The effect of virus infection on the organism of pregnant mice and their posterity was studied in experiment. The animals were infected with the prototype strain A13 (Flores) of Coxsackie virus which was administered on days 4, 7, 11, 15 and 19 of pregnancy. It has been demonstrated that pregnant mice are much more sensitive to the virus than non-pregnant females and that the placenta, along with the striped muscles, is the main reservoir of the virus. The obtained results also suggest that the virus penetrates into the tissues of the embryo most intensively in the second half of pregnancy and that the duration of manifestation of the virus in the tissues of the embryo depends on the period of intrauterine development. The study of the model system (long-term organ culture of the tissues of the organism) enabled us to establish a new fact of the cytoproliferative activity of A13 Coxsackie virus in the organ culture and in the placenta of mice infected in vivo, and also in the organ culture of the liver of their newborn, which is important for the confirmation of clinical observations presuming a high probability of intrauterine infection by the mentioned virus with its subsequent protracted persistence in the organism of the newborn.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
NAPQI is absent in the mouse brain after Sub-hepatotoxic and hepatotoxic doses of acetaminophen.
Toxicol Sci
March 2025
Summer Research Internship Program, University of Arkansas for Medical Sciences, Little Rock, AR, 72205, USA.
Acetaminophen (APAP) is the most-used over-the-counter analgesic among pregnant women. However, concerns have arisen over the safety of APAP exposure during gestation. In particular, it's been speculated that the hepatotoxic metabolite of APAP, N-acetyl-p-benzoquinone imine (NAPQI), forms in the brain after maternal use of therapeutic APAP doses and leads to neurodevelopmental disorders (NDDs).
View Article and Find Full Text PDFN,N-dimethylacetamide blocks inflammation-induced preterm birth and remediates maternal systemic immune responses.
Sci Rep
March 2025
Longo Center for Perinatal Biology, Loma Linda University School of Medicine, Loma Linda, CA, 92350, USA.
The common excipient, N,N-dimethylacetamide (DMA), prevents imminent endotoxin-induced preterm birth in mice. The present study hypothesized that DMA forestalls preterm birth to term (defined as day 18.5 or later) by attenuating bacterial endotoxin lipopolysaccharide (LPS)-induced maternal systemic inflammatory responses and cervix remodeling.
View Article and Find Full Text PDFThe myometrium plays a critical role during pregnancy as it is responsible for both the structural integrity of the uterus and force generation at term. Emerging studies in mice indicate a dynamic change of the myometrial epigenome and transcriptome during pregnancy to ready the contractile machinery for parturition. However, the regulatory systems underlying myometrial gene expression patterns throughout gestation remain largely unknown.
View Article and Find Full Text PDFThe use of cannabis during pregnancy and nursing is a growing public health concern, and the multigenerational impacts of perinatal cannabis exposure remain largely unknown. To address this knowledge gap, we sought to examine the long-term consequences of perinatal cannabis use on reproductive function and how it might impact subsequent generations. Pregnant female mice were exposed to control vehicle or cannabis extract [25, 100, or 200 mg/ml Δ9-tetrahydrocannabinol (THC) in the cannabis extract] from gestational day 1 to postnatal day 21 (twice/day), encompassing the duration of pregnancy through weaning.
View Article and Find Full Text PDFIL-1β stimulates ADAMTS9 expression and contributes to preterm prelabor rupture of membranes.
Cell Commun Signal
March 2025
Tianjin Key Laboratory of Human Development and Reproductive Regulation, Tianjin Central Hospital of Gynecology Obstetrics, Tianjin, 300100, China.
Background: Preterm prelabor rupture of membranes (pPROM) is a leading cause of neonatal morbidity and mortality. While intra-amniotic infection is a well-established driver of pPROM, the role of sterile intra-amniotic inflammation remains unclear. Recent evidence suggests that interleukin-1 beta (IL-1β) promotes extracellular matrix (ECM) remodeling via downstream effectors, a disintegrin-like and metalloproteinase domain with thrombospondin type 1 motif 9 (ADAMTS9), while protein O-fucosyltransferase 2 (POFUT2) facilitates its O-fucosylation and secretion, amplifying ECM degradation.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!