Fetal Life Research Articles

Дебют системной красной волчанки во время беременности

For a long time, systemic lupus erythematosus remains an insufficiently studied problem of rheumatology, the factors influencing the development and progression of the disease are not clear. The hormonal factor remains one of the possible triggers in the development of the disease in predisposed individuals. The course of pregnancy in patients with systemic lupus erythematosus is always associated with multiple risks. The onset of the disease during pregnancy often leads to the death of the fetus and the threat to the life of the mother. At the present stage, thanks to the possibilities of modern diagnostics and treatment, the prognosis for the life and health of both mother and fetus has improved. A case of the development of systemic lupus erythematosus during pregnancy and successful therapy with corticosteroids and belimumab is presented.

Recurrent Nonimmune Fetal Hydrops Due to a Novel Pathogenic Variant in PIEZO1 Gene: A Case Report from South India

AbstractNonimmune fetal hydrops (NIFH) has underlying diverse etiology with generalized lymphatic dysplasia being one such cause. Lymphatic malformation-6 is a type of lymphatic dysplasia that is due to homozygous or compound heterozygous variants in the PIEZO1 gene. The clinical features associated with this condition during fetal life are nonimmune fetal hydrops that manifests with widespread lymphatic edema, with other systemic manifestations like pericardial/pleural effusions, chylothorax along with lymphangiectasia seen primarily in lungs and intestines. We present a case of recurrent NIFH in a family due to a novel pathogenic mutation in PIEZO1 gene. This variant was identified in homozygous state in all the three affected fetuses and in heterozygous state in both the parents. The couple were counseled regarding recurrence of this condition and given reproductive options for future pregnancies.

Making a good egg: human oocyte health, aging, and in vitro development.

Mammalian eggs (oocytes) are formed during fetal life and establish associations with somatic cells to form primordial follicles that create a store of germ cells (the primordial pool). The size of this pool is influenced by key events during the formation of germ cells and by factors that influence the subsequent activation of follicle growth. These regulatory pathways must ensure that the reserve of oocytes within primordial follicles in humans lasts for up to 50 years, yet only approximately 0.1% will ever be ovulated with the rest undergoing degeneration. This review outlines the mechanisms and regulatory pathways that govern the processes of oocyte and follicle formation and later growth, within the ovarian stroma, through to ovulation with particular reference to human oocytes/follicles. In addition, the effects of aging on female reproductive capacity through changes in oocyte number and quality are emphasized, with both the cellular mechanisms and clinical implications discussed. Finally, the details of current developments in culture systems that support all stages of follicle growth to generate mature oocytes in vitro and emerging prospects for making new oocytes from stem cells are outlined.

Preventing and Treating Torsades de Pointes in the Mother, Fetus and Newborn in the Highest Risk Pregnancies with Inherited Arrhythmia Syndromes.

The number of women of childbearing age who have been diagnosed in childhood with ion channelopathy and effectively treated using beta blockers, cardiac sympathectomy, and life-saving cardiac pacemakers/defibrillators is increasing. Since many of these diseases are inherited as autosomal dominant, offspring have about a 50% risk of having the disease, though many will be only mildly impacted during fetal life. However, highly complex delivery room preparation is increasingly needed in pregnancies with inherited arrhythmia syndromes (IASs). However, specific Doppler techniques show meanwhile a better understanding of fetal electrophysiology. The advent of fetal magnetocardiography (FMCG) now allows the detection of fetal Torsades de Pointes (TdP) ventricular tachycardia and other LQT-associated arrhythmias (QTc prolongation, functional second AV block, T-wave alternans, sinus bradycardia, late-coupled ventricular ectopy and monomorphic VT) in susceptible fetuses during the second and third trimester. These types of arrhythmias can be due to either de novo or familial Long QT Syndrome (LQTS), Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT), or other IAS. It is imperative that the multiple specialists involved in the antenatal, peripartum, and neonatal care of these women and their fetuses/infants have the optimal knowledge, training and equipment in order to care for these highly specialized pregnancies and deliveries. In this review, we outline the steps to recognize symptomatic LQTS in either the mother, fetus or both, along with suggestions for evaluation and management of the pregnancy, delivery, or post-partum period impacted by LQTS.

Genes in loci genetically associated with polycystic ovary syndrome are dynamically expressed in human fetal gonadal, metabolic and brain tissues.

