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Graham J Burton - One of the best experts on this subject based on the ideXlab platform.
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ORIGINAL ARTICLE Placental Structure in Type 1 Diabetes Relation to Fetal Insulin, Leptin, and IGF-I
2013Co-Authors: Scott M. Nelson, Graham J Burton, Philip M. Coan, Robert S. LindsayAbstract:OBJECTIVE—Alteration of placental structure may influence fetal overgrowth and complications of maternal diabetes. We examined the placenta in a cohort of offspring of mothers with type 1 diabetes (OT1DM) to assess structural changes and determine whether these were related to maternal A1C, fetal hematocrit, fetal hormonal, or metabolic axes. RESEARCH DESIGN AND METHODS—Placental samples were analyzed using stereological techniques to quantify volumes and surface areas of key placental components in 88 OT1DM and 39 control subjects, and results related to maternal A1C and umbilical cord analytes (insulin, leptin, adiponectin, IGF-I, hematocrit, lipids, C-reactive protein, and interleukin-6). RESULTS—Intervillous Space volume was increased in OT1DM (OT1DM 250 � 81 cm 3 vs. control 217 � 65 cm 3; P � 0.02) with anisomorphic growth of villi (P � 0.025). The placentas showe
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rheological and physiological consequences of conversion of the maternal spiral arteries for uteroplacental blood flow during human pregnancy
Placenta, 2009Co-Authors: Graham J Burton, Eric Jauniaux, Andrew W Woods, John KingdomAbstract:Physiological conversion of the maternal spiral arteries is key to a successful human pregnancy. It involves loss of smooth muscle and the elastic lamina from the vessel wall as far as the inner third of the myometrium, and is associated with a 5–10-fold dilation at the vessel mouth. Failure of conversion accompanies common complications of pregnancy, such as early-onset preeclampsia and fetal growth restriction. Here, we model the effects of terminal dilation on inflow of blood into the placental Intervillous Space at term, using dimensions in the literature derived from three-dimensional reconstructions. We observe that dilation slows the rate of flow from 2 to 3 m/s in the non-dilated part of an artery of 0.4–0.5 mm diameter to approximately 10 cm/s at the 2.5 mm diameter mouth, depending on the exact radius and viscosity. This rate predicts a transit time through the Intervillous Space of approximately 25 s, which matches observed times closely. The model shows that in the absence of conversion blood will enter the Intervillous Space as a turbulent jet at rates of 1–2 m/s. We speculate that the high momentum will damage villous architecture, rupturing anchoring villi and creating echogenic cystic lesions as evidenced by ultrasound. The retention of smooth muscle will also increase the risk of spontaneous vasoconstriction and ischaemia–reperfusion injury, generating oxidative stress. Dilation has a surprisingly modest impact on total blood flow, and so we suggest the placental pathology associated with deficient conversion is dominated by rheological consequences rather than chronic hypoxia.
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endometrial glands as a source of nutrients growth factors and cytokines during the first trimester of human pregnancy a morphological and immunohistochemical study
Reproductive Biology and Endocrinology, 2004Co-Authors: Joanne Hempstock, Tereza Cindrovadavies, Eric Jauniaux, Graham J BurtonAbstract:Background The maternal circulation to the human placenta is not fully established until 10–12 weeks of pregnancy. During the first trimester the Intervillous Space is filled by a clear fluid, in part derived from secretions from the endometrial glands via openings in the basal plate. The aim was to determine the activity of the glands throughout the first trimester, and to identify components of the secretions.
