%0 Journal Article
%~ Pubmed
%A Fujita, Yasuyuki
%A Athayde, Neil
%A Tokunaga, Shoji
%A Trudinger, Brian
%T Measurement of cardiac contractility using fetal isovolumetric contraction time in fetal tachyarrhythmia.
%B Ultrasound in medicine & biology
%D 2011
%V 37
%N 2
%P 184-8
%@ 1879-291X
%X The isovolumetric contraction time (ICT) is known to be an index of cardiac contractility. In this study, we examined the relationship between the fetal ICT and fetal heart rate (FHR) and evaluated the usefulness of ICT in the assessment of fetal cardiac contractility in cases with fetal tachyarrhythmia. Seven cases with fetal tachyarrhythmia between 32 and 40 weeks' gestation were included in this study. The fetal ICT was measured using a continuous Doppler device and digital filters. The relationship between the fetal ICT and FHR was analyzed using the Spearman's rank correlation test in each fetus. Based on the FHR and ultrasound findings of hydrops at the measurement of ICT, the obtained data were divided into three groups: normal, tachyarrhythmia only and hydrops. The clinical usefulness of ICT was assessed using the random effect model. In 7 fetuses, a total of 60 data points were obtained. A significant correlation between fetal ICT and FHR was not noted in each fetus. The ICT of the hydrops group was significantly prolonged compared with those of the normal and tachyarrhythmia-only groups (p < 0.01). An association between the fetal ICT and FHR is not noted and the fetal ICT might have some utility to detect impaired fetal cardiac contractility even in fetuses with tachyarrhythmia.
%Z FOR Codes: 1114



%0 Journal Article
%~ Pubmed
%A Turner, A J
%A Trudinger, B J
%T A modification of the uterine artery restriction technique in the guinea pig fetus produces asymmetrical ultrasound growth.
%B Placenta
%D 2009
%V 30
%N 3
%P 236-40
%@ 0143-4004
%X To evaluate the use of diathermy ablation of branches of the uterine artery to produce growth restriction in the fetal guinea pig, and to compare this new approach with the more conventional use of uterine artery ligation. The development of growth restriction was documented by measuring fetal biparietal diameter (BPD) and the resistance index (RI) of the umbilical artery blood flow velocity waveform.
%Z FOR Codes: 111401



%0 Book Section
%A Trudinger, Brian
%T Doppler ultrasonography and fetal well-being
%B Clinical Obstetrics: The Fetus & Mother, Third Edition
%D 2007
%C United States
%I Blackwell Publishing Ltd
%V 
%N 
%P 59
%@ 9781405132169
%E Reece, E. Albert
%E Hobbins, John C.
%X 
%Z FOR Codes: 111402 110320



%0 Journal Article
%~ Pubmed
%A Wang, X
%A Athayde, N
%A Trudinger, B
%T Egr-1 transcription activation exists in placental endothelium when vascular disease is present.
%B BJOG
%D 2006
%V 113
%N 6
%P 683-7
%@ 1470-0328
%X OBJECTIVE: To seek evidence of early vascular injury in the placental villous microcirculation in placental insufficiency identified by a high-resistance umbilical Doppler study by examining for expression of fibroblast growth factor receptor-1 (FGFR-1), its transcription factor, early growth response factor-1 (Egr-1) and plasma fibroblast growth factor-2 (FGF-2). DESIGN: Case-control study. SETTING :University teaching hospital. SAMPLE: Placentas and umbilical vein blood were collected at delivery from 12 women with normal pregnancy delivered at term and 14 with placental vascular disease defined by an abnormal umbilical artery Doppler study. METHODS: Microvascular endothelial cells were isolated from fresh human placentas using collagenase digestion and Dynabeads coated with monoclonal antibody against CD31. RNA was extracted from the isolated endothelial cells. The messenger RNA (mRNA) expression of FGFR-1 and Egr-1 production were assessed by reverse transcription polymerase chain reaction and factored relative to 18S ribosomal RNA. To confirm that FGF-2 was playing a significant role in this microvascular endothelial cell injury in the placenta, we also measured the soluble fraction of FGF-2 in fetal plasma from same groups of pregnancies using an enzyme-linked immunosorbent assay. MAIN OUTCOME MEASURES: Microvascular endothelial cells expression of Egr-1mRNA, FGFR-1 mRNA and presence of soluble FGF-2 in fetal plasma. RESULTS: The soluble level of FGF-2 in the fetal placental circulation from pregnancy with placental vascular disease was increased when compared with normal pregnancy (median 10.15 pg/ml and interquartile range 5.34-21.83 pg/ml versus 4.46 pg/ml and 3.69-5.66 pg/ml; P < 0.05). Microvascular endothelial cells from the placental villi with placental vascular disease showed upregulation of both FGFR-1 mRNA expression (median 0.72 and interquartile range 0.40-1.64 versus 0.34 and 0.19-0.71; P<0.05) and Egr-1 expression (median 0.79 and interquartile range 0.27-1.86 versus 0.23 and 0.17-0.67; P<0.05) in comparison with normal pregnancy. CONCLUSIONS: Endothelial cells from the placental villi are upregulated for expression of Egr-1 transcription factor gene in placental vascular disease. The FGFR-1 activation and increase in FGF-2 in the fetal circulation are known to be very early features of the response of endothelium to injury. Egr-1 is a promoter of many key pathophysiologically relevant target genes, which influence the development of subsequent vascular lesions. This change may occur before the pathological features recognised on microscopy.
%Z FOR Codes: 111401



