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Biomedical subjects

G E Rice

Publications and source records attributed to G E Rice.

At least 91 records · Page 5Linked to original sources
PubMed1993

Elevated plasma interleukin 6: a biochemical marker of human preterm labour.

Maternal peripheral venous plasma interleukin 6 (IL-6) concentrations were determined during human pregnancy and labour at term and preterm. During preterm labour, IL-6 concentrations were significantly elevated (p < 0.02) compared to gestationally matched, non-labouring controls (53.7 +/- 15.7 pg/ml, n = 17, and 15.4 +/- 6.4 pg/ml, n = 23, respectively). IL-6 concentrations did not vary significantly during normal pregnancy and labour at term. These data support a role for IL-6 in the pathogenesis of human preterm labour, are evidence for the contention that preterm labour is mechanistically distinct at a biochemical level from normal labour at term and identify maternal peripheral venous plasma IL-6 as a biochemical marker of this condition.

Biomarkers↗
PubMed1993

Interleukin 8 concentrations in amniotic fluid and peripheral venous plasma during human pregnancy and parturition.

To establish the gestational and labour-associated changes in interleukin 8 (IL-8) release, we have determined the concentration of this cytokine in maternal peripheral plasma and amniotic fluid from 15 weeks of gestation to term and in association with spontaneous-onset labour at term and preterm. No statistically significant changes in peripheral plasma IL-8 concentration were observed during pregnancy or in association with labour onset (mean concentration 56.5 +/- 14.5 ng/l, N = 64). The IL-8 concentrations in amniotic fluid were up to 50-fold greater than those observed in peripheral plasma (p < 0.05) and increased significantly (p < 0.05) during pregnancy. At term, but before the onset of labour, amniotic fluid concentrations of IL-8 averaged 969.2 +/- 553.5 ng/l (N = 12). In association with labour at term, IL-8 concentrations increased to 3895.8 +/- 1414.4 ng/l (N = 6, p < 0.03). The concentration of IL-8 in amniotic fluid obtained from women in preterm labour averaged 1854.7 +/- 1352.6 ng/l (N = 6) but was not statistically different from the concentration of IL-8 in amniotic fluid obtained from gestational aged-matched non-labouring controls. Although the precise role of intrauterine IL-8 at the time of parturition awaits elucidation, these data support the concept that this cytokine may be involved in the biochemical events associated with the onset and/or propagation of normal labour in the human.

Amniotic Fluid↗
PubMed1992

Elevated maternal plasma immunoreactive phospholipase A2 in human preterm and term labour.

Peripheral plasma concentrations of immunoreactive phospholipase A2 (irPLA2) (Type II, non-pancreatic) were determined in 110 women during pregnancy. The concentration of irPLA2 did not significantly change during pregnancy (5.7 +/- 0.6 ng/ml, n = 72) until the onset of labour. When compared with non-labouring women, irPLA2 concentrations were significantly elevated in association with both preterm labour (13.3 +/- 2.4 ng/ml, n = 15, p less than 0.02) and labour at term (10.4 +/- 1.7, n = 23, p less than 0.02). These data suggest that maternal plasma irPLA2 may be reflective of the mechanism(s) underlying the labour-associated increase in human gestational tissue eicosanoid formation.

Female↗
PubMed1992

Lipopolysaccharide priming potentiates calcium ionophore stimulated human placental prostaglandin E2 release in vitro.

In this study, the effect of bacterial endotoxin (lipopolysaccharide; LPS) and of LPS priming on the in vitro release of PGE2 from human placental explants was investigated. Both LPS and the calcium ionophore A23187 significantly stimulated PGE2 release (P less than 0.05). Simultaneous exposure of placental explants to both LPS and A23187 revealed no additive or synergistic stimulation of PGE2 release. LPS priming of placental tissue significantly increased A23187-stimulated PGE2 release when compared to non-LPS-primed tissues. The addition of exogenous arachidonic acid (the substrate for PGE2 synthesis) also significantly (P less than 0.05) stimulated PGE2 release. There was, however, no significant further stimulation of PGE2 release following LPS priming in arachidonic acid treated explants. These data suggest that LPS not only increases basal PGE2 release in human placentae, but also potentiates agonist-stimulated PGE2 release, possibly by increasing tissue capacity for endogenous arachidonic acid liberation.

