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Biomedical subjects

A Golander

Publications and source records attributed to A Golander.

At least 19 recordsLinked to original sources
PubMed1989

Superoxide dismutase activity in the erythrocyte of the term newborn and premature.

Superoxide dismutase (SOD) activity was determined in the erythrocytes of 16 full-term and 12 preterm neonates and the mothers of these babies. Blood samples were obtained from the umbilical cord (or within the first 12 h and samples were again obtained 48 h after delivery. The results of the study show that SOD activity in the erythrocytes of the full-term newborn is identical to the SOD activity in the erythrocytes of their mothers. Exposing the newborn to atmospheric oxygen for 48 h caused no change in the activity of SOD. The activity of SOD in the erythrocytes of the preterm was not different from that of the full-term neonate.

Adult↗
PubMed1989

Insulin stimulates the synthesis and release of prolactin from human decidual cells.

Insulin-like growth factor I (IGF-I) and insulin have been implicated in the regulation of differentiated functions in many cells. We have reported that IGF-I stimulates the release of decidual PRL, acting through the type I IGF receptor (1). To determine whether insulin regulates the synthesis and secretion of decidual PRL, monolayer cultures of human decidual cells were exposed to insulin at concentrations ranging from 10 ng to 10 micrograms/ml for up to 5 days. Insulin stimulated a dose-dependent increase in PRL release (half-maximal concentration, 50 ng/ml), beginning 48 h after initial exposure. Insulin-exposed cells released 62 +/- 2% (mean +/- SEM), 97 +/- 3% and 82 +/- 6% more PRL than control cultures on days 3, 4, and 5, respectively. Insulin also stimulated de novo PRL synthesis. During the final 24-h culture period, insulin-exposed cells released 73 +/- 7% more immunoprecipitable [35S]-methionyl PRL than control cells, comparable to the 60 +/- 7% increase in PRL (by RIA) during the same period. Insulin effects were relatively specific to PRL, since insulin had a much smaller effect on the synthesis of total trichloroacetic acid-precipitable proteins. Additionally, insulin had no significant effect on cell number, total DNA, or total cellular protein. Specific and saturable insulin-binding sites were observed in decidual cells, and polyclonal antibodies to the insulin receptor acted as insulin agonists, stimulating an increase in PRL release comparable to that produced by insulin alone. These observations suggest that the responses to insulin are mediated through the insulin receptor. Furthermore, our studies suggest that insulin may have a role in the regulation of PRL synthesis and release from human decidua.

Binding, Competitive↗
PubMed1989

Tuftsin stimulates IL-1 production by human mononuclear cells, human spleen cells and mouse spleen cells in vitro.

Human peripheral adherent cells from splenectomized subjects, human spleen cells and mouse spleen cells were tested for IL-1 production in vitro in presence or absence of synthetic tuftsin (Thr-Lys-Pro-Arg). Application of synthetic tuftsin to peripheral blood adherent cells from normal donors as well as from splenectomized subjects induces IL-1 production. In splenectomized subjects the extent of induction was more evident than in controls. In human splenic cells tuftsin stimulates IL-1 production without KLH or LPS. In mouse spleen cells tuftsin alone did not stimulate the IL-1 secretion. However, addition of tuftsin to mouse spleen cells incubated with KLH augmented significantly the IL-1 secretion. As removal of the spleen leads to tuftsin deficiency, our present findings may perhaps explain the fulminant nature of the postplenectomy sepsis and some immune disturbances described in the postplenectomy state.

Animals↗
PubMed1988

Decidual prolactin (PRL)-releasing factor stimulates the synthesis of PRL from human decidual cells.