Polycystic ovary syndrome (PCOS) is a heterogeneous disorder, affecting around 10% of women of reproductive age, with infertility, depression or anxiety, obesity, insulin resistance and type 2 diabetes as risk factors. The cause of PCOS is not known but there is a predisposition to developing PCOS in adult life that arises during fetal or perinatal life. PCOS also has a genetic predisposition and a number of genetic loci associated with PCOS have been identified. These loci contain 25 candidate genes which are currently being studied to define the syndrome. Although the name PCOS suggests a syndrome of the ovary, PCOS has also been associated with the central nervous system and other organ systems in the body due to the wide variety of symptoms it presents. Here, we examined the expression patterns of PCOS candidate genes in gonadal (ovary and testis), metabolic (heart, liver and kidney) and brain (brain and cerebellum) tissues during the first half of human fetal development and postnatally until adulthood using public RNA sequencing data. This study is an initial step for more comprehensive and translational studies to define PCOS. We found that the genes were dynamically expressed in the fetal tissues studied. Some genes were significantly expressed in gonadal tissues, whilst others were expressed in metabolic or brain tissues at different time points prenatally and/or postnatally. HMGA2, FBN3 and TOX3 were highly expressed during the early stages of fetal development in all tissues but least during adulthood. Interestingly, correlation between expression of HMGA2/YAP1 and RAD50/YAP1 were significant in at least 5 of the 7 fetal tissues studied. Notably, DENND1A, THADA, MAPRE1, RAB5B, ARL14EP, KRR1, NEIL2 and RAD50 were dynamically expressed in all postnatal tissues studied. These findings suggest that these genes have tissue- or development-specific roles in multiple organs, possibly resulting in the various symptoms associated with PCOS. Thus the fetal origin of a predisposition to PCOS in adulthood could arise via the effects of PCOS candidate genes in the development of multiple organs.

A conceptual framework for selecting appropriate populations for public health interventions.

This article suggests a conceptual framework for choice of target populations for public health interventions. In short, who should benefit? Taking the seminal work of Geoffrey Rose on "individuals at risk" versus the "whole population approach" as a point of departure, we explore later contributions. Frohlich and Potvin introduced the notion of "vulnerable populations" applying relevant social determinants as the defining selection criterion. Other interventions focus on a "physical space" (spatial demarcations) such as a neighborhood as a means to define intervention populations. As an addition to these criteria, we suggest that the life-course perspective entails an alternative means of selecting target populations based on a "temporal" perspective. A focus on the various age phases ranging from fetal life and infancy to old age may guide selection of population segments for targeted public health interventions. Each of the selection criteria has advantages and disadvantages when used for primary, secondary, or tertiary prevention. Thus, the conceptual framework may guide informed decisions in public health planning and research regarding precision prevention versus various approaches to complex community-based interventions.

Transuterine Ultrasound-Guided Fetal Embolization of Vein of Galen Malformation, Eliminating Postnatal Pathophysiology.

Transuterine Ultrasound-Guided Fetal Embolization of Vein of Galen Malformation, Eliminating Postnatal Pathophysiology.

Persistent left superior vena cava without right superior vena cava during fetal life.

Enlarged coronary sinus detected during cardiac examination in the prenatal period is the first finding that raises suspicion for persistent left superior vena cava. In this report, a patient was presented who was referred with the prediagnosis of cor triatriatum sinister in the antenatal period and diagnosed with isolated persistent left superior vena cava (SVC).

Three-dimensional spatiotemporal imaging correlation in the diagnosis of isolated infracardiac total anomalous pulmonary venous connection in fetal life.

Total anomalous pulmonary venous connection (TAPVC) is a critical congenital heart disease which is often missed on prenatal echocardiography because of the decreased pulmonary blood flow in fetal life. Improvement in technology has resulted in increasing prenatal diagnosis of this condition. We report a foetus with infra cardiac TAPVC in whom prenatal diagnosis was facilitated by the use of STIC technology.