%0 Journal Article
%~ Pubmed
%A Fujita, Y
%A Trudinger, B
%T Fetal isovolumetric contraction time in a case of fetal tachyarrhythmia.
%B Ultrasound in Obstetrics and Gynecology
%D 2006
%V 28
%N 6
%P 854-5
%@ 0960-7692
%X 



%0 Journal Article
%~ Pubmed
%A Wang, Xin
%A Athayde, Neil
%A Trudinger, Brian
%T Placental vascular disease and toll-like receptor 4 gene expression.
%B American Journal of Obstetrics and Gynecology
%D 2005
%V 192
%N 3
%P 961-6
%@ 0002-9378
%X OBJECTIVE: Vascular disease in the placenta, which is identified by the study of umbilical artery Doppler flow velocity waveforms, is associated with endothelial cell activation and a proinflammatory cytokine response in the villous placental circulation. We studied toll-like receptor 4 expression (the ligand is lipopolysaccharide) to examine whether infection may cause these inflammatory components of placental vascular disease through an innate immune response. STUDY DESIGN: Microvessel endothelial cells were isolated from human placentae with collagenase digestion and then extracted with Dynabeads that were coated with monoclonal antibody against CD31. We studied 13 placentae from normal pregnancies that were delivered at term and 15 pregnancies with umbilical placental vascular disease that was defined by an abnormal umbilical artery Doppler study. We extracted RNA from the isolated endothelial cells. The messenger RNA expression of toll-like receptor 4 production was assessed by reverse transcriptase-polymerase chain reaction and factored relative to the glyceraldehyde-3-phosphate dehydrogenase and 18S ribosomal RNA genes. RESULTS: Microvessel endothelial cells from placental villi with placental vascular disease showed up-regulation of toll-like receptor 4 expression (toll-like receptor 4/18S, 1.92 +/- 0.37 vs 0.99 +/- 0.19; P < .05; toll-like receptor 4/glyceraldehyde-3-phosphate dehydrogenase, 2.20 +/- 0.36 vs 1.25 +/- 0.22; P < .05) in comparison with normal pregnancy. CONCLUSION: Up-regulation of toll-like receptor 4 gene in the endothelium of the placental villi is present in placental vascular disease, which may result from exposure of this endothelium to the toll-like receptor 4 ligand lipopolysaccharide in vivo. Directly extracted endothelial cells were used to avoid the possibility for change in behavior in tissue culture. We conclude that Gram-negative infection and lipopolysaccharide stimulation may cause placental vascular disease.



