OBJECTIVE: Rates of maternal morbidity in the US are accelerating partly due to increasing comorbidities among pregnant women. Proposals to adopt levels of maternal care (LOMC), similar to neonatal care, would direct patients to riskappropriate care earlier in pregnancy, theoretically reducing maternal transports, optimizing resources, and improving outcomes. The objective of this study is to describe characteristics and indications for maternal transport by LOMC within a state transport system. STUDY DESIGN: This is a retrospective cohort study of all maternal transports from Sept '15 e Jun '19 to Johns Hopkins Hospital (JHH, one of two Level IV centers within Maryland) or JH Bayview (JHB, Level III). Data were extracted from transport logs and electronic medical records; transports for neonatal indication were excluded. Continuous variables were compared using ANOVA, categorical variables using Chi-square, and a p-value < 0.05 used for statistical significance. RESULTS: 652 transports for maternal indication were recorded. Transport indication varied significantly by LOMC (P< 0.001): hospitals with 'no L&D' most commonly transported for
Individually prescribed exercise according to guidelines for pregnant women does not adversely alter uterine artery Doppler values, suggesting that uterine blood flow is not reduced as a result of exercise.
to placentation at embryonic day (E) 7.5 and in placenta at E10.5. We used quantitative (q) RT-PCR to assess mRNA expression of the following genes: complement 1 (C1); complement 3 (C3), the common point of the complement pathway; Ptgs, marker of decidualization; Flt-1 and sFlt-1, angiogenic genes altered in PE. To assess C3 deposition, we performed immunofluorescence (IF) on frozen sections (4 independent samples) with antibodies against C3. To quantify C3 deposition, corrected total cell fluorescence (CTCF) was measured using Image J software. RESULTS: At E7.5, increased Ptgs expression in BPH/5 mice is consistent with abnormal decidualization (Figure 1). Similarly, C3 expression and deposition at the mesometrial pole where the placenta develops were increased in BPH/5 mice at E7.5 (Figures 1 and 2). Mean C3 CTCF in decidual vasculature was significantly higher in BPH/5 mice compared to controls (27.09 v. 4.97, P< 0.05). In the placenta at E10.5, C3 expression was significantly increased in BPH/5 mice. Placental expression of sFlt-1 was also significantly increased, suggestive of abnormal placental angiogenesis seen in PE (Figure 1). CONCLUSION: In BPH/5 mice, C3 expression and deposition are increased at the MF interface in the uterus pre-placentation and in the placenta. These findings early in gestation implicate abnormal complement activation in the pathogenesis of PE.
Amlodipine does cross the placenta in measurable quantities, but is not detected in breast milk or infant plasma at 24-48 h of life indicating that it is likely safe to use during the peripartum period.
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