VERY RARE COMBINATION OF PATENT VITELLOINTESTINAL DUCT WITH PATENT URACHUS

Introduction - The vitelline duct is the embryological narrow channel connecting the yolk sac with the intestine. During the foetal life, vitelline duct tends to obliterates itself till to disappear. The partial failure of this obliteration can lead to the development of a duct, a ligament, or a diverticulum known as a Meckel's diverticulum. A Patent omphalomesenteric duct occurs because of the complete lack of vitelline duct.[3] The urachus is an embryological remnant of the allantois. Between the fourth and fth month of gestation, the foetal bladder tends to descend gradually and its apical portion creates the urachus. The urachus obliterates itself, becoming the median umbilical ligament. Its persistence after intrauterine life can manifest as urachal remnants. A patent urachus is because of complete lack of obliteration of urachus [1,3]. The incidence of these anomalies PU was 1-2 per 10000 while PVD is 1 in 5000 to 8000 deliveries [1,3,5]. The association of both anomalies is very rare [7]. Case discussion- A 12-years-old male presented with complaints of pain in abdomen, multiple episodes of vomiting. Patient was tachycardiac with tenderness in right iliac fossa with palpable lump with ultrasonography suggestive of perforated appendix with lump formation and was managed conservatively and asked for interval appendicectomy with CECT abdomen. CECT was suggestive of normal and compressible appendix with infected urachal cyst. But after 4weeks patient had similar complaints hence posted for emergency operation with McBurney's incision not by midline incision to avoid injury to urachal cyst. Intra operative ndings-1) patent Vitello intestinal duct 2) patent urachus 3)15cc pus discharge near umbilical end of urachus 4) normal appendix and small bowel. Resection of Vitello intestinal duct and urachus with ileoileal anastomosis done and specimen sent for histopathology which was suggestive of patent vitello intestinal duct with changes of gangrene. The Patent Vitello Conclusionintestinal duct with patent urachus is very rarely seen in combination and its diagnosis may be missed preoperatively and should be kept as a possibility in patients with patent urachus with or without infection

Phenylketonuria and the brain

Classic phenylketonuria (PKU) is caused by defective activity of phenylalanine hydroxylase (PAH), the enzyme that coverts phenylalanine (Phe) to tyrosine. Toxic accumulation of phenylalanine and its metabolites, left untreated, affects brain development and function depending on the timing of exposure to elevated levels. The specific mechanisms of Phe-induced brain damage are not completely understood, but they correlate to phenylalanine levels and on the stage of brain growth. During fetal life, high levels of phenylalanine such as those seen in maternal PKU can result in microcephaly, neuronal loss and corpus callosum hypoplasia. Elevated phenylalanine levels during the first few years of life can cause acquired microcephaly, severe cognitive impairment and epilepsy, likely due to the impairment of synaptogenesis. During late childhood, elevated phenylalanine can cause alterations in neurological functioning, leading to ADHD, speech delay and mild IQ reduction. In adolescents and adults, executive function and mood are affected, with some of the abnormalities reversed by better control of phenylalanine levels. Altered brain myelination can be present at this stage. In this article, we review the current knowledge about the consequences of high phenylalanine levels in PKU patients and animal models through different stages of brain development and its effect on cognitive, behavioural and neuropsychological function.

Reprogramming adult hematopoietic progenitors towards fetal-restricted lymphopoiesis via Cbfb2gene dosage

Abstract Hematopoietic Stem Cells (HSC) hold the potential to self-renew and differentiate into most immune cell subsets throughout life. However, some specialized immunocytes like microglia, B-1 B cells and γδ T cells emerge only during fetal life, and they cannot be generated by adult HSC. We discovered that CBFβ isoform 2 (CBFβ2), an evolutionarily conserved component of the RUNX transcription factor complex, reprograms adult HSC into acquiring fetal hematopoietic potential. While Cbfb2heterozygous mice generated normal numbers of mature IL-17 producing γδ T (Tγδ17) cells, we found that they lacked DN1d cell containing Tγδ17 precursors. Thus, Cbfb2gene dosage is critical for imprinting Tγδ17 differentiation potential in distinct precursor cells. In line with this reprogramming, Cbfb2haploinsufficient adult bone marrow (BM) progenitors, which are normally inefficient at Tγδ17 cell generation, became permissive for innate T cell development. Analysis of transcriptional profiles of HSCs and lymphoid progenitors (LMPPs and CLPs) from adult BM revealed that, among hemopoietic progenitors, LMPPs from Cbfb2heterozygous mice were the most affected by Cbfb2gene dosage and upregulated genes implicated in embryonic hematopoiesis. Using In Utero Transplantation of adult hematopoietic progenitors into the fetal liver of E14.5 pregnant dams’ fetuses, we were able to successfully reconstitute Tγδ17 cells and confirm an unprecedent bias in Tγδ17 development underpinned by reduced CBFβ2-dependent transcriptional activity. Our findings identify gene network architectures that impose temporal restriction on hematopoietic pluripotency and that could be exploited for the generation of fetal-derived lymphocytes in adult life.

