Maternal nutrition and gut microbiome composition are central regulators of fetal development and perinatal outcomes, modulating immune signaling, oxidative balance, and epigenetic programming. The authors searched PubMed, Scopus, the Cochrane Library, and Web of Science for full-text, peer-reviewed articles published in English between 2010 and 2025, using keywords relevant to maternal diet, gut microbiome, epigenetic modifications, oxidative stress, reactive oxygen species (ROS), short-chain fatty acids (SCFAs), placental function, and perinatal outcomes. Selected studies provided detailed insights into how maternal dietary patterns and microbiome-derived metabolites influence placental function, fetal growth, and neonatal health. Integration of the microbiome, epigenetics, and nutritional factors reveals key molecular and metabolic networks that shape perinatal health. Targeted modulation of these networks provides a foundation for personalized strategies to improve neonatal outcomes.

Objectives: To compare pregnancy prolongation and neonatal outcomes in women with signs of threatened preterm birth (PTB) and intact membranes by administration of low-doses of prednisone for 3 weeks compared to women who received standard protocols of tocolysis and respiratory distress syndrome (RDS) prophylaxis in a pilot randomized controlled trial. Methods: We randomized 26 women with signs of threatened PTB and intact membranes between 24 and 34 weeks of gestation to either continued prednisone administration for 3 weeks following the initiation of the standard protocol (intervention group) or standard therapy for threatened PTB (control group). The primary outcome was the gestational length in women with and without using low-doses of prednisone. The secondary outcome included incidence of RDS, intraventricular hemorrhage, necrotizing enterocolitis, the need for mechanical ventilation, and perinatal mortality in newborns from both study groups. Results: Participants in the intervention group had significantly longer pregnancy prolongation than the control group (65.38 vs. 40.54 days, p=0.001). Although the difference was not statistically significant (p=0.153), the gestational age at delivery in the intervention group (38.35 weeks) was 10 days longer than in the control group (36.89 weeks). There were no significant differences between the groups in neonatal outcomes. Conclusions: The first pilot randomized controlled study on low-dose prednisone in threatened PTB and intact membranes suggests it may prolong pregnancy without adverse neonatal outcomes. Due to the small sample size and single-centre design, these preliminary findings should be interpreted with caution and confirmed in larger, adequately powered trials.

Parental microbiome composition and nutritional and metabolic status have been studied in relation to in vitro fertilization (IVF), but their contribution to recurrent implantation failure (RIF) remains uncertain. This narrative review examines maternal and paternal microbial profiles, nutrition, inflammation, oxidative stress, and epigenetic regulation, distinguishing human observational and interventional findings from animal experiments, in vitro studies, and proposed mechanisms. The literature search was conducted in PubMed/MEDLINE, Scopus, and Web of Science, covering publications from 2000 to 2026. Search concepts included “in vitro fertilization”, “recurrent implantation failure”, “reproductive tract microbiota”, “gut microbiome”, “parental nutrition”, “oxidative stress”, and “sperm epigenetics”. Associations between reproductive-tract microbial profiles and pregnancy outcomes vary across populations and analytical methods. Endometrial findings require particular caution because low microbial biomass increases susceptibility to contamination. Evidence linking parental gut microbiota to epigenetic programming of human preimplantation embryos remains indirect, and paternal gut–testis mechanisms are supported predominantly by experimental research. Randomized probiotic studies have produced inconsistent results and have not established a reproducible improvement in implantation or live birth across IVF populations. Nutritional adequacy and management of relevant metabolic disorders belong within established preconception care, whereas microbiome testing, targeted microbial manipulation, and proposed epigenetic interventions remain investigational for RIF. The available evidence supports further study of these relationships but does not establish parental dysbiosis as a cause of RIF or demonstrate that microbiome modification prevents implantation failure.