%0 Journal Article
%~ Pubmed
%A Athayde, Neil
%A Wang, Jun
%A Wang, Xin
%A Trudinger, Brian
%T Fetuses delivered following preterm prelabor rupture of the membranes are capable of stimulating a proinflammatory response in endothelial cells.
%B Journal of the Society for Gynecologic Investigation
%D 2005
%V 12
%N 2
%P 118-22
%@ 1071-5576
%X OBJECTIVE: Preterm premature rupture of the membranes (PROM) has been attributed to ascending infection and a choriodecidual inflammatory response (ie, on the maternal side). However, on the fetal side those most at risk of morbidity have a systemic proinflammatory cytokine response. We have recently defined a similar proinflammatory response in pregnancies complicated by vascular disease on the fetal side of the placenta. A factor(s) present in fetal plasma from these pregnancies can stimulate human umbilical vein endothelial cells (HUVECs) to express mRNA for the proinflammatory cytokines, interleukin (IL)-6 and IL-8. The hypothesis of this study was that a similar factor(s) was present in preterm PROM. METHODS: A standard culture of HUVECs was incubated with fetal plasma, obtained immediately following delivery, from normal pregnancies delivering vaginally at term (n=16) and pregnancies delivering following preterm PROM (n=19). Expression of mRNA for IL-6 and IL-8 was assessed by reverse transcription polymerase chain reaction (RT-PCR) and standardized to GAPDH mRNA expression. RESULTS: Endothelial cell expression of IL-6 mRNA (median [25-75th centile] 0.295 [0.252-0.507] vs term vaginal delivery 0.208 [0.151-0.307]; P=.009) was enhanced in response to the fetal plasma from PROM cases compared to pregnancies delivering vaginally at term. In contrast, mRNA expression of IL-8 (median [25-75th centile] preterm PROM 0.41 [0.21-0.78] vs term vaginal delivery 0.49 [0.16-0.68]; P=.46) was not different in the two groups. CONCLUSIONS: We have demonstrated that in fetuses delivered following preterm PROM there is a factor(s) capable of stimulating a local endothelial cell proinflammatory cytokine (IL-6) response. This factor(s) that we have demonstrated may be responsible for the increased cytokine production seen in fetuses with the fetal inflammatory response syndrome.



%0 Journal Article
%~ Pubmed
%A Wang, Xin
%A Athayde, Neil
%A Trudinger, Brian
%T Microvascular endothelial cell activation is present in the umbilical placental microcirculation in fetal placental vascular disease.
%B American Journal of Obstetrics and Gynecology
%D 2004
%V 190
%N 3
%P 596-601
%@ 0002-9378
%X OBJECTIVE: Fetal growth restriction is associated with an abnormal umbilical artery Doppler study. A vascular disease is present in the fetal umbilical placental microcirculation. We hypothesized that the local production of factors that are injurious to microvessel endothelium is responsible for this vascular disease and that endothelial cell activation is a feature of this. Because the expression of the cell adhesion molecules is associated with endothelial cell activation, we isolated endothelial cells from the microvessels of the umbilical placenta and examined them for evidence of gene expression of cell adhesion molecules. STUDY DESIGN: Endothelial cells from the microcirculation of human placenta were isolated and purified with collagenase digestion and extraction with superparamagnetic beads that were coated with monoclonal antibody against CD31. Microvessel endothelial cells were isolated from the placentae of 13 women with a normal pregnancy and delivery at term and 10 placentas with umbilical placental vascular disease that was defined by abnormal umbilical artery Doppler study. Total RNA was extracted from isolated endothelial cells. The messenger RNA expressions of cell adhesion molecules (intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and platelet endothelial cell adhesion molecule-1) were assessed by semiquantitative reverse transcription-polymerase chain reaction. RESULTS: Microvessel endothelial cells from the fetal placentae of pregnancies that were complicated by umbilical placental vascular disease showed an enhanced expression of intercellular adhesion molecule-1 messenger RNA (2.12+/-0.45 vs 0.92+/-0.25) and platelet endothelial cell adhesion molecule-1 messenger RNA (4.29+/-0.87 vs 2.41+/-0.42) in comparison to normal pregnancies. There was no significant difference in expression of vascular cell adhesion molecule-1 messenger RNA (1.55+/-0.37 vs 1.68+/-0.38). CONCLUSION: We have shown that vascular disease in the fetal umbilical placental circulation is associated with an increase in the expression of intercellular adhesion molecule-1 and platelet endothelial cell adhesion molecule-1 by microvessel endothelial cells. We postulate that locally released factors cause injury and activation to microvessel endothelial cells. In this regard, the process in the fetus is similar to that of atherothrombotic vascular disease of later life.



