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Cesarean delivery is an abdominal surgical procedure performed for child delivery when the vaginal route is not feasible or desired due to maternal/fetal indications. All childbirth facilities should be able to safely perform a cesarean, which is not the current reality. For planned cesarean delivery, the facility must be prepared for the patient. In contrast, for unplanned arrivals at the facility, FIGO's Prep‐for‐Labor triage method allows rapid decision‐making on whether cesarean delivery can be safely performed on site or whether transfer to an advanced care center is needed. A checklist of staff/tools for safe on‐site cesarean delivery is provided to enable timely decision‐making. Maternal complications following cesarean are three‐fold higher than vaginal delivery. To prevent nonmedically indicated cesarean by favoring vaginal delivery, up‐to‐date safe and effective guidance is provided, defining labor, second stage length, and status before an arrested labor is confirmed. Whether cesarean delivery is planned or emergency, the Misgav Ladach simplified procedure is proposed as it is suitable for both low‐ and high‐risk cases, including twins, thereby reducing both operative morbidity and postoperative recovery. A trial of labor after first cesarean (TOLAC) should be pursued when feasible, for which the indications, contraindications, safeguards, and steps of safe labor induction are delineated. Implementation of these good practice recommendations will improve childbirth by reducing excessive nonindicated cesareans, while precisely defining the resources and postoperative care required for safe performance on site. Enabling safe childbirth by cesarean and TOLAC, even at sites with low rates currently, will significantly improve maternal and fetal outcomes. Synopsis: Cesarean delivery rates remain high. FIGO's Prep‐for Labor triage method defines site suitability, staff/tools, indications, methods, and how to minimize risks. Redefining labor arrest and trial of labor after cesarean reduces rates. [ABSTRACT FROM AUTHOR]

Childbirth is an intense event in which decisions may need to be made in seconds to guarantee the health of both mother and newborn. Despite health systems and care approaches varying widely according to real-life scenarios, availability of facilities, beliefs, resources, staff, and geography, among others, optimal outcomes should be ensured worldwide. Triaging low-risk pregnancies from high-risk pregnancies is the first step to ensure proper allocation of resources. From this need, we developed FIGO's Prep-For-Labor triage methods, a series of 2-minute labor and delivery bundles of care, with special regard given to low-and middle-income countries and rural settings. Around 80% of women, once properly triaged, can pursue vaginal delivery with minimal intervention, while those at risk can either be managed on site or transferred promptly to an advanced care site. FIGO's bundles of care and good practice recommendations for labor and delivery and immediate newborn triage cover four clinical scenarios: (1) preterm labor; (2) induced or spontaneous labor at term; (3) cesarean delivery; and (4) newborn care. From rapid triage of the mother (low vs high risk) to the list of required equipment, description of skilled staff, and coordination of resources, the recommendations for care are introduced across these four areas in this overview article. Implementing the proposed management steps described in each summary can improve maternal and neonatal outcomes. [ABSTRACT FROM AUTHOR]

Prenatal infections that have been exhaustively studied help frame the current Severe Acute Respiratory Syndrome related coronavirus-2 (SARS-CoV-2) pandemic, with the caveat that asymptomatic SARS-CoV-2 infected patients are not tested, while those symptomatic are delivered and/or treated with drug(s) available on-site. Thus, management and therapy are still heterogeneous. SARSCoV-2 induced respiratory infection remains mostly local, unless severe, which lessens transplacental vertical transmission (VT). Vaccination prior to or during pregnancy significantly changes the prognosis for both the mother and newborn. The virus spread to the fetus can be binding to ACE2 and TMPRSS2 protein receptors. A recent study demonstrated ACE2 and TMPRSS2 fetal expression in the intestine from the second trimester. Most placental infections are subclinical unless severe villitis and apoptosis are observed. The placenta is rarely tested, and it is highly probable that most are positive for the virus, requiring sophisticated diagnostics to document. Other VT modalities, such as vaginal, rectal or through amniotic fluid contamination, are very rare. Therefore, vaginal delivery is preferable when clinically feasible. It has not yet been determined whether the placenta is a shield or if it transmits infection, while, on the other hand, recent data support fetal resilience, which is plausible due to themajor difference between the placental and fetal rates of infection: only 3%-5% of documentable VT compared with up to 100% expected placental exposure to viremia. Newborn Polymerase Chain Reaction (PCR) from nasal swab is more practical as an option for VT diagnosis compared to ocular or anal swab, with low yield. The maternal infection leads to antiviral IgG production of 100% in severe cases, which is transferred to the fetus and breast milk. Postpartum-documenting VT is difficult since horizontal viral transmission may be common and minimized by mother/staff/family-preventive measures. Breastfeeding is safe and encouraged because, beyond nutrition, it promotes protective antibody transfer and maternal bonding. Lessons learned from other Betacorona viruses (SARS-CoV and Middle East Respiratory Syndrome related coronavirus [MERS-CoV]) virulence are relevant since mutations can increase or decrease vulnerability. Overall, data support fetal/newborn resilience against SARS-CoV-2 VT. However, viremia monitoring by sensitive tests and assessment for delayed sequelae shown in adults is necessary. [ABSTRACT FROM AUTHOR]

