Preeclampsia (PE) is a hypertensive disorder that affects 2–8% of pregnancies and is one of the main causes of fetal, neonatal, and maternal mortality and morbidity worldwide. Although PE etiology and pathophysiology remain unknown, there is evidence that the hyperactivation of maternal immunity cells against placental cells triggers trophoblast cell apoptosis and death. It has also been reported that placenta-derived extracellular vesicles (EV) carry Fas ligand (FasL) and Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and trigger apoptosis in Jurkat T cells. This study aimed to quantify and compare FasL and TRAIL expression in EV derived from cultures of placenta explants from women with PE (early versus late) and women with uncomplicated pregnancies. Also, the study assessed EV capacity to induce apoptosis in Jurkat T cells. The authors isolated EV from placenta explant cultures, quantified FasL and TRAIL using ELISA, and analyzed EV apoptosis-inducing capability by flow cytometry. Results showed increased FasL and TRAIL in EV derived from placenta of women with PE, and increased EV apoptosis-inducing capability in Jurkat T cells. These results offer supporting evidence that EV FasL and TRAIL play a role in the pathophysiology of PE.

In Latin America and the Caribbean, hypertensive pregnancy disorders are responsible for almost 26% of all maternal deaths [1] and, in Colombia, they account for 59% of all severe maternal morbidity (SMM) cases, and 59.7% of all SMM cases in adolescents [2]. One of the most important hypertensive pregnancy disorders is preeclampsia (PE). Lives can be saved, if PE is prevented, or detected early and properly managed. Prevention and detection depend on identifying the risk factors associated with PE, and, as these have been shown vary by population, they should be determined on a population-by-population basis. The following study utilized the nested case-control model to evaluate 45 potential PE risk factors of a cohort in Bogotá, Colombia, making it perhaps the most comprehensive study of its kind in Colombia. It found PE to have a statistically significant association with 7 of the 45 factors evaluated: 1) pre-gestational BMI >30 kg/m2, 2) pregnancy weight gain >12 kg, 3) previous history preeclampsia/eclampsia, 4) previous history of IUGR-SGA (Intrauterine Growth Restriction-Small for Gestational Age), 5) maternal age <20 or ≥35 years (20–34 was not associated), and 6) family history of diabetes. Finally, prenatal consumption of folic acid was found to lower the risk of PE. We recommend that, in Colombia, factors 1–6 be used to identify at risk mothers during pregnancy check-ups; that mothers be encouraged to take folic acid during pregnancy; and, that Colombia's health system and public policy address the problem of pregestational obesity.

Purpose: To identify micro-RNAs (miRNAs) expression profiles in peripheral blood plasma that could play a role as potential biomarkers in patients who progressed to castration-resistant prostate cancer (CRPC). Liquid biopsy analysis of miRNAs is a fast-developing field with a considerable likelihood to predict tumor progression and metastasis by targeting genes involved in oncogenesis. Patients and Methods: Differential expression analysis of miRNAs profile in CRPC patients was performed by creating small RNA libraries of circulating miRNAs using HiSeq2500 Illumina platform. A secondary analysis of aligned reads with miRNA identification and quantification was performed using miARmaSeq. Using the Bowtie algorithm, the selected variants were compared to reference nucleotide sequence GRCh38 and miRbase. Novel miRNA sequences were structurally analyzed using mirDeep2^®. Results: A total of 16 patients with CRPC were included for analysis. Identified circulating miRNAs were hsa-miR-885-3p, hsa-miR-4467, hsa-miR-4686, hsa-miR-146a-3p, hsa-miR-6514-5p. Genes identified as regulated by these miRNAs were GPR56, BDNF, CTNND1, C17orf62, and DTNA. Conclusion: We explored the miRNA expression profile in patients with CRPC, identifying five miRNAs implicated in the regulation of genes involved in prostate cancer (PCa) oncogenesis and progression. We also found miRNA 855– 3p in peripheral blood for the first time, which has a critical role in tumor growth mechanisms and higher expression profile than in healthy individuals.