%0 Journal Article
%~ Pubmed
%A Wang, Xin
%A Athayde, Neil
%A Trudinger, Brian
%T Maternal plasma from pregnant women with umbilical placental vascular disease does not affect endothelial cell mRNA expression of nitric oxide synthase.
%B Journal of the Society for Gynecologic Investigation
%D 2004
%V 11
%N 3
%P 149-53
%@ 1071-5576
%X OBJECTIVE: In placental vascular disease identified by umbilical artery Doppler study we have shown the existence of a factor in fetal plasma that causes activation of endothelial cells in culture with expression of cell adhesion molecules and nitric oxide synthase, apoptosis, and proinflammatory cytokine production. The present work was carried out to investigate a maternal origin for this factor active in the fetal circulation. METHODS: We collected maternal plasma from pregnant women with Doppler-defined umbilical placental vascular disease and examined its effect on endothelial cells in culture. Aliquots from a common culture of human umbilical vein endothelial cells (HUVEC) were incubated with maternal plasma from women with normal pregnancy (n = 23), umbilical placental vascular disease defined by abnormal umbilical artery Doppler (n = 30, with or without preeclampsia), and preeclampsia with normal umbilical artery Doppler (n = 14). The expression of mRNA for inducible and endothelial constitutive nitric oxide synthase (iNOS and ecNOS, respectively) was assessed by reverse transcriptase polymerase chain reaction. RESULTS: There was no significant increase in either the iNOS or the ecNOS mRNA expression by HUVEC cultured with maternal plasma from pregnancies with umbilical placental vascular disease compared with normal pregnancy (iNOS 1.49 +/- 0.35 versus 1.38 +/- 0.25; ecNOS 1.51 +/- 0.35 versus 1.25 +/- 0.27; P >.05). In the placental vascular disease group the results were similar for the presence or absence of maternal preeclampsia. In the samples from women with preeclampsia with normal umbilical Doppler, both iNOS and ecNOS mRNA expression (iNOS 1.42 +/- 0.53; ecNOS 1.46 +/- 0.39; P >.05) did not differ from normal. CONCLUSION: Maternal plasma from pregnancies with umbilical placental vascular disease did not affect endothelial cell expression of nitric oxide synthase. This finding does not support a maternal origin for the factor demonstrated in fetal plasma. These results suggest separate pathogenic pathways for the endothelial cell activation seen in preeclampsia and fetal growth restriction associated with abnormal umbilical artery Doppler flow velocity waveforms. These findings are also consistent with the concept that the vascular pathology in the fetal placenta may be primary and that the uteroplacental circulation is reduced in response rather than acts as a constraint.



%0 Journal Article
%~ Pubmed
%A Mindel, A
%A Marks, C
%A Tideman, R
%A Taylor, J
%A Seifert, C
%A Berry, G
%A Trudinger, B
%A Cunningham, A
%T Sexual behaviour and social class in Australian women.
%B International Journal of STD & AIDS
%D 2003
%V 14
%N 5
%P 344-9
%@ 0956-4624
%X Sexual behaviour is determined by social, cultural and personal factors. Sexual behaviour studies have been conducted in many countries. However, information from Australia is limited. This study was conducted in Obstetrics Department, Westmead Hospital, Sydney. Questionnaire-derived demographic and behavioural characteristics for public and private patients were compared using bivariate and logistic regression analyses. Of the patients, 3036 were public, and 595 private. On bivariate analysis some significant differences were private patients more likely to be born in Australia and have a higher education level whereas public patients were more likely to have had a greater number of lifetime sexual partners and younger age at first sex. Public patients were more likely to be herpes simplex virus type 2 (HSV-2) antibody positive (12%) than private patients (6%). On logistic regression significant variables included country of birth, being HSV-2 antibody positive, and age at first sex. A number of sexual and social variables were significantly different, comparing patients in the public and private sectors. Evaluation of interventions to reduce the sexual risk to women in the public sector should be considered, including encouraging young women to delay their sexual debut, and reducing the number of sexual partners.



%0 Journal Article
%A Trudinger, BJ
%A Song, JZ
%A Wu, ZH
%A Wang, J
%T Placental insuffuency is characterized by platelet activaton in the fetus
%B Obstetrics And Gynecology
%D 2003
%C 360 PARK AVE SOUTH, NEW YORK, USA, NY, 10010-171
%I Elsevier Science Inc
%V 101 (5)
%N 
%P 975-981
%@ 0029-7844
%X 



