DESIGN AN “IN HOUSE” SOFTWARE FOR SCREENING PREECLAMPSIA BY MATERNAL FACTORS AND MEAN ARTERIAL PRESSURE AT 11 – 13 WEEKS IN COMMUNE HEALTH CENTERS.

2015 ◽  
pp. 115-126
Author(s):  
Viet Nhan Nguyen ◽  
Ngoc Thanh Cao ◽  
Thi Minh Thi Ha ◽  
Van Duc Vo ◽  
Quang Vinh Truong ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Gestational Hypertension ◽  
Area Under The Curve ◽  
Health Centers ◽  
Maternal Factors ◽  
Good Tool ◽  
Uterine Artery Doppler ◽  
Study Results ◽  
In Pregnancy

Objective: Design an “in house” software for screening preeclampsia by maternal factors and mean arterial pressure at 11 – 13 gestational weeks in commune health centers. Methods: Based on the algorithms for calculating the risk of preeclampsia (PE) by maternal factors and mean artirial pressure at 11 - 13 gestational weeks in the study results of the authors, an “in house” software was deigned in Excel. The results of prediction preeclampsia by The Fetal Medicine Foundation (FMF)(version 2.3) were compared with the results by “in house” software in 1110 singleton pregnant women. Results: The “in house” software met the requirements for calculating the risks of PE and save data. FMF risk for gestational hypertension disorder in pregnancy by maternal factors, mean arterial pressure,uterine artery Doppler and PAPP-A has an area under the curve of 0.68 (95%CI: 0.59 – 0.78). The “in house” software risk for gestational hypertension in pregnancy by maternal factors, mean arterial pressure has an area under the curve of 0.643 (0.55 – 0.73) There was no statistically significant different between two programs (p:0.52). The risk cut-off 1:50 in the prediction of gestational hypertension of the “in house” software was used to identify the group of high risk with detetion rate (DR) 28.6% (95%CI: 14.9-42.2) comparing to 40.5% (95%CI:25.6-55.3) of FMF. Conclusion: The FMF version 2.3 is better but in the absence of Doppler ultrasound and PAPP-A test in the commune health cares, the “in house” software for screening PE is a good tool for councelling, following up and early intervention for PE.

scholarly journals Placental ischemia-stimulated T-helper 17 cells induce preeclampsia-associated cytolytic natural killer cells during pregnancy

2018 ◽  
Vol 315 (2) ◽  
pp. R336-R343 ◽  
Author(s):  
Corbin A. Shields ◽  
Maggie McCalmon ◽  
Tarek Ibrahim ◽  
Dakota L. White ◽  
Jan M. Williams ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Natural Killer ◽  
Cell Activation ◽  
Fetal Weight ◽  
T Helper ◽  
T Helper 17 ◽  
Placental Ischemia ◽  
In Pregnancy

Previous studies have demonstrated that T-helper 17 (TH17) cells and cytolytic natural killer (cNK) cells are increased in women with preeclampsia. In this study we investigated the role of placental ischemia-stimulated TH17 cells in induction of cNK cells in pregnancy. We further assessed the role of TH17 cell-mediated oxidative stress in facilitation of cNK cell activation in pregnancy by treating rats with the SOD mimetic tempol. CD4+/CD25− cells were isolated from reduced uterine perfusion pressure (RUPP) rats and differentiated into TH17 cells in vitro. On day 12 of gestation ( GD12), 1 × 106 placental ischemia-stimulated TH17 cells were injected into normal pregnant (NP) rats (NP + RUPP TH17 rats), and a subset of rats were treated with tempol (30 mg·kg−1·day−1) from GD12 to GD19 (NP + RUPP TH17 + tempol rats). On GD19, cNK cells, mean arterial pressure, fetal weight, and cNK cell-associated cytokines and proteins were measured. Placental cNK cells were 2.9 ± 1, 14.9 ± 4, and 2.8 ± 1.0% gated in NP, NP + RUPP TH17, and NP + RUPP TH17 + tempol rats, respectively. Mean arterial pressure increased from 96 ± 5 mmHg in NP rats to 118 ± 2 mmHg in NP + RUPP TH17 rats and was 102 ± 3 mmHg in NP + RUPP TH17 + tempol rats. Fetal weight was 2.37 ± 0.04, 1.95 ± 0.14, and 2.3 ± 0.05 g in NP, NP + RUPP TH17, and NP + RUPP TH17 + tempol rats, respectively. Placental IFNγ increased from 1.1 ± 0.6 pg/mg in NP rats to 3.9 ± 0.6 pg/mg in NP + RUPP TH17 rats. Placental perforin increased from 0.18 ± 0.18 pg/mg in NP rats to 2.4 ± 0.6 pg/mg in NP + RUPP TH17 rats. Placental levels of granzymes A and B followed a similar pattern. Treatment with tempol did not lower placental cNK cytokines or proteins. The results of the present study identify TH17 cells as a mediator of aberrant NK cell activation that is associated with preeclampsia.

