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R N Taylor

Publications and source records attributed to R N Taylor.

At least 73 records · Page 4Linked to original sources

Interleukin-8 concentrations are elevated in peritoneal fluid of women with endometriosis.

OBJECTIVE: To investigate the presence of interleukin-8 (IL-8), a macrophage-derived angiogenic factor, in peritoneal fluid (PF) of women with and without endometriosis. DESIGN: Case-control study. SETTING: University hospital. PATIENTS: Eighteen women with laparoscopic findings of mild to severe endometriosis, and nine women with no visual evidence of pelvic pathology. MAIN OUTCOME MEASURES: Peritoneal fluid IL-8 levels were determined using an ELISA. Interleukin-8 concentrations were compared among women with and without endometriosis. Correlation between PF IL-8 concentration and endometriosis stage was investigated. RESULTS: Interleukin-8 was detectable in the PF of a majority of women (67%). Interleukin-8 concentrations were higher in the PF of women with endometriosis than in matched normal controls. A significant correlation between PF IL-8 concentration and endometriosis stage was noted. CONCLUSIONS: We hypothesize that IL-8 is an important angiogenic factor that contributes to the pathogenesis of endometriosis by promoting the neovascularization of ectopic endometrial implants.

Adult↗

Which plasma factors bring about disturbance of endothelial function in pre-eclampsia?

The characteristic pathophysiological changes in pre-eclampsia are thought to be related to abnormalities of the maternal vascular endothelium. We suggest that the blood components that affect the risk of such damage are very-low-density lipoproteins (VLDL), which injure the endothelium, and toxicity-preventing activity (the pl 5.6 form of plasma albumin), which protects against VLDL-induced injury.

Cells, Cultured↗

Plasma cellular fibronectin as a measure of endothelial involvement in preeclampsia and intrauterine growth retardation.

OBJECTIVE: Our purpose was to determine the presence and degree of endothelial injury, by measuring plasma concentrations of cellular fibronectin, in pregnancies complicated by preeclampsia or intrauterine growth retardation. STUDY DESIGN: A matched, nested, case-control study design was used. Plasma was collected prospectively from pregnant women throughout gestation. At least 12 weeks after delivery women with preeclampsia, both preeclampsia and intrauterine growth retardation, or intrauterine growth retardation alone were identified. Normal controls were matched to these patients by age, race, and gestational age. Stored plasma, which had been obtained in the third trimester, was assayed for cellular fibronectin by means of a sensitive and specific enzyme immunoassay. After an appropriate transformation of the data results were compared with one-way analysis of variance with Fisher's post hoc test. RESULTS: Patients with preeclampsia (n = 18) had higher plasma cellular fibronectin concentrations than did control patients (n = 68) with median values of 2.8 and 1.4 micrograms/ml, respectively (p < 0.001, using transformed data). Patients with intrauterine growth retardation alone (n = 10) had 2.3 micrograms/ml cellular fibronectin, significantly higher than values of controls (p < 0.02 using transformed data) and significantly lower than those of patients with preeclampsia (p < 0.05 using transformed data). CONCLUSION: Pregnancies complicated by preeclampsia had significantly higher plasma cellular fibronectin concentrations than did pregnancies with intrauterine growth retardation alone, which in turn had significantly higher plasma cellular fibronectin concentrations than did control pregnancies. We speculate that endothelial involvement in intrauterine growth retardation is confined to the uteroplacental circulation, whereas it is systemic in preeclampsia.

Adult↗

Cyclosporine impairs release of endothelium-derived relaxing factors in epicardial and resistance coronary arteries.

BACKGROUND: Cyclosporin A is reported to impair endothelium-mediated vasorelaxation and induce endothelin release in some noncoronary vascular beds. We wished to determine whether acute cyclosporine administration induces endothelial dysfunction in coronary conductance or resistance arteries. METHODS AND RESULTS: We examined the effect of intracoronary acetylcholine, N omega-nitro-L-arginine methyl ester (L-NAME), L-arginine, nitroglycerin, and adenosine before and after acute cyclosporine administration (3 mg/kg IV over 30 minutes) in anesthetized dogs. Flow velocity was measured with a 0.014-in Doppler wire to assess resistance vessel responses, and epicardial coronary lumen area was simultaneously measured with a 4.3F, 30-MHz imaging catheter inserted over the Doppler wire. In 6 dogs, acetylcholine-induced increase in flow velocity was attenuated by cyclosporine in vehicle (137% to 55% at 10(-5) mol/L, P < .001), as was acetylcholine-induced epicardial vasodilation (14.1% to 6.7% at 10(-5) mol/L, P < .001). Vasodilation in response to intracoronary nitroglycerin (200 micrograms) and adenosine (6 mg) were unchanged by cyclosporine. Epicardial vasoconstriction with L-NAME (10(-4) mol/L) was reduced by cyclosporine (Pre, 7.4 +/- 0.9%; Post, 2.6 +/- 1.2%; P = .04), but L-arginine (10(-4) mol/L) had no effect after cyclosporine. In another 5 dogs, pure cyclosporine impaired acetylcholine-induced vasodilatation to the same degree as cyclosporine in vehicle (Cremophor); vehicle infusion did not impair endothelial function. In 5 more dogs, cyclosporine did not increase either arterial or coronary sinus concentrations of endothelin-1. CONCLUSIONS: The present study shows that cyclosporine acutely impairs release of endothelium-derived relaxing factor in canine conductance and resistance coronary arteries and provides evidence for decreased epicardial nitric oxide release after cyclosporine. The potential contribution of acute cyclosporine-induced coronary endothelial dysfunction to posttransplant vasculopathy needs further study.

