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Salomon, L. J., N. Siauve, D. Balvay, C. A. Cuénod, C. Vayssettes, A. Luciani, G. Frija, Y. Ville, and O. Clément. "IRM fonctionnelle placentaire : etude de la perfusion et de la permeabilite du placenta murin." Journal de Radiologie 85, no. 9 (September 2004): 1395. http://dx.doi.org/10.1016/s0221-0363(04)77283-2.
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Ceccaldi, P. F., L. Mandelbrot, R. Farinotti, F. Forestier, and S. Gil. "Apports de la perfusion ex vivo du cotylédon humain dans l’étude du passage placentaire des médicaments." Journal de Gynécologie Obstétrique et Biologie de la Reproduction 39, no. 8 (December 2010): 601–5. http://dx.doi.org/10.1016/j.jgyn.2010.06.010.
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Reyna-Villasmil, Eduardo, Gabriel Mayner-Tresol, and Pedro Herrera-Moya. "Exosomas placentarios y preeclampsia." Revista Peruana de Ginecología y Obstetricia 63, no. 2 (July 11, 2017): 219–25. http://dx.doi.org/10.31403/rpgo.v63i1989.
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El éxito del embarazo se asocia con una correcta placentación, esencial para el crecimiento y desarrollo del feto. El sincitiotrofoblasto en el embarazo normal produce y secreta una variedad de elementos necesarios para lograr este objetivo, entre ellos, los exosomas placentarios. Estos llevan proteínas citoplasmáticas y ligadas a la membrana y ácidos nucleicos que pueden reprogramar a las células receptoras. Dependiendo de sus interacciones con el sistema inmune pueden dividirse en inmuno-estimulantes o inmuno-supresores. La producción y secreción de exosomas placentarios inmunosupresores provoca un efecto protector en la unidad feto-placentaria. Aquellos aislados del plasma materno son activos in vitro y se incorporan a las células diana por endocitosis. Su efecto está regulado por factores que incluyen tensión de oxígeno y se correlaciona con la perfusión placentaria. La preeclampsia es un síndrome caracterizado una disminución del flujo sanguíneo útero-placentario asociado a una invasión trofoblástica alterada que puede conducir a hipoxia placentaria y disfunción endotelial, liberando materiales nocivos en la circulación, lo que ocasiona daños en la función endotelial. Se han reportado cambios en la liberación, concentración en plasma materno, composición y actividad de exosomas placentarios en asociación con la preeclampsia. En esta revisión se analiza el origen de los exosomas placentarios y cómo podrían estar involucrados en la fisiopatología de la preeclampsia.
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Hernandez, Elisa, Orlando Rodas, Juan C. Barrios, Camilo Carías, and Vivian Pérez. "Falta de evidencia de transmisión vertical y hallazgos histopatológicos en restos placentarios de pacientes con diagnóstico de Síndrome Respiratorio Agudo Severo por Coronavirus 2 (SARS-CoV-2) en Guatemala." Ciencia, Tecnología y Salud 7, no. 3 (November 26, 2020): 495–500. http://dx.doi.org/10.36829/63cts.v7i3.998.
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El primer caso de infección por el virus SARS-CoV-2, fue reportado en la ciudad de Wuhan, China en diciembre de 2019. Desde entonces la enfermedad se ha dispersado a más de 188 países, confirmándose más de 53 millones de casos a nivel mundial. El 13 de marzo de 2020 se reportó el primer caso de COVID-19 en Guatemala y, a mediados del mes de noviembre, se han reportado más de 116,000 casos, 4,000 fallecidos y 106,000 recuperados; con una tasa de mortalidad de 23 por cada 100,000 habitantes y una letalidad del 3.4%. Hasta ahora, la literatura científica disponible abarca ciertos aspectos de salud reproductiva, mientras se continúa recopilando más información que permita conocer más de su impacto real durante el proceso infeccioso y las secuelas derivadas de éste. La presente es una revisión histopatológica de restos placentarios de tres mujeres con resultado positivo para SARS-CoV-2, ingresadas en un hospital privado de la Ciudad de Guatemala. El examen histopatológico del tejido placentario aporta información importante sobre la salud de la madre y del feto. Todos los casos revelaron signos macroscópicos y microscópicos de disfunción placentaria por mala perfusión vascular materna, con formación de infartos hemorrágicos y daño placentario asociado con efectos adversos en el embarazo. Agregando a esto, dos neonatos presentaron un resultado negativo para SARS-CoV-2 y uno falleció. Es de suma importancia el estudio de la placenta de madres positivas a SARS-CoV-2 para conocer el rol de esta durante el embarazo y también, indagar en la posibilidad de transmisión vertical.
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Pacora, Percy, Enrique Oyarzún, Cristián Belmar, Lilia Huiza, Álvaro Santiváñez, and Roberto Romero. "La preeclampsia-eclampsia es un síndrome maternofetal multifactorial." Revista Peruana de Ginecología y Obstetricia 50, no. 4 (May 5, 2015): 223–31. http://dx.doi.org/10.31403/rpgo.v50i423.
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Durante el embarazo normal, el citotrofoblasto convierte su fenotipo epitelial a un fenotipo endotelial (proceso denominado pseudo-vasculogénesis) e invade las arterias maternas espiral. Esta transformación fisiológica de las arterias espirales miometriales aumenta el flujo sanguíneo y el suministro de nutrientes al feto al final del primer trimestre. Factores vasculares, tales como el factor de crecimiento endotelial vascular (VEGF), el factor de crecimiento placentario (PIGF), el receptor soluble tirosinaquinasa-1 similar al fms (sFlt1), participan en este proceso. En el origen de la preeclampsia participan proteínas angiogénicas circulantes. Además, el suero de las mujeres preeclámpticas reduce la viabilidad del trofoblasto, lo que se relaciona a cambios en la sensibilidad del trofoblasto a la apoptosis mediada por Fas, lo que podria ser mediado por citoquinas proinflamatorias, las que han sido encontradas aumentadas en pacientes con preeclampsia. En la preeclompsia, existe una pseudovasculogénesis defectuosa y la isquemia placentaria resultante se ha propuesto que facilita la liberación de factores derivados de la placenta. Los factores estresantes intervendrían en forma aislada o simultánea sobre el organismo vivo materno-placenta/embrión-feto. El organismo vivo respondería ante el estrés, de acuerdo a su predisposición genética, con una respuesta inflamatoria, el síndrome metabólico, la disminución de la perfusión placentaria, el aumento del estres oxidativo y la deficiencia de la relación prostaciclina/oxido nítrico. Por tanto, la hipertensión arterial es una respuesta adaptativa de la unidad materno-fetal, y sería una consecuencia y no la causa de la enfermedad. La toxemia del embarazo o preeclampsia-eclampsia es un síndrome multifactorial de origen materno-fetal, con un clínico variado, en el que la hipertensión arterial no siempre está presente.
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Read, MA, WB Giles, IM Leitch, AL Boura, and WA Walters. "Vascular responses to sodium nitroprusside in the human fetal-placental circulation." Reproduction, Fertility and Development 7, no. 6 (1995): 1557. http://dx.doi.org/10.1071/rd9951557.
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This study examined the activity of sodium nitroprusside (SNP) in the human fetal-placental circulation in vitro in pathological and experimental conditions in which vascular function may be impaired. SNP (13-3400 nM) caused a concentration-dependent reduction in fetal arterial perfusion pressure (FAP) in Krebs' perfused placental cotyledons, at basal tone and following pre-constriction with prostaglandin F2 alpha (PGF2 alpha). SNP-induced reduction in FAP in the PGF2 alpha pre-constricted fetal-placental circulation was enhanced approximately six-fold (5.85) in those placentae pre-treated with the nitric oxide (NO) synthase inhibitor N omega-nitro-L-arginine (100 microM). Reductions in FAP in the preconstricted fetal-placental vasculature caused by SNP were not altered by prior infusion of ouabain (100 nM) into the fetal circulation or during low oxygen perfusion (O2 tension < 50 mmHg). No differences were observed in the responses obtained to SNP in placentae obtained from women with normotensive pregnancies or those associated with (i) pregnancy-induced hypertension, (ii) intra-uterine growth retardation, or (iii) an elevated umbilical-artery Doppler-ultrasound systolic/diastolic ratio, in either preconstricted placentae or those at basal tone. These findings are consistent with an up-regulation of guanylate cyclase/cGMP-mediated vasodilatation in the fetal-placental vasculature following complete blockade of endogenous NO production.