Aims Neutrophil trafficking within the vasculature strongly relies on intracellular calcium signalling. Sustained Ca2+ influx into the cell requires a compensatory efflux of potassium to maintain membrane potential. Here, we aimed to investigate whether the voltage-gated potassium channel KV1.3 regulates neutrophil function during the acute inflammatory process by affecting sustained Ca2+ signalling. Methods and results Using in vitro assays and electrophysiological techniques, we show that KV1.3 is functionally expressed in human neutrophils regulating sustained store-operated Ca2+ entry through membrane potential stabilizing K+ efflux. Inhibition of KV1.3 on neutrophils by the specific inhibitor 5-(4-Phenoxybutoxy)psoralen (PAP-1) impaired intracellular Ca2+ signalling, thereby preventing cellular spreading, adhesion strengthening, and appropriate crawling under flow conditions in vitro. Using intravital microscopy, we show that pharmacological blockade or genetic deletion of KV1.3 in mice decreased neutrophil adhesion in a blood flow dependent fashion in inflamed cremaster muscle venules. Furthermore, we identified KV1.3 as a critical component for neutrophil extravasation into the inflamed peritoneal cavity. Finally, we also revealed impaired phagocytosis of Escherichia coli particles by neutrophils in the absence of KV1.3. Conclusion We show that the voltage-gated potassium channel KV1.3 is critical for Ca2+ signalling and neutrophil trafficking during acute inflammatory processes. Our findings do not only provide evidence for a role of KV1.3 for sustained calcium signalling in neutrophils affecting key functions of these cells, they also open up new therapeutic approaches to treat inflammatory disorders characterized by overwhelming neutrophil infiltration. [ABSTRACT FROM AUTHOR]

Abstract Background Viable embryos secrete preimplantation factor (PIF), a peptide that has autocrine effects where levels correlate with cultured embryos development. sPIF (PIF synthetic analog) promotes implantation by regulating decidual-cells immunity, adhesion, apoptosis and enhances trophoblastic cell invasion. Herein sPIF priming effects on non-decidualized endometrium and decidualized-stroma are investigated, assessing elements critical for effective embryo-maternal cross-talk, prior to and at implantation. Methods We tested sPIF effect on human non-pregnant endometrial epithelial and non-decidualized stroma α2β3 integrin expression (IHC and flow cytometry), comparing with scrambled PIF (PIFscr-control). We examined sPIF effect on decidualized non-pregnant human endometrial stromal cells (HESC) determining pro-inflammatory mediators expression and secretion (ELISA) and growth factors (GFs) expression (Affymetrix global gene array). We tested sPIF effect on HESC Phospho-kinases (BioPlex) and isolated kinases activity (FastKinase). Results sPIF up-regulates α2β3 integrin expression in epithelial cells, (P Conclusions sPIF post-fertilization primes endometrial-epithelium, while during implantation creates a beneficial pro-inflammatory milieu. PIF acts by balancing decidual pro-implantation properties while controlling excessive pro-proliferative and inflammatory signals expression. Overall, PIF influences critical peri-implantation events in a sequential coordinated fashion which facilitates embryo implantation.