scholarly journals Prediction of pre-eclampsia by a combination of maternal history, uterine artery Doppler and mean arterial pressure

2008 ◽  
Vol 32 (7) ◽  
pp. 877-883 ◽  
Author(s):  
N. Onwudiwe ◽  
C. K. H. Yu ◽  
L. C. Y. Poon ◽  
I. Spiliopoulos ◽  
K. H. Nicolaides
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Uterine Artery ◽  
Maternal History ◽  
Uterine Artery Doppler

scholarly journals Multivariate multilevel spline models for parallel growth processes: application to weight and mean arterial pressure in pregnancy

2012 ◽  
Vol 31 (26) ◽  
pp. 3147-3164 ◽  
Author(s):  
Corrie Macdonald‐Wallis ◽  
Debbie A. Lawlor ◽  
Tom Palmer ◽  
Kate Tilling
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Growth Processes ◽  
Spline Models ◽  
In Pregnancy ◽  
Parallel Growth

scholarly journals MEAN ARTERIAL PRESSURE AS A PREDICTOR OF GESTATIONAL HYPERTENSION AND PREECLAMPSIA

2016 ◽  
Vol 3 (68) ◽  
pp. 3715-3720
Author(s):  
Vidhya Ravi ◽  
Sivaranjani Panneer Selvam P ◽  
Bama S Ramesh
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Gestational Hypertension

scholarly journals Impaired acetylcholine-induced cutaneous vasodilation in young smokers: roles of nitric oxide and prostanoids

2013 ◽  
Vol 304 (5) ◽  
pp. H667-H673 ◽  
Author(s):  
Naoto Fujii ◽  
Maggie C. Reinke ◽  
Vienna E. Brunt ◽  
Christopher T. Minson
Keyword(s):  
Nitric Oxide ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Local Heating ◽  
Area Under The Curve ◽  
Daily Consumption ◽  
Cutaneous Vasodilation ◽  
Cox Inhibitor ◽  
Young Smokers ◽  
Synthase Inhibitor

Cigarette smoking attenuates acetylcholine (ACh)-induced cutaneous vasodilation in humans, but the underlying mechanisms are unknown. We tested the hypothesis that smokers have impaired nitric oxide (NO)- and cyclooxygenase (COX)-dependent cutaneous vasodilation to ACh infusion. Twelve young smokers, who have smoked more than 5.2 ± 0.7 yr with an average daily consumption of 11.4 ± 1.2 cigarettes, and 12 nonsmokers were tested. Age, body mass index, and resting mean arterial pressure were similar between the groups. Cutaneous vascular conductance (CVC) was evaluated as laser-Doppler flux divided by mean arterial pressure, normalized to maximal CVC (local heating to 43.0°C plus sodium nitroprusside administration). We evaluated the increase in CVC from baseline to peak (CVCΔpeak) and area under the curve of CVC (CVCAUC) during a bolus infusion (1 min) of 137.5 μM ACh at four intradermal microdialysis sites: 1) Ringer (control), 2) 10 mM NG-nitro-l-arginine methyl ester (l-NAME; NO synthase inhibitor), 3) 10 mM ketorolac (COX inhibitor), and 4) combination of l-NAME + ketorolac. CVCΔpeakand CVCAUCat the Ringer site in nonsmokers were greater than in smokers (CVCΔpeak, 42.9 ± 5.1 vs. 22.3 ± 3.5%max, P < 0.05; and CVCAUC, 8,085 ± 1,055 vs. 3,145 ± 539%max·s, P < 0.05). In nonsmokers, CVCΔpeakand CVCAUCat the l-NAME site were lower than the Ringer site (CVCΔpeak, 29.5 ± 6.2%max, P < 0.05; and CVCAUC, 5,377 ± 1,109%max·s, P < 0.05), but in smokers, there were no differences between the Ringer and l-NAME sites (CVCΔpeak, 16.8 ± 4.3%max, P = 0.11; and CVCAUC, 2,679 ± 785%max·s, P = 0.30). CVCΔpeakand CVCAUCwere reduced with ketorolac in nonsmokers (CVCΔpeak, 13.3 ± 3.6%max, P < 0.05; and CVCAUC, 1,967 ± 527%max·s, P < 0.05) and smokers (CVCΔpeak, 7.8 ± 1.8%max, P < 0.05; and CVCAUC, 1,246 ± 305%max·s, P < 0.05) and at the combination site in nonsmokers (CVCΔpeak, 15.9 ± 3.1%max, P < 0.05; and CVCAUC, 2,660 ± 512%max·s, P < 0.05) and smokers (CVCΔpeak, 11.5 ± 2.6%max, P < 0.05; and CVCAUC, 1,693 ± 409%max·s, P < 0.05), but the magnitudes were greater in nonsmokers ( P < 0.05). These results suggest that impaired ACh-induced skin vasodilation in young smokers is related to diminished NO- and COX-dependent vasodilation.

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