Previous studies from our laboratory demonstrated that the acute release of PRL from human decidual tissue is stimulated by a 23.5 kilodalton placental protein which we designated decidual PRL-releasing factor (PRL-RF). To determine whether PRL-RF may also affect the synthesis of PRL and/or cause a secondary increase in PRL release, we have examined the effects of purified PRL-RF on the synthesis and release of PRL over a 96-h period. Exposure of dispersed decidual cells to PRL-RF (0.5 microgram/ml) stimulated a biphasic increase in PRL release with acute transient stimulation during the first 0.5 h and a delayed and sustained stimulation beginning about 8 h after exposure which persisted for the duration of the 96 h. The amounts of PRL released from PRL-RF-exposed cells after 0.5, 8, 12, 24, and 96 h were 321.2 +/- 36.2 (mean +/- SEM, n = 3), 110.2 +/- 5.3, 138.2 +/- 7.2, 194.5 +/- 11.2, and 201.5 +/- 14.2% that of control cells. Studies of the de novo synthesis of [35S]methionyl PRL indicated that the increase in PRL release after the first few hours of exposure to PRL-RF was secondary to an increase in PRL synthesis. Somatostatin (100 nM) inhibited the acute stimulatory effect of PRL-RF, but had no effect on the delayed stimulation of PRL release. On the other hand, cycloheximide (20 microM) completely inhibited the secondary increase in PRL release in response to PRL-RF but had no effect on the acute release. These results demonstrate that PRL-RF stimulates both the synthesis and release of decidual PRL.

Cells, Cultured↗
PubMed1988

Insulin-like growth factor I stimulates the synthesis and release of prolactin from human decidual cells.

Recent studies suggest a role for insulin-like growth factor I (IGF-I) in the regulation of hormone release from placental, gonadal, and pituitary tissues. To examine whether IGF-I may also regulate the release of PRL from human decidual tissue, we have investigated the effect of recombinant human IGF-I on PRL release from monolayer cultures of human decidual cells exposed to IGF-I for up to 4 days. IGF-I (10-1000 ng/ml) stimulated a sustained dose-dependent increase in PRL release (half-maximal concentration, 25 ng/ml) beginning 48 h after initial exposure, but had no effect on the intracellular PRL content. The amounts of PRL released from maximally stimulated cultures on days 3 and 4 were 168 +/- 3% (mean +/- SEM) and 258 +/- 8% of control values, respectively. IGF-I-mediated effects were inhibited by cycloheximide (3.6 microM), suggesting that the increase in PRL was the result of newly synthesized hormone. The increase in PRL release was not due to a generalized effect on protein release, since IGF-I had no effect on the release of trichloroacetic acid-precipitable [35S]methionyl proteins. Radioligand competition studies indicate that the biological actions of IGF-I are mediated through interaction with the IGF-I receptor. Binding of radiolabeled IGF-I to decidual cells in suspension was specific, saturable, and displacable by unlabeled IGF-I, with a potency nearly 10 times greater than that of insulin. Furthermore, exposure of decidual cells to a monoclonal antibody to the IGF-I receptor (alpha-IR3) completely inhibited both IGF-I-mediated PRL release and specific binding of [125I]IGF-I to decidual cells. Since the actions of IGF-I occurred at physiological concentrations, these findings strongly support a role for IGF-I in the regulation of PRL secretion by human decidua.

Antibodies, Monoclonal↗
PubMed1988

Prolactin stimulates creatine kinase activity and DNA synthesis in explants of human amnion.

To characterize the action of hPRL and human placental lactogen on the amnion, decidua and placenta, we examined the effects of these hormones on the brain type isozyme of creatine kinase in cultured explants of these tissues from normal deliveries. In the amnion, hPRL (1 mg/l) caused a 1.8-fold increase in creatine kinase specific activity in 24 h, whereas hGH (1 mg/l) or human placental lactogen (1 mg/l) had no effect; oPRL (1 mg/l) also caused a 2.5-fold increase in creatine kinase activity. Neither hPRL, human placental lactogen nor hGH had a significant effect on creatine kinase activity in the placenta or decidua. [3H]thymidine incorporation into DNA increased in parallel to the stimulation of creatine kinase activity. The predominant isozyme of creatine kinase in both the unstimulated and stimulated explants was the brain type isozyme. Creatine kinase activity in the amniotic tissue increased significantly 2 h after hPRL treatment and reached its highest value at 4 h. The enzyme activity in the amnion rose with increasing hPRL dose and showed a significant increase at physiologic concentrations as low as 0.01 mg/l. This study, therefore, provides evidence for biological action of prolactin in amniotic tissue, suggesting that the amnion is physiologically responsive to prolactin.