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Delforce, Sarah J., Eugenie R. Lumbers, Stacey J. Ellery, Padma Murthi, and Kirsty G. Pringle. "Dysregulation of the placental renin–angiotensin system in human fetal growth restriction." Reproduction 158, no. 3 (September 2019): 237–45. http://dx.doi.org/10.1530/rep-18-0633.
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Fetal growth restriction (FGR) is a pregnancy complication wherein the foetus fails to reach its growth potential. The renin–angiotensin system (RAS) is a critical regulator of placental function, controlling trophoblast proliferation, angiogenesis and blood flow. The RAS significantly influences uteroplacental blood flow through the balance of its vasoconstrictive and vasodilatory pathways. Although the RAS is known to be dysregulated in placentae from women with preeclampsia, the expression of the RAS has not yet been studied in pregnancies compromised by FGR alone. This study investigated the mRNA expression and protein levels of RAS components in placentae from pregnancies compromised by FGR. Angiotensin II type 1 receptor (AGTR1) and angiotensin-converting enzyme 2 (ACE2) mRNA levels were reduced in FGR placentae compared with control (P = 0.012 and 0.018 respectively). Neprilysin (NEP) mRNA expression was lower in FGR placentae compared with control (P = 0.004). mRNA levels of angiotensinogen (AGT) tended to be higher in FGR placentae compared with control (P = 0.090). Expression of prorenin, AGT, angiotensin-converting enzyme (ACE) or ACE2 proteins were similar in control and FGR placentae. The renin-AGT reaction is a first order reaction so levels of expression of placental AGT determine levels of Ang II. Decreasing levels of ACE2 and/or NEP by limiting the production of Ang-(1-7), which is a vasodilator, and increasing placental Ang II levels (vasoconstrictor) may result in an imbalance between the vasoconstrictor and vasodilator arms of the placental RAS. Ultimately this dysregulation of the placental RAS could lead to reduced placental perfusion that is evident in FGR.
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Lacunza Paredes, Rommel Omar, and Jorge Ávalos Gómez. "Angioarquitectura placentaria y los orígenes de la patología monocorial." Revista Peruana de Ginecología y Obstetricia 61, no. 3 (November 12, 2015): 255–61. http://dx.doi.org/10.31403/rpgo.v61i1853.
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Los gemelos coriangiopagos (fetos que comparten una placenta) pueden tener de manera exclusiva asimetría en la distribución de territorios placentarios, con alta incidencia de inserción marginal y algunas veces en velamento del cordón umbilical; además, transfusiones interfetales (agudas o crónicas) que se producen por la presencia de comunicaciones sanguíneas (anastomosis placentarias). Resulta así una serie de fenotipos fetales que solo se presentan en este tipo de embarazos, en orden de frecuencia, el síndrome de transfusión feto-fetal, restricción del crecimiento intrauterino selectivo, síndrome de anemia-policitemia y la secuencia arterial reversa (twin reversed arterial perfusion - TRAP), pudiendo coexistir más de uno en un mismo embarazo. Es importante entonces el estudio de la angioarquitectura placentaria en los gemelos monocoriónicos, para comprender el comportamiento y el fenotipo que resultara en cada embarazo.
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Gude, NM, RG King, and SP Brennecke. "Endothelin: release by and potent constrictor effect on the fetal vessels of human perfused placental lobules." Reproduction, Fertility and Development 3, no. 4 (1991): 495. http://dx.doi.org/10.1071/rd9910495.
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Human placental lobules were bilaterally perfused with a modified Krebs solution at constant flow rates of 5 mL min-1, and fetal inflow perfusion pressure was recorded. The effect of infusions of endothelin-1 and endothelin-3 (ET-1 and ET-3) on the perfusion pressure was assessed and compared with that for the thromboxane A2-mimetic U46619 and prostaglandin F2 alpha (PGF2 alpha). All substances caused significant increases in pressure, ET-1 being the most potent, followed in order by U46619, ET-3 and PGF2 alpha. In addition, ET-like immunoreactivity was identified in the fetal effluent of placental lobules during 4 h of basal perfusion. The mean ET-1 equivalent immunoreactivity at 1 h of perfusion was 0.6 +/- 0.2 fmol min-1 g-1 of wet lobule weight for 10 placentae. These data suggest that human fetal placental endothelial cells are capable of synthesizing ETs and that ETs are potent constrictors of the fetal placental vessels. Thus, endothelins may play a role in the control of fetal vascular tone in the human placenta in normal and/or pathological conditions.
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Pacheco Romero, José. "Disfunción endotelial en la preeclampsia." Anales de la Facultad de Medicina 64, no. 1 (March 11, 2013): 43. http://dx.doi.org/10.15381/anales.v64i1.1421.
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Desconocemos aún la etiología de la preeclampsia, pero ahora sabemos que no es sólo una hipertensión inducida por el embarazo, sino que existe interacción entre una perfusión placentaria disminuida y la alteración en la función endotelial materna, probablemente por razones inmunológicas de rechazo parcial a la placentación normal. La contribución materna es de factores que anteceden al embarazo, influenciados por las adaptaciones metabólicas usuales. No existe un gen único que pueda explicar la preeclampsia, pero conocer la predisposición materna permite prevenir la preeclampsia en un grupo de mujeres.
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Rodda, C. P., M. Kubota, J. A. Heath, P. R. Ebeling, J. M. Moseley, A. D. Care, I. W. Caple, and T. J. Martin. "Evidence for a novel parathyroid hormone-related protein in fetal lamb parathyroid glands and sheep placenta: comparisons with a similar protein implicated in humoral hypercalcaemia of malignancy." Journal of Endocrinology 117, no. 2 (May 1988): 261–71. http://dx.doi.org/10.1677/joe.0.1170261.
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ABSTRACT Parathyroid hormone (PTH)-like bioactivity, assayed as adenylate cyclase response in UMR 106-01 osteogenic sarcoma cells, was present in extracts of sheep fetal and maternal parathyroid glands and placenta. Preincubation of extracts with PTH(1–34) antiserum inhibited approximately 40% of the bioactivity in fetal parathyroid extracts, 50% in maternal parathyroid extracts, but only 10% of the bioactivity in the placental extract. Partial purification of placental extracts by chromatography yielded fractions containing PTH-like bioactivity which were similar in behaviour to that of PTH-related protein (PTHrP) from a human lung cancer cell line (BEN). An antiserum against synthetic PTHrP(1–16) partially inhibited the bioactivity of the placental extract and synthetic PTHrP(1–34), but had no effect on the bioactivity of bovine PTH(1–34) or bovine PTH(1– 84). The placental PTH-like bioactivity was higher in mid- than in late gestation. Fetal parathyroid glands contained the highest PTH-like bioactivity. Thyroparathyroidectomy of one fetal twin lamb in each of 16 ewes between 110 and 125 days of gestation resulted in decreases of the plasma calcium concentration and reversal of the placental calcium gradient that existed between the ewe and the intact fetus. Perfusion of the placenta of each twin in anaesthetized ewes was carried out sequentially with autologous fetal blood in the absence of the exsanguinated fetus. The plasma calcium concentration in the blood perfusing the placenta of each twin increased, but reached a plateau at a lower concentration in the perfusing blood of thyroparathyroidectomized fetuses than in that of the intact fetuses. Addition of extracts of fetal parathyroid glands or of partially purified PTHrP resulted in further increases in plasma calcium in the autologous blood perfusing the placentae of thyroparathyroidectomized fetuses, but addition of bovine PTH(1–84) or rat PTH(1–34) had no effect. The presence of this PTH-like protein in the fetal parathyroid gland and placenta may contribute to the relative hypercalcaemia of the fetal lamb. This protein, which is similar to PTHrP associated with humoral hypercalcaemia of malignancy, stimulates the placental calcium pump responsible for maintaining a relative fetal hypercalcaemia during gestation. J. Endocr. (1988) 117, 261–271
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Bainbridge, Shannon A., and Graeme N. Smith. "The effect of nicotine on in vitro placental perfusion pressure." Canadian Journal of Physiology and Pharmacology 84, no. 8-9 (September 2006): 953–57. http://dx.doi.org/10.1139/y06-037.
