Biomedical subjects

D M Olson

Publications and source records attributed to D M Olson.

At least 91 records · Page 5Linked to original sources

PubMed1986

Relationships between experiences, processing style, and sex-related differences in performance on spatial tests.

53 female and 45 male undergraduates were administered the Spatial Antecedents Questionnaire (Activities, Academic Courses, Self-assessments, and Environmental Mapping subscales), the Spatial Dimensionality Test (Embedded Figures, Card Rotations, Paper Folding, Surface Development, Horizontal/Vertical Rotations, and Cube Perspectives subtests), and Revised-Individual Differences Questionnaire of Paivio. Scores from the Academic Courses and Self-assessment scales accounted for the most variability in spatial performance. Visual processing style correlated with performance on spatial tests for men, but not for women. Different patterns of activities and experiences correlated with spatial test performance for men and women.

Adolescent↗

PubMed1985

Prostanoid concentrations in maternal/fetal plasma and amniotic fluid and intrauterine tissue prostanoid output in relation to myometrial contractility during the onset of adrenocorticotropin-induced preterm labor in sheep.

Prostanoid [prostaglandin (PG)] concentrations were measured in ovine maternal and fetal plasma and amniotic fluid during the onset of preterm labor induced by the administration of a pulsatile infusion of ACTH-(1-24) (P-ACTH; 66.7 ng/min for 15 min every 2 h) to the fetus and in saline-infused controls. P-ACTH administration stimulated a change in intra-uterine pressure from type A-activity, characterized by sustained increases of low amplitude, to type B labor-like activity of short duration, high amplitude (greater than or equal to 10 mm Hg) increases which occurred between 12 and 8 h before the onset of labor. PGF2 alpha and/or PGFM (13,14-dihydro-15-keto PGF2 alpha) concentrations increased consistently in all fluids 16 h or earlier before labor. All PGs increased in fetal carotid arterial plasma (PGE2 greater than PGF2 alpha) and amniotic fluid, and the relative increases in each PG were similar. However, PGF2 alpha and PGFM selectively increased in maternal vena caval and aortic plasma, whereas smaller or negligible increases in the prostacyclin hydrolysis metabolite 6-keto PGF1 alpha (6KF) and PGE2 were noted. The output of PGs E2 and F2 alpha (picograms per 10(5) cells/8 h) increased 1.6- and 1.7-fold, respectively, by cells dispersed from the chorioallantois of P-ACTH-treated animals compared to that in control animals infused with saline for 100 h. From fetal cotyledons, these increases were 2.4-fold (P less than 0.05) and 3.6-fold, respectively. No significant changes occurred in 6-keto PGF1 alpha output from any tissue or PGE2 or PGF2 alpha output from amnion or maternal cotyledons. We conclude 1) that PGs increase in all fluids before the increase in uterine mechanical activity during induced preterm labor, implying that PGs mediate this event and are not a result thereof; 2) that syntheses of PGs E2 and F2 alpha increase similarly in intrauterine tissues with the onset of labor; and 3) that a selective increase in PGF2 alpha, a myometrial stimulatory PG, occurs exclusively in maternal plasma, suggesting that endoperoxide conversion to PGF2 alpha is specifically enhanced during parturition or suggesting the existence of an intrauterine tissue source of 9-keto PG reductase.

6-Ketoprostaglandin F1 alpha↗

PubMed1985

Transduction by leukotriene B4 receptors of increases in cytosolic calcium in human polymorphonuclear leukocytes.