Acetylcholine↗

Isolation, characterization, and comparison of human endometrial and endometriosis cells in vitro.

Endometriosis is a common gynecological disorder of unclear pathogenesis. We have established an in vitro model to investigate phenotypic similarities and differences between normal endometrial and endometriosis cells. Highly purified cultures of epithelial and stromal cells were isolated from normal endometrium and endometriosis implants. Morphological features as well as immunocytochemical markers confirm these isolates as epithelial and stromal cells. Potential hormone responsiveness was established by the documentation of estrogen receptor mRNA in epithelial and stromal cells isolated from both tissue types. Expression of this receptor protein was verified in stromal cells by competitive radioligand binding, revealing comparable receptor numbers and dissociation constants. CA-125 is selectively secreted in similar concentrations by epithelial cells isolated from both tissue types. PRL secretion is selectively exhibited by progestin-stimulated stromal cells from both tissue types. Our findings demonstrate that highly purified epithelial and stromal cells cultured from normal endometrial and endometriosis tissues express the same phenotypic and functional markers as their in vivo counterparts. These cultures provide useful models to identify endometriosis-specific cell products that contribute to the pathogenesis of this disorder.

Adult↗

Evaluation of plasma insulin-like growth factor-binding protein-3 as a potential predictor of preeclampsia.

OBJECTIVE: Elevated growth factor activity in women with preeclampsia is caused by an acid- and heat-labile protein complex with a native molecular mass of 150,000. The major plasma insulin-like growth factor-binding protein-3 has identical molecular characteristics. We hypothesized that increased endothelial cell release or decreased proteolytic degradation of insulin-like growth factor-binding protein-3 in preeclampsia would result in higher circulating levels of insulin-like growth factors and hence in increased mitogenic activity. STUDY DESIGN: Plasma insulin-like growth factor-binding protein-3 concentrations were determined by iodine-125 insulin-like growth factor-II radioligand blots of nonreducing gels in 16 normal and 16 preeclamptic patients collected from a prospective, case-control study. Enzyme-linked immunosorbent assays also were performed with a specific anti-insulin-like growth factor-binding protein-3 antiserum. RESULTS: Insulin-like growth factor-binding protein-3 concentrations were not different between women with normal versus preeclamptic pregnancies (p = 0.23). Enzyme-linked immunosorbent assays confirmed these results in a subset of patients. CONCLUSIONS: The findings indicate that insulin-like growth factor-binding protein-3 concentrations do not account for the elevated mitogenic activity observed in plasma from women with preeclampsia and are not a useful screening test for preeclampsia risk.

Adult↗

Peritoneal fluid concentrations of the cytokine RANTES correlate with the severity of endometriosis.

OBJECTIVE: Endometriosis is a common gynecologic disorder in which the concentration and activation of peritoneal macrophages are increased. The goal of this study was to quantify pelvic fluid concentrations of two cytokines involved in macrophage recruitment and activation. STUDY DESIGN: A case-control study of women undergoing pelvic surgery was conducted by collecting peritoneal fluid from 12 women without evidence of endometriosis (controls), 12 with mild, and 12 with moderate to severe endometriosis. Concentrations of RANTES and interferon gamma, soluble cytokines known to recruit and activate macrophages, were quantified by enzyme-linked immunosorbent assays. RESULTS: Pelvic fluid concentrations of RANTES are elevated in women with endometriosis and the levels correlate with the severity of disease. By contrast, concentrations of interferon gamma appear unaffected by the presence of or severity of endometriosis. CONCLUSION: The findings indicate that RANTES, a cytokine with potent chemotactic activity for human monocytes, may play an important role in the recruitment of peritoneal macrophages in endometriosis.

Adult↗

Characterization and ontogeny of endothelin receptors in human placenta.