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Cigarette smoking throughout pregnancy is associated with several negative outcomes, of which an increased incidence of intra-uterine growth restriction (IUGR) is most pronounced. Gestationally age-matched infants born to smoking mothers are, on average, 200 g lighter at birth, per pack smoked per day. The mechanisms and specific tobacco compounds responsible for the increased risk of IUGR among smokers have yet to be identified; however, it is widely accepted that smoking women have compromised placental perfusion throughout gestation due to the vasoconstricting effect of nicotine on uterine and placental blood vessels. Despite the universal acceptance of this theory, very little work has been completed to date examining the vasoactive properties of nicotine within the human placenta. The objective of this study was to determine the effect of nicotine on placental vascular function. Normal-term human placentae were obtained after elective cesarean sections. An in vitro placental perfusion system was used; increasing doses of nicotine (20–240 ng/mL) were added to either the maternal (n = 5) or fetal (n = 3) circulation. The basal feto-placental perfusion pressure was 39.87 ± 4.3 mmHg and was not affected by nicotine. This finding supports the hypotheses that nicotine does not directly affect placental microvascular function and that any contribution to fetal growth restriction is likely at the level of placental function (i.e., amino acid transport) and (or) uterine vascular function.
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Moore, J. M., B. Nahlen, A. V. O. Ofulla, J. Caba, J. Ayisi, A. Oloo, A. Misore, A. J. Nahmias, A. A. Lal, and V. Udhayakumar. "A simple perfusion technique for isolation of maternal intervillous blood mononuclear cells from human placentae." Journal of Immunological Methods 209, no. 1 (November 1997): 93–104. http://dx.doi.org/10.1016/s0022-1759(97)00162-2.
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Hirschmugl, Birgit, Simone Perazzolo, Bram G. Sengers, Rohan M. Lewis, Michael Gruber, Gernot Desoye, and Christian Wadsack. "Placental mobilization of free fatty acids contributes to altered materno-fetal transfer in obesity." International Journal of Obesity 45, no. 5 (February 26, 2021): 1114–23. http://dx.doi.org/10.1038/s41366-021-00781-x.
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Abstract Background Metabolic changes in obese pregnant women, such as changes of plasma lipids beyond physiological levels, may subsequently affect fetal development in utero. These metabolic derangements may remain in the offspring and continue throughout life. The placenta mediates bidirectional exchange of nutrients between mother and fetus. The impact of prepregnancy obesity on placental transfer of lipids is still unknown. Objective We aimed to examine materno-to-fetal free fatty acid (FFA) transfer by a combined experimental and modeling approach. Flux of 13C-labeled FFA was evaluated by ex vivo perfusion of human placentae as a function of prepregnancy obesity. Mathematical modeling complemented ex vivo results by providing FFA kinetic parameters. Results Obesity was strongly associated with elevated materno-to-fetal transfer of applied 13C-FFA. Clearance of polyunsaturated 13C-docosahexaenoic acid (DHA) was most prominently affected. The use of the mathematical model revealed a lower tissue storage capacity for DHA in obese compared with lean placentae. Conclusion Besides direct materno-to-fetal FFA transfer, placental mobilization accounts for the fetal FA supply. Together, with metabolic changes in the mother and an elevated materno-fetal FFA transfer shown in obesity, these changes suggest that they may be transmitted to the fetus, with yet unknown consequences.
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Alva-Menesses, Carlos, Santiago Llatas-Delgado, and Karín Montenegro-Díaz. "Acardia fetal en un embarazo triple." Revista del Cuerpo Médico del HNAAA 10, no. 1 (September 8, 2018): 40–42. http://dx.doi.org/10.35434/rcmhnaaa.2017.101.44.
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Se presenta el caso de una paciente de 24 años que ingresa al Hospital Regional de Lambayeque con una gestación doble bicorial biamniótica de 34 semanas 4 días por ecografía de II trimestre, en cuya ecografía al ingreso se evidenciaba una imagen dependiente de placenta probable teratoma placentario. Es hospitalizada con diagnósticos: Amenaza de parto pretérmino, feto 2 en transverso. Habiendo recibido tocólisis y maduración pulmonar se culmina la gestación por cesárea por parto pretérmino, obteniéndose dos recién nacidos de adecuado peso para la edad gestacional con dos placentas y una masa sólida de tejido embrionario con cordón procedente de una de las placentas, cuya anatomía patológica concluye: feto acárdico amorfo, producto de una perfusión feto fetal.
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Hnat, Michael, and Roger E. Bawdon. "Transfer of Meropenem in the ex Vivo Human Placenta perfusion Model." Infectious Diseases in Obstetrics and Gynecology 13, no. 4 (2005): 223–27. http://dx.doi.org/10.1155/2005/961356.
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Objectives.To determine maternal-fetal transplacental passage of meropenem in the ex vivo human perfusion model.Study design.Term placentae (n= 6) were collected immediately after delivery. A single cotyledon was localized, perfused and stabilized with physiologic Eagles minimal essential medium containing 3% bovine albumin and heparin as described by Chalier (Chalier JC. Criteria for evaluating perfusion experiments and presentation results. Contrib Gynecol Obstet 1985; 13:32–39). Meropenem was added to the maternal medium in concentrations similar to maternal serum peak and trough levels, then perfused through the maternal circulation of the cotyledon. To assess transfer and accumulation, fluid aliquots from both the maternal and fetal compartments were collected over an hour at defined intervals in an open and closed system. AntipyrineC14was added to the medium in order to calculate the transport fraction and clearance indexes. Meropenem and antipyrineC14concentrations were determined by High-pressure Liquid Chromatography and liquid scintillation, respectively.Results.Mean antipyrine transport fraction was 2.33 + 0.25. Maternal and fetal mean meropenem peak concentrations were 54.3 + 3.3μg/ml and 2.2 + 0.18μg/ml, respectively. Whereas, maternal and fetal mean trough concentrations were 12.7 + 1.3μg/ml and 0.41 + 0.10μg/ml, respectively. Mean peak clearance index was 0.077 + 0.007 and the mean trough was 0.052 + 0.015. Mean accumulation for the peak and trough concentrations of meropenem were 0.9 and 2.95μg/ml, respectively.Conclusions.Transplacental passage of meropenem was incomplete in the ex vivo human placental perfusion model. Accumulation was also noted in the fetal compartment
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Bapat, Priya, Reuven Kedar, Nir Melamed, Jeremy Matlow, Angelika Lubetsky, Katarina Aleksa, Howard Berger, and Gideon Koren. "The Transfer Of Dabigatran and Rivaroxaban Across a Dually Perfused Isolated Human Placental Cotyledon – Implications For Therapy In Pregnancy." Blood 122, no. 21 (November 15, 2013): 1142. http://dx.doi.org/10.1182/blood.v122.21.1142.1142.
