scholarly journals OC005: Ultrasound bioeffects: Quantification of cellular damage in animal fetal liver after use of Doppler pulse to measure ductus venosus

2008 ◽  
Vol 32 (3) ◽  
pp. 244-244
Author(s):  
B. Pellicer ◽  
S. Herraiz ◽  
T. S. Russell ◽  
A. Montllor ◽  
V. Felipo ◽  
...  
Keyword(s):  
Fetal Liver ◽  
Cellular Damage ◽  
Ductus Venosus ◽  
Ultrasound Bioeffects

Ultrasound bioeffects in rats: quantification of cellular damage in the fetal liver after pulsed Doppler imaging

2011 ◽  
Vol 37 (6) ◽  
pp. 643-648 ◽  
Author(s):  
B. Pellicer ◽  
S. Herraiz ◽  
E. Táboas ◽  
V. Felipo ◽  
C. Simon ◽  
...  
Keyword(s):  
Fetal Liver ◽  
Doppler Imaging ◽  
Cellular Damage ◽  
Pulsed Doppler ◽  
Ultrasound Bioeffects

Role of ductus venosus in distribution of umbilical blood flow in human fetuses during second half of pregnancy

2000 ◽  
Vol 279 (3) ◽  
pp. H1256-H1263 ◽  
Author(s):  
Maria Bellotti ◽  
Giancarlo Pennati ◽  
Camilla De Gasperi ◽  
Frederick C. Battaglia ◽  
Enrico Ferrazzi
Keyword(s):  
Blood Flow ◽  
Fetal Liver ◽  
Color Doppler ◽  
Liver Perfusion ◽  
Normal Pregnancy ◽  
Left Lobe ◽  
Ductus Venosus ◽  
Venous Circulation ◽  
Umbilical Blood ◽  
Umbilical Blood Flow

Color Doppler sonography was used to study umbilical and ductus venosus (DV) flow in 137 normal fetuses between 20 and 38 wk of gestation. Hepatic flows were also evaluated. In all parts of the venous circulation examined, blood flow increased significantly with advancing gestational age. The weight-specific amniotic umbilical flow did not change significantly during gestation (120 ± 44 ml · min−1 · kg−1), whereas DV flow decreased significantly (from 60 to 17 ml · min−1 · kg−1). The percentage of umbilical blood flow shunted through the DV decreased significantly (from 40% to 15%); consequently, the percentage of flow to the liver increased. The right lobe flow changed from 20 to 45%, whereas the left lobe flow was approximately constant (40%). These changes are related to different patterns of growth of the umbilical veins and DV diameters. The present data support the hypothesis that the DV plays a less important role in shunting well-oxygenated blood to the brain and myocardium in late normal pregnancy than in early gestation, which leads to increased fetal liver perfusion.

Ductus venosus-associated pericytes form a niche regulating hematopoietic stem cell proliferation in the fetal liver

2014 ◽  
Vol 42 (8) ◽  
pp. S19
Author(s):  
Jalal Ahmed ◽  
Yuya Kunisake ◽  
Sandra Pinho ◽  
Anna Arnal ◽  
Miriam Merad ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Stem Cell ◽  
Hematopoietic Stem Cell ◽  
Fetal Liver ◽  
Ductus Venosus ◽  
Hematopoietic Stem ◽  
Stem Cell Proliferation

scholarly journals Investigation of Clinical Safety of Human iPS Cell-Derived Liver Organoid Transplantation to Infantile Patients in Porcine Model

2020 ◽  
Vol 29 ◽  
pp. 096368972096438
Author(s):  
Tomonori Tsuchida ◽  
Soichiro Murata ◽  
Shunsuke Hasegawa ◽  
Satoshi Mikami ◽  
Shin Enosawa ◽  
...  
Keyword(s):  
Clinical Trials ◽  
Portal Hypertension ◽  
Portal Vein ◽  
Fetal Liver ◽  
Portal Pressure ◽  
Ductus Venosus ◽  
Portal Vein Ligation ◽  
Ips Cell ◽  
Liver Organoids ◽  
Human Ipsc