Calcimycin↗
PubMed1991

Gestational changes in electrolyte transport, electrical activity, and permeability of the porcine placenta.

1. The electrolyte transport capacities of the porcine placenta and fetal membranes (amnion, chorion, and allantois) during gestation (47-112 days) were assessed in vitro and in the absence of electrochemical, osmotic, or hydrostatic driving forces. Net transmural transport of 22Na and 36Cl across sections of porcine allantochorion-endometrium (ALCE), amniochorion-endometrium (AMCE), and allantoamnion (AA) mounted in Ussing chambers could not be detected at any stage of gestation. 2. These tissues were characterised throughout gestation by low electrical potential difference (PD; less than 5 mV, fetal side positive with respect to maternal side) and short circuit current (SCC; less than 16 microA.cm-2) which were amiloride and iodoacetate sensitive. 3. A periparturitent reversal in the polarity of PD to fetal side negative and a change in the direction of the SCC was observed in tissues obtained from sows (n = 3) at 111-112 day gestation. These changes were accompanied by a 73% increase in electrical resistance (R) and a 2-10-fold decrease in the permeability of tissues to Na and Cl. 4. Morphological studies revealed a decrease in the thickness of allantoamnion and a decrease in the height of epithelia from ALCE, AMCE, and AA during gestation, indicating a decrease in activity. These morphological changes only partly explained the pre-term electrophysiological changes in these tissues.

Animals↗
PubMed1991

The effects of free radical scavengers on arachidonic acid metabolism by ovine placental microsomes.

1. The effect of free radical (superoxide and hydroxyl) and hydrogen peroxide scavengers on the formation of prostaglandin E2 by ovine placental microsomes was investigated. 2. Of the free radical scavengers tested only Mn Desferal, a low molecular weight (712 Da) superoxide scavenger, at concentrations of 0.5-5 mmol/l significantly (P less than 0.001) stimulated PGE2 formation by ovine placental microsomes. 3. This observation is consistent with the involvement of superoxide radicals in the inactivation of prostaglandin G/H synthase (PGHS). 4. The results obtained further suggest that if superoxide radicals are important regulators of PGHS activity in the ovine placenta, they are not accessible to large molecular weight free radical scavengers.

Animals↗
PubMed1991

Arachidonic acid metabolites in pregnant rat uterus.

Production of prostaglandin E2 (PGE2), F2 alpha (PGF2 alpha) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) by pregnant rat uterus were measured in vitro. At mid-pregnancy, myometrium incubated with decidua attached released more prostanoids into the culture medium than when incubated without. As pregnancy progressed to 21 days more prostanoids were detected in the culture medium. However, no significantly increased conversion of exogenous arachidonic acid (AA) by myometrium was found.

Animals↗
PubMed1991

Tumor cell surface alpha 4 beta 1 integrin mediates adhesion to vascular endothelium: demonstration of an interaction with the N-terminal domains of INCAM-110/VCAM-1.