A study to assess the effect of maternal hemoglobin level on foetal outcome among antenatal mothers in selected maternity hospitals at Mangalore

In developing countries maternal anemia during pregnancy has been reported to increase the risk of unfavorable foetal outcome. According to the standard laid down by WHO, anemia in pregnancy is present when the hemoglobin concentration in the peripheral blood is 11gm\100ml or less. In India its prevalence has been found to be in the range of 50-90% in 3rd trimester of pregnancy according to different studies conducted in rural areas. Maternal anemia in pregnancy is commonly considered as risk factor for poor pregnancy outcome and can threaten the life of mother and foetus. However, the extent to which the maternal hemoglobin concentration affects the foetal weight and foetal outcome is still uncertain. In the present study the researcher will investigate the possible effects of abnormal maternal hemoglobin level on foetal outcome. Interpretation and Conclusion: The findings of the present study revealed that there is a relationship between maternal hemoglobin level and fetal outcome such as birth weight, color of the new born, muscle tone, pre term birth and gestational age of the new born. A review of previous studies done showed that the risks of preterm delivery and LBW increased in proportion to the severity of maternal anemia. A comprehensive community based intervention with iron supplementation, helminthes treatment and increase in knowledge regarding information, education and communication through effective strategies, to improve the hematological status of pregnant women in each trimester, is needed and there by reduces maternal and fetal mortality and morbidity.

"Heart of the Matter": Cardiac Dysfunction in Congenital Diaphragmatic Hernia.

Despite advances in caring for neonates with congenital diaphragmatic hernia (CDH), mortality and morbidity continues to be high. Additionally, the pathophysiology of cardiac dysfunction in this condition is poorly understood. Postnatal cardiac dysfunction in neonates with CDH may be multifactorial with origins in fetal life. Mechanical obstruction, competition from herniated abdominal organs into thoracic cavity combined with redirection of ductus venosus flow away from patent foramen ovale leading to smaller left-sided structures may be a contributing factor. This shunting decreases left atrial and left ventricular blood volume, which may result in altered micro- and macrovascular aberrations affecting cardiac development in the prenatal period. Direct mass effect from herniated intra-abdominal contents restricting cardiac growth and/or reduced left ventricular preload may contribute independently to left ventricular dysfunction in the absence of right ventricular dysfunction and or pulmonary hypertension. With variable clinical phenotypes of cardiac dysfunction, pulmonary hypertension, and respiratory failure in patients with CDH, there is increased need for individualized diagnosis and tailored therapy. Routine use of therapy such as inhaled nitric oxide and sildenafil that induces significant pulmonary vasodilation may be detrimental in left ventricle dysfunction, whereas in a patient with pure right ventricle dysfunction, they may be beneficial. Targeted functional echocardiography serves as a real-time tool for defining the pathophysiology and aids optimization of vasoactive therapy in affected neonates. KEY POINTS: · Cardiac dysfunction in neonates with CDH is multifactorial.. · Postnatal cardiac dysfunction in patients with CDH has its origins in fetal life.. · Right ventricular dysfunction contributes to systemic hypotension.. · Left ventricular dysfunction contributes to systemic hypotension.. · Supportive therapy should be tailored to clinical phenotype..

Association of umbilical cord serum TARC/CCL17 with childhood allergies: A birth cohort study

BackgroundEarly identification of infants at high risk of allergies can improve the efficacy of preventive interventions. However, an established quantifiable risk assessment method in the early postnatal period does not exist. TARC (or CCL17) is a Th2 chemokine used as an activity marker for atopic dermatitis (AD). Therefore, we evaluated the association between cord blood TARC (cTARC) and the development of allergic diseases in childhood. MethodsThis is a high-risk birth cohort for allergy, consisting of children with a family history of allergy. We collected 263 pairs of maternal and child cord blood samples perinatally and child blood samples at ages 1, 2, and 5 years. TARC and allergen-specific immunoglobulin E levels were measured, and the relationship between allergic diseases was analyzed. ResultsThe median cTARC was 989 pg/mL (interquartile range [IQR]: 667–1430 pg/mL). The cTARC levels in children who developed AD were higher than those in children who did not develop AD, and the association strengthened with younger age (median [IQR] at 1 year: 1285 [816–1965] vs. 933 [662–1330] pg/mL, p < 0.01; at 2 years: 1114 [787–1753] vs. 950 [660–1373] pg/mL, p = 0.02). In the multivariate analysis, cTARC was associated with AD, egg white sensitization, food allergy, allergic rhinitis, and Japanese cedar pollen sensitization. ConclusionscTARC was associated with the development of allergic diseases and allergen sensitization in early childhood. These results suggest that, infantile AD-mediated atopic march starts during fetal life, and this immune status is reflected in the cTARC at birth.