%0 Journal Article
%~ Pubmed
%A Wang, Xin
%A Wang, Jian
%A Trudinger, Brian
%T Gene expression of nitric oxide synthase by human umbilical vein endothelial cells: the effect of fetal plasma from pregnancy with umbilical placental vascular disease.
%B BJOG
%D 2003
%V 110
%N 1
%P 53-8
%@ 1470-0328
%X OBJECTIVE: To determine whether endothelial cell injury would be produced by factor(s) released into the fetal circulation, manifested by altered messenger RNA expression of nitric oxide synthase. DESIGN: Case-control study. SETTING: University teaching hospital. SAMPLES: Fetal plasma was collected from 34 normal pregnancies, 44 pregnancies with umbilical placental vascular disease identified by an abnormal umbilical Doppler and 11 pregnancies with maternal pre-eclampsia but with normal umbilical Doppler studies. METHODS: Aliquots from a common culture of human umbilical vein endothelial cells (HUVECs) were incubated with fetal plasma from the members of the three patient groups. The total RNA was extracted from the endothelial cells and mRNA for nitric oxide synthase was measured by reverse transcription and semi-quantitative polymerase chain reaction (RT-PCR). This was standardised by comparison of the amplified inducible nitric oxide synthase (iNOS) or endothelial constitutive nitric oxide synthase (ecNOS) to glyceraldehyde 3-phosphate dehydrogenase (GAPDH). MAIN OUTCOME MEASURE: Endothelial cell gene expression of iNOS and ecNOS. RESULTS: The mRNA expression of iNOS and ecNOS were significantly higher (P < 0.05) in HUVECs stimulated by fetal plasma from pregnancies with umbilical placental vascular disease [iNOS 1.12 (0.16); ecNOS 1.78 (0.18)] when compared with normal pregnancies [iNOS 0.56 (0.06); ecNOS 1.06 (0.10)]. In the maternal pre-eclampsia group, the NOS expression [iNOS 0.76 (0.11); ecNOS 1.39 (0.26)] did not differ from normal pregnancy. In the vascular disease group, there was no difference in NOS expression between the subgroups with and without maternal pre-eclampsia. CONCLUSIONS: Our study demonstrates that umbilical placental vascular disease is associated with a factor(s) in fetal plasma that produces an increase in the expression of iNOS and ecNOS mRNA by endothelial cells. Our findings raise the possibility that the release of factors causing an up-regulation of iNOS and ecNOS in the endothelium in the fetal placenta may occur as part of an inflammatory response of the vascular endothelium to injury.
%Z FOR Codes: 111402



%0 Journal Article
%~ Pubmed
%A Koga, Tsuyoshi
%A Athayde, Neil
%A Trudinger, Brian
%T A new ultrasound technique to measure the isovolumetric contraction time as an index of cardiac contractility: fetal lamb validation.
%B Journal of the Society for Gynecologic Investigation
%D 2003
%V 10
%N 4
%P 194-9
%@ 1071-5576
%X OBJECTIVE: We developed a noninvasive Doppler technique for measuring fetal cardiac isovolumetric contraction time (ICT). The purpose of this study was to determine how well our method reflects real cardiac performance using fetal lamb as an instrumented model. METHODS: The true ICT was measured by simultaneous recording of the pressure waves of the left ventricle and ascending aorta. The maximum first derivative of the left ventricular pressure wave (Max dp/dt) was calculated. The Doppler ICT was measured in the appropriately filtered Doppler cardiac signals. Positive and negative inotropic agents were administered to change the cardiac contractility. RESULTS: There was an inverse relationship between the Doppler ICT and the Max dp/dt. Excellent linear correlation was found an absolute value and changes from control value between the true ICT and the Doppler ICT (r = 0.959, r = 0.962). CONCLUSIONS: The Doppler ICT measurement provides useful information about changes in ventricular performance.
%Z FOR Codes: 111402



