Polymorphonuclear Leukocytes in the Fetal Membranes are Activated in Patients with Preterm Delivery: Ultrastructural and Enzyme-histochemical Evidence

Placenta ◽  
1999 ◽  
Vol 20 (2-3) ◽  
pp. 185-188 ◽  
Author(s):  
S. Matsubara ◽  
T. Yamada ◽  
H. Minakami ◽  
T. Watanabe ◽  
T. Takizawa ◽  
...  
Keyword(s):  
Preterm Delivery ◽  
Polymorphonuclear Leukocytes ◽  
Fetal Membranes ◽  
Histochemical Evidence

The Role of Calcium, Copper, Iron and Zinc in Preterm Delivery and Premature Rupture of Fetal Membranes

1984 ◽  
Vol 17 (4) ◽  
pp. 194-201 ◽  
Author(s):  
P. Kiilholma ◽  
M. Grönroos ◽  
R. Erkkola ◽  
P. Pakarinen ◽  
V. Näntö
Keyword(s):  
Preterm Delivery ◽  
Fetal Membranes ◽  
Premature Rupture ◽  
Iron And Zinc

The Role of Calcium, Copper, Iron and Zinc in Preterm Delivery and Premature Rupture of Fetal Membranes

1984 ◽  
Vol 39 (11) ◽  
pp. 679
Author(s):  
P. KIILHOLMA ◽  
M. GRÖNROOS ◽  
R. ERKKOLA ◽  
P. PAKARINEN ◽  
V. NÄNTÖ
Keyword(s):  
Preterm Delivery ◽  
Fetal Membranes ◽  
Premature Rupture ◽  
Iron And Zinc

scholarly journals Candidate Gene and MicroRNA Expression in Fetal Membranes and Preterm Delivery Risk

2015 ◽  
Vol 23 (6) ◽  
pp. 731-737 ◽  
Author(s):  
Daniel A. Enquobahrie ◽  
Mark Hensley ◽  
Chunfang Qiu ◽  
Dejene F. Abetew ◽  
Karin Hevner ◽  
...  
Keyword(s):  
Candidate Gene ◽  
Preterm Delivery ◽  
Microrna Expression ◽  
Fetal Membranes

Morphological features of the state of fetoplacental complex in women with early preterm birth after assisted reproductive technologies

2016 ◽  
pp. 79-81
Author(s):  
A.S. Mandrykova ◽  
Keyword(s):  
Preterm Birth ◽  
Preterm Delivery ◽  
Assisted Reproductive Technologies ◽  
Reproductive Technologies ◽  
Main Group ◽  
Fetal Membranes ◽  
Control Group ◽  
Premature Rupture ◽  
Fetoplacental Complex ◽  
Early Preterm Birth

The objective: the study of morphofunctional changes of the fetoplacental complex at 28–33 weeks of gestation in women with early preterm delivery after the application of ART. Patients and methods. We have examined 130 patients whose pregnancy occurred after the use of ART. This is the woman who gave birth at 28–33 weeks of gestation. Of these, 80 women had early premature births in the background premature rupture of fetal membranes, 50 – patients with early preterm delivery and timely rupture of fetal membranes (control group 2). The main group included 4 groups of 20 women with regard to the duration of anhydrous interval: 1.1 – anhydrous interval 5–6 hours (main group 1); 1.2 – anhydrous span 24 hours; 1.3 – anhydrous interval 45–48 hours; 1.4 – anhydrous period 5 days after PRFM. Results. Thus, the results of the research indicate that the main cause of early preterm birth in women after using ART are structural dezorhanization changes of collagen fibers of the connective tissue amnion and chorionic which lead to the appearance of microscopic defects – delamination its surface, causing premature rupture of fetal membranes the launch stage localized focal immediate type hypersensitivity reactions and restructuring epithelial cell membranes. Neutrophil macrophage properties in this case reduced and programmed to perform a cycle of incomplete phagocytosis, which increases the synthesis of inflammatory cytokines in the area of rupture of fetal membranes. Сonclusion. Reduced activity of neutrophils increases the effect of abuse and cytokine balance in favor predictor of early spontaneous labor at 28-33 weeks of gestation. Key words: morphological changes of the fetoplacental complex, early preterm birth, expectant tactics of childbirth.

Immunoreactive 15-hydroxyprostaglandin dehydrogenase (PGDH) is reduced in fetal membranes from patients at preterm delivery in the presence of infection

Placenta ◽  
1996 ◽  
Vol 17 (5-6) ◽  
pp. 291-297 ◽  
Author(s):  
C.A. Van Meir ◽  
R.K. Sangha ◽  
J.C. Walton ◽  
S.G. Matthews ◽  
M.J.N.C. Keirse ◽  
...  
Keyword(s):  
Preterm Delivery ◽  
Fetal Membranes

scholarly journals Prokineticin 1 induces a pro-inflammatory response in murine fetal membranes but does not induce preterm delivery

Reproduction ◽  
2013 ◽  
Vol 146 (6) ◽  
pp. 581-591 ◽  
Author(s):  
Tamsin R M Lannagan ◽  
Martin R Wilson ◽  
Fiona Denison ◽  
Jane E Norman ◽  
Rob D Catalano ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Mrna Expression ◽  
Preterm Delivery ◽  
Inflammatory Responses ◽  
G Protein Coupled Receptors ◽  
Fetal Membrane ◽  
Fetal Membranes ◽  
Term Labour ◽  
G Protein Coupled

The mechanisms that regulate the induction of term or preterm delivery (PTD) are not fully understood. Infection is known to play a role in the induction of pro-inflammatory cascades in uteroplacental tissues associated with preterm pathological parturition. Similar but not identical cascades are evident in term labour. In the current study, we used a mouse model to evaluate the role of prokineticins in term and preterm parturition. Prokineticins are multi-functioning secreted proteins that signal through G-protein-coupled receptors to induce gene expression, including genes important in inflammatory responses. Expression of prokineticins (Prok1andProk2) was quantified in murine uteroplacental tissues by QPCR in the days preceding labour (days 16–19).Prok1mRNA expression increased significantly on D18 in fetal membranes (compared with D16) but not in uterus or placenta. Intrauterine injection of PROK1 on D17 induced fetal membrane mRNA expression of the pro-inflammatory mediatorsIl6,Il1b,Tnf,Cxcl2andCxcl5, which are not normally up-regulated until D19 of pregnancy. However, intrauterine injection of PROK1 did not result in PTD. As expected, injection of lipopolysaccharide (LPS) induced PTD, but this was not associated with changes in expression ofProk1or its receptor (Prokr1) in fetal membranes. These results suggest that althoughProk1exhibits dynamic mRNA regulation in fetal membranes preceding labour and induces a pro-inflammatory response when injected into the uterus on D17, it is insufficient to induce PTD. Additionally, prokineticin up-regulation appears not to be part of the LPS-induced inflammatory response in mouse fetal membranes.

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