Hematogenous metastasis involves adhesive interactions between blood-borne tumor cells and the vessel wall. By the use of in vitro assays, the adhesion of human melanoma, osteosarcoma, and kidney carcinoma (but not colon carcinoma) cell lines was shown to involve the cytokine-inducible endothelial cell surface protein inducible cell adhesion molecule 110 (INCAM-110) and the alpha 4 beta 1 integrin, molecules normally involved in endothelial-leukocyte interactions. Tumor adhesion to human endothelial cell monolayers was increased 1.9- to 8.2-fold by endothelial activation with the cytokine tumor necrosis factor (TNF) and inhibited by the anti-INCAM-110 monoclonal antibody (mAb) E1/6. Each of these tumor cells expressed members of the beta 1 integrin family of adhesion molecules, and antibodies to the alpha 4 and beta 1 integrin subunits inhibited tumor-endothelial adhesion (48-87% inhibition). A cDNA encompassing the three N-terminal Ig-like domains of vascular cell adhesion molecule 1 (VCAM-1) encoded a protein recognized by the anti-INCAM-110 mAb E1/6 and, when captured onto plastic, supported melanoma cell adhesion by an alpha 4 integrin-dependent mechanism. In contrast to mAb E1/6, a second anti-INCAM-110 mAb Hu8/4 neither inhibited adhesion to activated endothelium nor bound the first three Ig-like domains of INCAM-110/VCAM-1. These data indicate that the adherence of several human tumors to activated endothelium is mediated by an interaction of alpha 4 beta 1 integrin and the N-terminal Ig-like domains of endothelial INCAM-110/VCAM-1. Tumor acquisition of the alpha 4 integrin subunit and endothelial expression of INCAM-110 may affect the frequency and distribution of metastasis.

Antibodies, Monoclonal↗
PubMed1991

Vascular and nonvascular expression of INCAM-110. A target for mononuclear leukocyte adhesion in normal and inflamed human tissues.

Inducible cell adhesion molecule 110 (INCAM-110), is a 110-kd adhesion receptor for lymphocytes and monocytes identified on cytokine-activated endothelium. Using immunoperoxidase techniques, little or no INCAM-110 was detected on endothelium in normal human tissues. In contrast, INCAM-110 was expressed in postcapillary venules in a variety of active inflammatory processes. In acute appendicitis, INCAM-110 was found coincident with strong expression of endothelial leukocyte adhesion molecule 1 (ELAM-1), a cytokine-inducible molecule that functions in neutrophil adhesion. However, in certain chronic inflammatory processes (eg, sarcoidosis), INCAM-110 was observed without simultaneous ELAM-1 expression. Anti-INCAM-110 antibody E1/6 also marked several extravascular cell types, including lymphoid dendritic cells, some tissue macrophages, synovial lining cells, and reactive mesothelial cells. These data suggest a role for endothelial INCAM-110 in the pathophysiology of both acute and chronic inflammatory reactions. Furthermore INCAM-110 may function as an adhesion molecule for mononuclear leukocytes in a variety of extravascular sites.

Acute Disease↗
PubMed1990

Adhesion of human B cells to germinal centers in vitro involves VLA-4 and INCAM-110.

Human B lymphocytes localize and differentiate within the microenvironment of lymphoid germinal centers. A frozen section binding assay was developed for the identification of those molecules involved in the adhesive interactions between B cells and lymphoid follicles. Activated human B cells and B cell lines were found to selectively adhere to germinal centers. The VLA-4 molecule on the lymphocyte and the adhesion molecule INCAM-110, expressed on follicular dendritic cells, supported this interaction. This cellular interaction model can be used for the study of how B cells differentiate.

Antibodies, Monoclonal↗
PubMed1990

Inducible cell adhesion molecule 110 (INCAM-110) is an endothelial receptor for lymphocytes. A CD11/CD18-independent adhesion mechanism.

Inducible cell adhesion molecule 110 (INCAM-110) is a 110-kD glycoprotein expressed on cytokine-activated human vascular endothelial cells. mAb blocking studies indicate that INCAM-110 and intercellular adhesion molecule 1 (ICAM-1) independently support the adhesion of lymphocytes to activated human umbilical vein endothelial cell monolayers. Anti-CD11a/CD18 antibodies with anti-INCAM-110 mAb E1/6 produce greater inhibition of lymphocyte adhesion than either reagent alone, suggesting that INCAM-110 and LFA-1 are not an obligate receptor-ligand pair. Blood monocytes, but not polymorphonuclear leukocytes, also appear to bind endothelial INCAM-110. Endothelial expression of INCAM-110 is upregulated at sites of inflammation, suggesting a role in the recruitment of mononuclear leukocytes.

Antibodies, Monoclonal↗
PubMed1990

Identification of luteinizing hormone releasing hormone-like immunoactivity in ovine cotyledons.