Because of the potent mitogenic and vasoactive properties of endothelin-1 (ET-1) and the presence of its receptor in third trimester placenta, we postulated that ET-1 might be involved in human placental growth and vascularization during development. As an initial approach to test this hypothesis, placental ET receptors were characterized and quantified in each trimester of pregnancy. Membrane-rich particulates were prepared from first-, second-, and third-trimester villous human placenta obtained immediately after pregnancy termination or delivery. ET receptors were characterized by radioligand saturation analysis, ligand competition, and reverse transcription-polymerase chain reaction (RT-PCR) to determine the concentration, affinity, and specificity of ET binding sites, and to document the presence of specific ET-receptor subtype mRNA transcripts in placentas from each trimester. Kinetic determinations of 125I-labeled ET-1 binding yielded a Kd = 61 pM, consistent with the equilibrium determinations of 34 +/- 6 pM (n = 11). The concentration of ET receptors decreased significantly from 682 +/- 94 fmol/mg protein (n = 4) in the first trimester to 266 +/- 89 fmol/mg protein (n = 4) in the third trimester. Competition studies with unlabeled ET-1 indicated a single class of binding sites with a Ki = 49 +/- 5 pM (n = 9), whereas competition with ET-3 demonstrated binding sites with two affinities. The predominant sites had a Ki = 84 +/- 14 pM, similar to that for ET-1. The RT-PCR data confirmed that both ETA and ETB receptors mRNA transcripts are expressed in human placenta.(ABSTRACT TRUNCATED AT 250 WORDS)

Base Sequence↗

New insights into the etiology of pre-eclampsia.

Pre-eclampsia is a pregnancy-specific syndrome of unknown etiology, defined by clinical findings of elevated blood pressure combined with proteinuria and oedema. The decidual portion of the spiral arteries of women who later develop pre-eclampsia does not undergo the normal pregnancy-induced remodelling that converts these vessels to high volume-low resistance conduits. We have postulated that this failure leads to vascular spasm, restricted blood flow, placental ischaemia and the release of toxic substances that enter the maternal circulation, resulting in multi-organ disease. The complex and interwoven pathways of endocrine, paracrine and autocrine factors appear to result in a vicious cycle of endothelial cell dysfunction, which is expressed clinically as pre-eclampsia.

Endothelins↗

Quality of laboratory performance in testing for human immunodeficiency virus type 1 antibody. Identification of variables associated with laboratory performance.

To identify factors that may affect the quality of laboratory performance of human immunodeficiency virus type 1 (HIV-1) antibody testing, the Centers for Disease Control and Prevention Model Performance Evaluation Program surveyed laboratories in 1989 that performed enzyme immunoassay (EIA) and Western blot tests for HIV-1 antibody. Panels of 10 HIV-1-antibody-positive and antibody-negative plasma samples, some of which were duplicates, were mailed to program-participating laboratories. Laboratories were also mailed survey questionnaires to ascertain their laboratory characteristics and testing practices. Using 1988 data, researchers previously found that the overall analytic performance of laboratories performing HIV-1 antibody testing was independently associated with the following: (1) requiring a minimum degree of testing personnel; (2) having written criteria for identifying unsatisfactory specimens; (3) requiring in-house training for testing personnel; (4) having tested more than 10,000 specimens; (5) being identified as an "other" laboratory type; (6) having more than 24 months of testing experience; (7) laboratory uses specific (Abbott) materials for EIA; and (8) testing specimens collected by family-planning clinics. To verify these findings, we performed multivariate analysis on 1989 performance data. For the 1989 EIA analytic sensitivity, significant positive (P < or = .05) associations were detected with having written criteria for identifying unsatisfactory specimens and with having tested more than 10,000 specimens. For the 1989 overall EIA analytic performance, a significant negative (P < or = .05) association was found with using specific (Abbott) EIA materials, and a significant positive (P < or = .05) association was found with having tested more than 10,000 specimens. For Western blot results, the only significant (P < or = .05) associations were for both analytic sensitivity and overall analytic performance and having tested more than 10,000 specimens.

Blotting, Western↗

Cytogenetic evidence for enhanced selective miscarriage of trisomy 21 pregnancies with advancing maternal age.

The effect of advancing maternal age on the risk of death of fetuses with certain chromosome abnormalities has been tested by comparing their frequency at the time of chorionic villus sampling (CVS) with that at amniocentesis. The frequency of chromosome abnormalities among women whose sole risk factor for a chromosome abnormality was advanced maternal age (> or = 35 years old) was determined in a pooled group of 15,147 CVS cases, of whom > 1/3 were from the initial 7,500 CVS cases at the University of California, San Francisco, and compared with a pooled group of 74,851 amniocentesis cases collected from the literature. The frequency of trisomy 21 not only increased with advancing maternal age as expected, but the slope of the increase was about 25% greater in the CVS group than in the amniocentesis group (P = 0.08 for the difference in slopes by a logistic statistical model and P = 0.04 by a normit model). Similar patterns were seen for trisomies 18 and 13, but the P values for the differences in slopes were much higher. These results suggest that the miscarriage rate of trisomy 21 during the gestational interval studied is selectively greater with advancing maternal age. The basis for the enhanced selective loss of trisomy 21 with maternal age may be a reduced ability of the ageing "maternal compartment" to compensate for abnormal conceptuses.