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maternal arterial connections to the placental Intervillous Space during the first trimester of human pregnancy the boyd collection revisited
American Journal of Obstetrics and Gynecology, 1999Co-Authors: Graham J Burton, Eric Jauniaux, Adrian WatsonAbstract:OBJECTIVE: We sought to determine morphologically when the maternal uterine circulation to the human placenta is established. STUDY DESIGN: We performed a histologic review of 12 early-pregnancy hysterectomy specimens contained within the Boyd Collection, ranging from 43 to 130 days' gestation. RESULTS: Before the eighth week of pregnancy, maternal arterial connections with the Intervillous Space are restricted to tortuous networks of intercellular Spaces. Only after this period can direct channels be observed. Initially, these are of small caliber, but they become sizable and clearly delineated after 11 to 12 weeks. CONCLUSION: The maternal circulation to the placenta must be extremely sluggish before the eighth week of pregnancy but will be gradually established over the next few weeks. It is unlikely to be substantial until at least 12 weeks. The implication is that development of the human fetoplacental unit during most of the first trimester takes place in a low-oxygen environment.
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star volume estimates of the Intervillous clefts in the human placenta how changes in umbilical arterial pressure might influence the maternal placental circulation
Journal of developmental physiology, 1993Co-Authors: A L Karimu, Graham J BurtonAbstract:The study estimated the mean volume of the clefts between adjacent villi in the normal term human placenta, and the effect on this of increasing the fetal perfusion pressure, using a new stereological tool called the 'star volume estimator'. This enables the measurement of irregular and complex structures, including both particles and cavities, in a mathematically defined and unbiased manner. To achieve this, a total of ten term placentae delivered by caesarean section were obtained. Four fetal arteries supplying opposite quadrants of the placental disc were perfusion-fixed under standard pressures of 40, 60, 80 and 100 mmHg respectively. Stereological estimates relating to the star volume of the clefts between the villi, and to the volume density of the Intervillous Space were obtained. There was a significant rise in the star volume of the Intervillous clefts from 26.8 x 10(4) m3 at 40 mm Hg to 75.1 x 10(4) m3 at 100 mmHg (F = 75, df = 1.38, P < 0.05). The volume density of the Intervillous Space remained unchanged, thus obviating the possibility of fluid leakage into the Intervillous Space accounting for this change. It is concluded that the fetal vasculature provides hydraulic support to the villous tree, and that changes in the umbilical perfusion pressure can therefore alter the disposition of the villi within the Intervillous Space. As fetal blood pressure rises, for example during acute hypoxic episodes, the villi will move apart. The enlargement of the clefts between adjacent villi will have a secondary effect upon the maternal circulation, promoting more even perfusion of the Intervillous Space at higher overall flow rates.(ABSTRACT TRUNCATED AT 250 WORDS)
Eric Jauniaux - One of the best experts on this subject based on the ideXlab platform.
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Human Reproduction vol.9 no. 12 pp.2432-2437. 1994 Comparison of colour Doppler features and pathological findings in complicated early pregnancy
2016Co-Authors: Eric Jauniaux, Jamal Zaidi, Davor Jurkovic, Stuart Campbell, Jean HustinAbstract:^ o whom correspondence should be addressed Resistance index (RI) and pulsatility index (PI) in the uterine and spiral arteries, uterine artery peak systolic velocity and Intervillous blood flow were recorded by transvaginal colour Doppler imaging in 30 missed abortions and 30 normal pregnancies matched for menstrual age. Pathological examination was performed in both groups within 24 h of Doppler investigation. The mean uterine PI was significantly (P < 0.01) higher in missed abortions compared to normal controls, whereas the mean uterine RI and peak systolic velocity and spiral RI and PI did not differ. A continuous Intervillous flow was found in 16 out of 23 (69.6%) of the complicated pregnancies before 12 weeks of gestation whereas it was not found in controls. In the missed abortion cases, the trophoblastic shell was fragmented or absent in 53 % and trophoblastic infiltration and physiological changes in the spiral arteries were reduced or absent in 43 and 63%, respectively. These findings were not related to