Luteinizing hormone releasing hormone (LHRH)-like immunoactivity has been identified in cotyledonary extracts prepared from pregnant ewes. This activity displayed similar physico-chemical properties as synthetic LHRH, as determined by reverse-phase HPLC and size-exclusion HPLC. Under reverse-phase conditions, cotyledonary LHRH-like immunoactivity displayed a retention time (10.5 +/- 0.1 min) which was not significantly different from that of synthetic LHRH. When subjected to size-exclusion HPLC, cotyledonary LHRH-like immunoactivity eluted in fractions which corresponded to a molecular weight range of 1100-1200 Da, which was not significantly different from the elution profile observed for synthetic LHRH. The cotyledonary tissue content of LHRH-like immunoactivity averaged 94 +/- 24 pg/mg (n = 6). The results of this study demonstrate the presence of LHRH-like immunoactivity in ovine cotyledons. Although placental synthesis of LHRH-like immunoactive material has been demonstrated in other species, it remains to be established whether this activity, demonstrated in ovine placenta, is the consequence of de novo placental synthesis or represents uptake from the maternal (and/or fetal) circulation.

Animals↗
PubMed1990

Prostaglandin E2 and F2 alpha in mid-pregnant rat uterus and at parturition.

Prostaglandin E2 (PGE2) and F2 alpha (PGF2 alpha) produced by 15 days pregnant rat myometrium, by parturient rat myometrium and myometrium plus endometrium were measured in vitro. The results showed that the PGs produced by parturient myometrium were higher than these obtained during mid-pregnancy. Myometrium with endometrium released more PGs than myometrium alone, and the addition of arachidonic acid (AA) at 10 DM did not show any significant effect. Exogenous progesterone or estradiol-17b at a concentration of 1 Dmol had no effect on parturient uterine PG secretions.

Animals↗
PubMed1990

Gestational tissue phospholipase A2 messenger RNA content and the onset of spontaneous labour in the human.

Considerable evidence supports a central role for prostaglandins in the genesis of uterine activity and cervical dilatation at the time of human labour. The first step in prostaglandin synthesis is the liberation of arachidonic acid from glycerophospholipids by phospholipase A2. In this study, we examined the periparturitional gene expression of PLA2 in human placentae and fetal membranes, using a cDNA clone for non-pancreatic PLA2. PLA2 gene expression was found to be significantly increased (P less than 0.05) in placentae obtained after spontaneous-onset labour and normal vaginal delivery as compared with placentae from elective Caesarean section. In both of these groups, PLA2 expression in amnion and chorion was significantly less than that in placenta. The results of this study suggest that placental PLA2 gene expression increases in association with spontaneous-onset of labour in the human. This conclusion is consistent with the finding of increased levels of prostaglandins in gestational tissues, amniotic fluid and blood plasma at the time of labour.

Amnion↗
PubMed1990

Gestational profile of the stimulatory effects of porcine amniotic and allantoic fluids on prostaglandin G/H synthase activity.

The effects of porcine fetal fluids (amniotic and allantoic) on microsomal prostaglandin G/H synthase (PGHS) activity were assessed. Both amniotic and allantoic fluids obtained from late-gestation sows stimulated PGHS activity (as indicated by increased formation of radiolabelled prostaglandin) in a dose-dependent manner. At the maximum dose tested, amniotic and allantoic fluids stimulated prostaglandin (PG) formation by 55.5 +/- 1.5 and 58.5 +/- 4.7%, respectively (n = 3, P less than 0.01). Based upon ED50 values, amniotic fluid was approximately threefold more effective than allantoic fluid in stimulating PG formation. The stimulatory effect of amniotic but not allantoic fluid increased significantly (P less than 0.01) during gestation (Days 47-112). The observed changes in the stimulatory effect of amniotic fluid on microsomal PG formation parallels the in vivo changes that occur in intra-uterine PG synthesis. Amniotic fluid stimulatory activity may contribute to this gestational increase in PG synthesis.

Allantois↗