Abortion, Spontaneous↗

Extraplacental human fetal tissues express mRNA transcripts encoding the human chorionic gonadotropin-beta subunit protein.

The glycoprotein hormone human chorionic gonadotropin (hCG) is synthesized in large quantities by the developing placenta, reaching peak concentrations in maternal blood during the late first trimester and early midtrimester of pregnancy. In general it is believed that the alpha-subunit of this dimeric hormone is expressed in pituitary gonadotropes, thyrotropes, and trophoblasts, while the beta-subunit is expressed exclusively by trophoblasts. Studies from our laboratory and other laboratories have shown that some midtrimester human fetal tissues, in addition to the placenta, can synthesize proteins that appear to be very similar to the beta-subunit of hCG. To define precisely the nature of this putative hCG-beta-subunit in extraplacental fetal tissues, we have examined the mRNA from a variety of human fetal and adult tissues using nucleic acid hybridization and reverse transcription-polymerase chain reaction (PCR) methods. Our results demonstrate that midtrimester fetal kidney and adrenal tissues contain hCG-beta mRNA transcripts at concentrations comparable to that of placenta, while fetal lung, brain, muscle, and adult adrenal contain only trace to undetectable levels of hCG-beta mRNA. By restriction endonuclease mapping of PCR fragments from fetal tissue cDNAs, we show that the hCG-beta transcript expressed in midtrimester human fetal organs is a bone fide copy of hCG-beta gene No. 5 of the beta-subunit gene family located on chromosome 19.

Base Sequence↗

Circulating concentrations of fetal fibronectin do not reflect reduced trophoblastic invasion in preeclamptic pregnancies.

This prospective, nested, case-control study investigated whether maternal plasma fetal fibronectin reflects reduced trophoblastic invasion at 16 to 20 weeks in women who later have preeclampsia. Concentrations of fetal fibronectin were 8.7 +/- 2.6 micrograms/ml in women with preeclampsia and 8.1 +/- 2.5 micrograms/ml in matched controls (p greater than 0.5). These results are discussed.

Case-Control Studies↗

Increases in plasma atrial natriuretic peptide concentration antedate clinical evidence of preeclampsia.

Atrial natriuretic peptide (ANP) concentrations are typically elevated in hypervolemic states. However, ANP levels have been reported to be increased in the peripartum period in women with preeclampsia, a disorder characterized by central hypovolemia. We postulated that ANP levels are elevated in preeclamptic patients before clinically evident disease. ANP concentrations were determined in three groups: uncomplicated pregnancies, pregnancies complicated by preeclampsia, and non-pregnant reproductive-aged women. The former groups were matched for gestational age at plasma sampling and delivery. The plasma samples, obtained prospectively from each patient during the first, second, and third trimesters and within 72 h postpartum, were frozen before RIA. A significant gestational increase in ANP was noted in both groups of pregnant women, with third trimester levels exceeding first trimester levels (P less than 0.05). Consistent with previous reports, ANP levels were elevated in overtly preeclamptic patients vs. matched controls in the third trimester. The ANP concentration was also significantly increased during the second trimester in women destined to develop preeclampsia. Postpartum ANP values decreased in the preeclamptic group to approach the level in normal patients postpartum. Thus, it appears that the stimuli of ANP secretion differ in uncomplicated and preeclamptic patients. Moreover, an elevation of plasma ANP is detectable before the onset of clinical evidence of preeclampsia.

Atrial Natriuretic Factor↗

Analytic sensitivity and specificity of enzyme immunoassay results in testing for human immunodeficiency virus type 1 antibody.

In 1986, a performance evaluation program at the Centers for Disease Control was implemented to assess the quality of performance of laboratories testing for human immunodeficiency virus type 1 antibody and to identify problems that occur during the testing process. Laboratories participating in the Centers for Disease Control Model Performance Evaluation Program for human immunodeficiency virus type 1 antibody testing furnished enzyme immunoassay results after they tested performance evaluation panels that were sent to them in August and November 1989. The panels consisted of 10 individual samples containing antibody-negative and antibody-positive samples, some of which were duplicates. Not all laboratories received the same panel of samples. Low false-negative and false-positive rates, as well as high intrashipment and intershipment reproducibility, indicate that most laboratories did not experience difficulty in testing performance evaluation samples sent to them in August and November 1989.

Evaluation Studies as Topic↗

Information about AIDS.

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Acquired Immunodeficiency Syndrome↗