normal or abnormal Doppler indices. Extended dislocation of the trophoblastic shell and a massive infiltration of the Intervillous Space and placental bed by maternal blood was also found in cases presenting with a continuous Intervillous blood flow before 12 weeks of gestation. These findings suggest that abnormal flow velocity waveforms in early pregnancies complicated by embryonic death are related to deficient placentation and dislocation of the trophoblastic shell that follows embryonic demise. The premature entry of maternal blood into the Intervillous Space disrupts the materno-embry-onic interface and is probably the final mechanism causing abortion. Key words: anembryonic/Doppler/missed abortion/placenta/ pregnanc
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rheological and physiological consequences of conversion of the maternal spiral arteries for uteroplacental blood flow during human pregnancy
Placenta, 2009Co-Authors: Graham J Burton, Eric Jauniaux, Andrew W Woods, John KingdomAbstract:Physiological conversion of the maternal spiral arteries is key to a successful human pregnancy. It involves loss of smooth muscle and the elastic lamina from the vessel wall as far as the inner third of the myometrium, and is associated with a 5–10-fold dilation at the vessel mouth. Failure of conversion accompanies common complications of pregnancy, such as early-onset preeclampsia and fetal growth restriction. Here, we model the effects of terminal dilation on inflow of blood into the placental Intervillous Space at term, using dimensions in the literature derived from three-dimensional reconstructions. We observe that dilation slows the rate of flow from 2 to 3 m/s in the non-dilated part of an artery of 0.4–0.5 mm diameter to approximately 10 cm/s at the 2.5 mm diameter mouth, depending on the exact radius and viscosity. This rate predicts a transit time through the Intervillous Space of approximately 25 s, which matches observed times closely. The model shows that in the absence of conversion blood will enter the Intervillous Space as a turbulent jet at rates of 1–2 m/s. We speculate that the high momentum will damage villous architecture, rupturing anchoring villi and creating echogenic cystic lesions as evidenced by ultrasound. The retention of smooth muscle will also increase the risk of spontaneous vasoconstriction and ischaemia–reperfusion injury, generating oxidative stress. Dilation has a surprisingly modest impact on total blood flow, and so we suggest the placental pathology associated with deficient conversion is dominated by rheological consequences rather than chronic hypoxia.
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endometrial glands as a source of nutrients growth factors and cytokines during the first trimester of human pregnancy a morphological and immunohistochemical study
Reproductive Biology and Endocrinology, 2004Co-Authors: Joanne Hempstock, Tereza Cindrovadavies, Eric Jauniaux, Graham J BurtonAbstract:Background The maternal circulation to the human placenta is not fully established until 10–12 weeks of pregnancy. During the first trimester the Intervillous Space is filled by a clear fluid, in part derived from secretions from the endometrial glands via openings in the basal plate. The aim was to determine the activity of the glands throughout the first trimester, and to identify components of the secretions.
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maternal arterial connections to the placental Intervillous Space during the first trimester of human pregnancy the boyd collection revisited
American Journal of Obstetrics and Gynecology, 1999Co-Authors: Graham J Burton, Eric Jauniaux, Adrian WatsonAbstract:OBJECTIVE: We sought to determine morphologically when the maternal uterine circulation to the human placenta is established. STUDY DESIGN: We performed a histologic review of 12 early-pregnancy hysterectomy specimens contained within the Boyd Collection, ranging from 43 to 130 days' gestation. RESULTS: Before the eighth week of pregnancy, maternal arterial connections with the Intervillous Space are restricted to tortuous networks of intercellular Spaces. Only after this period can direct channels be observed. Initially, these are of small caliber, but they become sizable and clearly delineated after 11 to 12 weeks. CONCLUSION: The maternal circulation to the placenta must be extremely sluggish before the eighth week of pregnancy but will be gradually established over the next few weeks. It is unlikely to be substantial until at least 12 weeks. The implication is that development of the human fetoplacental unit during most of the first trimester takes place in a low-oxygen environment.