%0 Journal Article
%~ Pubmed
%A Daniel, Art
%A Athayde, Neil
%A Ogle, Robert
%A George, Alice M
%A Michael, Jonathan
%A Pertile, Mark D
%A Bryan, Jennifer
%A Jammu, Vapinder
%A Trudinger, Brian J
%T Prospective ranking of the sonographic markers for aneuploidy: data of 2143 prenatal cytogenetic diagnoses referred for abnormalities on ultrasound.
%B The Australian and New Zealand Journal of Obstetrics and Gynecology
%D 2003
%V 43
%N 1
%P 16-26
%@ 0004-8666
%X OBJECTIVE: To design a scheme to rank sonographic anomalies as indicators of aneuploidy and record the distribution of data from 2143 prenatal amniotic fluid/chorionic villous sample diagnoses referred for karyotyping because of fetal anomalies detected with ultrasound. METHODS: In all cases the records of sonographic anomalies were obtained prior to karyotyping. A cascade of seven prospective categories of ultrasound anomalies was chosen and the data were included in the highest compatible sonography category. The categories were in descending order: (I) combined central nervous system (CNS)/cranial shape and cardiac anomalies (excluding spina bifida and anencephaly); (II) key anomaly present (exomphalos/ intrauterine growth restriction/duodenal atresia/cystic hygroma/fetal hydrops/talipes--with other multiple anomalies); (III) CNS +/- other abnormality (excluding choroid plexus cyst, spina bifida, anencephaly); (IVa) increased nuchal translucency--first trimester +/- other abnormality; (IVb) increased nuchal thickening--second trimester +/- other abnormality; (V) cardiac anomaly +/- other abnormality; (VI) other markers of aneuploidy (pyelectasis/two vessel cord/echogenic bowel/short femur); and (VII) other (mostly isolated) malformations. RESULTS: There were 412/2143 (19.2%) chromosome abnormalities detected in this sonographically abnormal group. Overall, the prevalence of aneuploidy significantly ranged from 51 to 3% according to the above I-VII ultrasound categories and from approximately 1-80% for individual ultrasound anomalies. Likelihood ratios were derived for many ultrasound anomalies for several aneuploidy groups: trisomies of 13; 18; and 21; 45,X and 45,X mosaics; triploidy; other autosomal duplications and/or deletions; and other (than 45,X) sex chromosomal aneuploidies. CONCLUSION: It is suggested this data could be used to assist pre-procedural counselling of patients after the ultrasound scan in tertiary referral centres for prenatal cytogenetic diagnosis.
%Z FOR Codes: 111402



%0 Journal Article
%~ Pubmed
%A Wang, Xin
%A Athayde, Neil
%A Trudinger, Brian
%T A proinflammatory cytokine response is present in the fetal placental vasculature in placental insufficiency.
%B American Journal of Obstetrics and Gynecology
%D 2003
%V 189
%N 5
%P 1445-51
%@ 0002-9378
%X OBJECTIVE: Vascular disease in the umbilical placental circulation is associated with fetal growth restriction and adverse outcome. It may be identified antenatally by the study of umbilical artery Doppler flow velocity waveforms. The cause of this vascular disease is unknown. We have previously provided indirect evidence for endothelial cell activation and a proinflammatory cytokine response. Recently, a family of inhibitors of cytokine signaling has been identified, referred to as the suppressors of cytokine signaling (SOCS). Activation of SOCS occurs when cytokines are produced in stimulated cells. We tested the hypothesis that endothelial cell activation was present in umbilical placental vascular disease and was associated with production of proinflammatory cytokines and members of the family of SOCS. STUDY DESIGN: Placentas were collected at delivery and microvascular endothelial cells were isolated. We studied 13 normal pregnancies and 10 with umbilical placental vascular disease identified by an abnormal umbilical artery Doppler study. Placental pieces were digested with collagenase and purified by adherence to Dynabeads coated with monoclonal antibody against CD31. The RNA was extracted from isolated endothelial cells. The messenger RNA expression of cytokine production (interleukin-6 and interleukin-8) and the members of SOCS family (CIS, SOCS1, SOCS2, and SOCS3) were assessed by use of semiquantitative reverse transcriptase-polymerase chain reaction. RESULTS: In the microcirculation of the placenta, endothelial cell expression of interleukin-6 messenger RNA (2.50+/-0.60 vs 1.25+/-0.26) and interleukin-8 messenger RNA (2.83+/-0.55 vs 1.58+/-0.27) was up-regulated in umbilical placental vascular disease in comparison to normal pregnancy. The endothelial cell mRNA expression of SOCS2 (3.36+/-0.77 vs 1.76+/-0.29) and SOCS3 (2.77+/-0.60 vs 1.48+/-0.26) was enhanced in placental vascular disease. There was no significant difference in expression of CIS and SOCS1 in microvessel endothelial cells. CONCLUSION: We have demonstrated that microvessel endothelium of the fetal placental vasculature produces both the proinflammatory cytokines (interleukin-6 and interleukin-8) and members of SOCS family (SOCS2 and SOCS3) in umbilical placental vascular disease. This cytokine production may play a key role in the interaction of endothelial cells of the placenta villi with neighboring cells. The up-regulation of SOCS2 and SOCS3 indicates these are the major negative regulators in umbilical placental microvessel endothelial cell activation pathways. By its occurrence, this also confirms the presence of a proinflammatory cytokine response.
%Z FOR Codes: 111402