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Abstract Background Anticoagulant therapy is often required in cases of high-risk pregnancy for the prophylaxis of venous thromboembolism following surgery, atrial fibrillation, and congestive heart failure, and for the prevention of pregnancy loss in thrombophilic women. During pregnancy, the concentrations of many blood-clotting factors rise, thereby increasing the need for anticoagulants that are safe to use throughout gestation. Dabigatran (Pradaxa®) and rivaroxaban (Xarelto®) are newer generation oral anticoagulants that are increasingly being prescribed to women of reproductive age for the treatment of thromboembolic disorders. Dabigatran acts by directly inhibiting thrombin, and rivaroxaban acts as a direct factor Xa inhibitor. However, the information regarding fetal safety and placental transfer of these drugs is currently lacking. If there is limited transfer of either drug across the placenta, then it may not increase the risk of bleeding in the fetus. The objective of this study was to determine the transplacental kinetics of dabigatran and rivaroxaban. Methods Placentae were obtained with informed consent after elective caesarean section of healthy term pregnancies in Toronto, Ontario. The transplacental transfer of dabigatran and rivaroxaban were separately assessed using ex vivo dual perfusion of an isolated human placental cotyledon. Dabigatran, at a concentration of 35 ng/ml, was added to the maternal circulation at the start of the experimental phase. Maternal and fetal samples were taken throughout the pre-experimental (1 h) and experimental (3 h) phases for measurement of dabigatran and markers of placental viability. Separate placenta perfusions with rivaroxaban were conducted at an initial maternal concentration of 250 ng/ml. The perfused drug was measured in maternal and fetal samples using liquid chromatography-mass spectrometry (LC/MS). Results There was slow transfer of dabigatran from the maternal to fetal circulation. The fetal-to-maternal (F:M) concentration ratio was 0.33 ± 0.13 after 3 hours (n=3). In contrast, the transfer of rivaroxaban from maternal to fetal circulation was much more rapid, as characterized by a F:M ratio of 0.72 ± 0.12 at 3 hour (n=4), suggesting rapid equilibrium between maternal and fetal circulations. Placental viability markers for all perfusions were within normal ranges. Conclusions This is the first direct evidence of the transfer of dabigatran and rivaroxaban across the human placenta from the mother to fetus. It suggests less fetal exposure to dabigatran. Disclosures: No relevant conflicts of interest to declare.
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Valdivia, Julio. "Disfunción endotelial en la preeclampsia." Anales de la Facultad de Medicina 64, no. 3 (March 11, 2013): 199. http://dx.doi.org/10.15381/anales.v64i3.1444.
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Estimado Dr. José Pacheco R.: Soy el Dr Julio Valdivia Silva de la Universidad Nacional San Agustin de Arequipa, pertenesco al Grupo de Investigación en Inmunología y a la División dentro del mismo de Bilogía Vascular. He leído con mucho interés la revisión realizada por Ud. sobre Disfunción endotelial y preeclampsia, publicada en la revista Anales de la Facultad de Medicina UNMSM Vol.64 páginas 43-54, en la cual establece una relación de baja perfusión placentaria como gatillo inicial en la fisiopatología de preeclampsia provocada principalmente por un rechazo parcial inmune a la invasión trofoblástica. Durante su revisión a nombrado una serie de factores humorales disrregulados que tendrían que ver al final con el aumento de la presión arterial y la aparición de los diferentes signos en preeclampsia-eclampsia.
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Holt, Daphne E., and Rekha Bajoria. "The role of nitro-reduction and nitric oxide in the toxicity of chloramphenicol." Human & Experimental Toxicology 18, no. 2 (February 1999): 111–18. http://dx.doi.org/10.1177/096032719901800208.
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1 Recent work on the toxicology of chloramphenicol suggests that its propensity to cause damage to the blood forming organs may be related to its potential for nitro-reduction and the subsequent production of nitric oxide. 2 In this study both aerobic and anaerobic nitro-reduction of chloramphenicol by human foetal and neonatal liver results in the production of the amine derivative. However intermediates of the reaction nitroso-or glutathionesulphinamido-chloramphenicol could not be detected by hplc. 3 Perfusion of chloramphenicol through isolated lobules of human placentae caused a decrease in blood pressure at a time which coincided with a peak of nitric oxide production. However, although the pressure drop could be reversed by an inhibitor of nitric oxide synthetase, the nitric oxide profile remained the same. 4 These observations suggest that involvement of the para-nitro group of chloramphenicol could cause both hemotoxicity and hypotension in susceptible individuals.
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King, RG, NM Gude, Iulio JL Di, and SP Brennecke. "Regulation of human placental fetal vessel tone: role of nitric oxide." Reproduction, Fertility and Development 7, no. 6 (1995): 1407. http://dx.doi.org/10.1071/rd9951407.
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Factors affecting fetal vessel resistance have been studied in vitro in bilaterally perfused lobules of human placentae. Potent and efficacious constrictors in this preparation (in order of potency) include endothelin-1 > the thromboxane mimetic U46619 > endothelin-3 > prostaglandin F2 alpha. Inhibitors of eicosanoid synthesis did not affect fetal vessel basal perfusion pressure, nor did they potentiate the effects of the vasoconstrictor U46619. In contrast, the nitric oxide inhibitors N omega-nitro-L-arginine (NOLA), haemoglobin and methylene blue all increased fetal vessel basal perfusion pressure and also increased U46619-induced constriction. Similarly, NOLA markedly potentiated the constrictor effects of endothelin-1, angiotensin II, 5-hydroxytryptamine and bradykinin. These studies therefore provide evidence that NO is important in the maintenance of low basal fetal vessel impedance and also reduces the effects of a number of vasoconstrictor autacoids. Nitric oxide synthase (NOS) activity of human placental homogenates has been measured and shown to be mainly calcium-dependent. Human placental NOS activity was not affected by labour state but was reduced in pre-eclampsia. No evidence was found that in pre-eclampsia raised concentrations of the endogenous NOS inhibitor asymmetric dimethylarginine were responsible for the reduced placental NOS activity. Hence, these studies provide evidence that NO is an important endogenous dilator of the fetal vessels of the human placenta and that reduced NOS activity could contribute to the pathogenesis and/or effects of pre-eclampsia.
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Karimu, AL, and GJ Burton. "The distribution of microvilli over the villous surface of the normal human term placenta is homogenous." Reproduction, Fertility and Development 7, no. 5 (1995): 1269. http://dx.doi.org/10.1071/rd9951269.
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The study was carried out to estimate stereologically whether regional differences exist in the distribution of microvilli between vasculo-syncytial (VSM) and non-vasculo-syncytial (non-VSM) areas of the villous surface in normal term placenta. In ten placentae a normal lobe was perfusion-fixed at a pressure of 60 mm Hg, and the intervillous space was perfused at 10 mm Hg. The tissue was routinely processed for ultrastructural examination. Stereological estimates relating to the length and diameter of microvilli, and to the villous surface amplification factor in adjacent but contrasting (VSM and non-VSM) regions, were obtained. A paired 't' test showed no significant difference in the villous surface amplification factor between the two regions (5.18 +/- 0.54 and 5.22 +/- 0.54 respectively, mean +/- s.e.m. P > 0.05). In addition, there were no significant differences between the length and diameter of microvilli in both regions (P > 0.05 in both). The results confirm that the normal term placenta has a continuous and even covering of microvilli over the syncytium.
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Olaya-Contreras, Mercedes, William Vargas-Moreno, and Jaime Eduardo Bernal-Villegas. "Una aproximación desde la física a las consecuencias patológicas de la longitud excesiva del cordón umbilical." Revista Colombiana de Obstetricia y Ginecología 66, no. 1 (March 30, 2015): 53. http://dx.doi.org/10.18597/rcog.8.
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<p>Introducción: el cordón umbilical es una estructura incomprendida a pesar de transportar todo lo que un feto necesita para crecer y subsistir. Cada una de sus características es relevante, y la principal es la longitud, la cual, cuando está alterada, se relaciona con pobre pronóstico neurológico y muerte fetal.<br />Materiales y métodos: con base en la revisión de principios físicos, se proponen fórmulas que podrían explicar la importancia de la longitud del cordón por sus repercusiones hemodinámicas.<br />Resultados: se analizó la circulación fetal desde el corazón hasta la red capilar vellositaria en el plato placentario y, por medio de fórmulas físicas, se plantea la importancia de la longitud del cordón en la perfusión fetal.<br />Conclusiones: las complicaciones clínicas conocidas para la excesiva longitud del cordón umbilical fueron analizadas desde el punto de vista de la física, dejando listas las fórmulas para ser alimentadas con datos reales provenientes de doppler fetales y mediciones del cordón umbilical.</p><p> </p>
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Holcberg, G., A. Amash, O. Sapir, E. Sheiner, S. Levy, L. Myatt, and M. Huleihel. "Perfusion with lipopolysaccharide differently affects the secretion of interleukin-1 beta and interleukin-1 receptor antagonist by term and preterm human placentae." Placenta 29, no. 7 (July 2008): 593–601. http://dx.doi.org/10.1016/j.placenta.2008.03.008.