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maternal circulation in the first trimester human placenta myth or reality
American Journal of Obstetrics and Gynecology, 1997Co-Authors: Richard Jaffe, Eric Jauniaux, J HustinAbstract:The classic theory of development of the uteroplacental and Intervillous circulation determined that maternal blood enters the Intervillous Space in high-pressure streams from the early first trimester. This theory has recently been challenged and our hypothesis to be presented is that the Intervillous circulation is not fully established until the end of the first trimester. Ex vivo studies of hysterectomy specimens have demonstrated that trophoblastic plugs obstruct blood flow into the Intervillous Space in early pregnancy and only at 12 to 13 weeks do these plugs become loose and allow for continuous maternal blood flow into the Intervillous Space. This concept is supported by many other experimental findings. In complicated early pregnancies the uteroplacental circulation demonstrates flow characteristics that are strikingly different from those of normal early pregnancies. In abnormal pregnancies increased flow within the Intervillous Space is demonstrated by color Doppler imaging. Our hypothesis supports other studies that have shown that the embryo favors an environment low in oxygen during early development and that oxygen levels in placental tissue are low in the early first trimester. The classic drawing of placental circulations is based on second- and third-trimester studies, and its applicability to the early first trimester should be revisited because we will show that new data support the hypothesis that the development of the early Intervillous circulation is a progressive phenomenon.
V. Tsatsaris - One of the best experts on this subject based on the ideXlab platform.
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Computational Fluid Dynamic Simulations of Maternal Circulation: Wall Shear Stress in the Human Placenta and Its Biological Implications
PLoS ONE, 2016Co-Authors: E. Lecarpentier, M. Bhatt, G. Bertin, B. Deloison, L. Salomon, P. Deloron, T. Fournier, Abdul I Barakat, V. TsatsarisAbstract:In the human placenta the maternal blood circulates in the Intervillous Space (IVS). The syncytiotrophoblast (STB) is in direct contact with maternal blood. The wall shear stress (WSS) exerted by the maternal blood flow on the STB has not been evaluated. Our objective was to determine the physiological WSS exerted on the surface of the STB during the third trimester of pregnancy.
Poels, Lambert G. - One of the best experts on this subject based on the ideXlab platform.
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Tertiary villi (human placenta, late midpregnancy)
2011Co-Authors: Poels, Lambert G.Abstract:: (A) Left: stain: Hematoxylin - azophloxine. (B) Right: electron microscopy (low magnification). At the left (A) multinucleated syncytiotrophoblast cells (STCs, 1) and vaguely cytotrophoblast cells (CTCs, 2) cover the loose fetal stroma (4). A large and a small arteriole (3) are embedded with stroma. Free cells such as fibroblasts and Hofbauer cells (5) (fetal phagocytes) are present. On ageing, dilated capillaries (6) tend to get localised near the basal membrane of the placental barrier (so-called vasculosyncytial membranes). At the right (B) a low magnification of a few terminal (tertiary) villi is shown: these villi are lined by STCs (1) that contain several distinct nuclei. A single CTC (2) is still present. Several capillaries are located close to the basal lamina of the placental barrier (6) forming the so-called vasculosyncytial membranes. At asterisk a large venule filled with erythrocytes. (5) points to a free fetal phagocyte (Hofbauer cell). (7) indicates Intervillous Space. Background: The placental barrier is formed on the one hand by the CTCs, STCs and a supporting basal lamina and on the other hand by the endothelial cells and basal laminae of the fetal blood capillaries. This barrier separates fetal vessels from the circulating maternal blood in the Intervillous Space, regulates as a membrane the transport of gases, hormones and nutrients in both directions. Embryonic/fetal waste products also pass from embryonal/fetal blood to maternal blood as well. Especially the trophoblastic layers (CTCs and STCs) play an important role in these processes. The barrier partially prevents penetration of foreign material as bacteria, toxins e.a. from maternal blood to fetal blood. However some maternal antigens and numerous viruses (e.g. HIV virus, rubella virus) as well as various drugs are still able to cross this barrier
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Anchoring villi (human placenta, early midpregnancy)
2011Co-Authors: Poels, Lambert G.Abstract:Stain: Hematoxylin -azophloxine. Survey (A) and detail (B). The maternal side at the bottom shows reddish matrix-type fibrinoid accumulations (1) (Rohr's fibrinoid layer) close to an anchoring villus (2) and the cytotrophoblastic cell columns (3). The anchoring villus is lined by cytotrophoblasts (4) which are covered at the outer side by multinuclear syncytiotrophoblasts (5). Intervillous Space is marked by (6). (See also POJA-L1227). (7) is a phagocytic Hofbauer cell, (8) infiltrating extravillous cytotrophoblast cells between the fibrinoid deposits; (9) points to the trophoblasts of the cytotrophoblast shell that covers part of the anchoring villus (3). Arrow (10) indicates a multinuclear trophoblast cell that develops into a placental bed giant cell