Amnion↗
PubMed1987

Antibodies to insulin receptor followed by anti-idiotype. Antibodies to insulin in child with hypoglycemia.

A child presenting severe hypoglycemia despite low or normal secretion of insulin was found to have IgM antibodies to the insulin receptor. These antibodies stimulated lipogenesis in fat cells in vitro and competed with insulin for binding to insulin receptors. After treatment with glucocorticoids, the anti-receptor antibodies and the hypoglycemia both disappeared, and antibodies to insulin appeared in the patient's serum. The anti-insulin antibodies were isolated by affinity chromatography and were found to inhibit the anti-insulin-receptor antibodies that were present earlier. The interaction between the patient's anti-insulin antibodies and his anti-receptor antibodies suggests that these two species of antibodies are related as idiotypes and anti-idiotypes. We also studied the interaction of the hypoglycemic patient's anti-receptor antibodies with anti-insulin antibodies of a diabetic patient and with anti-insulin antibodies of mice immunized to insulin. The hypoglycemic patient's anti-receptor antibodies were neutralized by the diabetic patient's anti-insulin antibodies, indicating that anti-insulin antibodies with a common idiotype may arise in both diabetes and hypoglycemia. Moreover, mouse anti-insulin antibodies that interacted with mouse anti-receptor antibodies neutralized the hypoglycemic patient's anti-receptor antibodies. In contrast, mouse anti-insulin antibodies that did not interact with the mouse anti-receptor antibodies did not neutralize the hypoglycemic patient's anti-receptor antibodies. Thus, the human anti-insulin antibodies share an idiotype with a specific class of mouse anti-insulin antibodies.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Stimulation of creatine kinase activity in rat organs by human growth hormone in vivo and in vitro.

Intraperitoneal injection of human GH (hGH) (4 micrograms/g BW) into 21-day-old rats causes, 24 h later, an increase in creatine kinase (CK) specific activity in kidney (1.7-fold), liver (1.6-fold), and in epiphyseal cartilage (1.8-fold). Similar stimulation was obtained when tissue explants were incubated for 24 h with hGH (1 microgram/ml); CK activity rose 1.8-fold in kidney, 1.9-fold in the liver, and 2.6-fold in epiphyseal cartilage. Highly significant stimulation of CK specific activity was obtained in these same organs in hypophysectomized rats. The increase in CK specific activity in the kidney, to some extent in the liver, but not in the epiphyseal cartilage, was also obtained on in vivo treatment with either human placental lactogen or ovine PRL. Stimulation of CK in these three organs by hGH is followed by a parallel increase in DNA synthesis. Dexamethasone, which was also found to increase CK activity in rat kidney and liver, did not affect the increase of CK by hGH in the kidney, stimulated the effect of hGH in the liver, and partially inhibited the effect of hGH in the epiphyseal cartilage. Diethylaminoethyl cellulose chromatography revealed that the basal and induced activity of CK in all cases was due to the brain type isozyme. On the basis of this evidence for a direct effect of hGH on CK brain type activity, we suggest that its stimulation is potentially a convenient and sensitive assay for biological activity of GH.

Animals↗
PubMed1986

Characterization and partial purification of a serum protein which stimulates the release of human placental lactogen in vitro.