Transplantation of liver organoids has been investigated as a treatment alternative to liver transplantation for chronic liver disease. Transportal approach can be considered as a method of delivering organoids to the liver. It is important to set the allowable organoid amount and verify translocation by intraportal transplantation. We first examined the transplantation tolerance and translocation of porcine fetal liver-derived allogeneic organoids using piglets. Fetal liver-derived organoids generated from the Kusabira Orange-transduced pig were transplanted to the 10-day-old piglet liver through the left branch of the portal vein. All recipients survived without any observable adverse events. In contrast, both local and main portal pressures increased transiently during transplantation. In necropsy samples, Kusabira Orange-positive donor cells were detected primarily in the target lobe of the liver and partly in other areas, including the lungs and brain. As we confirmed the transplantation allowance by porcine fetal liver-derived organoids, we performed intraportal transplantation of human-induced pluripotent stem cell (iPSC)-derived liver organoid, which we plan to use in clinical trials, and portal pressure and translocation were investigated. Human iPSC-derived liver organoids were transplanted into the same 10-day-old piglet. Portal hypertension and translocation of human iPSC-derived liver organoids to the lungs were observed in one of two transplanted animals. Translocation occurred in the piglet in which patent ductus venosus (PDV) was observed. Therefore, a 28-day-old piglet capable of surgically ligating PDV was used, and after the PDV was ligated, human iPSC-derived liver organoids with the amount of which is scheduled in clinical trials were transplanted. This procedure inhibited the translocation of human iPSC-derived liver organoids to extrahepatic sites without no portal hypertension. In conclusion, human iPSC-derived liver organoids can be safely transplanted through the portal vein. Ligation of the ductus venosus prior to transplantation was effective in inhibiting extrahepatic translocation in newborns and infants.

scholarly journals Placental corticotrophin releasing hormone is a modulator of fetal liver blood perfusion

2020 ◽  
Author(s):  
Satoru Ikenoue ◽  
Feizal Waffarn ◽  
Masanao Ohashi ◽  
Mamoru Tanaka ◽  
Daniel L Gillen ◽  
...  
Keyword(s):  
Blood Flow ◽  
Body Composition ◽  
Fetal Growth ◽  
Fetal Liver ◽  
Umbilical Vein ◽  
Liver Blood Flow ◽  
Late Gestation ◽  
Ductus Venosus ◽  
Maternal Circulation ◽  
Releasing Hormone

Abstract Context Variation in fetal liver blood flow influences fetal growth and postnatal body composition. Placental corticotrophin-releasing hormone has been implicated as a key mediator of placental-fetal perfusion. Objective To determine whether circulating levels of placental corticotrophin-releasing hormone across gestation are associated with variations in fetal liver blood flow. Design Prospective cohort study Methods Fetal ultrasonography was performed at 30 weeks’ gestation to characterize fetal liver blood flow (quantified by subtracting ductus venosus flow from umbilical vein flow). Placental corticotrophin-releasing hormone was measured in maternal circulation at approximately 12, 20 and 30 weeks’ gestation. Multiple regression analysis was used to determine the proportion of variation in fetal liver blood flow explained by placental corticotrophin-releasing hormone. Co-variates included maternal age, parity, pre-pregnancy BMI, gestational weight gain, and fetal sex. Results A total of 79 uncomplicated singleton pregnancies were analyzed. Fetal liver blood flow was 68.4 ± 36.0 ml/min (mean ± SD). Placental corticotrophin-releasing hormone concentrations at 12, 20 and 30 weeks were 12.5 ± 8.1, 35.7 ± 24.5 and 247.9 ± 167.8 pg/ml, respectively. Placental corticotrophin-releasing hormone at 30 weeks, but not at 12 and 20 weeks, was significantly and positively associated with fetal liver blood flow at 30 weeks (r = 0.319, p = 0.004), and explained 10.4% of the variance in fetal liver blood flow. Conclusions Placental corticotrophin-releasing hormone in late gestation is a possible modulator of fetal liver blood flow, and may constitute a biochemical marker in clinical investigations of fetal growth and body composition.

scholarly journals Fetal Ductus Venosus Pulsatility Index and Diameter during Second and Third Trimester of Gestation

2017 ◽  
Vol 56 (205) ◽  
pp. 124-131 ◽  
Author(s):  
Pratit Pokharel ◽  
Mukhtar Alam Ansari
Keyword(s):  
Gestational Age ◽  
Pulsatility Index ◽  
Fetal Liver ◽  
Umbilical Vein ◽  
Vena Cava ◽  
Cross Sectional Study ◽  
Ductus Venosus ◽  
Third Trimester ◽  
Cross Sectional ◽  
The Mean

Introduction: The ductus venosus is a small funnel shaped vessel found posterior to the fetal liver connecting the intra-abdominal umbilical vein and the inferior vena cava. It is one of the three physiological shunts in the fetus. The main objective of this study is to construct the reference table and normogram for fetal ductus venosus Pulsatility Index and diameter with gestational age. Methods: This was a prospective cross sectional study conducted during August 2011 to July 2012 taking 294 uncomplicated pregnancies using systemic random sampling method. Three measurements were made for ductus venosus diameter and Pulsatility Index in each fetus during period of fetal quiescence. Results: The ductus venosus diameter at <20weeks, 20-25 weeks, 25-30 weeks, >30 weeks were 1.16, 1.31, 1.62, 1.81 and Pulsatility Index at <20weeks, 20-25 weeks, 25-30 weeks, >30 weeks were 0.41, 0.44, 0.41 and 0.41 respectively. Conclusions: The mean diameter of the ductus venosus was linear across gestational age. The Pulsatility Index shows a scattered distribution across the gestational age. Keywords: ductus venosus diameter; gestational age; Pulsatility Index.

