Publications by authors named "Christopher L Dixon"

Objective: This study determined the cord plasma-derived extracellular vesicle (exosomes; 30-160 nm particles) proteomic profile in patients who had spontaneous preterm birth (PTB) or preterm premature rupture of membranes (pPROM), compared to those who delivered at term regardless of labor status.

Methods: This is a cross-sectional analysis of a retrospective cohort that quantified and determined the proteomic cargo content of exosomes present in cord blood plasma samples in PTB or pPROM, and normal term in labor (TL) or term not in labor (TNIL) pregnancies. Exosomes were isolated by differential centrifugation followed by size exclusion chromatography.

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Problem: Fetal inflammatory signals can be propagated to maternal tissues to initiate labor via exosomes (extracellular vesicles; 30-150 nm). We tested the hypothesis that fetal membrane cells exposed to infectious and inflammatory mediators associated with preterm birth (PTB) produce exosomes with distinct protein cargo contents indicative of underlying pathobiology.

Methods Of Study: Fetal membrane explants (FM) as well as primary amnion epithelial (AEC) and mesenchymal cells (AMC), and chorion cells (CC) from term deliveries were maintained in normal conditions (control) or exposed to LPS 100 ng/mL or TNF-α 50 ng/mL for 48 hours.

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Exosomes are membrane-bound nanovesicles that transport molecular signals between cells. This study determined changes in maternal plasma exosome proteomics contents in term and preterm births. Maternal plasma (MP) samples were collected from group 1: term not in labor (TNIL, n = 13); group 2: term in labor (TL, n = 11); group 3: preterm premature rupture of membranes (pPROM, n = 8); and group 4: preterm birth (PTB, n = 13).

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Article Synopsis
  • - Oxidative stress (OS) during term and preterm birth activates a specific pathway in fetal tissue that leads to cell aging, mediated by the p38 MAPK enzyme.
  • - The study examined how cigarette smoke extract triggers two pathways of p38 MAPK activation in amnion epithelial cells, one involving the dissociation of a protein complex and another through TGF-beta signaling.
  • - Results show that TGF-beta signaling and the protein TAB1 are crucial for the p38 MAPK activation, while ASK1 does not directly influence this process, providing insights for potential strategies to mitigate pregnancy-related risks.
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Parturition is defined as the action or process of giving birth to offspring. Normal term human parturition ensues following the maturation of fetal organ systems typically between 37 and 40 weeks of gestation. Our conventional understanding of how parturition initiation is signaled revolves around feto-maternal immune and endocrine changes occurring in the intrauterine cavity.

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Problem: We investigated p38MAPK activation-induced fetal membrane cell senescence in response to inflammation (tumour necrosis factor-alpha [TNF-α]) and infection (lipopolysaccharide [LPS]), factors associated with spontaneous preterm birth.

Method Of Study: Primary amnion epithelial cells (AECs) were exposed to TNF-α, 50 ng/mL and LPS, 100 ng/mL. Cigarette smoke extract (CSE), a known OS inducer, was used as positive control.

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Objective: To evaluate the effect of a "hard stop" on elective induction prior to 39 weeks at a large volume obstetrics hospital.

Study Design: From July 1, 2011, to June 30, 2013, there were 27,435 deliveries at our institution. We performed a retrospective chart review of all elective inductions I year before and after the implementation of a 39 week "hard stop" .

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