The factors that regulate the release of human placental lactogen (hPL) are poorly understood. To determine whether hPL is regulated by a factor(s) in pregnancy serum, placental explants were exposed for up to 9 h to a pool of serum samples from 50 women in the third trimester. In static explant cultures, the addition of the serum (0.6-10.8 mg protein/ml) caused a dose-dependent and reversible increase in hPL release during a 6-h period. The maximum release by the explants exposed to pregnancy serum was 200-250% greater than that of control explants, and the half-maximal dose was 2-3 mg/ml. Perifusion of placental explants with 15% pregnancy serum (final concentration, 10.5 mg protein/ml) also caused a significant release in hPL within 15 min, which reached a maximum of 200-225% above control levels. Two other pools of pregnancy serum samples as well as individual samples from four pregnant women also stimulated hPL release. Although pregnancy serum significantly stimulated hPL release, there was no increase in either the release of hCG or trichloroacetic acid-precipitable 35S-labeled proteins. Serum from nonpregnant women and men, as well as bovine serum, also stimulated hPL release, but their potencies were only 20-25% that of pregnancy serum. Chicken and porcine serum (10.8 mg/ml each) caused only small (less than 10%) increases in hPL release, and purified human albumin and ovalbumin had no effect. Dialysis or ultrafiltration of pregnancy serum using membranes with mol wt exclusions of 10K daltons caused no loss of activity. Delipidation of pregnancy serum with acetone-ethanol or acid-charcoal also caused no loss of activity, but treatment with trypsin caused greater than 95% loss of activity. Purification of the stimulatory activity by successive chromatographies on Sephadex G-150, Cibacron blue, and Sephadex G-75 resulted in an approximately 800-fold increase in specific activity. Approximately 90% of the total activity eluted from Sephadex G-75 with an apparent mol wt of 31,000, the remainder eluted in the void volume. Although partially purified pregnancy serum stimulated hPL release, the active fractions did not affect the release of rat LH, FSH, or GH from rat pituitary cells or the release of PRL from human decidual explants. Incubation of placental explants in calcium-deficient medium blocked the stimulatory effect of the partially purified pregnancy serum by greater than 90%. These studies indicate that human serum contains a protein(s) that causes a specific, rapid, dose-dependent, and reversible increase in hPL release.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1986

Stimulation of creatine kinase activity by calcium-regulating hormones in explants of human amnion, decidua, and placenta.

We have used stimulation of the activity of the brain type creatine kinase (CK) isoenzyme as a response marker to examine the effects of vitamin D metabolites, PTH, and calcitonin in cultured explants of placenta, decidua, and amnion from normal human deliveries. We found a biological response to PTH in placenta and amnion and to vitamin D metabolites in all three tissues. In the amnion, CK activity increased 2.3-fold after 24 h of incubation in 2.5 nM 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3], 3.8-fold when incubated with 12.5 nM 24,25-dihydroxyvitamin D3 [24,25-(OH)2D3] and 2.7-fold when incubated with 10 U/ml bovine PTH. In the decidua, 24,25-(OH)2D3, but not 1,25-(OH)2D3 or bPTH caused a 1.7-fold increase in CK activity. In contrast, the placenta responded to 1,25-(OH)2D3 with a 1.6-fold increase in CK activity and to bPTH, with a 1.7-fold increase but did not respond to 24,25-(OH)2D3. Bovine calcitonin (100 ng/ml) had no effect on CK activity in any of the three tissues. Nearly all CK in both the unstimulated and stimulated explants was the brain type isoenzyme. CK activity increased significantly between 1 and 4 h after hormonal treatment in all experiments. The enzyme activity rose steeply with dose and reached a significant increase, and usually a plateau, at hormone concentrations considered to be physiological in vivo. [3H]Thymidine incorporation into DNA increased in parallel to stimulation of CK activity in all experiments, except that PTH did not increase DNA synthesis in the placenta. PTH did cause an increase in cAMP production in explants of amnion (1.5-fold) and placenta (2.6-fold).

Amnion↗
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↗
PubMed1985

Decreased prolactin secretion by decidual tissue of pre-eclampsia in vitro.