The uptake of Quin-2 by human polymorphonuclear (PMN) leukocytes permitted accurate fluorimetric quantification of the cytosolic concentration of intracellular calcium [( Ca+2]in), without altering the expression of the two subsets of leukotriene B4 (LTB4) receptors, as assessed by the binding of [3H]LTB4. Chemotactic concentrations of LTB4 elicited a rapid increase in [Ca+2]in, which reached a peak within 0.6 to 1 min and then decayed back to baseline levels by 6 to 10 min. The maximal increase and the half-maximal increase in [Ca+2]in were achieved by LTB4 at mean concentrations of 5 X 10(-10) M and 2 X 10(-10) M, respectively, where the binding of LTB4 to high-affinity receptors predominates. A rank order of potency of LTB4 greater than 5(S),12(S)-6-trans-LTB4 greater than 12(S)-LTB4 was established for the elicitation of increases in [Ca+2]in, which reflects the binding of the isomers to low-affinity receptors. PMN leukocytes were preincubated with 10(-8) M LTB4 to induce chemotactic deactivation, which eliminates the expression of high-affinity receptors without altering the expression of the low-affinity receptors for LTB4. LTB4 elicited an increase in [Ca+2]in in the deactivated PMN leukocytes with an EC50 of 3 X 10(-8) M, which is similar to the Kd for LTB4 binding to the low-affinity receptors. Two lines of cultured human leukemic cells, IM-9 and HL-60, did not bind LTB4 specifically and did not show any change in [Ca+2]in upon the addition of 3 X 10(-8) M LTB4. The HL-60 human promyelocytic leukemia cell line was induced to differentiate in 1% dimethyl sulfoxide to leukocytes with more mature myelocytic characteristics. Differentiated HL-60 cells expressed an average of 54,000 low-affinity receptors for LTB4 per cell with an average dissociation constant of 7.3 X 10(-8) M and concurrently developed the capacity to respond to LTB4 with an increase in [Ca+2]in. The binding of LTB4 to either high-affinity or low-affinity receptors appears to be sufficient to initiate an increase in [Ca+2]in in human PMN leukocytes and differentiated HL-60 cells. The specificity of LTB4 receptors in transducing maximum increases in [Ca+2]in is determined by the subset of receptors that predominate as a result of the concentration of LTB4 and the state of the responding cells.

Aminoquinolines↗

PubMed1984

Follicular and uterine prostaglandin levels in relation to uterine contraction and the first ovulation of a sequence in the hen.

Changes in the concentration of progesterone, estrone, estradiol, prostaglandins (PG) E2, 6-keto F1 alpha and 13,14-dihydro-15-keto F2 alpha (PGFM) were measured in peripheral plasma, and in venous effluent from the shell gland and the largest (F1) and the second largest (F2) preovulatory follicles. Tissue concentrations in the F1, F2 and the most recently ruptured follicle and the shell gland also were determined. Changes in these criteria were compared to changes in uterine contraction before the first ovulation of a sequence. Significant increases of PGF2 alpha and PGFM in the peripheral plasma were observed when the frequency of uterine contraction reached a maximum, about 1 h before ovulation. Relative to peripheral plasma, the concentrations in F1 plasma of progesterone, PGF2 alpha and PGFM were increased 20-fold, 150-fold and 15-fold, respectively, at the time of the maximum frequency of uterine contraction. The highest tissue concentrations of PGs were also observed in the F1 follicle. These results suggest that the largest preovulatory follicle is the major source of PG synthesis and release. These PGs may stimulate uterine contraction and may also play a role in follicular rupture and release of the ovum.

Animals↗

PubMed1984

Early changes in prostaglandin concentrations in ovine maternal and fetal plasma, amniotic fluid and from dispersed cells of intrauterine tissues before the onset of ACTH-induced pre-term labour.

The changes with time in intrauterine tissue production and concentrations of PGE-2, PGF-2 alpha, 6-keto PGF-1 alpha and PGFM (13,14-dihydro-15-keto PGF-2 alpha) in maternal and fetal plasma and amniotic fluid were investigated during the first 72 h of pulsatile administration of ACTH1-24 to chronically catheterized fetal sheep. By 72 h there were no changes in the frequency, maximum amplitude or duration of uterine contractions compared to preinfusion values. Basal concentrations of PGE-2 in maternal and fetal plasma were generally higher than those of PGF-2 alpha, while 6-keto PGF-1 alpha values were intermediate. The concentrations of all PGs increased in amniotic fluid during ACTH infusion. In fetal plasma and in maternal vena caval plasma, however, there were significant increases only in PGF-2 alpha and PGFM. No changes were observed in plasma concentrations for any PG during saline infusion. The mean output of PGE-2, PGF-2 alpha and 6-keto PGF-1 alpha by dispersed cells prepared from chorioallantois and fetal and maternal cotyledons was consistently higher after ACTH for 72 h than from saline-infused animals, although significance (P less than 0.05) was achieved only for PGE-2 in chorioallantois . There are 3 conclusions. (1) Increases in ovine intrauterine tissue PG production precede the occurrence of increased myometrial contractile activity after ACTH treatment of fetal sheep. The results imply a causal relationship between rising PG and later myometrial contractions, rather than PG changes resulting from enhanced uterine activity. (2) The major site(s) of increased PG output in vitro from endogenous precursors are fetal structures, especially the chorio-allantoic membranes. (3) Although PGE-2 may be the major circulating PG during late gestation, there is a selective increase in plasma PGF-2 alpha concentrations before the onset of delivery.