Introduction: The VEGF family has been identified as abnormal in preeclampsia (PE). Hypertensive disorders of pregnancy (HDP) are major contributors to maternal and neonatal morbidity and mortality worldwide; likewise, umbilical cord anatomical abnormalities (UCAA) are linked to poor neonatal outcomes. Based on the relationship described between PE and UCAA and the role of the VEGF family in PE, this study explored VEGF expression in placental and UC tissued from patients with PE and with UCAA. Methods: We performed an observational, analytical study on placentas, comparing protein and mRNA expression in four groups: patients with PE, patients with UC abnormalities, patients with both, and patients with none of them. Using immunohistochemistry, we studied VEGF A, VEGF R1 (FLT1), MMP1, and PLGF. With quantitative reverse transcription polymerase chain reaction we described mRNA expression of PLGF, VEGF and sFLT1, and sFLT1/PLGF ratio. Results: Forty newborns were included. Sixty-seven percent of mothers and 45% of newborns developed no complications. Immunohistochemistry was performed on UC and placental disc paraffin-embedded tissue; in the latter, the mRNA of the VEGF family was also measured. Statistically significant differences were observed among different expressions in both HDP and UCAA groups. Interestingly, the UCAA group exhibited lower levels of sFLT1 and VEGF-A in comparison with other groups, with significant P-value for sFLT1 (P=0000.1). Conclusion: The origin of UCAA abnormalities and their relation with HDP are still unknown. VEGF family alterations could be involved in both. This study provides the first approach related to molecules linked to UCAA.

In December 2019, the novel Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) rapidly spread to become a pandemic. To date, increasing evidence has described the potential negative impact of SARS-CoV-2 infection on pregnant women. Although the pathophysiology of coronavirus disease 2019 (COVID-19) is not entirely understood, there is emerging evidence that it causes a severe systemic inflammatory response associated with vascular alterations that could be of special interest considering some physiological changes in pregnancy. Additionally, these alterations may affect the physiology of the placenta and are associated with pregnancy complications and abnormal histologic findings. On the other hand, data about the vaccine against SARS-CoV-2 are limited, but the risks of administering COVID-19 vaccines during pregnancy appear to be minimal. This review summarizes the current literature on SARSCoV2 virus infection, the development of COVID-19 and its relationship with physiological changes, and angiotensin-converting enzyme 2 (ACE2) function during pregnancy. We have particularly emphasized evidence coming from Latin American countries.

INTRODUCTION: Preeclampsia has a global frequency of 2–8% and a frequency of 10% in developing countries. In Colombia, preeclampsia causes 42% of maternal mortality. Alterations in placental homeostasis have been proposed to be involved in its pathophysiology. The aim of this study was to compare mRNA and protein levels of tissue factor (F3) and thrombomodulin (THBD) and the histopathological findings of placentas. MATERIALS AND METHODS: We studied 16 placentas from patients with preeclampsia and 19 term placentas with uncomplicated pregnancy. An expert pathologist, who was masked to the group assignment, conducted an evaluation to determine specific histological changes. Assessments of mRNA and protein levels of F3 and THBD were performed using real-time PCR and ELISA, respectively. RESULTS: Cases and controls differed in the frequency of decidual arteriopathy ( p = 0.027), acute infarction ( p = 0.001) and hyperplasia of the syncytiotrophoblast ( p = 0.0017). Cases had increased levels of F3 mRNA ( p = 0.0124) and protein ( p < 0.0001) and THBD mRNA ( p < 0.0001) and protein ( p < 0.0001). CONCLUSION: In placenta of patients with preeclampsia, we detected abnormal expression of F3 and THBD with increased protein and mRNA levels. The role of these molecules in the pathogenesis of this disease and in alterations of hemostatic and histopathological aspects of placentas need further studying.