In vitro prolactin (hPrl) secretion by explants of decidual tissue was studied in pre-eclampsia and normal controls. Our results indicate diminished hPrl production by decidua of pre-eclampsia as compared to the normal controls. Incubation of normal decidual tissue in the presence of serum obtained from pre-eclamptic patients did not induce an inhibitory effect on hPrl production.

Culture Media↗
PubMed1984

Rapid diagnosis of congenital adrenal hyperplasia by high performance liquid chromatography.

This manuscript describes methods for the quantitation of serum concentrations of 17-hydroxyprogesterone and 11-deoxycortisol (Compound S) employing reverse-phase high-performance liquid chromatography (HPLC) and ultraviolet (UV) absorbance which are applicable to the diagnosis of congenital adrenal hyperplasia due to deficiencies of 21- and 11-hydroxylase activities, respectively. These methods are simple, specific, precise and rapid. Data obtained by the HPLC-UV methods are highly correlated (p less than 0.001) with radioimmunoassay measurements.

17-Hydroxycorticosteroids↗
PubMed1981

Suppression of lymphocyte reactivity in vitro by a soluble factor secreted by explants of human decidua.

The immunologic mechanisms that protect the fetus from rejection were the subject of numerous investigations. Reports showing the uterus as a favorable site of implantation focused our attention to the decidua which is the maternal tissue intimately attached to fetal structures. Explants of human decidua were cultured for periods of 24 h and incubation media tested for their immunosuppressive activity. The incubation medium of human decidua when added to cultures of human lymphocytes suppressed both their reactivity to lectins and their activity in the mixed lymphocyte reaction. The results of these experiments suggest that decidual tissue releases a soluble factor which is a potent inhibitor of cell-mediated immunity.

Amnion↗
PubMed1981

Human placental lactogen release in vitro: paradoxical effects of calcium.

To study the effects of calcium on the release of human placental lactogen (hPL), placental explants were exposed to media containing lower or higher concentrations of calcium than normally available to the placenta. Explants exposed for 2 h to calcium-poor medium or medium containing either 2 mM EDTA or 2 mM EGTA released 160, 248, and 253% more hPL, respectively, than control explants. In contrast, explants exposed to medium containing higher than normal calcium concentrations released the same amounts of hPL as the control explants. At lower than normal extracellular calcium concentrations, the increased hPL release was inversely proportional to the calcium concentration. The increased release in calcium-poor medium was inhibited by subsequent exposure of the explants to medium containing calcium and was prevented by either barium or magnesium. Changes in barium or magnesium concentrations, however, had no effects on hPL release in the presence of normal extracellular calcium concentrations. Methoxyverapamil (D 600), an inhibitor of calcium flux, stimulated hPL release. Because low extracellular calcium and methoxyverapamil both inhibit calcium influx, these experiments suggest that calcium influx inhibits hPL release. The role of calcium in the regulation of hPL release therefore appears to be different from that reported in other release systems.

Barium↗
PubMed1981

Immunological functions in children years after recovery from protein calorie malnutrition (PCM) in their early infancy.

The immune functions were evaluated in 30 children, aged one year to 9 8/12 years, who had suffered during their early infancy from protein-calorie malnutrition (PCM) as the result of intractable diarrhea. Twelve healthy children matched for age and sex served as controls. All 42 children responded normally to intradermal injections of tuberculin and candida antigens. The reduction of nitrous blue tetrazolium (NBT) by the polymorphonuclear leucocytes (PMN) was normal. Apart from the lower concentrations of IgM in the post-PCM group--145 +/- 67 mg % as compared to 212.8 +/- 46 mg % (p less than 0.005)--no differences were noted in the other serum immunoglobulin and complement levels. The response to phytohaemagglutinins (PHA) in two different concentrations was significantly enhanced in the post-PCM group (p less than 0.05). The per cent of T cells in both groups was normal. The results of this study indicate that most immunologic parameters return to normal after a healthy nutritional status has been achieved, with the exception of some abnormalities in IgM production and lymphocyte reactivity to PHA. These need further investigation.

Child↗