Correction: Immunohistochemical expression and predictive value of PAX3 and FOXO1 proteins in high-grade serous ovarian carcinoma. Dejan Tirić,Dragan Soldo,Vajdana Tomić,Nikolina Penava,Kristina…

Laboratory diagnostics of iron homeostasis during pregnancy typically rely on routine parameters, which often inadequately reflect the actual maternal iron status. This study aimed to evaluate the investigative and diagnostic utility of soluble transferrin receptor (sTfR) and ferroportin (Fpn) concentrations as key indicators of iron dysregulation in women with normal early pregnancy and those experiencing missed abortion. These primary biomarkers were assessed in conjunction with standard laboratory parameters of iron status across the study groups. Notably, Fpn concentration had not previously been determined in women with either normal or abnormal pregnancies. The study enrolled 45 women with missed abortion and 45 women with normal first-trimester pregnancies. Peripheral blood concentrations of iron (Fe), unsaturated iron-binding capacity (UIBC), ferritin, hemoglobin (Hb), transferrin, and sTfR were measured using automated analyzers, while hepcidin and Fpn were quantified using ELISA kits. Transferrin saturation (TSAT), the sTfR/log ferritin index (sTfR-F index), and the ferroportin to soluble transferrin receptor ratio (Fpn/sTfR) were calculated. In the missed abortion group, Fpn (p < 0.001), Fe (p = 0.008), TSAT (p = 0.018), and Fpn/sTfR (p < 0.001) were significantly decreased, whereas sTfR (p = 0.001) and the sTfR-F index (p = 0.003) were significantly increased compared to women with normal pregnancies. Proposed multiparameter models incorporating sTfR and Fpn, or sTfR, hepcidin, and Fpn, accurately classified over 80% of cases and demonstrated excellent area under the curve (AUC) values of approximately 0.9. These findings indicate that Fpn and sTfR may serve as valuable investigative biomarkers for identifying dysregulation of iron homeostasis in early pregnancy.

In vitro fertilization (IVF) often requires multiple cycles before successful implantation and live birth are achieved. Although embryo quality and technical factors have traditionally been emphasized, emerging evidence suggests that parental microbiome composition and nutritional status are important, but under-recognized, determinants of reproductive success. Dysbiosis of the vaginal and endometrial microbiota in women is associated with reduced implantation rates, chronic low-grade inflammation, and altered endometrial receptivity, while maternal gut microbiota imbalance may contribute to systemic metabolic inflammation, oxidative stress, and epigenetic modifications affecting early embryonic development. Paternal factors are increasingly rec-ognized as equally important, as altered gut microbiota, obesity, insulin resistance, and micronu-trient deficiencies may affect sperm DNA integrity, methylation patterns, and small noncoding RNA profiles, potentially influencing embryonic developmental programming. This review aims to evaluate the interconnected mechanisms linking parental microbiome composition, nutritional and metabolic status, inflammation, oxidative stress, and epigenetic regulation with assisted reproduction and recurrent IVF failure. A comprehensive literature search was performed using PubMed/MEDLINE, Scopus, and Web of Science, covering the period from 2000 to 2025, with predefined keywords and Medical Subject Headings related to in vitro fertilization, recurrent implantation failure, maternal gut microbiome, reproductive tract dysbiosis, paternal gut-testis axis, oxidative stress, sperm epigenetics, DNA methylation, short-chain fatty acids, and preconception nutritional optimization. We considered peer-reviewed articles published in English, including original research, meta-analyses, and high-impact reviews providing mechanistic and translational insights. The evidence indicates that parental dysbiosis and nutritional and metabolic im-balances may converge on inflammatory, oxidative, mitochondrial, and epigenetic pathways, creating a biological environment that compromises implantation and may influence early em-bryonic programming. Importantly, these potentially modifiable factors support preconception microbiome modulation, nutritional optimization, and metabolic conditioning for both partners before IVF. In conclusion, an integrated preconception approach addressing parental microbiome, nutritional, metabolic, inflammatory, and epigenetic factors may represent a promising strategy for improving reproductive outcomes and potentially supporting the long-term health of the offspring.