%0 Journal Article
%~ Pubmed
%A Wang, Xin
%A Athayde, Neil
%A Trudinger, Brian
%T Fetal plasma stimulates endothelial cell production of cytokines and the family of suppressor of cytokine signaling in umbilical placental vascular disease.
%B American Journal of Obstetrics and Gynecology
%D 2003
%V 188
%N 2
%P 510-6
%@ 0002-9378
%X OBJECTIVE: We have shown that fetal plasma from pregnancies with placental vascular disease that were identified by an abnormal umbilical artery Doppler study causes endothelial cell activation. We investigated the hypothesis that this would be associated with endothelial cell production of cytokines and their natural regulators, the suppressor of cytokine signaling family. Activation of suppressor of cytokine signaling at the time of cytokine release confirms the fact that cytokine production is occurring in a stimulated cell. STUDY DESIGN: Aliquots from a common culture of human umbilical vein endothelial cells were incubated with fetal plasma from normal pregnancy (n = 29 pregnancies), from umbilical placental vascular disease defined by abnormal umbilical artery Doppler waveforms (n = 38 pregnancies), and from preeclampsia with normal umbilical artery Doppler scans (n = 10 pregnancies). The expression of messenger RNA for the cytokines interleukin-6 and interleukin-8 and the members of suppressor of cytokine signaling family (cytokine-inducible SH2-containing protein, suppressor of cytokine signaling 1, 2, and 3) were assessed by reverse transcriptase-polymerase chain reaction. RESULTS: Endothelial cell expression of interleukin-6 messenger RNA (1.94 +/- 0.24 vs 1.31 +/- 0.16) and interleukin-8 messenger RNA (2.62 +/- 0.33 vs 1.64 +/- 0.22) were enhanced in response to incubation with fetal plasma from placental vascular disease in comparison to incubation with fetal plasma from normal pregnancy. The messenger RNA expression of suppressor of cytokine signaling-2 (2.03 +/- 0.23 vs 1.37 +/- 0.16) was up-regulated significantly in placental vascular disease. Differences for cytokine-inducible SH2-containing protein, suppressor of cytokine signaling-1, and suppressor of cytokine signaling-3 were not significant. The expression of cytokines and the suppressor of cytokine signaling family did not differ from normal in the group with maternal preeclampsia and a normal umbilical study. Interestingly, in the umbilical placental vascular disease group, the results were similar in the subgroups, with or without preeclampsia in the mother. CONCLUSION: We have shown that factors that cause endothelial cell injury are present in the fetal circulation in umbilical placental vascular disease. This study is the first report of cytokine production and release and activation of the suppressor of cytokine signaling family by endothelial cells in response to fetal plasma in placental vascular disease. The role of all members of the suppressor of cytokine signaling family in this process must be investigated further. The fact that both the agonist (cytokines) and the antagonist (suppressor of cytokine signaling-2) are produced points to a significant role of endothelial cells in this disease.
%Z FOR Codes: 111402



%0 Journal Article
%~ Pubmed
%A Trudinger, Brian
%A Song, Jenny Z
%A Wu, Zhan H
%A Wang, Jun
%T Placental insufficiency is characterized by platelet activation in the fetus.
%B Obstetrics and gynecology
%D 2003
%V 101
%N 5 Pt 1
%P 975-81
%@ 0029-7844
%X OBJECTIVE: To investigate whether activation of circulating platelets was present in the fetal and maternal circulation in cases with vascular disease in the fetal-umbilical-placental circulation as identified by umbilical artery Doppler study. METHODS: We studied 20 mother-fetus pairs with an abnormal umbilical artery Doppler study indicating umbilical-placental pathology and 9 normal pregnancy pairs. All pregnancies in these two groups had elective cesarean delivery. We also studied 15 healthy nonpregnant women. Blood was collected at delivery, and flow cytometry was used to measure platelet activation. The platelet population was specified by the antiglycoprotein IIIa (CD61) antibody and activated platelets by the anti-P selectin (CD62) antibody. Platelet activation in response to thrombin (0.03 to 0.25 U/mL) was also assessed. RESULTS: In the normal, healthy, nonpregnant women, there was no evidence of platelet activation in the fetal circulation (median, 0.63% of platelet population). Platelet activation was present in the fetal circulation in pregnancies with placental insufficiency (median, 4.57%) compared with normal pregnancies (median, 1.19%) (P =.034). The fetal platelets from pregnancies complicated by placental insufficiency also showed resistance to challenge with increasing thrombin concentration compared with normal fetal platelets (at 0.25 U/mL thrombin concentration, placental insufficiency pregnancy 69.82% and normal pregnancy 81.49%, P =.003). In the maternal circulation there were no differences in platelet activation (normal 4.89%, placental insufficiency 5.16%, P =.33) and sensitivity to thrombin challenge. CONCLUSION: In the fetal circulation, the presence of Doppler-detected umbilical-placental vascular disease was associated with significantly enhanced fetal platelet activation and resistance to thrombin challenge. These changes were not noted in the maternal circulation. This provides further evidence of a primary vascular pathology in the fetal-placental circulation independent of disease in the uteroplacental circulation when the umbilical Doppler flow velocity waveform reveals a high resistance pattern.
%Z FOR Codes: 111402