Testicular toxicity in mice exposed to terephthalic acid in utero and during lactation.

Terephthalic acid (TPA) is a worldwide aromatic compound widely used to manufacture resins and the raw material for the polymerization reaction with ethylene glycol to produce polyethylene terephthalate, known as PET. The use of TPA extends to the synthesis of phthalates, plasticizers used in various industrialized products such as toys and cosmetics. The present study aimed to evaluate the testicular toxicity of terephthalic acid on male mice exposed in utero and during lactation to TPA in different developmental windows. The animals were treated intragastric with TPA at stock dispersal dosages corresponding to 0.0014g/ml and 0.56g/ml of TPA in 0.5% v/v carboxymethylcellulose as well as the control dose, composed solely of dispersion of carboxymethylcellulose (0.5% v/v). Four experimental windows were established: group I-treatment in utero, in the fetal period (gestational day-GD 10.5-18.5), with euthanasia at GD 18.5; group II-treatment in utero, in the fetal period (GD 10.5-18.5) and the lactational period (postnatal day (PND-15)), with euthanasia at 15days; group III-treatment in utero in the fetal period (DG 10.5-18.5) with euthanasia at 70days (age of sexual maturity, PND 70); group IV-treatment in utero, in the fetal period (GD 10.5-18.5) and the lactational period (PND-15), with euthanasia at 70days (PND70). The results indicate that TPA changes the reproductive parameters (testicular weight, GI, penis size, and anogenital index) only at the dose of 0.56g/ml in the fetal period. Data on the volumetric ratio of the testis elements show that the dispersion with the highest concentration of TPA significantly altered the blood vessel/capillary, lymphatic vessel, and connective tissue percentages. Only at the dose of 0.56g/ml TPA was it effective in decreasing the Leydig and Sertoli cell numbers of the euthanized animals at GD 18.5. In group II, TPA increased the diameter and lumen of seminiferous tubules, which indicates that TPA accelerated the maturation process of Sertoli cells without changing the number and the nuclear volume of these cells. The Sertoli and Leydig cell numbers of the 70-day animals exposed to TPA in the gestational and lactational period were similar to the control. Therefore, the present study is the first in the literature to show that TPA presents a testicular toxicity during fetal (DG18.5) and postnatal life (PND15), without repercussion in adulthood (70days).

Arrhythmia Profile in Children Presenting at a Tertiary Care Centre in India - From Fetal Life to Fifteen Years of Age Prabhu Shakuntala, Prabhshara

Many of the arrhythmias tend to be asymptomatic and detected incidentally, while some others may be picked up too late after a catastrophic presentation. The goal of this study was to document the arrhythmia profile in children presenting to our tertiary care hospital in India. We also reviewed the early and late outcomes of arrhythmias in these patients (including in isolated and post cardiac surgical patients). Amongst 100 patients with arrhythmias, 35% were detected incidentally for presentations like breathlessness (29%) and refusal to feed. A majority of patients (70%) did not have any underlying structural defect and had no cardiomegaly on chest X-Ray. Of those with structural defects, 90% were congenital with the majority being acyanotic (58%) and would have gone clinically undetected. 19 children (20%) presented with heart failure. Tachyarrhythmias (61%) were more common, and all the immediate deaths were from this group. Bradyarrhythmias were mostly complete heart blocks. Almost half the patients required emergency antiarrhythmics. Holter study was done to check for antiarrhythmic efficacy and to decide regarding pacing. In 48% cases, clinical management was changed based on the Holter report. Almost half the patients required emergency antiarrhythmics (adenosine, isoprenaline, amiodarone). The long-term outcomes were favorable with 50% of the patients not requiring long term antiarrhythmics and most remained asymptomatic. The need for interventional therapy like pacemaker insertion and radiofrequency ablation was less than 2%. Arrythmias in children have varied symptoms and pediatricians need to be aware about this. With optimal management, long term outcomes for these children are usually favorable.

