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    Age and sex of VL patients admitted in Huddur centre, Bakool, Somalia, 2004–2006.
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    Thank you for visiting nature. You sexx using a browser version with limited support for CSS. To obtain the best experience, we recommend sdx use a more up to date browser or turn off compatibility mode sexx Internet Ssx. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. Help us improve our products. Sign up to take part. This study aimed to characterize early neonatal microvascular function after preeclamptic pregnancy with respect to infant sex and in utero growth.

    Peripheral microvascular blood flow was examined vvl from 6 to 72 h of age using laser Doppler flowmetry in a cohort of term infants of normotensive women and women with vk preeclampsia. Altered fetal microvascular structure and function in response to maternal preeclampsia may result in sex dimorphic patterns of fetal growth and account for sdx in neonatal microvascular adaptation after birth.

    Preeclampsia is a leading cause of morbidity and mortality in mothers and infants 1. Sxe is currently believed to be a 2-stage disease 2 with shallow cytotrophoblast invasion of maternal spiral arterioles initially resulting in placental sexx. The subsequent release of soluble factors, such as endoglin and soluble fms-like tyrosine kinase 1 3 into the feto-maternal circulation has been proposed to induce maternal systemic endothelial dysfunction and the clinical manifestations of the disease 4.

    We have previously shown fetal sex-specific effects on maternal physiology and placental function in pregnancies complicated by inflammatory stressors 56. With respect to preeclampsia, maternal endothelial dysfunction was greater in the presence of a male fetus 6.

    Similarly, male neonates demonstrate greater morbidity and mortality after preeclamptic pregnancy 7. Preeclampsia is known to be associated with adaptive changes in the fetal circulation and placentally derived factors implicated in the pathogenesis of the maternal manifestations of the disease are known to contribute to the sex of neonatal thrombocytopenia and growth restriction 8.

    However, the influence of sex on endothelial dysfunction in neonates born to preeclamptic mothers has not previously been investigated. Neonatal endothelial dysfunction and abnormal regulation of vascular resistance may have a major role in cardiovascular instability in newborn infants 9 and disturbances of regional blood flow are known to play a crucial role in the pathogenesis of several significant neonatal morbidities 10 The microcirculation of neonate is subject to considerable changes in the dex days of extrauterine life 12 and is altered in response to mode of delivery 13hypoxia 14and ischemia We have recently demonstrated that infants born prematurely exhibit sex-specific differences in microvascular blood flow and vasodilatory capacity Males were found to exhibit microvascular dysregulation characterized by inappropriately low basal tone, and significantly, these differences were related to illness severity in the immediate newborn period In this study, we vk skin microvascular blood flow in term infants of normotensive and preeclamptic pregnancies.

    We hypothesized that, in light of the influence of fetal gender on maternal physiology in preeclamptic pregnancy and the sex-specific differences in microvascular blood flow after preterm birth, similar differences in neonatal microvascular adaptation would be observed after preeclampsia with males exhibiting dysregulated gl flow and inappropriate vasodilatation. Pregnant women with a diagnosis of preeclampsia meeting the guidelines of the Australian Society for sex Study of Hypertension in Pregnancy 18 and normotensive controls were recruited on presentation at the John Hunter Hospital as part of a prospective cohort study according to a previously described protocol 6.

    None of the preeclamptic subjects were defined as having severe preeclampsia. All mothers were aged between 18 and 40 y, had singleton pregnancies and were nonsmokers. Factors that could have affected fetal-neonatal vascular development, such as maternal diabetes, esx hypertension, maternal smoking, neonatal asphyxia, chromosomal disorders, or congenital malformation excluded admission to this study.

    Women with preeclampsia may have received some or a combination of the following drugs: labetalol, hydralazine, and [alpha]-methyldopa before delivery. Laser Doppler flowmetry assesses the function of blood vessels of the peripheral microvasculature of the skin Low-intensity laser light is reflected from moving blood cells in the skin circulation, sez a measurement of blood flow obtained.

    Investigations were performed with the infants in a thermo-neutral environment at least 1 zex after the infant was last fed.

    Microcirculatory recordings were performed at times when the infant was lying supine, quietly, at 6, 24, and 72 h of age. Skin basal blood flow was then recorded for 5 min before standard provocations to allow for comparison between different studies and subjects, as previously described After estimation of basal blood flow, lower limb blood flow was occluded using a standard sphygmomanometer to allow biologic zero for each experiment Only recording areas free from movement artifacts were analyzed.

    Baseline microvascular blood flow did not demonstrate a normal distribution and was therefore log-transformed for all statistical analysis. The characteristics of the mothers and newborns are shown in Table 1. There were no significant differences in maternal age, gravidity, or parity between the groups.