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Tertiary villi (human placenta, early pregnancy)
2011Co-Authors: Poels, Lambert G.Abstract:Stain: (A, left) Azan. (B, right) Immunoperoxidase staining with diaminobenzidin (DAB) and hematoxylin counterstaining for human anti-chorionic gonadotrophin (hCG-DAKO 231 antibody). (A) shows blue grey-stained postmitotic multinucleated syncytiotrophoblast cells (STC, 1b), partially cut tangentially (1a). These lining cells display an extensive brush border along the whole surface. Some lysed cells are observed within the Intervillous Space (4).The cytotrophoblasts (2) form a single row of lightly stained cells (CTCs or Langhans cells) closely adhering to the STC, as part of the placental barrier. (3) Loose embryonic connective tissue. (B) The right picture shows that the STCs (1) exclusively are stained positively (brown) for hCG. The CTCs (2), however, remain negative and appear not to be involved in the production of hCG. Due to the DAB-reaction an enhanced staining of the population of dark-brown lysosomal granules of the STCs is obtained
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Anchoring villi (human placenta, early midpregnancy)
2024Co-Authors: Poels, Lambert G.Abstract:Stain: Hematoxylin -azophloxine. The maternal side at the bottom shows reddish matrix-type fibrinoid accumulations (1) (Rohr's fibrinoid layer) close to an anchoring villus (2) and a cytotrophoblastic cell column (3). The anchoring villus is lined by cytotrophoblasts (4) which are covered at the outer side by multinuclear syncytiotrophoblasts (5). Intervillous Space is marked by (6). (See also POJA-L1227). (7) phagocytic Hofbauer cell, (8) decidua cells; (9) points to the trophoblasts of the cytotrophoblast shell that expands laterally and covers the areas between the anchoring villi (3)
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Chorioamnionitis (human)
2024Co-Authors: Poels, Lambert G.Abstract:Histologically chorioamnionitis describes the progression of the inflammatory process. Bacteria firstly colonized the chorioamniotic surface. In first two days polymorphonuclear granulocytes (PMN) migrate to the chorion (chorionitis) marginate and adhere to the bottom of the chorionic plate (stage 1). Subsequently they penetrate the plate in the following days (stage 2) and ultimately may reach the amnion (stage 3, true chorioamnionitis, not shown here) and eventually the amnion epithelium becomes necrotic (necrotizing chorioamnionitis, not shown here). Stain: Hematoxylin-eosin. (A) left side partly teared chorionic plate 1) with two chorionic vessels (2) and infiltration of PMN (3). To the right reddish subchorionic fibrinoid (Langhans, 4) infiltrated by PMN. (5) Intervillous Space with some chorionic villi. (B, C) at higher magnification: A continuous lining of amnion epithelium (6) on a compact layer of acellular stroma (7) followed by a diffuse infiltrate of PMN (3) of varying density and depth of penetration in the chorionic plate (1). Deeper towards the Intervillous Space (5) a band of PMN (3) close to the subchorionic fibrinoid (4) is also present. (Arrows, C) point to diffuse aggregations of likely bacteria. Background. Chorioamnionitis is the most important acute inflammatory disorder of the placenta because of its frequencey (about 20 % of all placentas). The placental and fetal infection occurs via ascending (transcervical route), hematogeneous (transplacental route) or via the oviduct. Ascending infections are mostly bacterial (normal flora of the cervix/vagina) and involve fetal membranes, amniotic fluid and umbilical cord . Generally the amnion cells, chorionic cells and decidual cells produce uterotonins a.o. prostaglandins for uterine contractions. A programmed-weakening process such as collagen remodeling of the cervix occurs under the influence of matrix metalloproteinases with an increased apoptosis in the amnion cells. Together with the result of stretch and shear forces of uterine contractions all these processes result in regular labor with the rupture of fetal membranes. An infection for the fetus causes inflammation resulting in intrauterine hypoxia (villous edema) as well as preterm delivery. Bacterial colonization with release of endo/exotoxins induces production of pro-inflammatory cytokines (IL-1, αTNF with IL-6, IL-8). This leads to neutrophilic activation and stimulation of synthesis/release of uterotonins and activation of matrix metalloproteinases. Preterm labor in fact results from these processes. (By courtesy of G. P. Vooijs MD, PhD, former Head of the Department of Pathology, University Medical Center, St. Radboud University, Nijmegen, The Netherlands
John Kingdom - One of the best experts on this subject based on the ideXlab platform.
