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In growth restricted fetuses before 34 weeks of gestation, absent or reversed end-diastolic velocity of the umbilical artery (AREDV) increases the odds for fetal death. AREDV is associated with increased placental resistance to blood flow resulting in an increased fetal cardiac afterload with fetal and neonatal consequences.
Fetal death diagnosed after 20 weeks of gestation accounts for more than half of annual infant deaths in the U.S. Since birthweight has been considered a surrogate of fetal growth, and a small for gestational age neonate is associated with fetal death, fetal growth restriction is frequently cited as a precedent of antepartum stillbirth.
The majority of preterm births have no clear risk factor. Intense effort has been directed to the discovery of biomarkers that can identify subclinical pathological changes before symptoms and signs of a specific obstetrical syndrome appear.
Coronavirus disease 2019 (COVID-19) is an illness caused by a novel coronavirus, now called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Such virus canonically utilizes the angiotensin-converting enzyme 2 (ACE2) receptor and the serine protease TMPRSS2 for cell entry.
Researchers at the Wayne State University School of Medicine and the Perinatology Research Branch of National Institute of Child Health and Human Development/National Institutes of Health in Detroit have found that placental cells minimally express the instructions, or mRNA, to generate the cell entry receptor and protease required by the virus that causes COVID-19 to invade human cells.