Obesity is a major, modifiable driver of endometrial carcinogenesis. This review distills how excess adiposity promotes malignant change and synthesizes prevention strategies across the hyperplasia–cancer continuum. Three converging axes underpin risk: aromatase-mediated estrogen excess; insulin resistance with hyperinsulinemia activating PI3K–AKT–mTOR signaling; and adipokine-driven low-grade inflammation with downstream NF-κB/STAT3 activity. Within this framework, EIN is the key precursor in which these pathways coalesce. Risk can be attenuated through progestin-based therapy (levonorgestrel-releasing intrauterine system or continuous oral regimens), structured weight management, and metabolic adjuncts in selected phenotypes (e.g., metformin for insulin resistance; incretin-based anti-obesity agents as emerging options). Bariatric surgery produces substantial weight loss and favorable metabolic shifts, though evidence for cancer risk reduction is largely observational. Overall, a practical precision-prevention approach—combining progestins with durable weight control and metabolic optimization under guideline-concordant surveillance—appears feasible in routine gynecologic care. Future research should establish causal effects, durability, and optimal sequencing/combination of interventions in trials with endometrial endpoints.

Premature rupture of membranes (PROM) and cervical incompetence (CI) are major contributors to preterm birth, a leading cause of neonatal morbidity and mortality. Background/Objectives: Disorders of the vaginal microbiota, such as bacterial vaginosis, have been associated with an increased risk of PROM, CI, and subsequent preterm birth. Probiotics, particularly Lactobacillus strains, have been proposed as a preventive strategy to restore and maintain a healthy vaginal microbiome. This review aims to summarize the latest evidence on the role of probiotics in the prevention of PROM and CI. Methods: A comprehensive review was conducted to evaluate the effectiveness of probiotic interventions in the prevention of PROM and CI, yielding 1809 records from 2005 to 2024. Seven relevant studies were selected by searching medical databases and focusing on studies that investigated the restoration of healthy vaginal flora, the reduction of pathogenic bacteria colonization, and the modulation of immune responses by probiotics. Results: The studies analyzed suggest that probiotics may help restore healthy vaginal flora, reduce pathogenic bacterial colonization, and modulate immune responses, thereby reducing the risk of membrane rupture and cervical insufficiency. Evidence from randomized controlled trials and observational studies shows that the use of probiotics is associated with a lower incidence of PROM and preterm birth, especially in high-risk groups. Conclusions: Probiotics emerge as a potential non-invasive and cost-effective strategy to improve pregnancy outcomes in women at risk of preterm birth due to PROM. According to our research, probiotic prophylaxis of cervical insufficiency has not yet been sufficiently investigated. Despite the promising findings, further research is needed to determine standardized probiotic formulations, optimal timing, and routes of administration. Personalized probiotic therapies may represent the future of preterm birth prevention as they offer targeted interventions based on individual microbiome composition.

(1) Background: The aim of our study was to assess the involvement of the sympathetic nervous system in the progression of patients with gastric carcinoma by analyzing the sympathetic neuronal fibers and beta 2 adrenoreceptors. (2) Methods: We performed a retrospective study in which we analyzed the clinical, biological, and histological data from a total of 104 patients diagnosed with stomach cancer. (3) Results: After analyzing the immunoreactivity of beta 2 adrenoreceptors, we observed increased values in patients with tumors larger than 5 cm in diameter (p = 0.0371), with a deeper degree of tumor invasion T3–4 (p = 0.0159), invasion in more than two lymph nodes (p = 0.0462), or a TNM stage III–IV. Regarding the survival analysis, better survival rates (65%) were observed for patients with a low value of beta 2 adrenoreceptors (B2A−), compared to B2A (+) patients, in which survival at 3 years of follow-up was only 43%. In addition, the analysis of intra-tumoral sympathetic fibers showed a better survival rate (83%) for patients with a low value of density compared to patients with increased density, in whom the survival rate was only 24%. (4) Conclusions: The findings of this study indicate that patients with stomach cancer have a more unfavorable prognosis when they have a higher density of sympathetic nerve fibers and an increased expression of beta 2 adrenergic receptors inside the tumor.

Background/Objectives: Fetal growth restriction (FGR) is one of the main causes of perinatal morbidity and mortality, and in most cases the mechanism is placental dysfunction of vascular origin. Hereditary thrombophilias have been evaluated as factors that favor maternal vascular malperfusion, but the data in the literature remain contradictory. The objective of the study was to evaluate the association between the PAI-1 4G/5G, MTHFR C677T and factor V Leiden G1691A polymorphisms and fetal growth restriction, as well as to analyze the dose–effect relationship between the number of thrombophilic variants and the severity of restriction. Methods: This was a retrospective case–control study including 480 singleton pregnancies: 240 cases with fetal growth restriction and 240 pregnant women with eutrophic fetuses, followed up for a period of five years. Cases were defined biometrically as an estimated fetal weight below the 10th centile, without Doppler confirmation, and the phenotype therefore corresponds to small-for-gestational-age rather than to the full consensus definition of fetal growth restriction; a secondary analysis restricted to cases below the 5th centile, performed in response to review, is reported. Maternal characteristics, genotypes, perinatal outcomes, and cumulative pattern of thrombophilic variants were analyzed. Results: PAI-1 4G allele carriers were significantly more frequent in the growth restriction group compared to the control group (70.8% vs. 44.6%; OR 3.02; 95% CI 2.07–4.40; p < 0.001), as were MTHFR C677T allele carriers (57.1% vs. 39.2%; OR 2.07; 95% CI 1.44–2.97; p < 0.001) and factor V Leiden carriers (33.3% vs. 12.1%; OR 3.64; 95% CI 2.27–5.83; p < 0.001). Carrier prevalence increased progressively with severity of restriction for the PAI-1 4G allele and, most steeply, for factor V Leiden (from 12.1% in controls to 75.0% below the 3rd centile; trend test p < 0.001); for the MTHFR 677T allele the increase was confined in the two case strata above the 3rd centile, and the estimate in the smallest subgroup was uninformative. The risk of growth restriction increased with the number of coexisting thrombophilic variants: OR 2.12 (95% CI 1.24–3.64) for one variant, OR 5.60 (95% CI 3.21–9.78) for two, and OR 24.42 (95% CI 7.87–75.78) for all three, compared with the absence of any variant. In multivariable analysis, the three polymorphisms remained independent predictors, with the strongest adjusted association being that of factor V Leiden (adjusted OR 3.33; 95% CI 2.03–5.47). Carriage of each variant was associated with a lower birth-weight centile: −12.3 points for PAI-1 4G, −10.2 for factor V Leiden and −8.0 for MTHFR C677T (all p < 0.001). Conclusions: In this study, PAI-1 4G/5G, MTHFR C677T, and factor V Leiden polymorphisms were independently associated with fetal growth restriction. The results are compatible with a contribution of hypofibrinolysis and inherited thrombophilia to the placental insufficiency phenotype, most clearly in the more severe strata, but they are associative and require confirmation in prospective cohorts incorporating Doppler assessment and placental histopathology.