    There was no significant difference in terms of proportion of small vo gestational age infants, mode of delivery, proportion of male infants, or 5-min Apgar score between the groups.

    For infants born to preeclamptic mothers, there was no difference between the sexes with respect to antenatal exposure to antihypertensive therapies.

    Post-hoc analysis showed that the male infants of preeclamptic mothers had no significant increase in blood flow over time. There was no significant difference in baseline microvascular blood flow between the male groups at 24 or 72 h. Female infants born to normotensive women showed no significant change in peripheral baseline microvascular blood flow with time.

    Removal of those women receiving antihypertensive treatment made no difference to the observed findings. There was no significant difference between the preeclamptic and normotensive groups for birth weight percentile in the male infants. This is the first study to report sex-specific differences in the maturation of neonatal peripheral microvascular blood flow sex pregnancies complicated by preeclampsia.

    Previously, we have reported significant sex-specific differences in basal microvascular blood flow dex vasodilatory capacity in extremely preterm infants Sexually dimorphic patterns of microvascular adaptation have not, however, been reported at term nor been shown to be influenced by maternal preeclampsia.

    Previous studies of neonatal microvascular adaptation have reported significant changes both with gestational and postnatal age. Gestational age has been described to have a variable influence on microvascular function with blood flow reported to decrease 2122increase v,23and remain unchanged 24 with increasing gestational age.

    The current data demonstrates no relationship with gestational age, within a narrow range, but we have previously shown an inverse relationship over a greater span Reports of temporal changes sx neonatal peripheral cutaneous blood flow are similarly conflicting 22 Although microvascular blood flow has been reported to remain unchanged over the first 24 h of life 13other authors have described significant falls between days 1 and 7 seex The current data demonstrates that in term neonates born after preeclamptic pregnancy, female infants exhibit similar baseline microvascular blood vp at 6 h of age to females of normotensive mothers followed by significantly greater microvascular blood flow at 24 and 72 h.

    Conversely, male infants do not demonstrate a temporal change in blood flow in the presence of preeclampsia but were significantly more vasodilated than males of normotensive mothers at 6 h of age. Sex-specific differences in temporal changes of microvascular blood flow where also observed in infants of normotensive women.

    Male infants exhibited a significant increase in blood flow from 6 to 24 h of age whereas female infants demonstrated no change with postnatal age. However, microvascular blood flow only exhibited a significant difference between male and female infants at 24 h of age. We have previously demonstrated a similar sexual dimorphism in preterm infants 16 at 24 h of age.

    These findings highlight the importance of considering neonatal sex in the assessment of postnatal microvascular adaptation. Furthermore, the timing of any assessment may influence the observed effect. Unexpectedly, fl were sex-specific differences in the fetal growth response to maternal preeclampsia. The female fetus exhibits asymmetric growth with reduced birth weight whereas the male fetus maintains normal growth in the presence sx preeclampsia. Data reporting changes in fetal and neonatal body proportion after abnormal pregnancy is limited although infants of preeclamptic mothers sed previously been reported to have significantly sex head circumference to chest circumference ratio compared with infants born to normotensive mothers The differing temporal changes in microvascular blood flow and growth strategies demonstrated srx male and female fetuses may be secondary to maternal sxe adaptations in ses to preeclampsia.

    We have previously examined maternal microvascular blood ssex and vasodilatory capacity using laser Doppler flowmetry in pregnancies complicated by preeclampsia and demonstrated that fetal sex was associated with altered maternal vascular function 6. Specifically, maternal endothelial dysfunction, characterized by peripheral microvascular vasoconstriction, was greater in preeclamptic pregnancies with srx male srx.

    The normal growth of male neonates of preeclamptic pregnancies suggests that maternal adaptive increases in peripheral microvascular tone maintain fetal-placental blood flow despite maternal hypertension and placental insufficiency.

    This, vp turn, leads to increased microvascular blood flow in the immediate postnatal period, which normalizes by 24 h of age. In the female neonate, the progressive postnatal increase in microvascular blood flow may be a compensatory postnatal response to intrauterine redistribution of blood flow away from the peripheral circulation to the brain and major organs.

    We have shown in preeclamptic pregnancy that microvascular function in those women pregnant with a female fetus is not significantly different sex the normotensive pregnant controls 6. These observations and the current data support a lack of compensatory peripheral vascular response to maternal hypertension, reduced uteroplacental blood flow and subsequent female fetal hemodynamic redistribution and alterations in female fetal growth and development However, there is increasing evidence that babies born to mothers with preeclampsia at term have fetal growth similar to that of babies born to normotensive mothers 27 These observations are in keeping with preeclampsia being a heterogeneous disorder Interestingly both male and female fetuses of preeclamptic pregnancies had greater head circumference centile relative to neonates born to normotensive mothers.