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Lattanzi, Wanda, Rosa P. De Vincenzo, Fabio De Giorgio, Egidio Stigliano, Arnaldo Capelli, and Vincenzo Arena. "An Acephalus Acardius Amorphous Fetus in a Monochorionic Pregnancy With Sex Discrepancy." Twin Research and Human Genetics 9, no. 5 (October 1, 2006): 697–702. http://dx.doi.org/10.1375/twin.9.5.697.
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AbstractAcephalus acardia is among the most severe malformations described in fetuses, with an incidence of about 1 in 35,000 births and is due to twin-to-twin transfusion syndrome, frequently occurring in monochorionic twin pregnancies. The severity of the syndrome depends upon the type of the anastomoses arising between the vascular networks of the two fetuses, usually configuring the ‘twin reverse arterial perfusion syndrome’. No clear and univocal etiological explanation is known, though few cases with chromosomal abnormalities have been reported so far. In some cases the fusion of two or more separate placentae of dizygotic fetuses occurs, leading to monochorionic twinning. Few cases of acardius amorphous with complete autoptical examination have been described so far. We report a case of acephalus acardius amorphus fetus, showing features of extremely severe sistemic immaturity with very few structured organs. Defined external and autoptic examinations have been performed on the dismorphic twin, along with the histological examination of tissue samples. Kariotype analysis showed sex discrepancy between the twins, as a normal female kariotype had been detected in the acephalus acardius while the living co-twin was a normal healthy male. The analysis of the placenta showed the vascular anomalies leading to the twin-to-twin transfusion syndrome.
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Jakoubek, Vít, Jana Bíbová, Jan Herget, and Václav Hampl. "Chronic hypoxia increases fetoplacental vascular resistance and vasoconstrictor reactivity in the rat." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 4 (April 2008): H1638—H1644. http://dx.doi.org/10.1152/ajpheart.01120.2007.
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An increase in fetoplacental vascular resistance caused by hypoxia is considered one of the key factors of placental hypoperfusion and fetal undernutrition leading to intrauterine growth restriction (IUGR), one of the serious problems in current neonatology. However, although acute hypoxia has been shown to cause fetoplacental vasoconstriction, the effects of more sustained hypoxic exposure are unknown. This study was designed to test the hypothesis that chronic hypoxia elicits elevations in fetoplacental resistance, that this effect is not completely reversible by acute reoxygenation, and that it is accompanied by increased acute vasoconstrictor reactivity of the fetoplacental vasculature. We measured fetoplacental vascular resistance as well as acute vasoconstrictor reactivity in isolated perfused placentae from rats exposed to hypoxia (10% O2) during the last week of a 3-wk pregnancy. We found that chronic hypoxia shifted the relationship between perfusion pressure and flow rate toward higher pressure values (by ∼20%). This increased vascular resistance was refractory to a high dose of sodium nitroprusside, implying the involvement of other factors than increased vascular tone. Chronic hypoxia also increased vasoconstrictor responses to angiotensin II (by ∼75%) and to acute hypoxic challenges (by >150%). We conclude that chronic prenatal hypoxia causes a sustained elevation of fetoplacental vascular resistance and vasoconstrictor reactivity that are likely to produce placental hypoperfusion and fetal undernutrition in vivo.
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Orrego G., Jaime, Juan Camilo Mosquera-Hernández, Santiago Ardila-Giraldo, Laura Torres-Canchala, Edgar Alzate, and Juan Pablo Benavidez. "Técnica EXIT como manejo de la vía aérea en masas gigantes congénitas de cuello." Revista Chilena de Pediatría 91, no. 3 (June 19, 2020): 398. http://dx.doi.org/10.32641/rchped.v91i3.1385.
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Las masas congénitas de cabeza y cuello se asocian a asfixia perinatal e injuria cerebral con elevada mortalidad. La técnica EXIT (Ex Útero Intrapartum Treatment) consiste en asegurar la vía aérea del neonato, sin interrumpir la oxigenación y perfusión materno-fetal a través del soporte placentario. Esta técnica no ha sido estandarizada en países de medianos ingresos.Objetivo: Describir el caso clínico de 2 neonatos manejados mediante la técnica EXIT.Caso Clínico: Se reportan dos casos, uno con malformación linfática diagnosticada a la semana 20 gestación y el segundo con tiromegalia y polihidramnios diagnosticados a la semana 35 de gestación. En ambos casos, durante la cesárea se realizó la técnica EXIT con un equipo conformado por neonatólogo, ginecólogo, anestesiólogo, cirujano pediatra, otorrinolaringólogo, enfermero y terapeuta respiratorio. En los dos pacientes se logró asegurar la vía aérea mediante intubación orotraqueal al primer intento. En el caso 1 se confirmó la malformación linfática y recibió escleroterapia, y en el caso 2 se diagnosticó hipotiroidismo congénito asociado a bocio, que fue manejado con levotiroxina. Los pacientes se mantuvieron 7 y 9 días con ventilación mecánica invasiva respectivamente y egresaron sin complicaciones respiratorias.Conclusiones: La técnica EXIT en estos casos fue un procedimiento seguro, llevado a cabo sin inconvenientes. Se necesita un equipo multidisciplinario y la disponibilidad de una unidad de cuidados intensivos neonatales, con el objetivo de reducir potenciales complicaciones y garantizar el manejo postnatal. Para lograr su ejecución, es indispensable el diagnóstico prenatal oportuno.
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GUDE, N. M., J. L. STEVENSON, E. K. MOSES, and R. G. KING. "Magnesium regulates hypoxia-stimulated apoptosis in the human placenta." Clinical Science 98, no. 4 (February 24, 2000): 375–80. http://dx.doi.org/10.1042/cs0980375.
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Apoptosis (programmed cell death) in the human placenta is likely to play a major role in determining the structure and function of that organ. Fetal growth restriction (FGR) has been shown to be associated with increased levels of placental apoptosis. Altered regulation of apoptosis may play an important pathophysiological role in FGR. As reduced placental perfusion and reduced oxygenation are features of FGR, one aim of this study was to determine the effects of hypoxia on apoptotic activity, as assessed by DNA laddering, of placental tissue in vitro. In addition, levels of placental apoptosis may be affected by pharmacological agents routinely used in obstetric patient management. Thus an additional aim of this study was to determine the effects of several relevant pharmacological agents on the levels of DNA laddering during in vitro incubation of human placentae under hypoxic conditions. Incubation of normal placental explant tissue at 37 °C for 1–2 h under hypoxic conditions significantly increased placental DNA laddering compared with that in non-incubated tissue, whereas levels of DNA laddering during incubation for up to 2 h under normoxic conditions were not significantly higher than those in non-incubated tissue. The DNA laddering activity of placental explants after 2 h of incubation under hypoxic conditions was significantly increased with increased concentrations of magnesium, but remained unchanged by the inclusion of pethidine, aspirin, nifedipine, dexamethasone, heparin or indomethacin in the incubation mixture. These results suggest that hypoxia may stimulate apoptotic activity in cultured human placental tissues, and that hypoxia-stimulated placental apoptosis may be further increased by increasing the extracellular magnesium concentration.
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Vangrieken, Philippe, Salwan Al-Nasiry, Aalt Bast, Pieter A. Leermakers, Christy B. M. Tulen, Ger M. J. Janssen, Iris Kaminski, et al. "Hypoxia-induced mitochondrial abnormalities in cells of the placenta." PLOS ONE 16, no. 1 (January 12, 2021): e0245155. http://dx.doi.org/10.1371/journal.pone.0245155.