Abstract Background PreImplantation Factor (PIF), a novel peptide secreted by viable embryos is essential for pregnancy: PIF modulates local immunity, promotes decidual pro-adhesion molecules and enhances trophoblast invasion. To determine the role of PIF in post-fertilization embryo development, we measured the peptide's concentration in the culture medium and tested endogenous PIF's potential trophic effects and direct interaction with the embryo. Methods Determine PIF levels in culture medium of multiple mouse and single bovine embryos cultured up to the blastocyst stage using PIF-ELISA. Examine the inhibitory effects of anti-PIF-monoclonal antibody (mAb) added to medium on cultured mouse embryos development. Test FITC-PIF uptake by cultured bovine blastocysts using fluorescent microscopy. Results PIF levels in mouse embryo culture medium significantly increased from the morula to the blastocyst stage (ANOVA, P = 0.01). In contrast, atretic embryos medium was similar to the medium only control. Detectable - though low - PIF levels were secreted already by 2-cell stage mouse embryos. In single bovine IVF-derived embryos, PIF levels in medium at day 3 of culture were higher than non-cleaving embryos (control) (P = 0.01) and at day 7 were higher than day 3 (P = 0.03). In non-cleaving embryos culture medium was similar to medium alone (control). Anti-PIF-mAb added to mouse embryo cultures lowered blastocyst formation rate 3-fold in a dose-dependent manner (2-way contingency table, multiple groups, X2; P = 0.01) as compared with non-specific mouse mAb, and medium alone, control. FITC-PIF was taken-up by cultured bovine blastocysts, but not by scrambled FITC-PIF (control). Conclusions PIF is an early embryo viability marker that has a direct supportive role on embryo development in culture. PIF-ELISA use to assess IVF embryo quality prior to transfer is warranted. Overall, our data supports PIF's endogenous self sustaining role in embryo development and the utility of PIF- ELISA to detect viable embryos in a non-invasive manner.

Worldwide, health systems and care approaches vary widely due to local reality, distance to facilities, cultural norms, resources, staff availability, geography, and politics. Consequently, globally maternal–newborn dyad care and outcomes are highly variable, leading to approximately 800 maternal deaths daily with a 100‐fold difference among high‐ and low‐resource countries. Irrespective of where care is received, maternal safety and wellbeing should be preserved. Despite ongoing efforts, however, this is not the case. Large gaps exist between spending and clinical outcomes. Segmented health care, coupled with poor planning and inadequate resource distribution, results in failure to provide essential life‐saving treatment. The proposed solution is a regional integrated care model from midwife to advanced level III/IV care and the newborn unit, achieved through effective coordination by site, staff, and clinicians. This model has been successfully implemented in high‐ to low‐resource countries in the past 20 years. In the large diverse population of the United States, constructive steps have been implemented to reduce high maternal mortality in black and rural communities. The COVID‐19 pandemic demonstrates the feasibility of rapid resources coordination to provide effective advanced care. The proposed integration of resources will have a major positive impact on the maternal–newborn dyad. Fragmented‐care resource‐independent policies put the maternal–newborn dyad at high risk. Integration of healthcare resources even in low‐income countries can improve global dyad outcomes. [ABSTRACT FROM AUTHOR]

Preterm birth (PTB) is the leading cause of neonatal morbidity and mortality and spontaneous PTB is a major contributor. The preceding inflammation/infection contributes not only to spontaneous PTB but is associated with neonatal morbidities including impaired brain development. Therefore, control of exaggerated immune response during pregnancy is an attractive strategy. A potential candidate is synthetic PreImplantation Factor (sPIF) as sPIF prevents inflammatory induced fetal loss and has neuroprotective properties. Here, we tested maternal sPIF prophylaxis in pregnant mice subjected to a lipopolysaccharides (LPS) insult, which results in PTB. Additionally, we evaluated sPIF effects in placental and microglial cell lines. Maternal sPIF application reduced the LPS induced PTB rate significantly. Consequently, sPIF reduced microglial activation (Iba-1 positive cells) and preserved neuronal migration (Cux-2 positive cells) in fetal brains. In fetal brain lysates sPIF decreased IL-6 and INFγ concentrations. In-vitro, sPIF reduced Iba1 and TNFα expression in microglial cells and reduced the expression of pro-apoptotic (Bad and Bax) and inflammatory (IL-6 and NLRP4) genes in placental cell lines. Together, maternal sPIF prophylaxis prevents PTB in part by controlling exaggerated immune response. Given the sPIF'FDA Fast Track approval in non-pregnant subjects, we envision sPIF therapy in pregnancy. [ABSTRACT FROM AUTHOR]