%0 Book Section
%A Koga, T
%A Athayde, NP
%A Trudinger, BJ
%A Nakano, H
%T A new and simple Doppler method for measurement of fetal cardiac isovolumetric contraction time
%B Ultrasound In Obstetrics & Gynecology
%D 2001
%C Germany
%I Springer-Verlag
%V 
%N 
%P 5-26
%@ 3540672680
%X 



%0 Journal Article
%~ Pubmed
%A Tideman, R L
%A Taylor, J
%A Marks, C
%A Seifert, C
%A Berry, G
%A Trudinger, B
%A Cunningham, A
%A Mindel, A
%T Sexual and demographic risk factors for herpes simplex type 1 and 2 in women attending an antenatal clinic.
%B Sexually Transmitted Infections
%D 2001
%V 77
%N 6
%P 413-5
%@ 1368-4973
%X OBJECTIVE: To establish risk factors for the presence of HSV-2 and HSV-1 infections in pregnant women. DESIGN, POPULATION, AND SETTING: A prospective study of 3306 women attending the antenatal department Westmead Hospital, Sydney, between June 1995 and April 1998. METHODS: Women completed a self administered questionnaire to establish risk factors for the presence of HSV-2 and HSV-1. Sera were tested for antibodies to HSV-2 and HSV-1. Data were analysed using SPSS and SAS. MAIN OUTCOME MEASURES: Seroprevalence of and risk factors for HSV-2 and HSV-1. RESULTS: 375 (11.3% (95% CI 10.3-12.5)) women were HSV-2 antibody positive. Increasing age, Asian country of birth, lower education level, public hospital status, confirmed genital herpes, a partner with genital herpes, early age of first sex, more than one lifetime sexual partner, and previous chlamydia infection were independently associated with HSV-2 seropositivity. Of 408 women tested for HSV-1 antibodies, 323 (79.2% (95% CI 74.9-83.0)) were positive. Oral herpes, oral blisters or sores, and being HSV-2 seropositive were independently associated with HSV-1 seropositive status. When the logistic regression model was rerun without HSV-2 status, parity of two or more and one or more sexual partners in the past 3 months were significant predictors of HSV-1 seropositivity. CONCLUSIONS: The presence of antibodies to HSV-2 and HSV-1 is related to a number of sexual and demographic risk factors. Public health campaigns directed at encouraging young people to delay the onset of sexual activity and reduce the number of sexual partners need to be evaluated. However, the possible availability of an HSV-2 vaccine that is able to protect over 70% of women offers the best hope for control of genital herpes.



%0 Journal Article
%A Rowlands, S
%A Bell, R
%A Donath, S
%A Morrow, S
%A Trudinger, BJ
%T Misoprostol versus dinoprostone for cervical priming prior to induction of labour in term pregnancy: a randomised controlled trial
%B Australian & New Zealand Journal of Obstetrics & Gynaecology
%D 2001
%C 24-28 Oval Rd, London, England, Nw1 7Dx
%I Academic Press Ltd
%V 124
%N 
%P 159-164
%@ 0021-9975
%X 



%0 Journal Article
%A Koga, T
%A Athayde, NP
%A Trudinger, BJ
%T The fetal cardiac isovolumetric contraction time in normal pregnancy and in pregnancy with placental vascular disease: the first clinical report using a new ultrasound technique
%B British Journal of Obstetrics and Gynaecology
%D 2001
%C 
%I 
%V 8
%N 
%P 314-323
%@ 
%X 



%0 Journal Article
%A Mindel, A
%A Taylor, J
%A Tideman, RL
%A Seifert, C
%A Berry, G
%A Wagner, K
%A Page, J
%A Marks, C
%A Trudinger, BJ
%A Cunningham, AL
%T Neonatal herpes prevention: a minor public health problem in some communities
%B Sexually Transmitted Infections
%D 2000
%C 
%I British Medical Journal Publishing Group
%V 76
%N 
%P 287-291
%@ 1368-4973
%X