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Introduction Impaired utero-placental perfusion is a well-known feature of early preeclampsia and is associated with placental hypoxia and oxidative stress. Although aberrations at the level of the mitochondrion have been implicated in PE pathophysiology, whether or not hypoxia-induced mitochondrial abnormalities contribute to placental oxidative stress is unknown. Methods We explored whether abnormalities in mitochondrial metabolism contribute to hypoxia-induced placental oxidative stress by using both healthy term placentae as well as a trophoblast cell line (BeWo cells) exposed to hypoxia. Furthermore, we explored the therapeutic potential of the antioxidants MitoQ and quercetin in preventing hypoxia-induced placental oxidative stress. Results Both in placental explants as well as BeWo cells, hypoxia resulted in reductions in mitochondrial content, decreased abundance of key molecules involved in the electron transport chain and increased expression and activity of glycolytic enzymes. Furthermore, expression levels of key regulators of mitochondrial biogenesis were decreased while the abundance of constituents of the mitophagy, autophagy and mitochondrial fission machinery was increased in response to hypoxia. In addition, placental hypoxia was associated with increased oxidative stress, inflammation, and apoptosis. Moreover, experiments with MitoQ revealed that hypoxia-induced reactive oxygen species originated from the mitochondria in the trophoblasts. Discussion This study is the first to demonstrate that placental hypoxia is associated with mitochondrial-generated reactive oxygen species and significant alterations in the molecular pathways controlling mitochondrial content and function. Furthermore, our data indicate that targeting mitochondrial oxidative stress may have therapeutic benefit in the management of pathologies related to placental hypoxia.
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Mateus, Julio. "¿Cuál es el efecto de las nuevas definiciones de hipertensión arterial en el adulto sobre el diagnóstico y manejo de esta condición en la gestante y de los trastornos hipertensivos del embarazo?" Revista Peruana de Ginecología y Obstetricia 64, no. 2 (July 16, 2018): 205–9. http://dx.doi.org/10.31403/rpgo.v64i2079.
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El American College of Cardiology (ACC) y el American Heart Association (AHA) publicaron nuevas guías para la prevención, detección, prevención, evaluación y manejo de la hipertensión en el adulto en el 2017 basadas en una revisión comprensiva sistemática de la literatura por parte de un comité científico de expertos. En las definiciones del ACC/AHA, hipertensión arterial se divide en estadio 1 (presión arterial sistólica (PAS) 130-139 mmHg y presión arterial diastólica (PAD) 80-89 mmHg) y estadio 2 (PAS ≥ 140 mmHg y PAD ≥ 90 mmHg). Los objetivos primarios del ACA/AHA son la detección temprana de la enfermedad, evaluación rápida, manejo oportuno y prevención de la enfermedad cardiovascular. Con estos cambios, se estima un aumento del 15 a 20% de la prevalencia de la hipertensión en los Estados Unidos (EE. UU.) en los próximos años. También, se espera un aumento considerable del número de gestantes que van a concebir con el diagnóstico de hipertensión arterial. No se han publicado aun actualizaciones en la clasificación de hipertensión pregestacional y gestacional por parte de organizaciones profesionales como el American College of Obstetricians & Gynecologists (ACOG), pero podrían ser publicadas próximamente. Mientras tanto, nosotros debemos continuar siguiendo las guías clínicas actuales de manejo de estas condiciones. En los EE. UU. se recomienda seguir las guías clínicas publicadas por el ACOG en el 2013, las cuales especifican la clasificación, predicción y manejo de la hipertensión durante el embarazo. En estas guías, hipertensión se define como una presión arterial (PA) ≥ 140/90 mmHg. Según el ACOG, el objetivo en el manejo médico de la hipertensión es mantener la presión arterial (PA) en <160/105 mmHg. Se recomienda el control estricto de la PA < 140/90 mmHg solamente en pacientes con hipertensión, comorbilidades como diabetes pregestacional y daño de órgano blanco. Para las otras pacientes, no se recomienda control estricto de la hipertensión, debido a la falta de evidencia científica de los beneficios y los posibles efectos negativos sobre la perfusión placentaria y el crecimiento fetal. Se espera que el estudio clínico pragmático aleatorizado multicéntrico que se está realizando en los EE. UU. (ClinicalTrials.gov Identifier: NCT02299414) suministre información acerca del mejoramiento de los resultados maternos y perinatales asociados con el control estricto de la PA en pacientes con hipertensión crónica. Por ahora, los especialistas en obstetricia deben continuar siguiendo las recomendaciones del ACOG o de otras organizaciones profesionales y estar atentos a nuevos comunicados por parte de estas organizaciones o expertos en el tema.
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Richards, Claire, Kimberly Sesperez, Michael Chhor, Sahar Ghorbanpour, Claire Rennie, Clara Liu Chung Ming, Chris Evenhuis, et al. "Characterisation of cardiac health in the reduced uterine perfusion pressure model and a 3D cardiac spheroid model, of preeclampsia." Biology of Sex Differences 12, no. 1 (April 20, 2021). http://dx.doi.org/10.1186/s13293-021-00376-1.
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Abstract Background Preeclampsia is a dangerous cardiovascular disorder of pregnancy that leads to an increased risk of future cardiovascular and metabolic disorders. Much of the pathogenesis and mechanisms involved in cardiac health in preeclampsia are unknown. A novel anti-angiogenic protein, FKBPL, is emerging as having a potential role in both preeclampsia and cardiovascular disease (CVD). Therefore, in this study we aimed to characterise cardiac health and FKBPL regulation in the rat reduced uterine perfusion pressure (RUPP) and a 3D cardiac spheroid model of preeclampsia. Methods The RUPP model was induced in pregnant rats and histological analysis performed on the heart, kidney, liver and placenta (n ≥ 6). Picrosirius red staining was performed to quantify collagen I and III deposition in rat hearts, placentae and livers as an indicator of fibrosis. RT-qPCR was used to determine changes in Fkbpl, Icam1, Vcam1, Flt1 and Vegfa mRNA in hearts and/or placentae and ELISA to evaluate cardiac brain natriuretic peptide (BNP45) and FKBPL secretion. Immunofluorescent staining was also conducted to analyse the expression of cardiac FKBPL. Cardiac spheroids were generated using human cardiac fibroblasts and human coronary artery endothelial cells and treated with patient plasma from normotensive controls, early-onset preeclampsia (EOPE) and late-onset preeclampsia (LOPE); n = 3. FKBPL and CD31 expression was quantified by immunofluorescent labelling. Results The RUPP procedure induced significant increases in blood pressure (p < 0.001), collagen deposition (p < 0.001) and cardiac BNP45 (p < 0.05). It also induced a significant increase in cardiac FKBPL mRNA (p < 0.05) and protein expression (p < 0.01). RUPP placentae also exhibited increased collagen deposition and decreased Flt1 mRNA expression (p < 0.05). RUPP kidneys revealed an increase in average glomerular size (p < 0.05). Cardiac spheroids showed a significant increase in FKBPL expression when treated with LOPE plasma (p < 0.05) and a trend towards increased FKBPL expression following treatment with EOPE plasma (p = 0.06). Conclusions The rat RUPP model induced cardiac, renal and placental features reflective of preeclampsia. FKBPL was increased in the hearts of RUPP rats and cardiac spheroids treated with plasma from women with preeclampsia, perhaps reflective of restricted angiogenesis and inflammation in this disorder. Elucidation of these novel FKBPL mechanisms in cardiac health in preeclampsia could be key in preventing future CVD.
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Badachhape, Andrew A., Laxman Devkota, Igor V. Stupin, Poonam Sarkar, Mayank Srivastava, Eric A. Tanifum, Karin A. Fox, Chandrasekhar Yallampalli, Ananth V. Annapragada, and Ketan B. Ghaghada. "Nanoparticle Contrast-enhanced T1-Mapping Enables Estimation of Placental Fractional Blood Volume in a Pregnant Mouse Model." Scientific Reports 9, no. 1 (December 2019). http://dx.doi.org/10.1038/s41598-019-55019-8.