Transplacental Transport of Artificial Sweeteners

The prevalence of obesity is increasing, and the origins of obesity and metabolic dysfunction may be traced back to fetal life. Currently, overweight pregnant women are advised to substitute sugar-sweetened beverages with diet drinks containing artificial sweeteners. Recent evidence suggests that the consumption of artificial sweeteners during pregnancy increases the risk of obesity in the child, but the mechanism is unknown. We hypothesized the transportation of artificial sweeteners across the placenta into the fetal circulation and the amniotic fluid. We included 19 pregnant women who were given an oral dose of acesulfame, cyclamate, saccharin, and sucralose immediately before a planned caesarean section. Nine women were included as controls, and they refrained from an intake of artificial sweeteners. The maternal and fetal blood and amniotic fluid were collected during the caesarean section, and concentrations of artificial sweeteners were measured using mass spectrometry. We found a linear relationship between the fetal plasma concentrations of artificial sweeteners and the maternal plasma concentrations, with adjusted coefficients of 0.49 (95% CI: 0.28–0.70) for acesulfame, 0.72 (95% CI: 0.48–0.95) for cyclamate, 0.51 (95% CI: 0.38–0.67) for saccharin, and 0.44 (95% CI: 0.33–0.55) for sucralose. We found no linear relationship between amniotic fluid and fetal plasma concentrations, but there were positive ratios for all four sweeteners. In conclusion, the four sweeteners investigated all crossed the placenta and were present in the fetal circulation and amniotic fluid.

Review of the Literature on Ramadan Fasting and Health in 2022

Abstract Objectives The literature on health and disease during Ramadan fasting (RF) is widely spread in many journals making it not readily accessible to those interested in the subject. Here, we provide an overview of the research on the interplay of RF with various aspects of well-being published in 2022. Materials and Methods A narrative, nonsystematic review of the international literature from a single major medical online database, PubMed, in one calendar year (2022) was conducted. The search term “Ramadan fasting” was used to retrieve the appropriate records. The relevant literature with substantial data-based content was presented in a concise thematic account, excluding those concerned with diabetes. Results Themes that emerged from the review included the pathophysiology of metabolic changes during RF, nutritional aspects including body composition and energy metabolism, cardiovascular disease and risk factors, renal function and structure, endocrinology (mainly thyroid), neurological disorders, mental health, pregnancy and fetal life, and infections (including COVID). Some miscellaneous clinical themes were identified, such as patients' and professional perspectives. Conclusions In 2022, the medical interest in RF was again widely spread across specialties. Cardiovascular disease and risk factors attract the most interest in terms of original articles and professional guidelines. We hope with this review to present a concise summary of the scholarly work on the subject in this year.

Vascular Stem Cells and the Role of B-Raf Kinase in Survival, Proliferation, and Apoptosis.

Neovascularization is an essential process in organismal development and aging. With aging, from fetal to adult life, there is a significant reduction in neovascularization potential. However, the pathways which play a role in increased neovascularization potential during fetal life are unknown. Although several studies proposed the idea of vascular stem cells (VSCs), the identification and essential survival mechanism are still not clear. In the present study, we isolated fetal VSCs from the ovine carotid artery and identified the pathways involved in their survival. We tested the hypothesis that fetal vessels contain a population of VSCs, and that B-Raf kinase is required for their survival. We conducted viability, apoptotic, and cell cycle stage assays on fetal and adult carotid arteries and isolated cells. To determine molecular mechanisms, we conducted RNAseq, PCR, and western blot experiments to characterize them and identify pathways essential for their survival. Results: A stem cell-like population was isolated from fetal carotid arteries grown in serum-free media. The isolated fetal VSCs contained markers for endothelial, smooth muscle, and adventitial cells, and formed a de novo blood vessel ex vivo. A transcriptomic analysis that compared fetal and adult arteries identified pathway enrichment for several kinases, including B-Raf kinase in fetal arteries. Furthermore, we demonstrated that B-Raf- Signal Transducer and Activator of Transcription 3 (STAT3)-Bcl2 is critical for the survival of these cells. Fetal arteries, but not adult arteries, contain VSCs, and B-Raf-STAT3-Bcl2 plays an important role in their survival and proliferation.