Adrenocorticotropic Hormone↗

PubMed1983

Stimulation of ovine myometrial activity by 6-keto prostaglandin E1.

6-keto prostaglandin E1 (6KE) is a metabolite of PGI2, which we have shown previously inhibits spontaneous myometrial activity. In the present study we examined the effects of 6KE on uterine electrical and mechanical activity in non-pregnant ovariectomized sheep. 6KE stimulated uterine activity in a dose-dependent fashion. The effect was enhanced by pre-treatment with estradiol (E2). It was not influenced by pre-treatment with meclofenamic acid and was not associated with significant changes in the concentrations of 13,14 dihydro 15-keto PGF2 alpha in vena cava plasma. After E2 treatment, 6KE had 0.2-0.3 of the stimulatory activity of PGF2 alpha. In the absence of E2, the uterine response to both 6KE and PGF2 alpha was decreased. In animals in which spontaneous myometrial activity was inhibited by PGI2, the uterus remained responsive to 6KE. We conclude that in the ovariectomized non-pregnant sheep 6KE stimulates uterine activity, and that the effect is independent of endogenous PG production.

Alprostadil↗

PubMed1983

Estradiol-17 beta and 2-hydroxyestradiol-17 beta-induced differential production of prostaglandins by cells dispersed from human intrauterine tissues at parturition.

Prostaglandin (PGE, 6-keto PGF1 alpha) output by cells dispersed from human amnion and decidua in the presence of increasing levels (0-5000 ng/ml) of estradiol-17 beta (E2) or 2-hydroxyestradiol-17 beta (2-OH E2) was studied in relation to parturition. Tissues were obtained from women at term either before (CS) or after (SL) spontaneous labor and vaginal delivery. In the absence of estrogens, the output of both PGs from amnion increased significantly with labor. No significant increase in decidua PG output occurred with labor. Neither estrogen influenced CS amnion PG output. However, both E2 and 2-OH E2 stimulated SL amnion PGE output (2-OH E2 greater than E2) while having no affect on 6-keto PGF1 alpha output. Only the highest dose of 2-OH E2 stimulated PGE output in CS decidua, but both estrogens significantly inhibited 6-keto PGF1 alpha output in this tissue. In SL decidua only 2-OH E2 significantly stimulated PGE, and neither estrogen affected 6-keto PGF1 alpha output. These results might suggest that estrogens modulate PG biosynthesis at the level of endoperoxide to primary PG conversion.

6-Ketoprostaglandin F1 alpha↗

PubMed1983

Prostaglandin synthesis by human amnion is dependent upon extracellular calcium.

Prostaglandin (PG) E and F output was studied in collagenase-dispersed amnion cells to determine the effect of extracellular Ca2+ upon PG synthesis. In the presence of 2.5 mM CaCl2, PGE and PGF output (picograms per 10(5) cells per 3 h) by cells obtained at term prior to labour following elective cesarean section (CS) was 183 +/- 39 and 127 +/- 23, respectively. This increased to 435 +/- 111 (p less than 0.025) and 241 +/- 49 (p = 0.056) from cells obtained after spontaneous labour and delivery at term (SL). Exclusion of CaCl2 from the medium (plus 0.1 mM EGTA) significantly reduced (p less than 0.025) PGE output in CS and SL cells (83 +/- 22 and 183 +/- 47, respectively) and PGF output in CS cells (70 +/- 17). PGE output in both CS and SL cells was unchanged when CaCl2 concentrations in the medium were decreased from 2.5 to 0.25 mM, but significantly attenuated (p less than 0.01) when extracellular CaCl2 was decreased from 0.25 to 0 mM. The voltage-sensitive Ca2+ channel blocker, D-600, decreased PGE output in the presence of (2.5 mM) CaCl2 to levels observed in the absence of CaCl2. Ionophore A23187 restored PGE output in the presence of D-600 and Ca2+. PGE output from CS amnion cells was stimulated by A23187 and elevated extracellular K+ (40 mM). In each case, exclusion of CaCl2 from the medium eliminated the response. These results suggest that PG output by human amnion is dependent, in part, upon the presence of extracellular Ca2+ and that Ca2+ may enter the cell via a potential-sensitive mechanism.