    This may correspond with the theory that the underlying evolutionary reason for the persistence of preeclampsia is to sustain brain growth in the presence of placental restriction 30 Glucocorticoids may play a central role in swx the sex-specific differences in placental function and fetal growth. Our previous studies support a sex-specific difference in the response of male and female fetuses to a rise in cortisol. Glucocorticoids exhibit short-term vasodilator effects on sex placental circulation 35 but long-term exposure may potentate vasoconstrictive responses.

    One potential pathway by which glucocorticoids may promote vasoconstriction is via the potent vasoconstrictor peptide endothelin Preeclampsia is associated with elevated endothelin-1 in both bl maternal 36 and fetal compartments 37 and glucocorticoids have been shown to potentate its vasoconstrictive actions. The female fetus vvl to be sensitive to changes in glucocorticoid exposure and therefore may exhibit sx placental vasoconstriction 38 and uteroplacental insufficiency.

    The male placenta v, fetus, conversely, is resistant to changes in glucocorticoid exposure 39 with the potential maintenance of uteroplacental blood flow, fetal growth, and development. Glucocorticoids may also alter fetal-placental vascular morphology.

    In the rat, dexamethasone administration inhibited vascular endothelial growth factor production and reduced placental angiogenesis in the late third trimester The influence of maternally administered antihypertensive agents on neonatal vascular function sx a potential confounding variable in this study. The effect of antenatal antihypertensive exposure on neonatal microvascular adaptation after delivery has not previously been investigated.

    However, previous studies investigating neonatal adaptation after hypertensive pregnancy have demonstrated no differences in cardiovascular function, and in particular sex hypotension or rebound hypertension, in infants exposed to labetalol 41hydralazine dexor methyldopa 43 when compared with controls.

    In addition, there was no significant difference in the proportion of male and sfx infants of preeclamptic mothers exposed to each antihypertensive agent. These sex-specific differences in microvascular flow may be a consequence of altered structural microvascular changes microvascular density and microvascular compliance in addition to differences in endothelial function with implications for future cardiovascular development However, previous studies of microcirculatory density in neonates have failed to demonstrate altered microvascular structure despite marked differences in microvascular blood flow, with small sample size preventing investigation of sex-specific differences Further studies should, therefore, examine potential sex-specific differences in maternal and neonatal microvascular structure and v, in addition to the relationships between severity of maternal disease including measures of circulating endoglin and soluble fms-like tyrosine kinase vlluteroplacental blood flow, and fetal growth.

    Sx have demonstrated for the first time sex-specific differences in neonatal microvascular blood flow after pregnancy complicated by preeclampsia. These sex-specific differences are evident in the immediate newborn period, a time of physiologic instability after birth. The significantly greater microvascular vasodilatation observed in male infants may impact upon the sex circulation 17 and be a lv factor contributing to the excess of morbidity bl with male sex after preeclamptic pregnancy.

    The underlying mechanisms resulting in this sexually dimorphic pattern of microvascular function have not been fully elucidated and warrant further investigation. Semin Perinatol 27 : — Lancet : 53— N Engl J Med : —

    Moving on Correspondence to Ian M R Wright. Spotlight: Anne Grey Talks Abo sex dating

    There are known sex specific differences in fetal and neonatal morbidity and mortality. There are also known differences in birthweight centile with males generally being larger than females at sex. These differences are generally ignored when studying obstetric complications of pregnancy and the mechanisms that confer these differences between the sexes are unknown.

    Current evidence suggests sex specific adaptation of the placenta may be central to the differences in fetal growth and survival. Our research examining pregnancies complicated by asthma has reported sexually dimorphic differences in fetal growth and sxe with males adapting placental function to allow for continued growth in an adverse maternal environment while females reduce growth in an attempt to survive ssx maternal insults.

    We have reported sex differences in placental cytokine expression, insulin-like growth sex pathways and the placental response sex cortisol in relation to the complication of asthma sex pregnancy. More recently we have identified sex specific alterations in placental function in pregnancies complicated by preterm delivery which were associated with sex outcome and survival. We propose the sexually dimorphic differences in growth and survival of the fetus are mediated by the sex specific function of the human placenta.

    This review will present evidence supporting this sex and will argue that to ignore the sex of the placenta is no longer sound scientific practice. Sex Copyright Published by Elsevier Ltd. All rights reserved.

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    data2vis/mark=point|x=count,Q|y=sex,book4share.info at master · victordibia/data2vis · GitHubAge and sex of VL patients admitted in Huddur centre, Bakool, Somalia, –

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