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AbstractNon-invasive methods for estimating placental fractional blood volume (FBV) are of great interest for characterization of vascular perfusion in placentae during pregnancy to identify placental insufficiency that may be indicative of local ischemia or fetal growth restriction (FGR). Nanoparticle contrast-enhanced magnetic resonance imaging (CE-MRI) may enable direct placental FBV estimation and may provide a reliable, 3D alternative to assess maternal-side placental perfusion. In this pre-clinical study, we investigated if placental FBV at 14, 16, and 18 days of gestation could be estimated through contrast-enhanced MRI using a long circulating blood-pool liposomal gadolinium contrast agent that does not penetrate the placental barrier. Placental FBV estimates of 0.47 ± 0.06 (E14.5), 0.50 ± 0.04 (E16.5), and 0.52 ± 0.04 (E18.5) were found through fitting pre-contrast and post-contrast T1 values in placental tissue using a variable flip angle method. MRI-derived placental FBV was validated against nanoparticle contrast-enhanced computed tomography (CE-CT) derived placental FBV, where signal is directly proportional to the concentration of iodine contrast agent. The results demonstrate successful estimation of the placental FBV, with values statistically indistinguishable from the CT derived values.
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Awoyemi, Toluwalase, Carolina Motta-Mejia, Wei Zhang, Lubna Kouser, Kirsten White, Neva Kandzija, Fatimah S. Alhamlan, et al. "Syncytiotrophoblast Extracellular Vesicles From Late-Onset Preeclampsia Placentae Suppress Pro-Inflammatory Immune Response in THP-1 Macrophages." Frontiers in Immunology 12 (June 7, 2021). http://dx.doi.org/10.3389/fimmu.2021.676056.
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Syncytiotrophoblast derived Extracellular Vesicles (STBEV) from normal pregnancy (NP) have previously been shown to interact with circulating monocytes and B cells and induce pro-inflammatory cytokine release. Early-onset preeclampsia (EOPE) is associated with an exacerbated inflammatory response, yet there is little data regarding late-onset PE (LOPE) and immune function. Here, using a macrophage/monocyte cell line THP-1, we investigated the inflammatory potential of STBEV, comprising medium/large-STBEV (>200nm) and small-STBEV (<200nm), isolated from LOPE (n=6) and normal (NP) (n=6) placentae via dual-lobe ex-vivo placental perfusion and differential centrifugation. THP-1 cells bound and internalised STBEV isolated from NP and LOPE placentae, as revealed by flow cytometry, confocal microscopy, and ELISA. STBEV-treated THP-1 cells were examined for cytokine gene expression by RT-qPCR and the cell culture media examined for secreted cytokines/chemokines. As expected, NP medium/large-STBEV significantly upregulated the transcriptional expression of TNF-α, IL-10, IL-6, IL-12, IL-8 and TGF-β compared to PE medium/large-STBEV. However, there was no significant difference in the small STBEV population between the two groups, although in general, NP small STBEVs slightly upregulated the same cytokines. In contrast, LOPE STBEV (medium and large) did not induce pro-inflammatory responses by differentiated THP-1 macrophages. This decreased effect of LOPE STBEV was echoed in cytokine/chemokine release. Our results appear to suggest that STBEV from LOPE placentae do not have a major immune-modulatory effect on macrophages. In contrast, NP STBEV caused THP-1 cells to release pro-inflammatory cytokines. Thus, syncytiotrophoblast extracellular vesicles from LOPE dampen immune functions of THP-1 macrophages, suggesting an alternative mechanism leading to the pro-inflammatory environment observed in LOPE.
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Bongaerts, Eva, Leonie Aengenheister, Battuja B. Dugershaw, Pius Manser, Maarten B. J. Roeffaers, Marcel Ameloot, Tim S. Nawrot, Hannelore Bové, and Tina Buerki-Thurnherr. "Label-free detection of uptake, accumulation, and translocation of diesel exhaust particles in ex vivo perfused human placenta." Journal of Nanobiotechnology 19, no. 1 (May 17, 2021). http://dx.doi.org/10.1186/s12951-021-00886-5.
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Abstract Background Pregnant women and developing fetuses comprise a particularly vulnerable population as multiple studies have shown associations between prenatal air pollution exposure and adverse pregnancy outcomes. However, the mechanisms underlying the observed developmental toxicity are mostly unknown, in particular, if pollution particles can cross the human placenta to reach the fetal circulation. Results Here, we investigated the accumulation and translocation of diesel exhaust particles (DEPs), as a model particle for combustion-derived pollution, in human perfused placentae using label-free detection by femtosecond pulsed laser illumination. The results do not reveal a significant particle transfer across term placentae within 6 h of perfusion. However, DEPs accumulate in placental tissue, especially in the syncytiotrophoblast layer that mediates a wealth of essential functions to support and maintain a successful pregnancy. Furthermore, DEPs are found in placental macrophages and fetal endothelial cells, showing that some particles can overcome the syncytiotrophoblasts to reach the fetal capillaries. Few particles are also observed inside fetal microvessels. Conclusions Overall, we show that DEPs accumulate in key cell types of the placental tissue and can cross the human placenta, although in limited amounts. These findings are crucial for risk assessment and protection of pregnant women and highlight the urgent need for further research on the direct and indirect placenta-mediated developmental toxicity of ambient particulates.
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Guillard, A., E. Gaultier, C. Cartier, L. Devoille, J. Noireaux, L. Chevalier, M. Morin, et al. "Basal Ti level in the human placenta and meconium and evidence of a materno-foetal transfer of food-grade TiO2 nanoparticles in an ex vivo placental perfusion model." Particle and Fibre Toxicology 17, no. 1 (October 7, 2020). http://dx.doi.org/10.1186/s12989-020-00381-z.
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Abstract Background Titanium dioxide (TiO2) is broadly used in common consumer goods, including as a food additive (E171 in Europe) for colouring and opacifying properties. The E171 additive contains TiO2 nanoparticles (NPs), part of them being absorbed in the intestine and accumulated in several systemic organs. Exposure to TiO2-NPs in rodents during pregnancy resulted in alteration of placental functions and a materno-foetal transfer of NPs, both with toxic effects on the foetus. However, no human data are available for pregnant women exposed to food-grade TiO2-NPs and their potential transfer to the foetus. In this study, human placentae collected at term from normal pregnancies and meconium (the first stool of newborns) from unpaired mothers/children were analysed using inductively coupled plasma mass spectrometry (ICP-MS) and scanning transmission electron microscopy (STEM) coupled to energy-dispersive X-ray (EDX) spectroscopy for their titanium (Ti) contents and for analysis of TiO2 particle deposition, respectively. Using an ex vivo placenta perfusion model, we also assessed the transplacental passage of food-grade TiO2 particles. Results By ICP-MS analysis, we evidenced the presence of Ti in all placentae (basal level ranging from 0.01 to 0.48 mg/kg of tissue) and in 50% of the meconium samples (0.02–1.50 mg/kg), suggesting a materno-foetal passage of Ti. STEM-EDX observation of the placental tissues confirmed the presence of TiO2-NPs in addition to iron (Fe), tin (Sn), aluminium (Al) and silicon (Si) as mixed or isolated particle deposits. TiO2 particles, as well as Si, Al, Fe and zinc (Zn) particles were also recovered in the meconium. In placenta perfusion experiments, confocal imaging and SEM-EDX analysis of foetal exudate confirmed a low transfer of food-grade TiO2 particles to the foetal side, which was barely quantifiable by ICP-MS. Diameter measurements showed that 70 to 100% of the TiO2 particles recovered in the foetal exudate were nanosized. Conclusions Altogether, these results show a materno-foetal transfer of TiO2 particles during pregnancy, with food-grade TiO2 as a potential source for foetal exposure to NPs. These data emphasize the need for risk assessment of chronic exposure to TiO2-NPs during pregnancy.