scholarly journals Uncovering the Role of Heme Oxygenase 1 in the Pathophysiology of β-Thalassemia

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 1364-1364 ◽  
Author(s):  
Daniel Garcia-Santos ◽  
Marc Mikhael ◽  
Monika Horvathova ◽  
Prem Ponka
Keyword(s):  
Heme Oxygenase ◽  
Conflicts Of Interest ◽  
Fetal Liver ◽  
Thalassemia Major ◽  
Severe Form ◽  
Cellular Damage ◽  
Heme Oxygenase 1 ◽  
Globin Chains ◽  
Thalassemia Minor ◽  
Free Heme

Abstract Thalassemias are a heterogeneous group of red blood cell disorders ranging from a clinically severe phenotype requiring life-saving transfusions (thalassemia major) to a relatively moderate symptomatic disorder, sometimes requiring transfusions (thalassemia intermedia). Thalassemia minor, the least severe form of the disorder, is characterized by minimal to mild symptoms. While thalassemia minor and intermedia are vastly more prevalent than thalassemia major, the latter is often fatal when not treated. Though considered a major cause of morbidity and mortality worldwide, there is still no universally available cure for this severe form of thalassemia. A reason for this is at least in part due to the lack of full understanding of pathophsyiology of thalassemia. The underlying cause of pathology in thalassemia is the premature apoptotic destruction of erythroblasts causing ineffective erythropoeisis. Normally, the assembly of adult hemoglobin (consisting of a tetramer of two α- and two β-globin chains) features a very tight coordination of α- and β-globin chain synthesis. However, in β-thalassemia, β-globin synthesis is decelerated causing α-globin accumulation; while in α-thalassemia the opposite scenario occurs. Unpaired globin chains that accumulate in thalassemic erythroblasts are bound to heme. In addition, in β-thalassemia an erythroid specific protease destroys excess α-globin chains, likely leading to the generation of a pool of “free” heme in erythroblasts. “Free” heme is toxic, but this toxicity will likely be augmented, if heme oxygenase 1 (HO-1) can release iron from heme. To date, virtually no information about the expression of HO-1 in erythroblasts has been produced; however, we have recently provided unequivocal evidence that this enzyme is present in several model erythroid cells1. Based on this novel and important finding, we hypothesize that in β-thalassemic erythroblasts HO-1 mediated release of iron from heme is the major culprit responsible for cellular damage. To test this hypothesis we exploited the mouse model of β-thalassemia, th3/th3. Thus far, our data indicates that HO-1 expression is increased in liver, spleen and kidney of β-thalassemic mice compared to wild type mice. Importantly, we observed that Epo-mediated erythroid differentiation of fetal liver (FL) cells isolated from β-thalassemic fetuses, display increased levels of HO-1 at mRNA and protein levels as well as decreased phosphorylated eiF2-α. Ferritin levels are also increased in these cells suggesting increased heme catabolism and iron release. Altogether, these results indicate that β-thalassemic erythroblasts have inappropriately high levels of unbound heme that is continuously degraded by HO-1. Further research is needed to determine whether HO-1 liberated iron is responsible for the damage of β-thalassemic erythroblasts. 1Garcia-Santos D, et al. Heme oxygenase 1 is expressed in murine erythroid cells where it controls the level of regulatory heme. Blood 123 (14): 2269-77, 2014. Disclosures No relevant conflicts of interest to declare.

Teratological Aspects of Dental Amalgam

1992 ◽  
Vol 6 (1) ◽  
pp. 114-119 ◽  
Author(s):  
K.S. Larsson
Keyword(s):  
Placental Transfer ◽  
Fetal Liver ◽  
Animal Experiments ◽  
Mercury Vapor ◽  
Dental Amalgam ◽  
Teratogenic Effect ◽  
Ductus Venosus ◽  
Genetic Constitution ◽  
Target Tissue ◽  
Metallic Mercury

The teratogenic effect is determined by four factors: (1) the agent, (2) the dose, (3) the stage of embryonic development, and (4) the genetic constitution of the embryo. The first two factors are of particular interest and warrant further comment. It should be emphasized that the mercury released from dental amalgam is mainly metallic mercury vapor. The dose of mercury vapor from dental amalgam fillings in the order of 5 ug/day is very low compared with the doses in a teratological study and is not likely to exceed the threshold necessary for a teratogenic effect to occur. The concentration of the teratogen at the target tissue is determined not only by the degree of placental transfer but also by other factors, such as the distribution within the maternal organism, the affinity to the fetal liver and blood, the hematocrit value, and the passage through the ductus venosus. These factors might help to explain toxicological mechanisms and species differences and have to be considered if the results of animal experiments are to be extrapolated to human conditions. Neither epidemiological data nor animal experimental data indicate that the release of metallic mercury vapor from dental amalgam therapy should cause teratogenic effects. A comparison with the incorporation of the fetotoxic methyl mercury might be justified.

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