Letter - Why do the fetal membranes rupture after fetoscopy? – Comments on proposed mechanisms and adding the fetus as a potential culprit

It has never been taken into account that the fetus itself, by being trapped within the iatrogenic openings in the amniotic membrane from a previous intervention, can tear her home to pieces. As early rupture of membranes within hours or days after percutaneous fetoscopic surgery for spina bifida occurs in less than 10% of our cases, I would attribute most ruptures later in gestation to this effect. Fetal fingers and toes fit all too easily and – with advanced gestational age (the mean age of PROM after my approach to fetoscopic spina bifida surgery occurs around 30 weeks of gestation) – the fetus becomes certainly strong enough to achieve this mischievous feat. Supporting this notion of the (trapped) fetus as a potential culprit, many expectant mothers report a period of stronger fetal movements shortly prior to the occurrence of PROM.

Inflammatory changes in the placenta in ischemic-cervical insufficiency

Introduction. The high frequency of inflammatory changin the placenta in isthmic-cervical insufficiency may be primarily associated with an ascending infection as a result of a violation of the barrier function of the cervix, however, premature remodeling of the cervix may also be secondary due to an already existing process. The study of the features of the spread of the infectious process and thnature of the inflammatory reaction in various structures of the placenta and fetal membranes can contribute to the understanding of pathogenetic mechanisms of preterm birth in isthmic-crvical insufficiency. Aim of the study — to evaluate the frequency and structure of inflammatory changes in the placenta in women with isthmic-cervical insufficiency. Materials and methods. A prospective cohort study was conduct, which included 154 pregnant women taken by the continuous sampling method. All patients were divided into two groups: group 1 consisted of 100 pregnant women with isthmic-cervical insufficiency, group 2 — pregnant women without isthmic-cervical insufficiency. All women after childbirth underwent a pathomorphological examination of the afterbirth. Results and discussion. In women with isthmic-cervical insufficiency, inflamatory changes in the placenta were detected in 71% (71) of cases, which was significantly more frequent compared to group 2 — 38.9% (21). Membranitis was significantly more frequent in isthmic-cervical insufficiency, amounting to 16% (16) versus 3.7% (2) comparison group (OR=4.32, 95% СI=1.03-18.09, p=0.023). Chorioamnionitis was 6 times more common in the afterbirth in women of group 1, accounting for 12% (12), versus 1.9% (1) in group 2 (OR=6.48, 95% CI=0.87-48.51, p=0.031). Involvement of the umbilical cord in the inflammatory process occurred only in pregnant women with isthmic-cervical insufficiency: funiculitis was combined with membranitis in 4% (4) of cases (p=0.137), the combination of funiculitis with choriomnionitis was detcted in 7% (7) of women p=0.047). Conclusion. The frequencof detection of inflammatory changes in the placenta in ICN was 71% (71). In the structure of inflammatory changes of the afterbirth in patients with ICN, the defeat of the fetal membranes prevails, which may indicate a predominatly ascending path of infection in this pathology. Damage membranes prevails, which may indicate a predominatly ascending path of infection in this pathology. Damage to the umbilical cord in ICN can occur both wth total inflammation of all structures of the placenta, and directly through the fetal membranes, without involving the chorion in the process.

The Association of Calcium Profiles at Calving with Health and Performance of Holstein Cows and Their Calves

The aim of this study was to assess the association of hypocalcemia at calving with health and performance of Holstein cows and their calves. Data were collected January 1st 2017 to December 31st 2020. A total of 431 lactating Holstein Friesian cows (118 primiparous and 313 multiparous) from a research of hypocalcemia was 2 groups (hypo and non-hypo). The overall prevalence of hypocalcemia was 3.4% for first-lactation cows and 18% for multiparous cows. Lactating dairy cows with hypocalcemia had greater proportion of cows with Retained Fetal Membranes (RFM) metritis and culling within 60 days in milk (DIM), compared with non-hypocalcemia respectively. For the first 2 official milk tests milk yield and components (% fat, % protein on SCC) did not differ between hypo and non-hypo cows. The days in milk at first service, mastitis, dystocia and pregnancy at first service were not different between hypo and non-hypo groups. The proportion of stillbirth, survival at 60 days of age in calves did not differ between calves born from hypo or non-hypo cows. Calves born from Hypo cows had greater incidence of diarrhea (38.3%) than calves born (22.3%) from non-hypo cows. The results of this study show that hypocalcemia in calving has significant health implications for both dams and their calves.

Dysregulated non-coding telomerase RNA component and associated exonuclease XRN1 in leucocytes from women developing preeclampsia-possible link to enhanced senescence

Senescence in placenta/fetal membranes is a normal phenomenon linked to term parturition. However, excessive senescence which may be induced by telomere attrition, has been associated with preeclampsia (PE). We hypothesized that the telomerase complex in peripheral blood mononuclear cells (PBMC) and circulating telomere associated senescence markers would be dysregulated in women with PE. We measured long non-coding (nc) RNA telomerase RNA component (TERC) and RNAs involved in the maturation of TERC in PBMC, and the expression of TERC and 5′–3′ Exoribonuclease 1 (XRN1) in extracellular vesicles at 22–24 weeks, 36–38 weeks and, 5-year follow-up in controls and PE. We also measured telomere length at 22–24 weeks and 5-year follow-up. The circulating senescence markers cathelicidin antimicrobial peptide (CAMP), β-galactosidase, stathmin 1 (STMN1) and chitotriosidase/CHIT1 were measured at 14–16, 22–24, 36–38 weeks and at 5-year follow-up in the STORK study and before delivery and 6 months post-partum in the ACUTE PE study. We found decreased expression of TERC in PBMC early in pregnant women who subsequently developed PE. XRN1 involved in the maturation of TERC was also reduced in pregnancy and 5-year follow-up. Further, we found that the senescence markers CAMP and β-galactosidase were increased in PE pregnancies, and CAMP remained higher at 5-year follow-up. β-galactosidase was associated with atherogenic lipid ratios during pregnancy and at 5-year follow-up, in PE particularly. This study suggests a potential involvement of dysfunctional telomerase biology in the pathophysiology of PE, which is not restricted to the placenta.

Roles of Two Small Leucine-Rich Proteoglycans Decorin and Biglycan in Pregnancy and Pregnancy-Associated Diseases

Two small leucine-rich proteoglycans (SLRP), decorin and biglycan, play important roles in structural–functional integrity of the placenta and fetal membranes, and their alterations can result in several pregnancy-associated diseases. In this review, we briefly discuss normal placental structure and functions, define and classify SLRPs, and then focus on two SLRPs, decorin (DCN) and biglycan (BGN). We discuss the consequences of deletions/mutations of DCN and BGN. We then summarize DCN and BGN expression in the pregnant uterus, myometrium, decidua, placenta, and fetal membranes. Actions of these SLRPs as ligands are then discussed in the context of multiple binding partners in the extracellular matrix and cell surface (receptors), as well as their alterations in pathological pregnancies, such as preeclampsia, fetal growth restriction, and preterm premature rupture of membranes. Lastly, we raise some unanswered questions as food for thought.