Amnion↗

PubMed1983

Avian shell gland contractility: interaction of PGF2 alpha and arginine vasotocin with Ca2+.

The effects of prostaglandin F2 alpha (PGF2 alpha) and arginine vasotocin (AVT) on the isometric contractile activity of avian shell gland longitudinal muscle strips were studied in relation to the role of extracellular Ca2+. PGF2 alpha and AVT stimulated contractile tension in a dose-related manner. This was attenuated when either of the Ca2+ channel blockers verapamil or R33956 was added to the muscle chamber baths. Ca2+-free solution containing 1 mM ethyleneglycol-bis (beta-aminoethylether)-N,N'-tetraacetic acid completely prevented contraction in response to increasing doses of PGF2 alpha or AVT. Washing of the strips with Ca2+-free solution eliminated spontaneous contractile activity, but replenishment of CaCl2 to the medium (0.1-5.0 mM) restored it. Addition of PGF2 alpha to the Ca2+-free medium enhanced contractile tension during Ca2+ replenishment, whereas AVT had no effect on tension generation at low extracellular Ca2+ concentration (0.1-0.5 mM) but increased it at higher extracellular Ca2+ concentration (1.0-5.0 mM). PGF2 alpha stimulation was sensitive to extracellular Na+ concentration, whereas AVT-induced activity was not. Potassium depolarization (20 mM K) potentiated PGF2 alpha-stimulated activity, whereas the response to AVT was unaffected. At 127.5 mM K, AVT-stimulated activity was inhibited. PGF2 alpha-enhanced Ca2+-dependent tension generation was right shifted in a dose-related manner by AVT. These results suggest that extracellular Ca2+ is necessary for the full expression of PGF2 alpha- and AVT-stimulated muscle contraction and suggest that each agonist has a different mechanism of action.

Animals↗

PubMed1983

Prostaglandin output in relation to parturition by cells dispersed from human intrauterine tissues.

Collagenase-dispersed cells from human amnion, chorion, decidua, and placenta have been maintained in short term cultures to study prostaglandin (PG) biosynthesis in relation to parturition. Cells retained metabolic function during the 6-h incubation period, as determined by the apparently linear utilization of radioactive glucose and the formation of tritiated water. All cells synthesized PGs (E, F, and 6-keto F1 alpha) from endogenous precursors. The output of all three PGs significantly increased in amnion and chorion, but not in decidua or placenta, obtained from women who had entered labor spontaneously at term and delivered vaginally (SL) when compared to women at term, but not in labor, delivered by elective cesarean section (CS). For example, PGE output (picograms per 10(5) cells/6 h) increased from 207 +/- 77 (n = 5) to 908 +/- 334 with labor (mean +/- SEM). The addition of indomethacin (10(-7)-10(-5) M) to SL amnion cells significantly decreased (P less than 0.001, by analysis of variance) PGE and PGF, but not 6-keto PGF1 alpha output. Comparison of PGF output with its metabolite, 13,14-dihydro-15-keto PGF2 alpha (PGFM); indicated that PGF values were similar to or higher than PGFM for all tissues other than CS chorion, where PGFM output was significantly greater (142 +/- 63 vs. 486 +/- 95; n = 5; P less than 0.05). PGFM levels in amnion increased with labor [104 +/- 51 (n = 5) to 341 +/- 96 (n = 5); P less than 0.05], suggesting that PG output increased with labor in the fetal membranes as a result of increased synthesis and not decreased metabolism.

6-Ketoprostaglandin F1 alpha↗

PubMed1981