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rheological and physiological consequences of conversion of the maternal spiral arteries for uteroplacental blood flow during human pregnancy
Placenta, 2009Co-Authors: Graham J Burton, Eric Jauniaux, Andrew W Woods, John KingdomAbstract:Physiological conversion of the maternal spiral arteries is key to a successful human pregnancy. It involves loss of smooth muscle and the elastic lamina from the vessel wall as far as the inner third of the myometrium, and is associated with a 5–10-fold dilation at the vessel mouth. Failure of conversion accompanies common complications of pregnancy, such as early-onset preeclampsia and fetal growth restriction. Here, we model the effects of terminal dilation on inflow of blood into the placental Intervillous Space at term, using dimensions in the literature derived from three-dimensional reconstructions. We observe that dilation slows the rate of flow from 2 to 3 m/s in the non-dilated part of an artery of 0.4–0.5 mm diameter to approximately 10 cm/s at the 2.5 mm diameter mouth, depending on the exact radius and viscosity. This rate predicts a transit time through the Intervillous Space of approximately 25 s, which matches observed times closely. The model shows that in the absence of conversion blood will enter the Intervillous Space as a turbulent jet at rates of 1–2 m/s. We speculate that the high momentum will damage villous architecture, rupturing anchoring villi and creating echogenic cystic lesions as evidenced by ultrasound. The retention of smooth muscle will also increase the risk of spontaneous vasoconstriction and ischaemia–reperfusion injury, generating oxidative stress. Dilation has a surprisingly modest impact on total blood flow, and so we suggest the placental pathology associated with deficient conversion is dominated by rheological consequences rather than chronic hypoxia.
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oxygen and placental villous development origins of fetal hypoxia
Placenta, 1997Co-Authors: John Kingdom, P KaufmannAbstract:Abstract The increasing practice of preterm delivery in the fetal interest for conditions such as pre-eclampsia or intrauterine growth restriction (IUGR) has provided an opportunity to study placental structure in pregnancies with prenatal evidence of fetal compromise. These data suggest that the origin of fetal hypoxia in IUGR with absent end-diastolic flow in the umbilical arteries is due to a failure of oxygen transport from Intervillous Space to umbilical vein. Failure of the fetoplacental circulation to extract oxygen from the Intervillous Space under such circumstances means Intervillous P o o is closer to maternal arterial values than under physiological conditions. Correspondingly the placental villi are chronically exposed to a higher oxygen tension than under normal circumstances — the term ‘hyperoxia', relative to normal intraplacental oxygenation, is proposed to describe this situation. Both the trophoblast and villous core react to increased oxygen despite fetal hypoxia. These results challenge the generally accepted concept of ‘placental hypoxia' in all circumstances where fetal hypoxia might arise. Therefore three categories are proposed for the origins of fetal hypoxia: (1) preplacental hypoxia; (2) uteroplacental hypoxia; and (3) postplacental hypoxia. Examples for these three disease states are listed in this review and the structural reaction patterns of placental villi to these differences in oxygenation are discussed.