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Jester, Andrea L., M. Reza Saadatzadeh, Brian Johnstone, Victor Njoku, Janak K. Bhavsar, Richard H. Ofstein, Zachary S. Tempel, et al. "Abstract 231: Allogeneic Mesenchymal Stromal Cells Derived from the Chorionic Villi of Human Placentae Are a Superior Source of Progenitor Cells for Angiogenic Therapies." Arteriosclerosis, Thrombosis, and Vascular Biology 32, suppl_1 (May 2012). http://dx.doi.org/10.1161/atvb.32.suppl_1.a231.
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Introduction: Autologous bone marrow mesenchymal stromal cells (ABMSCs) have been the focus for the treatment of myocardial and limb ischemia. The utility of ABMSCs is limited because, in addition to requiring an invasive procedure to harvest, the number and the regenerative capacity of ABMSCs decrease with age and comorbid conditions. A redirected focus on alternative sources of MSCs is warranted. Here we compare MSCs from adipose tissue (ASCs) and human placenta (pMSCs) for angiogenic therapies. Methods: ASCs and pMSCs were characterized using culture assays, flow cytometry and immunofluorescent staining. Immunodulatory properties were assessed using mixed lymphocyte reactions (MLR). Inflammatory and angiogenic cytokines were quantified using ELISA. The ability of ASCs and pMSCs to restore perfusion in a murine model of hindlimb ischemia was compared. Results: ASCs and pMSCs expressed cell surface antigens consistent with MSCs. In permissive cultures, ASCs and pMSCs stained positive for Oil Red O (adipogenic), Alcian Blue (chondrogenic) and alkaline phosphatase (osteogenic) in addition to neural and myogenic lineages. Immunofluorescent staining demonstrated that PMSCs but not ASCs express embryonic stem cell antigens Oct-3/4, Nanog, SSEA-3 and SSEA-4. ASCs and pMSCs demonstrated immunosuppressive properties in MLRs (n=3). There was a significant reduction of MNC proliferation when cultured with pMSCs (96.5 ± 3.7 % reduction; p < 0.001) or ASCs (93.27 ± 2.3 % reduction; p < 0.001). When compared to ASCs, pMSCs (n=3) secrete significantly greater quantities of VEGF (4.4 ± 0.13 vs. 2.5 ± 0.031 ng/mL; p < 0.001), HGF (2.4 ± 0.114 vs. 1.6 ± 0.173 ng/mL; p < 0.001), and Ang-1 (4.6 ± .23 vs. 1.6 ± 0.016 ng/mL; p < 0.001) in hypoxia. In NOD/SCID mice with femoral artery ligation (n=6), those treated with pMSCs demonstrated a significant improvement in perfusion compared to those treated with ASCs at 35 days post-treatment (56.18 vs. 40.82; p < 0.001). Conclusion: In conclusion, while both ASCs and pMSCs have potent immunosuppressive properties, pMSCs are superior in the production of angiogenic cytokines and restoration of perfusion in ischemic tissue. PMSCs can be banked and thus made readily available for the treatment of acute ischemic syndromes.
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Kushwaha, Monika, and Sanjeev Narang. "SIGNIFICANCE OF PLACENTAL HISTOPATHOLOGICAL FINDINGS IN PRETERM/TERM BIRTH." International Journal of Medical and Biomedical Studies 4, no. 5 (May 27, 2020). http://dx.doi.org/10.32553/ijmbs.v4i5.1143.
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Background: This study is cross-sectional, observational and comparative study, at Index Medical College, Hospital & Research Centre, Indore, Madhya Pradesh from July 2017 to July 2019 with sample size 100 placentae.
Method: The placenta received was evaluated blinded of maternal pregnancy outcome. The pattern of morphology was evaluated both qualitatively (type of lesion) and quantitatively (number of lesions).
Result: In Present study 79% of the deliveries were term deliveries and 21% were preterm deliveries. On placental macroscopy, placenta weight was significantly low among the neonates of preterm deliveries (370.00±60.49) as compared to term deliveries (440.89±55.22). Preterm placenta had higher number of abnormal placental lesion compared to term pregnancies.
Conclusion: The uteroplacental insufficiency defined as placental infarct, fibrosis of chorionic villi, thickening of blood vessels, and poor vascularity of chorionic villi. Placental histopathological lesions are strongly associated with maternal under perfusion and uteroplacental insufficiency. These are the reasons for preterm birth. Thus, knowledge of the etiological factor can be use to reduce maternal and neonatal morbidity and mortility.
Keywords: Placenta, Term & Preterm.
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Carmach Ananias, Gabriela Valentina, and Camila Fernanda Escobar Jaramillo. "Resultados obstétricos y perinatales asociados a la infección por COVID-19: una revisión de la literatura." Matronería Actual 1, no. 1 (March 5, 2021). http://dx.doi.org/10.22370/rev.mat.1.2021.2509.
Full textAbstract:
Objetivo: Determinar los resultados obstétricos y/o perinatales que se asocian a la infección por COVID-19, a través de una revisión de la literatura.Metodología: Se realizó una búsqueda avanzada en Pubmed, relacionada con los conceptos paciente e intervención y con los resultados de 67 términos, entre ellos “pregnant”, “newborn”, “Covid-19”, “abortion” y “placental pathology”. Se aplicaron como filtro los años 2019 y 2020 y se encontraron 506 estudios que, a su vez, se filtraron por título, resumen y tipo de estudio, seleccionando aquellos cuya muestra fueran embarazadas y/o neonatos diagnosticados con COVID-19, y que reportaran resultados obstétricos y/o perinatales negativos. Finalmente, se seleccionaron 42. Resultados: Los resultados que destacan por prevalencia o severidad fueron: parto prematuro, patología placentaria, anticuerpos IgM y/o IgG para COVID-19 aumentados en gestantes y recién nacidos, estado fetal no tranquilizador, COVID-19(+) en leche materna, en líquido amniótico o hisopado vaginal, probable transmisión intraparto, ingreso a UCIN, mala perfusión vascular fetal o materna y cesárea por condición materna asociada al virus.Conclusiones: Sugerimos instaurar medidas de prevención oportunas en las gestantes para evitar el contagio por COVID-19 durante y después de la gestación, con el propósito de evitar el riesgo de complicaciones asociadas al virus, las que conllevan importantes consecuencias para la madre y/o el recién nacido.
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Eddy, Adrian C., Heather Chapman, David T. Brown, and Eric M. George. "Differential regulation of sFlt-1 splicing by U2AF65 and JMJD6 in placental-derived and endothelial cells." Bioscience Reports 40, no. 2 (February 2020). http://dx.doi.org/10.1042/bsr20193252.
Full textAbstract:
Abstract Despite years of study, the gestational disorder preeclampsia (PE) remains poorly understood. One proposed mechanism of PE development is increased soluble VEGF receptor-1 (sFlt-1), ultimately causing angiogenic imbalance and endothelial dysfunction. The soluble protein is an alternative splice variant of FLT1, which also encodes for the full-length receptor Flt-1. The mechanism of the alternative splicing, and the reason for its inappropriate increase in preeclampsia, is not well understood. U2 auxiliary factor 65 (U2AF65) and jumonji C domain-containing protein 6 (JMJD6) have been implicated in the splicing of sFlt-1. Using siRNA knockdown and plasmid overexpression in immortalized placental trophoblasts (BeWo) and primary endothelial cells (HUVECs), we examined the role these proteins play in production of sFlt-1. Our results showed that U2AF65 has little, if any, effect on sFlt-1 splicing, and JMJD6 may enhance sFlt-1 splicing, but is not necessary for splicing to occur. Utilizing a hypoxic environment to mimic conditions of the preeclamptic placenta, as well as examining placentae in the reduced uterine perfusion pressure (RUPP) model of PE, which exhibits increased circulating sFlt-1, we found increased expression of JMJD6 in both hypoxic cells and placental tissue. Additionally, we observed a potential role for U2AF65 and JMJD6 to regulate the extracellular matrix enzyme heparanase, which may be involved in the release of sFlt-1 protein from the extracellular matrix. It will be important to study the role of these proteins in different tissues in the future, as changes in expression had differential effects on sFlt-1 splicing in the different cell types studied here.