated hPL release by perifused trophoblast cells that had been previously frozen at -70 degrees C for four weeks was identical to that of freshly dispersed cells from the same placenta. These experiments indicate that perifused trophoblast cells may be used as a model system to examine the dynamics of hPL release under basal conditions and in response to provocative stimuli.
Cells, Cultured↗
Cyclic AMP as a second messenger for prorenin release from human decidual cells.
The possible roles of cyclic AMP and protein kinase C in the release of renin from human decidual cells were investigated by examining renin release from monolayers of decidual cells exposed for 72 h to agents that increase intracellular cAMP or activate protein kinase C. Dibutyryl cAMP (10-1000 microM caused a dose-dependent stimulation of renin release after a 24-h exposure. Maximal stimulation, 410 per cent greater than that of control cells, occurred at 72 h, and 98 per cent of the renin released into the medium was in the form of prorenin. Forskolin (10-1000 microM) and cholera toxin (CT. 20-1000 ng/ml), both of which stimulate adenyl cyclase, also stimulated prorenin release. Phorbol myristate acetate (PMA), an activator of protein kinase C, had little effect on basal prorenin release at 100 nM but potentiated the stimulation of prorenin release by cAMP and CT. The effects on prorenin release were paralleled by stimulation of active renin release. The results of this study therefore implicate cAMP and protein kinase C in the regulation of prorenin release from decidual cells and suggest that prorenin release from the decidua and other tissues is regulated by the same second messengers.
Analysis of Variance↗
Regulation of the synthesis and release of decidual prolactin by placental and autocrine/paracrine factors.
Human decidual tissue synthesizes and secretes a protein that is identical to pituitary prolactin in its chemical, biological and immunological properties. Nevertheless, the factors that regulate the synthesis and release of prolactin from the decidual tissues appear to be different to those regulating the synthesis and release of pituitary prolactin. Studies from our laboratory over the past few years indicate that the synthesis and release of decidual prolactin are regulated, at least in part, by factors released by placenta, fetal membranes and decidua. The placenta releases a 23.5 KMr protein [decidual prolactin-releasing factor (PRL-RF)] that stimulates a rapid release of prolactin within the first few minutes of exposure and a sustained, prolonged, increase in the synthesis and release of prolactin beginning 6-8 h after exposure. The acute release of prolactin in response to PRL-RF is inhibited by decidual prolactin release-inhibitory factor (PRL-IF), a 35-45 K Mr protein that is released by the decidua. The secondary increase in the synthesis and release of prolactin in response to PRF-RF is blocked by lipocortin I, which is synthesized by both the placenta and decidua. IGF-I, insulin and relaxin also stimulate the synthesis and release of prolactin. However, the stimulation in response to these factors does not occur until 24-48 h after exposure. The cellular mechanisms involved in the release of decidual prolactin are as yet unknown. However, recent studies implicate activation of adenylate cyclase, phospholipase C-mediated phosphoinositide hydrolysis and phospholipase A2-mediated arachidonic acid release in the regulation of prolactin release. The finding that the synthesis and release of decidual prolactin are regulated, at least in part, by PRL-RF, IGF-I, insulin, relaxin and lipocortin I strongly suggests that there is novel feedback regulation between the placenta, fetal membranes, and decidua in the regulation of the synthesis and release of decidual prolactin.
Annexins↗
Prolactin release from perifused human decidual explants; effects of decidual prolactin-releasing factor (PRL-RF) and prolactin release-inhibitory factor (PRL-IF).
The dynamics of prolactin release from human decidual explants were studied under basal conditions, in response to decidual prolactin-releasing factor (PRL-RF), and in response to PRL-RF in the presence of decidual prolactin release-inhibitory factor (PRL-IF) or other factors known to inhibit prolactin release in static cultures. Explants were perifused with medium at a rate of 6 ml/h, and the medium was collected at 5 min intervals. The explants released prolactin for up to 20 h without evidence of cell necrosis, with the rate of prolactin decreasing gradually from 3.9 +/- 0.1 ng/5 min during the first 2 h to 2.2 +/- 0.1 ng/5 min during the last 2 h of exposure. PRL-RF, a 23.5 KMr protein released by the placenta, stimulated a dose-dependent increase in prolactin release from the perifused explants that occurred within the first 5 min of exposure and persisted until the exposure to the releasing factor was discontinued. PRL-IF, a 35-45 K Mr protein released by the decidua, caused a dose-dependent inhibition of PRL-RF-mediated prolactin release. Dibutyryl cAMP, cholera toxin, sn-1, 2-dioctonylglycerol, PMA, and arachidonic acid, which inhibit basal prolactin release from static decidual cultures, also caused a dose-dependent inhibition of prolactin release in response to PRL-RF. In each instance, the maximal dose of the agents tested inhibited PRL-RF-mediated prolactin release by greater than 84 per cent. These results indicate that the stimulation of prolactin by PRL-RF is inhibited by PRL-IF and pharmacologic agents that inhibit basal prolactin release.(ABSTRACT TRUNCATED AT 250 WORDS)
Arachidonic Acid↗
Infection due to Leuconostoc species: six cases and review.
Leuconostocs, members of the family Streptococcacae, have only recently been recognized as potential pathogens. We describe six cases of leuconostoc bacteremia and review 11 additional cases of infection reported in the literature. Fifteen patients with bacteremia ranged from neonates to persons aged 78 years. Almost all were hospitalized with significant underlying diseases, had received previous antibiotic therapy, and had undergone procedures that interrupted the normal integumentary defense. Leuconostoc bacteremia was associated with fever, leukocytosis, and gastrointestinal complaints. Eight of 15 patients had polymicrobial bacteremia, seven of these eight with staphylococcal species. Clinical isolates of Leuconostoc were frequently misidentified, usually as viridans streptococci. All clinical isolates identified to date--and most agricultural isolates--demonstrate a high level of resistance to vancomycin. Successful regimens for treatment of Leuconostoc include high-dose penicillin, clindamycin, and where appropriate, removal of infected intravascular catheters. Susceptibility testing of all gram-positive bacteria isolated from normally sterile body sites is recommended.
Adolescent↗
Antibiotic tolerance among clinical isolates of bacteria.
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Animals↗
Growth hormone and prolactin secretion in the carcinoid syndrome.
We evaluated plasma growth hormone (GH) and plasma prolactin (PRL) levels in ten patients with metastatic carcinoid tumors and the carcinoid syndrome ("active tumors") and seven patients with metastatic carcinoid tumors without the carcinoid syndrome ("inactive tumors"). The patients with active tumors had elevated serum serotonin levels and increased urinary 5-hydroxyindoleacetic acid (5-HIAA) while these values were normal in patients with inactive tumors. Forty-five per cent of patients with active tumors had elevated fasting plasma GH levels that were either not suppressed or showed a paradoxical increase in response to I.V. glucose. There was a positive correlation between the plasma GH levels and serotonin production by the tumor. Twenty-eight per cent of patients with inactive tumors had elevated fasting plasma GH levels. GH levels were decreased by the administration of serotonin antagonists in some but not all of the patients. Parachlorophenylalanine (PCPA) an inhibitor of serotonin synthesis caused a paradoxical rise in GH levels. GH release in response to insulin hypoglycemia was normal. Plasma prolactin levels were normal in most of the patients with metastatic carcinoid tumors. PCPA administration did not systematically alter plasma prolactin levels. We conclude that elevated plasma GH levels are frequently present in patients with the carcinoid syndrome. Both serotonin produced by the tumors and the tumor itself may be responsible for the elevated GH levels.
Adult↗